USACHP

G

Oc

DISTRIBUTION RESTRICT

distribution is unlimited
INTENTIONALLY LEFT BLANK
 Walter Reed Army 

(http://wrair-www.a

 U.S. Army Resear

(http://www.usarie

 U.S. Army Medica

Diseases

(http://www.usamr

 U.S. Army Medica

(http://chemdef.ap

Global epidemiologic inform

selecting and appropriately 

herein was provided by the 

Center (http://mic.afmic.det

additional tools to U.S. mili

specific diseases in specif

Use of trademarked n

the U.S. Army but is in

of a specific product.
INTENTIONALLY LEFT BLANK
Approach to the Patie

Approach to the Patie

 (Pneumonitis) ------

Specific Diseases

Acute Eosinophilic Pn

Brucellosis -------------

Crimean-Congo Hemo

Dengue Fever and De

Filariasis ----------------

Hepatitis (Viral) --------

Leishmaniasis, Cutan

Leishmaniasis, Viscer

Leptospirosis-----------

Malaria ------------------

Meningococcal Diseas

Q Fever ------------------

Rabies -------------------

Relapsing Fever -------

Sand Fly Fever --------

Schistosomiasis, Acut

Streptococcal Infectio

Tuberculosis (TB) -----

Typhoid and Paratyph

Typhus, Endemic (Mu

Typhus, Epidemic (Lou

Tick Typhus ------------
Venezuelan Equine Encephalitis -------------------------- 12

Viral Hemorrhagic Fevers (VHF) --------------------------- 12

Decontamination ---------------------------------------------- 13

BW Agent Characteristics ---------------------------------- 13

BW Agents – Drug Therapy and Prophylaxis ----------- 13

PART THREE: EXPOSURE TO CHEMICAL WARFARE AGENTS

Chlorine --------------------------------------------------------- 13

Hydrogen Cyanide and Cyanogen Chloride ------------- 14

Mustard (Sulfur Mustard) ------------------------------------ 14

Nerve Agents (GA, GB, GD, GF, VX) --------------------- 14

Phosgene – Carbonyl Chloride ----------------------------- 15

PART FOUR: TOXIC INDUSTRIAL CHEMICALS (TICs)

Basic Principles ----------------------------------------------- 15

Irritant Gases -------------------------------------------------- 16

Corrosives ------------------------------------------------------ 16

Asphyxiants ---------------------------------------------------- 16

Organic Vapors [Hydrocarbons (HC) and Halogenated

 Hydrocarbons (H-HC)] ------------------------------------- 17

Cholinergics ---------------------------------------------------- 18

Respiratory Protection --------------------------------------- 18

Deployment Chemical Exposure Questionnaire ------- 18

Summary of Common Acutely Toxic Industrial

 Chemicals from Inhalation Exposure ------------------- 18
Cold Weather

Freezing Injury (Frostb

Non-Freezing Cold Inj

Hypothermia -----------

Heat

Heat Cramps -----------

Heat Exhaustion ------

Heat Stroke -------------

Preparation of 0.1 Per

PART SIX: DEPLOYMEN

Terminology ------------

Dermatologic Examina

Eczemas and Dermat

Acne and Related Dis

Papulosquamous Diso

Fungal Infections ------

Viral Infections ---------

Bacterial Skin Infectio

Growths (Cancerous a

Miscellaneous ---------

Referral and Telederm

Tips ----------------------
WORLD 30

H—TREATMENT GUIDELINES FOR SELECTED SKIN

CONDITIONS ------------------------------------------------- 30

I—EMERGENCY DERMATOLOGY HEALTH KIT ----------- 30

Glossary ------------------------------------------------------------- 30
INTENTIO

definitive source of medic

referred to the Armed Forc

(AFMIC) for the most curr

Diseases outlined herein 

primary care internal med

mentioning:

 Focus is on initia

of the hospital. A

worst-case evacu

distribution of this 

generally lack lab

supply of drugs, s

would be extraord

conditions, comp

mentioned to help 

clinical decisions 

and predictability 

 Determination of 

limitations are left 

of the information 

support.

 This is not a comp

countermeasures

patient or comma

available, military 

individual, small-u

USACHPPM We
part of daily practice in the continental United St

(CONUS) and would not be unique in the operati

setting (example: sexually transmitted diseases

(STDs)).

¡ Morbidity or epidemic potential of the diseases, 

in the acute phase, would typically not be great

(examples: intestinal helminth infections and hu

immunodeficiency virus infection).

¡ Medical management of the conditions is typica

conservative, with emphasis on self-care and uni

prevention strategies (examples related to cold w

operations: cold urticaria, chilblains, solar kerat

sunburn, and eczema).

¡ Immunity in U.S. military populations (including

vaccine-induced) is reliably universal (examples:

tetanus, diphtheria, measles, and poliomyelitis).

 Within categories that are covered, some specific dis

are not included even though it is possible they will b

encountered in the CENTCOM AOR. This was prima

the interest of prioritizing to keep the manual reasona

sized, and to minimize delays in revision and publica

Examples include West Nile encephalitis, tickborne

encephalitis, hemorrhagic fever with renal syndrome, 

Rift Valley Fever. Still, some of these are included in 

regarding differential diagnosis.
Ophthalmology: eye.consu

The following references ha

strongly encouraged that yo

deployment.

Chemical Exposure Guideli

U.S. Army Center for Health 

May 2003 with January 200

Control of Communicable D

P-5038), 18th Edition, Ame

Emergency War Surgery, Th

Handbook

Field Operations Guide for 

of Foreign Disaster Assistan

opment, 1998

Special Operations Medical 

Command & Center for Tota

Foundation, 2001

Medical Management of Ch

Medical Research Institute 

Ground, Maryland, July 200

Medical Management of Bio

Medical Research Institute 

Maryland, August 2004

Textbook of Military Medicin

Military Dermatology, Office 

the Army, August 2004
INTENTIONALLY LEFT BLANK
Specific Diseases

Acute Eosinophilic Pn

Brucellosis -------------

Crimean-Congo Hemo

Dengue Fever and De

Filariasis ----------------

Hepatitis (Viral) --------

Leishmaniasis, Cutan

Leishmaniasis, Viscer

Leptospirosis-----------

Malaria ------------------

Meningococcal Diseas

Q Fever ------------------

Rabies -------------------

Relapsing Fever -------

Sand Fly Fever --------

Schistosomiasis, Acut

Streptococcal Infectio

Tuberculosis (TB) -----

Typhoid and Paratyph

Typhus, Endemic (Mu

Typhus, Epidemic (Lou

Tick Typhus ------------
Crimean-Congo hemorrhagic fever (CCHF) and dengue

hemorrhagic fever (DHF) may not appear until at or near 

time of defervescence.
Look fo r h e m orrh a gic sign s:

B le e din g from ve n ipu n ctu re si

Pe te ch iae , pu rpu ra, e c ch y m os

Epistaxis, oral m u cosa ble e din 

He m atu ri a, u te ri n e bl ee di n g, h

Is m a l a ri a a di a g n o s tic po s s i bi l i

N o 

N o

C l in i ca l e vi de n ce fo r do x y cy cl in 

Le ptos pi ros i s : C on ju n cti val 

m yo sitis, h x 

Rick e ttsiae : Acu te on se t se v

C l in ical e vide n ce of ab dom i n a

N o

C l in i ca l e vi de n ce fo r re s pi ra t

S tre p pharyn gitis, acu te b

a ty pica l pne um onia

N o

A c ute ly ill fe b rile pa

T = 101 °F (38 .5 °C 

C lin ical e vide n ce for acu te ar 

A bru pt o nse t h e adach e with 

in cre ase d with m ove m e n t of 

N o

A 
eat on the local economy. Efficacy is of brief du

inadequate for sustained operations. After initial 

weeks of protection, prophylaxis with antibiotics 

associated with increased incidence of diarrhea 

disruption of protective normal bowel flora and wi

gence of drug-resistant pathogens. Furthermore

prudent to reserve the best prophylactic drugs

(fluoroquinolones) for treatment to ensure its effe

when needed.

Public Health Measures - Command emphasis is esse

 Adequate sanitary facilities.

 Personal hygiene, especially hand washing.

 Water purification and individual water discipline.

 Use of food obtained only from medically approve

sources.

Incubation:

 Varies with specific pathogen. Ranges from hou

lococcal enterotoxins) to several weeks (giardias

amebiasis).

Diagnosis:

 Specific pathogen identification is not usually req

effective management of individual patients.

 The following algorithm provides an effective, effic

approach.
Mi

1-2 stools/day

no sym

+/- lopera

Loperam

Resol

Definition/Note: 1) Uncomfortable 2) Antibiotic Rx is 3) Self Rx encour4) Significant nau5) More gradual o6) Consider mala7) Campylobacte

outbreak), then 

8) For continued * For oral rehydration 

antidiarrheal mAzithromycin.
♦ Kaopectate is ineffective.

♦ Diphenoxylate with atropine (Lomotil) is less 

able than loperamide due to a higher inciden

effects.

 Fluoroquinolone choices, in order of preference, 

♦ Ciprofloxacin 500 mg PO BID for 3 days.

♦ Levofloxacin 500 mg PO QD for 3 days.

♦ Gatifloxacin 400 mg PO QD for 3 days.

♦ A single day of fluoroquinolone therpay has p

effective in relatively mild causes.

♦ In event of fluoroquinolone clinical failure, 1 g

Azithromycin as a single dose may be used
eosinophilic pneu

separately. The o

or confirmed case

 A number of addit

been diagnosed a

patients have reco

have fallen into tw

process and a cla

process is charac

upper respiratory 

malaise, fever, co

(CXR) demonstra

infiltrates, and a c

low white blood c

thrombocytopenia 

cases quickly res

by leukocytosis, f

alveolar infiltrates 

proven to be) a ba

respond well to an

Case definition

For purposes of standardi

confirmed by presence of 

for severe pneumonia incl

presence of bilateral alveo

ment for mechanical venti

guideline is directed towar

present with severe pneum
to link specific pathogens to clusters of cases, to exclu

causes of pneumonia, and to identify unusual pathogen

 History. A detailed history of each case of pne

required to document date of onset, duration of 

before seeking medical care, symptomatology, 

(e.g., dust, chemicals, and smoke), MOS, work 

ment, and geographic location. The EPICON t

prepared a detailed questionnaire that includes 

interview (clinical situation permitting) for each 

pneumonia (uncomplicated and severe) to esta

with other cases throughout the area of operati

a health care worker (HCW) should administer 

tionnaire (i.e., interview the patient). Additiona

capture forms in the EPI Data Collection Instru

included to record laboratory test results and ra

findings for transfer to the U.S. Army Center for 

Promotion and Preventive Medicine (USACHPP

CONUS.

 Diagnostic work-up. Although definitive identif

pathogen is often elusive, it is imperative to co

specimens for epidemiologic purposes, especi

cause of a suspected outbreak is unknown. Th

recommendations are based upon medical and 

assets available at Combat Support Hospitals 

order to minimize the logistical burden to clinic

to facilitate the timely transfer of specimens fro

clinical laboratory to Landstuhl Regional Medic

(LRMC) and/or CONUS. Severe cases of pn
(militar

CSH in 

charac

• Throat 

cocci (

assay 

• Throat 

transp

• Urine s

pneum

antigen 

• Group 

tic kits 

facilitie

♦ Radiolog

vs. bilater

pattern, a

Treatment and Case 

 Prognostic indicat

disease vs. progre

nately, there are n

patients who will p

mechanical ventila

who have bacteria

normal mental sta

tory rate <24/minu

mmHg, temperatu

sick” appearance 

therapy.
ppg 

as Azithromycin (Zithromax) or Levofloxacin 

practice and often effective. Depending on th

clinical status, the physician may elect to in

intravenous therapy followed by changeover t

therapy when possible. It is imperative that c

tion broad-spectrum antibiotics be avoided in 

with uncomplicated pneumonia to prevent em

of multi-drug resistant organisms.

♦ Severe pneumonia. Without a definitive micr

diagnosis, combination antibiotic therapy adm

intravenously is frequently required as empiri

ment:

3rd generation cephalosporin (ceftriaxone, cef

AND

Respiratory tract quinolone (levofloxacin (500

IV QD) >> preferred over ciprofloxacin) OR

azithromycin (500 mg IV QD)

AND

doxycycline (100 mg IV BID)

Alternatives to levofloxacin are gatifloxacin and moxifloxa

Doxycycline is included because a number of cases of in

with Coxiella burnetii (causative agent of Q fever) have be

ported. There is no strong recommendation for the additio

imipenem to the above regimen. However, if imipenem is 

seriously ill patient requiring mechanical ventilation, this s

used as a substitute for the cephalosporin.
diagnose

that the p

♦ Pressure

pressure

those exp

may need 

tation for 

proper m

require h

sures (45

ation, pa

needed b

tion.

♦ Evacuati

of patien

immedia

dent upo

port). Th

patients w

> 7 days; 

require e

analysis 
Diagnosis:

 Symptoms/Signs (abrupt onset; indistinguishable fro

community-acquired pneumonia (CAP)):

♦ Shortness of breath (89%).

♦ Fever/chills (67%).

♦ Cough (67%).

♦ Fatigue (67%).

♦ Chest pain (56%).

♦ Myalgias/arthralgias (56%).

♦ Inspiratory crackles.

♦ Hypoxemia.

♦ Respiratory failure.

 Laboratory findings:

♦ Hematology: Eosinophilia (= 250 cells x 103

/mL

♦ Microbiology: Negative.

♦ Serology: Negative.

♦ BAL: Eosinophilia (= 5%).

 Radiology:

♦ CXR: Alveolar and/or interstitial infiltrates (bilate

56%); pleural effusions uncommon (6%); no ade

thy.

♦ CT: Dense alveolar consolidation and pulmonary

edema; injury usually follows a bronchovascular 

bution; no adenopathy.

Duration: Abrupt onset of symptoms and rapid deterioration 

function; may require intubation with increasing requirements 

oxygen, positive end expiratory pressure (PEEP) >15, and hi

peak pressures >40. Untreated cases may recover with care
cefotaxime)

A

♦ Respiratory tra

IV QD) or Azit

A

♦ Doxycycline (

 Corticosteroids

♦ Solumedrol 80 

taper over 2-4 

 Pressure-control v

 Evacuation from th

Disposition: Evacuate fro

status in 4-6 weeks, but pa

theater. Returning a Servic

he/she was potentially exp

is NOT recommended.

Prognosis: Most recover 

Early administration of ste

broad-spectrum antibiotics

can prevent respiratory fail

Prevention and Public H

 Although the expo

not fully understoo

particulates (dust) 

Servicemembers s

ing, especially non

tion of the habit an

tobacco use durin
tobacco products in the patient’s possession; and an

personal effects that can be acquired.
 Isolation: standar

 Prophylaxis: none 

communicability f

Incubation: 2-3 weeks (1 

Diagnosis: systemic infe

tions; no diagnostic c

critical. Screen for:

♦ ingestion of unpas

of cheese, and

♦ exposure to anim

Classic presentation o

brucellosis infection co

ated with peripheral a

spondylitis.

 Symptoms/Signs

♦ Systemic (alm

• Fever as 

• Weaknes

• Night swe

• Weight lo

• Malaise.

• Lymphad

♦ Gastrointestin

• Nausea a

• Splenome

• Constipat

• Abdomina
• Osteomyelitis.

♦ Genitourinary (2-40%):

• Unilateral epididymo-orchitis.

• Pyelonephritis.

• Acute interstitial nephritis.

• Prostatitis (very uncommon).

♦ Pulmonary: cough (15-25%)

♦ Neurological (2-5%):

• Meningitis, encephalitis.

• Psychosis.

• Meningoencephalitis.

• Depression.

• Myelitis.

• Headaches.

• Paresis.

♦ Cardiovascular:

• Endocarditis - 2% (most common cause of d

♦ Cutaneous (5%) - many nonspecific findings

such as:

• Red-violet papules.

• Diffuse erythema.

• Abscesses.

• Erysipelas-like lesions.

• Erythema nodusum.

♦ Ocular:

• Keratitis.

• Uveitis.

• Papilledema.

• Optic neuritis.
gy

followed by Ig

indicates past 

 Radiology:

♦ CXR abnorma

aerosol: hilar 

lesions, lung a

pneumothorax

♦ Spondylitis wi

tis; erosion an

vertebral body 

involvement m

involvement.

 Invasive procedur

required in therapy 

 “Gold Standard”fo

♦ Isolation of pa

♦ Titer > 1:160 w

clinical finding

Duration:

 Treated: week to 

 Untreated: month

Complications: see Sym

Treatment:

 Uncomplicated: d

rifampin 600 mg/d

 Complications: se
Untreated: 30% complications, prolonged hospitaliza

and convalescence with occasional deaths due to end

tis.

Prevention and Public Health Measures:

 Locate contaminated products, if implicated, and

destroy.

 Educate commanders and troops not to drink or eat u

teurized dairy products.

 Report case as a reportable event using theater medi

surveillance reporting channels.
♦ Onset of illne

possible expo

 Isolation: Standa

(see Standard Pre

appendix A).

 Prophylaxis:

♦ No prophylax

♦ The antiviral d

immediate, po

available, it sh

and transporta

patients with 

then 400 mg 

Incubation: 1-3 days (ra

Diagnosis:

 Symptoms:

♦ Sudden onse

(especially low

♦ Marked anore

♦ Flushing of fa

♦ Pharyngeal hy

on soft palate

♦ Conjunctival i

♦ Signs of hem

♦ Ecchymoses 

(gums, nose, 

♦ Abdominal pa

♦ Backache (90
♦ Hypotension (70-90%).

♦ Oliguria (80%).

♦ Hepatomegaly (80-100%).

♦ Disturbed consciousness (80%).

♦ GI bleeding (hematemesis or melena) (70%).

♦ Epistaxis (50%).

♦ Vaginal bleeding (>50% of women).

♦ Edema (50%).

♦ Meningeal irritation (40%).

♦ Blooding gums (40%).

♦ Relative bradycardia (20%).

♦ Conjunctival injection (20%).

♦ Palmar erythema (20%).

♦ Gingival ulcers (16%).

 Laboratory findings:

♦ Hematologic:

• Anemia (as condition deteriorates).

• Leukopenia (60%).

• Thrombocytopenia (100%).

• Atypical lymphocytes (60%).

♦ Chemistry:

• Hyperbilirubinemia.

• Elevated transaminases.

♦ Urinalysis:

• Hematuria (90%).

• Proteinuria (90%).

♦ Microbiologic:

• Unavailable in most clinical laboratories.

• Viral isolation possible by specialized lab

with sophisticated containment and viral c

capabilities.
 X-rays: nonspeci

 Diagnostic confirm

Duration:

 Treated: undefine

and markedly abb

 Untreated: 10-14 

requiring several w

Complications:

 Sepsis, shock, re

 Relapse does not 

Treatment:

 Treatment regime

 Ribavirin may be b

intravenously ove

part of an investig

Germany).

 Ribavirin to be ad

and infused over 3

schedule:

♦ Loading dose

gm),

♦ Days 1-4: 16 

IV Q6H,

♦ Days 5-10: 8 

IV Q8H.
 Summary of immediate objectives:

♦ Prevent secondary cases (institute barrier pr

tions against blood and secretions ASAP).

♦ Initiate evacuation procedures.

♦ Consider treatable diseases in differential dia

Falciparum malaria Mefloquine 1250 mg

(5 tabs) given in a

divided PO dosing

schedule with 3 tabs

initially followed by

2 tabs 8-24 hours

later OR Malarone

4 adult tabs PO

QD for 3 days

Meningococcemia Ceftriaxone 50 mg/k

per day (2 gm max)

IM for 14 days

Leptospirosis Doxycycline 100 mg

PO BID for 10 days

Typhus Doxycycline 200 mg

PO single dose

Septicemia Ceftriaxone 50 mg /k

per day (2 gm max)

IM for 14 days

Plague Doxycycline 100 mg

PO BID for 10 days

Hemorrhagic Fever

With Renal Syndrome Ribavirin (Huggins e

al. J Infect Dis

164:1119-27, 1991)
Typhus 

Septicemia 

Plague 

Disposition:

 Local hospitalizatio

possible. If evacuat

strict isolation must 

 Depending on clinic

convalescence afte

 Rapidly recovered c

Prognosis:

 Treated: unknown.

 Untreated: 10-70% 

associated with hig

 Survivors generally 

Prevention and Public He

 Investigate possible 

 Identify and clinical

 Report case as a re

surveillance reportin
Incubation period: 3-14 days, commonly 4-7 days.

Diagnosis: Primary infection of adults with dengue virus 

viruses results in an undifferentiated febrile syndrome 

as dengue fever (DF). A positive tourniquet test or sp

ous epistaxis may occur in DF. Secondary dengue c

persons who may have previously had a dengue infec

manifest with critical hemorrhagic manifestations tha

aggressive clinical management (dengue hemorrhagic 

DHF). Very rarely does primary dengue infection res

significant hemorrhagic diathesis or capillary leakage 

shock. Therefore, extensive petechiae, ecchymoses 

significant bleeding should prompt immediate conside

more serious diseases, such as DHF or CCHF; see F

Algorithm.

 Symptoms (abrupt onset):

♦ Fever, may be biphasic (saddleback).

♦ Chills.

♦ Headache, diffuse.

♦ Eye pain.

♦ Intense long bone and joint pain.

♦ Myalgias.

♦ Anorexia.

♦ Nausea.

♦ Vomiting.

♦ Lassitude.

♦ Cutaneous hyperesthesia.
Fever Algorith

 Tourniquet Test - 

(www.cdc.gov/ncid

♦ Inflate blood p

systolic and d

♦ After deflating 

to its normal 

♦ Positive test: 

(6.25 cm2).

 Laboratory finding

♦ Hematologic:

• Hb/Hct: 

• WBC: le

• Platelets

♦ Chemistry, U

Coagulation: 

♦ Serology: Di

ELISA OR pa

14 days apar

 Diagnostic confirm

viruses endemic i

nesses which are 

grounds. These c

paired serology o

gen. Exact diagn

control, treatmen

there are exceptio

contact with infec

a vaccine availab

hemorrhagic feve

spread, and for w
py ppy

volume and correct electrolyte abnormalities, and 

ter analgesics and antipyretics (NSAIDs are not r

mended for DHF). DO NOT OVERHYDRATE. Ap

fluid hydration decreases DHF mortality; consider 

transfusion if Hct falls below 30%. Although plate

transfusions are generally not effective in reducing 

complications, consider if platelet count is less th

10,000.

Disposition: May be hospitalized in theater; most will be 

return to duty in 1 week, but there may be need for up 

days of convalescence. Development of severe syste

symptoms may require evacuation.

Prognosis:

 Mortality:

♦ DF is a nonfatal disease; complete recovery

is expected.

♦ DHF is associated with a 0.5 to 15% mortalit

rate.

 Subsequent dengue virus infection is more likely 

complicated by hemorrhage and shock.

 Patients may experience fatigue, weakness, and

depression for several weeks.

q

Incubation period: 3-12 months.

Diagnosis: Symptoms and signs can be grouped as infla

chronic obstructive or atypically hypersensitive.

 Symptoms/Signs (acute inflammatory, most likely 

seen in our nonimmune troops):

♦ An acute attack of localized pain, tenderness

and erythema is the hallmark of lymphatic fila

Genitalia (42%), arms (25%), legs (11%).

♦ Fever, sweats, chills, headache, lethargy, we

myalgias, and arthralgias after the lymphaden

♦ A retrograde lymphangitis follows within hour

strongly diagnostic for filariasis.

♦ Painful, swollen, tender testicle and/or

epididymis.

 Symptoms/Signs (chronic obstructive, requires pr

exposure over years following multiple acute atta

be seen in endemic populations):

♦ Chronic lymphedema.

♦ Hydrocele/chylocele.

♦ Lymph varices.

♦ Lymph scrotum.

♦ Elephantiasis.

♦ Chyluria.

 Laboratory findings:

♦ Routine labs are not necessary. Eosinophilia 

quently accompanies the acute phase sympt
- Place 

With 

♦ Serology: on

Duration:

 Treated: Curative

 Untreated: variab

enitis/lymphangiti

Complications: chronic o

and untreated.

Treatment: diethylcarbam

(Mectizan®) - not ava

may be beneficial in th

Prognosis: Excellent.

Disposition: Evacuate al

suspected or confirm

facility such as Walt

(WRAMC) or Nation

tropical medicine ex

__________

® Nucleopore is a register

tion, Pleasanton, Californi

® Mectizan is a registered 

Inc., Whitehouse Station, 

♦ Hepatitis B, h

contracted by 

products, oth

activity. Hepa

acute hepatit

hepatitis B.

 Isolation:

♦ Hepatitis A, E

washing.

♦ Hepatitis B, d

♦ Infectiousnes

tion period an

may persist w

periods.

 Prophylaxis:

♦ Hepatitis A: V

vaccine.

♦ Hepatitis B: V

vaccine.

♦ Hepatitis C: N

♦ Hepatitis E: N

Incubation:

 Hepatitis A: 30 da

 Hepatitis B: 70 da

 Hepatitis C: 50 da

 Hepatitis D: less 

hepatitis B.

 Hepatitis E: 40 da
♦ Fever (low grade).

 Signs:

♦ Icterus/jaundice.

♦ Tender hepatomegaly (mild-moderate).

♦ Splenomegaly (uncommon).

♦ Palmar erythema.

♦ Spider angiomata.

♦ Jaundice.

♦ Dark urine.

♦ Light color (acholic) stools.

♦ Low-grade fever (although fever is usually

absent).

 Laboratory findings:

♦ Hematologic:

• Hgb/Hct: usually normal; hemolysis occ

uncommonly.

• WBC:

- normal or mild leukopenia.

- mild lymphocytosis with or without a

lymphocytes may occur.

• Platelets: normal.

♦ Chemistry:

• Transaminases:

- rise 5-100 times normal.

- ALT (SGPT) > AST (SGOT).

- ALT usually >1000 in acute viral

hepatitis.

• Bilirubin: rises 1-20 times normal.
• Anti-hepa

hepatitis 

• Hepatitis 

active inf

chronic.

• Hepatitis 

infectious

• Anti-hepa

immunity 

• Anti-hepa

acute infe

(IgG: pas

• Anti-hepa

ongoing i

• Anti-hepa

E, (IgG p

♦ Coagulation:

• Generally 

viral hepa

• Prothrom

hepatitis.

 X-rays: nonspeci

 Invasive procedur

 Diagnostic confirm

Duration:

 Icteric phase: 1-3 

 Convalescent pha

months.
y

 Progression to chronic hepatitis:

♦ Hepatitis A or E: none.

♦ Hepatitis B: 5-10%.

♦ Hepatitis C: up to 50-70%.

 Pancreatitis.

Treatment:

 No specific treatment is available for acute viral

hepatitis.

 Rest is important.

 Discontinue any nonessential medications.

Disposition:

 Mild cases may be hospitalized in theater, as som

able to return to duty in 2-3 weeks.

 Evacuate moderate or severe cases.

Prognosis:

 Mortality: less than 1%, (except hepatitis E, up t

normal hosts, greater in pregnancy).

 Chronic disease: see complications above.
protection.

♦ Screening of 

and C.

♦ Use of standa

when dealing 

 Immune globulin 

globulin (HBIG) c

prophylaxis in pre

 Report all cases u

reporting channel
tropica) is more common with Afghanistan expos

although few cases have been found to date in Am

military personnel.

Incubation period: usually 2-8 weeks, but may be long

usual past 6 months).

Diagnosis:

 Symptoms/signs: Chronic inflammatory papule/n

that slowly increases in size and ulcerates over s

weeks. Base will crust over but the ulcer spread

the edge of a firm and raised border. Lesions are 

on exposed skin and are rarely seen on the palm

soles. Secondary bacterial infection with pus (ot

unusual with leishmaniasis alone) can be seen w

delay healing and lead to lesion enlargement.

 Laboratory confirmation: requires parasite demo

Follow procedures as outlined in the Leishmania 

and Biopsy Procedures appendix. Note: Optim

parasite should be demonstrated for definitive dia

since clinical diagnosis is less accurate. Clinica

ment should be used in the situation of a lesion t

seems to be healing (completely epithelialized) a

whether diagnostic procedures should be implem

Treatment: The diagnosis must be confirmed parasitolo

before treatment is offered (see above).

 Small lesions (< 2 cm total diameter) that are few 

number (less than 5-10) may not need treatment 
tropica or L. infan

two Leishmaniasi

of Pentostam® (p

treatment centers 

ton, DC) and Broo

Centers (WRAMC

on-line at www.pd

sis).

Disposition: Evacuate pa

treatment centers 

requires a 10-20 d

under a research 

proved, although 

more than 50 yea

Complications: Seconda

streptococcal bacte

cellulitis. Leishman

treatment may decr

small joints may pe

leishmaniasis is rare

then usually due to 

__________

TMThermomed is a tradem

gies Inc., Phoenix, Arizon

®Pentostam is a registere

Research Triangle Park, N
 Insecticide applications to sand-fly habitats.

 Reservoir host (rodents and canines) control.

 Protection of patients from sand-fly bites.

 Individuals who have a confirmed diagnosis of cuta

visceral leishmaniasis are prohibited from blood do

life according to recent policies of both military an

blood banks. This policy is based on the motivatio

banks to eliminate all possible transfusion-associa

infection risk. The likelihood that an individual, wh

of active disease, either naturally or by specific tre

will remain infectious and able to transmit leishma

blood donation is rare to theoretical in the case of 

However, the simplest course of action to eliminat

possibility of transfusion-associated leishmaniasis 

deferral. The number of persons affected by this p

relatively few compared to the size of the donor po

the impact of donor deferral for leishmaniasis to th

pool is trivial. It is important to explain the reason

deferral to those who have been infected with leish

otherwise, they may think that they remain infecti

stated above, almost all cases to date in the Ame

forces in Iraq have been L. major, and there has ne

reported case of transfusion-associated leishmani

caused by L. major.

 Report case as a reportable event using theater m

surveillance reporting channels.
‘Phlebotomus papatasi’ o

Multiple sand fly bites.
Impetiginous secondary infection of cutaneous leishmanias

Large ulcerated lesion.
A lesion after it has crusted 

Skin scraping with giemsa 
etcatasssoooteto

fetus.

 Isolation: generally not required. In forward area

field conditions where continued exposure to san

may occur, personal measures to protect the pat

sand fly bites, including insect repellents and per

impregnated netting, should be used.

 Prophylaxis: no immunoprophylaxis, chemoprop

vaccine available.

 Has been reported from the CENTCOM AOR, pa

Afghanistan, and is quite common in India.

Incubation: normally 3-8 months (range: from 10 days 

than 10 years).

Diagnosis: Acute visceral leishmaniasis in an immunolo

naive adult will frequently present as an acute febrile 

is often confused with malaria. There are no pathogn

signs or symptoms that will distinguish this febrile illn

many other causes. Patients are often described as 

even with fever > 400C. The acute presentation can re

progress to kala-azar, or evolve to a chronic syndrom

abdominal complaints, diarrhea, night sweats, weigh

fatigue. Consider visceral leishmaniasis in the differe

diagnosis of all acutely febrile patients.

 Symptoms:

♦ Onset may be insidious or abrupt.

♦ Fever: high intermittent or remittent, can be 

ated with chills or prostration.

♦ Sweats.
♦ Splenomegaly (

worsens).

♦ Hepatomegaly (

splenomegaly).

♦ Lymphadenopa

generalized).

♦ Fever (39 to 400

♦ Skin:

• trophic chan

dryness, ha

• polymorphi

ulcers (rare

• petechiae, p

♦ Eye: retinal hem

anterior uveitis (

♦ Jaundice (in adv

♦ Nodules or ulce

mucosa (rare).

♦ Edema (associa

with proteinuria)

♦ Bleeding: epista

sites.

♦ Ascites (advanc

 Laboratory findings:

Note: In early illness th

transaminase elevation. 

seen in advanced diseas

♦ Hematologic:

• anemia (no

• leukopenia.

• thrombocyto
y

• proteinuria (occasional).

• hematuria (occasional).

♦ Microbiologic: standard microbiologic techniq

not applicable.

♦ Serologic: Serologic diagnosis available.

♦ Coagulation:

• bleeding and clotting times are generally

normal.

• prothrombin time (PT) may be mildly prolo

seconds more than control).

 X-ray:

♦ Standard examinations are nonspecific.

♦ Hepatomegaly and splenomegaly can be dete

appropriate imaging modalities (sonogram, C

 Invasive procedures:

♦ Aspiration/biopsy of bone narrow, spleen,

liver, or lymph nodes.

♦ Attempt to visualize amastigotes on Wright o

Giemsa stained smears of tissue

and /or (+) culture.

 Skin testing: Leishmanin skin test will be negativ

disease and is not useful for diagnosis.

 Diagnostic confirmation:

♦ Diagnosis must be confirmed by the demonst

parasites in a tissue aspirate or biopsy.

♦ Culture of organism from tissue aspirate spec

possible with specialized technique (NNN or

Schneider’s media), but this should only be a

in facilities with experience in culturing leishm
 Hepatic:

♦ Acute liver fai

♦ Cirrhosis (rare

 Disseminated intra

 Hemorrhage.

 Secondary infectio

cases with accom

♦ Tuberculosis.

♦ Pneumonia.

♦ Dysentery.

♦ Measles, in pr

individuals.

♦ Herpes Zoste

 Persistent post-di

Treatment: visceral leish

disease acutely. How

confirmed visceral leis

CONUS facilities (WR

treated in theater or in 

 Standard therapy:

♦ Liposomal am

days 1-5, day 

__________

®AmBisome is a registere

Inc., Nutley, New Jersey.
Disposition: evacuate all patients with suspected or con

visceral leishmaniasis. This disease is slowly progre

should not be so far advanced in U.S. military person

emergency treatment is required.

Prevention and Public Health Measures:

 Command emphasis on use of personal protectio

(repellent, impregnated netting, application of per

to clothes and netting if not previously treated).

 Insecticide applications to sand fly habitats locat

troop areas.

 Control of wild canids and feral dogs (foxes, jack

may be natural reservoirs of infection; probably in

domestic dogs as well).

 Protection of patients from further sand fly bites, 

aborting possibility of epidemics based on human

reservoirs.

 Report all cases through preventive medicine

channels.
 Chemoprophylax

effective in areas 

exposure.

Incubation: 10 days, (ran

Diagnosis: Infection is ty

atic leptospirosis usua

biphasic illness. Less 

renal failure and hemo

including contact with 

wading, or drinking) o

may be helpful.

 Symptoms (abrup

♦ Fever (100% 

♦ Myalgia (97% 

♦ Headache (95

♦ Chills (85%).

♦ Sore throat (1

♦ Nausea/vomit

♦ Eye pain (50%

♦ Cough (25-50

♦ Diarrhea (23%

 Signs:

♦ Conjunctival i

♦ Muscle tende

♦ Hepatospleno

♦ Lymphadenop

♦ Pulmonary fin
• CPK increased.

♦ Urinalysis:

• proteinuria.

• pyuria.

• microscopic hematuria.

♦ Microbiologic: Culture is seldom useful in init

sis. Unique media needed is not routinely ava

although some standard blood culture system

support growth.

♦ Serologic: Field diagnosis is limited to rapid 

kits (dipstick and EIA) when available. Definit

diagnosis is obtained with microscopic agglut

testing (MAT). This test is performed only at 

labs and usually with paired acute and conva

serum (2-3 weeks apart).

 X-ray: variable in those with symptomatic pulmon

disease, most often small patchy, peripheral infiltr

Duration: 3 days to 3 weeks.

Complications:

 Anicteric leptospirosis: Aseptic meningitis, menin

cephalitis, uveitis, myocarditis, and iridocyclitis.

 Icteric leptospirosis (Weil’s disease): Jaundice, r

failure, hemorrhage (especially pulmonary), and d

Treatment:

 All cases should receive either doxycycline 100 m

for 7 days; or if severely ill, high dose parenteral a

penicillin G 110,000 U/kg per day (6-8 million U/d

four divided doses every 6 hours. Ceftriaxone and
 For mild cases, h

 For complicated c

renal insufficiency

medical facilities.

Prognosis:

 Anicteric leptospi

 Icteric leptospiros

mostly due to rena

pletely. Protracte

Prevention and Public H

 Command empha

swimming, wadin

 Control local rode

 Report case as a 

surveillance repor

 Consider troop pr

confirmed cases: 

during periods of 
Governorate 

Eritrea Year-round Variable Up to 11 – 50% 85

P. 

P. 

oc

Ethiopia Year-round Variable Up to 11 – 50% 85

P. 

P. 

P. 

Iran March – November Variable Up to 1% P. 

P. 

m

at 

Iraq May – November Variable Up to 2 – 10% 99

1% 

Jordan Risk does not 

currently exist 

Kazakhstan May – September Variable Infrequent cases Pr

bu

an

als

Kenya Year-round Countrywide 11 – 50% 90

P. 

P. 

P. 

Kyrgyzstan June – September Variable Infrequent cases Pr

bu

an

als
Saudi Arabia Year-round 

Somalia Year-round 

Sudan Year-round 

Tajikistan April – October 

Turkmenistan April – September 

United Arab 

Emirates 

 

Uzbekistan June – September 

Yemen Year-round 
INTENTIONALLY LEFT BLANK
others in the hosp

impregnated bed 

isolation is require

 Prophylaxis: Indiv

malaria patients d

 Chemoprophylaxi

♦ Chemoproph

considered fo

endemic. In C

accounts for 

predominates

described in t

no confirmed 

Multiple case

quired in Afgh

♦ Recommend

Chief (CINC) 

tions. FDA ap

• Chloroqu

starting 2 

and conti

after depa

OR

• Mefloquin

beginning 

country a

(4 doses) 

OR

• Doxycyc

beginning 
chloroquine, in symptomatic patients with docum

smear positive P. vivax malaria is referred to as “

cure.” Primaquine must not be given to pregnan

deficient individuals because of the risk of hemo

anemia. Different strains of vivax parasites have 

tolerances to primaquine; therefore, dosage reco

tions may vary by geographical region. Studies o

refugees indicate that 30 mg daily for 14 days is 

to reduce relapse rates for vivax infections from t

region. When used for radical cure, give primaqu

phosphate (30 mg primaquine base) by mouth da

days to individuals known to be G6PD normal.

• Use of primaquine, concurrently with an anti-

drug, in asymptomatic patients when they le

endemic area is referred to as anti-relapse th

(also called terminal prophylaxis). Individual

to take primaquine because they are G6PD 

should not be given primaquine for anti-relap

therapy.

• The current FDA approved dose regimen for 

maquine for both the radical cure and anti-re

therapy indications is 15 mg (base) PO QD X 

days. Recently, an expert panel recommend

higher dose of 30 mg (base) PO QD X 14 da

strains of P. vivax known to require higher do

cure, and this is the current Center for Disea

Control (CDC)-recommended, first-line regim

Current DOD Force Health Protection (FHP) 

does not allow use of FDA approved drugs w

unapproved dose regimens. Therefore, the u

primaquine for FHP should be limited to the a
sion seas

P. vivax, p

medicatio

considere

last poss

occurred

Incubation: Malaria can 

in an endemic area, a

of continuous exposu

 P. falciparum: 12 

 P. vivax: 14 days 

 P. malariae: 28 d

Diagnosis: Malaria MUS

If not diagnosed and t

fatal. Disease can oc

blood smear, but pati

will have a detectable 

illness. Patients with 

smear exams every 8

malaria. Persons on e

very low parasitemias 

 Symptoms:

♦ Prodrome of 

precede febri

♦ Paroxysm ch

chills, rigors, 

myalgia, abdo

diarrhea (ma

falciparum.
• Eosinophilia not seen.

• Thrombocytopenia (to <150,000/mm3).

• Blood smears intra-erythrocytic parasite

smears of peripheral blood.

o SMEAR MUST BE PREPARED AND 

INED 2-3 TIMES DAILY FOR 48 HO

RULE OUT MALARIA.

o Thick smears are more sensitive (ab

for finding parasites; thin smears are 

accurate for identifying parasite spec

o Thick smear: place one drop of bloo

slide; with the corner of another glas

spread drop until it is about dime siz

newsprint below slide can barely be 

until thoroughly dry. DO NOT METH

FIX; stain with Giemsa stain.

o Thin smear: prepare film as for norm

fix in methanol, use Giemsa stain.

♦ Chemistry:

• Hypoglycemia (may be severe, especial

quinine therapy, and may be recurrent).

• Electrolyte abnormalities, including hype

(from RBC lysis), and hyponatremia (from 

free water clearance).

• Elevated transaminases (alkaline phosph

normal).

• Azotemia (pre-renal).

• Hyperbilirubinemia.

♦ Urinalysis: may be normal; but increased pr

urobilinogen, and conjugated bilirubin may oc
Duration:

 Treated: 3-5 day

recrudesce within 

 Untreated:

♦ P. falciparum 

nonimmune p

♦ P. vivax rarely 

50% of cases

weeks to 1 ye

latency up to 

eliminated wi

laxis).

♦ P. malariae is 

not treated.

Complications: The follo

infection with P. falcip

 Hyperparasitemia

ized; correlates w

immune patient, t

lower degrees of p

 Cerebral malaria:

♦ Altered ment

argy, stupor, 

♦ Neurologic im

hemiplegia, c

hypoglycemia

♦ Treatment is 

supportive ca

♦ Mortality is hi

neurologic se
ventilation with positive pressure.

 Splenic rupture/hemorrhage:

♦ Spontaneous or from palpation of the spleen

cially with VIVAX malaria.

♦ Treatment is emergent blood replacement an

cal control of hemorrhage.

Treatment:

 Treatment of choice:

♦ Chloroquine plus primaquine for P. vivax mala

♦ Initial treatment for patients with P. falciparum 

able to tolerate oral medication should be Ma

4 tablets PO QD for 3 days (if not already on

Malarone prophylaxis).

• If mefloquine is the only anit-malarial dru

able, then it should be used at a dose of 

PO (5 tablets). The FDA approved dose 

tablets as a single dose. This regimen i

tolerated. The dose should be split and 

least 8-12 hours apart to reduce toxicity

Mefloquine should not be the first choice 

treatment because other, better tolerated 

are currently available.

♦ Alternatives:

• Quinine 650 mg PO TID for 3 days PLUS 

cline 100 mg PO BID X 7 days or Fansid

tablets PO one time.

__________

®Fansidar is a registered trademark of Hoffman-La Roch

Nutley, New Jersey.
complete 7 da

100 mg PO Q

♦ Quinidine glu

loading dose 

over 4 hours Q

switch to oral 

♦ Quinine dihyd

Q8H for 7 day

agents as liste

use IV quinidi

formulation of 

be available i

 Specific Precautio

♦ Monitor patie

quinine shoul

the QRS com

if the QT inter

potension dev

challenge.

♦ Monitor patie

immediately i

or IV quinine 

promptly can 

complications

Disposition for uncompl

48-72 hours w

drug therapy 

patient should 

splenomegaly 

patient to retu
ceftriaxone 250 mg IM one dose, OR Cip

500 mg PO one dose,

PLUS

• meningococcal vaccine, unless this has b

received within 2 years prior to the incide

exposure.

♦ Casual contacts need not receive prophylaxis

♦ Prophylaxis is not uniformly effective. Even a

receiving prophylaxis, close contacts with ind

who develop symptoms suggestive of mening

disease should be rapidly evaluated.

Incubation: 3-4 days (range 1-10 days).

Diagnosis: meningococcal infection may be asymptoma

may present either as a self-limited flu-like illness (withou

quelae), as meningitis, as fulminant septicemia (meningococcemia), or as combined meningitis-septicemia. Clinic

and symptoms will vary with the type of presentation. Ser

meningococcus is prevalent in Asia, therefore, vaccination 

should not preclude a possible diagnosis of acute mening

 Symptoms:

♦ Meningococcemia (very abrupt onset with fulm

course):

• Fever.

• Headache.

• Malaise.

• Diarrhea (occasionally may be severe).
• Altered m

• Petechiae

mucosal) 

of cases. 

and ische

faint, mor

purpura o

hours of o

for menin

♦ Meningitis:

• Headache

• Fever.

• Meningis

• Cranial n

VI, and V

• Altered m

• Seizures

• Positive K

 Laboratory finding

♦ Hematologic:

• Meningoc

o HGB

o WBC

nia im

o throm

• Meningiti

o HGB

o WBC

nia su
• Blood culture: positive in 50-60%.

• Organisms are fragile: smear and culture

be prepared as soon as CSF is obtained f

patient.

♦ Serology: not applicable.

♦ Coagulation: prothrombin time (PT) and partia

plastin (PTT) time may be prolonged in menin

mia. Evidence of DIC, including decreased fib

levels, and elevated levels of fibrin degradation 

may be seen.

 X-ray: nonspecific.

 Invasive procedure:

♦ In presence of meningitis or suspected menin

mia, lumbar puncture for CSF should be perfo

immediately, unless papilledema or other foca

logic signs suggestive of either intracranial ma

increased intracranial pressure are present.

♦ CSF should be tested for glucose, cell count, 

stain, and culture. Abnormal CSF results incl

are not limited to:

• glucose < 40 mg/dl (in 75% of cases).

• protein > 150 mg/dl (range 25-800).

• WBC > 1000 cells/mm, neutrophils predo

(range 10- 65,000; lymphocyte predomina

seen in <10%; poor prognosis associated 

absence of WBCs in CSF, as may be cau

WBC lysis from large amounts of mening

 Diagnostic confirmation: culture of organism from 

specimen (from CSF, or petechial aspirate). Choc

plates required.
Treatment must be initiate

meningococcal d

evaluation to proc

treatment regime

♦ Obtain rapid 

contraindicat

♦ While establi

hemoglobin, 

studies.

♦ Perform LP if 

♦ Administer on

otic. Duration 

cally 10-14 d

• cefotaxim

• ceftriaxo

• penicillin 

• ampicillin 

*For PCN alle

• gatifloxac

• chloramp

♦ Provide hemo

as needed.

♦ Proceed with 

tion, and eva

 If pneumococci a

500-750 mg IV Q

(*Note: This dose 

other indications, b

meningitis.)

 If H. influenzae a

ceftriaxone 2 gm 
 Treated: In properly treated cases, residual mor

not unusual, hearing loss may

persist, and mortality may be as high as 5-10%.

 Untreated: Mortality may range from 50-85%.

Prevention and Public Health Measures:

 Vaccination of susceptible populations. An effect

quadrivalent vaccine (affording protection against 

A, C, Y, and W-135) is available. Vaccination wit

past 3 years is regarded as protective. An approv

vaccine for serogroup B meningococci is not avai

 Antibiotic prophylaxis of close contacts, as abov

 Prevent overcrowding in troop shelters, and provid
Incubation: 20 days (ran

Diagnosis:

 Symptoms (gradu

♦ Fever to 40°C 

♦ Headache, se

♦ Fatigue (98%

♦ Chills (88%).

♦ Myalgia (68%

♦ Nausea, eme

♦ Pleuritic ches

♦ Diarrhea (21%

♦ Retroorbital p

♦ Nonproductive 

 Signs:

♦ Inspiratory cra

♦ Hepatomegal

(~50%).

♦ Mental status 

♦ Relative brady

♦ Hypoxemia, i

pneumonia ra

docarditis with 

 Laboratory finding

♦ Hematology: 

♦ Chemistry: h

2-3 times nor
Duration: clinical manifestations usually resolve within 2

in absence of specific treatment. However, therapy is 

to prevent development of complications (i.e., chronic 

Complications: endocarditis (chronic Q fever), granulom

hepatitis, and rarely, osteomyelitis, aseptic meningitis

cephalitis, hemolytic anemia, pericarditis.

Treatment:

 Doxycycline 200 mg PO BID for 2 weeks.

 Tetracycline 250 mg PO QID for 10 days.

 Ciprofloxacin 500 mg PO TID for 10 days.

Disposition: local hospitalization, anticipate return to dut

6 weeks. Complicated cases should be evacuated

Prognosis: most recover uneventfully and without relaps

ties rare in acute disease.

Prevention and Public Health Measures:

 Avoidance of slaughterhouses and birth products

of animals.

 Ingestion of only pasteurized dairy products.

 Report case as a reportable event using theater

medical surveillance reporting channels.
Incubation period: 14-6

95% are within 1 year

Diagnosis:

 Symptoms/Signs

fatigue, headache

and paresthesia a

merges to an acut

and hyperactivity 

muscles and hydr

 Laboratory: diagn

antibody staining 

diagnostic finding

although corneal 

the neck above th

cent antibody, can 

Duration:

 Treated: death in 

 Untreated: death 

symptoms.

Complications: usual mu

patient.

Treatment:

 No specific antirab

is directed solely 

 Pre-exposure pro

CINC surgeon.
(HRIG), 20 IU/kg or 9 IU/lb body weight; all o

should be infiltrated into the bite site if anato

possible. Any residual dose can be given int

larly in the gluteal area. (HRIG should NEVE

in the same syringe or into the same site as 

vaccine.) AND

♦ Give Human Diploid Cell Vaccine (HDCV) in f

mL doses, IM (deltoid area), on days 0, 3, 7

28. HDCV administration concurrent with ma

chemoprophylaxis with chloroquine may resu

decreased HDCV vaccine efficacy.

♦ Other approved rabies vaccines may be

available.

Disposition:

 Exposure: full duty with supervised HRIG and

HDCV.

 Clinical illness: EVAC.

 Nonavailability of HRIG and HDCV: EVAC.

Prognosis:

 Treated potential exposure: excellent.

 Treated or untreated clinical illness: uniformly

fatal.

the Borrelia spp.) is transmitted by the bite of 

nymph or adult soft ticks of the genus Ornitho

Transmission of infection may occur within m

tick attachment.

♦ Transfusion of infected blood transmits diseas

♦ Transplacental infection occurs.

 Isolation:

♦ Delouse patients with insecticide, taking care 

crushing lice or abrading skin.

♦ Direct person-to-person transmission does no

isolation other than measures to avoid transfe

not needed.

♦ Ticks should be identified and carefully remov

♦ Standard precautions.

 Prophylaxis: Following tick or louse bites in a hig

setting, a single dose of tetracycline 500 mg PO 

administered.

Incubation:

 Louse-borne relapsing fever: 4-8 days (range

2-10 days).

 Tick-borne relapsing fever: 2-14 days.

Diagnosis:

 Symptoms: The characteristic feature of relapsin

abrupt severe fever lasting several days, terminat

crisis by rapid defervescence, severe sweating an

ness ; then, after an interval of days (rarely weeks

ring one or more times.
cially calv

• Chills/rigo

• Severe he

• Dizziness 

• Nausea (

• Vomiting 

• Cough (5

• Prostratio

• Severe dy

• Anorexia

♦ Tick-borne rel

Initial episode 

persist up to 1

and more freq

at least one re

average, and 

Relapses ave

symptoms mo

disease. Oth

severe than, t

 Signs:

♦ Louse-borne r

• Petechia

more pro

extremitie

• Jaundice

• Fine eryth

• Liver tend

• Spleen te

• Iritis.

• Meningis
♦ Hematologic:

• Wright or Giemsa-stained blood smears s

carefully examined for extracellular spiroc

louse-borne disease, spirochetes should b

on smears, but they may too low in conce

detect by this method in tick-borne diseas

and thin malaria smears are satisfactory f

nation. Spirochetes are not detectable du

intervals between fevers.

• Anemia.

• Thrombocytopenia, often < 50,000.

• WBC: usually WNL, but may rise to

15,000-30,000.

♦ Chemistry: elevated transaminases; elevated 

both conjugated and unconjugated.

♦ Urinalysis: albuminuria, microhematuria, pyur

♦ Microbiologic:

• Dilute one drop of blood with one drop of n

saline, cover with cover slip, and examine 

darkfield or phase contrast microscopy. T

corkscrew rotation of spirochetes can be s

• Specialized culture techniques or animal i

are required for isolation.

♦ Serologic: not clinically available.

♦ Coagulation: PT and PTT may be prolonged.

 Radiology: nonspecific.

 Invasive Procedures: lumbar punctures show eleva

opening pressure; pleocytosis, and elevated CSF p

typical. Both polys and mononuclear cells may be

seen.
antibiotics, a s

pressure elev

sharp rise in f

headaches an

urinary incont

cemia, leukop

The severity o

greater if antib

♦ Treatment of J

• Meptazin

mg IV giv

minutes a

onset of f

drops bel

ameliorat

relapsing 

use nor a

• Pretreatm

is of ques

• Naloxone 

with isoto

saline) is 

necessar

sion refra

 Myocarditis with p

and congestive he

 Coincident typhus 

borne relapsing fev
• doxycycline 200 mg PO, single dose.

• erythromycin 500 mg PO, single dose.

♦ Parenteral regimens:

• tetracycline 250 mg IV, single dose.

• erythromycin, 250 mg IV, single dose.

 Tick-borne:

♦ Oral regimens:

• tetracycline 500 mg PO Q6H for 6 days 

pregnant women or children < 8 years old

• doxycycline 100 mg PO BID for 10 days

• erythromycin 500 mg Q6H for 10 days.

♦ Parenteral regimens:

• penicillin G 3 million units IV Q4H for

10 days.

• ceftriaxone 2 gm IV Q6H for 10 days.

Disposition: Local hospitalization, with subsequent retu

Consider restricted duty with no hard physical activity 

days to allow associated splenomegaly to resolve. E

may be needed for cases with complications.

Prognosis:

 Louse-borne:

♦ Treated: complete recovery in > 95% of cas

♦ Untreated: mortality variable; usually 2-10%

reach 70% in epidemic conditions.

 Tick-borne:

♦ Treated: complete recovery in > 95% of cas

♦ Untreated: mortality low, less than 10%.
 Reservoir eradica

♦ Louse-borne 

treat.

♦ Tick-borne di

treat and con

 Report case as re

surveillance repor
also make effective barriers for sand flies.

 Prophylaxis: none required.

Incubation: 3-6 days.

Diagnosis: Widespread outbreaks have occurred in milit

campaigns when nonimmune soldiers entered endem

 Symptoms:

♦ Fever to 400C.

♦ Headache.

♦ Myalgia.

♦ Supraorbital pain (intense) or retrobulbar pain

with eye movement.

♦ Limb stiffness.

♦ Malaise.

♦ Gastrointestinal symptoms (nausea, vomitin

♦ Facial congestion.

♦ Neck stiffness.

 Signs:

♦ Fever.

♦ Conjunctival injection.

♦ Papilledema (occasional).

♦ No adenopathy.

♦ Erythematous flush but no rash.

 Laboratory findings:

♦ Hematologic: leukopenia on day 4 - 5

of fever.

♦ Chemistry, urinalysis, microbiology, and

coagulation: not applicable.
depression, and easy 

Treatment:

 No specific treatm

 Provide supportive 

Disposition: limited duty 

resolves, then full dut

prolonged and some p

Prognosis: full recovery. 

immunity against same se

Prevention and Public H

 Insecticide sprayi

and entrenchmen

 Troop education.

 Command empha

measures (use of 

permethrin insect

treated). Mosquit

effective controls 

density is no large

 Report outbreaks 

authorities.
tailed cercariae. Clinical syndrome of acute schistos

occurs after 2 weeks to 3 months.

Diagnosis:

 Characteristically associated with S. japonicum a

sometimes with S. mansoni. S. haematobium is 

associated with an acute syndrome.

 While schistosomiasis is not a threat in most of C

Asia, it does occur in the Arabian Peninsula and 

Southwest Asia. Outbreaks of swimmer’s itch tha

occurred in Central Asia are attributable to animal

dent schistosomes for which humans are not prim

hosts.

 Symptoms:

♦ Fever (all).

♦ Chills.

♦ Sweating.

♦ Headache.

♦ Cough (most).

♦ Diarrhea (50%).

♦ Weight loss.

 Signs:

♦ Lymphadenopathy.

♦ Hepatomegaly (50%).

♦ Splenomegaly (10%).

 Laboratory findings:

♦ Hematology: eosinophilia very common.

♦ Microbiology: stool or urine exam may but u

does not show schistosoma eggs in patients 

acute schistosomiasis.
Complications:

 Rare reports of de

infection.

 If not recognized o

chronic manifesta

infections must be 

not.

Treatment:

 Praziquantel (Bilt

following a meal; 

on the same day.

 Praziquantel may 

ness; side effects 

 Treatment of acut

schistosomicidal 

possibly life-threa

transient complica

administration of 

by an equivalent c

 Swimmer’s itch ca

an antipruritic.

Disposition: limited duty 

severity; evacuation m

__________

®Biltricide is a registered t

Haven, Connecticut.

be considered. Al

penicillin can be e

Incubation: 2-4 days for 

Diagnosis: clinical strept

pharyngitis, scarlet fev

pyoderma (impetigo). 

syndrome occurs, but 

 Pharyngitis:

♦ Symptoms: so

malaise.

♦ Signs: pharyn

hyperplasia; e

(in 50%), tend

favor > 1010

F 

♦ Laboratory: m

cultures. Antig

but somewha

laboratory sup

 Scarlet fever:

♦ Usually occur

seen with stre

♦ Symptoms: t

fever, rash, an

toxicity or a to
enitis. Progresses rapidly. May evolve to ab

gangrene, or septicemia.

 Erysipelas:

♦ Symptoms: chills, fever, systemic toxicity.

♦ Signs: red, edematous, sharply demarcated, 

ing skin lesion.

 Impetigo:

♦ Signs: pustules that rupture easily and enlar

shallow skin ulcers or erosions, typically with 

colored crusts. Usually occur on exposed sk

such as the mid-face or beard area or at site

bites or other preexisting rashes. Highly con

 Streptococcal toxic shock:

♦ Signs: sepsis syndrome, shock, acute renal 

ARDS.

Duration:

 Pharyngitis: treated 1-4 days; untreated 3-5 day

 Scarlet fever: rash persists 4-5 days; subsequen

mation persists 2-4 weeks.

 Erysipelas/cellulitis:

♦ Treated: improvement in 24-48 hours.

♦ Untreated: may proceed to fatality.
tis, meningitis, br

necrotizing fascit

Treatment:

 Pharyngitis:

♦ Benzathine P

dose; preferre

♦ Penicillin V 2

to compliance 

♦ Erythromycin 

penicillin alle

 Scarlet fever:

♦ Treat primary 

skin) as appro

♦ Supportive ca

 Erysipelas/celluli

♦ Penicillinase-

possible stap

ing on severit

1-2 days afte

Minimum 10-

♦ Erythromycin 

occurs, trans

Q6H to comp

cin; OR

♦ Vancomycin 

course.
♦ Intensive supportive care.

 For penicillinase producing streptococcal organism

are resistant to penicillin, alternate therapies inclu

macrolides such as clarithromycin or the second g

tion quinolones such as lofloxacin.

Disposition:

 Local hospitalization required for scarlet fever, erys

or severe pharyngitis.

 Mild pharyngitis or impetigo may be returned to

duty.

 Evacuation required for rheumatic fever, glomerulo

toxic shock, necrotizing fascitis or other advanced 

tious complications.

Prognosis:

 Treated: excellent prognosis.

 Untreated: complication will be associated with

serious sequelae in some cases.

♦ Scarlet fever and erysipelas: may be fatal if n

properly treated.

_________

®Keflex is a registered trademark of Dista Products and E

Company, Indianapolis, Indiana.

®Septra is a registered trademark of Burroughs, Wellcome

search Triangle Park, North Carolina.

®Bactroban is a registered trademark of GlaxoSmithKline

search Triangle Park, North Carolina.
producing strain 

 Food handler pre

personnel will mi

infections.
 For development of primary lesion: 4-12 weeks.

 For progressive, reactivation or extrapulmonary d

Progressive disease can occur soon after exposu

although this is unlikely unless the exposed pers

immunosuppressed. Lifetime risk of reactivation 

10%. Half of this (5%) is the first 2 years after in

exposure (infection).

Diagnosis:

 Symptoms:

♦ Initial infection is usually asymptomatic.

♦ Fever (may be intermittent) night sweats, ano

weight loss, fatigue, cough (productive or non

for more than 3 weeks), hemoptysis, chest p

(pleuritic), dyspnea.

♦ Symptoms produced by extrapulmonary tube

depend on the organ system involved. Extrap

sites, listed here in order of decreasing frequ

include lymphatics, pleura, genitourinary trac

joint, meninges, peritoneum, liver, pericardium

ear, and brain.

 Signs:

♦ Signs may be absent, especially in early dis

general, they are nonspecific and less signifi

would be expected from extent of disease.

♦ Rales, especially post-tussive: dullness to p

and diminished breath sounds.

♦ Other signs depend on the site(s) of extrapul

involvement.
♦ Urinalysis:

• Usually n

• In presen

see steril

♦ Microbiologic

• Observat

(sputum, 

presump

organism

eases). A 

significan

slide are 

o Fluo

effici

o Alter

Kinyo

• Radiome

can reve

• Standard 

to 12 wee

• In presen

obtain AF

urine.

♦ Serology: no

♦ Coagulation: 

__________

®BACTECis a registered 

Company, Franklin Lakes
no sputum can be produced.

♦ Bronchoscopy, with washings for cultures, ma

diagnostic when TB is a consideration but org

cannot be recovered by less invasive means.

♦ The choice of other specific invasive procedur

including thoracentesis, lumbar puncture, or b

is guided by clinical evidence of extrapulmona

 Skin testing:

♦ In previous nonreactors TB skin test (PPD)

may become positive in 4-10 weeks.

♦ PPD may be negative in early or primary dise

overwhelming disease, or in patients with imm

pression from other disease.

♦ Up to 25% of patients with pulmonary TB may 

negative skin tests; 5% of patients may have 

tive anergy (negative PPD and positive anergy 

♦ In persons exposed to others with active pulm

TB, and those with abnormal chest xrays (bu

active disease) or immunosuppression, >5 m

tion is considered positive.

♦ In an area of high prevalence, PPD skin tests 

mm induration are considered positive.

♦ Prior BCG vaccination should not be consider

interpreting PPD results.

 Diagnostic confirmation: successful culture of my

ria from clinical specimens.
tion of the involved 

 Recurrence, poss

occur in inadequa

adequately treate

occur.

Treatment:

 Treatment should 

patient shows evid

meningitis, or is o

recovery of the or

important for corre

be available in the

 If initiated, therapy 

regimen of rifamp

ethambutol. Initia

field is discourage

Disposition: EVAC.

Prognosis: excellent in p

Prevention and Public H

 Isolation and treat

 Prophylaxis of co

surgeon.

 Persons with susp

wear a surgical m

is likely.
(p) y p

 Report case as a reportable event using theater

medical surveillance reporting channels.
♦ Standard and 

♦ Disinfection o

♦ Since excretio

several week

more than 1 y

ing patients s

turned to field 

 Prophylaxis:

♦ For househol

administer va

within 3 years

♦ Household co

handlers unle

negative for s

hours apart.

Incubation:

 Average: 1 week

 Range: 3 days to 

 Larger inoculum is 

incubations.

Diagnosis:

 Symptoms: insid

present with simil

for considerations

♦ Fever (75-100

♦ Headache* (5

♦ Anorexia (39-

♦ Cough (28-86
 Signs:

♦ Fever: remittent, 104oF (40oC); (75-100%); le

in early phase.

♦ Pulse slow relative to fever.

♦ Rose spots: 2-8 mm blanching, erythematou

maculopapular lesions; occur in crops of abo

located on upper abdomen; persist several ho

several days; appear 2-4 weeks into illness, (

♦ Hepatomegaly: (15-50%).

♦ Splenomegaly: often tender; (40-64%).

♦ Neurological/mental status changes: lethargy

coma seizures, delirium, and meningismus; (

 Laboratory findings:

♦ Hematologic:

• HGB/HCT: anemia common, worsens pr

sively over first 3 weeks.

• WBC: normal in 75% (range 1,200-20,00

• Platelets: usually normal, occasionally l

• ESR: typically elevated.

♦ Chemistry:

• SGOT, LDH: mild/moderate elevation in

about 33%.

• Alkaline phosphatase: mild elevation

common.

• Bilirubin: mild elevation (twofold) commo

cient to cause jaundice, uncommon.

• CPK: occasionally elevated.

♦ Urinalysis: nonspecific.
illness.

• Urine cul

second w

specimen

• Skin snip

cultures o

♦ Serologic: lim

nonspecific.

♦ Coagulation: 

coagulopathy

be seen.

 X-Ray: chest x-ra

 Invasive procedur

♦ Bone marrow 

♦ Skin snip or b

above.

 Diagnostic confirm

blood, marrow, or 

case is presumpt

Duration:

 Treated: 3-10 day

 Untreated: 4-wee

complicated.

Complications:

 Intestinal perforat

♦ Incidence: 1-

week of illnes

♦ Mortality: 25
♦ Mortality: low if recognized and treated.

♦ Typically occurs during second or third week

of illness.

♦ Treatment is supportive, including transfusion

cal intervention should be reserved for massiv

persistent bleeding.

 Local abscess/infection:

♦ Incidence: < 1%.

♦ May occur in any tissue, notably bone, soft ti

meninges, heart, pericardium, lungs, liver, spl

kidneys, thyroid, or breast.

 Other complications:

♦ Hemolytic anemia (2%).

♦ Typhoid pneumonia (8-10%).

♦ Peripheral neuropathy.

♦ Relapse (5-20%).

Treatment:

 Preferred regimens:

♦ Ciprofloxacin 500 mg PO BID for 10-14 days (

detected early); OR

♦ Ceftriaxone (Rocephin®) 1-2 g IV QD for

7 days.

 Supportive fluid and nutritional therapy is essentia

 Avoid heparin and antipyretics.

__________

®Rocephin is a registered trademark of Hoffman-LaRoche 

Nutley, New Jersey.
 Vaccinate all milit

 Command empha

♦ Strict sanitati

♦ Hand washing

♦ Strict water pu

♦ Fly control:

• Insecticid

• Screenin

• Proper ga

 Epidemiologic inv

required.

 Report case as a 

medical surveillan
 Symptoms: onset variable, but more commonly

sudden.

♦ Fever (90-100%).

♦ Chills.

♦ Headache (severe) (85% or more).

♦ Myalgia (85%).

♦ Nonproductive cough (50-60%).

♦ Nausea.

♦ Vomiting.

♦ Marked weakness/prostration.

♦ Sore throat.

♦ Chest pain.

 Signs:

♦ Fever (100%) up to 1050F (400C) for 12-16

days duration.

♦ Rash (60-80%).

• Initial: pink macules on upper thorax and 

men, rapidly spreads to the rest of the bo

spares face, palms, and soles; appears o

3-5 of illness.

• Later: remains central, macules become 

rhagic and gangrene may ensue, duration 

days.

♦ Conjunctival injection (50%).

♦ Splenomegaly (30%).

♦ Mental status changes (20%).

♦ Photophobia (10-20%).

♦ No eschar present.
for epidemiologic 

application of indir

cross-absorption o

antigen from othe

Duration:

 Treated: 2-3 days

 Untreated: up to 1

Complications: very unc

Treatment:

 Standard: Doxycy

3 days after deferv

 Alternatives: Tetr

3 days after deferv

 Relapse: rare in m

original regimen.

Disposition: local hospita

weeks.

Prognosis: excellent; eve

sequelae.

Prevention and Public H

 Insecticide applica

kill fleas.

 After effective inse

measures includin

 Rat-proofing huma
Incubation: 12 days (range 5-23 days).

Diagnosis:

 Symptoms (abrupt onset):

♦ Sustained fever > 400C.

♦ Severe headache.

♦ Prostration.

♦ Back pain.

♦ Limb pain.

♦ Nonproductive cough.

♦ Photophobia.

♦ Anorexia.

♦ Constipation.

♦ Nausea (uncommon).

♦ Vomiting (uncommon).

♦ Diarrhea (uncommon).

 Signs:

♦ Rash (90%); onset on 5th or 6th day of illness

in axillary folds, on abdomen and chest. Cent

spread later. Initially roseolar, macular; becom

petechial. Rarely involves palms, soles or fac

eschar is seen. Rash is similar to endemic ty

less severe. Also:

♦ Profound lethargy/stupor.

♦ Delirium.

♦ Facial congestion.

♦ Conjunctival injection.

♦ Splenomegaly.

♦ Hypotension.

♦ Tachycardia.
♦ Microbiology

centers but n

hospitals.

♦ Serology ava

♦ Coagulation: 

(PPT).

 Invasive procedu

 X-ray: CXR may 

Complications: sepsis, 

myocarditis, CHF, ven

Treatment:

 Doxycycline, 200 

 Tetracycline, 250 

vescence (avoid i

 Relapse: repeati

Disposition:

 Initial: hospitaliza

 Post treatment:

♦ prompt respo

♦ complicated c

sponse to tre
ppy pp

Prevention and Public Health Measures:

 Insecticides:

♦ Application of insecticide to clothing of all pe

at risk of exposure.

♦ Use of persistent insecticide for application 

clothing of individuals at particular risk.

 Hygiene: command emphasis on personal hygie

cleanliness of clothing.

 Disease reporting to higher echelon medical

authorities.

 Report case as a reportable event using theater

medical surveillance reporting channels.
 Symptoms:

♦ Fever (100%)

♦ Headache, se

♦ Myalgia (35%

♦ Dyspnea.

♦ Weakness, fa

♦ Cough.

 Signs:

♦ Fever (100%) 

untreated.

♦ Rash (>95%)

• Initial: pa

site of inf

abdomen

followed 

• Later: ma

fever, loca

soles) the

untreated

severe ca

♦ Conjunctival i

♦ Hepatomegal

 Laboratory finding

♦ Hematology: 

♦ Chemistry: hy

SGOT.

♦ Microbiology: 

conditions.

♦ Urinalysis: pr

♦ Serology: ava
Complications: deep venous thrombosis, digital gangren

carditis, renal failure, hemorrhage.

Treatment: Doxycycline 100 mg PO BID or Tetracycline 

PO Q6H until 1 day after defervescence.

Disposition: local hospitalization, anticipate return to dut

weeks. Evacuate cases with complications.

Prognosis: excellent, most show rapid clinical

 improvement after 46 hours of therapy.

Prevention and Public Health Measures:

 Avoid contact with ticks or tick-infested animals if

possible.

 Use of DEET repellent and permethrin impregnate

by all personnel will reduce risk of exposure.

 Report case as a reportable event using theater

medical surveillance reporting channels.
Tularemia ---------------

Venezuelan Equine E

Viral Hemorrhagic Fev

Decontamination ------

BW Agent Characteris

BW Agents – Drug Th
; g pyg

dysphagia, and oral / tonsillar lesions). Significant

lymphadenopathy (mediastinal in inhalational disea

in others) is characteristic.

Diagnosis: Physical findings are nonspecific. A widene

mediastinum may be seen on CXR in later stages o

The organism is detectable by Gram stain of the blo

blood culture late in the course of illness.

Prophylaxis: Oral Ciprofloxacin or doxycycline for kno

imminent exposure. An FDA-licensed vaccine is av

Soldiers going to areas of increased threat should a

vaccinated. Vaccine schedule is 0.5 mL SC at 0, 2

then 6, 12, and 18 months (primary series), followed 

boosters.

Isolation and Decontamination: Standard precaution

After an invasive procedure or autopsy is performed 

possible), the instruments and area used should be 

disinfected with a sporicidal agent (hypochlorite). In

anthrax does not seem to be transmissible from pe

person.
g ) 

million U IV Q4H) 

available. Publish

health consensus 

initial therapy. Th

antibiotic sensitivi

cycline. Tetracycl

recommended in 

mended treatmen

changed to oral th

Supportive therap

adequacy of airwa

__________

Note: More information av

anthrax/
should be suspected if multiple casualties simultaneo

present with progressive descending flaccid paralysis

confirmation can be obtained by bioassay (mouse neu

tion) of the patient’s serum. Other helpful labs include

for antigen in environmental samples, PCR for bacteria

environmental samples, or nerve conduction studies a

electromyography.

Prophylaxis: Pentavalent toxoid vaccine (types A, B, C, 

is available as an IND product for those at high risk of 

sure.

Isolation and Decontamination: Standard precautions f

HCWs. Toxin is not dermally active and secondary ae

are not a hazard from patients. Decontaminate with s

water. Botulinum toxin is inactivated by sunlight withi

hours. Heat (80OC for 30 minutes, 100OC for several m

and chlorine (>99.7% inactivation by 3 mg/L free availa

chlorine (FAC) in 20 minutes); also destroy the toxin.

Treatment: Early administration of trivalent licensed antit

heptavalent antitoxin (types A, B, C, D, E, F and G), a

only as an IND product, may prevent or decrease prog

to respiratory failure and hasten recovery. Intubation a

ventilatory assistance for respiratory failure. Tracheos

may be required.

 Supportive care, including prompt respiratory sup

be lifesaving. Respiratory failure due to paralysis 

respiratory muscles is the most serious effect and
Antitoxin: Early administ

since the antitoxin can 

patients with symptom

symptom progression 

and the antitoxin has 

effective in food-borne 

continues to be absor

experiments show tha

antitoxin is very effect

signs. If the antitoxin 

symptoms, it does no

 Three different an

United States. A 

antitoxin is availab

and Prevention fo

product has all the 

product, including 

sickness. A mono

available from the 

vices for infant bot

offers a heptavale

 Use of the equine 

serum sensitivity 

performed by inje

physiological salin

patient’s forearm 

the injection site a

reaction for 20 mi
y g 

ously, doubling the previous dose every 20 minute

1.0 - 2.0 mL can be sustained without any marke

tion. Preferably, desensitization should be perfor

an experienced allergist. Medical personnel adm

the antitoxin should be prepared to treat anaphyla

epinephrine, intubation equipment, and IV access
many infections prese

are asymptomatic. La

blood culture with prol

cultures produce a hig

phage-typing, oxidativ

dures. ELISA, followe

Prophylaxis: There is no 

brucellosis, although a

laxis is not recommen

demic disease. Treat

exposure to the poten

body fluids and aeroso

confirmed biological w

Isolation and Decontam

by body fluids and aer

appropriate for HCWs

been reported via tiss

Environmental decont

0.5% hypochlorite sol

Treatment: Antibiotic the

weeks is usually suffic

regimens may be requ

meningoencephalitis, 
gpg py 

tetracycline, and an aminoglycoside is recommen

some experts for patients with meningoencephalit

endocarditis.
Both diseases are alm

Diagnosis: Methylene bl

reveal scant small bac

ance. Standard cultur

mallei and B. pseudom

small multiple lung ab

lungs, with consolidat

may be normal or elev

diagnosis, but low tite

exclude the diagnosis

Prophylaxis: Currently, n

prophylaxis is availabl

Isolation and Decontam

health care person-to-

unlikely, although sec

improper handling of i

tions are indicated wh

ment. Environmental 

pochlorite solution is e

Treatment: Therapy will v

clinical presentation. 

be managed with oral 

severe illness may req

prolonged treatment.
TMP / sulfa for 60-150 days. If extrapulmonar

rative disease is present, then therapy should 

for 6-12 months. Surgical drainage of absces

be required.

 For severe disease, parental therapy with Ceftazid

mg/kg/day in three divided doses combined with T

(TMP 8 mg/kg/day – sulfa 40 mg/kg/day) in four di

doses for 2 weeks, followed by oral therapy for 6 m

 Other antibiotics that have been effective in experi

infection in hamsters include doxycycline, rifampin

Ciprofloxacin. The limited number of infections in 

has precluded therapeutic evaluation of most of th

otic agents; therefore, most antibiotic sensitivities 

on animal and in vitro studies. Various isolates ha

markedly different antibiotic sensitivities; therefore

isolate should be tested for its own resistance pat
the pneumonic form. 

evidence of a bubo, an

Diagnosis: Suspect plag

healthy individuals dev

nia, especially if hemo

diagnosis can be mad

Wayson stain of blood

rates. Definitive diagn

from those sites. Imm

Prophylaxis: For asymp

aerosol or to a patient 

give doxycycline 100 

duration of risk of expo

ics include Ciprofloxac

No vaccine is currently 

previously available lic

against the most likely 

against aerosol expos

Isolation and Decontam

bubonic plague, and re

suspected pneumonic 

environment for varyin

disinfectants, and exp

effective if decon is ne

disease cycles if vecto

present.
♦ gentamicin, 5 mg/kg IM or IV once daily, or

 2 mg/kg loading dose followed by 1.75 mg/kg IM 

 every 8 hours;

♦ doxycycline 200 mg initially, followed by 100 mg e

 12 hours.

Duration of therapy is 10-14 days. While the patient is typica

afebrile after 3 days, the extra week of therapy prevents relap

Results obtained from laboratory animal, but not human, exp

ence, indicate that quinolone antibiotics, such as Ciprofloxac

ofloxacin, may also be effective. Recommended dosage of

Ciprofloxacin is 400 mg IV twice daily. Chloramphenicol,

25 mg/kg IV loading dose followed by 15 mg/kg IV four times 

for 10-14 days, is required for the treatment of plague mening

 Usual supportive therapy includes IV crystalloids and

hemodynamic monitoring. Although low-grade DIC m

occur, clinically significant hemorrhage is uncommo

the need to treat with heparin. Endotoxic shock is c

mon, but pressor agents are rarely needed. Finally, 

rarely require any form of local care or surgical draina

but instead recede with systemic antibiotic therapy. 

incision and drainage poses a risk to others in conta

the patient; aspiration is recommended for diagnostic

purposes and may provide symptomatic relief. It is s

dard practice to first inject saline to mobilize aspirate

contents.
serologically.

Prophylaxis: Chemoprop

incubation period may 

symptoms. Therefore

started 8-12 days pos

This regimen has bee

inactivated whole cell 

protection against exp

this vaccine may be s

immunity. Therefore, 

mended to detect pres

Isolation and Decontam

recommended for HC

rare. Patients expose

a risk for secondary co

organism. Decontam

water or a 0.5% chlori

skin decontamination 

Treatment: Q fever is gen

without treatment, but 

given orally for 5-7 day

disease. Q fever endo

treat.

be unusual for infectio

secretions should be s

(ELISA). Acute and co

diagnosis. Nonspecifi

include leukocytosis a

Prophylaxis: There is cu

antitoxin available for 

appears promising in 

chemical protective m

against inhalation.

Isolation and Decontam

HCWs. Ricin is nonvo

expected to be a dang

taminate with soap an

sodium hypochlorite) 

Treatment: Management 

treatment for pulmona

cathartics are indicate

value for large molecu

in discriminating betwe

(See “CDC Protocol fo

www.bt.cdc.gov/agent

Prophylaxis: Immediate 

undertaken for all pers

Isolation and Decontam

tions for a minimum of 

contacts. Patients sh

scabs separate and q

civilian setting, strict q

may prove to be impra

reasonable alternative 

their temperatures dai

during the 17-day peri

case would suggest th

contact should then b

home, until smallpox i

remain in isolation un

Treatment: At present, th

Cidofovir is under inve

case remains support

__________

More information available 
Diagnosis: Diagnosis is clinical. Patients present with a 

respiratory syndrome without CXR abnormalities. La

bers of patients presenting in a short period of time w

symptoms and signs of SEB pulmonary exposure wo

suggest an intentional attack with this toxin.

Prophylaxis: Use of military chemical protective mask. 

currently no human vaccine available to prevent SEB 

tion.

Isolation and Decontamination: Standard precautions 

SEB is not dermally active and secondary aerosols a

hazard from patients. Decontaminate with soap and 

Destroy any food that may have been contaminated.

Treatment: Treatment is limited to supportive care. Arti

ventilation might be needed for very severe cases, an

to fluid management is important.

 Currently, therapy is limited to supportive care. C

attention to oxygenation and hydration is importa

severe cases with pulmonary edema, ventilation 

positive end expiratory pressure, vasopressors a

might be necessary. Acetaminophen for fever, an

suppressants may make the patient more comfo

value of steroids is unknown. Most patients wou

expected to do quite well after the initial acute ph

illness, but generally would be unfit for duty for 1

Severe cases risk death from pulmonary edema 

respiratory failure.
oily fluids contaminati

Confirmation requires 

mental samples.

Prophylaxis: The only de

wearing a military che

topical skin protectan

immunotherapy or che

field.

Isolation and Decontam

removed and exposed 

water. Eye exposure 

irrigation. Secondary 

contact with contamin

secondary dermal exp

warranted until decon

Then, standard preca

Environmental decont

pochlorite solution un

sodium hypochlorite a

time.

Treatment: There is no s

ive. Soap and water w

can significantly reduc

hour may prevent toxi

should be given orally 
administered to victims of an unprotected aeroso

Respiratory support may be necessary. The eyes 

be irrigated with normal saline or water to remove 
mediastinal lymphade

culture is possible but 

established retrospec

Prophylaxis: A live, atten

investigational new dru

It is administered onc

Ciprofloxacin given as 

prophylaxis when give

Isolation and Decontam

HCWs. Organisms ar

mild heat (55°C for 10 

Treatment: Administratio

gentamicin) with early 

 Appropriate thera

otics:

♦ Gentamicin 3 

♦ Ciprofloxacin 

oral Ciproflox

patient is clini

of a 10- to 14-

♦ Ciprofloxacin 

10-14 days.

♦ Streptomycin 

10-14 days.
rates.

___________

* This number may only be answered during regular office 

Monday-Friday, 8:30 AM to 5:30 PM, EST.
Diagnosis: Clinical and ep

findings nonspecific. T

striking leukopenia and 

made from serum, and 

Both neutralizing or IgG 

specific IgM present in a 

infection.

Prophylaxis: A live, attenu

gational new drug. A se

vaccine is available for 

receiving the first vaccin

immunoprophylaxis. Alp

animal models. There a

Isolation and Decontamin

tine is not required. Sta

vector control while the 

of direct human-to-huma

The virus can be destro

standard disinfectants.

may be transmitted to hum

entry. Although evidence f

many of these viruses, the

their potential for aerosol d

likelihood for confusion wi

weaponized.

Symptoms/Signs: VHFs 

flushing of the face an

hypotension, and sho

vomiting, and diarrhea 

fevers.

Diagnosis: Definitive diag

techniques. Significa

hemorrhagic fever syn

a VHF.

Prophylaxis: The only lic

vaccine. Prophylactic 

protocol) may be effec

CCHF, and possibly he

(HFRS).

Isolation and Decontam

addition of a surgical m

coming within 3 feet o

or proven Lassa fever, 

tory protection should 

including the use of a 
namic, hematologic, pulmonary, and neurologic m

tions of VHF, regardless of the specific etiologic a

Only intensive care will save the most severely ill 

Health care providers employing vigorous fluid res

of hypotensive patients must be mindful of the pro

some VHFs (e.g., HFRS) for pulmonary capillary 

Pressor agents are frequently required. The use o

cular devices and invasive hemodynamic monitori

be carefully considered in the context of potential 

versus the risk of hemorrhage. Restlessness, con

myalgia, and hyperesthesia should be managed b

vative measures, and the judicious use of sedative

analgesics. Secondary infections may occur as w

patient undergoing intensive care utilizing invasive 

dures and devices, such as IV lines and indwelling 

eters.

 The management of clinical bleeding should follow 

same principles as for any patient with a systemi

coagulopathy, assisted by coagulation studies. In

cular injections, aspirin, and other anticoagulant d

should be avoided.

 The investigational antiviral drug ribavirin is availab

compassionate use protocols for therapy of Lassa 

HFRS, CCHF, and Rift Valley fever. Separate Pha

efficacy trials have indicated that parenteral ribavir

duces morbidity in HFRS, and lowers both the mo

and mortality of Lassa fever. In the HFRS field tria

ment was effective if begun within the first 4 days o

and continued for a 7-day course. A compassiona

protocol, utilizing IV ribavirin as a treatment for La
Omsk HF and Kya

 Argentine HF resp

of convalescent p

neutralizing antibo

This therapy is inv

protocol.
in the control of infectious diseases. However, we are ofte

to use the most efficient means of rendering microbes har

(e.g., toxic chemical sterilization), as these methods may 

people and damage materials which are to be decontamin

agents can be decontaminated by mechanical, chemical, 

physical methods:

 Mechanical decontamination involves measures to 

but not necessarily neutralize an agent. An exam

filtering of drinking water to remove certain water-b

pathogens (e.g., Dracunculus medinensis), or in 

context, the use of an air filter to remove aerosoliz

anthrax spores, or water to wash agent from the s

 Chemical decontamination renders BW agents ha

the use of disinfectants that are usually in the for

liquid, gas or aerosol. Some disinfectants are ha

humans, animals, the environment, and materials

 Physical means (heat, radiation) are other metho

can be employed for decontamination of objects.

Dermal exposure to a suspected BW aerosol should 

diately treated by soap and water decontamination. Caref

ing with soap and water removes nearly all of the agent fro

skin surface. Hypochlorite solution or other disinfectants 

reserved for gross contamination (i.e., following the spill o

liquid agent from a munition directly onto the skin). In the 

of chemical or gross biological contamination, these will c

additional benefit, may be caustic, and may predispose to 
6-ounce ampules of calciu

These solutions evaporat

they are made in advance

containers. Also, the chlo

distinctly marked containe

difference between the 5% 

solution.

To mix a 0.5% sodium 

Clorox and nine parts wat

a 5.25% sodium hypochlo

applied with a cloth or swa

daily with the pH in the alk

Chlorine solution mus

wounds, as it may lead to 

and spinal cord injuries. H

into noncavity wounds and 

appropriate disposal cont

contaminated solution will 

Subsequent irrigation with 

should be performed. Pre

sprayed into the eyes, as 

For decontamination 

hypochlorite solution shou

equipment, a contact time 

is required. This is corros

most fabrics, so rinse thor

after completion.
chemical agents. Aerosolized particles in the 1-5 μm siz

will remain suspended due to Brownian motion; suspend

agents would be eventually inactivated by solar UV light, 

tion, and oxidation. Little, if any, environmental residues 

occur. Possible exceptions include residua near the diss

line, or in the immediate area surrounding a point-source 

BW agents deposited on the soil would be subject to deg

by environmental stressors and competing soil microflora

Simulant studies at Dugway Proving Ground suggest that 

ary reaerosolization would be difficult, and would probably 

a human health hazard. Environmental decontamination 

is costly and difficult and should be avoided, if possible. 

contaminated terrain, streets, or roads must be passed, t

dust-binding spray to minimize reaerosolization may be c

ered. If it is necessary to decontaminate these surfaces, 

calcium or lye may be used. Otherwise, rely on the natu

processes which, especially outdoors, lead to the decont

of agent by drying and solar UV radiation. Rooms in fixe

are best decontaminated with gases or liquids in aerosol 

(e.g., formaldehyde). This is usually combined with surfa

disinfectants to ensure complete decontamination.
Glanders Low Assumed 

Pneumonic 

Plague 

High 100-500 

organism

Tularemia No 10-50 

organism

Q Fever Rare 1-10 

organism

Smallpox High Assumed 

(10-100 

organism

Venezuelan 

Equine 

Encephalitis 

Low 10-100 

organism

Viral 

Hemorrhagic 

Fevers 

Moderate 1-10 

organism

Botulism No 0.001 μg/

LD50 for t

A 

Staph 

Enterotoxin B 

No 0.03 μg/ 

person 

incapacit

Ricin No 3-5 μg/kg 

LD50

in mice 

T-2 

Mycotoxins 

No Moderate 
term) 

 Tetracycline 500 mg Q6H x 3 d Alternates for 

erythromycin, 

 Doxycycline 300 mg once, or 

100 mg Q12H x 3 d 

 trimethoprim a

sulfamethoxaz

and furazolido

 Ciprofloxacin 500 mg 

Q12H x 3 d 

 Quinolones fo

tetra/doxy resi

strains 

 Norfloxacin 400 mg Q12H x 3 d 

Q Fever Tetracycline 

500 mg PO Q6H x 5-7 d 

continued at least 2 d after 

afebrile 

Tetracycline 

500 mg PO QID x 5 d (start 

8-12 d post-exposure) 

Currently testi

vaccine to 

determine the 

necessity of sk

testing prior to 

 Doxycycline 

100 mg PO Q12H x 5-7 d 

continued at least 2 d after 

afebrile 

Doxycycline 

100 mg PO BID x 5 d (start 

8-12 d post-exposure) 

Glanders Antibiotic regimens vary 

depending on localization and 

severity of disease - refer to text 

Post-exposure prophylaxis 

may be tried with TMPSMX 

No large thera

human trials h

been conducte

owing to the ra

naturally occu

disease. 

Plague Streptomycin 30 mg/kg/d IM in 

2 divided doses x 10–14 d 

 or 

Gentamicin 5mg/kg IM or IV 

once daily x 10-14 d 

 or 

Ciprofloxacin 400mg IV Q12H 

until clinically improved then 

750 mg PO BID for total of 

10–14 d 

Doxycycline 

100 mg PO BID x 7 d or 

duration of exposure 

Ciprofloxacin 

500 mg PO BID x 7 d 

Chlorampheni

plague mening

required 

25 mg/kg IV, t

15 mg/kg QID 

 Doxycycline 200 mg IV then 

100 mg IV BID, until clinically 

improved then 100mg PO BID 

for total of 10-14 d 

Tetracycline 500 mg PO 

QID x 7 d 

Alternate Rx: 

trimethoprimsulfamethoxaz
 Ciprofloxacin 750 m

Q12H for 10 - 14 d 

Viral 

encephalitides 

Supportive therapy: 

analgesics and 

anticonvulsants prn 

Viral 

Hemorrhagic 

Fevers 

Ribavirin (CCHF/La

(IND) 

30 mg/kg IV initial d

16 mg/kg IV Q6 H x 

8 mg/kg IV Q8H x 6 

 Passive antibody fo

BHF, Lassa fever, a

Smallpox No current Rx other 

supportive; Cidofovi

(effective in vitro); a

studies ongoing 

Botulism DOD heptavalent eq

despeciated antitox

serotypes A-G (IND

(10 mL) IV 

 CDC trivalent equin

for serotypes A, B, E 

(licensed) 

Staphylococcus 

Enterotoxin B 

Ventilatory support f

inhalation exposure 

Ricin Inhalation: supporti

therapy G-I : gastric 

superactivated char

cathartics 

T-2 Mycotoxins 


aso poduce a seee dyspea, tpuoay ede

vomiting, headache, syncope also seen. Very high do

produce sudden death without obvious pulmonary lesi

possibly via laryngospasm. All recognized exposures 

referred for direct observation/care.

Patient Evaluation:

 Victim should be immediately removed from the to

environment by fully masked personnel. The M40 

insufficient respiratory protection at the point of re

where chlorine concentrations may be very high. 

protective clothing is required for liquid/solution ex

 Liquid contamination causes eye and skin burns 

Contaminated clothing should be removed/dispose

Treatment:

 General: Persons with inhalational exposures mu

at immediate rest. Exertion increases the extent 

and hastens the onset of pulmonary edema. Sym

trouble breathing are experienced before signs ma

Casualties must be observed for 6 hours after exp

before they can be cleared for discharge.

 Eyes: Liquid exposures should be flushed with co

quantities of water; medical attention should be so

Vapor exposures, if symptomatic, should be flush

water. Medical attention should be sought if sym

 Skin: Liquid exposures should be flushed with co

quantities of water. Contaminated clothing should 

removed/disposed of. Vapor exposures require no 

therapy unless symptomatic. Intense exposure p

burns; wash with water.
p

gospasm may be 

intubation may be 

be required. Med

If stridorous/hoars

vision since laryng

above). Medical a

If dyspnea/cough/

for impending pulm

bronchospasm su

exchange that wh

should be sought. 

help. Be wary of s

pressure ventilatio

pulmonary edema

Fluid managemen

due to fluid shifts f

Rehydration using 

should hypotensio
If becomes symptomatic, treat as above.

If still asymptomatic, lesser observation for additio

6 hours, since some bronchospasm may appear la

If hypoxic from bronchospasm: bronchodilators an

mental oxygen (oxygen may be utilized with positiv

pressure; e.g., PEEP 5-7 cm or intubation).

If pulmonary edema (occurs with moderate to seve

exposures): Treat as noncardiac pulmonary edem

with PEEP 5-7 cm and/or intubation. Control hypo

with fluids, not vasoactive drugs. Diuretic therapy 

severe hypotension if intubation is required.

If infection: Inhalational exposures may produce p

infiltrates, fever, and white blood cell elevations lea

erroneous diagnosis of (presumed bacterial) pneum

Prophylactic antibiotics are not indicated. Surveilla

bacteriologic cultures are obtained anticipating an 

mate 50% risk of nosocomial pneumonia at days 3

If pain: Airway discomfort may benefit from codein

wary of sedation.
cyanide appear w

exposed person h

5-30 minutes afte

ment. Liquid exp

to manifest even a 

poisoning.

 Clues to cyanide 

depression (cyan

and apnea ensue

sions, pink color, 

history of exposu

difficult to distingu

Hydrogen sulfide 

therapeutically id

 Severe cyanide p

If cyanide poison

not have moderat

cyanide poisonin

diagnosis should 

Patient Evaluation: leve

heart rate, convul

 Exposure to a hig

followed by convu

gradual decrease 

(3-5 minutes) and 

minutes).
Treatment:

 For a mild exposure (conscious and breathing): rem

further exposure and observe; no antidotes; oxyge

given to young or old or in presence of heart diseas

patient with mild symptoms.

 Severe exposure (unconscious, decreased respirat

and acidotic): immediately receive 100% oxygen a

as needed. Antidotes should be administered as s

possible (see below). It is important to note that p

oximeter results are completely unreliable in the se

methemoglobinemia, which is induced by amyl nitr

sodium nitrite therapy. Rapid initiation of therapy i

 Cyanide antidotes are packaged in kits containing 

globin formers (amyl and sodium nitrite) and sulfur 

(thiosulfate). Kit contents are appropriate as packa

adults. Antidote is used for severely affected perso

not for mildly affected persons.

 If casualty is seriously affected, and IV/IO line is no

ately available, use amyl nitrite ampules while esta

access. Crush the ampule for casualty to inhale. 

wrapped in gauze and inserted into a nostril, put in

ventilation mask, or inserted into the ET tube. Mon

hypotension and temporarily discontinue use if exc

Once blood pressure responds, restart the nitrite (a

IV). Amyl nitrite is irritating to naïve users and as t

recover they will push it away.
ampules of 300 m

 Follow with 12.5 g

over 20 minutes. 

♦ If initial dose i

initial dose. I

levels are we

minutes if no 

of Antidote Ki

therapy is usu

♦ Seizing patien

therapy with b

lorazepam, m

♦ The earliest s

acidosis towa

aerobic meta

pressure. Ale

to recover.

 If patient continue

continue oxygen t

 Transfer apneic o

facility.

 Patients often rec

occurred. Heada

acetaminophen (T

peripheral nerves 

to months.
__________

* For all ages, crush amyl nitrite ampule and allow it to be inh

up to 3 minutes. If patient is endotracheally intubated, place 

some of its contents in the large end of the ET tube where it c

to the Ambu bag or the ventilator. If amyl nitrite use is to cont

beyond 3 minutes, use a new vial approximately every 3 minu

patient recovers or until sodium nitrite can be administered. 

venous access is established and sodium nitrite is available

ter sodium nitrite and discontinue use of amyl nitrite as soon 

possible.
toxic environmen

 Physical remova

with just copious 

wasting time to p

be removed, and 

immediately avai

tion is a dry abso

The M291 kit follo

decontamination

water rinse is exc

household bleach 

cool water, or tho

acceptable altern

plus wet wipes an

Full strength blea

mustard penetrat

should be flushed 

exposure is to va

oughly wash as a

 If there is a histor

patient becomes 

become impossib

facility for observa

Patient Evaluation: Initi

exposure):

 Eyes: irritation, fe

affected organ. S

swelling may ens

Severe eye injury 

corneal destructio
and assisted ventilation with oxygen should be sta

This patient should be evacuated to an intensive c

as quickly as possible.)

Treatment:

 There is nothing to do for these patients until effec

except to decontaminate. Tissue is damaged with

minutes, so decontamination must be done imme

 Eyes: Acute mustard (both vapor and liquid) casu

should ALWAYS have their eyes copiously irrigate

sterile solution PRIOR to administration of any add

ophthalmic solutions or medications. If copious ir

is not done initially, it may well not be possible lat

eyelids have swollen shut over the eye. Any comm

eye solution may relieve the irritation from a mild e

If significant eye exposure is expected, initiate top

or systemic steroid and antibiotic therapy immedi

redosing frequently (every 15 minutes for topical) f

first day with earliest evacuation to ophthalmic spe

More severe effects: a mydriatic BID or QID (depe

the length of action of the drug) may provide pain r

vaseline on lid edges BID; sunglasses if photopho

present. Control pain with systemic, not topical, a

sics. Visual loss is usually due to lid edema and 

pharospasm, not eye damage.

 Skin: A soothing lotion (e.g., calamine) for erythem

itching. Leave small blisters intact. Do not unroo

of any size until it can be done under sterile condi

(Echelon III). If blisters are flaccid, debride and red

with topical antibiotic. It is very critical to avoid inf

it will increase the depth of injury. Any burns on th
least daily for organ

identified). Second

to develop.

 Systemic absorptio

cause bone marrow 

Monitor lymphocyte 

to severely intoxicat

enough to require m

as soon as possible

first 24-36 hours pre

patients should be e

Within about 5 days 

and septic, and with

platelet counts. Ad

stimulating factor (G

magnitude of granu

Granulocyte counts 

count less valuable
sphere. Physical removal by the fastest available me

even with just copious amounts of water, is far better 

wasting time to prepare a dilute bleach solution. If liq

contact, clothing should be removed and skin deconta

with whatever is immediately available that is clean. U

friction plus a liquid. The M291 kit followed by a wet w

good for gross decontamination. Warm soapy water 

by warm water rinse is excellent. 0.5% hypochlorite (

household bleach mixed with 9 parts water), soap and 

water, or thoroughly flushed with water alone are acce

alternatives. Full strength bleach must not be used fo

enhance mustard penetration and further injure the sk

should be flushed with large amounts of saline. If exp

to vapor alone, remove clothing and thoroughly wash a

All casualties require complete nakedness and full wa

protect the treating personnel.

Patient Evaluation: If conscious, note ventilatory status 

about nausea. If unconscious, note ventilatory status and 

(heart rate may be high, low, or normal in a nerve agent ca

Initial effects differ depending on whether exposure was to 

to liquid.

 Vapor: Effects start within seconds to a minute o

♦ Mild to moderate: Miosis (possible redness 

pain, and complaints of dim or blurred vision, 

rhinorrhea, excess secretions, dyspnea (mild 

severe). Nerve agents cause severe broncho

and bronchorrhea, the worst conceivable asth

attack.
Treatment:

 Initial managemen

♦ Mild to moder

one or two do

of pralidoxime 

of the dyspne

below for size 

with oxygen, 

repeated at 5- 

ment is noted

mouth, no de

to administer 

trointestinal e

in the same m

eye pain is se

FOR SELF-C

• Mild expo

• Moderate 

symptom

atropine a

symptom

• Severe ex

MARK 1 

already s

Repeat a

respirato

MARK 1’s 

respirato

PAM per 
(CANA) must be administered in ALL of 

situations.

♦ Severe: Administer three doses of atropine IM 

IV in hypoxic patient) and start one dose of

pralidoxime by slow IV drip over 20 minutes. 

rapid administration will cause hypertension.) 

“Recommended adult doses” below for size o

Intubate and ventilate with oxygen. Initial ven

will be difficult because of airway resistance; 

pine will relieve this. Administer diazepam if c

ing. Suction for secretions. Repeat one dose 

atropine (IM until hypoxia is improved, then IV

5 minutes until:

• secretions diminish or

• airway resistance is less or is normal.

Failure to respond (i.e., no dry mouth, no dec

in secretions) confirms the need to administe

additional doses of atropine. Monitor via puls

oximeter; cardiac monitoring should also be d

Cardiac arrhythmias are uncommon after atro

given. Acidosis may develop after seizures o

period of hypoxia and will require therapy. Pa

should be medically evacuated to a hospital a

stabilization (adequate drug therapy and initia

ventilation).

♦ Eyes: Do not treat miosis unless eye/head p

severe. Use topical, not systemic, anticholin

relieve pain. Papillary constriction may persi

to 2 months.
 Further care.

♦ Give atropine 

ing comfortab

secretions ar

exposure, thi

even days.

♦ Mild to mode

who is breath

hospitalized a

should be foll

weeks). Afte

observed in h

absorbed from 

♦ Severe: Con

atropine follo

present. If pa

recovery of a

over 1-3 hour
and causes noncardiogenic pulmonary edema. Develop

pulmonary edema within 4 hours of exposure is a very po

prognostic sign.

Patient Evaluation:

 Victim should be immediately removed from the tox

environment by fully masked personnel (full-face pos

pressure apparatus).

Treatment: Maintain at rest at least 6 hours.

 Eyes: Gas exposures, if symptomatic, should be

flushed with water.

 Skin: Gas exposures require no specific therapy

unless symptomatic.

 Breathing: symptoms precede signs. Casualties m

complain of dyspnea on exertion. Evaluate respirat

cyanosis. Oxygen always used –

If apneic: CPR with intubation. Be aware that laryngosp

may be present with intense exposures; hence, intubati

be very difficult and tracheostomy required.

If stridorous/hoarse: Consider intubation under direct vis

since laryngospasm maybe imminent (see above).

If dyspnea/cough/chest tightness: Consider intubation f

impending pulmonary edema.
Steroids: methylpredniso

Theophylline: load 150 m

If asymptomatic: Maintai

 6 hours;

If becomes symptomatic, 

If still asymptomatic, lesse

If hypotensive (will occur r

Immediate volume replac

or crystalloid may be used 

sion.

If infection: Inhalational e

infiltrates, fever, and WBC 

diagnosis of (presumed b

antibiotics are not indicate

are obtained anticipating 

mial pneumonia at days 3

If hypoxia: Commonly fro

occasionally from broncho

If pain: Airway discomfort 

sedation.
ATROPINE at 1 mg/ml drug

concentration

(0.02 mg/kg Pediatric, 2 mg adult) 2 mL

ATROPINE at 2 mg/mL drug

concentration

(0.02 mg/kg Pediatric, 2 mg adult) 1 mL

PRALIDOXIME (2-PAM,

Protopam®) at 50 mg/mL

(for IV use)

(50 mg/kg Pediatric, 1000 mg adult) 20 mL

PRALIDOXIME (2-PAM, Protopam)

 at 300 mg/mL (for IM use)

 (40 mg/kg Pediatric, 600 mg adult)

(Reconstitute by adding

3 mL sterile water to a 1 g vial

of pralidoxime) 20 mL

SODIUM NITRITE at 3%

(300 mg/ 10 mL)

(Pediatric 0.3 mL/kg for Hgb 11 g/dL,

adult 10 mL) 10 mL

SODIUM THIOSULFATE at 25%

concentration

(Pediatric 1.65 mL/kg, adult 50 mL)

®Protopam is a registered trademark of Wyeth Ayerst L

Madison, New Jersey.
y 

 Chemicals from Inha
 Uncontrolled or poorly controlled occupational ex

deployed military personnel, and in specific occup

groups, is quite possible. The resulting health ef

not be clearly linked with such exposures unless 

(fire, ruptured tanks, etc.) occurs that makes the 

of exposure evident. Based on the presenting cli

signs or symptoms, health care practitioner (HCP

remember to inquire about the possibility of occup

exposures to TICs to their patients and to others 

with. The “Chemical Exposure Questionnaire” loc

the end of Part Four should be used as a screeni

patients whose complaints or clinical signs are p

related to an occupational or environmental expos

during deployment. The practitioner should attem

positive answers to the questions with signs and 

toms found during the clinical encounter, thus pro

any appropriate interventions. Known exposures 

documented in the medical record.

 When a TIC release is either accidental or due to 

or warfare event, and casualties are obvious, it is 

always practical to consider every specific chem

may have been present for early casualty manage

One can, however, consider major classes of che

that were likely and how they are expected to affe

exposed population, thus guiding general treatme

measures. This part of the TG is organized arou

of chemicals and their toxic syndromes (“toxidrom

♦ Toxidrome classes include irritant gases, cor

asphyxiants, organic vapors (hydrocarbons a

chlorinated hydrocarbons), and cholinergics.
commerce with 

♦ Inhalation and 

most chemical 

However, terro

and water supp

♦ The Table (Sum

Industrial Chem

located at the e

tial information 

industrial chem

Its use is inten

and characteri

as provide exp

health effects a

more chronic e

teratogenicity.

♦ A few chemica

which will be p

♦ There are chem

initial treatmen

toxicities (e.g., 

will be pointed 

look up informa

as time permits 

 Products of combu

unknown and toxic 

tered in a wartime/d

toxidrome categori

are irritant gases a
from trauma and chemical exposures.

 Other important basic principles to bear in mind:

♦ The incident site should be organized to provid

immediate decontamination, triage and care fo

persons, but at the same time protect the res

from exposure/injury themselves.

• Organize control zones (“hot,” “warm,” “co

zones).

• Firefighters and other rescuers should we

protective equipment to avoid becoming c

themselves.

• Except for immediate life-saving procedur

ABCs), decontamination of chemically co

nated patients is the priority in the warm z

(Removal of contamination prevents furthe

tion, as well as secondary contamination 

others.)

• Finish the primary survey (ABCDE), resus

triage and transport in the cold zone.

♦ Characterize what happened, types of exposu

document who the exposed personnel are as 

possible.

 Acute and chronic effects can vary among differen

populations (e.g., occupational groups, including m

personnel, are typically healthier than many of the 

residents who may have more preexisting sensitiv

susceptibilities).

 It is difficult to determine if a substance is a corro

irritant in a particular concentration or circumstan

 Irritants are substances that cause inflammation 

swelling, but not cellular death and tissue damag

corrosive would cause cellular damage and death

Acute Effects:

 Throat, eye, nose or skin irritation (rhinorrhea, lac

choking feeling, burning feeling, coughing, tachyp

wheezing.

 Headache, and nasal dryness and hemorrhage.

 Skin: Redness, swelling, and pain may occur.

 To determine potential severity of the exposure, c

ize the circumstances (e.g., what particular subs

involved, duration of exposure, determination of if 

occurred in a confined space, and if the patient h

of consciousness).

 Highly water soluble irritant gases cause immedia

irritation of the upper respiratory mucosa. Most p

find this unpleasant enough to get away before gr

damage is done. However, if they are trapped an

breathe or be in contact with high concentrations 

enough periods, damage will occur. Eyes and sk

burn and necrose. Upper airway will be affected 

prolonged high concentration will affect lower airw

well. Patient may have trouble with breathing and 

absorption, hyperreactive airways (asthma), glott

esophageal edema, hoarseness, stridor and laryn

(danger of airway obstruction). Development of p

edema may be delayed by 1-3 days. Circulatory 

can occur in severe cases.
and nervous syst

seizures, decreas

likely be due to th

system damage (

Chronic Effects:

 Reactive airways 

persistent asthma 

♦ Onset within 2

♦ Positive meth

♦ Persistence o

hyperreactivi

♦ Symptoms si

ing, and dysp

♦ Airflow obstru

function tests

 Skin: Allergic con

repeated exposur

Treatment:

 Using wide-range 

stance if possible

 Move patient to fr

tress. If symptom

administer oxyge

Use 100% humid

sisted ventilation 

prolonged. Cons

ing upper airway o
bia persist, an ophthalmologic examination sh

be performed including a slit lamp exam after

thorough irrigation.

♦ Administration of topical antibiotics, cyclople

mydriatics, and patching may be necessary i

instances of abrasion.

 Support respiratory and cardiovascular function. 

or difficulty in breathing develops, evaluate for res

tract irritation, bronchitis, or pneumonitis. Carefu

observe patients with inhalation exposure for the d

ment of any systemic signs or symptoms and ad

ter symptomatic treatment as necessary. Espec

with low solubility irritant exposures, if there is evi

of pulmonary edema within 4 hours, intensive car

likely be needed. If no symptoms are observed w

hours and the CXR is normal, acute lung injury is

unlikely to develop. If acute lung injury is possibl

patient must have strict bedrest without exertion.

Physical exertion can exacerbate the severity of t

inflammation.

 Evacuate patients with moderate symptoms, che

signs, or impaired oxygenation. Observe for at lea

hours if exposure has been to substances known 

cause delayed onset of pulmonary symptoms. C

ray may be needed. Crystalloid solutions must b

administered cautiously to avoid a net positive flu

balance. The use of corticosteroids is controvers
♦ Irritants are s

swelling, but 

A corrosive w

♦ Examples of 

phosphoric, a

♦ Examples of b

sodium hydro

♦ Examples of c

dioxide, hydro

peroxide, and 

♦ Examples of a

red, and white 

Toxidrome: local chemic

membranes that come 

Acute Effects:

 Swelling, redness 

at mucous memb

susceptible. Lung 

 Headache, nasal 

rhinnorhea, lacrim

 Lung irritation sym

difficulty breathing

 Upper airway sign

and throat tightne

hoarseness, strido

upper airway obst

fest wheezing and 

larynogospasm, b
anemia due to hemolysis or methemoglobin forma

absorbed systemically (e.g., chromates, nitrates/

nitrites). Tachycardia and other reflexive cardiovas

reactions would be expected.

♦ Cardiac effects (e.g., pump failure or dysrythm

are possible with white phosphorus (WP) and

hydrogen fluoride (HF) due to hypocalcemia (b

direct cardiotoxicity (WP).

 Nervous system effects can result from hypoxemi

hypovolemia or anemia (anxiety, confusion, agitat

seizures, decreased level of consciousness, com

death) or hypocalcemia (tetany, seizures).

 Skin and eyes: Pain and irritation, or corrosion a

burn site (acids produce a coagulation burn, base

produce a liquifactive necrosis (slippery burn or sa

cation).

 Systemically absorbed WP can cause kidney or l

damage.

Chronic Effects: Scarring; RADS (see irritant gases).

Treatment:

 Move patient to fresh air. Administer 100% humid

supplemental oxygen with assisted ventilation as

required. Airway intubation if needed – sooner ver

later if signs of impending airway obstruction are p

(see above). Cardiac monitoring or support as ind

and available.

 Decontamination by diluting and irrigating is critic

♦ Remove clothing and promptly irrigate skin wi

copious amounts of water.
comfort.

 Monitor for respir

breathing develop

tion, bronchitis, pn

 Consider and trea

effects (see notes 

 Labs as indicated 

electrolytes, liver 

urinalysis).

 Evacuate patients 

signs, or impaired 

hours if exposure 

cause delayed on

 Specific systemic 

♦ Acids produc

and hardened 

limit deeper p

are possible w

the anion is m

hydrogen ion

acid is a relat

ion is very tox

Chromic acid 

oxidizer (and 

on this), and 

poisoning.

♦ Bases produc

fies and dest

penetrate dee

however, bas

systemic effe
(secondary to pigment release).

 White phosphorus spontaneously combusts on co

with air. It produces both chemical and thermal bu

Immersion in water stops the burning. It is unlike

inhaled, but its reactive combustion products, suc

phosphorus pentoxide and related oxyacids, could 

inhaled.

♦ On the skin, it causes serious burns and syst

toxicity. It can be absorbed through the burne

to produce kidney and/or liver damage.

♦ Liver damage and even failure, and renal insuff

and even failure, can be delayed development

♦ Before liver or kidney damage is apparent, the

be rapid cardiovascular collapse due to hypovo

from the burns, and direct cardiotoxicity with p

failure (cardiogenic shock) and dysrhythmias.

♦ It also combines with endogenous calcium to

produce hypocalcemia (can lead to prolonged 

torsade de pointes, and negative inotropy with

decreased cardiac output).

♦ It is damaging to eyes and mucous membrane

can cause blindness.

 White phosphorus is often embedded in skin and s

be removed. To better visualize:

♦ Use a black light in a dark room (phosphoresc

♦ Apply 1-3% copper sulfate solution (color cha

bluish copper phosphide). Use sparingly as s

temic absorption can cause hemolysis.

♦ Immerse removed WP in water to prevent spon

ous combustion.
also very serious 

 Hydrogen fluoride 

administration of 

should be contac

the procedures be

♦ Inhalation ex

solution of ca

nebulizer. (D

♦ Topical applic

gel form, or u

involved.

♦ Local subcut

titrated to reli

skin surface 

subcutaneou

♦ IV injection fo

gluconate 10

control cardia

calcium chlo
with hemoglobin-mediated oxygen transport: 

amines, organic nitro compounds, or inorgani

or nitrate salts such as amyl nitrite, aniline, is

nitrite, nitrobenzene, nitroglycerine, and sodiu

nitrite.

♦ Carbon monoxide (CO) interferes with hemogl

mediated oxygen transport and oxygen utiliza

mitochondrial cytochrome oxidase.

♦ Cyanides, cyanogenic compounds (acetonitri

acrylonitrile, cyanogens, cyanogen chloride), 

(such as hydrogen, potassium, and sodium s

and azides (such as hydrogen, lead, and sod

azide) interfere with oxygen utilization by mito

drial cytochrome oxidase.

Toxidrome: Inadequate oxygenation of tissues, especial

those with high aerobic metabolic demand (e.g.,

cardiovascular and central nervous system).

Acute Effects:

 The neurologic and cardiopulmonary systems will 

first to show effects as they are the most depende

oxygen.

♦ Mild symptoms include dizziness, weakness

fatigue, headache, nausea.

♦ Vision changes can include decreases in nigh

vision, visual acuity, and visual fields (tunnel v

♦ More severe symptoms include dyspnea, tach

dia, tachypnea, air hunger, hyperventilation, a
♦ Cyanosis is no

may interfere w

transport in blo

red, but causin

azide poisoning

♦ Methemoglobi

brown-colored 

appears bluish 

methemoglobi

♦ Skin appearan

exposure) doe

cherry red.

♦ There may also 

activity such a

 Effects of lack of ox

to escape from the 

 Some agents caus

ported in compress

frostbite on direct s

Chronic Effects: If hypoxia 

exists for anoxic damag

injury, eye/vision damag

transient blindness, reti

(acute tubular necrosis, 

Treatment:

 Removal from expo

humidified oxygen 

whatever other ven

quired. Arterial blo
patients with inhalation exposure for the developm

any systemic signs or symptoms and administer

symptomatic treatment as necessary (e.g., seizu

 Patients with severe or prolonged exposure shou

carefully evaluated for neurologic and other seque

 Freeze injury associated with dermal exposure to

compressed or liquid forms (i.e., propane) is unlik

frostbite in that the damage occurs within second

rewarming is not beneficial. Freeze injuries of th

nature should be managed much like a thermal b

 If a patient appears with characteristic symptoms 

particular asphyxiant (or is known to have been e

posed) which has an antidote, administration of t

timely manner can be lifesaving.

 Specific antidotes:

♦ There are specific antidotes to some of the s

temic asphyxiant exposures (e.g., a cyanide

poisoning antidote kit, or hyperbaric oxygen f

but it may be difficult in the field setting to m

specific diagnoses regarding a mixed exposu

♦ Note: This list is to remind you that these a

exist. There are specific instructions and cav

regarding how to administer these antidotes w

should be obtained from your local consultan

packaging inserts, or medical texts:

• Carbon monoxide: hyperbaric oxygen (H

may be lifesaving.

• Methemoglobin-forming compounds: me

blue. Methemoglobinemia results in a ch

late brownish-colored blood when viewed 
(to form m

 Special notes:

♦ Hydrogen sulf

immediate los

down” (needs 

nerve gas kno

(see irritant ga

and possibly l

♦ Hydrogen sulf

though they h

“olfactory fatig

after a short p

♦ Hydrogen azi

irritant gas (se

lower respirat

without as mu

♦ Nitrites and n

direct vasodila

headache, hy

cope, and cer

infarction due 

♦ Smoke/produ

burning buildi

as componen

Examples: cy

are also comp

♦ Some asphyx

and hydrogen 

settle in low p
Some hydrocarbons such as methane and pr

are also dangerous because they are highly f

mable and can form explosive mixtures with 

 Stages of exposure for simple asphyxiants: Fou

are described, depending on the arterial oxyg

saturation. All early effects may decrease ab

self-rescue from the toxic environment.

♦ INDIFFERENT STAGE:

• %O2 Saturation: 90%

• Night vision: decreased

♦ COMPENSATORY STAGE:

• %O2 Saturation: 82 to 90%

• Respiratory rate: compensatory increas

• Pulse: compensatory increase

• Night vision: decreased further

• Performance ability: somewhat reduced

• Alertness: somewhat reduced

• Above symptoms may begin earlier in th

with significant preexisting cardiac, pulm

or hematologic diseases.

♦ DISTURBANCE STAGE:

• %O2 Saturation: 64 to 82%

• Compensatory mechanisms become ina

(air hunger; fatigue, tunnel vision, dizzine

headache, belligerence, euphoria, reduce

visual acuity, numbness and tingling of e

ties, hyperventilation, poor judgment, me

loss, cyanosis, decreased ability for esc

from toxic environment).

 Examples of HHCs include (halogenated can b

chloride, bromide, fluoride, iodide)—

♦ methylene chloride.

♦ chloroform.

♦ carbon tetrachloride.

♦ trichloroethane (TCA).

♦ trichloroethylene (TCE).

♦ perchloroethylene (PCE).

♦ vinyl chloride.

Toxidrome: sleepiness, even to the point of narcosis (de

stupor or coma), and cardiac irritability with premature

ventricular contractions (PVCs) and even ventricular ta

cardia (VT) or ventricular fibrillation (VF).

Acute Effects:

 Exposures in confined spaces with poor ventilatio

be deadly.

 Neurologic: CNS depression (headache, dizzine

a sense of intoxication, confusion, decreased lev

consciousness, sleepiness), general anesthesia 

narcosis, possibly to respiratory depression and 

coma, and death. (Some H-HCs used to be used 

general inhalational anesthesia.)

♦ Most likely from vapors of halogenated, arom

other higher molecular weight hydrocarbons, 

volatile petroleum distillates.

♦ Halogenated and aromatic hydrocarbons can

produce CNS depression following ingestion.
short chain molec

and butane) can a

with dyspnea, cou

hypoxemia.

 Skin:

♦ Liquid HCs an

solvents and 

branes with a

defatting derm

and cracking

♦ With extensiv

can be absor

ute to system

♦ Frostbite can 

fied gases (e.

♦ HC and H-HC

drying to the 

tract.

 Eyes can be injur

tion, blurred vision

ation. Mild to mod

ocular injury may 

carbons.

 Ingestion is not th

“accidents” but ke

can have some st

aspiration pneum

the patient’s exha

pneumonia may h

sputum productio

breath sounds, hy
can cause headache, dizziness, weakness, confu

agitation, seizures, coma, and even death. Tachy

and tachypnea would be expected.

 Liver or kidney toxicity: Many H-HCs are metabo

in the liver and kidney and can cause toxicity and

failure. Kidney effects can also occur due to hypo

♦ Liver: elevated transaminases possible. Sign

cantly hepatotoxic H-HCs: carbon tetrachlorid

chloroform, 1,1,2-trichloroethane (vinyl trichlor

Less hepatotoxic: trichloroethylene, tetrachlo

ylene and 1,1,1-trichloroethane. Carbon tetra

ride can cause fatty liver.

♦ Renal effects (acute renal tubular necrosis, pr

teinuria, or hematuria) occur infrequently follow

acute exposure to petroleum distillates and o

unsubstituted hydrocarbons. Many H-HCs are

potentially nephrotoxic.

 Disseminated intravascular coagulation, hemolyti

anemia, and pancytopenia have occasionally bee

reported following vapor inhalation, aspiration, or i

tion of HCs. Rhabdomyolysis has been reported.

Chronic Effects:

 Long-term or repeated exposure to certain aroma

chlorinated HCs can result in hematologic (e.g., b

zene), hepatotoxic (e.g., chlorinated HCs), renal (

chlorinated HCs), neuropsychiatric (e.g., toluene)

neurological (e.g., n-hexane) and carcinogenic (e

known: benzene, vinyl chloride; suspected: carb

tetrachloride, chloroform, methylene chloride, me
Treatment:

 Treatment involve

tamination, oxyge

support as neede

 Move patient to fr

supplemental oxy

required. Monito

difficulty in breath

tract irritation, bro

tract irritation, if s

edema, which ma

hours after expos

 Support respirato

nephrine and othe

used with caution 

of the myocardium 

 Decontaminate:

♦ Remove all co

absorption.

♦ Wash all exp

soap and wat

♦ Exposed eye

amounts of te

normal pH if 

phenol or ani

lacrimation, o

should have a

 A physician may 

areas if irritation o

clinician experien
In cases of significant inhalational abuse, chlorinat

exposure, prolonged unconsciousness and hypox

prolonged and extensive dermal exposure to liquid 

HC injection:

♦ Monitor CBC, urinalysis, and liver and kidney f

tests, and serum CPK in patients with signific

exposure.

♦ Monitor fluids and electrolytes.

♦ Monitor arterial blood gases, pulmonary functi

chest x-ray for patients with significant exposu

 Benzene may particularly produce abnormalities o

hematopoietic system. Monitor the complete bloo

for patients with significant exposure.

 Monitor methemoglobin level in cyanotic patients w

not respond to oxygen and who may have been ex

to aniline or nitrobenzene.

 Special notes:

♦ Natural gas and petroleum are the sources of 

HCs, and they can be aliphatic (straight or bra

chained), aromatic (with at least one benzene 

or substituted with a chemical constituent in p

the hydrogen, such as hydroxyl or nitro or am

groups or halogenated (having a halide constit

such as chlorine, fluorine, bromine or iodine). T

are many HC, substituted HC, and H-HC comp

and besides having certain effects in common

have their own unique toxicities.

♦ HCs can be gaseous, liquid or solid (physical 

dependent upon chain length/molecular weigh

shorter chains/lower MWs tending to exist as 

and longer chains/higher MWs tending to exis
 Other specific ch

♦ N-hexane: lon

neuropathy, w

from a single 

♦ Phenol is rap

the skin lead

thetic on the s

can result alo

dysrhythmias 

death.

♦ Aniline produ

hepatotoxicity

♦ Pentachlorop

oxidative pho

and allow sub

tachypnea, h

and cardiac ir

and cardiovas

♦ Benzene is a 

exposure als

pancytopenia

♦ Methylene ch

CO and can p
♦ Chemical warfare nerve agents (CWA) are als

cholinesterase inhibitors.

♦ Major differences between OP pesticides and 

agents involve vapor pressure, timing for “agin

[making a permanent bond with acetyl cholin

erase (Ach-ase) – becoming irreversible] and 

of antidote needed. OP pesticides are, in gen

more oily and less volatile, take a longer time 

aging, and require much more antidote over ti

(even though the nerve agents are acutely mo

toxic. OPs have a slower onset of toxicity bu

effects last longer.) Carbamates do not age (

always reversibly bound to Ach-ase).

Toxidrome: PNS muscarinic: diarrhea, urination, miosis

bradycardia, bronchorhea, bronchospasm, emesis, la

tion, salivation, secretion, sweating (DUMBELS) and/

nicotinic: mydriasis, tachycardia, weakness, hyperte

hyperglycemia and fasciculations (MTWTF), and/or C

confusion, convulsions, coma.

Acute Effects:

 Cholinergic nerve endings or synapses (nicotinic a

muscarinic) occur in the central nervous system (

and peripheral nervous system (PNS). PNS inclu

the sympathetic and parasympathetic ganglia, ne

muscular junctions and neuroeffector junctions (p

sympathetic). Some of the effects can be contra

and competing.

♦ PNS muscarinic effects are also remembered 

SLUDGE (salivation, lacrimation, urination, de
respiratio

due to CN

paralysis

• Cardiova

sympathe

parasymp

bradydys

predomin

• Other eff

(pupillary 

but usua

♦ Opthalmic eff

headache, an

♦ CNS effects i

confusion, ag

death.

♦ Skin: most o

irritation, exc

OPs absorb w

membranes (

or dusts). Ca

sorbed. Swe
exposure. It manifests as burning or tingling, then

progressive distal weakness and ataxia in the low

limbs. Flaccid paralysis, spasticity, ataxia or qua

gia may ensue. Recovery may be slow or incomp

 Sequelae may also include subtle neuropsycholog

deficits. Decreased vigilance, defects in expressiv

language and cognitive function, impaired memory

depression, anxiety or irritability and psychosis ha

been reported as delayed effects.

 The HC diluent may contribute to the overall toxic

Refer to HCs management for further information.

Treatment:

 Remove to fresh air. Ensure adequate ventilation 

oxygenation (100% oxygen as indicated). Airway

suction and/or intubation may be needed. Cardia

monitoring and support as needed. Treat seizures 

valium or lorazepam. Provide specific antidotes a

needed, promptly.

 Decontaminate:

♦ Remove all contaminated clothing to prevent f

absorption.

♦ Wash all exposed areas of the body thorough

soap and water.

♦ Exposed eyes should be irrigated with copiou

amounts of tepid water for at least 15 minutes
Patients who have 

those who develo

more likely to deve

a worse prognosi

 Specific antidotes

♦ Atropine:

• Symptom

only. It w

fasciculat

respirato

acetylcho

• Initial dos

every 5 m

orrhea, br

Severely 

doses – u

weeks.

♦ Pralidoxime (2

• Reactivat

“aged”) if 

dosage. 

needed fo

sure wha

• Infuse SL

1-2 gram

infusion o

RBC cho

discontin

 Soldiers are fit-tes

issued to them fo

mask with the C2

other reactive ma

 The M-40 series m

to be used by sol

various potential w

ing CWA, BWA, r

TICs that are also 

mask filters are te

and are required t

CWAs besides ne

agents (hydrogen 

agents (phosgene

(orthochlorobenzy

chloroacetopheno

cyanide and cyan

phosgene, are als

military protective 

protection against 

 The only TICs in t

specifically design

are hydrogen cya

gene; for tactical s

doctrine should be 

simulation studies 

series mask filter 

other TICs (e.g., s

Industrial Chemic

For various reason
into consideration what all of the confounding facto

in a deployed situation. See footnote I of Summar

Common Acutely Toxic Industrial Chemicals from I

tion Exposure table.

 When NIOSH-approved commercial respirators are

available and indicated, each type has specific gui

on fit testing, proper use, and maintenance. Soldie

should be trained and properly fit tested. When re

tors are indicated for occupational duties, as much 

practicable in the military-unique setting, a respira

protection program should be in place.
j

− New or different exposu

(chemical/biological/radi

(Inquire from list below abo

− Is ventilation adequate w

− Increased stress? 

− Do you get the material(

− Can you smell the chem

− Do you wash your hands 

− Do you use—or were yo

such as gloves, masks, 

(Specify the equipment.) 

− Were you instructed in th

Environmmental factors at 

Is your deployment locatio

commercial business, dum

concern? 

Is air pollution a problem? 

Are pesticides or herbicide

What is your source of drin

bottled water, other) 

Is the water purified prior to 

Any unusual or irritating ex

[If answered ‘yes’ t
[Review of systems as appropriate.] 

Exposures about which to inquire (and examples in parenthes

During your deployment, have you been exposed to the following? 

Metals? (arsenic, beryllium, cadmium, chromates, lead, mercury

nickel) 

Dust or fibers? (asbestos, coal dust, fiberglass, rock dust, silica 

talc) 

Fumes or mists? (welding fumes) 

Workplace chemicals? [gasoline, solvents, oils, acids, alkalis, 

industrial alcohols, ketones, pesticides – try to name specific 

chemicals (see list below)] 

Chemical warfare agents? 

Army-specific chemicals? [explosives, fogs (trinitrotoluene)] 

Radiation? (x-rays, lasers) 

Biologicals? (molds, viruses, insects, Anthrax, Smallpox, Bot tox

Ricin, tularemia) 

Loud noise, vibration, extreme heat or cold? 

Specific chemicals for query: ammonia, benzene, ca

tetrachloride, chlorinated naphthalenes, chloroform, dichlorobenz

ethylene dibromide, ethylene dichloride, halothane, isocyana

ketones, methylene chloride, perchlorethylene, phenol, phosg

styrene, toluene, TDI or MDI, trichloroethylene, vinyl chloride, PC

PBBs. 
Summary of Common Acutely Toxic Indu

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

Ph

(O

Thr

Acrolein 107-02-8 

Irritant vapor/ corrosive 

Colliqu

(1.8 pun(0.5 

Acrylonitrile 107-13-1 

Asphyxiant (cyanide; antidote!) (this effect can be delayed) Irritant vapor/corrosive; other systemic effects possible

Colyell(1.6 onio

Allyl alcohol 107-18-6 

Irritant vapor/corrosive; other systemic effects (liver, kidney) 

Col

(1.7 

mus

(6 p
Summary of Common Acutely Toxic Ind

Chemical/ 

CASRN Toxidrome Class(es) and Other Prominent Effects 

(

Ammonia 7664-41-7 Irritant gas C

(

puo

(11

Arsine 7784-42-1 

Primary effect: hemolysis Secondary renal failure; Effects may be delayed for hours. (arsenic) 

Cmo(0

Boron trifluoride 7637-07-2 

Irritant gas. Treat as hydrogen fluoride; also boron toxicity 

Cpuo
Summary of Common Acutely Toxic Indust

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

D

(Odo

an

Th

nas

Bromomethane 74-83-9 

(aka methyl bromide); irritant gas; halogenated hydrocarbon. Alkylating agent. Multisystem effects – neuro/psych (seizures); liver, skin vesicant etc. Effects can be delayed by hours. 

Colorchlorat higconceppm) 

Carbon monoxide 630-08-0 

Asphyxiant (antidote!) 

Colorgas. (
Summary of Common Acutely To

Chemical/ 

CASRN Toxidrome Class(es) and Other Promine

Effects 

Chlorine 7782-50-5 Irritant gas Cyanogen chloride 506-77-4 

Asphyxiant (cyanide, antidote!); irritangas 

Diborane 19287-45-7 

Irritant gas; (possible neuro, liver, kidney) (boron) 
Summary of Common Acutely Toxic Industr

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

P

De

(Odor 

and 

Thr

nasa

Dimethylamine 124-40-3 

Irritant gas/corrosive 

Colorlan ammlike odppm) j

Ethylene oxide 75-21-8 

Irritant gas; corrosive; alkylating agent. neuro (seizures, irreversible damage), GI- N, V, etc., skin irritant/ vesicant 

Colorlliquid with aodor. (420 p490 ppsweet/odor)M 
Summary of Common Acutely Toxic Indu

Chemical/ 

CASRN Toxidrome Class(es) and Other Prominent Effects 

(O

n

Fluorine 7782-41-4 Strong irritant gas Pa

grepuodrea

pp

(25na

Formaldehyde 50-00-0 

Irritant gas; corrosive; (poss.neuro, kidney, metab.acidosis acutely); (allergic reactions) 

Newisu(0

(0ey
Summary of Common Acutely Toxic Industr

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

De

(Odo

and 

Thr

nas

Hydrazine 302-01-2 

Irritant vapor/corrosive; (can have delayed effects) [asphyxiant (metHb poss.)] Hemolysis;CNS excitation/ seizures; liver; kidney; GI-n,v,d; blood sugar Antidotes! :pyridoxine-Vit B6; methylene blue prn 

Coloroily libelow (3.7 pammo

Hydrogen bromide 10035-10-6 

Irritant gas 

Colorsharpodor. 

(5 ppm throat
Summary of Common Acutely Toxic Ind

Chemical/ 

CASRN Toxidrome Class(es) and Other Prominent Effects 

(

Hydrogen chloride 7647-01-0 Irritant gas C

ypo

(3

Hydrogen cyanide 74-90-8 

Asphyxiant (antidote!) 

Cb(abo

Hydrogen fluoride 7664-39-3 

Irritant gas/corrosive (hydrofluoric acid); systemic effects – hypocalcemia, etc – antidote!). 

Cfu(bso

(5 n
Summary of Common Acutely Toxic Indus

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

D

(Od

an

Th

na

Hydrogen selenide 7783-07-5 

Irritant gas; (poss. delayed 2-12 hrs: GI – n,v,d, chills, malaise, etc.; ?cor) (garlic odor on breath) 

Coloan odecaradis

(1.5 

Hydrogen sulfide 7783-06-4 

Irritant gas; asphyxiant (“knock down”); possible antidote! 

Colo(0.000.00rotte

(50-
Summary of Common Acutely Toxic Indu

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

Mercury 7439-97-6 (see other resources for most mercury cmpds. Here discussed: elemental mercury vapor-acute effects) 

pulmonary irritant (pneumonitis), kidney (ATN); neuro (mostly with subacute and chronic exposures); gingivitis (delayed few days); within hours: weak, chills, GI-n,v,d etc. (consider chelation) 

Monomethylamine 74-89-5 

Irritant gas/corrosive 
Summary of Common Acutely Toxic Indu

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

(O

a

T

n

Methyl hydrazine 60-34-4 

Irritant vapor/corrosive; (can have delayed effects) [asphyxiant (metHb poss.)] Hemolysis;CNS excitation/ seizures; liver; kidney; GI-n,v,d; blood sugar Antidotes! :pyridoxine-Vit B6; methylene blue prn 

Fumliquam(0.9

Methyl isocyanate 624-83-9 

Strong irritant vapor/corrosive; (cyanide poisoning unlikely) (poss. liver, kidney, sensitization) 

Cola shodo

(2 p
Summary of Common Acutely Toxic Indu

Chemical/ 

CASRN Toxidrome Class(es) and Other Prominent Effects 

D

(O

a

T

na

Methyl mercaptan 74-93-1 Irritant gas; CNS depression, asphyxiant- siImilar to Hydrogen Sulfiide, poss. MetHB Col

(0.0d, 0r, roodo

Nitric acid 7697-37-2 

Irritant vapor/Corrosive; [poss. MetHb (see asphyxia) and hemolysis if nitric oxides formed in air from released acid] 

Colred, with suffppm

(62 

Nitrogen dioxide 10102-44-0 

Irritant gas (may be delayed effects up to 72 hrs or more); poss metHB (see asphyxia) 

Yelliqubro70°punSol(1 p(10
Summary of Common Acutely Toxic Ind

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

(

Parathion 56-38-2 cholinergic 

PabrgaSo(0

Phosgene 75-44-5 Irritant gas 

Csum1.

(1nath

Phosphine 7803-51-2 

Irritant gas (may be delayed onset of lung injury); systemic asphyxiant (brain, kidney, cor, liver) [beware: Al or Zn phosphide rodenticides and water!] 

C

(0ga
Summary of Common Acutely Toxic Industria

Chemical/ 

CASRN Toxidrome Class(es) and Other Prominent Effects P

Desc

(Odor 

and 

Thre

nasal

Phosphorus trichloride 7719-12-2 Irritant vapor/corrosive Colorle

fuming an odor hydroch(no data

Phosphorus oxychloride 10025-87-3 

Irritant vapor/corrosive (poss. liver and kidney) 

Clear, cyellow, with a pmusty obelow 34° F. 

Propylene oxide 75-56-9 

Irritant gas/corrosive; neuro/CNS depression (alkylating agent) 

Colorlegas (abo (45 ppm ppm GM odor)

M

(457 ppanimal)
Summary of Common Acutely Toxic I

Chemical/ 

CASRN

Toxidrome 

Class(es) and 

Other Prominent 

Effects

Sulfuric acid 7664-93-9 corrosive Sulfur dioxide 7446-09-5 

Irritant gas; (poss sulf.Hb) 

Sulfur trioxide 7446-11-9 

Irritant vapor/corrosive (similar effects to sulfuric acid) 
Summary of Common Acutely Toxic Indu

Chemical/ 

CASRN Toxidrome Class(es) and Other Prominent Effects 

(O

a

T

n

Toluene-2,4- diisocyanate 584-84-9 

Irritant vapor/corrosive; neuro/psych [allergic sensitization – lung (asthma)/skin (eczema)] 

Colyellliquwitpunppm
Planning Guidelines (ERPG

sure Level Guides Handboo

 3) U.S. Department of En

Limits (TEEL), Revision 20, 

c

 Interim AEGL

d Final AEGL

e Proposed AEGL

f

 ERPG

g TEEL

h Source = Agency for Toxic 

ToxFAQsTM, Toxicological P

lines, http://www.atsdr.cdc.g

I

 Environmental persistence 

j

 Source = National Library 

Bank (HSDB), accessed 11 

k

 Impairment = irreversible 

health effects or an impaire

tion of AEGL-2 in the Natio

ing Procedures for Develop

Hazardous Chemicals”, 20

l

 Mask effectiveness based 

canister presented in US A

Center, “Toxic Industrial Ch

Performance”, ECBC-TR-09

against cyanogen chloride 

information. “Poor”: Offers 

term limited protection. Op

be avoided. If the mask is 

“Marginal”: Use as an esca

nation or against brief, low 

immediately after chemical 

TIC effectively; filter change 

only TICs in the table that t
M Source = Odor Thresholds for Chemicals with Established O

tional Health Standards, AIHA, 1989.

N Sense of smell becomes fatigued with time & CANNOT be re

upon to warn of the continuous presence of the chemical (Sou

ACGIH, ATSDR, or Patty’s Toxicology, 5th Edition) O Warning Properties of Industrial Chemicals, Occupational H

Resource Center, Oregon Lung Association.

ND = no data available

r = recognition threshold

d = detection threshold

GM = geometric mean
Cold Weather

Freezing Injury (Frostb

Non-Freezing Cold Inj

Hypothermia -----------

Heat

Heat Cramps -----------

Heat Exhaustion ------

Heat Stroke -------------

Preparation of 0.1 Per
♦ Usually subsides over the course of 3-7 days.

♦ Can occur after acclimatization with rapid asc

higher altitude.

 Probable cause: hypoxia-induced subclinical cere

edema.

 Often precedes both high altitude cerebral edema 

and high altitude pulmonary edema (HAPE), but m

of cases do not progress to HACE or HAPE.

 Incidence and severity worsen with vigorous physi

activity during ascent or during the first 1-3 days a

altitude.

ALTITUDE INCIDENCE (%) 

MILD MODERATE SE

~ 7,000 ft (2,130 m) 0-40 0-10 

 ~10,000 ft (3,050 m) 60-70 0-40 

~12,000 ft (3,660 m) 10-40 40-80 

~14,000 ft (4,270 m) 20 60 

~18,000 ft (5,500 m) 0 10 

Symptoms/Signs (headache and nausea most commo

 Headache

♦ Usually symmetric, nonfocal, throbbing.

♦ Most intense at night and shortly after arising 

morning (increased hypoxemia caused by dec

ventilation during sleep).

♦ Worsened by strenuous exercise, changes in

position, valsalva.

♦ Sometimes helped by mild exercise (increase

ventilation).

♦ Anorexia, nausea, and vomiting.
higher altitude in t

 Differential:

♦ Viral gastroen

♦ Hangover.

♦ Exhaustion.

♦ Dehydration.

♦ CO poisoning

♦ HACE.

Prevention and Public H

 Staging and grade

altitude should no

(600 m/day) with a

4000 ft (600-1200 

 Avoid over exertio

 Acetazolamide 12

pre-ascent, contin

♦ Prevents AMS 

most of the ot

♦ Side effects: p

impairs physic

♦ Contraindicat

♦ High dose dex

Prevents sym

when the drug 
acetaminophen 325 mg PO Q4H to 1000 mg 

Q6H, ibuprofen 200 to 800 mg PO Q4-6H, or 

NSAIDs).

♦ Opioids may be more successful, but they s

not be used because of respiratory depressi

reduction of cognitive function.

♦ Prochlorperazine 5 to 10 mg PO Q6-8H can 

used to treat nausea and vomiting. Respirat

stimulation a potentially beneficial side effec

♦ Alcohol and other respiratory depressants sh

be avoided.
recognized early a

resolves rapidly a

quences.

 Often preceded by 

with HACE; most 

comitant HACE.

 Incidence relative

small units, can b

prognosis and nee

Incidence:

 Varies widely with 

specific circumsta

mates: 1/10,000 a

skiers), 1/50 at 20

ers), 15/100 at 11-

conflict).

 Increased risk in a

rapidly following s

altitude.

 Prior episodes ma

 Subclinical form o

♦ Manifested p

field.

♦ Rales found i

altitudes high

♦ Clinical signif

to frank pulmo

♦ Usually begin

ascent.
 Male sex.

 Obesity.

 Low hypoxic ventilatory response.

 Congenital absence of one pulmonary artery.

 Prior episode of HAPE.

Symptoms/Signs:

 Early pulmonary edema: nonproductive cough an

rales (common at high altitude even without HAPE

 Early hypoxemia: dyspnea on exertion, fatigue an

weakness with decreased tolerance for physical a

and increased time needed for recovery after phys

exertion.

 Resting tachycardia and tachypnea greater than t

induced by altitude alone.

 Nail beds and lips more cyanotic than others’ at th

same altitude.

 Cough may become productive of frothy, pink or bl

streaked sputum.

 Rales become more numerous and widespread, a

wheezing may develop.

 Lung sounds may progress to an audible gurgling 

airway that can be heard without a stethoscope, e

cially when the affected person is supine.

 Orthopnea may occur in some individuals (<20%)

 Progressive hypoxemia causes progressive dyspn

cyanosis.
, 

and an R-wave in le

Diagnosis:

 Presumptive:

♦ Two of the follo

• Dyspnea a

• Cough

• Weakness

• Chest tight

PLUS

♦ Two of the follo

• Rales or w

• Central cya

tachycardia 

 Differential:

♦ Pneumonia

♦ Congestive hea

♦ Pulmonary emb

♦ In a military set

warfare agents.

Prevention and Public He

 Adequate acclimati

pharmacologic prop

 Unacclimatized sol

as possible.

♦ Avoid cold expo

adequately acc

♦ Acetazolamide 
♦ Descent should be by passive means (exertio

cold, and anxiety can increase pulmonary art

pressure).

♦ Keep soldier as warm and comfortable as pos

and administer supplemental oxygen (4-6 L/m

improvement, then 2-4 L/min) during descent

♦ Soldiers with mild HAPE symptoms and who 

ambulatory may walk down slowly.

♦ Soldiers with any altitude illness should n

unaccompanied.

 Use portable hyperbaric chamber if descent not p

or oxygen unavailable (may require 4 or more hou

treatment in the chamber to be effective for HAPE

 Increase beneficial effect and conserve oxygen su

by:

♦ expiratory positive airway pressure mask (EP

♦ pursed-lips breathing

 Nifedipine: Start with a 10 mg immediate release c

sule orally then extended release formulation 30 m

Q12-24H.

altitude due to serious prognosis and the need fo

evacuation.

Incidence:

 Occurs in unacclimatized individuals who ascend 

from low to high altitude, or from high to higher al

♦ Overall incidence (1% of rapid ascenders) low

that of AMS or HAPE.

♦ Majority of cases occur above 12,000 ft (3,60

 Risk factors same as for AMS. AMS itself and pre

episode of HACE are risk factors.

 Time of onset following high altitude exposure gen

occurs later than AMS or HAPE. Mean duration 

exposure before onset of HACE symptoms may b

days with a range of 1-13 days.

 Progression to death if untreated: 12-72 hours.

Symptoms/Signs:

 Early (AMS signs):

♦ Severe headache, nausea, vomiting and extre

lassitude. None is invariably present.

♦ Cyanosis and general pallor.

♦ Mental status: confusion, disorientation, drow

ness, impaired mentation, withdrawal.

♦ Truncal ataxia and change in mental status h

differentiate early HACE from AMS. May pro

to ataxic gait.

♦ Coexisting HAPE symptoms.
present for a pres

after the first coup

 Differential: altitu

attack, infection, m

mia, substance a

hypoxia resulting 

Prevention and Public H

 No proven efficac

precludes adequa

 Based on hypoth

HACE, AMS prev

Treatment (should be st

tive diagnosis):

 Definitive treatme

 Outcome improve

1000 ft (300 m) m

descent to an altit

♦ Ambulatory p

panied.

♦ Portable hype

descent is un

6 hours of pre

 Continuous supp

min should alway

substitute for des

added to the air in

to increase its eff
may require intubation with hyperventilation and blad

catheterization.

 Evaluate for concomitant HAPE and treat immediate

present.
 Usually associate

weight gain of app

Diagnosis:

 Presumptive:

♦ Diagnosis ca

because it ten

ascents.

 Differential:

♦ Differential dia

allergic reacti

ties caused b

clothing.

Treatment:

 Can be treated su

 Definitive treatme
throughout any altitude deployment.

Symptoms/Signs:

 Fundoscopic exam will show hyperemia and engor

of the disc and increased tortuosity of retinal vesse

 Retinal hemorrhages appear as “splinter” and “flam

hemorrhages in the superficial layers of the retina, 

hemorrhages in the deeper layers can occur.

Diagnosis:

 Differential diagnosis includes hemorrhage from vas

disease, diabetes mellitus, septic infarcts or from h

caused by cardiac and respiratory disease.

Treatment:

 Self-limited resolve 1-2 weeks after descent; desce

not necessary for hemorrhages outside of the mac

 When a macular hemorrhage is diagnosed, descen

imperative to promote healing and prevent further he

rhage.

fort it causes to individual soldiers. Cough spasms 

cause soldiers to be easily detected by opposing f

in some tactical situations.

 Treatment involves ample hydration, steam inhalat

hard candies or soothing lozenges and a mild coug

suppressant.

 A mask or a porous, breathable silk balaclava as a 

covering to reduce respiratory heat and moisture lo

 Decongestant nasal sprays may relieve cold-induc

vasomotor rhinitis and lessen mouth breathing.
sleep disorders 

peripheral edem

dexamethasone AMS treatment 

HACE 

acetaminophen AMS headache 
triazolam insomnia 0.125 mg, PO QHS Short-term us

only. Possib

short-term 

memory 

loss 

temazepam insomnia 30 mg, PO QHS 

nifedipine HAPE treatment 

HAPE prevention 

10 mg sublingually, 

followed by 30 mg 

PO QID 

20 mg PO TID 

started, 24 H 

before ascent, 

continuing Q8H 

until 72 H after 

ascent 

prochlorperazine nausea/vomiting 5-10 mg Q6-8H PO 

or IV; or 25 mg PO 

BID 

Also stimulat

respiration 
ypg

 First degree frostb

♦ minor injury to 

♦ blanches whi

wheal, no blis

days

 Second degree fro

♦ whole epiderm

♦ limited motion 

♦ blisters form, 

♦ blood in bliste

♦ tissue under b

blister intact

 Third degree frost

♦ dermis to retic

♦ tissue is white

♦ deep tissues 

♦ skin loss thro

mummificatio

♦ residual cold 

 Fourth degree fros

♦ involves skin, 

bone

♦ with rewarmin

blisters may o

♦ rewarming br

♦ permanent an

 Corneal frostbite i
with warm skin. The groin or axillae are particula

effective areas for warming frozen tissue.

 Tissue must not be exposed to temperatures in e

of 102-103°F which will aggravate the injury. Do n

expose tissue to motor engine manifolds or exha

water, open flames, stove tops, or incandescent b

Many frostbite injuries have been substantially wo

by exposure to inappropriate warming techniques

 Frostbitten tissue is vulnerable to trauma and infec

should be carefully protected from physical injury 

evacuation.

Hospital Management:

 Warming of still-frozen tissue, treatment of variou

phases, of the injury as it evolves, and evaluation 

coincident injury and illness. If the tissue has alr

thawed on arrival at the MTF, additional active wa

should not be done.

 Digits or entire hands or feet can be warmed in a

temperature monitored water bath kept at 102-10

The face or ears can be warmed by towels kept w

water warmed to 102-104°F. Warming should be

continued until no further improvement in circulati

mobility is noted. This usually requires 15-45 min

depending on the initial temperature and size of t

injured part.

 After warming, the frostbitten tissue should be ca

and atraumatically dried, completely covered in b

dry dressings, and kept slightly elevated to decre

swelling.

 Establish IV access (dehydration and hypovolem
or twice daily in sk

Betadine.

For complete guidance 

and Management of Co

(www.usariem.army.mil
ggyp

not change after warming.

 Skin is frequently macerated and slightly edemato

The degree of injury is not completely apparent ea

 After several hours (occasionally as long as 24-36 

a marked hyperemia develops associated with seve

burning pain and reappearance of sensation proxim

but not distally; blanches with elevation; lasts a few 

to many weeks depending on the severity of the in

 Edema and blisters develop in the injured areas as

perfusion increases. Poorly perfused skin will slou

 Persistence of no pulse in an extremity after 48 ho

suggests severe deep injury and high likelihood of 

stantial tissue loss.

 Boots and socks should not be replaced until feet 

warm and have normal feeling.

 Injured extremity must be carefully protected durin

evacuation.

 Severe pain may develop during evacuation if warm

occurs, but extremity should not intentionally be de

of passive warming (dry covering and protection fro

cold). Soldiers performing the evacuation should b

equipped and trained to provide adequate analgesia

 Do not massage or actively warm extremity.

 NFCIs should be evacuated to a rear echelon hosp
For complete guidance 

and Management of Co

(www.usariem.army.mil
significant hypothermia. Withdrawal and irritability 

common. As hypothermia worsens, subtle menta

changes progress to frank confusion, lethargy, with

behavior, and obtundation. The degree of mental s

change is not a reliable guide to the degree of hypo

mia.

Clinical Manifestations:

 90-95°F (32-35°C)

♦ Mild hypothermia

♦ Shivering and vasoconstriction present

♦ Impaired fine and gross motor skills

♦ Mental processes slow, errors in judgment

♦ Bradycardia with PVCs possible

 82.5-90°F (28-32°C)

♦ Moderate hypothermia

♦ Shivering and vasoconstriction attenuated or g

♦ Lethargy, staggering gait

♦ Atrial arrhythmias

♦ Bradycardia

♦ Hypopnea

 < 82.5°F (< 28°C)

♦ Severe hypothermia

♦ Absent shivering or vasoconstriction

♦ Loss of consciousness

♦ Muscles and joints rigid

♦ Vital signs reduced or absent

♦ Risk of ventricular fibrillation/cardiac arrest

♦ Core temperature below 77°F (25°C) – spontan

ventricular fibrillation
 When indicated, e

does not seem to 

tion.

 Oxygen suppleme

of the low oxygen 

tion can be assist

 Treat dehydration 

ermic casualties)

 Victims of severe 

cardiac arrest; the

perceptible signs 

solid clinical indic

conversion of perf

fibrillation. Use ca

then take extra tim

slow and difficult t

 Give glucose/suga

Hospital Management:

 Casualties who ha

moderate degrees 

chance to rewarm 

spontaneously, th

They should be ad

given warmed hum

 Although virtually 

lavaged with warm 

(stomach, urinary 
requirements and carbon dioxide production will b

Ventilation needs to be guided by blood gas meas

ments to avoid excessive respiratory alkalosis. B

gas measurements can be interpreted as reported 

laboratory; temperature “correction” is no longer co

ered appropriate.

 As a general rule, antiarrhythmic and vasoactive d

are not useful during resuscitation from hypotherm

core temperatures exceed 90°F. Below that temp

drug effects are absent or unpredictable. Also, sin

metabolism is markedly slowed below 90°F, apply

American Heart Association Advanced Cardiac Life

Support (ACLS) drug protocols in hypothermia cau

the accumulation of drugs which have no manifest 

when administered, but which suddenly and dram

express themselves as they regain activity at high

temperatures. If drug therapy of ventricular fibrillat

required, bretylium at its usual doses would be the 

of choice.

For complete guidance please see TB MED 508, Prev

and Management of Cold-Weather Injuries

(www.usariem.army.mil/download/tbmed508.pdf).
able to pain

♦ despite the sa

cramps, frank 

tion are unus

♦ no significant 

heat cramps 

 Differential diagno

♦ tetany due to 

gastroenteriti

♦ compartment 

♦ strychnine po

♦ black widow s

♦ abdominal co

Management:

 Replenish salt ora

♦ Response to 

valuable in th

♦ Route of adm

of symptom r

♦ See Preparat

Methods.

♦ Salt tablets s

source.

For complete guidance 

Heat Stress Control and 

(www.usariem.army.mil
levels.

 The management of heat exhaustion is directed to

correcting the two pathogenic components of the 

excessive cardiovascular demand and water-elect

depletion. The load on the heart is reduced by res

cooling. Water-electrolyte depletion is corrected b

administering oral or parenteral fluids.

Heat exhaustion casualties retain the ability to cool sponta

ously if removed from the stressful circumstances. Howev

spontaneous cooling is necessarily observed only AFTER 

has occurred. Casualties with incipient heat stroke and he

exhaustion are hard to distinguish initially. THEREFORE, 

TIVE COOLING SHOULD BE PROVIDED FOR ALL CASU

TIES WHO ARE AT RISK FOR HEAT STROKE.

 Any loss of consciousness and mental status cha

need to be documented. Such patients need to b

evaluated as potential heat stroke cases.

 Normal saline should initially be given in 200-250 m

boluses to an amount sufficient to restore normal c

tory function. No more than 2 liters of NS should b

administered without laboratory surveillance if labo

support is available. Subsequent parenteral fluid r

ment should be D5/O.5 NS or D5/0.2 NS.

 A single episode of heat exhaustion does not imp

predisposition to heat injury. Repeated episodes o

exhaustion require thorough evaluation.

________________________________________________

For complete guidance see TB MED 507/AFPAM 48-15

Heat Stress Control and Heat Casualty Management

(www.usariem.army.mil/download/tbmed507.pdf).
Incidence:

 Heat stroke occur

produce different 

primary clinical di

exertional heat st

rhabdomyolysis w

♦ “Classical” he

quently with im

or medication

dehydration. 

young childre

heat waves.

♦ “Exertional” h

individuals ex

heat loads.

 Encephalopathy i

presentation rang

confusion to seizu

The etiology of en

 Coagulopathy due 

causes of DIC see

lium, rhabdomyol

activation causing 

sis is secondarily 

thermal injury to m

clotting factors.

 Hepatic injury is c

elevation, clotting 

be seen in the cou
should not be delayed to accomplish a diagnostic evaluat

Cooling and evaluation should proceed simultaneously.

Diagnosis:

 Heat stroke presents as collapse with variably se

encephalopathy and hyperthermia. There may be

clinical evidence of dehydration, coagulopathy or 

 Laboratory evaluation should be directed by the d

tial diagnosis appropriate for the clinical circumst

Patients with heat stroke require serial monitorin

platelets and plasma clotting factors, renal and h

function, and electrolyte and acid-base status.

 Differential includes: infection (particularly menin

cemia and P. falciparum malaria), pontine or hypo

lamic hemorrhage, drug intoxication (cocaine, am

amines, phencyclidine, theophylline, tricyclic ant

pressants), alcohol or sedative withdrawal, severe

hypertonic dehydration, and thyroid storm.

The patient with heat stroke requires early evacuation to m

facilities with intensive care capabilities. Active cooling s

be started immediately and continued during evacuation.

Treatment:

 Clinical outcome of patients with heat stroke is p

a function of magnitude and duration of temperatu

elevation.

♦ Most important therapeutic measure is rapid

reduction of body temperature.
in ventila

evaporat

the case 

nearly the 

often as 

♦ If immersion d

water can be 

 Cooling can also 

surface and acce

water can be app

thin conforming c

(Circulating cooling b

field situation—will als

cooling blankets have 

working environment, 

slower cooling than im

niques. Their best us

temperature in the pe

cooling where temper

 Invasive cooling t

enemas, peritone

recommended be

cooling, and they 

 Rectal temperatu

active cooling; dis

hypothermia.

 Heat stroke patie

fluid resuscitation

♦ Fluid requirem

hours are typ

AVOIDED.
intravenously, endotracheally or rectally.

 Hyperkalemia is the most life threatening early clin

problem.

♦ Measurement of plasma [K+] is an early priorit

available. Tall T-waves on the surface ECG are

consistent with hyperkalemia but not definitive

interpretation of plasma [K+] early in the clinic

course of heat stroke is difficult due to confoun

electrolyte and acid-base disturbances.

♦ Clinically significant hyperkalemia is manifeste

electrocardiographic changes including increas

wave amplitude, slowed A-V conduction with w

of the P-R interval, diminishing P-wave amplitu

“sine wave” ventricular rhythms.

♦ Hyperkalemia greater than 6.5 meq/L or with e

cardiographic changes should be treated. Glu

(50 gm slow IV), insulin (20 units of regular ins

and sodium bicarbonate (1-2 amps IV) will lowe

plasma [K+] within minutes. Serious ventricula

dysrhythmia should be treated with IV calcium

chloride (1-2 amps).

♦ Cardiac monitoring and electrocardiography ca

used to supplement laboratory monitoring for

changes in plasma potassium (T-wave amplitud

calcium (QT interval).

 Acute renal injury is common in exertional heat str

♦ Urinary catheterization to monitor urine output 

obtain urine for [Na+] should be done early.
either cooling 

 The effects of rhab

are renal injury du

hyperkalemia, hyp

dromes due to mu

renal perfusion an

toxic effects of my

♦ Hyperkalemia 

dialysis.

♦ Hypocalcemi

♦ Increasing ten

compartment 

intracompartm

of intramuscu

considered at 

may not signa

permanent da

 Prognosis is wors

of encephalopathy

develop after heat 

paresis, seizure d

♦ Management 

directed at mi

fluid overrepla

thermal and m

tol has been u

edema if rena

dexamethaso

cerebral edem
noncardiogenic pulmonary edema, and myocardia

infarction. Immuno-incompetence and infection ar

complications, particularly in patients with severe 

failure.

MEDICATIONS REPORTED TO INCREASE

HEAT ILLNESS RISK

Anticholinergics 

 Atropine 

 Scopolamine 

Antihistamines 

Diuretics 

Tricyclic antidepressants 

Major tranquilizers 

Amphetamines 

Cocaine 

Ergogenic aids (e

those containing 

Alcohol 

Beta-blockers 

For complete guidance see TB MED 507/AFPAM 48-15

Heat Stress Control and Heat Casualty Management

(www.usariem.army.mil/download/tbmed507.pdf).
 Prepare a saturat

and add specific q

solution to drinkin

Saturated salt sol

spoons of table sa

Saturated salt sol

saturated salt solu

0.1% salt solution 

solution added to 

following proportio

1/8 cante

canteen o

1/4 cante

canteen o

1 mess k

water

5 mess k

water

1/2 cante

4 canteen 

Growths (Cancerous a

Miscellaneous ---------

Referral and Telederm

Tips ----------------------
or ellipsoidal lesion (e.g., deep tumors).

 Vesicles: small (<1 cm), circumscribed, elevated 

that contains fluid. Walls are thin (translucent).

 Bullae: large (>1 cm) same as vesicle.

 Pustules: like a papule (raised, <1 cm) lesion tha

contains pus.

 Erosions: moist, circumscribed, usually depresse

lesion that results from loss of epidermis.

 Ulcer: lesion which there has been destruction of 

epidermis and at least the upper dermis.

 Cysts: a sac that contains liquid or semisolid ma

(e.g., epidermal inclusion cyst).

 Atrophy: diminution in the size of a cell, tissue, o

or part of the body (dermal or epidermal).

 Sclerotic: circumscribed or diffuse hardening or in

tion of the skin.

 Scale: abnormal shedding or accumulation of stra

corneum in perceptible flakes.

 Crusts: results when serum, blood or purulent ex

dries on the skin surface.

 Necrotic: dead tissue, usually sharply demarcate

black.

 Excoriations: superficial excavations of the epide

resulting in linear or punctate abrasions/ulceration

 Fissures: linear cleavages or cracks in the skin t

deep and usually painful.

6
 Examination

♦ Patient’s gene

♦ Number of les

able

♦ Primary lesion

• Type - ma

vesicle-b

cyst

• Shape - a

form, line

• Borders - 

demarcat

• Color - un

blanching

• Palpation 

mobility, t

♦ Distribution

• Number o

generaliz

• Pattern (s

(e.g., site

nous, ext

and soles

♦ Secondary le

erosion, fissu

lichenified, sc

♦ Comment wh

teeth, eyes, jo

to sweat
6
♦ Topical Manag

• Limit bath

5 minutes 

other day

is expose

worse the 

• Use a mil

Cetaphil)

impetigini

their skin, 

2000) can 

• Lubricate 

as Vaselin

shortenin

which are 

often che

addition o

may irrita

• For oozin

using alum

Domebor

quart of w

washcloth

water afte

the soaks 

creams ca

ointments 

stops.
(gp

cortisone, even though it is a lower percen

a fact that often confuses patients).

• Fluocinonide cream or ointment (mid-high

potency steroid) QD to BID for

stubborn plaques.

♦ Antihistamine Therapy • Sedating antihistamines probably just ma

patient too sleepy to know that he or she 

itchy: hydroxyzine (Atarax) 10-25 mg PO 

diphenhydramine (Benadryl) 25-50 mg PO 

chlorpheniramine (Chlortrimaton) 4-8 mg P

QHS.

• Nonsedating forms do not help significant

♦ Antibiotics - Only if 2° infection • Systemic - dicloxacillin, cloxacillin, cepha

for staph and strep coverage.

• Mupirocin (Bactroban) ointment TID.

♦ Other topical antipruritic preparations one can 

prn • Camphor/menthol preparations (Sarna, Sa

Vick’s Vaporub); pramasone (Prax).

• Avoid Caladryl because topical Benadryl p

may cause allergic sensitization.

• Avoid topical benzocaine because this als

induces frequent allergic contact dermatit

♦ Pediatric Eczema • Hydrocortisone 1% cream (hydrocortison

or desonide if eczema is severe). May us

courses of higher strength topical steroid 

6
help. Hav

lukewarm 

use mild c

than rub) 

apply the 

seal mois

• This is a c

obtain rea

tients nee

be cured. 

treatment 

vigorousl

medicatio

condition 

may have 

exacerba

 Acute Allergic C

This form of conta

often appears in li

cludes plants, suc

products; nickel a

preparations such 

Neosporin produc

the offending agen

ment:

♦ Mild - erythem

• Triamcino

♦ Moderate - er

• Cool tap w

• Apply mo
midback and pubic areas. Commonly confused w

lupus erythematosus and rosacea (if on face), an

psoriasis (if on scalp). Start with OTC Shampoos. They can be used to w

the seborrheic areas (scalp, face, etc). With all m

cated shampoos, keep shampoo on the hair for 1

minutes before rinsing. Use daily for best results

Shampoos can be rotated every 2-3 months to pre

tolerance. ♦ Tar containing (e.g., T-Gel, T-Sal, Ionil-T,

Pentrax Gold, Polytar)

♦ Zinc containing (e.g., DHS zinc, Head and

Shoulders)

♦ Sulfur and salicylate/salicylic acid (e.g., Ionil

Plus)

♦ Selenium sulfide 1% (e.g., Selsun Blue)

Prescription Shampoos - use only if the OTC

shampoos fail. ♦ Selenium sulfide 2.5% ♦ Ketoconazole (e.g., Nizoral - expensive) Topical Steroids ♦ For scalp: liquid mid-to-high strength cortison

such as fluocinonide BID for 7 days then QHS. ♦ Hydrocortisone 1%-2.5% cream or ointment b

mild face and body involvement. Moderate strengt

steroids may be used for 2 weeks. Topical Antifungals (e.g., clotrimazole but not Nys

may be helpful to control Pityrosporum (an organi

which may exacerbate seborrheic dermatitis in so

individuals).

6

(g, ) (, 

0.1%) or gel (0.01%, 0.025%). This age

drying, so patients need to build up a tole

start every 4th night for a week, then every 

night for a week, then every 2nd night for a 

then every night if tolerated.

• Tretinoin and BP inactivate each other. U

in the AM and tretinoin at night.

• Azeleic acid (e.g., Azelex) QD-BID is als

useful.

• Some practitioners add topical erythromy

clindamycin to the BP. There are comme

pre-mixed preparations, but these are rar

formulary because of cost. Having the pa

apply the antibiotic and BP at the same t

almost as effective, and a lot cheaper.

• Some patients will find it too drying to us

than one topical (e.g., tretinoin and BP).

♦ Moderate Acne (mostly papules and pustules

with few comedones or cysts). Combine a

topical regimen (as above), with one of the

following oral antibiotics:

• Tetracycline 250-500 mg PO BID (photos

ity; not in kids or in pregnancy).

• Doxycycline 100 mg PO QD (photosensi

nausea; take with food).

• Minocycline 100 mg PO QD (more expen

take with food; common side effects less

common, but severe side effects somewh

more common – although still very rare –

compared to plain tetracycline).

6
course; it 

tologists, 

sidering t

zone; if p

of conven

derm.con

Telederm

isotretino

rotates h

♦ Acne during p

• Can safe

topical be

clines an

A has not 

♦ Other points 

• Tretinoin 

skinned p

• Tretinoin 

often as 

simple, in

• Tretinoin 

30 minut

sized am

Some red

expected 

Tretinoin 

stopped 

dryness. 

arid clima

0.01% cr
 Rosacea – four types: telangiectatic, erythemat

papulopustular; and hyperglandular. May overlap/c

exist. Treatments:

♦ Metronidazole 0.75-1.0% cream (e.g., Noritat

Metrocream, Metrogel) BID, sulfa-based lotio

(e.g., Sulfacet-R) QD, or azeleic (e.g., Azelex

or tetracycline 250 mg PO QD-BID.

♦ Mixed reports on triggering substances (e.g.,

alcohol, spicy foods, coffee). Sunscreen may 

very important, especially in a sunny climate

 Pseudofolliculitis barbae (PFB)

The treatment for PFB in the field is to avoid shav

Keep the beard trimmed closely (1/4-inch) with sc

or clippers per regulations. A P2 profile is permitt

There is no benefit in expecting the service memb

repeatedly try to shave to see if the PFB has reso

spontaneously – it doesn’t. Treatment of choice 

laser hair removal, but until patient rotates home, 

use topical treatments like for acne (BP wash plu

tretinoin QHS), plus hydrocortisone 1% cream pr

soothe irritation.

 Acne keloidalis nuchae (AKN) is a form of scar

alopecia most common in young black men. It c

of firm folliculocentric keloidal papules on the occ

nuchal region. The papules may coalesce into gi

scarring plaques. Etiology is unclear.

♦ Avoid close haircuts on the nuchal/occipital re

Remind your gung-ho soldiers that 1/4 -1/2-in

is perfectly within regulations. Further remind 

that the creation of a permanently disfigured 

not worth the military glamour of a high-and-ti

6
y 

Kevlar helme

pressure on t

medical reten
subungual debris).

♦ Topical Steroids

• Face - hydrocortisone 1%-2.5% cream o

desonide BID.

• Scalp - same as for seborrheic dermatiti

• Trunk, feet, and hands - triamcinolone 0.

cream BID (mild involvement) to betamet

or clobetasol ointments for more severe 

• Intralesional triamcinolone (5 mg/mL) ca

effective for small plaques.

• For those patients who do not respond to 

steroids, try applying any mid-potency to

steroid to the trunk or extremity lesions (

ably when they are moist following a sho

then cover it with clear plastic wrap. Thi

occlusive therapy potentiates the topical 

cine and if used overnight for up to 2 wee

may help to improve or clear a problem a

• DO NOT USE SYSTEMIC STEROIDS.

♦ Tar Products

• Scalp - see seborrheic dermatitis. For th

plaques on the scalp, applying Baker’s P

solution overnight, especially under a pla

shower cap, may loosen scale.

• Trunk and extremities – products such a

Derm or Fototar QHS (warn patients tha

can cause photosensitivity and can stain

clothing).

6
trunk and proxima

afebrile and are o

the spring and fal

and its mode of tr

that no precaution

Treat with topical 

topical steroids. B

getting sunburned

Differentiation fro

two eruptions can 

feel poorly, have m

check for presenc

or other STDs. Ex

gitis, palmoplanta

Remember that tr

syphilis. Don’t he

 Lichen Planus

Although there ar

planus shows the 

rather than round)

(not red) papules

(wrist, ankle, and 

see lacy white lin

In addition, a lacy 

genital mucosa a
6
antifungal crea

clotrimazole). T

the point of clin

widespread or v

need griseofulv

for adults) QD w

Failures occur 

medicine, if the 

hair follicles, or 

applying the top

areas, so keep 

clean and dry a

such as hydroc

WEEK ONLY m

infection is clea

Drying powders 

wetness under 

application or d

the area has be

♦ Tinea unguium 

is best left untre

preparations ra

♦ Tinea capitis h

ringworm” is a 

shows abundan

“black dots.” A 
♦ Tinea versicolor appears as light to dark brown

powdery scaly discrete and coalescent macul

the back, neck, chest, shoulders, and upper a

This condition is due to a yeast that is a part o

normal skin flora and can recur in hot, humid

conditions. It is harmless. Remind patient tha

even if treated perfectly, TV will leave abnorma

pigmentation for up to several months beyond 

Relapses are near-inevitable. Treatment optio

• Apply Selsun-type shampoo from the nec

down to the waist and also to the arms 15

minutes prior to daily showering for 1 wee

repeat weekly for the next month.

• Clotrimazole or spectazole cream BID for 

weeks.

• Oral ketoconazole 200 mg PO QD for 1 w

very effective for resistant cases.

♦ Macerated tinea pedis is a painful inflammato

disorder usually caused by a polymicrobial infe

(mixed dermatophyte and bacterial). It appear

white, gooey cakes in the webspaces of toes.

• First gently remove as much of the macera

inflamed tissue as possible using hydroge

peroxide or saline on a gauze pad. Then t

the underlying fungal infection. For 1-2 we

use an anti-infective astringent (such as co

less Castellani’s paint or gentian violet, if t

agents are available) TID. Other drying so

tions include teabag soaks (two teabags

steeped in 6 oz of water and liquid allowed 

6

ment if located on the palms, soles, and 

periungual and subungual locations). Fre

time (amount of time you see white frost o

wart) needs to be 15-30 seconds with two

separate freeze-thaw cycles (freeze, let th

itself, then freeze again). Patients should 

informed of possible blister formation (eve

blisters) following the treatments and care 

treatment site (keeping it clean, applying

antibiotic ointment if needed, and sterile p

ing the blister if necessary).

• Occasionally you may choose to pare do

wart with a scalpel blade (particularly pain

hyperkeratotic plantar warts) but avoid su

and electrocautery of warts as this is pain

rarely effective, and may lead to scars tha

worse than the warts.

♦ Flat Warts - Common in children and young a

Hard to treat. Lesions appear as small, flat-to

skin-colored papules and are often found on th

hands, arms and legs. Treatments include liq

nitrogen (caution in dark skinned patients) and

tretinoin (e.g., Retin-A) 0.1% cream QHS. In

children, tretinoin can work quite well and leav

scarring; however, it is slow.

♦ Plantar Warts - Similar approach as for comm

warts. Avoid long freezes as this may impede

walking and running.

6
follow-up 

purified d

Apply pe

• Imiquimo

times/we

• Note: As

so that th

better ab

for genita

that genit

before cle

genital w

Advise th

 Molluscum Cont

umbilicated papu

immunocomprom

often sexually tra

removes/express

Such treatments 

topical salicyliate

Duofilm), or podo

eyelids in small c

prudent since les

(e.g., Cantharone

individual lesions

tape for 12-24 ho

discuss blister ca

sites clean, apply 

Often need to rep
♦ Recurrent outbreaks: Acyclovir (Zovirax) 400 

TID or Valacyclovir (Valtrex) 1 gram PO TID fo

5 days.

♦ If frequent recurrences (every 1-2 months) can 

Acyclovir (Zovirax) 400 mg PO TID or Valcyclo

(Valtrex) 500 mg – 1 gram/day as chronic sup

sion.

6
papules, may be 

 Furunculosis – 

acute, round, ten

suppuration. A ca

furuncles.

 Pyogenic paron

possible purulent 

 Staphylococcal 

streptococcal imp

 Staphylococcal 

same as streptoc
bleed. SCCs occur most commonly on ears, lips, 

dorsal hands. They don’t respond well to liquid nit

These require biopsy and surgical excision.

 Basal cell carcinomas are the most common sk

cancers. The most common appearance is pink to

reddish, pearly, somewhat translucent appearing p

and nodules, with rolled borders and fine telangiec

that frequently ulcerate and bleed. These also requ

surgical treatment.

 Seborrehic Keratoses rarely appear before age 3

then slowly appear in increasing numbers. They ra

in size from 0.5-3 cm, range in color from tan-to-da

brown-to-black, are velvety or verrucose-surfaced, a

usually appear to be “stuck on” to the skin. They a

rarely pruritic, sometimes inflamed if caught on clo

but are usually asymptomatic.

 Nevi are more common in lighter-skinned people a

those with a history of sun exposure. May be con

tal. Small (< 0.6 cm if acquired, may be any size 

congenital), tan to dark brown, flat or raised, regula

borders.

 Melanoma - Use the ABCDs to recognize suspic

lesions. These guidelines are good but not perfec

diagnosis is suspected on a clinical basis but mad

histopathology. A biopsy is necessary to establish 

diagnosis.

♦ Asymmetry (there is no exact limit, but symm

a good sign, asymmetry is a bad sign).

♦ Border irregularity (again, there is no exact lim

regular is a good sign, irregular is a bad sign).

6

oa eedes about oe seee types ob

Severe thermal burns require surgical interventio

and ICU-level care for fluid management. Electri

injury may require monitoring for cardiac dysfunc

and rhabdomyolysis. Chemical warfare agents a

discussed elsewhere.

♦ Ordinary chemical burns (i.e., not chemical warf

agents) require flushing with saline (or any availa

fluid) to neutralize the agent. Alkalines require m

more copious irrigation (several liters, even in a

minor exposure) than neutral or acid agents.

♦ Third degree burns need to be debrided to remov

devitalized tissue.

♦ Second degree burns – if the blisters can be pro

tected, they should be left intact, as they are a

perfect biological dressing. If they cannot be

protected, they should be ruptured under sterile 

at least clean) conditions. In either case, the wo

should first be cleaned (with saline or peroxide) a

covered with a sterile dressing. The wound can 

protected with Silver sulfadiazine (e.g., Silvaden

the patient is not allergic to Sulfas, polysporin, o

even just Vaseline). Contrary to what we were a

taught in Boy/Girl Scouts, the wound should not 

allowed to dry out and scab. The wound should b

cleaned, dressed, and inspected for signs of infe

tion QD-BID. If any evidence of infection, culture 

possible, and treat with cloxacillin or cephalexin

6
yy(

♦ Control insects 

Note: even when people are 

only one or a few will have ar

not.

 Lice (pediculosis a

♦ Lice infestation 

communicable, 

Body lice (Pedic

significant in ca

lice (P. h. capitis

eyebrows and e

direct contact o

especially in the 

asis pubis) gene

heavy infestatio

usually transmit

ted by other clo

♦ Lice can be tran

alive on the bod

of about 1 mont

up to 1 week wit

crab lice only 2 

viable for up to 1 

♦ Treatment:

• IN ALL CAS

- Need to tre

wash in ho

dry clean, 

month.
because lice die soon after leaving the ho

• HEAD AND PUBIC LICE (need to comb out 

after treatment)

- Permethrin 1% cream rinse (e.g., Nix) – r

into dry hair, and allowed to remain on for 

minutes (maybe 30-60 minutes if resistan

suspected), then toweled. Do not re-was

least 24 hours.

- Pyrethrin with piperonyl butoxide (e.g., Ri

shampoos, need to be left in for 10 minute

Less effective than permethrins. Must be

repeated 7-10 days later.

- Malathion lotions (e.g., Ovid) – rubbed int

scalp and hair; leave on for 8-12 hours, th

wash out with non-medicated shampoo.

- Lindane (gamma-benzene hexachloride)

shampoo, need to be left in for 4 minutes

to be used in children and pregnant wome

banned in California because of fears of

neurotoxicity.

• BODY LICE

- Mostly live in the clothing, so questionabl

need to treat patient. If so, use single

application of permethrin 5% cream (not c

rinse!) left on overnight. Treating the fomi

(clothing, bedding, etc) is the key.

• FOR MASS OUTBREAKS (Preventive medic

personnel need to get involved)

- Consider mass delousing

6
cases 

(iii) S

arms

(c) Di

perso

bedd

(d) Ad

in the 

 Scabies

♦ General

• Sarcopte

only hum

Adults ma

6 week pe

itching co

treatment 

in 1-2 wee

• Scabies le

papules, 

secondar

burrows. 

eruption o

webspace

and axilla

spares th

infants.

Note: It d

• Nodular s

appears a

diameter 
y y 

washed off thoroughly after 8 hours.

• Ivermectin orally at 0.2-0.4 mg/kg as a singl

May repeat in 1 week. Most useful in situat

where multiple individuals need to be treated 

treatment failure from permethrin.

♦ Tips about treatment

• Total body application requires 25-30 gm (1 

• Apply medication to all surfaces, not just aff

areas. Rub it under fingernails too.

• Permethrin is now the drug of choice becau

virtually free of side effects and because the

resistance to the other two medications.

Permethrin is safe in children and pregnant w

Lindane should not be used in children beca

neurotoxicity, or in pregnant woman because 

fetal risk of neurotoxicity and aplastic anemi

• Bedding and clothing must be washed and d

a hot-cycle or removed from body contact fo

least 72 hours.

• Retreatment is probably not necessary whe

permethrin. Nevertheless, usually recomme

retreatment after 1 week. It may be overkill 

gives patients peace-of-mind.

• Pruritus will persist for about 2-3 weeks beca

the dead mites remain in the stratum corneu

that long and continue to elicit an itch respo

Consider adding antihistamines, or topical S

or a topical corticosteroid to help control itch

6
 Melasma (or ch

brownish, macula

most commonly i

such as women w

Melasma often ar

hormone therapy 

gen).

♦ Patients nee

sun protectio

blockers in th

♦ First line trea

2-4% hydroq

Melanex, Eld

for 3 months 

♦ “Kligman form

cream and a 

0.1% cream, 

pea-sized tab

together, and 

♦ If making lim

(Azelex) in ad

♦ Not all patien

pigment is in 

♦ WARNING: 

darkening (ps

quinone so a

quinone alon

as a test site 
 Urticaria (

hives) are very pruritic, red, papulesto

plaques. Sometimes the center is a paler color. Th

finding is that individual lesions do not stay for more 

hours. Be specific when trying to get this history, be

the overall attack of urticaria can last any length of t

each lesion will last for less than 24 hours.

Urticaria is not a disease, but a reaction to somethin

That “something” can be an allergy, an infection, or a

anything else. Often, the cause was a subclinical in

a few days or weeks before the eruption started; mo

the cause is not found. Patients (and many doctors

focus on a new exposure that coincides with the eru

but more likely the inciting cause was a few weeks e

Ask about recent illnesses, environmental exposure

medications (including OTC, herbal, etc), and system

symptoms. As a rule of thumb, the cause will either 

easy to find or it will never be found. An elaborate wo

is not indicated in the field – acute urticaria resolves 

6 weeks, chronic urticaria requires a very extensive w

that will wait until the patient rotates home.

The goal in the short run is to make the patient comf

Start with non-sedating anti-histamines such as Alleg

Claritin, or Zyrtec. If these are not adequate, continu

using them in the morning, and add a sedating antih

mine at night such as diphenhydramine (Benadryl) o

hydroxyzine (Atarax). If need be, increase to the ma

doses. Remember that “non-sedating” is relative; ind

6
Physical agen

fewer irritant a

block both UV

not leave a re

allergic reactio

hours to be ef

intercept ultra

work.) Recom

UVB sunscre

agents can ca

but PABA cau

tured sunscre

chase agent m

chemical sun

containing avo

and are usual

♦ How much su

you got too m

probably got t

tan more eas

sensitive diso

worsens their 

day. Everyon

sure or use su

(1000h-1500h
, p, 

solution for warts, etc).

 Prompt Referrals – Referrals should be made prom

biopsy of suspected melanoma or for evaluation of w

spread blistering disorders; petechiae or purpura with

hypotension, fever, or renal failure; ulcers with fever; 

 Routine Referrals –Unless you are co-located with 

Dermatologist, suggest using Teledermatology (belo

rather than transporting patient across a high-risk ar

 Teledermatology – Now available for deployed prov

(not for self-referrals or non-providers). Email

derm.consult@us.army.mil. You will get a response 

24 hours. In the body of the email, include:

♦ Generic demographic data: age, race, gender, d

position, branch of service and your unclassified 

location. DO NOT include patient identifying info

tion (patient’s name or SSN).

♦ History including past and current treatment, me

tions, and their outcome.

List environmental factors affecting the pa

(heat, cold, arthropod, etc.)

Where did condition start? Has the patien

treated previously?

What does it look like? What is its’ distrib

Is it improving? Not responding to treatme

Comes and goes? Worsening?

What laboratory tests have been done?

♦ Your primary and/or differential diagnosis, if know

any specific questions you may have.

6
of both, fr

2nd image 

1

S

(

U

p

g

T

s

C

fo

c

a

♦ If you have an

program plea
sium permanganate, or topical bacitracin.

 Use creams rather than gels or ointments on open o

lesions such as an acute contact dermatitis.

 Neomycin should be avoided; it is a good broad-spe

antibiotic but it induces a contact allergy in 10% of p

tients. Topical Benadryl (Caladryl) also causes frequ

contact allergy. Avoid both of these. It should be no

that bacitracin sensitivity is also becoming common

Caladryl can be replaced by calamine.

 Vaseline and Crisco shortening are the cheapest effe

moisturizers.

 Refer to Sanford’s antibiotic guide.

 When confronting the typical round red itchy scaling 

in the field, most cases will be due to fungal infectio

course of clotrimazole TID x 2 weeks is a reasonabl

course of action. A skin scraping and KOH preparat

an easy method for confirming diagnosis. Avoid ster

anti-fungal combinations.

 Notes about antifungals:

♦ Nystatin will treat only candida infections (but no

dermatophyte or tinea versicolor).

♦ Griseofulvin will treat only dermatophytes (such 

tinea corporis but NOT tinea versicolor).

♦ Azole creams will treat candida, dermatophytes

tinea versicolor.

• Ketoconazole (oral) is more expensive; rare 

of fatal drug-induced hepatitis; and interacts

adversely with several medications. Recom

not using it routinely for tinea versicolor and 

dermatophytoses.

6
CLASS I (Super potent)

clobetasol propionate 0.05% 

betamethasone

 dipropinate 0.05% 

CLASS 2

amcinonide 0.1% 

fluocinonide 0.05% 

halcinonide 0.1% 

fluocinolone acetonide 0.2% 

betamethasone

 dipropionate 0.05% 

CLASS 3

triamcinolone 0.5% 

betamethasone

 dipropionate 0.05% 

CLASS 4

triamcinolone 0.25% 

hydrocortisone valerate 0.2% 

mometasone furoate 0.1% 

CLASS 5

triamcinolone 0.1% 

hydrocortsone valerate 0.2% 

betamethasone valerate 0.1% 

fluocinolone acetonide 0.05% 

halcinonide 0.025% 

fluticasone

 propionate 0.005% 
skin atrophy, telangiecactasias, hypopigmentatio

stretch marks.

♦ For body, use class 5, 4, or 3. The same side e

can occur here too.

♦ For hands and feet, use class 2 or 1. The same 

effects can occur here too; also a risk that large

amounts of topical steroids can be equivalent to 

oral steroids and long-term use can suppress HP

axis.

♦ For severe contact dermatitis (e.g., severe poiso

exposure etc.), consider oral steroids for 2-3 we

Do not use oral steroids routinely for unknown itc

disorders, and do not use for psoriasis.

6
G—SKIN DISEASES SEE

WORLD ----------------

H—TREATMENT GUIDEL

CONDITIONS ---------

I—EMERGENCY DERMAT

Glossary ---------------------

the use of a two-tiered app

1) Standard precautio

patients. Standard pr

procedures that are d

body surfaces and the

bloodborne pathogens

2) When caring for pa

epidemiologically imp

extra barrier or isolatio

These precautions wi

or airborne transmiss

instances when more 

need to be implement

Standard Precautions

These precautions apply w

skin or mucous membran

or excretions except swea

most effective means of p

infections. Hand hygiene 

soiled or disinfecting hand

irrespective of whether glo

take place immediately aft

between patient contacts

blood, or body fluids or co

handled. Gloves should b

branes, broken skin, cont

secretions, or excretions. 

between patients and befo

patient. During procedure
unavoidable, use a mechanical device or the one-handed

technique. HCWs must ensure that puncture-resistant

containers are designated and used for all used sharps

instruments. Patient and treatment rooms, cubicles, and

bedside equipment should be appropriately cleaned. The 

water and detergents in hospitals are sufficient to deconta

food service materials therefore no special precautions are

needed.

The tables below list examples of conditions necessitatin

isolation precautions and summarize the measures to be 

for the different isolation precautions.

A
infection

H erpes s

Droplet M eningit

H aem op

m eningit

pertussis

Parvovir

pharyngi

children 

S u m m a ry o f T ra n 

P re ca u tio n C o n ta c t 

Patient 

room 

P r iv a te 

G love s B efore 

Hand 

hygie ne 

S ta n d a rd 

G o w n If d ir e c t c o n ta 

w ith p a tie n t o 

environm e nt 

M asks Standard 

precautions 

O the r 

Excerpted from: Wenzel, 

Paul Butzler, (editors).

A Guide to Infection Contr

tional Society for Infectiou

2004. pp. 38-42.
clothing, dirt), highenergy projectiles (devitalized tissue, tiss

ischemia, hematoma), and delays in casualty evacuation. W

will likely become infected unless rapid, appropriate treatme

initiated.

Common microorganisms causing battlefield infections.

Gram-positive cocci - Staphylococcus species, Streptococc

Gram-negative rods (bacilli) - Escherichia coli, Proteus, Kle

 species.

Anaerobic gram-positive and gram-negative rods- Clostridiu

 Bacteroides, Prevotella species.

Nosocomial transmission - Pseudomonas, Enterobacter,

 Acinetobacter species.

Patterns of infection are dictated by area of injury.

Skin, soft tissue, muscle and bone - Staphylococcus,

Streptococcus,

 Clostridium species.

Intracranial injuries - Staphylococcus and gram-negative 

Orofacial and neck injuries - gram-positive cocci and mo

 anaerobes.

Thoracic cavity - staphylococcal empyemas and pneumo

 to Staphylococcus, Streptococcus and Pseudomonas 

 especially with prolonged intubation.

Intrabdominal injuries - Enterococcus, gram-negative rod

 anaerobic bacilli.

General principles of treatment focus on:

Treatment within 6 hours of injury.

Surgical debridement.

Copious irrigation.

B
S

F

F

Tactical a

echel

suppo

tactica

400 m

penet

shock

antibi

cefote

Medical t

surgic

table)
to infection control practices.

Minimal interventions include frequent hand w

ing, frequent use of alcohol hand gel, an

wearing surgical gloves with changing th

between patients.

Equipment that comes into direct contact w

patient should be cleaned between patie

Consider cohorting those patients undergoin

term in-hospital care.

Special battlefield wounds that may not require evacu

for surgical debridement.

Soft tissue injuries meeting all of the followin

criteria:

Non-mine injuries (due to potential co

nation).

Absence of fracture.

Entrance and exit wounds measuring 

than two centimeters in maximum

dimension.

Pleura or peritoneum not breached.

No major vascular injury.

No evidence of frank infection.

Treat with copious irrigation along with a dose of intravenous

antibiotic (cefazolin) or oral fluoroquinolone followed by 4 day

oral therapy or monitoring without oral antibiotics.

Table. Antimicrobial prophylaxis of battlefield wounds. These

recommendations are for empiric therapy of those with acute

battlefield wounds and do not apply to wound infections that

develop in personnel receiving long term medical care at eche

facilities.

B
Injury Potential paAbdominal, pelvic, upper thigh, gluteal region, HEENT wound or chest wound crossing mouth/esophageal/ sinus mucosa 

• Gram pos

(Streptoco

Staphyloc

• Gram neg

Enterobac

• Anaerobe

species, C

Extremity wound††, or HEENT wound or chest wound not crossing mouth/esophageal mucosa, penetrating brain injury 

• Gram pos

(Streptoco

StaphylocGroup A streptococ

• Gram pos

(ClostridiClostridiu

• If water e

consider Pspp, Aero
due to possible excess infection.

Duration of therapy: intracranial involvement- 5 days; open

fracture- 72 hours after the time of injury or not more than 24

hours after coverage of wound; perforated GI tract- continue f

only 24 hours after surgery in the presence of injury to any ho

viscus, if no hollow viscus involvement single preoperative do

adequate; oral cavity- 5 days.

B
CA-MRSA

Colonizes approxima

Often carries a gene t

invasive infections

Rarely recognized in 

of injury.

Typically remains sus

clindamycin, tetra

Prevention

Routine personal 

Consider as the i

infections do 

(cefazolin, ce

amoxicillin/cla

If infection likely, 

sulfamethoxa

Consider deconta

Nasal mupiro

Chlorhexidine

Multi-drug resistant bacte

Recognized among c

Etiology unknown but 

Skin colonization 

described bu

present.
frequent use of alcohol hand gel, and/or 

surgical gloves with changing them betw

patients.

Equipment that comes into direct contact w

should be cleaned between patients.

Consider cohorting those patients undergoin

in-hospital care.

In-theater nosocomial infections

Personnel receiving prolonged medical care in echelon II

are at risk of developing nosocomial infections. A nosoco

infection is defined as a new infectious syndrome, such a

nia, bacteremia, or urinary tract infection, after 72 hours o

ization. These infections often involve multi-drug resistan

(Acinetobacter baumannii, Pseudomonas aeruginosa, K

pneumoniae, MRSA).

Management

Initial empirical institution of broad spectrum ant

agents.

Vancomycin when gram-positive pathogens 

Carbapenems (meropenem or imipenem/cila

amikacin when gram-negative pathogen

Tailoring of antimicrobial therapy should be g

the results of bacterial culture and susc

data, if available.

For echelon III facilities without this real-time 

consider batch-testing cultures at anoth

that does have that capability, in order t

local susceptibilities and resistance tren

Emphasize infection control measures as mentio

Multi-drug resistant bacteria.

C
diseases, other fo

important to repo

i. Reportable Me

vital signs of any p

activity. These ar

in preventing dise

because of comm

ii. Medical evacu

manders want to 

is happening to th

iii. Occupational a

(OEHS) data from 

iv. Lost or modifie

support due to illn

c. These forms of su

below, with applic

for access.

II. Traditional (“Sick Call”

a. This information i

providers in detec

illnesses that repr

intervention and a

measures.
D
http://www.fhp.sm

iii. The JMeWS tra

available at: https:/

(unsecure).

iv. The FHP site n

but also contains l

activities discusse

AFIOH.

III. Reportable Medical E

UNSECURE

a. RMES is the vital 

serving as a sentinel 

preventable diseases 

b. Reporting of RME

ployed environment, 

for the garrison enviro

outlined below will im

c. RMES should be c

up the medical chain 

Division PM officer or 

medical chain of com

of the two following p

i. The JMeWS 

(JMeWS I do

or early summ

Annex Q repo

ii. Forward RME 

jmews@depl

helpdesk@fh

on to AMSA.
REPORTABLE MEDICAL EVENTS REPORTING FORM, 

D
REPORTABLE MEDICA
b. Landstuhl Regional Medical Center (LRMC) Join

Patient Tracking Application (JPTA) shows patie

information at LRMC. Available at: https://

dwmmc.lrmc.amedd.army.mil/PatientInformation

secured/logon.aspx

POC: DWMMC, LRMC, DSN 314-486-8127

V. Occupational and Environmental Health Surveillance

(OEHS).—SECURE

a. This information is useful in determining occupat

environmental exposures in deployed settings. S

often return to home station reporting exposures 

to deployment, such as asbestos in buildings or

drinking water contamination. The OEHS datab

the appropriate first resource for determining the 

of these claims.

b. The OEHS database is available via the USACH

secure website, at www.usachppm1.smil.mil, or 

from the FHP secure website.

D
Cholera 

Coccidioidomycosis 

Cold weather injury 

Cryptosporidiosis 

Cyclospora 

Dengue fever 

Diphtheria 

E. coli 0157:H7 

Ehrlichiosis 

Encephalitis 

Filariasis 

Giardiasis 

Gonorrhea 

Haemophilus influenzae, invasi

Hantavirus disease 

Heat exhaustion 

Heat stroke 

Hemorrhagic fever 

Hepatitis A 

Hepatitis B 

Hepatitis C 

Influenza 

Lead poisoning 

Legionellosis 

Leishmaniasis, unspecified 

Leprosy 

Leptospirosis
seen by the same practitioner and a decision ne

be made if there was any efficacy to the course 

antibiotics. If the lesion has persisted or worsen

scraping or biopsy should be performed.

- Photos of the lesion prior to scraping or biopsy b

done should be taken if the practitioner has the c

ity. E-mail these photos to WRAIR since this m

in the diagnosis (peter.weina@us.army.mil) and 

either derm.consult@us.army.mil or

id.consult@us.army.mil

2) Scraping procedure:

- Clean area with alcohol pads and allow to dry.

- Anesthetize with lidocaine 1% or 2% with epinep

1:100,000 (unless the epinephrine is contraindic

due to anatomic site).

- Two tissue smears are performed by horizontally

scraping (lightly enough to elicit an exudate, but 

vigorously enough to cause bleeding) the base o

underlying ulceration with a #15 blade (this often

requires removal of the overlying crusted debris)

dermal tissue is then thinly applied in a circular f

to a dime- to nickel-sized area in the center of th

slide. Minimize blood, epithelium (keratinocytes

purulence on the specimen.

- Additionally, material from the scrapings (and ev

overlying crusted debris) should be inserted into 

vial of 95-100% ethanol for PCR analysis.

- Ensure slides are labeled per the format of your

F
and approxim

lesion (see ph

Lesions on th

larger vessels 

extreme caut

(described ab

- The biopsy sp

clean, 2X2 dr

on the tissue 

the touch prep

- The tissue sh

impression sm

each biopsy) 

surface of the 

- Dry thorough

- The tissue bio

smears are m

small amount 

the specimen

transport tube

- The slides an

shipped per y

via DHL or Fe

The containe

specimens an

MTFs have pe

nostic specim

- Complete the 

below and inc

patient biopsi
Silver Spring, Maryland 209107500

Preferred biopsy area:

F
Places You 

Slept 

# Weeks 

or N/A 

Screens Or 

Windows? 

(Y/N) 

A/C 

(Y/N

Vehicle or 

Ground 

Tent Building 

Your Use of Insect 

Repellents 

Product Was Not 

Available to Soldier 

Bed Net, Treated w/ 

Permethrin 

Bed Net w/o Permethrin 

Permethrin Treated DCUs 

DEET (green tube) on Skin 

Commercial Insect 

Repellent 

If Yes, List in Box 

PART B – CLINICAL PROVIDER (Send fo

Lesion Location & #: ____________________

Antibiotic Treatment (type/dose/length): _____

Photos Taken? N / Y If Yes, sent to W

Procedures Done: Scrape Biopsy: N / Y 

 Culture: N / Y Prese

Date Eval: ___________ MTF: ___________

Clinician Name 

(stamp) ========================

Results: ( POS / NEG ) __________________

Notes: ________________
Infestations of scabies and Often secondarily infected

 head lice;

Tinea (pityriasis) versicolor Nearly universal in some

 populations

Pyoderma Primary infections or

 secondary infected sites

Dermatophytosis

Acne vulgaris

Pigmentary disorders Often pityriasis alba,

 melasma, and vitiligo

G
Burns, mild or moderate 

Bacterial infection, mild 

Fungal infection 

Scabies, noninfected 

Scabies, infected 
Antibiotics

Ampicillin, 250-mg tablets 

Ampicillin, 500-mg vials 

Penicillin benzathine, 

2.4-mU vials 

Penicillin procaine, 

3.4-mU vials 

Chloramphenicol, 

250-mg capsules 

Chloramphenicol, 1-g vials 

Nystatin, 100,000 IU tablet 

Tetracycline, 250-mg 

capsules 

Corticosteroids

Dexamethasone 

(injectable) 

Prednisolone (oral) 

Topicals and 

miscellaneous

Povidone iodine 10% 

solution 

Zinc oxide 10% ointment 

Benzoate 6% /salicyate 

 3%(Whitfield's) ointment 

Lidocaine 

I
Armed Forces Institute of 

ALT

alanine transaminase (SG

AMS

acute mountain sickness

AOR

area of responsibility

APG

Aberdeen Proving Ground

AKN

acne keloidalis nuchae

APHA

American Public Health A

ARDS

adult respiratory distress s

ASAP

as soon as possible

AST

aspartate transaminase (S

ATP

adenosine triphosphate

BAL

bronchio alveolar lavage

BDO

battle dress overgarment

BID

twice per day
Crimean-Congo Hemorrhagic Fever

CDC

Center for Disease Control

CINC

Commander in Chief

CNS

central nervous system

CONUS

continental United States

CPAP

continuous positive airway pressure

CPK

creative phosphokinase

CPR

cardiopulmonary resuscitation

CSF

cerebrospinal fluid

CSH

Combat Support Hospital

CXR

chest x-ray

DF

Dengue fever

DIC

disseminated intravascular coagulation

DNA

deoxyribonucleic acid

DNBI

Disease and Non-Battle Injury
EPICON

Epidemiologic Consultativ

ESR

erythrocyte sedimentation 

EVAC

evacuation (medical)

FAC

free available chlorine

FDA

Federal Drug Administrati

FHP

Force Health Protection

FM

field manual

GAS

Group A Streptococcus

GCSF

granulocyte colony stimul

GI

gastrointestinal

HACE

high altitude cerebral edem

HAPE

high altitude pulmonary ed

HARH

high altitude retinal hemor

HBIG

hepatitis B immune globu

HC

hydrocarbon
hemorrhagic fever with renal syndrome

HGB

hemoglobin

H-HC

halogenated hydrocarbon

HI

hemagglutination-inhibition

HRIG

human rabies immune globulin

HTH

high test hyprochlorite

ICU

intensive care unit

IFA

indirect fluorescent antibody (test)

IgG

immunoglobulin G

IgM

immunoglobulin M

IM

intramuscular

IND

investigational new drug

INH

isoniazid

IU/kg

international units per kilogram

IV

intravenous
y y

MTWTF

miosis, tachycardia, weak

MW

molecular weight

NATO

North Atlantic Treaty Orga

NBC

nuclear biological chemica

NFCI

non-freezing cold injury

NNMC

National Naval Medical Ce

NSAID

nonsteroidal antiinflammat

NTE

neuropathic target esteras

OCONUS

outside continental United 

OD

once per day

OEF

Operation Enduring Freedo

OEHS

Occupational and Environm

OIF

Operation Iraqi Freedom

OP

organophosphates

OSHA

Occupational Safety and H
by mouth

PPD

purified protein derivative

PPT

prolonged prothrombin time

PR

Petyriasis Rosea

PT

prothrombin time

PTT

partial thromboplastin time

PVC

premature ventricular contractions

QD

per day

QID

four times per day

RADS

reactive airways dysfunction syndrome

RBC

red blood cell

RMES

reportable medical events surveillance

RNA

ribonucleic acid

RPR

rapid plasma reagin

SCC

squamous cell carcinomas
trichloroethane

TCE

trichloroethylene

TG

technical guide

TIA

transient ischemic attacks

TIC

toxic industrial chemical

TID

three times per day

TMP

trimethoprim

UAE

United Arab Emirates

USACHPPM

U.S. Army Center for Heal

USAID

U.S. Agency for Internation

USAMRICD

U.S. Army Medical Resea

USAMRIID

U.S. Army Medical Resea

USARIEM

U.S. Army Research Instit

USCENTCOM

U.S. Central Command

URI

upper respiratory infection

UV

ultraviolet
WP

white phosphorus

WRAIR

Walter Reed Army Institute of Research

WRAMC

Walter Reed Army Medical Center

PART SIX: DEPLOYMENT DERMATOLOGY

APPENDIX A - STANDARD PRECAUTIONS AND ISOLATION

 PROCEDURES

APPENDIX B - MANAGEMENT OF BATTLEFIELD WOUNDS

APPENDIX C - RESISTANT BACTERIA/IN-THEATER

 NONSOCOMIAL INFECTIONS

APPENDIX D - DNBI AND HEALTH SURVEILLANCE

APPENDIX E - TRI-SERVICE REPORTABLE MEDICAL EVEN

APPENDIX F - LEISHMANIA SCRAPING AND BIOPSY

 PROCEDURES

APPENDIX G - SKIN DISEASES SEEN IN THE DEVELOPING

 WORLD

APPENDIX H - TREATMENT GUIDELINES FOR SELECTED

 SKIN CONDITIONS

APPENDIX I - EMERGENCY DERMATOLOGY HEALTH KIT