Chapter 78


Overview of American Trypanosomiasis

First Described: Chagas’ disease (American trypanosomiasis) was first described in humans in 1909 (Carlos Chagas).1

Cause: Trypanosoma cruzi, a protozoan parasite (phylum Sarcomastigophora, family Trypanosomatidae)

Affected Hosts: Dogs, humans, and more than 150 other domestic or wildlife mammalian species

Geographic Distribution: Central and South America; to a lesser extent southern United States (especially southeastern Texas)

Mode of Transmission: A bite from, or ingestion of, reduviid (kissing bug) vectors, primarily Triatoma species. Transmission through blood transfusion and vertical transmission can occur.

Major Clinical Signs: American trypanosomiasis in puppies manifests as lethargy, inappetence, mucosal pallor, lymphadenopathy, splenomegaly, arrhythmias, or sudden death. Neurologic signs such as pelvic limb ataxia and exaggerated spinal reflexes may also occur. Adult dogs may show lethargy, arrhythmias, signs of right- or left-sided congestive heart failure, or sudden death.

Differential Diagnoses: The differential diagnoses for suspected Chagas’ myocarditis include dilated cardiomyopathy of large-breed dogs, parvoviral myocarditis in puppies, canine monocytic ehrlichiosis, babesiosis, and leishmaniosis. The primary differential diagnoses for suspected Chagas’ meningoencephalitis in puppies are canine distemper virus infection and neosporosis, but other infectious and inflammatory causes of meningoencephalitis should also be considered.

Human Health Significance: Transmission to humans has the potential to occur after needle-stick injuries; caution is advised when handling tissues or clinical specimens from dogs with suspected trypanosomiasis.

American Trypanosomiasis

Etiology and Epidemiology

Chagas’ disease, or American trypanosomiasis, is caused by the flagellated protozoan Trypanosoma cruzi. In North America, disease in dogs usually manifests as cardiac disease typified by arrhythmias or myocarditis (acute or chronic), and, rarely, neurologic disease.2-7 However, many infected dogs are subclinically infected for life. Cats can become infected, but disease in cats has not been recognized. Trypanosoma cruzi is an important vector-borne zoonosis in the Americas, particularly South and parts of Central America, and is the leading cause of dilated cardiomyopathy in humans.8 Within the United States, most cases in dogs occur in Texas and especially involve working dogs that reside in southeastern Texas (Figure 78-1).911 A few affected dogs have been reported from other southern states,5,6,1214 and as far north as Missouri.15 The seroprevalence in dogs from Louisiana and Texas has generally been in the range of 12% to 22%, with seroprevalences of <10% in other states where canine disease has been identified.16 Canine Chagas’ disease is of importance to veterinary practitioners because it can be difficult to diagnose, is a potential zoonosis, and there is a lack of therapeutic options.

Trypanosoma cruzi exists in three morphologic forms. The form that circulates freely in the host’s peripheral blood is the trypomastigote. This form is 15 to 20 µm long, with a flattened spindle-shaped body and a centrally placed vesicular nucleus. A single flagellum originates near a large, subterminal kinetoplast (situated posterior to the nucleus) and passes along the body to project anteriorly (Figure 78-2). The host intracellular or amastigote form is approximately 1.5 to 4.0 µm in diameter, is roughly spheroid, and contains both a nucleus and a rod-like kinetoplast. A small flagellum is present, but this is rarely obvious under light microscopy. The third morphologic form, the epimastigote, is found in the arthropod vector, a reduviid or “kissing bug” (subfamily Triatomae). Epimastigotes are flagellated and spindle shaped with the kinetoplast situated anterior to the nucleus. When a vector is involved in transmission, infection occurs when trypomastigotes are deposited in the triatomine’s feces at the insect bite site. This is the main mode of transmission to humans in South America.

Transmission of T. cruzi in endemic countries depends on the confluence of vectors, reservoirs, parasites, and hosts (both people and animals) in a single habitat. Only three Triatomae species (Triatoma infestans [the main vector in South America], Triatoma dimidiata, and Rhodnius prolixus) that feed on man in endemic regions in South America display the appropriate behavior that enables them to transmit T. cruzi effectively. These species feed on blood from both people and domestic reservoir mammals (dog, cat, guinea pigs), reproduce prolifically while cohabiting close to people, and defecate soon after taking a blood meal, meaning that they are usually still on the host near the bite wound when they defecate.17 Infection rates in these vectors can be as high as 100% south of the equator. By contrast, domestic transmission cycles probably do not occur in the United States, except in areas of southeastern Texas where there is evidence to suggest that the dog can be involved in domestic transmission cycles involving vectors and man.18 Generally, though, the two principal vectors in the United States (Triatoma protracta and Triatoma sanguisuga) have low infection rates (20%), display different feeding habits, and defecate about 20 minutes after feeding, often when they have long fled the host.19 As a result, it is more likely that dogs in North America become infected when they eat infected triatomines or their excreta. Certainly, opossums20 and armadillos21 become infected by this route, and outbreaks have occurred in humans following ingestion of contaminated food or drinks.22 Blood transfusion and transplacental transmission can also occur, and infection after ingestion of infected milk from lactating bitches has been proposed.6 Whether ingestion of reservoir hosts leads to transmission is unclear.

Within the United States, the principal wildlife reservoir hosts of T. cruzi in the eastern seaboard states south from Maryland and in most other southern states (Texas, Louisiana, and Oklahoma, to name a few) are opossums and raccoons. Armadillos can also be infected.23 Various mouse, squirrel, and rat species are the main reservoir hosts in New Mexico and California.24 Isolates of T. cruzi from vectors and animal reservoirs in North America are less pathogenic in mice than South American isolates.23,25 Experimental inoculation of T. cruzi isolates from opossums and armadillos into dogs produces a disease consistent with naturally acquired acute and chronic canine trypanosomiasis, so it is likely that dogs in nature are infected with the same isolates as these wildlife hosts.26 Six genotypes of T. cruzi have been identified (TcI through TcVI, also known as discrete typing units or DTUs), which appear to differ in their vector preferences and the extent to which they cause disease.26

After infection, trypomastigotes enter macrophages, transform into amastigotes, and multiply by binary fission (Figure 78-3). Alternatively, they spread hematogenously from the site of infection, infect myocardiocytes, transform into amastigotes, multiply, and transform back into trypomastigotes. The host cell then ruptures and trypomastigotes are released back into circulation. Parasitemia in dogs appears as early as 3 days postinfection (DPI), peaks at 17 DPI, and is cytologically undetectable (subpatent infection) by 30 DPI.2 Clinical signs of acute myocarditis, should they occur, develop about 14 DPI with recovery occurring around 28 DPI.2 Rapid intracellular multiplication ensures a rapid rise in parasitemia before effective immunity develops. Parasitemia steadily rises as more and more intracellular multiplication cycles add to the number of circulating trypomastigotes. The vector becomes infected when it ingests circulating trypomastigotes, which transform into epimastigotes and multiply by binary fission. Transformation of the epimastigotes back into trypomastigotes occurs in the vector’s hindgut before the trypomastigotes are passed in the feces.

Clinical Features

Signs and Their Pathogenesis

As in humans, there are three phases of Chagas’ myocarditis in dogs: acute, indeterminate (or latent), and chronic.2-6 Acute myocarditis results from cell damage and inflammation as trypomastigotes rupture from myocardiocytes. Lethargy, fever, inappetence, generalized lymphadenopathy, slow capillary refill time with pale mucus membranes, and, in some cases, splenomegaly and hepatomegaly are the main signs in puppies. Diarrhea can also occur. In dogs over 6 months of age, parasitemia develops more slowly and clinical signs are often much less severe or not apparent at all. Sudden death, presumably from cardiac muscle failure or conduction system failures leading to malignant arrhythmias, is not a common occurrence. Although less common than signs referable to cardiac abnormalities, neurologic signs referable to meningoencephalitis (as a direct result of parasitic invasion of the neurologic system) may also occur and include weakness, pelvic limb ataxia, and exaggerated spinal reflexes suggestive of distemper. Humans with Chagas’ disease can also develop severe megaesophagus or megacolon due to parasympathetic denervation,22 but these have not been described in dogs.

Dogs that survive the acute phase enter a prolonged indeterminate phase typified by a lack of clinical signs. Parasitemia becomes cytologically undetectable at about 30 DPI, although it can still be demonstrated by blood culture. The ECG is usually normal during this phase, although ventricular arrhythmias can be induced by exercise.3 Although not all dogs progress to develop chronic disease, some develop chronic myocarditis with cardiac dilatation over the subsequent 8 to 36 months.2,3 ECG abnormalities become more prevalent in these dogs and may even result in sudden death. Clinical signs referable to right-sided and eventually, in some, left-sided heart failure occur and can include exercise intolerance, pulse deficits, ascites, pleural effusion, hepatomegaly, and jugular venous congestion.2 Chronic Chagas’ myocarditis is clinically indistinguishable from dilated cardiomyopathy of large breed dogs.46 The pathogenesis of the cardiomyopathy is unknown, but proposed mechanisms include damage to myocardiocytes or the autonomic nervous system by immune-mediated mechanisms or toxic parasitic products, and/or microvascular disease coupled with platelet dysfunction.27,28 Cardiac dilatation occurs when fibrosis no longer permits efficient compensatory hypertrophy.27,29 Some T. cruzi isolates that infect dogs in the United States are not pathogenic but produce a marked serologic response and a low-level parasitemia following immunosuppression.2,30 Reactivation of infection with immunosuppression can occur in human patients.22

Physical Examination Findings

The most common physical examination findings in puppies with Chagas’ disease are lethargy, generalized lymphadenomegaly, splenomegaly, pallor, and arrhythmias. Generalized subcutaneous edema has also been reported.31 Dogs with chronic Chagas’ disease may show signs of right- and/or left-sided congestive heart failure, with tachypnea, ascites, or jugular pulses. Cardiac murmurs and/or arrhythmias may be detected on auscultation of the heart.


The key to diagnosis of Chagas’ disease is a high degree of clinical suspicion. Chagas’ disease should be considered in any dog with signs of myocarditis or cardiomyopathy, particularly if it lives or has lived at any time—even years before evaluation—in an endemic region.

Laboratory Abnormalities

Complete Blood Count

During the acute T. cruzi infection, the CBC of some dogs may reveal anemia, leukocytosis due to a neutrophilia, eosinophilia, monocytosis, and lymphocytosis.32,33 Thrombocytopenia, leukopenia, and/or lymphopenia have also been documented.16 Dogs in the chronic phase of infection may have no hematologic abnormalities.

Diagnostic Imaging

Microbiologic Tests

Diagnostic assays for trypanosomiasis in dogs and cats are described in Table 78-1.

Cytologic Examination

During acute disease, trypomastigotes may be detected on blood smear examination (see Figure 78-2). However, only a few parasites may be present on the entire slide, demanding diligent examination, or some form of concentration technique may be used. High-power (400×) examination of the buffy-coat layer from a centrifuged microhematocrit tube may reveal the motile parasites. Examination of a thick-film buffy-coat smear stained with either Wright or Giemsa stains is more sensitive than examination of a blood smear. A highly effective concentration technique involves pelleting trypomastigotes from plasma (obtained by centrifugation of 10 to 50 mL of heparinized blood at 800 × g for 10 minutes) by further centrifugation (8000 × g for 15 minutes). The pellet from the final centrifugation may be examined microscopically after staining or be submitted for PCR analysis or culture. The larger the volume of the blood specimen collected, the greater the likelihood that organisms will be detected. Trypomastigotes may also be found on cytologic examination of lymph node aspirates and in abdominal effusions. Amastigotes were described in the lymph node of one affected dog that were cytologically indistinguishable from those of Leishmania.31

Serologic Diagnosis

Serology is extremely useful for the diagnosis of Chagas’ disease, especially during the indeterminate and chronic phases when trypomastigotes are very difficult to detect.34 Indirect fluorescent antibody, ELISA, and radioimmunoprecipitation assays are most commonly used. A rapid immunochromatographic dipstick test has also been developed.35 Serologic tests confirm the presence of antibodies to T. cruzi, but most cross-react with antibodies to Leishmania. Further, in rare situations in dogs, the clinical signs of Chagas’ disease and leishmaniasis overlap sufficiently that it is necessary to go to considerable lengths to establish a diagnosis.31 Therefore a detailed history of the likelihood of exposure to Leishmania must be known in order to accurately interpret serologic results. A higher antibody titer to Trypanosoma than to Leishmania may support a diagnosis of trypanosomiasis. Positive serology in association with consistent clinical signs is the most common means of diagnosis of Chagas’ disease in dogs. If possible, two different serologic assays should be used to confirm a positive titer, especially in regions of low prevalence. The serum titer usually becomes positive by 21 DPI, when parasitemia is declining, and persists for the life of the animal irrespective of whether clinical signs develop.30

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Jul 10, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Trypanosomiasis
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