American
Trypanosomiasis
Chagas Disease,
New World Trypanosomiasis,
South American Trypanosomiasis,
Mal de Chagas,
Chagas-Mazza Disease
Last Updated: September 2009
Importance
American trypanosomiasis (Chagas disease) is an important cause of heart
disease, megaesophagus and megacolon among people in Mexico, Central and South
America. Many mammals can be infected with the parasite that causes this disease;
however, among animals, clinical cases have been reported mainly in dogs. Chagas
disease is transmitted by the bites of triatomine insects, or “kissing bugs.” Some
infected insects occur in sylvatic environments, where humans are exposed only
occasionally. These “sylvatic cycles” are found from the U.S. through South America.
From Mexico through South America, triatomine insects have also become adapted to
human dwellings, particularly substandard housing where the insects hide in cracks
during the day and emerge to feed on humans and animals at night. Most human cases
are acquired from insects in these “domestic cycles,” and campaigns to eliminate the
bugs, together with testing to prevent congenital cases and transmission in blood
transfusions, have significantly reduced the incidence of Chagas disease. Antiparasitic
treatment is most effective early, before irreversible damage occurs to the heart or
gastrointestinal tract.
Etiology
Chagas disease results from infection with the protozoan parasite Trypanosoma
cruzi, a member of the family Trypanosomatidae. Most strains of this parasite can be
classified into two major groups, T. cruzi I and T. cruzi II, which can be separated
further into various lineages (e.g., T. cruzi IIa). Lineages tend to be associated with
certain host species, although this relationship is not absolute.
Geographic Distribution
T. cruzi can be found in the Americas from the U.S. to Chile and central
Argentina. In the U.S., this parasite is thought to be endemic in approximately the
southern half of the country, as well as in California.
Transmission and Life Cycle
Chagas disease is a vector-borne disease transmitted primarily by triatomine
insects, which are also called reduviid insects, “kissing beetles/ bugs” or “assassin
bugs.” More than 130 species of these insects appear to be capable of transmitting T.
cruzi, with the most important species in the genera Triatoma, Rhodnius and
Panstrongylus. The parasite usually completes its life cycle by cycling between an
insect species and a mammalian species with which the insect lives in close
association. The mammalian hosts include wildlife, domesticated animals and
humans.
In its mammalian host, T. cruzi can be found in the blood as trypomastigotes
(extracellular nondividing forms) and in cells as amastigotes (replicative forms).
When an insect takes a blood meal from an infected mammal, it ingests the
trypomastigotes. After 2 to 4 weeks of development, some of the parasites migrate to
the insect’s hindgut, where they are transformed into the infective metacyclic
trypomastigotes. The insect defecates after it feeds, releasing the trypomastigotes in
its feces. These parasites can enter the mammal’s body through mucous membranes
or breaks in the skin. Scratching may inoculate trypomastigotes into the bite wound,
or allow the parasites to enter through the scratches. Triatomine insect species that
exhibit delayed defecation after feeding are less likely to transmit Chagas disease than
species that defecate on the host. Humans and animals can also be infected if they eat
either the insect or uncooked food that contains insect feces.
There are three basic cycles of transmission for T. cruzi. In the sylvatic (wild)
cycle, this organism cycles between wildlife and triatomine insects that live in
sylvatic environments. Humans and domesticated animals are infected occasionally
when they contact these bugs in the wild. Under some conditions, the insects may also
invade houses or outbuildings when they are attracted to light, heat or certain odors,
and may contaminate food. Wild triatomine insects can also be transported
accidentally to human houses. The sylvatic cycle is responsible for relatively few
cases of Chagas disease. It is the only cycle in the U.S. A domestic transmission cycle
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American Trypansomiasis (Chagas Disease)
also exists in Mexico and parts of Central and South
America. In this cycle, some insect vectors have colonized
primitive adobe, grass and thatched houses, resulting in
transmission between humans and insects. Important
species in the domestic cycle include Triatoma infestans, T.
dimidiata and Rhodnius prolixus. Transmission cycles
between insects and domesticated animals (peridomestic
cycles) can also provide opportunities for the parasite to
infect humans.
T. cruzi is not spread between mammals by casual
contact; however, it can be transmitted directly via blood
(e.g., in a blood transfusion) and in donated organs.
Carnivores can acquire this organism when they eat
infected prey. Vertical transmission has been reported in
dogs and other animals, both in utero and in the milk.
Transmission in milk is very rare in humans, but
transplacental transmission can occur at each pregnancy,
and during all stages of infection. Laboratory infections
usually occur when the parasites contact mucous
membranes or broken skin, or are accidentally injected via
needlestick injuries, but aerosol transmission might be
possible in this setting.
Disinfection
T. cruzi is an obligate intracellular parasite. It is
destroyed by several hours of exposure to direct sunlight or
other harsh environments. T. cruzi is susceptible to many
disinfectants including 1% sodium hypochlorite, 70%
ethanol, iodine/alcohol solutions, glutaraldehyde and
formaldehyde. It can be inactivated by moist heat (121°C
for a minimum of 15 min) or dry heat (160 to 170°C for a
minimum of an hour).
Infections in Humans
Incubation Period
The incubation period is usually at least 5 to 14 days
after exposure to triatomine insect feces, and 20 to 40 days
after infection by blood transfusion. Many people do not
become symptomatic until the chronic stage, which can
occur 5 to 40 years after infection.
Clinical Signs
The acute phase is defined as the period during which
the parasites can be found easily in the blood. Many people,
particularly adults, are asymptomatic during this stage. The
symptoms of the acute phase are highly variable and may
include fever, headache, anorexia, malaise, myalgia, joint
pain, weakness, nausea, vomiting, diarrhea, hepatomegaly,
splenomegaly,
and
generalized
or
localized
lymphadenopathy. Edema, either generalized or localized to
the face and/or lower extremities, occurs in some cases.
Sometimes, a chagoma (a localized painless induration) is
seen where the parasite has entered through the skin. If
entry occurs via the ocular mucous membranes, there may
be painless edema of one or occasionally both eyes, often
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accompanied by conjunctivitis and enlargement of the local
lymph nodes. This syndrome, which is called Romaña’s
sign, usually persists for 1 to 2 months. Patients
occasionally develop a rash, but this usually disappears
within several days. In most cases, the clinical signs resolve
within weeks to months without treatment; however, some
acute cases can be fatal. Deaths are most likely to occur in
young children and patients who are immunosuppressed
(e.g., HIV-infected individuals), who may develop acute
myocarditis or meningoencephalitis.
The acute phase is usually followed by an
asymptomatic period of varying length; this stage is called
the indeterminate phase. During the indeterminate phase,
the parasites disappear from the blood. Although estimates
vary, approximately 70% to 90% of the patients in the
indeterminate phase never become symptomatic. Most of
the remaining patients enter the chronic phase after 5 to 15
years, but in a few patients, the indeterminate phase can last
as long as 40 years.
The chronic phase is typically represented by organ
failure, usually of the heart or digestive system. Heart
disease, the most common form of chronic Chagas disease,
may be characterized by arrhythmias and conduction
abnormalities, cardiac failure, apical aneurisms, embolic
disease including stroke or pulmonary embolism, and
sudden death. Signs of isolated left heart failure may occur
first. Biventricular congestive heart failure with peripheral
edema, hepatomegaly, pulmonary congestion and dyspnea
is common in the later stages. Some patients develop chest
pains without evidence of coronary artery disease.
Digestive system abnormalities lead to megaesophagus
and/or megacolon, which can occur concurrently with heart
disease. The symptoms of megaesophagus may include pain
during swallowing, excessive salivation, regurgitation and
chest pain. Dysphagia mainly occurs with dry, solid and cold
food. Aspiration pneumonitis can be a sequela and there is an
increased risk for cancer of the esophagus. In severe cases,
there may be weight loss or cachexia, and the esophagus may
rupture. The symptoms of megacolon include severe
constipation, which can last for a few days to months, and
abdominal pain that is often associated with episodes of
constipation. The abdomen may be asymmetrically
distended. Complications may include intestinal occlusion,
volvulus, fecalomas, ulceration, or intestinal perforation with
peritonitis. Patients with Chagas disease also have an
increased chance of developing gastric ulcers or chronic
gastritis, due to abnormalities in the stomach. Gall bladder
abnormalities may include mega-gallbladder or cholelithiasis.
Small intestinal dilatation is rare.
Women who are infected with T. cruzi can give birth to
infected children. Congenital infections may occur during
any of the woman’s pregnancies, whether she is
symptomatic or not. In congenitally infected infants, the
most common symptoms are premature birth,
hepatosplenomegaly, meningoencephalitis, changes in the
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American Trypansomiasis (Chagas Disease)
retina and signs of acute myocarditis/ cardiac insufficiency.
Transplacental infections are also associated with abortions.
Patients with AIDS suffer a more severe form of the
disease with a high percentage of neurological and cardiac
signs. Many of these patients develop T. cruzi brain
abscesses, which are not seen in immunocompetent patients.
HIV-infected
individuals
and
others
who
are
immunosuppressed, including those who receive organ
transplants, are at risk for reactivation of T. cruzi replication.
Serology
Serology is most often used to diagnose chronic
infections. Commonly used serological tests in humans
include
indirect
immunofluorescence
(IFA),
hemagglutination and enzyme-linked immunosorbent
assays
(ELISAs).
Other
tests
including
radioimmunoprecipitation and complement fixation may
also be used. Cross-reactions can occur with other parasites,
particularly Leishmania species.
Communicability
Molecular techniques
Polymerase chain reaction (PCR) techniques can be
used for diagnosis. Immunoblotting (Western blotting) is
another option.
Chagas disease is not spread from person to person by
casual contact, but infected humans can transmit the
parasite to the insect vectors. Congenital infections occur in
1-10% of infants born to infected mothers, and this may
occur at any stage of the disease. Transmission through the
milk is very rare. T. cruzi can also be spread in tissue
transplants or blood transfusions.
Diagnostic Tests
Chagas disease can be diagnosed by microscopy,
isolation of the parasite, serology or molecular techniques.
Microscopic examination
Light microscopy can sometimes detect T. cruzi in
Giemsa or Wright stained samples of blood, cerebrospinal
fluid or tissues. T. cruzi can be found in the heart, skeletal
and smooth muscle cells, and the glial cells of the nervous
system. It sometimes occurs in chagomas. In immunocompromised patients, parasites may also be detected in
atypical sites such as the pericardial fluid, bone marrow,
brain, skin and lymph nodes. Active parasitemia is much
more likely to be found during the acute than the chronic
stage. Either thick or thin blood smears may be examined,
but parasite morphology is clearer in thin smears. Blood
concentration techniques can increase the probability of
finding the parasites; examination of the buffy coat is often
used. T. cruzi can be difficult to distinguish from
Trypanosoma rangeli, which is avirulent.
Isolation of the agent
T. cruzi can be cultured from heparinized blood
samples or tissues. Various specialized media including
liver infusion tryptose medium or Novy-MacNeal-Nicolle
medium, as well as Vero cell lines can be used. Culture
may take 1 to 6 months. The agent can also be isolated by
inoculating the blood into a guinea pig, mouse or rat; this
procedure is often successful in chronic cases.
Xenodiagnosis is considered to be the gold standard where
it is available. In xenodiagnosis, laboratory-reared, T. cruzifree triatomine insects are allowed to feed on an infected
individual; the parasites may be found in the intestinal
contents of the insect 1 to 2 months later. Because these
methods of diagnosis are slow and labor-intensive, and
require highly trained personnel, they are generally used
only to confirm a diagnosis if other tests are inconclusive,
in research, or to isolate strains of parasites.
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Treatment
Acute Chagas disease can be treated with antiparasitic
drugs. In the U.S., drugs may be available only under an
Investigational New Drug protocol from the CDC Drug
Service. Treatment of acute or congenital cases is
recommended to prevent the development of chronic
disease. Antiparasitic drugs are less effective in the
indeterminate and chronic stages, and treatment
recommendations may vary with the age of the patient and
other factors. There are significant side effects with these
drugs, which must be given long term.
In the chronic stage, treatment of cardiomyopathy is
mainly symptomatic and similar to the treatment of other
causes of heart disease. A pacemaker may be necessary,
and a heart transplant can be considered. Surgery, balloon
dilation of the gastroesophageal junction and/or
symptomatic relief may be used for chagasic
megaesophagus or megacolon.
Prevention
Vaccines are not available for humans; however,
precautions can be taken to reduce the risk of infection,
particularly in countries where the prevalence of Chagas
disease is high. Triatomine insects usually feed at night and
withdraw to their hiding places in daylight. In endemic
areas, houses can be improved by plastering walls,
improving flooring and taking other measures to remove the
cracks where these insects hide. Triatomine insects are
often found in basements, which should be avoided.
Sleeping inside a screened area, under a permethrinimpregnated bed net, or in an air-conditioned room is
safest. Bed nets should be tucked tightly under the mattress
before dusk. Animal pens and storage areas should be kept
away from homes. Regular spraying of insecticides in and
around houses can reduce the number of insects, and in
some cases, eliminate them.
Some triatomine bugs such as Triatoma infestans and
Rhodnius prolixus have adapted to human dwellings, and
do not exist in the wild. These insects can be eliminated
completely by control measures, greatly reducing the risk
of Chagas disease. Since 1991, the Pan American Health
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American Trypansomiasis (Chagas Disease)
Organization and the World Health Organization have run
a joint program to eliminate T. infestans, the most
important vector for Chagas disease in humans. This
program has decreased the distribution of this insect by
more than 80%, although foci can still be found in some
regions. Triatomine species that occur in sylvatic cycles
but colonize human dwellings can also be controlled or
eliminated by insecticides and other measures, but they
may recolonize homes. Foods that might be contaminated
should be cooked.
Blood and organ donors should be screened to prevent
transmission by these routes. In the U.S., transfused blood
has been screened for Chagas disease since 2007. Pregnant
women can be tested to identify cases where congenital
transmission may occur, and the infant should be monitored
and treated if necessary.
People in occupational risk groups should take
additional precautions. Veterinarians and technicians should
protect their skin and mucous membranes from
contamination with parasites in blood or tissues. This
includes using gloves and/or other barriers while drawing
blood samples from T. cruzi-infected animals, taking care
of IV catheters or performing other invasive procedures.
Needles and other “sharps” must be handled and disposed
of properly to prevent needlestick injuries. Individuals who
work with wildlife and hunters should also take
precautions, especially when handling blood and tissues.
Laboratory personnel should use appropriate personal
protective equipment, including gloves and eye protection,
while processing blood samples, cultures or infected
insects. If an accidental exposure occurs, the site should be
disinfected immediately if possible, and antiparasitic drugs
may be given prophylactically.
Travelers to areas where Chagas disease is common
should wear thick clothing that covers as much of the body
as possible; heavy long-sleeved shirts, long pants, socks and
shoes are recommended. Sleeping in sub-standard housing
should, if possible, be avoided.
Morbidity and Mortality
Chagas disease is most common among people who
live in substandard housing. Most cases are acquired by
exposure to insects in domestic or peridomestic cycles, or
by congenital transmission. In some areas, outbreaks have
been linked to foods such as fresh fruit juices contaminated
by sylvatic triatomines. In endemic areas, many people
become infected in childhood. In South and Central
America, campaigns to control the vectors in the domestic
cycle have significantly decreased the number of new
human infections. Triatomine vectors for T. cruzi are
present in the U.S.; however, only a few locally acquired,
vector-borne cases have been diagnosed in people. The
lower prevalence rate in the U.S. is mainly due to higher
standards of living and the absence of triatomine species
that are well adapted to living in human houses. In addition,
some of the insects involved in sylvatic transmission in the
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U.S. exhibit delayed defecation after feeding, which may
reduce the risk of transmission.
The morbidity and mortality rates vary with the stage
of the disease. Approximately 5% of people infected with
T. cruzi develop acute symptoms. Estimates of the case
fatality rate for acute Chagas disease range from less than
5% to approximately 8%; among immunologically
competent individuals; deaths occur mainly in young
children with acute myocarditis or meningoencephalitis.
The CDC estimates that 20-30% of humans infected with
T. cruzi eventually develop chronic disease; estimates
from other sources vary from 10% to 50%. The reason for
the progression of disease in some patients but not others
is unknown. It may be related to host genetic factors, the
dose of the parasites, the number of inoculations, the
strain of the parasite, and immunological or nutritional
factors. Cardiac disease is often fatal. Occasionally, deaths
are also caused by volvulus of a dilated sigmoid
megacolon.
Infections in Animals
Species Affected
Trypanosoma cruzi occurs in more than 100 species of
mammals throughout the Americas; infections have been
reported among carnivores including dogs and cats, as well
as in pigs, goats, lagomorphs, rodents, marsupials, bats,
xenarthra (anteaters, armadillos and sloths) and non-human
primates. In the U.S., opossums, armadillos, raccoons,
coyotes, rats, mice, squirrels, dogs and cats are among the
most frequent hosts. Birds, reptiles and fish are not
susceptible to infection.
Incubation Period
The incubation period for acute disease in dogs appears
to be 5 to 42 days; in experimental infections, symptoms of
acute heart disease are usually reported after 2 to 4 weeks.
Like humans, some dogs may not develop clinical signs
until the chronic stage, which occurs after a few years; the
exact length of this period is not known.
Clinical Signs
Dogs
Acute, latent and chronic stages of infection occur in
experimentally infected dogs. Clinical signs reported in the
acute stage include fever, anorexia, lethargy, an unkempt
hair
coat,
lymphadenopathy,
hepatomegaly
and
splenomegaly. Anorexia, diarrhea, ascites and/or weight
loss may also be seen. Some dogs may have palpebral
edema. Chagomas appear to be rare, but they have been
reported in a few dogs inoculated with a South American
strain of T. cruzi. Cardiac dysfunction can occur during the
acute phase; acute myocarditis may cause arrhythmias or
sudden collapse and death. After the acute phase, infected
dogs enter the indeterminate (latent) stage, during which the
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American Trypansomiasis (Chagas Disease)
parasites are difficult to find and the animal is asymptomatic.
The indeterminate stage can be as short as 27 days in some
experimentally infected animals, but it seems to last for years
in some natural infections. Congestive heart failure is the
most common sign during the chronic stage. Right-sided
heart failure usually occurs first. Eventually, dogs with
heart disease develop chronic myocarditis with cardiac
dilatation and arrhythmias. Sudden death can occur.
Limited information is available from naturally
infected dogs. In one retrospective study from Texas,
sudden death was the most common presentation in more
than 500 confirmed cases. Other common clinical signs
included anorexia, lethargy, ascites, an enlarged heart,
cardiac conduction disturbances and respiratory
difficulties. Hepatomegaly, anemia, diarrhea, vomiting
and edema were reported less often. Heart disease was
the most common presentation in both puppies and
adults. In Mexico, only mild disease was reported in
naturally infected stray dogs, although ECG changes were
seen in some of these animals. A limiting factor in the
latter study is that stray dogs would be expected to have a
relatively short lifespan, and may not have lived long
enough to develop more severe signs.
Atypical cases have also been reported in dogs. In
one dog, the clinical signs included anorexia, lethargy,
weight loss, generalized lymphadenopathy, fever and
dependent, pitting edema, without cardiac signs or
lesions. Neurologic signs such as limping or coma have
occasionally been reported. One case of Chagas disease in a
13-month-old Doberman pinscher presented as slowly
progressive paraparesis with temporal, supraspinatus and
infraspinatus muscle atrophy, bilateral enophthalmos,
superficial inguinal lymphadenopathy, tachycardia with pulse
deficits, and chorioretinitis. In addition to neurologic
abnormalities in the hindlegs and forelegs, this dog had
cranial nerve deficits and a delayed gag reflex.
Experimentally
infected
dogs
can develop
histological abnormalities in the esophagus and stomach,
but unlike humans, megaesophagus and megacolon have
not been reported.
Cats
Symptomatic Chagas disease has been rarely described
in cats. Reported clinical signs include fever, edema, weight
loss and neurological signs such as convulsions and paresis.
Other species
There is little information about Chagas disease in
other species, including wild animals. Mild, histologically
evident myocarditis (without clinical signs of heart disease)
has been reported at necropsy in infected wild raccoons and
opossums. Naturally infected rats can develop arrhythmias
and more severe cardiac lesions. Infertility, fetal losses,
reduced birth weights, and early postnatal deaths have been
reported in pregnant mice.
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Post Mortem Lesions
Click to view images
In dogs, acute disease is characterized mainly by
cardiac lesions, which are particularly prominent on the
right side. The myocardium may be pale, and
subendocardial and subepicardial hemorrhages are often
present. Multiple yellowish-white spots and streaks, mainly
involving the coronary groove, may be found in the heart.
In addition, there may be secondary pulmonary edema,
congestion in the liver, spleen and kidneys, and a modified
transudate in the peritoneal cavity. Pericardial effusion has
been reported in some naturally infected dogs. Gross
lesions may be absent in some infected animals.
In chronic Chagas disease, the heart is bilaterally
enlarged and flaccid, with thinning of areas in the
ventricular walls. Atypical cases without cardiac lesions
have also been reported.
Mild myocarditis (multifocal interstitial inflammation)
has been reported in wild raccoons and opossums at
necropsy.
Communicability
Chagas disease is not contagious during casual
contact, but the parasite can be transmitted in blood or by
contact with tissues. Carnivores can be infected if they eat
T. cruzi-contaminated tissues. Many species of animals,
including dogs, can serve as amplifying hosts, and infect
the insect vectors. Vertical transmission can also occur in
some animals.
Diagnostic Tests
Chagas disease can be diagnosed by microscopy, isolation
of the parasite, serology and molecular techniques.
Microscopic examination
A presumptive diagnosis can be made if T. cruzi is
observed by light microscopy in a stained blood smear or
buffy coat sample, or in tissues such as the heart. The
trypomastigotes occur as either short, broad forms or long,
thin forms in the blood; in stained preparations, they form a
C-shape. Amastigotes, which are found inside cells, are
round or ovoid, and 1.5-4 µm in diameter. Differentiating T.
cruzi from the morphologically similar, non-pathogenic
species T. rangeli is difficult.
Isolation of the agent
T. cruzi can be cultured from blood samples or tissues;
culture is usually more successful in the acute stage. This
organism often occurs in the myocardium, but it can also
be isolated from other organs such as the lymph nodes,
liver, gastrointestinal tract, brain, cerebrospinal fluid and
adrenal gland. Various specialized media including liver
infusion tryptose medium or Novy-MacNeal-Nicolle
medium, as well as Vero cell lines may be used. The agent
may also be isolated by inoculating blood into a guinea
pig, mouse or rat. Xenodiagnosis is considered to be one
of the most accurate tests for Chagas disease in South
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American Trypansomiasis (Chagas Disease)
America, but it is of little practical importance for
veterinarians in the U.S. Isolation of the agent may take 1
to 6 months, and requires highly trained personnel.
Serology
Indirect immunofluorescence is the most commonly
used serological test. Other assays include radio-immunoprecipitation, direct and indirect hemagglutination,
complement fixation and ELISAs. Cross-reactions can occur
with other parasites, particularly Leishmania species.
Molecular techniques
Molecular detection methods including PCR and
western blot (immunoblot) analysis techniques can detect T.
cruzi DNA in tissues and blood.
Treatment
Occasionally, dogs have been treated with antiparasitic drugs. These drugs appear to be more effective in
the early stages; by the time of diagnosis, treatment may be
too late to prevent the progression of the disease.
Prevention
Dogs and cats should not be allowed to eat tissues from
potentially infected wild animals. Strict indoor housing in
well-constructed homes or other facilities reduces the risk
of infection. Housing animals indoors at night, when
triatomine insects are active, may also be helpful. Residual
insecticides sprayed regularly in kennels and surrounding
structures may decrease the number of insect vectors. In
breeding kennels, testing bitches for T. cruzi-might also
decrease the incidence of Chagas disease by reducing
vertical transmission. No vaccines are available.
Morbidity and Mortality
The prevalence rate can be high among wildlife in
endemic areas. Surveys of wildlife in the U.S., conducted
mainly in raccoons and opossums, have reported prevalence
rates from 2% to 62%. In one study, 19 of 134 coyotes in
Texas had antibodies to T. cruzi. In the U.S., the reported
seroprevalence rates in dogs from Texas, Oklahoma,
Louisiana, Georgia and other southern states vary from
1.1% to 8.8%. Over a 15-year period, more than 500
clinical cases of Chagas disease were reported among dogs
in Texas, suggesting that this disease occurs regularly in
some areas. In the Yucatan region of Mexico, one study
reported that 10-14% of dogs were seropositive, but when
both serology and PCR were used, the prevalence as high as
17%. The infection rate is highest among dogs that are
regularly exposed to wildlife and insect vectors. Cats are
frequently infected with T. cruzi in South America.
There is little information on the morbidity and
mortality rates in dogs, except in experimentally infected
animals, where these rates are high. In one study, 13 of 26
dogs infected with blood trypomastigotes died during the
acute phase. In another, 26 of 38 dogs died during the
acute phase, while the 12 survivors developed chronic
Last Updated: September 2009
© 2009
disease and lived for 1 to 2 years. In a study using North
American strains of T. cruzi from armadillos or opossums,
7 of 13 dogs died or were euthanized due to the severity of
acute disease. Based on human data, some sources suggest
that approximately 5% of naturally infected animals
would be expected to develop symptoms during the acute
stage. In naturally infected dogs with chronic cardiac
disease, the survival time after diagnosis ranged from 0
months to 5 years.
Internet Resources
Centers for Disease Control and Prevention (CDC)
http://www.cdc.gov/chagas/
Public Health Agency of Canada - Disease Information.
American Trypanosomiasis or Chagas Disease
http://www.phac-aspc.gc.ca/tmppmv/info/am_trypan_e.html
Public Health Agency of Canada - Transfusion Transmitted
Diseases/Infections
http://www.phac-aspc.gc.ca/hcai-iamss/ttiit/ttdi_e.html#chagas
Medical Microbiology
http://www.ncbi.nlm.nih.gov/books/NBK7627/
The Merck Manual
http://www.merck.com/pubs/mmanual/
The Merck Veterinary Manual
http://www.merckvetmanual.com/mvm/index.jsp
References
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Zoonoses and communicable diseases common to man and
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PAHO; 2003. Scientific and Technical Publication No. 580.
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Barr, SC, Brown CC, Dennis VA, Klei TR. Infections of inbred
mice with three Trypanosoma cruzi isolates from Louisiana
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Barr SC, Brown CC, Dennis VA, Klei TR. The lesions and
prevalence of Trypanosoma cruzi in opossums and armadillos
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Barr SC, Gossett KA, Klei TR. Clinical, clinicopathologic, and
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with North American Trypanosoma cruzi isolates. Am J Vet
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Barr SC, Van Beek O, Carlisle-Nowak MS, Lopez JW, Kirchhoff
LV, Allison N, Zajac A, de Lahunta A, Schlafer DH, Crandall
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