Final Diagnosis:  Toxoplasmosis in a juvenile cat

Gross findings:  Grossly, the cat was in poor body condition and moderately dehydrated.  The thymus was markedly atrophied.  Mesenteric lymph nodes were markedly swollen and bulged on cut section.

Histologic findings: The hepatic parenchyma contained numerous, variably sized foci of necrosis.  Affected foci contained anuclear and hypereosinophilic hepatocytes infiltrated by few macrophages and lymphocytes.  Few hepatocytes contained 25-35 µm in diameter protozoal cysts, characterized by a thin cyst wall containing numerous 1-2 µm in length, punctuate to elongate bradyzoites.  Protozoal organisms were consistent with Toxoplasma gondii  tissue cysts.

An intrahepatocyte Toxoplasma gondii tissue cyst containing numerous punctuate to crescent-shaped bradyzoites (H&E, 100X).  Note the lack of inflammation surrounding the tissue cyst.	A nodular aggregate of glial cells with central necrosis within the cerebrum (H&E, 20X).  Inflammation is most likely centered on extracellular tachyzoites.

The cerebral, cerebellar, and brainstem parenchyma contained numerous small, nodular foci of necrosis infiltrated by moderate numbers of glial cells and few macrophages and lymphocytes.  Rare protozoal cysts, not associated with the foci of necrosis, were observed within the cerebrum.

  The adrenal gland cortices contain multiple foci of necrosis and few intracellular protozoal cysts.

  Mesenteric lymph nodes contain multiple extensive foci of necrosis.

  Pulmonary alveolar septa were diffusely, markedly expanded by histiocytes and fewer lymphocytes, plasma cells, and neutrophils.  Alveoli were frequently lined by plump epithelial cells with large round nuclei and few prominent chromocenters (type II pneumocytes) and contained moderate numbers of histiocytes with abundant eosinophilic, vacuolated cytoplasm.

Ancillary testing:  No bacteria or viruses were isolated by bacterial culture and virus isolation of the lung, liver, kidney, lymph node, or spleen.

Discussion:  The presence of necrosis in multiple organs, including the liver, adrenal glands, lymph nodes, and brain, along with protozoal cysts within multiple organs supports a diagnosis of systemic toxoplasmosis in this cat.  Although Toxoplasma gondii and Neospora caninum are difficult to differentiate histologically, systemic Toxoplasma gondii infection is by far the most common cause of systemic protozoal disease in juvenile cats  Toxoplasma gondii  is an intracellular coccidian parasite that has a wide host range that includes all domestic species, rodents, birds, primates, and humans.  Domestic cats are the definitive hosts and the sexual stage of the parasite occurs within feline enterocytes.  Transmission to cats is thought to occur most frequently by ingestion of infected tissues.  Other routes of infection include congenital infection and ingestion of contaminated feces.  Oocysts, which may be shed in the feces of infected cats, mature into sporozoites, the infectious stage.  Once within the host, sporozoites divide and produce tachyzoites.  From the gastrointestinal tract, Toxoplasma is transported to tissues either free within the plasma, or intracellularly by lymphocytes, macrophages, and granulocytes.  Tachyzoites may infect almost any host cell to form a parasitophorus vacuole within the host cell membrane.  Proliferation of tachyzoites results in destruction of the host cell and subsequent release of infectious zoites.  These organisms may also encyst within cells to persist indefinitely as tissue cysts.

  The characteristic lesion associated with systemic toxoplasmosis in cats is necrosis.  Lesions may occur in almost any organ but are most commonly found in the brain, liver, lung, lymph nodes, heart, skeletal muscle (including the tongue), and eye.  Additionally, a nonsuppurative and proliferative interstitial pneumonia, as was observed in this case, may occur in disseminated disease.

  The majority of infected cats have clinically silent infection due to an appropriate humoral and cell-mediated immune response, and subsequent latency of the organism.  Development of systemic disease may be the result of multiple variables including age, infectious dose, host species, and immune status.  Immunosuppression secondary to stress, glucocorticoids, immunosuppressive drugs, or viral infection such as FIV, FeLV, and canine distemper virus in dogs, may predispose the animal to developing systemic disease.  Acute infection of pregnant animals, including women, ewes and does, may result in parasitemia, placentitis, and abortion or infection of the fetus.  Toxoplasma gondii should be considered as a potential cause of abortion in all domestic species.

  Prenatal or neonatal infection may result in acute death, or nonspecific signs such as lethargy, depression, and hypothermia.  Other clinical signs include fever, icterus, neurologic signs, pneumonia, lameness, and ocular abnormalities.

  Antemortem diagnosis of systemic Toxoplasma gondii infection can be extremely difficult.  Serology is frequently used despite obvious shortcomings.  A positive antibody titer indicates exposure but not acute infection, and titers may persist in latent infection due to the humoral response to tissue cysts.  Therefore, antemortem diagnosis should be based on a combination of history, serologic testing (preferably acute and convalescent titers) and clinical signs.

-by Dr. Ryan Jennings, ADDL graduate student

References:

1. Brown CC, Baker DC and Barker IK: 2007.  Alimentary system.  IN: Jubb, Kennedy and Palmer's Pathology of Domestic Animals.  Ed. Maxie.

2. Dubey JP, Mattix ME and Lipscomb TP: 1996.  Lesions of neonatally induced toxoplasmosis in cats.  Veterinary Pathology 33:290-295.

3. Dubey JP and Lappin MR: 2006.  Toxoplasmosis and Neosporosis.  In: Infectious Diseases of the Dog and Cat.  Ed. Greene.