Navy Medical Department

Pocket Guide to

MALARIA PREVENTION

AND CONTROL

NAVY ENVIRONMENTAL HEALTH CENTER

BUREAU OF MEDICINE AND SURGERY

NAVY ENVIRONMENTAL HEALTH CENTER

Technical Manual NEHC-TM PM 6250.1 (September 2000)
Navy Medical Department Pocket Guide

to Malaria Prevention and Control

September 2000

Adapted from NEHC TM92-1 by

CDR James E. LaMar II, MC, USN; the Preventive Medicine 

Directorate, NEHC; and the Navy Preventive Medicine Community.

Please send all correspondence concerning the 

content and style of this guide to the Production Editor, 

CDR M. O. Mann, MSC, USN at the address below.

Navy Environmental Health Center

2510 Walmer Avenue

Norfolk, Virginia 23513-2617

E-Mail: mannm@nehc.med.navy.mil
Navy Medical Department

Pocket Guide to

MALARIA PREVENTION AND CONTROL

TABLE OF CONTENTS

INTRODUCTION.......................................................................1

CHAPTER

1. Malaria: Disease, Life Cycle, Distribution...........................5

2. Prevention...................................................................... 11

Personal Protective Measures ................................... 12

Chemoprophylaxis ................................................... 15

Unit Protective Measures .......................................... 20

3. Diagnosis ...................................................................... 27

4. Treatment ...................................................................... 36

5. Glucose-6-Phosphate Dehydrogenase Deficiency.............. 51

6. Military Malaria Control Responsibilities............................ 57

APPENDIX

1. Information & Intelligence Sources; Consultants................ 67

2. Mosquito Vectors and Identification.................................. 77

3. Laboratory Diagnostic Techniques ................................... 82

4. Antimalarial Medications ................................................. 90

5. Supplies and Training Aids ............................................ 103

6. Glossary ..................................................................... 106

BIBLIOGRAPHY................................................................... 114

INDEX ................................................................................. 121

i
1

INTRODUCTION

The threat to health and readiness of sailors and Marines posed 

by malaria stimulated the creation of the Malaria “Blue Book” in 1984. 

Prevention and treatment of malaria is more complex due to the 

emergence of drug resistance, pesticide resistant mosquito vectors, 

and large populations of infected people in many areas of the world. 

The World Health Organization estimates that two billion people are at 

risk for malaria infection. Each year, malaria causes more than 300 

million clinical cases and over two million deaths. In 1995, children 

under the age of five accounted for 800,000 of those deaths. The 

direct and indirect costs associated with malaria infections are 

enormous; costs were over 1.8 billion dollars in 1995 in Africa alone. 

Malaria strikes during war, during deteriorating social and 

economic conditions, and after natural disasters; all situations where 

the military is called to serve. Deployed forces cannot afford loss of 

personnel or depletion of resources for cure and convalescence. 

Protecting and improving the health of airmen, soldiers, sailors, and 

Marines while serving in such operations requires thorough 

understanding of the prevention and treatment of malaria. This 

“Malaria Pocket Guide” includes information to help service personnel:

⇒ Understand the transmission and life cycle of malaria parasites.

⇒ Prevent malaria.

⇒ Diagnose and treat malaria. 

⇒ Persuade commanders to enforce malaria preventive measures.

Command Responsibility

Malaria control depends on directed discipline by those in 

command. In their role as advisors, medical personnel must identify 

threats, and present countermeasures and their benefits so those in 

command can make effective decisions. In World War II, Lieutenant 
2

General Sir William Slim stopped the longest, most humiliating retreat 

in the history of the British Army. When he assumed command in 

Burma in April 1942, the health of his troops was dismal. For each 

wounded man evacuated, 120 were evacuated with an illness. The 

malaria rate was 84 percent per year of total troop strength, even 

higher among the forward troops. In his memoirs, he describes his 

course of action:

“... A simple calculation showed me that at this rate 

my army would have melted away. Indeed it was doing so 

before my eyes.

Good doctors are of no use without good discipline. 

More than half the battle against disease is not fought by 

doctors, but by regimental officers. It is they who see that 

the daily dose of mepacrine (anti-malarial 

chemoprophylactic drug used in W.W.II) is taken...if 

mepacrine was not taken, I sacked the commander. I only 

had to sack three; by then the rest had got my meaning. 

Slowly, but with increasing rapidity, as all of us, 

commanders, doctors, regimental officers, staff officers, 

and NCOs united in the drive against sickness, results 

began to appear. On the chart that hung on my wall the 

curves of admissions to hospitals and malaria in forward 

units sank lower and lower, until in 1945 the sickness rate 

for the whole 14th Army was one per thousand per day.”

The threat to force readiness that challenged General Slim and 

his army similarly confronts our forces today. In 1993, a large 

percentage of Marines and soldiers in certain units participating in 

Operation Restore Hope in Somalia developed malaria. The 

explanation for the outbreak is complex, involving a number of factors. 

 The complex life cycle of malaria, lack of command support leading to 

poor execution of personal protective measures, and incomplete 

medical intelligence of the malaria threat all contributed. 

Available medical intelligence concluded that Plasmodium

falciparum was the predominant malaria threat in Somalia. Task 

Force medical planners were influenced by the Army’s policy of not 

performing G-6-PD screening on its personnel. The risk of 

precipitating a hemolytic reaction from terminal primaquine prophylaxis

had to be weighed against the chance that P. vivax and P. ovale were 
3

present. Based on those factors, Task Force medical planners did not 

recommend terminal primaquine prophylaxis.

Unfortunately, P. vivax was endemic in Somalia, and 75 soldiers 

developed malaria infections after they returned to the United States. 

After the first 30 soldiers were diagnosed with P. vivax malaria, 

terminal primaquine prophylaxis was instituted. Despite this 

precaution, another 45 soldiers developed malaria infections and had 

to be hospitalized and administered higher dosages of primaquine. 

Clearly P. vivax malaria is present in Somalia, and drug resistant

strains are developing. It should be just as obvious that poor 

execution of personal protective measures allowed these soldiers to be 

bitten by infective mosquitoes. Returning Marines also developed P. 

vivax infections. The reasons were difficult to quantify, but poor 

compliance with terminal primaquine prophylaxis and resistant strains 

of P. vivax were responsible.

The story does not end with the P. vivax malaria outbreak in 

returning soldiers and Marines. During Operation Restore Hope, 

medical surveillance revealed that half of all malaria and dengue cases 

were occurring in a single Marine battalion located in the Baardera

area. Investigation of these outbreaks found that the Marine 

commander did not enforce recommended countermeasures. 

Fortunately, consequences were minimal. The ill Marines recovered, 

and the unit was not involved in any significant engagements in its 

weakened condition.

The examples presented show that malaria is a formidable and 

deceptive foe to military units deployed into endemic areas. Resistant 

plasmodia strains exist in most areas of the world, and some species 

lie dormant and attack long after the threat is perceived to be absent. 

Drugs once commonly used to prevent and treat malaria are no longer 

effective. Persuading commanders to enforce personal protective 

measures is difficult. No vaccine is yet available, though a promising 

falciparum malaria vaccine is being tested.

However, all the necessary tools are present for successful 

prevention of malaria. Medical personnel must successfully 

communicate the threat. After convincing their commanders, medical 

 personnel must teach, supervise, and practice personal protective 

measures. At the same time, they must be able to diagnose and treat 

personnel stricken with malaria. It cannot be emphasized enough, 

as General Slim demonstrated, that success against malaria 

requires a unified effort enforced by commanders.
4
5

CHAPTER ONE

MALARIA: Disease, Life Cycle, Distribution

Definition

Malaria is both an acute and chronic disease caused by protozoa 

of the genus Plasmodium. Four species cause human malaria: P. 

falciparum, P. vivax, P. malariae, and P. ovale. The protozoa are 

transmitted to humans by female mosquitoes of the genus Anopheles. 

 (Transmission can also occur by direct inoculation of infected red 

blood cells via transfusion, needles, or congenitally). Some signs and 

symptoms of the illness are high fever, chills, headache, anemia, and 

splenomegaly. Most serious and fatal complications are caused by P. 

falciparum.

Life Cycle

The life cycle of malaria is complex (see Fig. 1-1) with 

developmental stages and corresponding symptoms differing according 

to the Plasmodium species involved (see Table 1-1). Sporozoites, the 

infective stage of plasmodia, are injected from the salivary glands of 

infected mosquitoes during feeding. Following inoculation, the 

sporozoites disappear from the blood within 30 minutes. Many are 

destroyed by white blood cells, but some enter liver cells.

Exoerythrocytic Phase. Sporozoites that enter liver cells 

multiply asexually in a process called exoerythrocytic schizogony. 

Thousands of uninucleate merozoites form, displacing the nucleus of 

the liver cell, but causing no inflammatory reaction in the liver. 

Eventually, invaded liver cells rupture, releasing thousands of 

merozoites into the bloodstream. This occurs 6 to 16 days after initial 

infection depending on the infecting Plasmodium species.

Dormant or Hypnozoite Phase. All infections due to P. 

falciparum and P. malariae have a single exoerythrocytic form. All

infected liver cells parasitized with P. falciparum and P. malariae

rupture and release merozoites at about the same time. 
6

In contrast, P. vivax and P. ovale have two exoerythrocytic forms. 

 The primary type develops, causes liver cell rupture, and releases 

merozoites just as described for P. falciparum and P. malariae. The 

other form, which develops concurrently, is known as the hypnozoite. 

Sporozoites that enter liver cells differentiate into hypnozoites that 

remain dormant for weeks, months, or years. At some future time, the 

hypnozoites activate and undergo exoerythrocytic schizogony, forming 

a wave of merozoites that invade the blood and cause a delayed case 

or a clinical relapse.

Erythrocytic Phase. Released merozoites invade red blood 

cells (erythrocytes), where they develop into trophozoites. After a 

period of growth, the trophozoites divide and develop, eventually 

forming 8-24 merozoites in each red blood cell. When this process is 

complete, the host red blood cells rupture, releasing mature 

merozoites. The symptoms associated with malaria occur at this 

point. 

The merozoites then invade fresh erythrocytes and another 

generation of parasites develops in the same manner. This process 

occurs repeatedly during the course of infection and is called 

eryrthrocytic schizogony. The length of this development cycle differs 

according to the species of parasite, varying from 48 hours in vivax, 

ovale, and falciparum malaria, to 72 hours in P. malariae infections. In 

the early stages of infection there is no characteristic periodicity as 

groups of parasites develop at different times. The febrile episodes

caused are inconsistent. Later, the erythrocytic schizogony 

development cycle becomes synchronized, and the febrile paroxysms

become more consistent. Some merozoites differentiate into sexual 

forms (female macrogametocytes, male microgametocytes) and 

develop in invaded red blood cells.

Vector Phase. Anopheles mosquitoes feeding on infected hosts 

ingest sexual forms developing in red blood cells. The
7

female macrogametocytes and male microgametocytes mature in the 

mosquito’s stomach and combine forming a zygote that undergoes 

mitosis. The products of mitosis are ookinetes, which force 

themselves between the epithelial cells to the outer surface of the 

stomach, and form into small spheres called oocysts. The oocysts 

enlarge as the nucleus divides, eventually rupturing and releasing 

thousands of motile sporozoites into the body cavity. The sporozoites 

migrate to the salivary glands, making the female mosquito infective. 

The vector phase of the life cycle, called sporogony, is complete in 8 

to 35 days depending on species and environmental conditions.

Environmental Factors. Anopheles mosquitoes are essential for 

development, multiplication, and spread of plasmodia. Therefore, any 

area harboring Anopheles mosquitoes may be at risk for 

Table 1-1. Selected Characteristics of the Four Species of

Human Malaria

P. falciparum P. vivax P. ovale P. 

malariae

Incubation days 

(range)

12 (9-14) 13 (12-17) 

or up to 6-12 

months

17 (16-18) 

or longer

28 (18-40) 

or longer

Exoerythrocytic

cycle (days) 5.5-7 6-8 9 12-16

No. of 

merozoites

per liver cell

40,000 10,000 15,000 2,000

Erythrocytic

cycle (hours) 48 42-48 49-50 72

Red blood cell 

preference

younger cells, but 

can invade cells of 

all ages

Reticulocytes Reticulocytes Older cells

Relapses No Yes Yes No

Fever 

periodicity 

(hours)

none 48 48 72

Febrile 

paroxysm

length (hours)

16-36 or 

longer

8-12 8-12 8-10

Severity of 

primary attack

severe in 

non-immune

mild to 

severe

mild mild
8

Drug 

Resistance

+++--
9

Figure 1-1. Malaria Life Cycle

 6. Mosquito vector ingests

gametocytes after biting

infected local inhabitants.

 4. Repeating Erythrocytic (red blood

cell) cycle. Merozoites develop

and release causing hemolysis.

 5. Some merozoites develop

into gametocytes.

 2. Transmission by

female Anopheles.

1. Oocyst / sporozoite

formationin mosquito gut.

 3. Exoerythrocytic (liver) cycle.

Sporozoites infect liver cells

and develop.

malaria transmission. Specific environmental conditions optimal for 

anopheline mosquito vector and parasite development include 

temperature between 200 and 300C and a mean relative humidity of 

60%. The sporogony phase requires temperatures between 160 and 

330C. High relative humidity increases mosquito life-span, thereby 

increasing the probability of mosquitoes becoming infective. Areas 

with high rainfall have increased malaria incidence because of an 

increase in breeding sites. The accompanying high humidity 

increases survival rates of female anopheline mosquitoes. Elevation, 

along with cooler temperatures and lower humidity, is also a factor as 

transmission rarely occurs above 2000-2500 meters.
10

Figure 1-2. Worldwide Distribution of Malaria

Chloroquine-resistant P. falciparum

Chloroquine-sensitive malaria

Distribution. The worldwide distribution of malaria is illustrated by the 

map in Fig 1-2. This is a general representation and not intended for 

threat assessment or countermeasure planning. Country-specific 

information can be obtained from the Medical Environmental Disease 

Intelligence and Countermeasures (“MEDIC”) compact disc, and the 
11

Navy Environmental and Preventive Medicine Unit responsible for a 

particular world area. (Further intelligence can be obtained from the 

agencies listed in Appendix One).

Malaria transmission occurs in more than 100 countries. 

Regions include Africa, Asia, islands of the South, west, and central 

Pacific Ocean, Latin America, certain Caribbean islands, and Turkey. 

These areas, all between 450 N and 400 S latitude (see Fig. 1-2), 

possess tropical or subtropical zones wherein anopheline mosquito 

habitats exist.
12

CHAPTER TWO

PREVENTION

Systematic applications of four tactics are essential to planning 

and carrying out disease and injury prevention in field and combat 

operations. Listed in order, they are applicable for prevention of 

malaria (or any other threat): 

1) Determine disease and injury threats in the area of operation 

before deployment.

2) Identify or develop countermeasures to reduce threats to an 

acceptable level.

3) Educate personnel regarding threats and train in correct use of 

countermeasures.

4) Command enforcement of countermeasures.

The next three sections of this chapter review effective malaria 

countermeasures available. Preventive countermeasures are divided 

into three sections: Personal Protective Measures, 

Chemoprophylaxis, and Unit Protective Measures. Medical 

personnel must seek information to answer the questions outlined 

below and determine which countermeasures to employ, and make 

recommendations for the same to commanders:

1) What type(s) of malaria is(are) present?

2) Which countermeasures will be effective in the area and 

situations the unit will encounter? 

3) How will the unit obtain the necessary supplies, personnel, and 

equipment needed?

4) Do unit personnel know how to apply the countermeasures

chosen? Will they apply them? What training is needed?

5) Does the entire chain of command understand its role and 

accountability in enforcing the countermeasures?
13

Section I. Personal Protective Measures

This section presents measures that prevent mosquitoes from 

biting and transmitting malaria. Applications of personal protective 

measures are effective against a wide range of disease vectors, 

not solely for prevention of malaria. In many military operations, 

they will be the only means of protection against biting arthropods. 

They are the first line of defense, are simple to teach and perform, and 

enable personnel to remain in endemic areas while maintaining their 

operational capabilities. The major drawback of personal protective 

measures is dependence on service member compliance. Persuasion 

by medical personnel, and enforcement by NCOs and commanders is 

necessary for their continuous proper application. Medical personnel 

must circulate among units teaching, examining, and improving 

personal protective measure practice, and also reporting their findings 

to those in charge. Commanders and NCOs must ensure compliance 

and lead via personal example.

DEET

Topical repellents are natural or synthetic compounds that repel 

arthropods. The use of vapor-active skin repellents by U.S. Armed 

Forces has a long history. It began with the use of oil of citronella in 

1910, continued with the discovery of dimethyl phthalate during WW II, 

and led to the development of diethyl toluamide or “DEET” in 1957. 

The duration of a repellent’s effectiveness decreases with activity, 

heat, and humidity. Since Anopheles mosquitoes inhabit warm 

tropical environments, military personnel need to re-apply repellent 

frequently to prevent biting. These products were selected based on 

their effectiveness. Contrary to public opinion, Avon Skin So SoftR and 

flea collars are not effective. As with all repellents and 

insecticides, carefully read and comply with the label 

requirements.

Available Military Supplies: Insect/Arthropod Repellent Lotion 

(NSN 6840-01-284-3982) is a 33 % DEET lotion developed to last 12 

hours, has low odor, and less damaging to plastics than previous 

formulations. Apply in the same manner as skin lotion; neglected skin 

is not protected.

Insect Repellent, Clothing and Personal Application (NSN 6840-

00-753-4963) is a 75% DEET, 25% alcohol liquid that must be applied 

every 1-2 hours in warm, humid conditions. It may cause skin 

irritation, is corrosive to plastics and paint, and is very flammable. 
14

Apply in the same manner as skin lotion; neglected skin is not 

protected. The liquid can also be used as a fabric impregnant, with 

effectiveness of up to 2 days if not removed by laundering, rain, or 

perspiration.

Permethrin Uniform Impregnants

Impregnants are compounds very similar to topical repellents. 

They are longer lasting, and cannot be applied to skin. Permethrin is 

an impregnant for fabric only, used by the military to treat tents and 

clothing. It is also a contact insecticide capable of reducing the biting 

population and attack rate in the immediate area of use. Permethrin is 

a synthetic compound modeled from a naturally occurring insecticide 

found in certain plants. It is quick acting, long lasting (12 years in 

unwashed, stored clothing), nearly odorless, and non-staining. 

Permethrin is resistant to degradation when exposed to heat, sunlight, 

wear, laundering, rinsing, and immersion in water. It is effective 

against crawling arthropods such as ticks, and flying insects such as 

mosquitoes and biting flies.

Available Military Supplies: Permanone Aerosol Spray ”Insect 

Repellent, Clothing Application” (NSN 6840-01-278-1336) is a 

formulation of 0.5% permethrin in 6 oz. aerosol cans for use on 

uniforms and mosquito netting. It is odorless, non-irritating, and can 

last through 3-5 washings. Apply the same way as spray paint (slow 

sweeping motion 6-8 inches from object) until the surface of the fabric 

appears moistened. Allow to dry for 2 hours before wearing. Do not 

apply to caps, socks or undergarments or while clothing is being worn.

IDAA Kit, “Insect Repellent, Clothing Application” (NSN 6840-01-

345-0237) is a field kit in which shirt and trousers are treated in 

separate plastic bags containing a 1% permethrin and water mixture. 

Treatment lasts through about 30 washings.
15

Protective Clothing and Netting

The basic utility or camouflage uniform treated with permethrin 

and worn with sleeves down, collars closed and trousers bloused over 

boots offers excellent protection from mosquitoes. Other types of 

protective clothing and netting are also available.

Available : DEET net jacket, known as Parka, Fabric Mesh, Insect 

Repellent, (NSN 8415-01-035-0848) is a waist length mesh jacket with 

extra long sleeves and a hood designed to cover a combat helmet. 

The fabric is polyester netting interwoven with cotton strands designed 

to absorb DEET. It is issued with a ziplock plastic bag and a bottle of 

the 75% DEET liquid (NSN 6840-00-753-4963). Before wearing, 

saturate the coat with the supplied DEET and store in the plastic bag 

for 24 hours. Protection should last 6 weeks if the jacket is stored in 

the ziplock pouch when not being worn. Impregnation with permethrin 

is also an option, which provides longer, more effective protection.

Insect Head Net (NSN 8415-00-935-3130) is a fine mesh nylon 

screen and cover that can be worn over a helmet, cap, or bare head. It 

is designed to be fastened to the uniform shirt collar and breast pocket 

buttons. For maximum protection, impregnate with permethrin or 

DEET liquid.

Mosquito Bed Nets, (NSN 7210-00-266-9736), and poles (NSN 

7210-00-267-5641) are a protective measure with a long history of use 

in tropical areas. They are designed for use with cots, bedrolls, 

hammocks, steel beds, and shelter half tents. Personnel should 

receive bed nets and be trained in their use before entry into an 

endemic area. If set up properly, they will not interfere with quick night 

exits. Bed nets should be treated with permethrin, set up before dusk 

and checked for tears or other spots where mosquitoes can enter. A 

training team to coach, inspect, and advise on the application of 

personal protective measures including bed net use should be 

established for each unit. 
16

Section II. Chemoprophylaxis

This section presents three frequently used chemoprophylactic

regimens. Choice of regimen is determined by two factors:

⇒ Drug resistance in specific locations.

⇒ Any allergic or other reaction to the anti-malarial drug of choice, 

or restriction by job (mefloquine is not authorized for prophylaxis 

in aviators and divers).

Excellent primary sources of information on malaria drug 

resistance are the Medical Environmental Disease Intelligence and 

Counter-Measures (“MEDIC”) compact disc, and the Navy 

Environmental and Preventive Medicine Unit responsible for that area of 

the world. (Agencies dedicated to supplying such information, along 

with all needed contact information and protocol are listed in Appendix 

1).

Unit personnel must be screened before malaria 

chemoprophylaxis is initiated. Personnel who had prior reactions or 

risk factors, and those in certain occupations need to be identified and 

provided with an appropriate regimen.

Chemoprophylaxis: Before, During, After. One of the least 

appreciated aspects of chemoprophylaxis is the requirement for taking 

the drug before, during, and after exposure to malaria. 

Chemoprophylaxis should begin 2 weeks before travel to endemic 

areas to allow adequate blood levels to develop. This is true for all 

malaria prophylaxis drugs except for doxycycline, which should be 

initiated 1-2 days before exposure. The two-week lead-time is also 

useful to monitor personnel for any drug reactions. Prophylaxis must 

be continued for four weeks after leaving an endemic area to ensure 

that suppressive cure results. The required four week time period is to 

ensure drug therapy exceeds the length of time needed for the 

incubation period in the liver. If a mosquito bites on the last day of 

deployment, protection is needed 2-3 weeks later, when parasites 

emerge into the blood stream.

Directly Obse rved Therapy (DOT). Directly observed therapy is 

recommended for all regimens. Chain of command support is required 

to carry out this method. A fellow service member supervised by a 

chain of command authority observes weekly or daily drug dosage.
17

 

Chemoprophylactic Regimens. The three regimens are described 

below; doses are listed in Table 2-1: 

Regimen A. For areas where chloroquine resistant P. falciparum has 

NOT been reported, once weekly use of chloroquine alone is 

recommended. Chloroquine is usually well tolerated, and the few 

personnel who have side effects may tolerate the drug better by taking 

it with meals, or in divided twice-weekly doses.. Chloroquine 500 mg 

salt (300 mg base)/wk should begin 2 weeks before entering endemic 

areas of operation, taken once a week while deployed, and once a 

week for four weeks after leaving. The related drug, 

hydroxychloroquine, is useful as an alternative and may be better 

tolerated. It is available by open purchase under the trade name 

PlaquenilR .

Regimen B. For areas where chloroquine resistant P. falciparum 

exists, mefloquine is recommended. Mefloquine is usually well 

tolerated at prophylactic dosage, but should not be taken by personnel 

with a history of seizures, severe psychiatric disorders, or those with 

cardiac conduction abnormalities. Aviators are prohibited from using 

it. Mefloquine 250 mg/wk should begin 2 weeks before entering 

endemic areas of operation, taken once a week while deployed, and 

once a week for four weeks after leaving.

If a two-week lead time prior to exposure is not possible, a 

loading dose of 250 mg/day on days 1, 2, 3, and 7 may be given. This 

is followed by the routine weekly regimen. This short interval loading 

dose period has been used with very few side effects. If this regimen 

is chosen, medical personnel should monitor unit members for side 

effects.

Regimen C. Doxycycline is also recommended for areas where 

chloroquine- resistant P. falciparum exists. If given under supervision, 

it is very effective. Doxycycline
18

Table 2-1. Drugs Used for Malaria Prophylaxis*

Drug Adult Dosage Pediatric Dosage

Mefloquine 

(LariamR)

250 mg salt

(228 mg base),

once/week

15-19 kg: 1/4 tab/wk

20-30 kg: 1/2 tab/wk

31-45 kg: 3/4 tab/wk

> 45 kg: 1 tab/wk

Doxycycline

100 mg 

once/day

> 8 yr. of age:

 2 mg/kg once daily,

 up to adult dose of

 100 mg/day

Chloroquine 

phosphate

(AralenR)

500 mg salt 

(300 mg base),

once/week

5 mg/kg base 

(8.3 mg/kg salt), once/wk 

up to 

maximum adult dose 

of 300 mg base

Primaquine

15 mg base

(26.3 mg salt),

once/day for 14 

days 

0.3 mg/kg base

(0.5 mg /kg salt),

once/day for 14 days 

(maximum 15 mg base)

Hydroxychloroquine

sulfate

(PlaquenilR)

400 mg salt

(310 mg base),

once/week

5 mg/kg base

(6.5 mg/kg salt),

once/week up to 

maximum adult dose of

310 mg base

Proguanil

(PaludrineR)

200 mg, once/day, 

in combination with 

weekly chloroquine

< 2 yr.: 50 mg/day

2-6 yr.: 100 mg/day

7-10 yr.: 150 mg/day

>10 yr.: 200 mg/day

*all are oral doses
19

100 mg/day is taken at approximately the same time of day, beginning 

1-2 days before entering endemic areas of operation, taken daily while 

there, and daily for four weeks after leaving. It is the drug of choice for 

chemoprophylaxis in most parts of Southeast Asia.

One of the most common side effects of doxycycline is adverse 

gastrointestinal symptoms, usually nausea or vomiting. This often 

leads to compliance problems. These side effects may be avoided by 

taking doxycycline with a meal. Other side effects include 

photosensitivity manifested by a severe sunburn reaction, and an 

increased frequency of monilial vaginitis. The sunburn reaction can be 

prevented by avoiding prolonged exposure to sunshine, or sunscreen 

use. Females taking doxycycline should be supplied with nystatin 

suppositories to treat possible yeast infections when they occur.

Terminal Primaquine Prophylaxis: Currently, primaquine is the 

only available drug for prevention of P. vivax and P. ovale relapse. As 

most endemic areas of the world have at least one of these species,

terminal primaquine prophylaxis is recommended to eradicate 

hypnozoites. It can be initiated immediately or soon after personnel 

depart the area of exposure, or during the last two weeks using 

Regimens A, B, or C. This ensures an overlap of medication to 

eradicate parasites of any stage that may be present. No other 

medication eliminates Plasmodia merozoites in the liver. Without 

primaquine therapy, personnel can harbor dormant parasites in the 

liver long after leaving the risk area. Terminal primaquine prophylaxis

is given to ensure a complete cure.

Dosage is 15 mg base (26.3 mg salt)/day for 14 days; DOT

recommended. Dosage may need to be increased to 30 mg if resistant 

P. vivax and P. ovale strains are present in the area. Personnel 

should be screened for G-6-PD deficiency before given primaquine. 

See Chapter 6 for details and recommendations. In certain instances, 

terminal primaquine prophylaxis may not be indicated. Consult with 

the cognizant Navy Environmental and Preventive Medicine Unit or 

other authorities for recommendations on need for terminal primaquine 

prophylaxis or increased dosages.

Prophylaxis During Pregnancy: Women who are pregnant should 

avoid travel to malarious areas. When travel must occur, chloroquine

is safe to use in pregnancy. No harmful fetal effects have been 

reported when given in the recommended doses for malaria 
20

prophylaxis. Proguanil has been used for several decades without 

adverse effects on the pregnancy or fetus.

Mefloquine is not recommended for use during pregnancy by the 

FDA. However, a review of clinical trials and reports of inadvertent use 

during pregnancy shows no association with adverse fetal or 

pregnancy outcomes. Mefloquine may be considered for use by 

females who are pregnant when exposure to chloroquine-resistant P. 

falciparum is unavoidable. 

Doxycycline is contraindicated for malaria prophylaxis during 

pregnancy. Fetal effects include discoloration and dysplasia of teeth 

and inhibition of bone growth. Tetracyclines are only indicated to treat 

life-threatening infections due to multi-drug resistant P. falciparum. 

Primaquine should not be used during pregnancy, as it can be 

passed transplacentally to a G-6-PD deficient fetus, causing in utero 

hemolytic anemia. Chloroquine can be given once weekly until 

delivery, at which time primaquine can be given.

Pediatric Prophylaxis: Children should avoid travel to areas with 

chloroquine-resistant P. falciparum, unless a highly effective drug such 

as doxycycline or mefloquine can be administered. Indications and 

dosage schedules are the same as for adults; dose is based on age or 

weight (see Table 2-1). 

Doxycycline is contraindicated in children under 8 years of age. 

Mefloquine is not recommended in children who weigh less than 15 kg, 

though recent data suggest it is safe for use in that group. 

Chloroquine and proguanil are safe for pediatric use.

Chloroquine is manufactured in the U.S. in tablet form only, and 

has a very bitter taste. Pharmacists can pulverize tablets into powder 

for mixing in food or drink, or prepare gelatin capsules. Oral 

suspensions of chloroquine are available overseas; parents should 

calculate dose because preparations vary. Overdose of anti-malarial 

drugs can be fatal. They must be stored in childproof containers out of 

reach of children.

Section III. Unit Protective Measures

Unit malaria protective measures consist of the following:

⇒ Discipline and training.
21

⇒ Treatment of equipment with permethrin.

⇒ Camp selection.

⇒ Vector control measures.

Discipline and Training

Avoiding malaria, other diseases, and non battle injuries is a 

team effort that must be supported by command authority. Medical 

personnel must be prepared to decisively advise those in command of 

such threats and their countermeasures, train personnel in the use of 

protective measure use, and monitor their application and 

effectiveness. Disciplined and correct use of the personal protective 

measures thus far presented is very effective in preventing malaria and 

other diseases. 

Equipment Treatment

Units should institute a program to treat uniforms, netting, and 

tents with Insect Repellent, Clothing Application (NSN 6840-01-334-

2666). This is a 40% concentrate in 5.1 oz. bottles that is mixed with 

water and applied using a 2-gallon sprayer to uniforms, netting, or 

tents. Other gear (camouflage netting, ground covers, sleeping bags, 

hammocks, and window drapes) should also be treated. 

Treat tents while erected, and uniforms and miscellaneous items 

while spread on the ground. Treated uniforms are ready to wear when 

dry; do not treat underwear or caps. Mark date of treatment on items. 

 Permethrin is very long lasting (12 years in unwashed, stored 

clothing), and such treatment could be done during routine field 

exercises. This approach would effectively prepare unit equipment 

months or years before use in an actual contingency.

Effectiveness in uniforms lasts through 30 washings. Tents and 

netting should be retreated every 6-9 months if regularly used. The 

impregnation of miscellaneous items (camouflage netting, ground 

covers, sleeping bags, hammocks, window drapes, and barrier nets) 

for protection is very effective.

Camp Selection
22

If the tactical situation permits, base camps should be located in 

areas where there is low risk of exposure to infected mosquitoes. The 

following factors affect the risk of exposure:

⇒ Presence of mosquito breeding sites.

⇒ Direction of prevailing winds.

⇒ Proximity of settlements with malaria infected inhabitants.

⇒ Length of time unit will be present in area.

Breeding areas vary depending on the specific species of 

Anopheles mosquito responsible for malaria transmission. Sunlit 

streams, shaded lagoons, rice fields, and marshes are all breeding 

habitats for different species of Anopheles mosquitoes. Campsite 

selection close to possible breeding sites of the mosquito known to 

transmit malaria in that region should be avoided. When camping near 

an area where a high density of Anopheles mosquitoes is unavoidable, 

camp where the prevailing winds will blow the mosquitoes away from 

camp.

A host population of infected humans is necessary to infect 

mosquitoes. If possible, locate base camps distant enough from 

settlements with infected inhabitants so as to be beyond normal flight 

range (2-3 kilometers) of the Anopheles mosquito vector .

Duration of deployment in the area is also important for planning 

permanent mosquito control measures. If military presence may be 

prolonged, establishment of a long-term base should be done with the 

preceding factors in mind or where elimination of mosquito breeding 

areas through engineering and control projects is feasible. 

Entomologists should be consulted to find the site most amenable for 

development by determining mosquito activity and identifying breeding 

areas. Improvement projects that impound water should be screened 

by entomologists and preventive medicine personnel to prevent 

creation of mosquito breeding areas.

Another unit protective measure to consider when operating in 

endemic areas is reducing troop exposure during peak biting times 

(dusk till dawn for most anophelines). Examples include:

1) Restrict showers and baths to hours when the mosquitoes are 

not biting.

2) Reschedule work parties and unit formations.

3) Allocate available screening material to buildings that protect the

largest number of personnel during peak mosquito biting times.

Malaria Vector Control Measures
23

Vector control includes two stages: surveillance and control. 

First, mosquito surveillance and analysis of collected data are 

performed. The analysis leads to choice of control measures most 

applicable to area and situation. Mosquito control is the employment 

of chosen vector control measures. 

Preventive medicine teams deployed in contingency situations 

are prepared to survey campsites for mosquitoes and other vectors, 

determine their breeding areas, and establish programs to control 

them. They are experienced at implementing sanitation and other 

public health measures and prepared to supervise and provide 

technical guidance to unit personnel (medical and non-medical) on unit 

protective measure management, if needed. These teams include 

medical entomologists. 

Medical entomologists supervise the two-stage process, first 

determining mosquito species, their abundance, and breeding sites. A 

control plan is then recommended, including specific control methods 

and their evaluation. Descriptions of common vector surveillance and 

control techniques used by medical entomologists follow.

Mosquito Surveillance Techniques 

Larval Mosquito Surveys. The goals of sampling for mosquito 

larvae are to identify their habitats, and later to evaluate control 

measures. All possible breeding areas are checked by sampling a 

uniform volume of water, and counting and identifying larvae present. 

From these data, the larval index, or average number of larvae 

collected per sample is calculated and recorded. This information is 

used to justify the use of permanent control measures such as filling 

or draining.

Anopheles larvae are found in areas of heavy surface vegetation 

where debris accumulates, usually in water less than one meter deep. 

 In larger ponds or lakes, they are found close to the shore.

Adult Mosquito Surveys. These are most frequently done 

because adult mosquitoes are often easier to collect and identify. 

These surveys determine the species present and their relative 

abundance, and the potential of a disease outbreak. For example, if 

no species of Anopheles mosquitoes are collected, the risk of malaria 

transmission will probably be low.

Biting Collections and Landing Counts. This is the most simple 

and direct method used to determine which vector species in a region 

is feeding on humans. Relative abundance, host preference, place and 

time of biting, and species are estimated. Mosquitoes are vacuumed 
24

into a container when they land. Counts continue for a designated 

period of time (usually 15-30 minutes). A standard area of skin is 

exposed, and the data are converted to “bites per man per hour” of 

each species collected for standard comparison. 

Success of mosquito control measures can be evaluated by 

comparing biting counts before and after application of mosquito 

control measures. The same “bait" collector, and location should be 

used for each collection to assure comparability of results.

A landing count survey is done to rapidly assess mosquito biting 

activity and abundance when populations are high. An index (landing 

rate) is obtained by recording the number of mosquitoes that land on 

clothing within a certain time interval (usually one minute). 

Resting Sites. Daytime inspections are useful for some 

anopheline mosquitoes. They rest in cool, dark, humid places 

protected from the wind during the day. From these sites, they are 

vacuumed into a container and provide a representative sample of the 

population. 

Pyrethrum Spray/Sheet Collection. Spread white sheets on the 

floor of a human or animal shelter and spray the overhead spaces 

above with pyrethrum or 2% d-phenothrin. Any mosquitoes resting

overhead will be killed, and can be collected from the sheets and 

identified. For best results, the technique should be used during 

midmorning hours.

Light Traps. Light traps are the most widely used method to 

sample adult mosquito populations. The New Jersey light trap has 

limited use in military situations because of its size and need for a 110 

volt power source. The solid state Army miniature light trap is more 

often used in the military setting. Traps are hung near wooded areas,

swamps, or potential breeding sites, 5-6 feet above ground and 30 feet 

away from buildings, avoiding areas exposed to strong winds or 

artificial light sources. They are scheduled a specific number of nights 

per week, and results are tabulated as to species, sex, and total 

number collected per night, per location. A trapping index (total 

females divided by number of trap nights) will detect changes in the 

population density of mosquitoes in an area.

Some Anopheles mosquito species are not attracted by light, but 

by carbon dioxide (CO2). If so, light traps are baited with a perforated 

container of dry ice mounted above the trap. Light traps and adult 

mosquito resting counts are initially unsatisfactory to monitor 

populations of Anopheles mosquitoes because these methods may 
25

not identify all potential vector species. Mosquito collections from 

landing counts should be done until medical entomologists are 

satisfied that they have identified all Anopheles species present in the 

area. Then, they determine which collection methods are sufficient to 

monitor area species.

Mosquito Control Measures. The goal of malaria vector control 

is to eliminate the anopheline population or reduce it below the number 

required to sustain disease transmission. There are three main 

methods used to reduce mosquito populations: 

⇒ Biological control.

⇒ Elimination of breeding sites.

⇒ Insecticides.

The use of insecticides to kill larvae and adult mosquitoes has 

been practiced in many military operations. Elimination of breeding 

sites and employment of biological control methods may take too long 

to have an effect or are too resource intensive to be practical in most 

military operations. However, they are quite effective as public health 

measures for control of malaria and may be employed in humanitarian 

operations. 

Biological control. Several methods of biological control currently 

exist. One involves the introduction of Bacillus thuringiensis 

israelensis, a mosquito bacterial pathogen, into a targeted mosquito 

population. Another requires the introduction of mosquito larvae-eating 

fish, Gambusia spp., into breeding areas.

Elimination of breeding sites. Breeding sites can be made 

unsuitable for mosquito larvae through a variety of methods. They 

include increasing water flow or ditching, removing protective aquatic 

vegetation, or other actions that completely destroy breeding areas 

(filling or draining). Aside from limiting water containers in bivouac 

areas or simple ditching to provide drainage, permanent removal of 

breeding sites requires careful and thorough engineering, heavy 

equipment, and personnel usually not available to an engaged military 

force.

Insecticides: Chemical Control of Larvae. Treatment of standing 

water with larvicides provides temporary control of mosquitoes and is 

more effective than adult control techniques. Unfortunately, the adult 

mosquito population is not immediately affected. Therefore, this may 
26

be a cost effective control method if troops are going to be located in 

the area for an extended period.

Solutions, emulsifiable concentrates, and suspensions are 

effective with ground operated or aerial dispersal equipment. They are 

also available in forms that can be applied by hand (briquettes or 

biodegradable plastic pouches). Medical entomologist supervision is 

essential. Considerations include larvicide formulation, delivery 

method, and amount and application rate. Method, amount, and 

formulation vary depending on geography, vegetation, species, level of 

insecticide resistance, and possible toxic effects on local inhabitants

and troops in the treatment area.

Insecticides: Chemical Control of Adult Mosquitoes, Outdoor 

Control. The treatment of choice to control adult mosquitoes is ultralow-volume spraying (ULV). ULV spraying provides adequate 

protection for limited periods of time. To provide continuous protection 

in large areas with many breeding sites, ULV insecticides must be 

applied on a repetitive schedule, typically twice daily, daily, or every 

other day. 

ULV insecticides should be applied when winds are calm (less 

than 6 knots), and when the ground is cooler than the air. Such 

temperature conditions usually occur at sunrise and sunset. However, 

many Anopheles mosquitoes are most active later in the evening. As 

ULV insecticides are most effective against flying insects, spraying 

operations should be planned for dusk, after dark, and early morning 

(near sunrise). When properly applied, ULV treatments do not leave 

dangerous or unsightly deposits on trees, bushes, or terrain.

Aerial application of insecticide requires special consideration. It 

requires the authorization of certified Department of Defense 

entomologists or applied biologists, and qualified pest control 

personnel must supervise the operation. Factors considered before 

use include size of treatment area, vegetation cover (canopy) and 

density, suitability of alternate measures, prevalence of vector borne 

diseases, and the prospects of increasing troop effectiveness.

Insecticides: Chemical Control of Adult Mosquitoes, Indoor 

Control. Indoor control of mosquitoes relies on aerosol space sprays 

that have only a short-term effect. They must be re-applied whenever 

new mosquitoes enter the space.

Another method of indoor control is application of residual sprays 

to surfaces where mosquitoes rest. Use permethrin or a long lasting 

spray recommended by a medical entomologist. For porous surfaces 
27

such as brick or unfinished wood, use a suspension made with a 

water-mixable powder or a microencapsulated formulation.

Insecticides: Chemical Control of Adult Mosquitoes, Barrier 

Treatments. Residual spray treatment of all vegetation surfaces within 

30 meters of small camps or bivouac areas can establish a barrier 

against mosquito re-infestation. Apply with backpack or hand held 

sprayers.
28

CHAPTER THREE

DIAGNOSIS

The definitive diagnosis of malaria is made by the identification of 

malaria parasites in a peripheral blood film. However, U.S. medical 

professionals are inexperienced in malaria diagnosis and treatment 

because they rarely encounter the disease. When confronted with 

malaria, Navy medical personnel have misdiagnosed it as “viral 

illness”, “gastroenteritis”, or “flu.” Malaria also may not be considered 

because it shares signs and symptoms with other tropical illnesses 

including typhoid fever, rheumatic fever, and bacterial meningitis. 

Therefore, diagnosis of malaria requires a raised level of suspicion and 

diligent screening. 

Screening. Screen all febrile patients possibly exposed to malaria 

transmission. This includes personnel who took malaria 

chemoprophylaxis medication while deployed to endemic areas, or air 

crew or travelers briefly exposed at airports in malaria endemic zones. 

The screening tool of choice for malaria diagnosis is microscopic 

examination of thick and thin blood smears. Thick smear examination 

detects the presence of any organisms; thin smear examination 

identifies the specific infecting Plasmodium species. Thick and thin 

smears can be prepared on the same microscope slide; see Appendix 

3 for description of this technique and further information on preparing 

and interpreting peripheral blood smears. 

Timing of Screening. Symptoms often precede detectable 

parasitemia by 1-2 days. Therefore, screen blood obtained through 

fingersticks or other techniques several times a day (frequency is more 

important than timing) until a diagnosis of malaria is made or ruled out. 

 Thin smear diagnosis for causal species is crucial, as P. falciparum

infections are life threatening and require specific treatment. After 

diagnosis, blood smears should continue to be monitored for response 

to therapy. Decreasing parasite count (concentration) signifies 

favorable response to therapy; frequency of testing depends on 

therapeutic response and severity of illness. For example, seriously ill 
29

patients should be tested 2-3 times daily until they significantly 

improve, then daily until parasite level is zero.

Early diagnosis and treatment is lifesaving; falciparum malaria

kills 25% of non-immune adults within 2 weeks if treatment is not 

started early in the infection. If the diagnosis of malaria is 

suspected, treat, then arrange for definitive diagnosis. The rest 

of this chapter describes the clinical manifestations of malaria to aid in 

early diagnosis and understanding of disease processes.

Clinical Manifestations

Symptoms (Table 3.1). Patients present with a variety of symptoms

depending on the stage of infection and the infecting species. Fever is 

virtually always present, and fever plus any other symptom might be

malaria if exposure occurred. Common complaints include mild to 

moderate malaise, fatigue, muscle aches, back pain, headache, 

dizziness, loss of appetite, nausea, vomiting, abdominal pain, and 

diarrhea. Dry cough and shortness of breath have been reported in 

some patients. Gastrointestinal complaints can be considerable, 

suggesting a diagnosis of gastroenteritis. Young children and semiimmune individuals may complain of fever and headache as their only 

symptoms.

Signs. Physical examination usually demonstrates an increased 

temperature, tachycardia, and warm flushed skin. The spleen is often 

palpable in initial infection, but this is more likely in subsequent 

attacks. It is usually soft and may be tender. The liver is often 

enlarged and may be tender; jaundice is not unusual. Orthostatic 

hypotension often occurs during initial infections. Mental confusion

and cyanosis are sometimes encountered.

Laboratory Findings (Table 3.2). Abnormal laboratory findings reflect 

the severity of hemolysis. Blood. A normocytic, normochromic 

anemia with leukopenia and thrombocytopenia is sometimes present 

on initial screening, but is almost always present following medication 

therapy with the resultant clearing of parasitemia. Massive P. 

falciparum infections cause acute decreases in hemoglobin, 

hematocrit, and an increase in reticulocyte count. Kidneys. Trace to 

moderate protein, urobilinogen, and conjugated bilirubin may be found 

on urinalysis. In severe P. falciparum infections, massive hemolysis

Table 3-1. Malaria Clinical Findings
30

Sign or Symptom Percent with Finding

• Fever & Chills 96

• Headache 79

• Muscle Pain 60

• Palpable Liver 33

• Palpable Spleen 28

• Nausea & Vomiting 23

• Abdominal Cramps/Diarrhea 6

combined with circulating immune complexes produces acute renal 

insufficiency or failure (“blackwater fever”) with laboratory findings of 

hemoglobinuria, proteinuria, and an elevated serum creatinine. Fever 

and dehydration may cause an increase in BUN and creatinine, but if 

serum creatinine rises disproportionately higher than BUN (BUN to 

creatinine ratio is normally 10 or 12 to 1), renal failure must be 

considered. 

Liver. Liver impairment may occur, though hyperbilirubinemia 

normally results from hemolysis. Abnormalities in liver function tests, 

increased ALT, AST, and prolonged prothrombin time, sometimes 

occur causing diagnostic confusion with viral hepatitis. Serum albumin 

is usually decreased.

Hypoglycemia, commonly seen in P. falciparum infections and 

pregnancy, is due to the 75-fold increase in glucose consumption by 

parasitized red blood cells. In addition, quinidine or quinine may 

stimulate insulin secretion, causing clinically significant hypoglycemia

when used for treatment, especially when given intravenously. If a 

patient deteriorates during convalescence, especially with a 

deterioration in neurologic function, hypoglycemia should be 

considered as a possible cause.

False positive serologic tests may be present, including syphilis 

(VDRL, RPR), rheumatoid factor, heterophil agglutinins, and cold 

agglutinins. These result from

Table 3-2. Malaria Laboratory Findings

Finding Normal 

Range

Percent with 

Abnormal 

Findings
31

• Reticulocytosis 3 - 18% 42

• Thrombocytopenia 12K-150K 36

• Bilirubin Increased 1 - 1.8 33

• VDRL Positive (-) 28 (+)

• Anemia 5.8 - 12 (Hgb) 28

• Leukopenia 3,000 - 4,700 26

• Alk. Phos. Increased 11-27 17

• SGOT Increased 40 - 108 10

a polyclonal increase in both IgG and IgM immunoglobulins, which are 

associated with appearance of specific malarial antibodies and 

reduced complement levels. Malaria does not cause eosinophilia.

Hyperparasitemia. Patients with P. falciparum infections that are 

hyperparasitemic have a higher risk of death. Hyperparasitemia is 

defined as a parasite count of greater than 250,000 per microliter 

(>250,000/?l), or as having greater than 5% of red blood cells 

parasitized. Risk of death is due to extensive microvascular disease, 

and severe metabolic effects from the parasite load.

Pathophysiology and Clinical Presentation

Clinical symptoms and signs of malaria occur shortly before or at 

the time of red blood cells lysis. Fever is caused by the release of 

merozoites, malarial pigment, parasite proteins and cellular debris. 

Chills or rigor, followed by high fever occur in a cyclical pattern in 

infections due to P. vivax, P. ovale, and P. malariae, but not P. 

falciparum, which is more likely to show continuous fever with 

intermittent temperature spikes. Clinical signs and symptoms 

described are those experienced by non-immune patients, such as will 

be seen in most U.S. military personnel. Clinical manifestations are 

not as severe in persons living in endemic areas. They are infected 

intermittently and develop partial immunity.

The malaria paroxysm is the defining clinical feature of the 

disease. That being said, it is often not present. Fever caused by 

malaria can have any pattern, and falciparum infections often present 

with a constant fever. The classic paroxysm typically has three 

stages, and is preceded in some patients by an initial period of 

nonspecific symptoms. Those symptoms include fatigue, muscle 

aches, loss of appetite, headache, and a slight fever of 2-3 day's 

duration. 
32

A paroxysm begins with the “cold” or “chilling” stage lasting 15 

minutes to several hours during which the patient feels cold and has 

shaking chills. The second “hot” stage lasts several hours and 

coincides with red blood cell rupture and merozoite release. During 

the second stage temperatures rise to 40OC (104OF) or higher. There 

is minimal sweating and the patient is at risk of febrile seizures or 

hyperthermic brain damage. Clinical signs and symptoms include 

tachycardia, hypotension, cough, headache, backache, nausea, 

abdominal pain, vomiting, diarrhea, and altered consciousness. Within 

2-6 hours, the patient enters the third “sweating” stage of the 

paroxysm with generalized sweating, resolution of fever, and marked 

exhaustion, usually giving way to sleep. Paroxysms occur in regular 

intervals, but take several days to emerge. 

As previously stated, the classic paroxysm described above is 

generally not how P. falciparum infections present. P. falciparum

malaria is more severe and qualitatively different from the other 

plasmodia that infect humans, and is the only type that causes 

microvascular disease. For those reasons, it will be discussed 

separately and in more detail.

Malaria due to Plasmodium falciparum Infection

Plasmodium falciparum malaria is a microvascular disease with a 

substantial metabolic element that damages tissue in the following 

manner: P. falciparum parasites mature in red blood cells causing 

knobs to form on their surface in effect making them “sticky”. This 

stickiness causes parasitized red blood cells to adhere to endothelial 

cells, lining capillaries and postcapillary venules of brain, kidneys, and 

other organs, obstructing blood flow. In addition to being “sticky," 

infected red blood cells are less flexible, adding to their obstructive 

potential. In obstructed capillaries and postcapillary venules, parasites 

consume glucose and produce lactate-causing acidemia and release 

of tissue necrosis factor-? (a cytokine produced by the immune 

system). Lack of oxygen and increased concentrations of toxic 

metabolites cause capillaries to become more permeable, allowing 

leakage of protein and fluids. This results in tissue edema and further 

anoxia due to the edema, leading to organ damage and death. In 

some cases, diagnosis of P. falciparum infection is made difficult 

because no parasites are seen on peripheral blood smears, as they 

are sequestered in the host’s microvasculature.
33

Cerebral Malaria. The principal manifestations of cerebral malaria 

are seizures and impaired consciousness, usually preceded by a 

severe headache. Neurologic examination may be unremarkable, or 

have findings that include contracted or unequal pupils, a Babinski

sign, and absent or exaggerated deep tendon reflexes. Cerebrospinal 

fluid examination shows increased pressure, increased protein, and 

minimal or no pleocytosis. High fever, 410 to 420C (1060 to 1080F), with 

hot, dry skin as seen in heat stroke can occur.

Manifestations of cerebral malaria are caused by microvascular

obstruction that prevents the exchange of glucose and oxygen at the 

capillary level, hypoglycemia, lactic acidosis, and high-grade fever. 

These effects impair brain function, yet cause little tissue damage in 

most cases, as rapid and full recovery follows prompt treatment. Ten 

to twelve percent of patients surviving cerebral malaria have persistent 

neurologic abnormalities upon hospital discharge.

Renal Failure. Renal failure, due to acute tubular necrosis, is a 

common complication of severe P. falciparum infections in nonimmune persons. Acute tubular necrosis in severe P. falciparum

infections is caused by two mechanisms: renal tubules become 

clogged with hemoglobin and malarial pigment released during 

massive hemolysis, and microvascular obstruction causes anoxia and 

glucose deprivation at the renal capillary or tissue level. Failure of 

urine production is a poor prognostic sign, requiring peritoneal or 

hemodialysis.

Pulmonary Edema. Often fatal, acute pulmonary edema can develop 

rapidly and is associated with excessive intravenous fluid therapy. 

Fast, labored respiration, with shortness of breath, a non-productive 

cough, and physical findings of moist rales and rhonchi are usually 

present. Chest X-rays usually show increased bronchovascular

markings. It is thought that the pulmonary edema is more related to 

release of tissue necrosis factor, than to the effects of microvascular

obstruction.

Gastroenteritis. Most patients with falciparum malaria complain of 

loss of appetite and nausea. However, in some patients (especially 

young children), additional symptoms including vomiting, abdominal 

pain, watery diarrhea, and jaundice are present leading to 

misdiagnosis of viral gastroenteritis or hepatitis. Clinical 

manifestations are associated with the adherence of parasitized red 

blood cells in the microvasculature of the gastrointestinal tract.
34

Anemia. Destruction of red blood cells upon merozoite release, and 

inhibition of hematopoesis by tissue necrosis factor-? cause the 

severe anemia often seen in P. falciparum infections. Also, P. 

falciparum parasites can infect red blood cells of all ages, which 

theoretically allows infection of all circulating red blood cells. 

Whereas, P. vivax and P. ovale require young red blood cells 

(reticulocytes) and P. malariae requires mature blood cells for 

infection.

Severe anemia is defined as a hematocrit of less than 21%, and 

clinical manifestations may include dark brown or red urine 

(hemoglobinuria), decrease in urine production, and jaundice. Renal 

failure, as previously discussed, may be a complication. Another 

cause of hemolysis and hemoglobinuria in patients with malaria is 

destruction of G-6-PD deficient red blood cells by oxidant anti-malarial 

drugs such as primaquine.

Malaria due to P. vivax (or P. ovale) Infection

Infections due to P. vivax and P. ovale are virtually the same. 

Both are less severe than falciparum malaria, and parasite blood levels 

are lower. Parasitized red blood cells do not develop knobs, therefore 

no microvascular obstruction with resultant brain, kidney, lung, or other 

organ complications occur in malaria due to P. vivax or P. ovale. 

P. vivax and P. ovale form a dormant stage in liver cells called 

hypnozoites. These parasites activate and cause delayed infections 

or a relapse (Table 3-3). A relapse usually occurs within 6 months of 

an acute attack. Some hypnozoites remain dormant much longer, and 

are virtually undetectable. If there is any suspicion that P. vivax or P. 

ovale is endemic in the area of exposure, presumptive treatment must 

be given to prevent illness. Currently, the only available treatment is 

primaquine; dosages are listed in Chapters 4, 5, and Appendix 4.

As previously stated, fever is virtually always present, and fever 

plus any other symptom might be malaria. P. vivax or P. ovale fevers 

may be erratic or continuous in the initial phase of illness. After 3 to 4 

days, if not treated, the fever then develops into a synchronous cycle 

of afternoon temperature increases every 48 hours. The fever can be 

as high as 40OC (104OF), and symptoms during this stage have been 

described as worse than falciparum malaria. Physical findings usually 

include an enlarged, tender spleen, and a palpable liver present by the 

second week of infection. Deaths have been reported due to rupture of 

an enlarged spleen.
35

Parasitemia levels are less for P. vivax or P. ovale because they 

infect only young red blood cells, unlike P. falciparum which can infect 

red blood cells of all ages. Fewer red blood cells are hemolyzed, but 

their loss stimulates replacement. This increases the number of 

young red blood cells (reticulocytes), which are susceptible to 

infection, leading to parasitemia levels greater than 1 to 2% in P. vivax

or P. ovale infections.

Malaria due to P. malariae Infection

P. malariae infection is the mildest and most chronic of all the 

human malaria infections. Invasion of red blood cells builds up slowly, 

so blood parasite levels are low, and symptoms are usually mild. 

Patients may have several febrile paroxysms before parasites are seen 

in the peripheral blood. As in P. vivax and P. ovale infections, febrile 

paroxysms develop in the afternoon, but cycle every 72 hours. P. 

malariae and P. falciparum do not have the hypnozoite stage, therefore 

relapses do not occur in infections with these species. 

Recrudescence can be seen with P. malariae infections many years 

after the initial infection. This is due to an increase in parasites after a 

chronic, low level of parasitemia in infected red blood cells that have 

persisted in tissue microcapillary circulation. Low-grade infections can 

persist up to 20-30 years. Splenomegaly is a common complication in 

those patients with low-grade infections of long duration.

P. malariae infection may produce a unique immune complex 

glomerulonephritis . Low-level parasitemia causes continuous antigen 

stimulation of host antibodies and formation of immune complexes, 

causing an immune complex glomerulonephritis. This manifestation 

usually presents 3-6 months after malaria transmission season, and 

can lead to nephrotic syndrome. Half the people who develop 

nephrotic syndrome had their first symptoms before the age of 15. 

Classic findings include persistent proteinuria, hypoalbuminemia, 

edema, and ascites. Patients who develop this complication do not 

respond to anti-malarial therapy, and response to corticosteroids is 

variable. 

Table 3-3. Characteristics of malaria relapse and 

recrudescence.

Relapse or Delayed 

Illness

Recrudescence
36

Species P. vivax, P. ovale P. malariae

Cause hypnozoites (persistent liver 

cell stage)

persistent undetectable 

parasitemia

Malaria in Pregnancy

Because of the immune suppression associated with pregnancy, 

recrudescence and relapse are frequent in the second and third 

trimester. Malaria can potentiate the anemia of pregnancy, and cause 

acute renal insufficiency and hypoglycemia in P. falciparum infections. 

 It is associated with increased numbers of abortions, miscarriages, 

stillbirths, and neonatal deaths.

Malaria in Children

In non-immune children, the initial attack can vary widely. 

Common symptoms include drowsiness, anorexia, thirst, headache, 

nausea, vomiting, and diarrhea. Common early signs include 

increased temperature (may be greater than 40OC), pallor, and 

cyanosis; enlarged liver and spleen occur later. Convulsions are 

frequent, and cerebral malaria is the most frequent complication. 

Anemia is a complication with repeated infections.

Children living in endemic areas develop limited immunity. 

Symptoms are milder and more difficult to detect. They include lowgrade anemia, restlessness, loss of appetite, weariness, sweating, 

and intermittent fever.
37

CHAPTER FOUR

 TREATMENT

Overview

After establishing the presence of a malaria infection, treatment 

should be initiated as soon as possible. Specific treatment regimen 

depends on whether the case is diagnosed as complicated or 

uncomplicated malaria. Severity of clinical illness and level of 

parasitemia determine this distinction. In addition, steps must be 

taken to identify the responsible species, and the area where 

transmission occurred as those factors influence treatment. Patients 

diagnosed with complicated malaria are at risk for morbidity and death. 

 Prompt treatment minimizes this risk. If possible, treatment of 

malaria should be done in consultation with a physician trained and 

experienced in treatment, with access to a tertiary care center.

Choice of treatment regimen, drug type, and selection of oral or 

intravenous administration, is based on the above factors. Two types 

of drugs are used to treat malaria. Blood schizonticides, which attack 

parasites in red blood cells, are used in acute infection to prevent or 

terminate the clinical attack. Tissue schizonticides are medications 

that act on the exoerythrocytic parasite stages (forming merozoites

and hypnozoites) in liver cells to prevent relapse. Treatment with 

tissue schizonticides, known as “radical” cure, is required for 

infections of P. vivax and P. ovale. An algorithm for malaria treatment 

is illustrated in Figure 4-1.

During treatment, patients must be monitored for response to 

therapy and complications from the infection or treatment. Repeated 

clinical assessment is important in cases of severe malaria, where 

early detection of complications and immediate intervention may be 

lifesaving. 
38

 no no

 

 yes yes

 

 no

 

 yes

 

 

 

no 

 yes

Complicated 

Malaria

Falciparum 

Malaria

Vivax or ovale

Malaria

IV Quinidine

(IV Quinine)

Patient able to take 

drugs by mouth

Use oral drug 

treatment

1. Mefloquine (1250 mg: 750 mg followed in 12 hrs by 500 mg), or

2. Halofantrine (500 mg q 6 hrs x 3 doses, repeat in 7 days), or

3. Quinine ( 600 or 650 mg tid to complete 7 days of therapy for 

complicated; or 600-650 mg for 3-7 days for uncomplicated), 

plus either

• Doxycycline 100 mg bid; or Tetracycline 250 mg qid to 

complete 7 days of therapy; or

• Pyrimethamine/sulfadoxine (FansidarR) (3 tablets in a 

single dose on last day of quinine.)

Vivax or ovale present as 

co-infection

Primaquine 

treatment

No further treatment 

needed

Chloroquine & 

Primaquine

Malaria due to

P. malariae

Chloroquine

Figure 4-1. Algorithm for Treatment of Malaria
39

Table 4-1. Uncomplicated Malaria Treatment

DRUG DOSE

 Chloroquine-sensitive

Chloroquine

Adults: 1.0 gm (600 mg base) initially, 500 mg 

(300 mg base) in 6 hrs, then 500 mg (300 

mg base) at 24 and 48 hrs

Children: 10 mg base/kg, 5 mg base/kg 6 hrs, 

later, then 5 mg base/kg at 24 and 48 hrs

 Chloroquine-resistant

Mefloquine*

 or

Adults: 1250 mg (750 mg followed in 12 hrs by 

500 mg).

Children: 25 mg/kg once (15 mg/kg followed in 

8-12 hrs by 10 mg/kg).

Halofantrine

 or

Adults: 500 mg every 6 hrs x 3 doses, not 

with meals*. Repeat dose in 7 days.

Children (<40kg): 8 mg/kg every 6 hrs x 3 

doses. Repeat dose in 7 days

Quinine

 plus either

Doxycycline*

 or

FansidarR

(500 mg sulfadoxine, 25 mg 

pyrimethamine)

Adults: 600 or 650 mg of the salt tid for 3-7 

days.

Children: 25 mg/kg/day of the salt divided into 3 

doses x 7 days.

Doxy :100mg bid x 7 days; do not use in 

children under 8. 

For children over 8, doxy 2 mg/kg bid x 7 days; 

not to exceed 100mg bid.

Adults: 3 tablets in a single dose. 

Children: 1⁄4 tab < 1 yr, 1⁄2 tab 1-3 yrs, 1 tab 4-8 

yrs, 2 tabs 9-14 yrs, 3 tabs > 14 yrs, all 

single dose.

* contraindicated for use in pregnant or lactating women, and those at 

risk of cardiac arrhythmia
40

Treatment

Uncomplicated Malaria. Chloroquine remains the medication of 

choice for patients with P. vivax, P. ovale, P. malariae, and 

uncomplicated chloroquine-sensitive P. falciparum infections. Drugs 

and dosages for treatment of uncomplicated malaria are listed in Table 

4-1. Chloroquine-resistant P. vivax has been reported in New Guinea, 

Indonesia, Myanmar, India, Irian Jaya, and the Solomon Islands; so it 

is important to consult with medical intelligence sources to obtain the 

latest information on drug resistance in the area of transmission. 

Chloroquine is safe, and the 3-day treatment course is well tolerated. 

If chloroquine therapy is not effective, or if infection was acquired in an 

area with chloroquine-resistant malaria, mefloquine is the next drug of 

choice, followed by quinine in combination with either doxycycline or 

pyrimethamine-sulfadoxine (FansidarR). Tetracycline may be used as 

an alternate to doxycycline. The regimen of tetracycline is an adult 

dose of 250 mg qid, and a pediatric dose of 5 mg/kg qid, not to exceed 

250 mg qid. Doxycycline and tetracycline are not to be used in 

children under 8. For uncomplicated malaria, quinine can be given as 

a 3 day course, except in Southeast Asia where a 7 day course is 

required because of an increase in relative resistance to quinine.

Febrile, acutely ill patients are prone to vomiting anti-malarial 

drugs, which are very bitter tasting. Administer an antipyretic such as 

TylenolR (acetominophen). This eases symptoms and helps patients 

tolerate anti-malarial drugs. Patients continuing to vomit require 

treatment by injection, administration of crushed tablets via 

nasogastric tube, or suppository. After administering an effective dose 

by one of these routes, patients can usually complete their course of 

therapy by mouth.

Complicated Malaria. Complicated malaria is almost always due to 

P. falciparum, and is associated with a mortality rate between 15 and 

25%. Its diagnosis is based on the severity of clinical manifestations 

and a parasitemia involving more than 1% or 2% of red blood cells. 

Patients presenting with any of the clinical manifestations listed in 

Table 4-2 should be treated for complicated malaria. Drugs and 

dosages for treatment of complicated malaria are listed in Table 4-3.

Treatment approach for complicated malaria is listed below:

• Start treatment as soon as diagnosis is suspected.

• Calculate dosage according to patient weight.
41

• Give medication intravenously.

• Give loading dose of medication (not indicated if patient has 

received quinine, quinidine, or mefloquine in the last 24 hours).

• If patient is comatose, place on his or her side and give a single 

parenteral dose of Phenobarbital (5-20mg/kg) to prevent 

convulsions.

• Measure parasite count and hematocrit every 6-12 hours.

• Exchange transfusion is indicated for patients with high level 

parasitemia (>15%) and should be considered for severely ill 

patients with parasitemia levels between 5 to 15% if it can be 

provided safely.

• Switch to oral medication as soon as patient can tolerate tablets, 

and response to treatment is confirmed.

• Observe patients carefully for drug toxicity and complications. 

Patients with complicated malaria should be treated with 

intravenous quinidine (parenteral quinine has not been available in the 

U.S. since 1991). Intravenous quinine or quinidine are potent blood 

schizonticides, and therapeutic plasma concentrations can be quickly 

and safely achieved by administration of a loading dose. Loading 

doses have been shown to decrease the duration of fever, parasitemia, 

and coma, and should be given if the patient has not received quinine, 

quinidine, or mefloquine in the last 24 hours.

Loading doses of quinine or quinidine should be given followed by 

continuous infusion. Baseline blood pressure and ECG should be 

obtained before initiating therapy, and periodically throughout 

treatment. Therapy should be discontinued if systolic blood pressure 

persists below 80 mm Hg, if either the QRS interval widens greater 

than 50% of baseline or the QT interval is greater than 0.6 seconds; or

if a cardiac arrhythmia arises.

Overdose of quinine or quinidine, particularly if too rapidly infused, 

can cause convulsions, hypotension, cardiovascular collapse, heart 

block, and ventricular fibrillation. If possible, plasma concentrations of 

quinidine or quinine should be monitored, and the maintenance dose 

should be reduced if plasma concentrations exceed 20μg/ml(mg/l). 

The maintenance dose should be reduced to one-third to one-half after 

48 hours to prevent accumulation and toxicity, unless the patient has 

improved and can tolerate oral medication. Therapeutic doses of both 

quinine and quinidine can cause hypoglycemia through stimulation of 

insulin release. All patients treated with intravenous quinidine or 

quinine should receive a continuous infusion of 5 to 10 % dextrose. 
42

Measure blood glucose periodically during treatment, every 4 to 6 

hours in unconscious patients, and give prompt treatment of 

intravenous dextrose if glucose levels fall below 40mg/dl (2.2mmol/l).
43

Table 4-2. Manifestations of Complicated Malaria

MAJOR SIGNS DESCRIPTION

Unarousable coma

Failure to localize or abnormal 

response to painful stimuli; coma

persisting for >30 min after 

generalized convulsion

Seizures More than two generalized 

convulsions in 24 hours

Severe anemia (normochromic, 

normocytic)

Hematocrit rapidly falling or <15%, 

or hemoglobin <5g/dl, with 

parasitemia level > 10,000 per ml, or 

with > 1 to 2% of RBCs involved

Severe bleeding abnormalities

Significant bleeding from gums, 

nose, GI tract, and/or evidence of 

disseminated intravascular 

coagulation

Pulmonary edema /adult 

respiratory distress syndrome

Shortness of breath, fast labored 

respiration, rales

Renal failure

Urine output <400 ml/24 hrs (<12 

ml/kg per 24 hrs in children); no 

improvement with re-hydration; 

serum creatinine >3.0 mg/dl (>265

?mol/l)

Hemoglobinuria

Black, brown, or red urine; not 

associated with effects of drugs or 

red blood cell enzyme defects 

(primaquine/G-6-PD)

Hypoglycemia Glucose <40mg/dl (<2.2 mmol/l)

Hypotension/shock

Systolic BP <50 in children aged 1-5 

or <80 in adults; core to skin 

temperature >100C difference

Acid base disturbances

Arterial pH <7.25 or plasma 

bicarbonate <15 mmol/l
44

Table 4-3. Regimens for treatment of Complicated Malaria

Drug Dose (Pediatric dose same unless indicated)

IV Therapies

Quinidine gluconate 10 mg of base/kg loading dose (max. 600 

mg) in normal saline infused over 1-2 

hours, followed by 0.02 mg/kg/min 

continuous infusion until oral therapy can 

be started. 

Quinine dihydrochloride

(available only 

outside the U.S.)

20 mg/kg loading dose IV in 5% dextrose 

over 4 hrs, followed by 10 mg/kg over 2-4 

hrs q8h (max. 1800 mg/d) until oral therapy 

can be started.

Oral Therapies

Mefloquine*

 Or

Adults: 1250 mg (750 mg followed in 12 

hrs by 500 mg); 

Children: 25 mg/kg (15 mg/kg followed in 

8-12 hrs by 10 mg/kg).

Halofantrine

 Or

Adults: 500 mg q 6 hrs x 3 doses, repeat 

in 7 days; 

Children: 8 mg/kg q 6 hrs x 3 doses, 

repeat in 7 days. 

Quinine

Plus either

Doxycycline 

 Or

FansidarR

(500 mg sulfadoxine, 25 mg 

pyrimethamine)

Adults: 600 or 650 mg salt tid; Children: 25 

mg/kg/d in 3 doses x 3-7d.

Adults: Doxy 100 mg bid, not indicated for 

children under 8. 

Children over 8: doxy 2 mg/kg bid, not to 

exceed 100 mg bid. 

Adults: 3 tablets in a single dose. 

Children: 1⁄4 tab < 1 yr, 1⁄2 tab 1-3 yrs, 1 tab 

4-8 yrs, 2 tabs 9-14 yrs, 3 tabs > 14 yrs, 

all single dose.

*delay initial dose until 12 hours after the last dose of quinidine or 

quinine 
45

 Intravenous therapy is continued until the patient is able to tolerate 

oral therapy. Regimens for oral therapy are given in Table 4-3. 

Tetracycline may be used as an alternate to doxycycline. The regimen 

of tetracycline is an adult dose of 250 mg qid, and a pediatric dose of 

5 mg/kg qid, not to exceed 250 mg qid. Doxycycline and tetracycline 

are not to be used in children under 8.

 Alternate treatments include intravenous chloroquine, intramuscular 

FansidarR, mefloquine or halofantrine tablets crushed and mixed with 

water given via nasogastric tube, or artemisinin derivatives. Intravenous 

chloroquine is less toxic than quinine or quinidine, but resistance to it 

is so prevalent that it is not used for treatment of severe malaria 

cases. This applies even to areas without resistant strains of malaria. 

 If oral therapy with mefloquine is chosen to complete the 

recommended 7 days of therapy, delay the intial dose for 12 hours 

after the last dose of quinidine or quinine. 

Halofantrine is a newly licensed drug developed by the Walter 

Reed Army Institute of Research. It should not be used in patients 

who developed P. falciparum infections while on mefloquine

prophylaxis because parasite resistance to both drugs is similar. In 

addition, fatalities have occurred when halofantrine has been used for 

treatment in patients who received mefloquine prophylaxis.

Intramuscular FansidarR (a combination drug containing 

sulfadoxine and pyrimethamine) has been shown to clear parasitemia

as quickly as chloroquine, but hypersensitivity reactions to 

sulfonamides are common and cause complications. 

Artemisinin, a compound known as qinghaosu in China, has been 

used with great success there and in trials in Thailand. It is available 

as heterogeneous compounds in suppository, intravenous, and tablet 

forms.

“Radical” Cure. To prevent relapse, P. vivax and P. ovale infections 

need to be treated to eradicate tissue schizonts (persistent liver cell 

stages known as hypnozoites). This is known as “radical” cure, and 

currently the only available effective drug is primaquine. It is a potent 

oxidant, and can cause severe hemolytic anemia in G-6-PD deficient 

patients. Therefore, before treating with primaquine, the G-6-PD status 

of patients must be checked, and an appropriate dosage regimen 

selected. Radical cure dosage schedules are listed in Table 4-4.
46

Table 4-4. Primaquine Treatment Regimens

G-6-PD NORMAL 1 tablet* per day x 14 days

G-6-PD deficiency

(Mild African form)

3 tablets per week for 8 weeks

G-6-PD deficiency

(More severe Mediterranean variety)

2 tablets per week for 30 

weeks

* 1 tablet consists of 26.3 mg pimaquine phosphate, 15 mg primaquine base.

Treatment Management

Monitoring. Complicated malaria patients are at risk for sudden 

decompensation and need to be closely monitored. If possible, these 

patients should be transferred to facilities with an intensive care unit 

(ICU) or equivalent. Treatment should be supervised by a physician. 

Initial patient monitoring should be frequent (every 1 to 2 hours), until 

the patient improves. Parameters to monitor include:

• Vital signs (temperature, pulse, blood pressure, respiration)

• Parasite concentration.

• Urinary output.

• Serum electrolytes.

• Blood glucose.

• Hematocrit/hemoglobin.

• ECG (required for quinidine treatment).

Response to therapy is monitored by serial blood smears. Fewer 

parasites will be seen on successive smears if treatment is effective. 

If no improvement in clinical symptoms or decrease in parasitemia is 

seen in the first 24 to 48 hours of treatment, resistance should be 

assumed and treatment with an alternate drug should be initiated. 

Providers should be vigilant and monitor other parameters to identify 

the common complications of malaria: cerebral malaria, 

hypoglycemia, anemia, renal failure, pulmonary edema, concurrent 

bacterial infection, and over-hydration. Prompt initiation of supportive 
47

measures (intravenous hydration, glucose administration, oxygen 

therapy, blood transfusion, etc.) is important in reducing permanent 

injury and mortality.

Cerebral Malaria. Generalized seizures occur in more than 50% of 

patients with cerebral malaria, and can lead to sustained neurological 

deterioration or aspiration pneumonia. Patients with impaired 

consciousness should be placed in the lateral decubitis position. If 

patient is unconscious, intubation with an endotracheal tube or 

placement of a rigid oral airway is indicated to maintain the airway. 

Vital signs, level of consciousness (modified Glasgow coma scale, 

see Table 4-5), and seizures should be monitored and recorded 

frequently. Seizures must be treated promptly with a benzodiazepine 

drug (diazepam, chlormethiazole, or lorazepam). A nasogastric tube 

should be placed to lower risk of aspiration pneumonia.

Deepening coma or signs of cerebral herniation are indications for 

further assessment with computed tomography (CT) or magnetic 

resonance imaging (MRI). If such techniques are not available, 

therapy to lower intracranial pressure should be attempted. 

Acceptable treatment measures include intravenous mannitol, 1.5 

mg/kg of 10-20% concentration given over 30 minutes, or 

hyperventilation to reduce arterial pCO2 below 4.0 pKa. Steroids have 

been proven ineffective when used in an attempt to lower intracranial 

pressure. 

Seizures may be prevented with a single intramuscular dosage of 

phenobarbital sodium (loading dose 15-20 mg/kg, total dose 60-200 

mg/kg/day). In an ICU, an alternate method is phenytoin, 10-15 mg/kg 

loading dose, followed by an adult maintenance dose of 100 mg every 

6 hours. Plasma phenytoin concentration should be monitored daily.

Hypoglycemia. This complication should be suspected in any 

patient who becomes unresponsive. Frequent monitoring of blood 

glucose is necessary in complicated malaria, particularly during 

intravenous quinine or quinidine administration. Hypoglycemia can be 

caused by two mechanisms, stimulation of insulin release caused by 

quinine or quinidine therapy, or from consumption of glucose by large 

numbers of parasites. If available, give a therapeutic trial of 50% 

dextrose followed by continuous infusion of 5 or 10 % dextrose 

solution.

Table 4-5. Modified Glasgow Coma Scale
48

Score

Best Verbal Response: Oriented 5

Confused 4

Inappropriate words 3

Incomprehensible sounds 2

None 1

Best Motor Response: Obeys commands 6

Localizes pain 5

Flexion to pain:

 Withdrawal 4

 Abnormal 3

Extension to pain 2

None 1

______

Total 2 - 11

Unarousable coma < 7

Pulmonary Edema. This complication results from either increased 

capillary permeability or fluid overload and resembles Adult Respiratory 

Distress Syndrome (ARDS). A patient with pulmonary edema needs 

treatment in an ICU, as positive pressure ventilation with positive end 

expiratory pressure/continuous positive airway pressure (PEEP/CPAP) 

is needed for adequate oxygenation. Fluid overload must be prevented 

by maintaining the central venous pressure between zero and 10-15 

cm H2O. If an ICU setting is not available, oxygen should be delivered 

by the most effective means available, and a rapid acting diuretic such 

as furosemide should be given intravenously.

Renal Failure. Renal complications are seen in one third of adult 

patients with severe falciparum malaria. Most patients will respond to 

cautious re-hydration with an increase in urine output. Dialysis is 

indicated for hyperkalemia, uremia, metabolic acidosis, or pulmonary 

edema. Treatment of intravascular hemolysis (blackwater fever) 

involves correction of uremia with dialysis, and avoidance of fluid 

overload due to blood transfusion. In cases of renal failure due to 

massive hemolysis, blood transfusion is usually necessary to prevent 

death.

Anemia. In most cases no intervention beyond treatment of the 

malaria infection is required. Transfusion should be considered if the 

hematocrit drops below 20%, or if it is falling rapidly and associated 
49

with clinical distress. Clinical manifestations indicating need for 

transfusion include shock, cardiac failure, hypoxia, and extreme 

lethargy. 

Transfusion has safely been used to correct anemia, but the 

volume given must be included in fluid balance calculations to prevent 

pulmonary edema. Diuretics (furosemide, 1-2 mg/kg) can be given to 

promote urine output to maintain fluid balance during transfusion. 

Plasma expanders (colloids), and administration of oxygen can be 

used if transfusion is not practical or available. 

Exchange transfusion for treatment of hyperparasitemia has been 

used for approximately 70 patients. Though most showed clinical 

improvement during and after the procedure, it has not been proven 

superior to optimal anti-malarial medication treatment. Manual 

exchange transfusion (alternating phlebotomy with transfusion), or 

continuous cell separation (hemophoresis) are methods of exchange 

transfusion that have been used. 

Septic Shock. Secondary bacterial infection is a frequent 

complication in severe malarial cases. Blood, urine, and CSF fluid, 

etc. should be routinely cultured. Broad-spectrum intravenous 

antibiotics combining an aminoglycoside and a later generation 

cephalosporin should be started immediately if a secondary bacterial 

infection is suspected. Other causes of shock to consider are 

hypovolemia from dehydration, pulmonary edema, or massive blood 

loss (gastrointestinal hemorrhage or ruptured spleen).

Ruptured Spleen. This potentially fatal complication should be 

considered in patients infected with P. vivax or P. falciparum. Clinical 

manifestations include complaints of abdominal pain, especially in the 

left upper quadrant, left shoulder pain, and hypotension without other 

signs of blood loss. Free blood in the peritoneal cavity or a torn 

splenic capsule can be detected by ultrasound or CT, and confirmed 

by needle aspiration of the peritoneal cavity. A trial of conservative 

management is currently recommended so the spleen and its 

immunological functions can be preserved. This includes blood 

transfusion, close observation in an ICU or equivalent setting, and rapid 

access to surgical consultation. 

Pregnancy. Treatment is essential for pregnant women to save their 

lives and prevent miscarriages. Falciparum malaria is associated with 

low birth weight, fetal distress, premature labor, miscarriage, stillbirth, 
50

and hypoglycemia. Treat as for any adult, suspect hypoglycemia, and 

do not give tetracycline or halofantrine.

Pediatrics. Most of the 1 to 3 million deaths from malaria each year 

are children, primarily in Africa. Common complications are 

convulsions, coma, hypoglycemia, metabolic acidosis, and severe 

anemia. Severe jaundice, acute renal failure, and pulmonary edema 

are unusual. Children tolerate anti-malaria drugs well, and treatment is 

virtually the same as for adults with appropriate dosage adjustments. 

Tetracycline drugs cause defects in forming teeth and bone, and 

should not be given to children under 8 or 9 years.

Completion of Treatment

Complicated malaria should be treated for a total of 7 days. 

Mefloquine can be given as a single dose when oral drugs can be 

tolerated, since therapeutic blood levels last for a week. Dosages of 

other oral medications indicated after intravenous therapy are shown in 

Table 4-3.

Uncomplicated malaria requires 3 days of chloroquine treatment 

in susceptible infections. Oral mefloquine or halofantrine can be used 

in resistant cases. If P. vivax or P. ovale were identified or suspected, 

“radical” cure to eradicate hypnozoites is indicated. Table 4-4 lists 

appropriate dosages for patient G-6-PD status.

Follow Up and Prognosis 

Once elimination of parasites has been documented on 

peripheral blood smears, routine repeat smears are not recommended. 

 Patients should be advised that malaria relapse is possible despite 

thorough treatment. If presenting for care with a febrile illness within a 

year, they should be advised to inform their provider that they were 

recently treated for malaria and it should be considered a potential 

cause of their present illness.
51

CHAPTER FIVE

GLUCOSE-6-PHOSPHATE

DEHYDROGENASE DEFICIENCY

Overview

The recognition of Glucose-6-Phosphate Dehydrogenase (G-6-

PD) deficiency was the direct result of investigations of the hemolytic 

effect of the drug primaquine in the 1950s. G-6-PD is the first enzyme 

of the hexose monophosphate shunt, a biochemical pathway crucial in 

the protection of red blood cells. Damage done to hemoglobin

molecules (See Table 5-1) by oxidizing drugs or chemicals is 

neutralized or reversed by substances that the hexose 

monophosphate shunt produces. 

Primaquine is the only currently available drug able to destroy 

dormant hypnozoites in liver cells and prevent relapse of P. vivax or P. 

ovale malaria. Unfortunately, it is a strong oxidizing agent, and can 

cause severe hemolytic anemia in G-6-PD deficient personnel. In the 

U.S. military population, 2 types of G-6-PD deficiency are common. 

Understanding the difference between these types, and the primaquine

treatment schedules available for each, can minimize or prevent 

complications from drug reactions, and allow treatment of the relapsing 

forms of malaria.

Physiology of G-6-PD Deficiency

Red blood cells are normally protected from oxidizing substances 

in a complex chemical pathway in which G-6-PD is an essential 

enzyme. In G-6-PD deficient red blood cells, this protective 

mechanism is compromised and oxidizing substances produced by 

infections or oxidant drugs damage hemoglobin molecules. In this 

harmful process, hemoglobin is denatured irreversibly and precipitates 

in clumps of protein called Heinz bodies. Heinz bodies attach to red 

blood cell membranes, 
52

deforming the cells, and are filtered from circulation by the spleen. 

Free hemoglobin is released into the blood

Table 5-1. Summary of Hemolysis in G-6-PD Deficiency

• Exposure of hemoglobin to oxidant

• Heinz body formation (denatured clumps of hemoglobin

inside red blood cells)

• Deformation of red blood cells caused by attachments of 

red cell membranes and Heinz bodies

• Removal and destruction of deformed red bloods cells by 

the spleen

• Decline in hemoglobin, hematocrit

• Increase in red blood cell production (reticulocytosis) to 

compensate for decrease in red blood cells

• Hemoglobinuria and symptoms if hemolysis severe 

(overcomes the liver’s ability to metabolize hemoglobin

breakdown products) 

from the destroyed red blood cells. If a large number of red blood cells 

are destroyed, the human body’s normal compensatory mechanisms

are overwhelmed. The amount of hemoglobin released into the 

bloodstream may be too great to be absorbed and metabolized by the 

liver, resulting in hemoglobinuria and kidney damage. Anemia may 

also occur if the loss of red blood cells is too great to be compensated 

by an increase in the rate of reticulocytosis. The extent of hemolysis

depends on the type and severity of G-6-PD deficiency, and the 

amount of exposure to oxidizing substances (see Table 5-2).

G-6-PD Types. The gene for G-6-PD is located on the X 

chromosome(s). Severe deficiency is fully expressed in males and 

rare in females. Over 200 variants have been identified. In the U.S. 

military, the two types that are often encountered are G-6-PD A-, found 

in 16% of Afro-American males, and the more rare G-6-PDMed found in 

Greeks, Sardinians, Sephardic Jews, Arabs, and other males of 

Mediterranean descent.
53

Table 5-2. Drugs and Chemicals that Should be Avoided by 

G-6-PD Deficient Individuals

Acetanilid

Furazolidone

Methylene blue

Nalidixic acid

Naphthalene

Niridazole (AmbilharR)

Isobutyl nitrite

Nitrofurantoin (FuradantinR)

Phenazopyridium (PyridiumR)

Phenylhydrazine

Primaquine

Sulfacetamide

Sulfamethoxazole (GantanolR)

Sulfanilamide

Sulfapyridine

Thiazolesulfone

Toluidine blue

Trinitrotoluene (TNT)

Urate oxidase 

As normal red blood cells age, the activity of G-6-PD decays 

slowly, reaching 50% of its original level in 60 days. Despite this loss, 

normal red blood cells retain enough activity to sufficiently protect red 

blood cells from oxidants. G-6-PD decay is significantly pronounced 

in deficient individuals. G-6-PD

A-

 declines to 50% of baseline activity 

in 13 days, while G-6-PDMed declines to 50% of baseline activity in 1-2 

days. In G-6-PD A- deficiency, young red blood cells have normal 

enzyme activity, while older cells are grossly deficient. In G-6-PDMed 

virtually all red blood cells are deficient. Thus, hemolysis is self 

limited in individuals with G-6-PDA-, ending when older red blood cells 

are destroyed. In G-6-PDMed hemolysis is much more severe, as all 

red blood cells are at risk (see Table 5-3).

Most cases of drug induced hemolytic reactions related to G-6-

PD Adeficiency are probably sub-clinical. During the Vietnam War, 

only 20 persons were documented to have developed a severe drug 

reaction because of G-6-PD deficiency. At that time, chloroquineprimaquine tablets were given weekly to service members as malaria 

prophylactic therapy, and routine G-6-PD testing was not done. As 

thousands of service members were required to take the weekly 

prophylaxis, 20 cases were much less than expected. It is probable 

that the reactions that occurred were due to G-6-PDMed, not G-6-PDA-.
54

Table 5-3. Clinical Comparison: G-6-PD Aand G-6-PDMed

G-6-PD A- G-6-PDMED

Frequency Common in 

Afro-American 

populations

Common in 

Mediterranean 

populations

Degree of Hemolysis Moderate Severe

Hemolysis with:

 Drugs

 Infection

Unusual

Common

Common

Common

Need for transfusions No Sometimes

Chronic Hemolysis No No

Signs and Symptoms of Hemolysis. Signs and symptoms appear 

1-3 days after initiation of drug therapy. Shortness of breath, rapid 

pulse, hemoglobinuria (brown or black urine), and fatigue are common 

clinical manifestations. In mild cases, shortness of breath, rapid 

pulse, and fatigue appear during or after physical exertion. A modest 

decline in hemoglobin (3-4 mg/dl) occurs without hemoglobinuria. 

Most of these cases are easily overlooked unless caregivers are alert.

If hemolysis is markedly severe, shortness of breath, rapid pulse, 

palpitations, and fatigue can present at rest. Some patients complain 

of abdominal or back pain. Signs include hemoglobinemia (pink to 

brown plasma), hemoglobinuria, and jaundice. Heinz bodies can be 

seen if red blood cells are stained using methyl violet.

Laboratory Analysis. Urine dipstick and hematocrit are simple and 

useful screening tools that can be done in the field. Hemoglobin 

(blood), bilirubin (urobilinogen), and protein should be monitored when 

using urine dipsticks to screen for hemolysis. It is important to 

differentiate the “blood” identified by urine dipstick as free hemoglobin

or as red blood cells (hematuria). Hemoglobin in urine is present when 

red blood cells are destroyed in the hemolytic process, while intact red 

blood cells are present due to another pathologic process. Hematocrit 

testing, if performed, should be compared to baseline values. If 

facilities are available, other useful laboratory tests include blood and 

plasma hemoglobin levels, plasma haptoglobin level, reticulocyte

count, lactose dehydrogenase level, and identification of Heinz bodies. 

Primaquine Use in G-6-PD Deficient Personnel
55

G-6-PD Screening and Documentation. All Navy and Marine Corps 

personnel are tested for G-6-PD deficiency. Testing is qualitative, 

determining the presence of G-6-PD deficiency, but not the type or 

severity. Members who test positive must be informed of the 

deficiency, the signs and symptoms they may experience and why 

they may occur, and the risks of taking oxidant medications. They 

also should be advised to consult with their unit corpsman or medical 

officer if malaria medications are administered to them. 

The results of G-6-PD screening must be recorded in individual 

medical records, along with an entry documenting individual 

counseling of their deficiency. Unit medical records should be 

checked periodically to ensure that G-6-PD and other important 

information such as immunization status, blood type, etc., are 

recorded. If the information is not available, testing should be 

repeated. Use of spreadsheet software and microcomputers is an 

excellent medium for maintenance of unit medical readiness data.

Current Navy policy prohibits primaquine prophylaxis of G-6-PD

deficient service members. If, in the future, treatment of G-6-PD 

deficient personnel is authorized, testing for the specific type of 

deficiency is recommended. Once tested, such personnel should be 

informed of the type and details of their deficiency. If test information 

is not available as to an individual’s specific type of deficiency when 

terminal primaquine prophylaxis is sanctioned, the dosage regimen 

should be given based on demographic data. These data support the 

assumptions that G-6-PD deficiency in Afro-American personnel is the 

G-6-PDA- type, and personnel of European descent have the G-6-PD

Med

type.

Terminal Primaquine Prophylaxis/Treatment. Primaquine 

remains the only drug available for treatment of the relapsing types of 

malaria. It can be used safely in G-6-PD deficient personnel under 

close medical supervi sion. Doses must be given less often and over a 

longer period of time to avoid a serious hemolytic reaction. Ensuring 

treatment compliance will be challenging, as the primaquine regimen 

consists of 24 doses over 8 weeks in G-6-PDAdeficient personnel, and 

60 doses over 30 weeks in G-6-PDMed deficient personnel (see table 5-

4).

Monitoring. If, in the future, primaquine prophylaxis of G-6-PD

deficient personnel is authorized, monitoring of deficient members is 

recommended. G-6-PD deficient personnel taking primaquine should 

be advised to seek medical evaluation if any symptoms or change in 
56

urine color occur. A simple urine dipstick and/or hematocrit performed 

3 to 4 days after the initial dose and checked periodically would 

identify severe cases of hemolysis.

Therapy of Drug Reaction. If hemolysis occurs, particularly in G-6-

PDA- deficient persons, transfusion is usually not required. Hemolytic 

episodes are usually self-limited, even if drug administration is 

continued. This is not the case with the more severe G-6-PDMed

deficiency and drug treatment should be stopped. If the rate of 

hemolysis is rapid, transfusion of whole blood or packed cells may be 

useful. Good urine flow should be maintained in patients with 

hemoglobinuria to prevent kidney damage. Folic acid may be 

beneficial as in other patients with increased bone marrow activity (an 

increase in bone marrow activity is caused by red blood cell 

formation).

Table 5-4. Primaquine Treatment Regimens

G-6-PD Normal 1 tablet* per day x 14 days

G-6-PDA- Deficiency 3 tablets per week for 8 weeks

G-6-PDMed Deficiency 2 tablets per week for 30 weeks

 *1 tablet consists of 26.3 mg primaquine phosphate, 15 mg primaquine base.
57

CHAPTER SIX

MILITARY MALARIA CONTROL 

RESPONSIBILITIES

Throughout history, diseases and non-battle injuries (DNBI) have 

resulted in more casualties to the Navy/Marine Corps team than 

combat. Historically, malaria has been the most formidable disease to 

prevent. The resources expended in its treatment, and the personnel 

hours lost due to malaria significantly decrease force readiness, 

especially in combat situations. 

Prevention of DNBI is arguably the most important mission of 

military medicine. Success is achieved only when line commanders

are convinced that principles of preventive medicine are an essential 

element in force protection. As Field Marshal Slim maintained (see 

Introduction), the countermeasures necessary to prevent malaria must 

be enforced by line commanders. Medical personnel must understand 

and practice the following three basic principles of Force Protection:

1) Threat assessment. 

2) Countermeasure selection and implementation. 

3) Reassessment of threats and countermeasures guided 

by outcome measurement and analysis.

After careful analysis of the deployment situation, appropriate 

countermeasure recommendations to commanders can be made. 

Then, with command support, countermeasure training and 

coordination can be instituted throughout the chain of command. 

Medical Surveillance. Medical personnel must actively track unit 

illnesses and injuries. A single case of malaria may constitute an 

outbreak and signals a breakdown in preventive measures. Cases 

must be investigated and analyzed by unit medical personnel. 

Recommendations to correct the problem should be made 
58

immediately to the unit commander and followed by the institution of 

corrective measures. 

This chapter will outline the application of the second and third 

principles to control malaria and other DNBIs by the chain of 

command. In general, malaria control is achieved through Personal 

Protective Measures, Mosquito Control, and Chemoprophylaxis. 

In military situations, personal protective measures and 

chemoprophylaxis are simple, effective, and successful. Mosquito 

control may be less suitable in contingency settings but can be 

particularly useful in long-term or humanitarian operations. Consult the 

cognizant medical entomologist. To prevent malaria, strong line 

involvement and enforcement is essential. Medical personnel must 

work closely with line commanders and staff to implement measures 

to prevent malaria.

I. Line Commander Responsibilities

CINCs and JTF Commanders. These commanders exercise 

authority over all assigned and attached forces in their area of 

operations. The decisions they make regarding medical guidance, 

assignment of medical tasks, and the joint medical concept of the 

operation are based on the advice received from CINC or Joint Task 

Force Surgeons. Prior to the operation, detailed medical guidance is 

published in Annex Q of the operation order. The malaria risk is 

characterized, and required countermeasures selected are included in 

that document. Annex Q is prepared by the CINC or JTF Surgeon 

staff, endorsed by the CINC or JTF commander. 

This process reveals the impact that medical advice has on 

military operations. Line commanders need their medical officers to 

supply accurate, clear advice to enable them to make decisions to 

keep their forces ready. Jonathan Letterman, the Medical Director for 

the Army of the Potomac during the Civil War, clearly defines that role 

in the following quote:

“A corps of medical officers was not established solely for the purpose 

of attending the sick and wounded...the labors of medical officers 

covers a more extended field. The leading idea, which should be 

constantly kept in view, is to strengthen the hands of the Commanding 

General by keeping his army in the most vigorous health, thus rendering 

it, in the highest degree, efficient for enduring fatigue and for fighting. In 

this view, the duties of the corps are of vital importance to the success 

of an army, and commanders seldom appreciate the full affect of their 

proper fulfillment.”
59

Fleet and Force Commanders. These service commands are 

responsible for training and equipping units in their service, and 

maintaining their operational readiness. In prevention of DNBI

(malaria control), their function is to provide all supplies 

necessary for implementation of countermeasures, as well as to 

ensure that all personnel are trained to employ personal 

protective measures. An example of this is First Marine 

Expeditionary Force’s readiness policy requiring every Marine 

deploying as part of a Marine Expeditionary Unit (MEU) to have 

three sets of utility uniforms pretreated with permethrin.

Unit Commanding Officers. The success of malaria control 

depends on the enforcement of personal protective 

measures by Commanding Officers (COs). Part of the 

responsibility of enforcing personal protective measures is 

ensuring that personnel are adequately trained and can employ 

them. Commanding Officers ultimately decide how 

chemoprophylaxis is administered, whether before a meal, by 

separate departments, or by employment of directly observed 

therapy (DOT). Finally, they must provide a surveillance report 

as directed in the Navy reportable disease instruction. Accurate 

surveillance data and analysis yield accurate reassessment of 

threats and countermeasures.

II. Medical Department Responsibilities

DNBI and malaria control efforts depend on medical 

department personnel. They provide the expertise to: 1) 

perform medical surveillance; 2) educate, train, and supervise 

the employment of personal protective measures and 

chemoprophylactic regimens; 3) diagnose and treat malaria, and 

other diseases and injuries; and 4) perform vector surveillance 

and control. Superior medical departments train their personnel 

to demonstrate and instruct other service members in the use of 

field hygiene and personal protective measures. In addition, 

they instruct corpsmen as well as medical officers to be familiar 

with the various chemoprophylaxis and treatment regimens, and 

the alternate treatments required for G-6-PD deficient individuals, 

pregnant service members, and persons who have had adverse 

reactions from anti-malarial drugs. 

Medical personnel also must understand the threat in order 

to counter it. Essential sources of medical intelligence are the 
60

Armed Forces Medical Intelligence Center, and Navy 

Environmental and Preventive Medicine Units. Appendix 1 

describes in detail these and other resources from which 

medical intelligence, threat assessments, and other information 

can be obtained.

Senior Medical Officers. Force and Fleet medical officers

have two priorities: 

1) Advising force commanders of DNBI threats, including 

malaria, and recommending appropriate 

countermeasures.

2) Preparing medical department personnel to counter 

identified threats. 

Advising force commanders of the appropriate 

countermeasures to employ requires medical commanders to 

characterize the DNBI threat. By combining medical 

intelligence on the area of operation with an understanding of 

mission operations, plans, and objectives, the risks to the force 

can be judged. Countermeasures are then recommended to 

reduce risks and ensure mission accomplishment. This is a 

synergistic process; countermeasures prevent illness and injury, 

increasing force readiness. 

Part of the process of recommending countermeasures is 

estimating the resources needed to employ them. This includes 

identifying and directing necessary training, along with 

identifying and procuring necessary supplies needed to 

implement recommended countermeasures. This information 

needs to be passed on as expeditiously as possible to the 

personnel responsible for action.

Unit Medical Officers. Unit medical officers, including 

Independent Duty Corpsmen, are essential in prevention of DNBI

and malaria. They advise their CO on all medical matters. 

Enforcement of personal protective measures and method of 

administration of chemoprophylaxis depend on the advice given 

the CO by the Unit medical officer. By doing continuous 

surveillance of malaria incidence rates, other DNBI rates, and 

proper employment of personal protective measures, Unit 

medical officers can monitor the success of countermeasures, 

and reassess the threats. Unit medical officers must also train 
61

and supervise the unit’s corpsmen to ensure optimal medical 

care is delivered. 

Flight Surgeons. Flight surgeon responsibility is the same as 

that of Unit medical officers, with special attention to the effects 

of malarial chemoprophylaxis medications on flight personnel. 

Continuous or periodic monitoring of flight personnel on 

medication may be required to ensure safety. Flight personnel 

under treatment for malaria cannot fly until completion of 

treatment and evaluation by a flight surgeon. It is important to 

note that chemoprophylaxis with mefloquine is not authorized for 

use in flight personnel.

Preventive Medicine Officers. The General Preventive 

Medicine Officer (PMO) serves as a source of information for all 

levels of the chain of command. Currently PMOs serve on all 

Marine Expeditionary Force staffs, and requests have been 

made to place PMOs on the staffs of the geographic CINCs. 

Knowledge of the general duties of all medical department 

personnel involved in malaria control (Medical Entomologists, 

Environmental Health Officers, Preventive Medicine Technicians) 

 allows them to consult and coordinate the provision of any 

needed training, supplies, or control measures with units in the 

field or in garrison. PMOs will usually deploy to the area of 

operation with a deployable lab, a resource able to aid in 

disease diagnosis and vector identification and surveillance.

One of their primary duties is to coordinate or assist in any 

illness or outbreak investigation. All surveillance data are 

monitored and analyzed by PMOs, forwarded to all unit and 

military treatment facility medical departments, and to 

commanders, along with pertinent recommendations. Current 

malaria prevalence, incidence, and any pattern of drug 

resistance in an operational area are included in these reports. 

(Reports are not limited to malaria statistics).

Hospital Corpsmen. The training and support of hospital 

corpsmen is of paramount importance to force readiness and 

must be emphasized at every level in the chain of command. 

Hospital corpsmen are the first line of defense in malaria and 

DNBI prevention. Unit corpsmen perform most of the personal 

protective measures training given to unit personnel. They live 

among them in the field and monitor the daily employment of 

countermeasures. They supervise administration of 
62

chemoprophylaxis, and are often the first to initiate the 

diagnosis and care of any malaria cases. 

Preventive Medicine Technicians (PMTs). These are 

specially trained hospital corpsman, and are directly involved in 

all aspects of malaria and DNBI control. They provide training in 

personal protective measures to hospital corpsmen and unit 

personnel. They also perform field vector surveillance, collect 

epidemiological data, and will supervise or conduct field 

sanitation and vector control measures if needed. They serve 

along side PMOs, and are excellent resources for preventive 

medicine information in the field.

Laboratory Personnel. Laboratory personnel assigned to 

deployable labs, fleet hospitals, Marine Medical Battalions, or 

any other unit that deploys to malaria endemic areas must be 

able to perform thick and thin peripheral blood smears and 

differentiate between the four plasmodia species that cause 

malaria in humans. They should be able to teach this 

diagnostic technique to interested medical personnel. 

An important responsibility is sending prepared duplicate 

blood smear slides to the Navy Environmental and Preventive 

Medicine Unit assigned to monitor the area of operation. Such 

samples enable update of the area threat assessment and 

diagnosis confirmation. The slides should be both stained and 

unstained, and accompanied by identifying information and the 

clinical history of the case. 

Environmental Health Officers (EHOs). Environmental Health 

Officers are often assigned to deployable labs, preventive 

medicine units, Marine Force Service Support Groups, Marine 

Divisions, Marine Air Wings, and Joint Task Forces. They 

assist in collection of epidemiological and entomological data, 

and evaluate the environmental conditions that affect malaria 

control. They also have a primary role in the training and 

supervision of PMTs. 

Medical Entomologists. Medical entomologists obtain the 

most current mosquito information and recommend applicable 

methods of vector control. They supervise adult and larval 

mosquito surveys, pesticide application, and train personnel in 

identification and control measures. They are assigned to 

Marine Force Service Support Groups to:
63

1) Recommend and ensure that personal protective measures

are employed.

2) Select optimum locations for bivouacs and base camps.

3) Recommend safe times for training and field exercises.

Preventive Medicine teams can deploy EHOs, Medical 

Entomologists, Epidemiologists, Laboratory Technicians, and 

Industrial Health Officers. These teams can provide varied and 

useful services to deployed forces.
64

III. Administrative Responsibilities

Medical Records. Medical records of Navy/Marine Corps 

service members are required to include:

G-6-PD Screening Results: A result, either deficient or 

normal, must be entered on a Standard Form 600 (SF 600). If 

deficient, this information must be highlighted on the Problem 

Summary List (NAVMED 6150/20). In addition, the 

“Sensitivities” block in the “Alert box” on the cover of their 

medical treatment record must be checked. Other health care 

beneficiaries, including civilian technical experts, should be 

offered this screening test if traveling to endemic areas.

Chemoprophylaxis. The date prophylaxis began and ended, drug 

type, and dosage should be entered on a SF 600. If terminal 

primaquine prophylaxis is given, entry of the same information is 

required. 

All personnel required to take chemoprophylaxis must be 

informed of the reason for taking the medication, common side 

effects of the drug, and when to take the medication. It should 

also be communicated clearly that taking prophylactic 

medication does not guarantee malaria prevention. 

Service members should be advised to seek medical 

evaluation if they suffer drug side effects or have symptoms of 

malaria. This information is usually presented at the unit level. 

When this information is presented, personal protective 

measures may be demonstrated, and DEET, permethrin, 

netting, and other necessary items may be issued.

Medical Event Reports. Medical Event Reports (MERs) are 

required, by instruction, on any member diagnosed with malaria. 

 The report should be generated using the Naval Disease 

Reporting System software package which can be downloaded 

from the NEHC homepage (http://www-nehc.med.navy.mil). If 

the software is unavailable, a message can be generated. The 

MERs are then sent to the Navy Environmental and Preventive 

Medicine Unit assigned to monitor the area of operation. The 

message should also “info” all military treatment facilities in the 

area, the nearest Navy Disease Vector Ecology and Control 

Center, and the Navy Environmental Health Center (NEHC). The 

information is important to monitor and update both the malaria 
65

threat and presence of drug-resistant malaria in the area of 

operation.

The following is the minimum information included in the 

MER:

1) Patient travel history 3 months prior to diagnosis.

2) Type and duration of chemoprophylaxis or treatment 

medications taken, if applicable.

3) Interpretation (diagnosis) of blood smears performed 

on the patient.

4) Date that blood smears were sent to a Navy 

Environmental and Preventive Medicine Unit for 

confirmation.

Medical Treatment Facilities. The staff of Military Treatment 

Facilities that may receive malaria patients should be 

familiarized with treatment. Commanders should arrange 

training from available sources such as the Internal Medicine or 

Infectious Disease department, or the nearest Navy 

Environmental and Preventive Medicine Unit. A general inservice training session that includes the following topics is 

recommended:

1) Diagnosis, treatment and monitoring.

2) Common complications of severe falciparum malaria

infections. 

3) The physiology of terminal primaquine prophylaxis

and G-6-PD deficiency.

4) Monitoring blood parasite concentration with 

peripheral blood smears for treatment response.

Another important aspect in the care of malaria patients is to 

send a timed and dated peripheral blood smear upon transfer, so 

the receiving facility can compare it with their initial blood smear, 

and confirm the diagnosis. 

Medical Board Evaluations. Service members who develop 

severe malaria complicated by a severe hemolytic reaction 

characterized by hemoglobinuria together with the diagnosis of 

“blackwater fever” and/or renal failure are required to be 

evaluated for fitness for further duty by a Medical Board. A 

Medical Board is also required on personnel who develop a 

similar severe hemolytic reaction as a result of taking malaria 

chemoprophylactic drugs. The complication of cerebral malaria 
66

does not require evaluation by a Medical Board unless 

permanent neurologic disability has occurred. 

Blood Donor Programs. Blood donation programs are subject 

to the guidance of BUMED P-5120, “Standards for Blood Bank

and Transfusion Services.” The directive is applicable to both 

military and civilian blood banks and requires that individuals 

treated for malaria wait three years from the date of completion 

of therapy to donate blood. Individuals who took malaria 

chemoprophylactic drugs while in endemic areas must also wait 

three years from completion of chemoprophylaxis to donate 

blood. The reason for the waiting period is to prevent donated 

blood from being contaminated by malaria parasites, not drugs.

Individuals who visited a malaria-endemic area without taking 

chemoprophylactic drugs and remained asymptomatic are required to 

wait 6 months before being eligible to donate blood. Persons placed on 

chemoprophylactic therapy in readiness, but who did not travel into a 

malaria endemic area, do not have a required waiting period to donate 

blood.
67

APPENDIX ONE

INFORMATION & INTELLIGENCE SOURCES; 

CONSULTANTS

Introduction. Resources listed in this appendix for malaria and DNBI

prevention are divided into two general sections, Medical Information 

and Medical Intelligence. Directions on how to acquire information, 

references, or software are included along with points of contact and 

Internet/E-mail addresses. Some of the Medical Intelligence products 

listed are classified and require a security clearance for access.

I. MEDICAL INFORMATION

1. Military Sources

 A. General Policy and Guidance

• Bureau of Medicine and Surgery

Division of Occupational and Preventive Medicine 

(MED-24B) 2300 E Street NW

Washington, DC 20372-5300 

Phone: (202) 762-3495; DSN: 294-3495; 

FAX: (202) 762-3490

• Navy Environmental Health Center 

Preventive Medicine Directorate

2510 Walmer Ave

Norfolk, VA 23513-2617

Phone: (757) 462-5593; DSN: 253-5593 

FAX: (757) 444-9691, DSN 564-

E-mail: prevmed@med.navy.mil
68

 B. Navy Environmental & Preventive Medicine Units

 (NEPMUs), four world-wide:

• Navy Environmental & Preventive Medicine Unit 2

 Epidemiology Department, Norfolk, VA 

 Phone: (757) 444-7671; DSN 564-

 Fax: (757) 444-1191; DSN 564-

 E-mail: epi-nepmu2-nor@nepmu2.med.navy.mil 

• Navy Environmental & Preventive Medicine Unit 5

 Epidemiology Department, San Diego, CA

 Phone: (619) 556-7070; DSN 526-

 Fax: (619) 556-7071; DSN 526-7071;

 E-mail: nepmu5@nepmu5.med.navy.mil

• Navy Environmental & Preventive Medicine Unit 6

 Epidemiology Department, Pearl Harbor, HI

 Phone: (808) 473-0555; DSN 315-

 Fax: (808) 473-9361; DSN 315-

 E-mail: nepmu6@nepmu6.med.navy.mil

• Navy Environmental & Preventive Medicine Unit 7

 Epidemiology Department, Sigonella NAS, Sicily, Italy

 Phone: From US 011-39-095-56-3781;

 From Italy 095-56-3781; 

 From Europe 0039-095-56-3781; DSN 624-3781

 Fax: from US 011-39-095-56-4100; DSN 624-4100

 E-mail: sig1pmu@sig10.med.navy.mil

⇒ NEPMUs Publications and Services available:

∗ Pre-deployment medical briefings.

∗ Courses on malaria, hepatitis, field sanitation, etc. 

∗ Consultation with representative of Epidemiology 

Department.

∗ PPM – Entomologist.

 C. Navy Disease Vector Ecology and Control Centers 

 (DVECCs), two within CONUS: 

• DVECC, Jacksonville: P.O. Box 43, Bldg. 937, Naval Air 

Station Jacksonville, FL 32212-0043 (904) 542-2424; DSN 

942-

 E-mail: dvj0ccj@jax10.med.navy.mil 
69

• DVECC, Bangor: 19950 Seventh Ave. Poulsbo, WA 98370-

7405 (360) 315-4450; DSN 322- Email:postmaster@ndvecc.navy.mil 

⇒ DVECC Publications and services available:

∗ “VECTRAPS,” or vector reports, descriptions of 

disease vectors and control measures worldwide. 

∗ Information on pesticide usage and resistance and 

personal protective measures.

 D. Navy Infectious Diseases Consultants

• National Naval Medical Center

 Infectious Diseases Division

 8901 Wisconsin Ave

 Bethesda, MD 20889-5600

 DSN: 295-4237

 Phone: (301) 295-4237

 Fax: -2831

• Naval Medical Center

 Infectious Diseases Division

 620 John Paul Jones Circle

 Portsmouth, VA 23708

 Phone: (757) 953-5179

 Fax: -7674

• Naval Medical Center

 Infectious Diseases Division

 34800 Bob Wilson Drive Suite 201

 San Diego, CA 92134-1201

 DSN: 522-7475

 Phone: (619) 532-7475

 Fax: -7478/8798

 E. Naval Medical Research Units

• Naval Medical Research Institute

Director for Malaria Programs

12300 Washington Ave

Rockville, MD 20852

Phone: (202) 295-2079; DSN 295-2079; 

Fax: (202) 295-6171

E-mail: hoffmans@nmripo.nmri.nnmc.navy.mil 
70

• U.S. Naval Medical Research Institute No. 3

PSC 452, Box 5000 FPO AE 09835-0007 

(Cairo, Egypt)

 Phone: ask overseas operator for Cairo, 820727

• U.S. Naval Medical Research Institute No. 2 

Box 3, APO AP 96520

 (Jakarta, Indonesia)

Phone: ask overseas operator for Jakarta, 414-507

• U.S. Naval Medical Research Institute Detachment

American embassy Unit 3800, APO AA 34031-0008

(Lima, Peru)

Phone: ask overseas operator for Lima, 52-1560, 9662

Within U.S.: 011-51-14-52-1562, 9662

F. Walter Reed Army Institute of Research

• Division of Preventive Medicine (202) 782-1334; DSN 662-

• Travel Medicine Clinic (202) 782-1302/1312; DSN 662-

G. Preventive Medicine Recommendations for specific

operations 

• Available from the JTF or CINC Surgeon’s office, Fleet or 

Force Surgeon’s office, or the Navy Environmental and 

Preventive Medicine Unit assigned to the area of operation.

• If involved in the planning phase for a regularly recurring 

exercise, contact the cognizant NEPMU to obtain 

recommendations for specific operation.

H. Armed Forces Medical Intelligence Center. See Medical 

Intelligence section for description of AFMIC products including 

the Medical Environmental Disease Intelligence and 

Countermeasures CD-ROM (“MEDIC”).

2. Civilian Sources

 A. Sources for Individual Travelers. These are commercial, 

computer-based, medically oriented travel risk information and 

recommendation services which are updated regularly.

• TravaxTM Shoreland, Inc. P.O. Box 13795 Milwaukee, WI, 

53213-0795; (800) 755-2301; (414) 774-4600; Fax-4060
71

• Travel CareTM, Care Ware, Inc. 9559 Poole Street, La Jolla, 

CA, 92037; (619) 455-1484; Fax -5429

• Centers for Disease Control and Prevention: Fax 

Information Service for International Travel. To receive a 

document call (404) 332-4565, and follow the prompts. To 

get a directory, call the fax number and enter "document 

number 000005" when prompted by the voice menu. This 

service is available year round, 24 hours a day.

B. Internet Homepages And Other Computer Related 

Sources:

• NEHC Web page: http://www-nehc.med.navy.mil/

• CDC: http://www.cdc.gov/travel/ 

• American Society of Tropical Medicine and Hygiene 

(ASTMH): http://www.ASTMH.org/ 

• PROMED: Intended to be an increasingly sensitive aid for 

detection of outbreaks worldwide: http://www.fas.org 

/promed/

• Medical Matrix: Huge database listing hundreds of Internet 

available information sources: http://www.slackinc.com/ 

matrix/

• Shoreland Travel Health Information Service: 

http//www.shoreland.com

• National Library of Medicine: 

http://www.ncbi.nlm.nih.gov/PubMed

• Rollins School of Medicine at Emory University, Public 

Health Resources on the web: 

http://www.sph.emory.edu/PHIL/

3. Textbooks and Publications

A) Medical Products for Supporting Military Readiness: 

Vaccines & Drugs (“The GO Book”), Nov 1996, U.S. Army 

Medical Research & Materiel Command: Secretary of the 

General Staff, USA-MC, Fort Detrick, Maryland, (301) 619-

7111, DSN: 343-

B) Pocket Book of Infectious Disease Therapy, Bartlett JG,

Williams & Wilkins, 1996 

C) Control of Communicable Diseases Manual, Chin, ed., 

American Public Health Association, 17th Edition, 2000
72

D) Hunter's Tropical Medicine, Strickland, ed., Saunders, 7th 

Edition, 1991

e) Principles and Practice of Infectious Diseases, Mandell et. 

al., Churchill Livingstone, 4th Edition, 1995

F) Manson's Tropical Diseases, Cook, ed., Saunders, 1996

G) Wilderness Medicine, Auerbach, ed., Mosby, 1995

H) The Sanford Guide to Antimicrobial Therapy, Sanford, ed., 

Antimicrobial Therapy, Inc., yearly

II. MEDICAL INTELLIGENCE

A. AFMIC. The primary source of medical intelligence products is 

the Armed Forces Medical Intelligence Center (AFMIC), a 

division of the Defense Intelligence Agency, located at Fort 

Detrick, Maryland. Described are the medical intelligence 

products AFMIC provides:

• Medical Environmental Disease Intelligence and 

Countermeasures CD-ROM (“MEDIC”). “MEDIC” 

provides worldwide disease and environmental health risks 

hyperlinked to Joint Service approved country-specific 

countermeasure recommendations and other pertinent 

military medical references. Also included in “MEDIC” are 

military and civilian health care delivery capabilities, 

operational information, arthropod vector information, an 

expanded poisonous snake section on some countries, an 

expanded section on poisonous and injurious plants, and 

significant portions of Control of Communicable Diseases 

Manual (included by permission from the American Public 

Health Association).

• Infectious Disease Risk Assessment, (IDRA) and 

Environmental Health Risk Assessment, (EHRA). 

Infectious Disease and Environmental Health Risk 

Assessments are unclassified risk assessments on 

individual countries without countermeasure 

recommendations. They are available in three media: by 

message, via the AFMIC bulletin board system (BBS), and 

on the “MEDIC” CD-ROM. The most current assessments 

are available through the BBS, and each month some 

countries are updated through a cyclic update process. 

Assessments are oriented for and available only to 

operational U.S. military personnel. lDRAs and EHRAs 
73

were formerly known as the Disease and Environmental 

Alert Reports (DEARs). 

• Disease Occurrence Worldwide (DOWW). Classified 

and unclassified supplements to IDRAs and EHRAs. The

DOWW is a monthly compilation of reports on disease 

outbreaks which serve as late-breaking updates to the 

IDRA. DOWW is published as an unclassified message 

with a classified supplement if necessary.

• AFMIC Wire. A bi-weekly message serving as an update 

of infectious disease and environmental risks worldwide. 

AFMIC’s version of Headline News, it is a current 

intelligence document, which presents analysis of new 

information of potential tactical interest. In addition to the 

scheduled wire, “Special Wires” may be produced 

periodically on topics of interest to deploying units.

• Medical Capability Studies (MEDCAP). Information on 

foreign country assets and medical infrastructure. It 

evaluates the ability of a country to support its armed 

forces in peace and war, and the suitability of facilities in 

the country to support U.S. operations. These studies are 

produced on countries of tactical significance, usually 

those with power projection capability.

• Health Services Assessment (HSA). Health Service 

Assessments are comprehensive evaluations of a 

country's health infrastructure, and may be considered a 

short form of the MEDCAP. HSA evaluates a country in 

less detail, and is designed to provide an overview of a 

country’s civilian and military/health care systems to 

support operational planning. 

• Urban Area Medical Capabilities Study. The Urban 

Study was recently redesigned to meet the needs of 

United States Special Operations Command (USSOCOM). 

 It includes a map of the urban area, general health 

information, and locations, descriptions, and photographs 

of key medical treatment facilities.

• AFMIC Bulletin Board System (BBS). The BBS is an 

automated on-line system for the dissemination of 

unclassified medical intelligence products. This system is 

designed to provide timely, user friendly access to finished 

AFMIC products. All textual components of the “MEDIC”
74

are available on the BBS. The BBS System Operator may 

be reached at (301) 619-2686 or DSN 343-2686. The BBS 

may be accessed by dialing: (301) 619-3625 or 2000 or 

DSN 343-3625 or 2000.

• Request for Information (RFIs). An RFI is a way to ask 

AFMIC for answers to questions not found in published 

studies, usually requiring AFMIC to assemble specific 

information. The RFI system is designed to respond to 

requests for specific information on countries or areas 

worldwide, 24 hours per day, 7 days per week. RFIs 

should be directed to AFMIC through unit intelligence 

sections by way of the Community On-line Intelligence 

System for End-Users and Managers (COLISEUM) or by 

contacting AFMIC Operations at their 24 hour contact 

number, (301) 619-7574 or DSN 343-7574. Their phones 

are secure via STU-III through the TS-SCI level. 

Procedures for obtaining the AFMIC wire, the DOWW, 

the IDRA, and the EHRA. AFMIC produces the AFMIC 

Wire under Address Indicator Group (AIG) 6623 for CONUS 

plus Alaska & Hawaii, and under AIG 12630 for OCONUS 

not including Alaska & Hawaii. The DOWW, IDRA, and 

EHRA are transmitted under AIG 12243 for CONUS plus 

Alaska & Hawaii and AIG 11829 for OCONUS not including 

Alaska & Hawaii. To be added to distribution for any of the 

AFMIC message products, please send name, 

organization, mailing address, routing indicator, plain 

language address, DSN and commercial telephone 

numbers, and a brief justification to: 

AFMIC

ATTN: MA-1 

Frederick, MD 21702-5004 

or 

DIRAFMIC FT DETRICK MD//MA-1

AFMIC can be reached at (301) 619-3837 or DSN 343-3837 

for information.

⇒ Procedures for receiving hardcopy AFMIC products 

and other intelligence products. Hardcopy publications 

produced by AFMIC are disseminated by the Defense 

Intelligence Agency through the Defense Intelligence 
75

Dissemination System (DIDS). An organization receives 

products based on requirements registered by the 

organization’s Intelligence Office (IN) in a Statement of 

Intelligence Interest (SII). Largely, the SII is maintained by 

the IN or Security Office. Once a document is published 

by AFMIC, it is automatically mailed to the organization’s 

IN or Security Office for distribution within the organization.

Once an organization has an SII registered distribution 

for AFMIC hardcopy products, but is not receiving some 

publications, its IN can modify the SII by adding the 

desired Intelligence Function Codes (IFCs) and country 

codes for those publications.

If an organization does not have an SII registered with 

DIA, follow the procedures as outlined in DIA Regulation 

No. 59-1, dated 12 June 1995, “DoD Intelligence 

Dissemination Program.”

B. CIA World Factbook. The CIA World Factbook is an 

unclassified publication that provides general political and 

economic data on all countries of the world. It is updated annually 

and available as a hardcopy publication or through the Internet 

CIA home page. There is also a classified supplement that 

provides information on military, security, and intelligence forces 

worldwide.

C. Military Capabilities Study (MCS). The MCS is designed to 

serve as a ready reference document for national, operational, 

and tactical planners and consumers. Each study presents a 

compilation of intelligence on forces and resources that 

contribute to the military security of each country, and on the 

political and economic factors affecting the country’s military 

capabilities.

D. Intelink. This is the classified Internet system, and functions in 

the same manner as NetscapeR or Internet ExchangeR, and 

documents can be easily downloaded and printed. Within the 

intelligence community it is rapidly becoming the preferred 

method of dissemination of information. 

The ultimate goal is to have INTELINK available to all 

battalion level and higher intelligence sections. National level 

intelligence organizations, including each of the Unified 

Command Joint Intelligence Centers and AFMIC have home 
76

pages on INTELINK. All AFMIC products, and most recent 

intelligence publications, may be found there.

E. Internet Sites. There are a number of unclassified sources 

available. The Central Intelligence Agency has a home page 

where users may access the World Factbook. The State 

Department home page contains State Department country fact 

sheets, embassy information, and travel advisories. Other 

commercial databases are available which address travel 

medicine. Take time to find and bookmark useful resources.

F. Joint Worldwide Intelligence Communication System 

(JWICS). This secure telecommunications system links sites 

throughout the intelligence and operations communities, and 

allows secure teleconferencing. In support of time sensitive or 

complex requirements, it may be possible to arrange a 

teleconference between medical planners and AFMIC analysts. 

To arrange a conference, contact the unit intelligence officer to 

determine if a JWICS site exists and is available, then work with 

the local site manager and AFMIC Operations on specifics.
77

APPENDIX TWO

MOSQUITO VECTORS AND IDENTIFICATION

Introduction. Human malaria is transmitted only by mosquitoes 

belonging to the genus Anopheles. Currently 422 species of 

Anopheles mosquitoes have been identified throughout the world, 70 of 

which transmit malaria. Of the 70 species that transmit malaria, only 

40 are of major significance. 

Anopheles mosquitoes are most frequently found in tropical 

regions, but are also found in temperate climates and in the Arctic 

during summer (see Appendix Table 2.1). As a rule, they are not 

found at elevations above 2000-2500 meters (6500-8200 ft).

Mosquito Life Cycle. Development time from egg to adult depends 

on species and temperature, ranging from 7 days at an average 

temperature of 31OC, to 20 days at an average temperature of 20OC. 

Life span is species specific, and is affected by temperature, humidity, 

and presence of natural enemies. When the temperature is over 35OC 

or the humidity is less than 50%, longevity is greatly reduced. 

Average life span of a female mosquito under favorable conditions is 

10-14 days, with some able to live as long as 3-4 weeks.

Eggs. Females lay their first batch of eggs 3-6 days after they emerge 

from the pupal stage. Anopheline eggs are laid singly on the type of 

water preferred by the particular species. They are blackish, 0.5 mm 

long, and have tiny air-filled floats that let them drift on the water 

surface. Eggs hatch 2-3 days after being laid. 

Larvae. Anopheles mosquito larvae have unique characteristics. 

They lack the prominent air tube or siphon found in other mosquito 

species larvae. They float horizontally on the surface of the water, and 

turn their heads 180O to feed. They move in sudden jerks, and sink 

below the surface if disturbed. After molting three times, they develop 

into pupae.

Appendix Figure 2-1. Differences between Anopheles, Aedes, 

and Culex mosquitoes at various stages of development.
78

Anophelines Culicines

Anopheles Aedes Culex

Eggs

with floats, laid 

singly on water

no floats, laid singly 

on dry/ damp 

surface

no floats, laid in 

rafts on water

Larva

no air tube

rest parallel to water 

surface, head 

rotated 180o when 

feeding

one tuft on short 

stout air tube

rest at angle to 

surface, head not 

rotated

several tufts on 

slender air tube

rest at angle to 

surface, head not 

rotated

Adult

resting position

resting position resting position

Pupae. Mosquito pupae are comma-shaped. There are two separate 

body regions: the cephalothorax (the head and thorax combined), and 

the abdomen (tail section). They do not feed, but come to the water 

surface to breathe through short paired respiratory trumpets. The 

pupal stage lasts 2-4 days, after which an adult mosquito emerges.

Adults. In order for eggs to develop, female mosquitoes require at 

least one, sometimes two blood meals. Male mosquitoes do not take 

a blood meal. Adult mosquitoes typically fly and bite within a twothree kilometer radius of breeding areas but strong winds have carried 

them as far as 30km. Peak biting time is between 1900-2100 hours 

for some species while other species such as A. gambiae are late 
79

feeders, biting between 2400-0300 hours. Control methods should be 

targeted to coincide with peak biting times when possible. The resting 

posture of adult mosquitoes differs by species (see Appendix Figure 2-

1).

Appendix Table 2-1. Anopheles species of importance in 

transmission of human malaria.

Region Description Major Vectors

North America From Great Lakes to 

southern Mexico

A. freeborni

A. quadrimaculatus

A. hermsi

Central America

Southern Mexico, 

Caribbean islands, 

fringe of South 

American coast

A. albimanus

A. argyritarsis

A. pseudopunctipennis

A. aquasalis

A. darlingi

South America

South American 

continent

A. pseudopunctipennis

A. punctimacula

A. albimanus

A. albitaris

A. aquasalis

A. darlingi

North Eurasia Europe and west 

Asia, Arctic south 

excluding 

Mediterranean coast

A. atroparvus
80

Appendix Table 2-1, continued. Anopheles species of importance 

in transmission of human malaria.

Region Description Major Vectors

Mediterranean South coast of 

Europe, North coast 

of Africa

A. atroparvus

A. labranchiae

A. sacharovi

A. superpictus

Africa-Arabia Saharan Africa, North 

Arabian peninsula

A. pharoensis

A. sergentii

Sub-Saharan 

Africa

South Arabian 

peninsula, Ethiopia, 

Somalia, tropical 

Africa, Madagascar

A. funestus

A. arabiensis

A. gambiae

A. melas

A. merus

India-Iran Northwest of the 

Persian Gulf, Indian 

subcontinent

A. culicifacies

A. fluviatilis

Indochina Indochinese 

peninsula

A. dirus

A. maculatus

A. fluviatilis

A. minimus
81

Appendix Table 2-1, continued. Anopheles species of importance 

in transmission of human malaria.

Region Description Major Vectors

Malaysia Indonesia, Malaysian 

peninsula, Philippines, 

Timor

A. campestris

A. donaldi

A. letifer 

A. aconitus

A. balabacensis

A. dirus

A. flavirostris

A. leucosphyrus

A. maculatus

A. sundaicus

China Korea, Taiwan, Japan,

and the Coast of mainland 

China

A. anthropophagus

A. sinensis

Australia-Pacific Northern Australia, Papua 

New Guinea, islands 

west of 1750 east latitude

A. farauti type 1

A. farauti type 2

A. koliensis 

A. punctulatus
82

APPENDIX THREE

LABORATORY DIAGNOSTIC TECHNIQUES

Introduction. Despite development of serological techniques, 

conclusive diagnosis of malaria continues to be made through 

microscopic examination of peripheral blood smears. This is the only 

method that can differentiate among the four species of plasmodia that 

cause human malaria.

Thick Smears. Red blood cells are hemolyzed in thick smears; 

leukocytes and any malaria parasites present are the detectable 

elements. The hemolysis and slow drying that occur in thick 

smear preparation cause distortion of plasmodia morphology, 

making differentiation of species difficult. Thick smears are used 

to detect infection, and estimate parasite concentration.

Thin Smears. Thin smears are fixed with methanol, preventing 

hemolysis. Red blood cells are intact, and any Plasmodia

present are less likely to be distorted, and remain within 

erythrocytes. Identification of specific species is usually done 

using thin smears after detection of parasites on the thick 

smears. 

Navy Environmental & Preventive Medicine Units offer training 

classes on preparation of thick and thin smears and microscopic 

examination for diagnosis of malaria. This appendix summarizes thick 

and thin blood smear preparation for field reference. 

Drawing Blood

• Anytime malaria is suspected.

• Repeat if smears are negative.

• Maximum frequency: once per hour.

Obtaining Blood

• Fresh blood is required from either fingerstick or venous 

phlebotomy
83

• Follow universal precautions (gloves, hand washing, proper 

handling and disposal of sharp instruments and other materials 

contaminated with blood)

• Fingerstick Method:

1) Clean end of finger with disinfectant solution.

2) Wipe fingertip with sterile material (remove remaining 

disinfectant that may interfere with diagnostic process).

3) Pierce fingertip with sterile lancet.

4) Allow blood to flow freely, do not squeeze finger.

• For venous blood obtained in a vacutainer, use a pipette to apply 

a drop of blood to slide(s) for thick and thin smears

Slide Preparation (see Appendix Figure 3-1)

⇒ Thick Smear

5) Wipe away first drop of blood at fingerstick site. Then touch 

a clean microscope slide near one end to the next blood 

drop that forms.

6) Spread drop of blood with corner of another slide to make an 

area about 1 cm in diameter.

• This is the thick smear. Correct thickness is attained when 

newsprint is barely legible through the smear.

⇒ Thin Smear

7) Touch a new drop of blood (smaller than the first) with the 

edge of a clean slide.

8) Bring the edge of the slide with the new drop of blood to the 

surface of the first slide. Place it at the far end, and wait 

until the blood spreads along the whole edge.

9) Holding the slide at an angle of 450, push it forward with a 

rapid, gentle movement.

• For preparation of separate slides for thick and thin smears, 

use a second slide in step 4. 

• Dry the smears. Air dry, allowing 10 minutes for the thin 

smear and 30 minutes for the thick smear.

• Mark slide with patient identification and date and time of 

collection. This can be done using a pencil on the thin 

smear after it has dried.
84

Fixing Thin Smears

• After drying, only thin smears are fixed. Fixing is done using 

methanol in one of two ways:

10) Dip thin smear into methanol for 5 seconds.

11) Dab thin smear with methanol-soaked cotton ball. 

• Do not fix the thick smear. Even exposure of the thick smear to 

methanol fumes will prevent hemolysis and make it unreadable. If 

using the one slide method, prevent exposure of the thick smear 

to methanol or methanol fumes by carefully dipping or dabbing 

the slide, and gently blowing the fumes away from the thick 

smear area.

Staining Slides

Giemsa stain is available in the military supply system, and this 

staining method is presented. Preparation of Giemsa staining solution 

is done with buffered water and Giemsa concentrate. Do not shake 

the Giemsa concentrate as this will cause suspension of particulate 

matter in the stain resulting in artifacts on final slides. Formation of 

artifacts renders slides difficult to interpret. 

Preparation of Giemsa staining solution

1) Prepare buffered water solution, pH 7.2:

• Mix capful of buffering salts into 1000 ml of distilled water.

• Check pH. Titrate with sodium hydroxide (NaOH) solution 

until pH is 7.2.
85

Appendix Figure 3-1. Thick and Thin Blood Smear Preparation.

2) Prepare Giemsa staining solution by mixing:

• 1 part unshaken Giemsa stain concentrate.

• 9 parts buffered water.

Slide Staining with prepared Giemsa solution

• Place slides flat in a staining rack or other suitable surface.

• Cover with 1-2 ml of Giemsa solution.

• Let stand for 10 minutes.

• Gently rinse by “floating” excess stain off slide with buffered 

water; be careful not to wash the blood smear away.

• Rinse until no more stain is seen in solution.

• Dry smear side down, making sure that smear does not touch 

the slide rack or other surface used for drying.

Slide Preparation Pointers

• Clean microscope slides before use. Blood will spread cleanly, 

stain will adhere properly, and no artifacts will impede diagnosis.

• Do not fix slides with a heat source. If overexposed to heat, 

parasites are destroyed, and cannot be seen microscopically.

• Parasites stain best at pH of 7.2. Check stain pH for optimal 

staining.

• Filter the Giemsa stain. Removal of particles and residue will 

make slides much easier to interpret.

Step 1 Step 2

Step 3

Step 4 Step 5 Thick Smear

Thin Smear
86

Microscopic Examination of Thick and Thin Blood Smears

Training and experience are essential for accurate reading. Slides 

should be examined for at least 20 minutes before being judged to be 

free of malaria parasites. Parasites are often not readily apparent, and 

quick visual scans are insufficient for diagnostic purposes. Appendix 

Table 3-1 shows selected microscopic characteristics of human 

malaria species.

Part of the diagnostic process is estimation of the extent of 

infection. Two methods are presented to estimate the parasite 

concentration or parasitemia. One requires the use of thick smears, 

and is called the Absolute Numbers Method. The other requires the 

use of thin smears, and is called the Percent Method.

Absolute Numbers Method (thick smear)

This method is based on the assumption that 8000 leukocytes (white 

blood cells) are found in a ml of blood. By counting the number of 

parasites seen in same visual fields needed to count either 200 or 500 

leukocytes, the parasite concentration per ml can be estimated. 

Perform the following steps to estimate parasite concentration:

1) Examine the equivalent of 0.25 ml of blood (100 visual fields using 

a 7X ocular lens and a 100X oil-immersion objective lens) to 

determine if an infection exists.

2) In a systematic manner of scanning visual fields, identify 200 

leukocytes, while counting the number of malarial parasites in 

those same visual fields.

3) If after 200 leukocytes have been identified and less than 9 

malarial parasites have been counted, continue the process until 

500 leukocytes have been identified.

4) If after 200 leukocytes have been identified and 10 or more 

parasites have been counted, record the number of parasites 

counted per 200 leukocytes.
87

Appendix Table 3-1. Selected microscopic characteristics

Species Stages found in 

circulating 

Blood

Appearance of

Red Blood Cells

 Size Stippling

Plasmodium

falciparum

Trophozoites

Gametocytes

Normal Maurer’s dots or 

clefts 

infrequently 

seen 

Plasmodium

vivax

All: Schizonts 

Trophozoites

Gametocytes

Enlarged, 

Maximum size 

may be 1.5-2 

times normal

Schuffner’s dots 

may be present

Plasmodium

ovale

All: Schizonts 

Trophozoites

Gametocytes

Enlarged, 

Maximum size 

may be 1.25-

1.5 times 

normal

Schuffner’s dots 

may be present

Plasmodium

malariae

All: Schizonts 

Trophozoites

Gametocytes

Normal Ziemann’s dots 

rarely seen

5) Once 500 leukocytes have been identified, record the number of 

parasites counted.

6) Convert the parasite count per leukocytes identified into parasite 

concentration per ml with one of the following formulas:

 Number of parasites x 8000 = parasites per ml

 Number of leukocytes counted 

or

 if 200 leukocytes were counted:

Number of parasites counted x 40 = parasites per ml

or

 if 500 leukocytes were counted:

Number of parasites counted x 16 = parasites per ml 
88

Appendix Table 3-1. Selected microscopic characteristics 

(con’t)

Appearance of Parasites

 No. of

 Cytoplasm Pigment merozoites

Double dots in rings 

common, rings small 

and delicate

Black

Coarse and conspicuous 

in gametocytes

6-32

Avg. = 10-24

Ameboid trophs light 

blue, has irregular 

“spread out” 

appearance in troph 

stage 

Golden-brown, 

inconspicuous

12-24

Avg. = 16

Rounded, compact 

trophs, dark to 

medium blue, usually 

dense; Chromatin is 

large

Dark brown, 

conspicuous

6-14

Avg. = 8

Rounded, compact 

trophs, dark blue with 

dense cytoplasm;

band form trophs

occasionally seen

Dark brown, coarse, 

conspicuous

6-12

Avg. = 8

“Rosette” 

occasionally seen

7) All parasite species and forms are tabulated together. This 

includes both sexual (gametocytes) and asexual (trophozoites, 

merozoites) forms. 

Percent Method (thin smear).

This method estimates the percentage of red blood cells infected with 

malarial parasites. It is based on the number of red blood cells found 

parasitized on a thin smear, and is executed in the following manner:

1) Locate an area in the thin smear where red blood cells are close 

together but not touching.

2) Scan in a systematic method (use the microscope stage control 

to scan one “row” at a time).
89

3) Count the total number of red blood cells in each row. At the 

same time, tabulate the number of red blood cells parasitized.

4) Count a total of 300-500 red blood cells.

5) Divide the number parasitized by the total number counted and 

multiply the result by 100 to obtain a percentage estimate of red 

blood cells parasitized:

 Red Blood Cells parasitized X 100 = Percent of Red Blood

 Total Red Blood Cells counted Cells parasitized

6) If occasional parasites are seen when scanning the smear, but 

none are identified during the process of counting 300-500 red 

blood cells, a percentage value of less than 1% of red blood cells 

parasitized is assigned.

7) An estimate of less than 1% of red blood cells parasitized does 

not need to be refined, since no clinical predictive value is gained. 

 It is values of 2-3% or above that are of clinical concern.

Future Diagnostic Techniques

New, easy to perform serum serology techniques for malaria 

diagnosis are being developed. Two such methods, now approved by 

the FDA (ParaSightRF, Becton Dickinson, Sparks, MD; ICT Malaria 

P.fR, ICT Diagnostics, Sydney, Australia), are designed for easy 

performance in field situations, and require no laboratory experience 

and little training. Both tools detect P. falciparum serologically using 

enzyme linked immunosorbent assay (ELISA), with results in 10 

minutes. Clinical trials show these methods detect P. falciparum

infections at parasite blood concentration of greater than 40 parasites

per microliter (>40 parasites/μl).
90

APPENDIX FOUR

ANTIMALARIAL MEDICATIONS

Antimalarial drugs are divided into 4 classifications corresponding 

to their action on the different plasmodium life cycle stages in human 

hosts (see Table 5-1). The 4 classes are listed below:

1) Blood schizonticides attack plasmodia in red blood cells 

preventing or terminating the clinical attack.

2) Tissue schizonticides attack the exoerythrocytic forms in the 

liver. . 

3) Gametocytocidal drugs attack the gametocyte stage in red blood 

cells.

4) Hypnozoiticidal drugs kill dormant P. vivax or P. ovale

hypnozoites in liver cells. 

All common drugs used worldwide for treatment of malaria are 

discussed in this chapter. As with treatment of tuberculosis, multidrug treatment regimens are becoming necessary as drug-resistant 

strains emerge. The status, availability, effectiveness, dosage, and 

side effects of each are presented. Drugs are listed by generic name 

in alphabetical order and divided into three sections; 1) anti-malarial 

drugs available

Table 5-1. Antimalarial Drugs classified by action on Plasmodia

Life Cycle Stages

Drug Class Drugs

Blood Schizontocide Chloroquine, Quinine, Quinidine, 

Mefloquine, Halofantrine, 

Sulfonamides, Tetracyclines, 

Atovaquone, Artemisinin compounds

Tissue Schizontocide Primaquine, Proguanil, Pyrimethamine, 

Gametocidal Primaquine

Hypnozoitocidal Primaquine

through the military supply system; 2) Anti-malarial drugs available in 

the U.S., but not in the military supply system; and 3) Anti-malarial 
91

drugs under development or available in foreign countries. An important 

avenue of treatment is nasogastric administration of oral anti-malarial 

medications. If intravenous treatment in severe malaria patients is not 

possible, oral anti-malarial medications pulverized, mixed with water, 

and delivered via nasogastric tube are absorbed well and effectively. 

Dosage for nasogastric treatment is the same as the oral dose.

Section 1. Antimalarial Drugs Available in the Military 

Supply System

Chloroquine Phosphate

Status: FDA approved.

Availability: Currently available.

Product: A 4-aminoquinoline compound, chloroquine is a blood 

schizonticide active against P. vivax, P. malariae, and P. ovale. It has 

limited activity against most P. falciparum infections. 

Description: 500 mg (300 mg base) tablets for oral administration.

Effectiveness: Chloroquine phosphate is indicated for suppressive 

treatment and for acute attacks of malaria due to Plasmodium vivax, 

P. malariae, P. ovale, and susceptible strains of P. falciparum. It 

does not prevent relapse in patients with P. vivax and P. ovale 

infections, because it does not eliminate persistent liver stage 

parasites. Primaquine must be given to achieve radical cure

(elimination of dormant hypnozoites in liver cells). Because of the 

increasing frequency of parasite resistance to chloroquine, its use as a 

prophylactic is limited to Mexico, Central America, and limited areas 

of the Middle East.

Dose & Administration: For prophylaxis: One 500 mg tablet weekly 

beginning 2 weeks prior to departure to endemic areas and continued 

for 4 additional weeks upon return. 

For treatment: An initial dose of two 500 mg tablets followed by 

one 500 mg tablet in 6-8 hours, then a single 500 mg dose on each of 

two consecutive days for a total of five tablets (2,500 mg) in 3 days.

Side Effects: The most frequently observed side effects are 

gastrointestinal and include anorexia, nausea, vomiting, diarrhea, and 

abdominal cramps. Mild and transient headache, tinnitus, and 

deafness have been reported. Ocular reactions including blurred 

vision, and reversible interference with visual accommodation or 

focusing of vision may also occur. Long-term or high-dosage therapy 

may result in irreversible retinal damage. 
92

Chloroquine may cause hemolysis when administered to patients 

with G-6-PD deficiency, but reactions are not as severe as those seen 

with primaquine. G-6-PD deficient service members taking chloroquine

prophylaxis should be informed of side effects (see Chapter 6), and 

advised to seek medical evaluation if they occur. For severe reactions, 

an alternate prophylactic regimen should be provided.

Doxycycline Hyclate

Availability: Currently available.

Product: A widely used antibiotic useful as an anti-malarial primarily 

for prevention of P. falciparum infections.

Description: Available as 100mg tablets for oral administration.

Effectiveness: Doxycycline is indicated for the prophylaxis of malaria 

due to P. falciparum; it is less effective against P. vivax infections. It 

is effective against asexual, erythrocytic forms of P. falciparum, but 

not gametocytes of the sexual stage. It is also indicated for treatment 

of resistant strains of falciparum malaria.

Dose & Administration: For prophylaxis: One 100 mg tablet daily 

beginning 1-2 days prior to departure to endemic areas, daily during 

stay in the area, and continued for 4 weeks after departure. 

For treatment: Doxycycline (100 mg twice daily for 7 days) or 

tetracyline (250 mg four times daily for 7 days) given as part of a multidrug regimen is effective in areas with drug resistant strains of 

falciparum malaria. Most often used with mefloquine. 

Side Effects: Most frequently observed side effects include nausea

and epigastric distress; less frequent are incidents of diarrhea and 

vomiting. Stomach and esophageal ulceration has been reported. The 

frequency and severity of gastrointestinal side effects may be reduced 

by taking doxycycline with meals. Absorption of this drug is impaired 

by antacids containing aluminum, calcium, magnesium, iron, or 

bismuth subsalicylate. Monilial vaginitis and increased sensitivity to 

sun exposure are also common side effects.

Halofantrine (Halfan7)

Status: FDA approved for treatment only.

Availability: Currently available in the UK, not yet marketed in the 

U.S.

Product: A phenanthrenemethanol discovered and developed by 

Walter Reed Army Institute of Research, and subsequently codeveloped by SmithKline Beecham.
93

Description: 250 mg tablets, indicated for the treatment of mild to 

moderate malaria caused by P. falciparum and P. vivax in adults who 

can tolerate oral medication.

Effectiveness: Halofantrine is effective against chloroquine-sensitive 

and chloroquine-resistant P. falciparum. It is also effective against P. 

vivax and some multi-resistant strains of P. falciparum. There may be 

cross-resistance to mefloquine in certain endemic areas.

Dose & Administration for Treatment: 500 mg (250 mg tablets x 2) 

every 6 hours for three doses (total first course dose 1500 mg). 

Repeat this course of therapy in 7 days. Halofantrine should be taken 

on an empty stomach (no food 2 hours before or 2 hours after each 

dose).

Side Effects: Generally well tolerated. May cause gastro-intestinal

symptoms, including diarrhea. In doses higher than normal or when 

taken with food containing fat, can cause prolongation of QT interval. 

Prior treatment with mefloquine increases the likelihood of QT interval 

prolongation. Can lead to torsade-de-pointes in individuals with 

congenital prolonged QT syndrome.

Mefloquine HCl (LariamR)

Status: FDA approved.

Availability: Currently available.

Product: An anti-malarial drug effective against P. falciparum and P. 

vivax infections. 

Description: Available as 250 mg tablets.

Effectiveness: Mefloquine HCl provides improved prophylaxis against 

chloroquine-resistant strains of P. falciparum and P. vivax. However, 

P. falciparum strains resistant to mefloquine have been reported.

Dose & Administration: For prophylaxis: One 250 mg tablet weekly, 

beginning 2 weeks prior to departure to endemic areas, and continued 

for 4 additional weeks after departure.

For treatment: Five 250 mg tablets (15-25 mg/kg) given as a 

single oral dose. The drug should be taken with at least 8 ounces of 

water with meals or a snack.

Side Effects: The most frequently observed side effect is vomiting, 

(3% incidence). It has also been associated with the occurrence of 

neurologic and psychiatric events after both prophylactic and 

therapeutic use. Minor neurologic events include dizziness, vertigo, 
94

headache, decrease in sleep, visual, and auditory disturbances. 

Serious adverse events such as seizures, disorientation, and toxic 

encephalopathy have been reported after therapeutic doses in patients 

with predisposing medical history (epilepsy, alcohol and drug abuse, 

or psychiatric disorder). Neurologic side effects have an incidence of 

less than 1%.

Primaquine Phosphate

Status: FDA approved.

Availability: Currently available.

Product: An anti-malarial drug for elimination of persistent P. vivax 

and P. ovale liver stage parasites (hypnozoites). 

Description: Available as 26.3 mg (15 mg base) tablets for oral 

administration.

Effectiveness: Primaquine phosphate is indicated for cure and 

prevention of relapse of P. vivax and P. ovale malaria.

Dose & Administration: For treatment and terminal prophylaxis: 

One tablet daily for 14 days in individuals who are not G-6-PD

deficient. The primaquine regimen must overlap at least one dose of 

chloroquine. Therefore, primaquine must be started no later than 1 

week after the last dose of chloroquine. 

Current Navy guidance directs that G-6-PD deficient service 

members are not to be given primaquine. Therefore, if, in the future, 

use of primaquine in G-6-PD deficient service members is authorized; 

give three tablets as a single dose once a week for 8 weeks in G-6-

PDA- deficient individuals, or two tablets as a single dose once a week 

for 30 weeks in G-6-PDMed deficient individuals. 

Side Effects: The most frequently observed side effects include 

abdominal discomfort, nausea, headache, interference with visual 

accommodation, and pruritus. Methemoglobinemia is common, but 

rarely necessitates interruption of therapy. Leukopenia and 

agranulocytosis occur rarely. Do not use during pregnancy. If used for 

treatment in G-6-PD individuals, caution service members of possible 

side effects (see Chapter 6). If side effects occur, advise members to 

seek medical evaluation and treatment.

Quinidine Gluconate

Status: FDA approved for treatment of cardiac arrhythmias and 

intravenous treatment of severe malaria.

Availability: Currently available.
95

Manufacturer: Generic.

Product: Quinidine is a cinchona alkaloid, the dextrostereoisomer of 

quinine. Used to treat cardiac arrhythmia, it is now the drug of choice 

for intravenous treatment of chloroquine-resistant falciparum malaria as 

intravenous quinine is no longer available in the U.S.

Description: 80 mg/ml (55mg base /ml) intravenous solution available 

in 10 ml vials as quinidine gluconate.

Effectiveness: Very effective and safe for intravenous treatment of 

severe malaria. No reports of resistance in any strains of Plasmodia.

Dose & Administration: For prophylaxis: Not indicated. 

For treatment: Loading dose of 10 mg/kg (6.2 mg base/kg) given over 

1-2 hours, followed by continuous infusion of 1.2 mg/kg/hour (0.72 mg 

base/kg/hour) for 72 hours or until patient can swallow. Intravenous 

quinidine can safely be administered by monitoring EKG, blood 

pressure, and infusion speed; quinidine blood levels should be kept 

between 3-7 mg/L if monitored. Life-threatening arrhythmias are rare 

with proper doses, but infusion should be stopped temporarily if the 

EKG shows prolongation of the QRS interval by >50%, or if the QT 

interval is prolonged >50% of the preceding R-R interval. Hypotension 

may occur if infusion is too rapid. Loading dose is not indicated if 

patient started quinine, quinidine, or mefloquine treatment within the 

preceding 24 hours.

Side Effects: Quinidine is toxic to the heart if given too quickly or in 

too high a dose. EKG changes including prolonged QT intervals are 

common, but life threatening arrhythmias are rare if proper dosages 

are used. Most side effects are gastrointestinal in nature and include 

nausea, vomiting, abdominal pain, diarrhea, and rarely, esophagitis. 

Symptoms of mild to moderate cinchonism (ringing in the ears, 

headache, nausea, and impaired vision) may appear in sensitive 

patients after one dose of the drug. Less frequent side effects include 

urticaria, skin flushing with intense itching, and hypersensitivity

reactions of angioedema, acute asthmatic episode, and liver toxicity.

Quinine (QuinammR)

Status: FDA approved.

Availability: Currently available in the U.S. in tablet form only.

Product: The first successful compound for treatment of malaria, it 

has been available for three centuries. With the introduction of 
96

chloroquine, the use of quinine fell dramatically, but the widespread 

emergence of chloroquine-resistant P. falciparum has increased its 

use. The intravenous form was last available in the U.S. in 1991.

Description: Available as 130, 200, 260, 300, and 325 mg capsules, 

and 260 and 325 mg tablets that have a very bitter taste. Indicated for 

treatment of all forms of malaria in patients able to swallow tablets. 

Effectiveness: Acts rapidly against asexual erythrocytic stages of all 

four Plasmodium species that infect humans. There is resistance 

reported in the rural, northern mountainous area of Thailand and West 

Africa. Quinine should be used as part of a multi-drug regimen in 

those areas.

Dose & Administration: For prophylaxis: Not indicated.

For treatment: Adults: 600-650 mg 3 times a day for 7 days.

Children: 10 mg/kg 3 times a day for 7 days. 

Side Effects: Quinine has the poorest therapeutic-to-toxic ratio of all 

of the anti-malarial drugs. Side effects are collectively known as 

cinchonism and include ringing in the ears, decreased hearing, 

headache, nausea, vomiting, and mild visual disturbances. These side 

effects are all dose related and reversible. Less common side effects 

include urticaria, angioedema of the face, itching, agranulocytosis, 

hepatitis, and hypoglycemia in patients with high P. falciparum

parasitemia.

Section 2. Antimalarial Drugs Available in the United States but 

not in the Military Supply System

Atovaquone

Status: Atovaquone is available as MepronR in the U.S., and is FDA 

approved for treatment of Pneumocystis carinii pneumonia. It is now 

FDA approved for treatment of malaria.

Availability: Atovaquone was recently introduced in the combination 

drug MalaroneR (atovaquone and proguanil) for treatment of malaria. 

MalaroneR has been distributed in partnership with WHO under close 

supervision only to patients resistant to conventional malaria 

treatment. MalaroneR is now available in the U.S. for prophylaxis and 

treatment.

Product: An antiprotozoal agent that is a synthetic derivative of 

hydroxynaphthoquinone, and may exert its effect by selectively 

inhibiting electron transport in mitochondria. 
97

Description: MepronR (250 mg; intravenous solution,750 mg/5ml), 

MalaroneR (atovaquone and proguanil).

Effectiveness: Atovaquone is indicated in the acute treatment of mild 

to moderately severe Pneumocystis carinii pneumonia in patients who 

cannot tolerate co-trimoxazole. Recent trials have shown that a 3 day 

course of 1000 mg of atovaquone and 400 mg of proguanil had a cure 

rate of 87% for chloroquine-resistant falciparum malaria.

Dose & Administration: For prophylaxis: One tablet MalaroneR (250 

mg atovaquone and 100 mg proguanil) daily. For treatment: For 

malaria, 1000 mg per day for 3 days in daily combination with 400 mg 

of proguanil. Atovaquone should be administered with food. 

Side Effects. Atovaquone is well tolerated. Common side effects

listed in order of occurrence are rash, nausea, diarrhea, headache, 

fever, and vomiting. 

Hydroxychloroquine Sulfate (PlaquenilR)

Status: FDA approved for prophylaxis and treatment.

Availability: Currently available.

Product: Also a 4-aminoquinoline compound, hydroxychloroquine

sulfate has the same actions, effectiveness, and indications as 

chloroquine phosphate. 

Description: 200 mg (155 mg base) tablets. 

Effectiveness: Like chloroquine, it is a blood schizonticide active 

against P. vivax, P. malariae, P. ovale, but with limited activity against 

most P. falciparum infections. It does not prevent relapse in patients 

with P. vivax and P. ovale infections, and must be followed with 

primaquine to effect radical cure of these diseases. As with 

chloroquine, because of increased parasite resistance, 

hydroxychloroquine sulfate is considered most useful for prophylaxis in 

Mexico, Central America, and limited areas of the Middle East.

Dose & Administration: For prophylaxis: Adults: 2 tablets (400 mg) 

each week beginning 2 weeks prior to exposure, and continued for 4 

weeks after leaving endemic area. If unable to begin two weeks prior, 

an initial double (loading) dose of 4 tablets (800 mg) may be taken in 2 

doses 6 hours apart. Children: Administration same as adults; 

dosage is 5 mg base/kg each week, not to exceed the adult dosage 

regardless of weight. If unable to begin prophylaxis 2 weeks before 

exposure, give an initial double (loading) dose of 10 mg base/kg in two 

doses 6 hours apart.
98

For treatment: Adults: Initial dose of 4 tablets (800 mg) followed by 2 

tablets (400 mg) in 6-8 hours, then 2 tablets (400 mg) on the next 2 

days for a total dose of 10 tablets (2000 mg). Children: Four doses 

as follows; dose 1: 10 mg base/kg; dose 2: 5 mg base/kg 6 hours 

after dose 1; dose 3: 5 mg base/kg 18 hours after dose 2; dose 4: 5 

mg base/kg 24 hours after dose 3.

Side Effects: Usually well tolerated. Side effects reported include 

mild and transient headache, dizziness, and gastrointestinal

complaints of diarrhea, loss of appetite, nausea, abdominal cramps, 

and rarely, vomiting.

Pyrimethamine/Sulfadoxine (FansidarR)

Status: FDA approved for treatment only.

Availability: Currently available.

Product: A combination drug containing the DNA synthesis inhibitors 

pyrimethamine and sulfadoxine. Each blocks a different enzyme in 

the synthesis of DNA from guanosine triphosphate.

Description: A tablet containing 25 mg pyrimethamine and 500 mg 

sulfadoxine.

Effectiveness: FansidarR is useful as an alternative treatment of 

chloroquine-resistant falciparum malaria. It is also often used to treat 

suspected malaria cases in areas where persons developing malaria 

symptoms cannot obtain prompt medical evaluation. It once was used 

as a weekly prophylaxis, but caused frequent, severe allergic 

reactions. In 1984, American travelers who took FansidarR in Kenya 

were as likely to die from FansidarR toxicity as from malaria.

Dose & Administration: For prophylaxis: Not indicated. For 

treatment: Adults: 3 tablets in a single dose. Children: 1⁄4 tab in 

those < 1 year old, 1⁄2 tab in children 1-3 years old, 1 tab in children 4-

8 years old, 2 tabs in adolescents 9-14 years old, 3 tabs in those >14 

years old. All treatments, adult and children, are single dose.

Side Effects: Fatalities have occurred due to severe reactions, 

including Stevens-Johnson syndrome and toxic epidermal necrosis in 

persons using FansidarR as a prophylaxis. No fatal reactions have 

been reported when it has been used for treatment (3 tablets in a 

single dose). Adverse reactions, rare when FansidarR is used for 

treatment, include urticaria, serum sickness, itching, conjunctival or 

scleral injection, nausea, vomiting, headache, and drug fever.
99

Section 3. Antimalarial Drugs under development or Available 

in Foreign Countries

Artemisinin

Status: Under investigation. 

Availability: Currently used in China and the Far East, not available 

in the U.S. 

Product: A sesquiterpene lactone derived from the Chinese 

wormwood plant Artemesia annua, artemisinin has long been used to 

treat febrile illnesses in China. There it is known as “qinghaosu.” 

Description: Artemisinin compounds can be administered enterally, 

intravenously, or intramuscularly. In China, the drug has been used in 

the following forms: 

Artemisinin suppositories represent a major advantage in treating 

severe malaria in patients unable to tolerate oral medications in 

situations where injections cannot be given. They have proved effective 

in cerebral and other severe falciparum infections. Sodium artesunate 

is a powder that is reconstituted just before intravenous injection. 

Artesunate is the tablet form, and has been efficacious in treatment of 

uncomplicated falciparum malaria. Artemether is the form used for 

intramuscular injection, and is given in an initial loading dose of 200 

mg, followed on the subsequent 6 days with a dose of 100 mg.

Effectiveness: Artemisinin compounds are blood schizonticides 

effective against parasites resistant to chloroquine and quinine. In a 

trial in Thailand, artensuate tablets (100 mg initial dose, followed by 50 

mg q 12 hrs for 5 days) combined with mefloquine (750 mg initial dose 

followed by 500 mg after 6 hrs), proved effective in curing adults with 

uncomplicated falciparum malaria and were more effective than

artensuate or mefloquine given alone. 

Dose & Administration: For prophylaxis: Not indicated. For 

treatment: Expected to be effective against all forms of human 

malaria, particularly severe and complicated falciparum malaria where 

rapid effects on parasites are needed. Dosage of each is under 

investigation. 

Side Effects: No severe adverse effects have been reported in clinical 

trials by over 4,000 patients. Mild adverse effects include transient 

first-degree heart block, mild decreases in reticulocyte and neutrophil 

counts, elevated liver transaminases, abdominal pain, diarrhea, and 

drug fever. 
100

Proguanil (Paludrine)

Status: Not approved by the FDA for use.

Availability: Available outside the U.S. 

Product: Proguanil is an antifolate agent, and was the first agent 

found to inhibit dihydrofolate reductase (an enzyme important in DNA 

synthesis) in plasmodia. It was also recently released as part of the 

combination drug MalaroneR (Atovaquone and Proguanil).

Description: 100 mg tablets.

Effectiveness: It is useful as a prophylactic agent against P. 

falciparum and P. vivax. It acts too slowly to be used alone for 

treatment of acute malaria, but has been used successfully as part of 

multi-drug regimens for treatment of uncomplicated malaria. See 

description of atovaquone for further information.

Dose & Administration: For prophylaxis: 200 mg daily, alone or in 

combination with chloroquine. For treatment: Useful in multi-drug 

regimens. MalaroneR(atovaquone and proguanil) given for 3 to 7 days 

has had success in treatment of P. ovale, P. malariae, and multi-drug 

resistant P. falciparum. 

Side Effects: Very safe at daily dosage levels. Side effects of 

nausea, vomiting, abdominal pain, and diarrhea have been experienced 

at higher dosages.

Pyrimethamine/dapsone (MaloprimR or DeltaprimR)

Status: Not released in the U.S.

Availability: The combination drugs MaloprimR and DeltaprimR are 

available in the UK. Pyrimethamine and dapsone are available as 

individual products in the U.S., but not as combined formulations.

Product: A combination drug containing pyrimethamine and dapsone.

Description: 25 mg pyrimethamine and 100 mg dapsone used as 

malaria prophylaxis.

Effectiveness: Often prescribed in the UK for suppressive treatment 

of malaria due to P. vivax, P. malariae, P. ovale, and P. falciparum. 

Though toxicity is very uncommon, hemolysis and 

methemoglobinemia limit the use of this drug. Risk of aplastic anemia 

limits use for prophylaxis when alternatives are available.

Dose & Administration: For prophylaxis: 1 tablet weekly. For 

treatment: Not indicated.

Side Effects: Hemolytic anemia, aplastic anemia, 

methemoglobinemia, Heinz body formation, and bone marrow

suppression. Contraindicated in persons with G-6-PD deficiency.
101
102

Intravenous Quinine 

Status: FDA approved.

Availability: Not available in the U.S. CDC stopped supplying 

intravenous quinine in 1991.

Product: See description in section 1.

Description: Intravenous concentrations vary, check when formulating 

intravenous solution for treatment. 

Effectiveness: Acts rapidly against asexual erythrocytic stages of all 

four Plasmodium species that infect humans. 

Dose & Administration: For prophylaxis: Not indicated.

For treatment: Adults: Loading dose of 20 mg salt/kg given over 4 

hours, then followed in 8-12 hours by 10 mg salt/kg given over 4 hours 

every 8-12 hours until patient can swallow and tolerate oral medication.

Children: Loading dose of 15 mg salt/kg given over 2 hours, then 

followed in 8-12 hours by 10 mg salt/kg given over 2 hours every 12 

hours until patient can swallow and tolerate oral medication.

Side Effects: Hypoglycemia is the most common severe side effect 

of quinine during treatment of malaria. When quinine is being given 

intravenously, blood glucose levels should be monitored. If there is 

any change in mental status, hypoglycemia should be suspected. 

See section 1 for description of other side effects. 

WR 238605 (Tafenoquine)

Status: Under investigation.

Availability: Clinical trials only.

Product: This is a new 8-aminoquinoline developed by Walter Reed 

Army Institute of Research now undergoing clinical trials.

Description: Not applicable.

Effectiveness: Similar in structure to primaquine, in initial tests it 

appears to be 10 times more active than that drug. It is a tissue 

schizonticide and has shown some blood schizonticide activity.

Dose & Administration: Pending. It is being developed as a less 

toxic alternative to primaquine to be used for radical cure of P. vivax

and P. ovale malaria. It is under consideration for potential use for 

malaria prophylaxis.

Side Effects: There are currently no data on the relative toxicity of 

this drug compared to primaquine in G-6-PD deficiency.
103

APPENDIX FIVE

SUPPLIES AND TRAINING AIDS

Following is an extensive list of useful items available through the 

Federal Supply System for personal protection, chemoprophylaxis, 

and treatment of malaria. Special circumstances (i.e., new drug 

development, new patterns of drug resistant plasmodia, significant 

product improvement, items required due to unique deployment or 

geographical contingencies) may necessitate purchase of civilian 

products. The nearest Navy Environmental and Preventive Medicine 

Unit or Navy Disease Vector Ecology and Control Center are excellent 

and knowledgeable sources of advice regarding such situations. 

Personal Protection Supplies

NSN ITEM

6840-00-753-4963 Insect repellent, clothing and personal, 75 percent 

DEET, 2 ounces

6840-01-067-6674 Insecticide, D-phenothrin, 2 percent

6840-01-278-1336 Insect repellent, clothing, Permethrin

aerosol, 6 ounce can

6840-01-284-3982 Insect repellent, personal, 33 percent DEET, 

2 ounces

7210-01-010-2052 Insect Bar (netting), cot type

7210-00-267-5641 Poles, insect bar (for suspending insect bar)

8415-01-035-0846 Parka, fabric mesh, insect repellent (DEET

jacket) – size small

8514-01-035-0847 Parka, fabric mesh, insect repellent (DEET

jacket) – size medium
104

8514-01-035-0848 Parka, fabric mesh, insect repellent (DEET

jacket) – size large

8415-00-935-3130 Head net, insect

Antimalarial Drugs

6505-00-117-6450 Chloroquine phosphate tablets, 0.5 gm, 

500’s

6505-00-913-7905 Chloroquine/Primaquine phosphate tablets, 

individually sealed, 150’s

6505-00-299-8273 Primaquine phosphate tablets, 1000’s

6505-01-132-0257 Pyrimethamine-sulfadoxine (FansidarR) 

tablets, 25’s

6505-00-957-9532 Quinine sulfate, 325 mg capsules, 100’s

6505-01-095-4175 Doxycycline, 100 mg tablets, 50’s

6505-01-078-3717 Chloroquine hydrochloride, injection

6505-00-864-6298 Quinidine gluconate, injection

6505-01-107-1480 Mefloquine hydrochloride, tablets 100’s (after 

stock depleted refer to next stock number)

6505-01-315-1275 Mefloquine hydrochloride, tablets, 25’s (use 

this stock number after previous stock 

number is depleted)

Training Aids

1. Bench Aids for the Diagnosis of Malaria. A set of eight 

glossy plates, available from World Health Organization 

Publications Center USA, 49 Sheridan Avenue, Albany, NY 

12210. (518) 436-9686. Cost is less than $15.00, which 

includes shipping and handling.

2. Audiovisual Aids

a) 801472 DN – Vector-Borne Diseases: Our Constant Enemy.
105

b) 802373 DN – Malaria Prevention

c) 504463 DD – Disease Vector Surveillance and Control in Arid 

Regions (Still in Development)

d) 802372 DN – Insect Repellent: Do It Yourself Protection 

From Vector-Borne Disease. (Still in Development)
106

APPENDIX SIX

GLOSSARY

anemia - decrease in number of red blood cells and/or quantity of 

hemoglobin. Malaria causes anemia through rupture of red blood cells 

during merozoite release. 

anorexia – lack of appetite, lack of desire or interest in food.

arthralgia – pain or aching of the joints.

chemoprophylaxis – method of disease prevention by taking specific 

medications. Malaria chemoprophylaxis requires drugs to be taken 

before, during, and after exposure. Very effective, but not absolute 

because of drug resistance and poor compliance. Chemoprophylaxis

is also called “suppressive treatment.”

cinchonism – side effects from quinine or quinidine, reversible with 

lower dosages or termination of the drugs. Effects include tinnitus, 

headache, nausea, diarrhea, altered auditory acuity, and blurred vision. 

 The term derives from cinchona bark, the natural source of quinine.

clinical cure – elimination of malaria symptoms, sometimes without 

eliminating all parasites. See “radical cure” and “suppressive cure.”

coma – decreased state of consciousness from which a person 

cannot be aroused. See “Glasglow coma scale,” Table 4-5 in Chapter 

4, page 46.

cure – see “clinical cure,” “radical cure,” and “suppressive cure.”

cyanosis, cyanotic – physical sign where the skin appears blue, 

caused by lack of oxygen.

delirious – mental state characterized by confusion and agitation. 

Delusions and hallucinations may also be present.
107

D.O.T. (directly observed therapy) – most effective method of ensuring 

drug compliance, where drug administration is observed by an 

appointed authority.

dyspnea – shallow, labored breathing.

eosinophilia – an increased number of eosinophils, a type of white 

blood cell. Greater than normal numbers of eosinophils are often 

associated with parasitic infections, but not malaria.

erythrocyte – a red blood cell.

erythrocytic stage – the malaria parasite’s life cycle when infecting 

and developing within red blood cells.

exoerythrocytic stage – stage in plasmodia life cycle when 

developing in liver cells (hepatocytes).

fever paroxysm – see “paroxysm.”

fluid overload – a condition in which an excessive amount of IV fluids 

(crystalloids, blood products) has been administered. In severe 

episodes causes pulmonary edema.

fluid resuscitation – administration of IV fluids to correct a loss or 

decrease in blood volume. The loss may be actual, relative, or both. 

Actual loss of blood volume is due to hemorrhage, sweating, or 

diarrhea. Relative loss of blood volume occurs when the vascular 

system dilates, increasing total volume. Fluid resuscitation is done 

with a variety of IV fluids, such as normal saline, lactated ringers, 

dextrose solutions, and blood products.

flush – capillary dilation causing skin to appear reddish in color.

gametocyte – sexual stage of malaria parasites which form in red 

blood cells. Macrogametocytes (female) and microgametocytes

(male) form in individual erythrocytes, are ingested by female 

mosquitoes, and unite in the mosquito’s stomach. Characteristic 

diagnostic features of P. falciparum gametocytes include their 

crescent or banana shape, and their overshadowing of the morphology 

of infected red blood cells.

hematemesis – vomiting of blood which may be either acute and 

bright red; or old and clotted appearing as coffee grounds.
108

hematochezia – passing blood rectally; blood may appear bright red, 

or dark red-black, and is usually foul smelling and sticky.

hematocrit – the amount of blood consisting of red blood cells,

measured as a percentage. Measured after a blood sample has been 

centrifuged or allowed to settle. Normal hematocrit values: Males 39-

49%; females 33-43%.

hemoglobin – the protein in red blood cells which carries oxygen. 

Normal range of hemoglobin values: Males – 13.6 - 17.2 g/dl; Females 

– 12.0 – 15.0 g/dl (136-173 g/L and 120-150 g/L).

hemolysis – destruction of red blood cells. Malaria causes hemolysis 

when malaria parasites mature and rupture red blood cells they 

infected.

hepatocytes – liver cells.

hepatomegaly – enlarged liver. An unusual physical finding in 

malaria.

hyperpyrexia – high fever greater than 105o F (40.5o C).

hyperthermic - elevated temperature. 

hypnozoite – a stage of malaria parasites found in liver cells. After 

sporozoites invade liver cells, some develop into latent forms called 

hypnozoites. They become active months or years later, producing a 

recurrent malaria attack. Only P. vivax and P. ovale species that 

infect humans develop latent stage hypnozoites. Primaquine is the 

only available drug active against hypnozoites.

hypoglycemia – blood glucose less than the lower value of normal 

(70-110 mg/dl [3.9-6.1 mmol/L in SI reference units]). Glucose levels 

of 40 and below constitute severe hypoglycemia, a life-threatening 

emergency. Hypoglycemia is common in malaria, as malaria 

parasitized red blood cells utilize glucose 75 times faster than 

uninfected cells. In addition, treatment with quinine and quinidine

stimulate insulin secretion, reducing blood glucose.

hyponatremia – serum sodium less than the normal lower limit, 

which is 135-147 mEq/L (135-147 mmol/L in SI reference units). 

Serum sodium levels approaching 120 and below constitute severe 
109

hyponatremia, a medical emergency. Hyponatremia can be seen in 

malaria, and is indicative of complicated malaria.

hypotension – see “orthostatic hypotension.”

icterus – yellow discoloration of the eyes due to an elevated bilirubin. 

Faint discoloration is seen when bilirubin blood levels rise to 2.5-3.0 

mg/dl (43-51 mmol/L in SI reference units). Often identified as scleral

icterus, because the sclera or “whites“ of the eyes turn yellow.

immunity – the body’s ability to control or lessen a malaria attack 

with antibodies and other protective reactions developed in response to 

previous malaria attacks. Semi-immune individuals live in malaria 

endemic areas and are repeatedly infected. Immunity developed does 

not prevent or cure malaria attacks, but controls the attack, minimizing 

symptoms. Such individuals typically have low blood levels of malaria 

parasites.

incubation period – time period beginning when malaria parasites

are injected by a mosquito bite, ending when symptoms develop. 

Incubation periods range from 7 to 40 days, depending on species.

jaundice – yellow discoloration of skin and eyes due to elevated blood 

levels of bilirubin. 

leukocytosis – total white blood cell count greater than 11,000 per 

cubic millimeter. Leukocytosis refers specifically to elevation in the 

number of polymorphonuclear leukocytes, which make up the majority 

of white blood cells. 

leukopenia – total white blood cell count of less than 5,000 per cubic 

millimeter. Leukopenia refers specifically to a reduction in the number 

of polymorphonuclear leukocytes, which make up the majority of white 

blood cells. 

lymphadenopathy – enlarged lymph nodes, which can be detected 

by physical examination. Lymphadenopathy is not a usual physical 

finding in malaria.

malaise – subjective feeling of being sick, ill, or not healthy. The 

feeling is generalized, varying from mild to severe in intensity. It may 

be the lone clinical manifestation of malaria, or may accompany other 

signs and symptoms.
110

merozoite – the end product of the asexual reproductive stage 

(schizogony) of the malaria parasite life cycle. Merozoite maturation 

takes place in erythrocytes or hepatocytes. Schizogony in 

erythrocytes ends in their rupture, releasing merozoites which infect 

other red blood cells. Schizogony in liver cells culminates in their 

rupture and merozoite release, which infect red blood cells. In P. vivax

and P. ovale infections, released merozoites can also infect other liver 

cells and develop into hypnozoites.

myalgia – muscle pain or ache.

obtunded – mental state in which reaction to stimuli is dulled or 

blunted, such as persons with severe alcohol intoxication.

oliguria – decrease of urine production.

oocyst – cysts located in the outer stomach wall of mosquitoes, 

where sporozoite development takes place. When mature, the 

oocysts rupture and release sporozoites. Sporozoites subsequently 

migrate to salivary glands, and get injected into the host when 

mosquitoes feed.

orthostatic hypotension – decrease in blood pressure occurring 

when an individual arises from a seated or lying position. A small 

decrease in blood pressure is normal, but large decreases are 

abnormal, especially if accompanied by clinical manifestations such 

as faintness, light-headedness, dizziness, or increased pulse. 

Orthostatic hypotension is a common finding in patients with malaria 

infections.

parasitemia – level of malaria parasites in blood. If no fever or other 

symptoms except for an enlarged spleen accompany finding of malaria 

parasites in blood, the condition is referred to as “asymptomatic 

parasitemia.”

paroxysm – a sudden attack or increase in intensity of a symptom, 

usually occurring in intervals. Malaria is classically described as 

producing fever paroxysms; sudden severe temperature elevations 

accompanied by profuse sweating. However, fever paroxysms are 

rarely exhibited in the majority of malaria cases in non-immune 

persons, while semi-immune local inhabitants are more likely to have 

them. Therefore, diagnosis should not be based on this finding in U.S. 

military personnel.
111

petechiae – small red or purple skin macules, usually 1-3 mm in 

diameter. They are manifestations of small subcutaneous bleeds and 

seen in minor trauma, when the platelet count is very low, or in clotting 

defects. They are also caused by immune complex deposits in the 

skin.

petechial rash – grouping of petechiae.

presumptive treatment – administration of anti-malarial drugs in 

suspected cases before results of laboratory tests are available to 

confirm diagnosis.

prophylaxis – see “chemoprophylaxis.”

prostration – a state characterized by an extreme loss of strength.

pulmonary edema – accumulation of fluid in lung alveoli due to 

leakage, resulting in difficulty breathing. It is generally due to 

breakdown of stability of membranes lining alveolar spaces and/or fluid 

overload.

QT interval - measured from the beginning of the QRS to the end of 

the T wave, it represents total duration of ventricular systole. As a rule 

of thumb, it should be less than 50% of the preceding R-R interval. A 

prolonged QT interval indicates delayed repolarization of ventricular 

myocardium. Development of serious ventricular tachyarrhythmias (R 

on T phenomenon), syncope, and sudden death are possible under 

this condition.

radical treatment – treatment intended to achieve cure of P. vivax or 

P. ovale malaria. Requires primaquine treatment, which destroys 

latent exoerythrocytic stage parasites (hypnozoites).

radical cure – complete elimination of malaria parasites from the 

body, specifically hypnozoites.

rales – crackling sounds heard at end inspiration during lung 

auscultation. An abnormal physical finding.

RBC – red blood cell.

recrudescence – a repeated attack of malaria (short term relapse or 

delayed), due to the survival of malaria parasites in red blood cells. 

Characteristic of P. malariae infections.
112

recurrence – a repeated attack weeks, months, or sometimes years, 

after initial malaria infection, also called a long-term relapse. Due to 

re-infection of red blood cells from malaria parasites (hypnozoites) that 

persisted in liver cells (hepatocytes).

relapse – a repeat attack of malaria.

resuscitation – see “fluid resuscitation.”

rigor – severe chill, characterized by shaking of the body.

sallow – pale, reddish-yellow in color.

schizogony – asexual reproductive stage of malaria parasites. In red 

blood cells, schizogony entails development of a single trophozoite 

into numerous merozoites. A similar process happens in infected liver 

cells.

scleral icterus – see “icterus.”

splenomegaly – an enlarged spleen. A common finding in malaria 

patients that sometimes can be detected by physical examination.

sporozoite – stage of malaria parasites injected into the bloodstream 

by biting infective mosquitoes. Sporozoites infect liver cells,

disappearing from bloodstream within 30 minutes.

stuporous – mental state characterized by lack of awareness of one’s 

surroundings.

suppressive treatment – treatment intended to prevent clinical 

symptoms or parasitemia through destruction of parasites in red blood 

cells. It does not prevent or eliminate malaria infection as parasites 

may persist in the liver and produce a relapse after drug therapy is 

stopped. Suppressive treatment is also called “chemoprophylaxis.”

tachycardia – increased heart rate, defined as greater than 100 beats 

per minute.

tachypnea - increased respiratory rate defined as greater than 20 

breaths per minute.

thrombocytopenia – low platelet count, defined as less than 

150,000. Low platelet counts can lead to impaired blood clotting, and 

counts below 50,000 increase the risk of spontaneous bleeding. 
113

Thrombocytopenia is typical in malaria, though spontaneous bleeding 

is rare.

tinnitus – ringing sound in the ears, a common side effect of quinine

treatment.

treatment – see “presumptive treatment,” “radical treatment,” and 

“suppressive treatment.”

trophozoite – early developmental stage of blood schizont.

urticaria – hives. Numerous swellings in skin, ranging from many 

localized lesions a few mm to a few cm in diameter, to large blotchy 

irregular swellings.

vasodilation – increase in diameter of small vessels of the vascular 

system. Net result is often a decrease in blood pressure, which may 

be significant.
114

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APPENDIX ONE: Information & Intelligence Sources, 

Consultants

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APPENDIX TWO: Anopheles Vectors: Identifcation

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APPENDIX THREE: Laboratory Diagnostic Techniques

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Bennett JE, Dolin R, editors. Mandell, Douglas and Bennett’s 

Principles and Practice of Infectious Diseases, 4th Edition. New York: 

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U.S. Army Medical Research and Materiel Command; 1996.

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APPENDIX FIVE: Supplies and Training Aids

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Prevention and Control, 2nd Edition. Norfolk: Navy Environmental Health 

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APPENDIX SIX: Glossary

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121

INDEX 

abdominal pain, 28, 31, 48

Absolute Numbers Method, 86

acetominophen, 40

acute pulmonary, 32

acute renal insufficiency, 29, 35

acute tubular necrosis, 32

Administrative Responsibilities, 64

Adult Mosquito Surveys, 23

AFMIC Wire, 73, 74

altered consciousness, 31

aminoglycoside, 49

anemia, 5, 30, 33, 42, 48, 106

Annex Q, 58

Anopheles, 5, 6, 7, 12, 21, 23, 24, 26, 77, 78, 79, 80, 81, 119

Armed Forces Medical Intelligence Center, 60, 72

arrhythmia, 38

artemisinin, 44, 90, 99, 100

Atovaquone, 90, 97, 100

aviators, 15, 16

Babinski, 32

back pain, 28, 54, 55

Bed Nets, 14

Biological control, 24, 25

blackwater fever, 29, 48, 65

Blood Donor, 66

Blood schizonticides, 36, 90, 91, 98, 100, 102

blood smears, 27, 32, 45, 50, 62, 65, 82

brain, 31, 32, 33

breeding sites, 21, 22, 24, 25

Bureau of Medicine and Surgery, 67

carbon dioxide (CO2), 24

CDC, 71, 116

Cerebral Malaria, 32, 35, 46, 66
122

Chemoprophylaxis, 2, 11, 15, 16, 18, 27, 58, 59, 60, 61, 62, 64, 65, 

66, 103, 106, 113

children, 1, 19, 28, 33, 35, 38, 39, 42, 43, 44, 49, 96, 98, 99

chills, 5, 29, 30, 31

chloroquine, 16, 17, 19, 37, 38, 39, 44, 49, 53, 90, 91, 92, 93, 94, 95, 

96, 97, 100, 101, 104

chloroquine resistant P. falciparum, 16

Chloroquine-primaquine, 53

cinchonism, 96, 106

citronella, 12

Clinical Findings, 29

coma, 40, 42, 46, 47, 106

Commanders, 58, 59

compliance, 3, 12, 18, 55

complicated, 36, 39, 40, 42, 43, 45, 49, 100, 101

Convulsions, 35, 40, 42, 49

Corpsman, 59, 60, 61, 62

cough, 28, 31, 32

countermeasures, 2, 3, 10, 11, 20, 57, 58, 59, 60, 61, 62,70, 72

cyanosis, 28, 35, 106

DEET, 12, 14, 64, 103, 104

dehydration, 29, 48

diarrhea, 28, 31, 33, 35, 91, 92, 93, 96, 97, 98, 100, 101, 106, 107

Directly Observed Therapy, 15, 59, 107

dizziness, 28, 94, 98, 110

DNBI, 57, 58, 59, 60, 61, 62, 67

dormant, 3, 5, 6, 18, 33, 51, 90, 91

DOT, 15, 18, 59

DOWW, 73, 74

doxycycline, 15, 16, 17, 18, 19, 37, 38, 39, 43, 44, 92, 104

drowsiness, 35

drug resistance, 1, 7, 15, 39, 61, 117

DVECCs, 68, 68

eggs, 77, 78

ELISA, 89

entomologists, 21, 22, 24, 25, 26, 58, 61, 63, 68

Environmental Health Officers, 61, 62

eosinophilia, 30, 107

erythrocytes, 6, 82, 107, 110
123

Erythrocytic, 6, 7, 92, 96, 102, 107, 111

Exchange transfusion, 40, 48

Exoerythrocytic, 5, 6, 7, 36, 90, 107

exposure, 21, 33, 92, 106

falciparum malaria, 4, 6, 28, 31, 33, 34, 37, 47, 49, 65, 92, 95, 97, 99, 

100, 114

Fansidar, 37, 38, 39, 43, 44, 98, 99, 104

febrile, 6, 7, 27, 31, 34, 39, 50

fetal, 19, 49

fever, 5, 7, 28, 29, 30, 31, 32, 34, 35, 40, 48, 65, 97, 107, 108, 110, 

111

Flight surgeon, 61

Folic acid, 56

force protection, 57

furosemide, 47, 48

G-6-PD, 3, 18, 19, 33, 42, 44, 45, 51, 52, 53, 54, 55, 59, 64, 65, 92, 

94, 95, 101, 102, 118

Gametocidal drugs, 90

gastrointestinal, 18, 28, 33, 48, 91, 92, 95, 98

Giemsa, 84, 85, 86

Glasgow coma scale, 46

glomerulonephritis, 34

glucose, 29, 31, 32, 41, 42, 45, 46, 47, 102, 108

halofantrine, 37, 38, 43, 44, 49, 90, 93

headache, 5, 28, 29, 31, 32, 35, 91, 94, 96, 97, 98, 99, 106

Heinz bodies, 51, 52, 54, 101

hematocrit, 28, 33, 40, 42, 45, 48, 52, 54, 56, 108

hematopoesis, 33

hemodialysis, 32

hemoglobin, 28, 32, 42, 45, 51, 52, 54, 56, 106, 108

hemoglobinuria, 29, 33, 42, 52, 54, 56, 65

hemolysis, 28, 29, 32, 33, 48, 52, 53, 54, 56, 82, 84, 92, 101, 108

host, 6, 21, 23, 32, 34, 90, 110

HSA, 73

humidity, 8, 12, 77

Hydroxychloroquine, 16, 17, 97, 98

hyperparasitemia, 30

hypersensitivity, 44, 96

hyperthermic, 31, 108
124

hypnozoites, 6, 18, 34, 35, 36, 44, 49, 51, 90, 91, 94, 108, 110, 111, 

112

Hypnozoitocidal drugs, 90

hypoglycemia, 29, 32, 35, 41, 42, 46, 47, 49, 96, 102, 108

hypotension, 28, 31, 40, 42, 49, 95, 109, 110

hypovolemia, 48

ICT Malaria P.fR, 89

IDRA, 72, 73, 74, 75

impregnant, 13

inhabitants, 21, 25, 111

Insecticides, 12, 13, 24, 25, 26, 103

insulin, 29, 41, 47, 108

intravenously, 29, 32, 36, 40, 41, 44, 46, 47, 48, 49, 91, 95, 96, 97, 

99, 100, 102

kidneys, 28, 31, 33, 52, 56

knobs, 31, 33

Laboratory Personnel, 62

Landing Counts, 23, 24

larvae, 22, 23, 24, 25, 63, 77, 78

larvicides, 25

lateral decubitis position, 46

Letterman, 58

leukopenia, 28, 30, 95, 109, 111

life cycle, 1, 2, 5, 7, 8, 77, 90, 107, 110

Light Traps, 24

loss of appetite, 28, 31, 33, 35, 98

lysis, 30

macrogametocytes, 6, 7, 107

malaise, 28, 110

MalaroneR, 97, 100, 101

mannitol, 46

Marine Expeditionary, 59, 61

MEDCAP, 73

MEDIC, 10, 15, 70, 72, 74

Medical Board, 65, 66

medical intelligence, 3, 39, 60, 67, 70, 72, 74

medical officers, 58, 59, 60, 61

mefloquine, 15, 16, 17, 19, 38, 39, 40, 43, 44, 49, 61, 90, 92, 93, 95, 

100, 104

merozoites, 5, 6, 7, 18, 30, 31, 33, 36, 88, 106, 110, 112
125

microgametocytes, 6, 7, 107

microvascular, 30, 31, 32, 33

Military Supplies, 12, 13, 84, 91, 97

miscarriage, 35, 49

mosquito control, 21, 22, 23, 24, 58

MRI, 46

muscle aches, 28, 31

nasogastric, 39, 44, 46, 91

nausea, 18, 28, 29, 31, 33, 35, 91, 92, 94, 96, 97, 98, 99, 101, 106

Navy Health Environmental Center (NEHC), 65

Naval Medical Research Units, 69

Navy Environmental and Preventive Medicine Unit, 10, 15, 18,60, 62, 

64, 65, 70, 103

Netting, 13, 14, 20, 21, 64, 103, 104

neurologic, 29, 32, 46, 66, 94

obtunded, 110

ookinetes, 7

Orthostatic hypotension, 28, 110

oxidant, 33, 44, 51, 52, 53, 55

P. falciparum, 3, 5, 6, 7, 9, 16, 19, 27, 28, 29, 30, 31, 32, 33, 34, 35, 

39, 44, 48, 89, 91, 92, 93, 96, 98, 100, 107

P. malariae, 5, 6, 7, 30, 33, 34, 35, 37, 39, 91, 98, 101, 112

P. ovale, 3, 5, 6, 7, 18, 30, 33, 34, 35, 36, 39, 44, 49, 51, 90, 91, 94, 

98, 101, 102, 108, 110, 111

P. vivax, 3, 5, 6, 7, 18, 30, 33, 34, 35, 36, 39, 44, 48, 49, 51, 90, 91, 

93, 94, 98, 100, 101, 102, 108, 110, 111

ParaSightRF, 89

parasitemia, 27, 28, 30, 34, 35, 36, 39, 40, 42, 44, 46, 48, 86, 96, 110, 

112

parasites, 1, 6, 8, 15, 18, 27, 28, 30, 31, 32, 33, 34, 36, 40, 44, 45, 

47, 50, 66, 82, 85, 86, 87, 88, 89, 91, 94, 98, 100, 106, 107, 108, 

109, 110, 111, 112, 114, 117

paroxysm, 6, 7, 30, 31, 34, 107, 110, 111

Percent Method (thin smear), 88

Permethrin, 13, 14, 20, 26, 59, 64, 103

personal protective measures, 3, 4, 11, 12, 14, 20, 58, 59, 60, 61, 62, 

63, 64, 69, 103

Phenobarbital, 40, 46

phenytoin, 46

Plaquenil, 16, 17, 97
126

Plasmodium, 2, 5, 27, 31, 87, 90, 91, 96, 102, 107, 114, 115, 116, 

117, 119

pregnancy, 19, 29, 35, 49, 95

Preventive Medicine Officer, 61

Preventive Medicine Technicians, 61, 62, 63

primaquine, 3, 17, 18, 19, 33, 34, 42, 44, 45, 51, 53, 55, 56, 64, 65, 

90, 91, 92, 94, 98, 102, 104, 108, 111, 114

Proguanil, 17, 19, 90, 97, 100

Protective Clothing, 14

proteinuria, 29, 35

prothrombin time, 29

psychiatric, 16, 94, 95

pupae, 77, 78

Pyrimethamine, 37, 38, 39, 43, 44, 90, 98, 101, 104

qinghaosu, 44, 99

QT, 40, 93, 95, 111

quinidine, 29, 40, 41, 43, 44, 45, 47, 90, 95, 104, 106,

quinine, 29, 37, 38, 39, 40, 41, 43, 44, 47, 90, 95, 96, 97, 100, 102, 

104, 106, 108, 113

radical cure, 36, 44, 45, 49, 91, 98, 102, 106, 111

recrudescence, 34, 35, 112

relapse, 6, 7, 18, 33, 34, 35, 36, 44, 50, 51, 91, 94, 98, 112

Repellents, 12, 13, 14, 20, 103, 104, 105

reticulocyte, 28, 33, 34, 54, 100

reticulocytosis, 52, 30

rheumatoid factor, 29

rigor, 30, 112

RPR, 29

R-R, 95, 111

schizogony, 5, 6, 110, 112

schizonticides, 36, 40, 90, 91, 98, 100, 102 

scleral, 99, 109, 112

seizures, 16, 31, 32, 42, 46, 94

side effects, 16, 18, 64, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100, 

101, 102, 106, 113

Signs, 5, 27, 28, 30, 31, 35, 42, 54, 55

spleen, 28, 29, 34, 35, 48, 49, 52, 110, 112

splenomegaly, 5, 34, 112

sporogony, 7, 8

sporozoites, 5, 6, 7, 108, 110, 112
127

sulfadoxine, 37, 38, 39, 43, 44, 98, 104

surveillance, 3, 22, 23, 37, 59, 61, 62, 63, 105

sweating, 31, 35, 107, 111

symptoms, 5, 6, 18, 27, 28, 30, 31, 33, 34, 35, 39, 45, 52, 54, 55, 56, 

64, 93, 99, 106, 109, 110, 112

systolic, 40, 42

tachycardia, 28, 31, 113

terminal primaquine prophylaxis, 3, 18, 55, 64, 65, 94

tetracycline, 19, 37, 39, 44, 49, 90, 92

thick smears, 27, 83, 84, 85, 86

thin smears, 27, 62, 82, 83, 84, 85, 86, 88

thrombocytopenia, 28, 30, 113

Tissue schizonticides, 36, 44, 90, 102

transfusion, 5, 46, 48, 40, 49, 54, 56, 66

transmission, 1, 5, 8, 10, 21, 23, 24, 27, 35, 36, 39, 79, 80, 81, 82

trophozoites, 6, 87, 88, 112, 113

Ultra-low-volume (ULV), 25, 26

uncomplicated, 36, 37, 38, 39, 49, 100, 101

Uniform, 13, 14, 20, 59

Unit Protective Measures, 11, 20, 22

urinalysis, 29

urticaria, 96, 99, 113

VDRL, 29, 30

vector, 1, 6, 7, 8, 12, 20, 21, 22, 23, 24, 26, 59, 61, 62, 63, 65, 68, 69, 

72, 79, 80, 81, 103, 105, 115, 119

vector surveillance, 22, 59, 62, 105

ventricular fibrillation, 40

Vital signs, 45, 46

vomiting, 18, 28, 29, 31, 33, 35, 39, 91, 92, 94,96, 97, 98, 99, 101, 

107