Canine Chagas' disease: update (Proceedings)

Article

Infection occurs when infected feces of a vector (Triatomin?, commonly called kissing or assassin bugs) are deposited in a wound (bite site of vector) or mucous membrane, or when a dog eats an infected vector (shown to occur in opossums and raccoons). Raccoons fed infected meat do not get infected so dogs probably not infected by eating meat from intermediate hosts in which the organism is sequestered in muscle. Transmission by contaminated blood transfusion also occurs.

OVERVIEW

     • Caused by the zoonotic hemoflagellate protozoan parasite Trypanosoma cruzi.

     • Infection occurs when infected feces of a vector (Triatominae, commonly called kissing or assassin bugs) are deposited in a wound (bite site of vector) or mucous membrane, or when a dog eats an infected vector (shown to occur in opossums and raccoons). Raccoons fed infected meat do not get infected so dogs probably not infected by eating meat from intermediate hosts in which the organism is sequestered in muscle. Transmission by contaminated blood transfusion also occurs.

     • Endemic (in both humans and pets) in South and Central America.

     • Most cases in dogs in the USA seenTexas, but also Louisiana, Oklahoma, South Carolina, and as far north as Virginia. Infected vectors and reservoir hosts also reported in the western (California, New Mexico), southern (Florida, Georgia) and southeastern (North Carolina, Maryland) states.

     • Six endemic human cases reported in the USA, the last in a Louisiana woman after Hurricane Katrina.

     • After local multiplication at site of entry (5 days post-infection - DPI), hematogenous spread occurs to most organs but mainly the heart (and much less extent, brain). Organisms become intracellular, multiply, then rupture out into the circulation to produce maximal parasitemias (14 DPI) associated particularly with acute myocarditis and, less commonly, diffuse encephalitis.

     • Parasitemias wane (sub-patent by 30 DPI), antibody titers rise (detectable by 26 DPI), and the dog enters a protracted asymptomatic period (can last for months to years) if he survives the acute myocarditis. During this time, there is progressive and insidious development of myocardial degeneration and eventual dilative cardiomyopathy of unknown pathogenesis.

     • Some isolates from dogs in the USA don't seem very pathogenic and just lead to very high antibody titers without disease.

SIGNALMENT

     • Commonly seen in young (acute form - usually under 2 years) but reported in old dogs (chronic form), hunting breeds, more often in males (dogs likely to contact vectors or reservoir hosts)

     • Cats can become infected, but no case has been reported in North America.

CLINICAL SIGNS

Two syndromes - acute (myocarditis or encephalitis in young dogs) or chronic (dilative cardiomyopathy in older dogs)

Historical Findings

Acute

     • Sudden death

     • Lethargy, depression, anorexia

     • Diarrhea

     • Weakness

     • Exercise intolerance

     • Mild to severe CNS dysfunction (like distemper)

     • Ataxia, seizures

Chronic

     • Weakness

     • Exercise intolerance

     • Syncope

     • Sudden death

Physical Examination Findings

Acute

     • Generalized lymphadenopathy

     • Signs of both left and right heart failure

     • Tachycardia with or without arrhythmias

     • Neurologic signs, weakness, ataxia, chorea, seizures (indistinguishable from distemper)

Chronic

Sustained or paroxysmal tachycardia

DIAGNOSIS

DIFFERENTIAL DIAGNOSIS

     • Cardiomyopathy

     • Congenital cardiac defects

     • Traumatic myocarditis

     • Distemper

     • Toxoplasmosis

     • Neosporosis

LABORATORY TESTS

     • Serology (available Centers for Disease Control - CDC, Parasitology Unit, US Dept. of Health and Human Services, Atlanta, GA 30333). Positive titer confirms infection although there can be cross reaction with Leishmania antibodies.

     • Cytology: see organisms on blood smear very early on infection (from 5 to 21 DPI) but not plentiful. May need to use some method of concentration such as microhematocrit tube: Using the 40 X microscope objective, examination above the buffy coat in a microhematocrit tube (spun down to read PCV) will reveal organisms during period of high parasitemia.

     • Organism isolation into liver infusion tryptose culture media (collect 50 ml heparinized blood).

Radiography

Acute

     • Dilated cardiac silhouette, pulmonary edema (rarely, mild pleural effusion)

Chronic

     • Cardiomegaly.

Echocardiography

Acute

     • Rarely shows chamber or wall abnormalities.

Chronic

     • Reduced ejection fraction/fractional shortening, thinning of right and left ventricular free wall.

Electrocardiography

Acute

     • First- and second-degree heart block, atrioventricular block, depression of R wave and QRS amplitude, right bundle branch block

Chronic

     • Depression of R wave and QRS amplitude, right bundle branch block, ventricular arrhythmias (initially unifocal ventricular premature contractions becoming multiform, then degenerating into various forms of ventricular tachycardia)

TREATMENT

     • Alert owner to possible zoonotic risk and potential for sudden death.

     • The acute form invariably develops into the chronic form, which is usually fatal.

     • THE INFECTED INTACT FEMALE COULD TRANSFER INFECTION TO OFFSPRING.

DRUGS

     • Several drugs have limited efficacy against the parasite during the acute stage, but none produces a clinical cure. Even treated animals may progress to chronic disease.

     • Benznidazole (Radamil, Roche 7-1051, NJ) at 5 mg/kg PO q24h for 60 days. Produces cures in people and dog so is considered the drug of choice in dogs. Available from the CDC.

     • Nifurtimox (Lampit, Bayer 2502): investigational drug available only from the CDC (dosage: 30 mg/kg PO q12h, for 90-120 days). Severe side effects negates is use.

     • Allopurinol, ketoconazole, verapamil have shown efficacy in other species but not dogs.

     • Cythioate (Proban, Cyanamid, NY) at 3.3 mg/kg PO every other day is effective in reducing vector populations.

     • Spot-on applications of fiprinol on the coats of dogs do not appear to prevent infections in dogs, or reduce the feeding of vectors but deltamethrin-treated collars do reduce Triatoma infestans feeding.

     • Supportive treatment of dilative cardiomyopathy (right and left cardiac failure) and ventricular arrhythmias.

ZOONOSIS

     • Chagas' disease has zoonotic potential, and because it is essentially incurable in humans, euthanasia of infected dogs is an option.

References

Dorn PL, Perniciaro L, Yabsley MJ, et al. Autochthonous transmission of Trypanasoma cruzi, Louisiana. Emerg Infect Dis 2007;13:605-607.

Barr SC. American trypanosomiasis. In: Greene CE (editor), Infectious diseases of the dog and cat, 2nd edition. Philadelphia: WB Saunders, 2006. p. 676-680.

Barr SC. Chagas' Disease (American Trypanosomiasis. In: Barr SC and Bowman DD (eds), Canine and Feline Infectious Diseases and Parasitology. Ames: Blackwell Pub, 2006. p. 113-119.

Reithinger R, Ceballos L, Stariolo R, et al. Extinction of experimental Triatoma infestans populations following continuous exposure to dogs wearing deltamethrin-treated collars. Am J Trop Med Hyg 2006;74:766-771.

Barr SC. Canine Chagas' Disease (American Trypanosomiasis) in North America. Vet Clin Nth Am: Small Animal Parasites: Biology and Control. 2009;39:1005-1064.

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