blood cells, where it multiplies asexually over
a period of about 48 or 72 hours, depending
on the species. After reaching maturity it
bursts from the red cell, releasing a large
number (usually 8 to 20) new parasites which
enter new red cells and reinitiate the cycle.
Typical malaria symptoms, chills and fever,
are associated with the rupturing of infected
ted cells and release of the parasites. This
process is often synchronous, which accounts
for the intermittent nature of the symptoms,
often occurring at about 48- or 72-hour
intervals (the so-called "tertian” or “quartan”
cycles). In addition to this asexual cycle in
humans, some of the parasites develop into
sexual forms, the male and female game-
tocytes. Infection of the mosquito takes place
when a receptive anopheline feeds on an
infected person who is carrying the gametocyte
Stages. The parasite then undergoes an
asexual cycle in the mosquito which requires
7 to 20 days and culminates with the invasion
of the mosquito salivary gland with numerous
microscopic, spindle-shaped forms known as
sporozoites. The human infection is initiated
when these forms are injected during the bite
of the infected mosquito. Before the asexual
cycle in the red cells is established, the
parasite must complete a 5- to 10-day period
of multiplication in cells of the liver.
Clinically, the malaria infection varies from
a moderately severe to a highly fatal illness,
depending on the species of parasite and the
host’s condition. In the absence of prompt
treatment, the so-called "malignant tertian"
malaria, caused by P. falciparum, is parti-
cularly severe and often fatal in infants and
young children and in those adults who possess
no partial immunity due to previous malaria
experience. The benign tertian Parasite, P.
vivax, generally causes a less severe illness
and a lesser rate of mortality. There appears
to be no true "immunity" conferred by a
malaria attack; persons in a highly endemic

i

area may be infected over and over again,
usually developing a tolerance for the parasite
which prevents severe clinical consequences,
but which does not prevent the continuation of
a chronic, often debilitating infection.

If insufficiently treated, a malaria infection
may persist in humans for many months or
years and have a continuing or periodically
renewed ability to infect mosquitoes, often in
the absence of symptoms or with a less severe
clinical attack. For two of the species, P.
vivax, and P. ovale, the continuation of
parasites in the liver cells for prolonged
periods may give rise to relapses by reinvasion
of the red blood cells from this source at
intervals for several years after the initial in-
fection. There is probably no such true
relapse mechanism for P. falciparum or P.
malariae. However, in the case of P. malariae
low-grade parasitemias may continue to be
present in persons who have developed a
tolerance for the infection. These parasitemias
are characteristically asymptomatic or with
infrequent mild symptoms and are less likely
to be treated with a specific drug for malaria
than would be the primary symptomatic attack
and, therefore, from time to time may provide
an unsuspected source of infection to
mosquitoes. The remaining hazard of malaria
transmission within the United States stems
from the possible importation of such cases, or
of cases recently acquired in endemic areas but
not yet clinically apparent, into receptive areas
of the country.

Despite the widespread presence of
anopheline mosquitoes throughout the United
States, a highly susceptible human population,
and the importation of thousands of cases of
malaria acquired overseas during World War
TI and the conflicts in Korea and Vietnam,
there have been reported between 1964 and
1990 a total of 79 cases in 16 episodes of
introduced malaria, i.e., malaria due to local
transmission from an infected individual who


ENDEMIC CYCLE

Other mosquitoes

a EPIDEMIC
\ Sq CYCLE

PHEASENT
EPIDEMIC ,

LOCAL WINTER,
‘TRESERVOIR?
cc

[Known portion
of eyele

BB specutve § VemeF
portion Northern

Southern
ofcycle bird migration §=—bird migration

EE virus cycle in U.S.

D> miGRANT BIRDS

LOCAL WINTER RESERVOIRS ? Known portion

of cycle

WEED Speculative
Portion of cycle

SLE virus cycle in U.S.

femme eeeeTM

(=@ Known portion of cycle
BS Speculative portion of cycle

Endemic cycle of VE*
“Representative of 10, (€, I. 1V antigensc subgroups

Local Winter Reservoks 7 SOUTHERN BIRD

Possibly: Birds, Catex tersalte, MIGRATION
AEXZ’ Known portion
MIGRANT ° specie
MIQRANT - Speculative

Portion of cycle

WE virus cycle in western U.S.

CE group virus cycle in U.S.

LaCrosse and Keystone aubtypes.
Jamestown Canyon subtype

SUMMER

INFECTION IN MAN
(Mortality less than 1%)

Mosquito Rodent Cycle ? + of cycle

Mosquito Equine Cycle?

Epidemic VEE virus cycle*
“Representative of 1A, 1B, and 1G

Figure 1. North American Mosquitobome Arboviral Encephalitis Cycles

tL


addition, antibodies to Everglades virus have
been found in Seminole Indians, hunters,
fishermen, and campers in localized areas in
southern Florida. The virulent epidemic type
1A and 1B viruses have been involved in
extensive epizootics in horses and epidemics in
humans in tropical America since 1935.

In 1971 an outbreak of the 1B type of VEE
occurred in Texas, in association with a
similar outbreak in Mexico, and more than
1500 equines were fatally infected. Although
only 19 human cases of VEE were reported to
the Center for Disease Control during 1971,
one authority places the number of cases in
Texas at 110, with no deaths (Bowen et al.
1976). Psorophora columbiae, Ps. discolor,
Aedes sollicitans, and Ae. thelcter were the
primary vectors in South Texas during the
1971 epidemic. Other species of Culex,
Anopheles, Mansonia and Deinocerites were
also found infected in Texas in 1971, and may
be important in other countries. The Texas
epidemic was controlled by a_ three-fold
program involving (a) vaccination of equines
with live, attenuated vaccine to protect horses
and to preclude them as a source of virus for
mosquito vectors; (b) quarantine of equines in
Texas and adjoining states; and (c) ultra-low
volume aerial application of technical
malathion to some 13.5 million acres of
mosquito-producing area along the Mexico-
Texas border and the Gulf Coast of Texas and
Louisiana (Sudia and Newhouse 1975). No
further Venezuelan equine encephalitis activity
has been reported in equines or humans in the
United States during the period of 1972 to
1975.

DENGUE

Dengue is a viral disease transmitted from
Person to person by mosquitoes. It may occur
in epidemic form in almost any part of the
tropics or subtropics. It is usually an acute,
nonfatal disease, characterized by sudden onset
of fever, headache, backache, joint pains,

nausea, and vomiting. There are four virus
serotypes (DEN 1-4). Three of the four
serotypes (DEN-1, DEN-2, and DEN-4) have
been circulating in the Americas since 1981.
Although endemic transmission of DEN-3 has
not occurred in the region since 1977, it could
be reintroduced. While most infections result
in relatively mild illness, some may cause the
severe forms of the disease, dengue
hemorrhagic fever (DHF) characterized by
severe rash, purpura, mild gum bleeding,
nosebleeds, gastrointestinal bleeding and
circulatory failure resulting in dengue shock
syndrome (DSS) and even death.

In the Western Hemisphere the principal
and perhaps the only mosquito responsible for
transmission of dengue in human populations
has been Aedes aegypti. Aedes albopictus has
been a vector in Hawaii, the Philippines, and
Southeast Asia and may become one in the
New World. The mosquitoes obtain the virus
from the blood of infected persons during the
period from the day before the initial fever
through the third or fourth day of illness. The
virus multiplies in the mosquito, which
becomes infective to man 8 to 14 days after
the infective blood meal. The mosquitoes may
remain infective for the rest of their lives with
the ability to transmit the disease-causing virus
during subsequent blood feedings on humans.
(Gubler, 1988).

Dr. Benjamin Rush reported one of the
earliest outbreaks of dengue in the United
States from Philadelphia in 1780. In 1922
there was a large epidemic from Florida to
Texas with an estimated 2 million cases, and
with perhaps a million cases in Texas alone.
Cases of dengue were reported in Louisiana in
1945. Dengue epidemics spread from Jamaica
in 1977, to Honduras in 1978, to Mexico in
1979, and to Texas in 1980 where 27 cases
were reported in people who apparently had
not been out of the country. Cases of dengue
contracted overseas but occurring in the


Eastern Equine Encephalitis

Eastern equine encephalitis (EEE) is found
along the Atlantic and Gulf Coasts and inland
in limited areas in New York and the
Midwest. As will be noted in Table 1, cases
usually occur in small numbers in any one
year. Cases generally occur in the late
summer and are concentrated in the young age
groups. There were localized epidemics in
Massachusetts in 1956 (12 cases), and in New
Jersey in 1959 (32 cases); 1968 (12 cases);
1982 (12 cases) and 1983 (14 cases). Eastern
equine encephalitis is the most deadly of the
North American mosquito-borne viral diseases,
with 50 to 75% of the human cases ending

ST. LOUIS

Sporadic or
focal infection
reported

fatally and leaving a high proportion of the
survivors with severe central nervous system
sequelae. The disease often occurs in horses
and in game farm pheasants and may be fatal
in up to 90% of these animals. The bird-to-
bird cycle of the virus is typically maintained
by Culiseta melanura, a mosquito whose
larvae are found in freshwater swamps.
Because this mosquito rarely bites humans or
horses, other mosquitoes, such as the eastern
salt marsh mosquito Aedes  sollicitans,
Coquillettidia pertubans, and Aedes vexans,
are probably the vectors responsible for
transmission of the disease to these dead end
hosts.

EASTERN

Figure 2. Distribution of 4 Types of Mosquitoborne Arboviral Encephalitis



encephalitis viruses but not by others. For ex-
ample, deaths due to EEE virus have been
reported in red-winged blackbirds, house
sparrows, whooping cranes, and pheasants.
SLE virus produces no outward signs in birds.
Schematic illustrations of the basic
transmission cycles of the five major types of
encephalitis viruses of North America are

presented in Figure 1. Portions of some of
these cycles are still speculative and await fur-
ther confirmation. The geographic distribution
of four of these viruses is shown in Figure 2.
The human cases of four major mosquito-
bome viral encephalitides of North America
reported by the states to the Centers for
Disease Control and Prevention since 1970 are
summarized in Table 1.

TABLE 1. REPORTED CASES OF ARBOVIRAL ENCEPHALITIS IN THE U. S.

TYPE OF ENCEPHALITIS
YEAR EEE SLE WEE LAC/CE TOTAL
1970 2 15 4 89 110
1971 4 57 11 58 130
1972 0 13 8 46 67
1973 7 5 4 75 91
1974 4 714 2 30 110
1975 3 1815 133 160 2111
1976 0 379 1 47 427
1977 1 132 41 65 239
1978 5 26 3 109 143
1979 3 32 3 139 177
1980 8 125 i) 49 182
1981 0 15 19 91 125
1982 12 34 9 130 185
1983 14 19 7 64 104
1984 5 33 2 89 129
1985 0 21 1 68 90
1986 1 43 7 64 115
1987 3 17 41 87 148
1988 1 0 0 41 1
1989 9 34 tt) 65 108
1990 5 240 0 62 245
1991 12 70 1 6 89
TOTALS 99 3199 297 1531 5126



on them.

Members of the Culex pipiens complex,
Culex pipiens pipiens (the northern house
mosquito) and Culex pipiens quinquefasciatus
(the southern house mosquito) are the main
urban vectors of St. Louis encephalitis. Culex
tarsalis is the chief vector in rural areas in
western states. Culex nigripalpus is the main
vector in Florida.

Culex salinarius and Culex restuans are
potential vectors in some localities, but this
observation requires confirmation.

LaCrosse Encephalitis/California

Encephalitis
Transmission of LaCrosse (LAC) and other
California serogroup _ viruses including

California encephalitis (CE) and Jamestown
Canyon (JC) to humans is rather constant. As
shown in Table 1, there are about 75 reported
cases nationally (range 30 to 160) each year.
Routine testing for and reporting of California
serogroup encephalitis was initiated widely in
the United States beginning in 1963.
"Between 1963 and 1984, 1611 cases of CNS
(central nervous system) illness, serologically
confirmed as CE, were reported to CDC....,
the vast majority of these cases undoubtedly
resulted from infection with LAC virus.”
(Grimstad, 1988). The greatest number of
cases of LaCrosse encephalitis have been
reported in the midwestern states of Ohio,
Indiana, and Wisconsin, in August and
September, usually in children under 16 years
of age, and more often in males than in
females. As shown in Table 1, each year
from 1970 to 1991 more cases of LAC/CE
were reported than cases of EEE or WEE, and
often than cases of SLE. Fortunately
infections with LAC virus cause a less severe
illness than is commonly found with other
mosquito-borne encephalitides. The mortality
rate is probably in the order of 4 per 1,000.
Human cases of California encephalitis (CE)

have been reported from California where the
CE virus has been isolated from Aedes
melanimon mosquitoes. Human cases of
Jamestown Canyon (JC) encephalitis have been
reported from Michigan, New York, and
Ontario. Aedes stimulans may be the principal
vector of JC virus. Other viruses in the
California encephalitis serogroup include
Keystone and Trivittatus--usually with Aedes
mosquito vectors.

LaCrosse encephalitis differs from Eastern
equine, Western equine, and St. Louis
encephalitis in that it has mammalian, rather
than an avian, vertebrate host system. The
major mammalian hosts are the eastern
chipmunk, tree squirrels, and foxes. The
principal vector is the eastern treehole
mosquito, Aedes triseriatus. The virus has
been shown to overwinter in the eggs of the
treehole mosquito and has been passed through
the eggs to larvae, pupae, females and males
(Watts et al. 1973). The virus is maintained
in woodland habitats and even within small,
isolated woodlots, which are quite numerous in
some north central states. There is a strong
association between the occurrence of human
LAC encephalitis cases and the presence of
Ae. triseritus in artificial containers, such as
tires, on patients’ premises. Detailed accounts
of the California encephalitis group, including
data on human cases and isolations of the
various subtypes from many species of
mosquito and vertebrate hosts, has been
published (Sudia ef al. 1971 and Calisher and
Thompson 1983).

Venezuelan Equine Encephalitis

Venezuelan equine encephalitis (VEE) is
caused by a number of subtypes of virus. The
endemic Everglades virus (EV) in Florida is of
low virulence and is transmitted by Culex
(Melanoconion) mosquitoes from wild rodents.
Three clinical human cases have been reported
in southern Florida (Ventura et al. 1974). In



SELF-STUDY COURSE 3013-G
Vector-Borne Disease Control

SELF-STUDY

MOSQUITOES

Of Public Health Importance
And Their Control

ee “y, U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES
Public Health Service
Centers for Disease Control and Prevention
Public Health Practice Program Office ‘CENTERS Fon CrsEAae CONTROL,
vera Atlanta, Georgia 30333

m,


and Galindo 1956) reaching as far north as
Mexico. The yellow fever virus may be
highly fatal to some of the species of monkeys
involved in the jungle cycle, while others
develop viremias with little or no apparent
illness. The potential for initiation of urban
transmission of the disease depends on the
return of a human who has become infected in
the forested area to an area where Aedes
aegypti is present to initiate and maintain
human-to-human. transmission. This has
occurred only rarely in the Americas and has
in no case resulted in an epidemic. Esta-
blishment of the urban cycle may occur with
some frequency in Sudan, Ethiopia and other
African areas (Monath 1988).

MALARIA

Although malaria had disappeared as a
significant problem within the United States by
the early 1950’s, it is still one of the most
important communicable diseases on a
worldwide basis. Malaria in humans is an
acute or chronic disease caused by any one of
four species of microscopic protozoan Parasites
in the genus Plasmodium (P. vivax, P.
falciparum, P. malariae and P. ovale). The
Parasite is transmitted from Person to person
by the bite of Anopheles mosquitoes.
Although there are 17 species of Anopheles in
the United States, only three served as
significant vectors of the disease: An.
quadrimaculatus east of the Rocky Mountains,
An. freeborni and An. hermsi in the West.

Malaria was the number one insect-borne
disease in the United States from colonial days
until the late 1940’s. As shown in Figure 3
malaria control has been a continuing battle
from 1930 to the present time. During the
Great Depression of the 1930's over 100,000
Cases were reported each year, but the number
was probably grossly underreported. In the
late 1930's the TVA, WPA, and other
governmental agencies began area-wide

malaria control programs and reduced the
number of cases to about 60,000 a year at the
beginning of World War I. During World
War II, a cooperative Program of PHS and
state and local health departments, the Malaria
Control In War Areas Program (MCWA),
helped control this disease, but the number
rose at the end of the war due to cases
contracted overseas in the China-Burma-India
and Mediterranean theaters of war. As the
result of a Malaria Eradication Program from
1945-1952, the number of cases dropped
dramatically, from over 60,000 cases in 1945
to 2,184 in 1950 (Fig. 3).

As Veterans returned from the Korean
conflict, many came down with malaria. The
number of cases rose to 5,600 in 1951 and
peaked at 7,023 in 1952, of which
approximately 50 were transmitted in the
United States. As the number of veterans
returning from malarious areas decreased, the
number of cases of malaria decreased,
Teaching a low of 132 in 1957, Beginning in
1965 soldiers returning from Vietnam came
down with malaria in this country and the
number of cases of malaria rose to a peak of
over 4,000 cases in 1970. Following
President Carter’s decision to admit up to
14,000 Asian refugees a month, the number of
cases rose to 1,864 in 1980, due in part to
infected Indochinese refugees. Since 1980
about a thousand cases of malaria have been
Teported each year, almost all of them
contracted overseas. However, migrant
agricultural ‘workers from Mexico (some
suffering from malaria) came across the border
and slept outdoors in California where they
were bitten by malaria mosquitoes which later
transmitted malaria to other migrants and
tesidents who had never been out of the
country. In San Diego county, California 27
malaria cases were reported in 1986 and 30
cases in 1988.

The malaria parasite inhabits the human red


United States have been reported for many
years, as 102 cases in 1990 (CDC, 1991).

Epidemics of dengue, some with cases of
dengue hemorrhagic fever (DHF) and dengue
shock syndrome (DSS) have occurred in the
Americas. The estimated cost of the DEN-2
and DEN-3 epidemic in Puerto Rico in 1977
was between $6 and $16 million (U.S.) in
medical costs, lost work, and control
measures. The 1981 DHF epidemic in Cuba
had an even greater economic impact with an
estimated cost of over $100 million (U.S.) in
control measures and medical costs during a 4-
month period from July through October.
Gubler (1988) reported 502,026 cases in 1977
in the Americas and 362,398 in 1981 with
116,143 persons hospitalized and 158 deaths,
with most of the 1981 cases from Cuba. Some
authorities have theorized that the severe
hemorrhagic forms of the disease (DHF and
DSS) occur only in persons experiencing a
second infection with a different (heterologous)
dengue serotype. For example, the 1981
Cuban epidemic of DHF caused by DEN-2
virus was preceded by a large DEN-1
epidemic in 1977.

Dengue is endemic in Puerto Rico with 11
outbreaks since 1963. Starting in 1986, from
6,000 to 11,000 cases of dengue-like illness
have been reported each year in Puerto Rico.

The most recent major epidemic of dengue
in the Americas occurred in Peru in 1990,
with 76,000 cases reported. The most recent
outbreak of dengue hemorrhagic fever (DHF)
occurred in Venezuela in 1989-90 involving
3,108 cases of severe dengue and 73 deaths
(CDC, 1991).

YELLOW FEVER
Yellow fever is a viral disease which is
transmitted to humans by mosquitoes. Illness
from this infection may be acute and fatal or
so mild as to be inapparent. There are two
distinct epidemiologic types of the disease in

the Americas: Urban yellow fever and jungle
yellow fever. In both the virus is the same,
and humans are protected from each by the
same vaccine; however, the mosquito vectors
and normal vertebrate hosts differ.

Urban Yellow Fever

In the classical urban type of yellow fever,
epidemics are the result of human-to-human
transmission of the virus by Aedes aegypti,
commonly called the yellow fever mosquito.
Although no epidemics have occurred in the
United States since the outbreak of 1905 in
New Orleans, epidemics were reported with
some frequency during the 18th and 19th
centuries from most of the larger seaports in
the eastern United States, even as far north as
Philadelphia, New York, and Boston. These
epidemics probably originated from the
importation of cases from infected areas of
Central and South America. Although Aedes
aegypti is commonly found in many areas of
the United States, importation of cases leading
to the establishment of epidemics in this
country is a theoretical but highly remote
possibility because of vaccine usage and the
absence of urban yellow fever elsewhere in the
Americas.

Jungle Yellow Fever

Jungle yellow fever, also called sylvan or
sylvatic yellow fever, is normally a disease of
monkeys and perhaps other wild animals,
transmitted most frequently by sylvan, treetop-
frequenting mosquitoes in the genera
Haemagogus, Sabethes and Aedes. Enzootic
and epizootic yellow fever is maintained in the
jungle primates by these vectors. Humans
usually become involved when they invade
jungle habitats for occupational or other
purposes and are bitten by the sylvan vectors.
Epizootics continue to occur in jungle areas.
The most recent extension of activity toward
the United States occurred in 1956 (Trapido



Western Equine Encephalitis

Western equine encephalitis (WEE) is found

in the states west of the Mississippi River,
Wisconsin, and Illinois, as shown in Figure 2.
As in Eastern equine encephalitis, cases are
concentrated in the young. There were many
major outbreaks in horses in the 1930's, with
thousands of cases and many deaths. The
largest human epidemic, probably over 3,000
cases, occurred in the western United States in
1941. Another large epidemic occurred in
1952, primarily in the Central Valley of
California (Reeves 1990). There were 141
cases in 1958 and 172 cases in 1965. In 1975
133 cases were reported, primarily in the Red
River Valley of Minnesota and South and
North Dakota. While deaths have been
reported in human cases of WEE, it is
generally a much milder disease than EEE.
Mortality has been reported as ranging from 1
to 5% of the cases. The death rate in horses
is considerably higher.

Culex tarsalis and Aedes melanimon are the
important mosquito vectors of Western equine
encephalitis. Isolations of WEE virus have
been made from many species of mosquitoes
and birds. (Reisen and Monath, 1988).

St. Louis Encephalitis

St. Louis encephalitis (SLE) was first
‘recognized during an epidemic in the St.
Louis, Mo., area in 1933, although
retrospectively the first known outbreak of the
disease was found to have occurred in 1932 in
Paris, Illinois. Since that time, human cases
of SLE have been reported from all of the
contiguous states, with the exception of the
New England area and South Carolina (Fig.
2). (Monath, 1980; Chamberlain, 1987; Tsai
and Mitchell, 1988).

The largest number of cases of SLE on
record for a single year occurred in 1975 when
1815 cases were reported from 30 States, the
majority of them in the Ohio and Mississippi

valleys. Human cases of SLE typically occur
in late summer and fall. During the Florida
epidemic of 1990, in order to prevent infection
from night-biting mosquitoes, people were
advised to stay indoors after dark and many
football games were rescheduled for afternoon

playing.

The following major outbreaks have
occurred:
Location Date Cases Deaths
St. Louis, MO 1933 1,097 221
St. Louis, MO 1937 431 107
Hidalgo Co., TX 1954 373 10
Louisville, KY 1956 10 «12
Cameron Co., TX 1957 114 3
Tampa Bay area, FL 1962 222 «(43
Houston, TX 1964 243° «(27
Dallas, TX 1966 172 22
Florida 1990 226 «10

St. Louis encephalitis is considered to be a
more serious disease than Western equine
encephalitis but less so than Eastern equine
encephalitis. The disease is more commonly
seen and is more severe in older people. Case
fatality rates for most outbreaks of SLE have
varied from 2 to 20%, and neurologic sequelae
have been reported in a small percentage of
cases. However, most infections of SLE virus
in humans do not result in illness, and many
mild cases show aseptic meningitis or fever
only.

St. Louis encephalitis virus exists primarily
as an infection of birds transmitted by
mosquitoes. It may be enzootic in some areas
but occasionally epizootics may occur in which
a large percentage of birds in the area become
infected. Birds develop the levels of viremia
needed to infect mosquitoes but do not suffer
ill effects from the disease. Humans and
horses acquire SLE infections from mosquitoes
which have previously fed on infected birds,
but apparently do not develop a sufficient
amount of virus to infect mosquitoes that feed


INTRODUCTION

Throughout history mosquitoes have
occupied a position of importance as a pest of
mankind, but not until the late 19th century
were these arthropods identified as the agents
responsible for transmission to man of some of
his more devastating diseases. During
subsequent years, knowledge of the
telationship of mosquitoes to disease has

expanded; and knowledge of methods for
controlling these disease vectors has often
provided us with means toward reducing or
eliminating the diseases in many areas. In this
manual the importance of mosquitoes to human
health in the United States is considered, along
with basic information on mosquito,
identification, biology, and control.

MOSQUITOES AS DISEASE VECTORS

World-wide, mosquitoes are responsible for
the transmission of disease to millions of
people each year. These diseases include
encephalitis, dengue, yellow fever, malaria,
and filariasis. In the past, most of these
diseases have been highly important as
endemic or epidemic diseases in the United
States, but presently only the arthropod-borne
encephalitides continue to occur with some
frequency in this country.

ENCEPHALITIS

A high proportion of the arthropod-borne
viruses known to affect humans are transmitted
to humans by mosquitoes. Several of these
viruses are responsible for encephalitis, a
disease affecting the central nervous system.
The five major types of arboviral encephalitis
in the United States are: Eastern equine
encephalitis (EEE), Western equine
encephalitis (WEE), St. Louis encephalitis
(SLE), LaCrosse encephalitis (LAC) and
Venezuelan equine encephalitis (VEE); each is
caused by a distinctly different virus or virus
complex. These viruses are normally
infections of birds or small mammals. During
the course of such infections the level of virus
may increase (amplification), facilitating
further extension of transmission. The
occasional infection of human or equine hosts

may result in severe illness or death. In most
cases, the human or equine host is a "dead
end" for the virus, with little or no possibility
of subsequent transmission of the disease from
these hosts because of their inability to infect
mosquitoes.

The viruses that cause Eastern equine,
Western equine, or St. Louis encephalitis are
normally transmitted from bird to mosquito to
bird, and less commonly from bird to
Mosquito to human or horse. The viruses that
cause LaCrosse encephalitis and Venezuelan
equine encephalitis are normally transmitted by
mosquitoes among small mammals, but
occasionally are transmitted to humans or, in
the case of VEE, to horses. Because of the
higher VEE viremias common in infected
horses, these hosts may provide a source for
the mosquito transmission of the virus to new
hosts.

Human cases of arbovirus infections range
from inapparent or mild to very severe
illnesses which may permanently damage the
central nervous system and, in some instances,
are fatal. Similarly, horses may have mild to
severe or fatal infections with EEE, WEE, or
VEE viruses. SLE virus causes only
asymptomatic infections in horses (they
develop antibodies but not clinical illness).
Birds may die of infection caused by some


came into the United States. All cases of
malaria in the United States which are sus-
pected as introduced cases are carefully
investigated by state and/or federal health
authorities to determine the exact origin. In the
event of introduced malaria, immediate steps
are necessary to prevent further spread, and
these include detection and treatment of cases
as well as mosquito surveillance and, if war-
ranted, localized mosquito contro] measures.

FILARIASIS

The World Health Organization estimates
that at least 250 million people are infected
with the filarial nematode parasites Wuchereria
bancrofti and Brugia malayi, transmitted by
mosquitoes (WHO 1974). The adult worms
live in various parts of the human lymphatic
system, causing the diseases known as Ban-
croftian and Brugian filariasis. Persons may
harbor the parasites with no apparent
symptoms, or the filarial worms may cause
inflammation and other complications. In
some persons who have had prolonged and
repeated infections, there may be extreme
enlargement of the external genitalia, breasts,
or legs, hence the clinical term elephantiasis
for pronounced enlargement of parts of the
body, often with a thickened rough skin.

The young filarial worms are transmitted
from person to person by various species of
mosquitoes. These nematodes undergo
developmental changes in the mosquito which
is an essential link in the cycle of trans-
mission. The immature worms, called
microfilariae, occur in the human bloodstream.
Here they are picked up by mosquitoes as they
feed. A minimum period of 10 to 11 days is
required for the developmental stages in the
mosquito thorax before infective forms migrate
to the mosquito proboscis, from which point
they reach the new host at the next feeding.
The infective filariae are not injected into the
new host by the mosquito but actively

12

penetrate the skin, perhaps at the site where
the mosquito punctured the skin. Important
vectors of Wuchereria bancrofti include
species of the genera Culex, Aedes, and
Anopheles. The generally accepted vectors of
Brugia malayi are mosquitoes in the genus
Mansonia.

Filariasis is widespread in many tropical
and subtropical regions throughout the world.
The Bancroftian type of filariasis is apparently
an increasing public health problem in many of
the larger cities in southeastern Asia. In the
Western Hemisphere it occurs in the West
Indies, Venezuela, Panama, and the coastal
portions of the Guianas and Brazil. Filariasis
control programs are based on control of the
mosquito vectors and treatment of the human
cases with diethylcarbamazine (Hetrazan).

A small endemic center existed for many
years near Charleston, SC, but this has now
disappeared. In many parts of the United
States, people who have recently left the
tropics may have the immature worms
circulating in their blood. However the
disease is not known to be naturally acquired
in the United States at the present time.

DOG HEARTWORM

The dog heartworm (Dirofilaria immitis) is
a common mosquito-transmitted _filarial
parasite of dogs which causes serious disease
in these animals along the Atlantic and Gulf
Coasts from Massachusetts to Texas and inland
at least to Illinois and Minnesota. This
nematode is also an occasional parasite of
man; during the past 15 years at least 35
human cases have been reported in the United
States (Gershwin et al. 1974). The parasite in
man is usually located in the lung and less
often in the heart. Other than as a lesion
which may simulate other diseases in medical
diagnosis, its clinical significance in man has
not been fully determined.

The mosquito vectors of dog heartworm are



CONTENTS

iii

Page

INTRODUCTION .. 2.222. eens 1
MOSQUITOES AS DISEASE VECTORS ...........2... 00.0000 ec eee eee 1
Encephalitis 1
Dengue 7
Yellow Fever... .. 8
Malaria ........ 9
Filariasis ....... 12

Dog Heartworm 12
GENERAL CHARACTERISTICS AND LIFE CYCLE OF MOSQUITOES ........... 13
Life History 13

Eggs .... 20.0... 02. eee eee eee 13

Larvae .. see saa see wee 15
Pupae 17

Adults 18

Habits of the Adult Mosquitoes .................. 19
Ecologic and Bionomic Types of Mosquito Life Histories 20
NOTES ON IMPORTANT SPECIES OF MOSQUITOES ....................... 22
The Genus Aedes ...... 2.0... 0002s 22

The Genus Anopheles : 31

The Genus Culex . . 35

The Genus Culiseta 39

The Genus Mansonia and Coquillettidia 40

The Genus Psorophora sae . 41

Other Mosquitoes 2... 6... eee eee eee eee 44
MOSQUITO SURVEYS ......... 00.0002 t een ene 44
Mosquito Control Maps .: 44

Adult Mosquito Surveys 45

Larval Mosquito Surveys 51
Mosquito Egg Surveys and Reiter Gravid Trap ................ 55
Utilization of Survey Data... 2... eee ene 57

THE CONTROL OF MOSQUITOES 58
Naturalistic Control... 2... ee eee 58
Biological Control 64
Chemical Control (Larval Control and Adult Control) 64
Personal Protection from Mosquitoes 72
Methods for Assessing Chemical Control of Mosquitoes 73
PUBLIC RELATIONS ........ 0200000 cee ee 74
PICTORIAL KEYS ... 0.2 ces 76-80
REFERENCES .... 2.21 eee 81-85


MOSQUITOES

Of Public Health Importance
And Their Control

Harry D. Pratt

and
Chester G. Moore

Prepared and Printed 1960
Revised 1969
Revised 1976
Revised 1977

Reprinted 1988
Revised 1992

Revised 1993

oe

,
H U.S. DEPARTMENT OF HEALTH & HUMAN SERVICES DC
Oe Public Health Service

“essa


NUMBER OF CASES

MALARIA- Reported Cases by Year, United States

200,000 +
100,000 +
50,000 4

10,000 +
5,000 +

1,000 ~
500 4

100 4

50

1930-1988

TVA Malaria Control Program

{ WPA Malaria Control Program

War Areas Control Program
{ Relapses-Overseas Cases

Mataria Eradication Program

PRIMAQUINE Treatment of Servicemen

Relapses From Korean Veterans
F Returning From Malarious Areas

Returning Vietnam Veterans
| Asian Refugees

Small epidemics
in California

T

T T T T T T T T T y u
1930 1935 1940 1945 1950 1955 1960 1965 1970 1975 1980 1985 1990

YEAR

Figure 3. Malaria -- Reported Cases by Year, United States. 1930-1988

10



not definitely known, but a list of infected
mosquitoes has been published (Ludiam et al.
1970), and includes Culex Salinarius, Aedes
aegypti and Ae. taeniorhynchus. Aedes

canadensis may be an important vector in the
northeastern United States. Aedes sierrensis is
a vector in California and Utah. Aedes
albopictus is a competent vector of D. immitis.

GENERAL CHARACTERISTICS AND LIFE CYCLE OF
MOSQUITOES

Mosquitoes are small, long-legged, two-
winged insects belonging to the Order Diptera
and the Family Culicidae. The adults differ
from other flies in having three characters in
combination: long, many-segmented antennae;
an elongate proboscis; and scales on the wing
veins and wing margin. This is a very large
group containing over 3000 species. There
are approximately 165 species and subspecies
in North America north of Mexico belonging
to 13 genera distributed among 3 subfamilies
according to Darsie and Ward (1981). Their
general classification of the mosquitoes
occurring in this area is outlined below:
Order Diptera (flies and mosquitoes)

Family Culicidae (mosquitoes)
Subfamily Anophelinae (anophelines)
Genus Anopheles-17 Species
Subfamily Culicinae (culicines)
Genus Aedes-79 species and
subspecies
Genus Coquillettidia (formerly
Mansonia) | species
Genus Culex-29 Species and
subspecies
Genus Culiseta-8 species
Genus Deinocerites-3 species
Genus Haemagogus-1 species
Genus Mansonia-2 species
Genus Orthopodomyia-3 species
Genus Psorophora-15 species
Genus Uranotaenia-3 species and
subspecies
Genus Wyeomyia-4 species
Subfamily Toxorhynchitinae

13

Genus Toxorhynchites (formerly
Megarhinus)-2 subspecies

LIFE HISTORY
Mosquitoes have four distinct stages in their
life history, the egg, larva, pupa, and adult
(Fig. 4). The first three Stages occur in water,
but the adult is an active flying insect that
feeds upon the blood of man and animals or
upon plant juices.

Eggs

Eggs are white when first deposited,
becoming dark within an hour or two. In
general, mosquito eggs fall into three distinct
groups: (a) those laid singly on the water
surface: (b ) those laid together to form rafts
which float on the water surface; and (c) those
laid singly on damp soil or vegetation. These
differences are reflected in the structure of the
egg.

Anopheline eggs are laid singly on the
water surface. They are elongate oval, usually
pointed at one end and provided with a pair of
lateral floats (Fig. 4). They average about
one-half millimeter in length. Hatching
usually takes place within 2 or 3 days. The
eggs of Toxorhynchites are also laid singly on
the water surface where they are kept afloat by
means of air bubbles which form among the
spines on the egg shell. The eggs of Culex,
Culiseta,  Coquillettidia, Mansonia and
Uranotaenia are \aid side by side to form a
raft often containing 100 or more eggs. They
remain afloat on the surface of the water until