Abbey Veterinary Services

DIAGNOSTIC HISTOPATHOLOGY AND CYTOLOGY

CASE OF INTEREST

A case of Toxoplasmosis in a Sand Cat (Felis margarita).

By Richard Fox, Veterinary Pathologist

Case donated by Lucy Genovese, Veterinary Pathologist.

A two year old Sand Cat presented with severe dyspnoea but died shortly after. Another Sand Cat did not show any clinical signs. A necropsy was performed soon after death. Obvious lesions were limited to lung lobes which were diffusely wet on cutting and hyperaemic with areas of haemorrhage. A pleural effusion (yellow and clear) was also evident with a specific gravity of 1.023 and total protein of 2.0 g/dl. Multifocal punctate areas of hyperaemia were also evident throughout the liver tissue. Sections of tissue were submitted for histopathological examination.

In sections of lung tissue there were multifocal areas of parenchymal necrosis. Alveoli were filled with proteinaceous material, fibrin and frequent activated macrophages containing phagocytosed debris and a few degenerate neutrophils were present. Some sloughed necrotic epithelial cells were also present. Some of these larger epitheliod cells, possibly macrophages and epithelial cells, contained tachyzoites. Free tachyzoites were occasionally identified within the alveolar space. Alveolar walls were thickened by engorged blood vessels, macrophages and due to the presence of type II pneumocytes.

Figure 1. Histological section of the lung displaying type II pneumocyte hyperplasia and intra-alveolar protein exudation and inflammation (x40 obj.). HE Stain.

Figure 2. Histological section of the lung identifying intra-cellular and free fusiform to crescent shaped tachyzoites in an alveolus. (x63 obj.). HE Stain.

In the liver, there was multifocal random hepatocellular necrosis but tending to be in the periacinar regions. There was also multifocal bile duct epithelial vacuolation and necrosis, sometimes associated with the presence of tachyzoites. Tachyzoites were also occasionally identified within areas of parenchymal necrosis. There was prominent canalicular bile plugging (cholestasis). Inflammation was limited to areas of necrosis (namely lymphocytes, macrophages and neutrophils) as well as a moderate portal infiltration.

Figure 3. Histological section of the liver displaying an area of hepatocelluar necrosis associated with haemorrhage, leukocytes and fibrin deposits. (x2.5 obj.). HE Stain.

In the stomach (fundus) further multifocal areas of necrosis with tachyzoites were identified within the deep mucosa.

Toxoplasma gondii is an obligate intracellular coccidian protozoan parasite, and its exposure is widespread among the human and domestic animal population. Toxoplasma gondii is a tissue protozoal organism with three life stages – tachyzoites, bradyzoites and sporozoites. Tachyzoites is acute, rapidly dividing stage of the organism that disseminates via blood or lymph during active phase of the infection but can infect almost all tissues. The tachyzoites replicate intracellularly until the infected cell is destroyed, releasing the organism.

Clinical signs develop as a result of the inflammation induced by the parasite in infected tissues. Toxoplasma organisms, when inhibited by immune responses, form tissue cysts may develop that contain the more slowly dividing bradyzoites. Bradyzoites can later be reactivated under conditions of immunosuppression to divide rapidly as tachyzoites, potentially resulting in clinical disease. Bradyzoites can persist in affected tissues for the lifetime of the host.

Cats are the only species able to complete the coccidian life cycle of T. gondii in the intestinal tract. After ingestion of bradyzoites (that are present as encysted organisms in ingested meat) intestinal epithelial cells are infected and several rounds of asexual replication occur followed by a sexual cycle. Sporulated oocysts, which are not infectious at this stage, are passed in the faeces. Sporozoites develop in the oocysts after one to five days of exposure to oxygen in conjunction with appropriate environmental temperatures and humidity.

Toxoplasmosis can be contracted via the oral route via infected food matter, ingestion of food or water contaminated with faeces that contain sporulated oocysts or due to transplacental transmission. Cats are the key animal species in the epidemiology of Toxoplasma gondii because they are the only hosts that excrete the infective, environmentally resistant oocysts in their faeces.

Respiratory tract involvement is one of the most common presentations and therefore associated clinical signs include dyspnea and coughing. Anorexia, malaise, lameness, icterus, fever, tonsillar enlargement, lymphadenomegaly, splenomegaly and evidence of encephalitis are often but not always observed . Muscle discomfort from myositis is frequently noted during physical examination and neurological signs can be present. Myocarditis and retinochoroiditis/anterior uveitis are sometimes involved in clinical disease. Secondary changes include vitreal hemorrhage, vitreal opacity, retinal detachment, iritis, iridocyclitis, hyphema, cataracts and corneal precipitates.

Diagnostic tests for toxoplasmosis include hematology, clinical chemistry, and urinalysis. Although there are no laboratory findings pathognomonic for toxoplasmosis, suggestive clinical history and the following laboratory abnormalities raise the index of suspicion: non-regenerative anaemia, neutrophilic leukocytosis, monocytosis, eosinophilia, elevated creatine kinase, elevated alkaline phosphatase, elevated alanine transferase, elevated lipase, hyperbilirubinaemia, hyperproteinaemia, proteinuria and bilirubinuria.

Cytological examination may reveal tachyzoites in blood, CSF, transtracheal wash fluid, peritoneal effusion, or pleural effusion from clinically ill animals.

Currently available drugs as the time of writing, which usually supress the replication of T. gondii are not completely effective in killing the parasites. Examples include Clindamycin, Potentiated Sulphonamides in cases of systemic infection. Enteroepithelial infection also includes treatment protocols which which include Monensin and Toltrazuril. Clindamycin is often regarded as the treatment of choice in cats. Several new drugs are available but are not licenced for veterinary use but have been used in experimental toxoplasmosis in mice which include roxithromycin, trimetrexate and aprinocid.

References:

1. Purdue 2003 Winter Newsletter: Link

2. J. B. Dubey & R. Lappin: Toxoplasmosis and Neosporosis. In: Greene CE, ed. Infectious diseases of the dog and cat. Philadelphia WB Saunders and Co, 2006;754-775.

3. C. C. Brown,D. C. Baker & I. K. Barker, Infectious and parastitic diseases of the respiratory tract (Fifth ed.) In: K.V.F. Jubb, P.C. Kennedy and N. Palmer, Editors, Pathology of Domestic Animalsvol. 2, Academic Press, San Diego (1985), pp. 270-272.