Page 182 - Small Animal Internal Medicine, 6th Edition

154 PART I Cardiovascular System Disorders

Trypanosomiasis (Chagas disease) is an important zoonosis Hepatozoon americanum, identified as a new species dis-
in Central and South America; within the United States, the tinct from Hepatozoon canis, was originally found in dogs
VetBooks.ir disease occurs mainly in young dogs in Texas, Louisiana, along the Texas coast but has a much wider range. Coyotes,
rodents, and other wildlife are an important wild reservoir.
Oklahoma, Virginia, and other southern states. The pos-
sibility for human infection should be recognized; Chagas
(Amblyomma maculatum) or through predation. Skeletal
myocarditis is the most common cause of human cardiomy- Dogs become infected by ingesting the organism’s tick host
opathy in the world. The organism is transmitted by blood- and cardiac muscles are the main tissues affected by H. amer-
sucking insects of the family Reduviidae and is enzootic in icanum. A severe inflammatory reaction to merozoites
wild animals of the region. Amastigotes of T. cruzi cause released from ruptured tissue cysts leads to pyogranuloma-
myocarditis with a mononuclear cell infiltrate and disrup- tous myositis and myocarditis. Clinical signs include stiff-
tion and necrosis of myocardial fibers. Acute, latent, and ness, anorexia, fever, neutrophilia, periosteal new bone
chronic phases of Chagas myocarditis have been described. reaction, muscle atrophy, and often death.
The acute stage can involve lethargy, depression, and other Leishmaniosis, endemic in certain regions, can cause
systemic signs, as well as various tachyarrhythmias, AV con- myocarditis, various arrhythmias, and pericardial effusion
duction defects, or sudden death. Clinical signs are some- with cardiac tamponade, as well as other systemic and cuta-
times subtle. The disease is diagnosed in the acute stage by neous signs. Babesiosis has also occasionally been reported
finding trypomastigotes in thick peripheral blood smears; to cause cardiac lesions in dogs, including myocardial hem-
the organism can be isolated in cell culture or by inocula- orrhage, inflammation, and necrosis. Pericardial effusion
tion into mice. Animals that survive the acute phase enter and variable ECG changes may be noted.
a subclinical latent phase of variable duration. During this Other causes
phase, the parasitemia resolves, and antibodies develop Rarely, fungi (Aspergillus, Cryptococcus, Coccidioides,
against both the organism and cardiac antigens. Chronic Blastomyces, Histoplasma, Paecilomyces, Inonota); non-
Chagas disease is characterized by progressive right-sided Bartonella rickettsiae (Rickettsia rickettsii, Ehrlichia canis);
or generalized cardiomegaly and various arrhythmias. Ven- algae-like organisms (Prototheca spp.); and nematode larval
tricular tachyarrhythmias are most common, but supraven- migration (Toxocara spp.) cause myocarditis. Except for
tricular tachyarrhythmias may occur. Right bundle branch Coccidioides immitis, an important cause of pericarditis and
block and AV conduction disturbances are also reported. pericardial effusion in the southwestern United States (see
Ventricular dilation and reduced myocardial function are p. 1505), affected animals are usually immunosuppressed
usually evident echocardiographically. End-stage disease is and have systemic signs of disease. Rocky Mountain spotted
indistinguishable from idiopathic DCM, although the RV is fever (R. rickettsii) occasionally causes fatal ventricular
generally preferentially affected in Chagas disease. Clinical arrhythmias, along with necrotizing vasculitis, myocardial
signs of right-sided or biventricular failure are common, and thrombosis, and ischemia.
sudden death can occur. Antemortem diagnosis in chronic
cases is usually made with a combination of serologic testing NONINFECTIVE MYOCARDITIS
and compatible clinical signs. Therapy in the acute stage is Occasionally myocarditis is diagnosed histopathologically
aimed at eliminating the organism and minimizing myo- with no obvious etiologic agent. Lymphocytic, lymphocytic-
cardial inflammation. Currently, the preferred treatment in plasmacytic, and eosinophilic myocardial inflammation
both humans and dogs is benznidazole; in the United States, have been described with no infectious agents noted on his-
this drug is available only through the Centers for Dis- topathology or serologic screening. It is unknown whether
ease Control and Prevention (CDC). In dogs with chronic myocarditis in these dogs is an immune-mediated or auto-
Chagas disease, antiparasitic treatments do not affect out- immune process, or a response to an infectious agent that
come. Therapy is aimed at supporting myocardial function, was not identifiable postmortem. Clinical findings in such
controlling CHF, and suppressing arrhythmias. Prevention cases often include high-grade AV block and sinus arrest,
strategies in endemic areas include limiting contact with vec- with sudden death being a common outcome.
tors and reservoirs, using insecticides, and screening canine
blood donors. Clinical Findings and Diagnosis
Toxoplasmosis and neosporosis can cause clinical myo- Unexplained onset of arrhythmias or CHF after a recent
carditis in conjunction with generalized systemic infection, episode of infective disease or drug exposure is the classic
especially in the immunocompromised animal. The organ- clinical presentation of acute myocarditis. However, defini-
ism becomes encysted in the heart and various other body tive diagnosis can be difficult because clinical and clinico-
tissues after the initial infection. With rupture of these cysts, pathologic findings are usually nonspecific and inconsistent.
expelled bradyzoites induce hypersensitivity reactions and A database including complete blood count, serum bio-
tissue necrosis. Other systemic signs, including encephalitis, chemical profile with creatine kinase activity, serum cardiac
pneumonia, and chorioretinitis, often overshadow signs of troponin I (and NT-proBNP) concentration, thoracic and
myocarditis. Diagnosis is based on serologic testing with abdominal radiographs, and urinalysis are usually obtained.
rising antibody titers. Antiprotozoal therapy with clindamy- ECG changes may include an ST segment shift, T-wave or
cin or trimethoprim sulfa is recommended. QRS voltage changes, AV conduction abnormalities, and