JPC SYSTEMIC PATHOLOGY

URINARY SYSTEM

January 2024

U-P04 (NP)

 

Signalment (JPC #1599299):  Bovine kidney

 

HISTORY:  Tissue from a cow in a herd experiencing an epizootic disease. Affected cattle became febrile, refused to eat and salivated profusely. Milk production dropped and the animals were found to be anemic with enlarged peripheral lymph nodes. Some cows died, others aborted, and many recovered after one to two weeks of clinical disease.

 

HISTOPATHOLOGIC DESCRIPTION:  Kidney: Diffusely within glomerular tufts, the mesangium is moderately hypercellular, and there is mild multifocal accumulation of fibrin and small amounts of necrotic debris. Multifocally, glomerular tufts are adhered to Bowman’s capsule (synechiae) with minimal visceral and parietal epithelial cell hypertrophy. Occasionally within the glomerular endothelium, there are one or more 20-30 um intracytoplasmic, thin-walled protozoal cysts (meronts) containing numerous 2-3 um diameter, oval basophilic merozoites. Multifocally expanding the cortical interstitium are infiltrates of predominantly lymphocytes and plasma cells, with occasional macrophages and neutrophils. Rarely, interstitial capillary endothelial cells contain the previously described intracytoplasmic protozoal cysts. Multifocally, perivascular lymphatics are mildly dilated, and connective tissue is mildly separated by clear space (edema). Multifocally, tubules are mildly ectatic, and there is mild interstitial hemorrhage and congestion.

 

MORPHOLOGIC DIAGNOSIS:  Kidney: Glomerulonephritis, endocapillary, acute, global, diffuse, mild to moderate, with mild multifocal interstitial nephritis and endothelial intracytoplasmic protozoal cysts, breed unspecified, bovine.

 

ETIOLOGIC DIAGNOSIS:  Renal sarcocystosis

 

CAUSE:  Sarcocystis sp.

 

GENERAL DISCUSSION:

• Sarcocystis is a genus of cyst-forming coccidia with an obligatory two-host life cycle, which includes an herbivorous intermediate host with stages in the vascular endothelium and then skeletal muscle, and a carnivorous definitive host with stages occurring in the small intestine
• Most definitive hosts are clinically unaffected but some species of Sarcocystis are pathogenic to the herbivore intermediate host causing myositis and muscle atrophy
• Sarcocystis spp. are members of the protistan phylum Apicomplexa, class Sporozoa, subclass Coccidiasina  
• In cattle, Sarcocystis spp. are highly prevalent and distributed worldwide; incidence of infection approaches 100%; grossly visible sarcocysts results in condemnation of the carcass
• S. cruzi is the most common and the most pathogenic in cattle; other less common pathogenic species include S. hirsuta and S. hominis 

 

PATHOGENESIS:

• Carnivores (definitive host): Ingestion of muscular or neural tissue of herbivores containing mature sarcocysts > digestion in the small intestine frees zoites > transformation into micro- and macro-gametes in epithelium or subepithelium > fertilization > sporont/sporozoites in oocyst, and sporulation within the lamina propria > sporocysts enter intestinal lumen and are passed in feces
• Herbivores (intermediate hosts): Ingestion of sporocysts frees sporozoites in small intestine > penetrate the mucosa and enter endothelium of small arterioles > differentiation into first‑generation schizonts (meronts) > maturation into many merozoites > differentiation into 2^nd generation schizont with about 25 merozoites > 2^nd generation merozoites enter bloodstream and travel to striated muscle or neural tissue > form sarcocysts containing infective bradyzoites
• Sarcocystis is the only coccidia that sporulates in the lamina propria of the villus tips of the intestine in the definitive host
• Acute fatal disease may occur in cattle, sheep and swine during endothelial phase
• Release of meronts correlates with clinical fever peaks

 

 

TYPICAL CLINICAL FINDINGS:

• Acute fatal disease in cattle, sheep and swine (vascular dissemination of sporozoites): Fever, petechiation of mucous membranes, edema, icterus, and macrocytic hypochromic anemia 3 - 5 weeks after initial infection and lasting 6 - 8 weeks
• As disease progresses in cattle the following clinical signs can be seen:

• Inappetence, weight loss, reduced milk yield, hyperexcitability, hair loss, and occasional nervous signs
• Abortion occurs in this phase in some species; abortion in this instance is associated with systemic disease

• Chronic (muscular and CNS sporocysts):  Most infected animals are asymptomatic; in massive infections there may be cachexia, muscle atrophy, hair loss, nystagmus, nervousness, and death  
• Some investigators believe degenerating sarcocysts cause chronic myositis, which leads to eosinophilic myositis 
• In some clinically normal cattle, meronts in the placenta and vascular endothelium of the fetal brain can cause a non-suppurative encephalitis and subsequent abortion

 

TYPICAL GROSS FINDINGS:

• Generalized serous atrophy of fat; excessive yellow fluid in all body cavities; watery blood; petechial hemorrhage in the heart and pericardium, serosa of the gastrointestinal tract and urinary bladder; edema and hemorrhage of lymph nodes; alternate pale and dark striping or mottling of skeletal muscles
• Chronically affected cattle, even those severely affected, often have no prominent gross lesions  
• Eosinophilic myositis: well-demarcated, green, focal stripes or patches in skeletal muscle  

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Acute lesions: Hemorrhage and inflammation (mostly lymphocytes, fewer macrophages, eosinophils, and plasma cells) in the cardiac perivascular and interstitial tissues, skeletal muscle, lung, liver, and kidney  
• Chronic lesions: Usually none because live sarcocysts do not elicit inflammation; possibly thin, linear collections of lymphocytes between muscle fibers near sarcocysts; degenerating sarcocysts surrounded by variable numbers of inflammatory cells (relatively few eosinophils), or, later, macrophages and granulation tissue
• Kidney: Thin walled meronts containing many oval basophilic merozoites; located within the cytoplasm of endothelial cells of blood vessels and glomerular capillaries
• Muscle: Thin walled cysts (sarcocysts) containing many basophilic bradyzoites; located within and separating myocytes
• Eosinophilic myositis (thought to be IgE mediated hypersensitivity reaction to the sarcocysts, relatively rare condition): Inflammatory infiltrate of large numbers of eosinophils with variable muscle fiber degeneration

 

ULTRASTRUCTURAL FINDINGS:

 

ADDITIONAL DIAGNOSTIC TESTS:

• In cattle, diagnosis is by seeing parasites in mononuclear cells in peripheral blood smears or in endothelial cells on tissue section  
• In carnivores, diagnosis is made by finding sporulated oocysts on a fecal exam or gametes and oocysts in the lamina propria of the small intestine on tissue section
• Western blot using equine serum can be 100% sensitive and 98% specific

 

DIFFERENTIAL DIAGNOSIS:

• Toxoplasma gondii - schizonts in feline intestinal cells are PAS positive and usually extravascular; thin-walled cysts are found in several tissues
• Neospora caninum – thick walled cysts and confined to the CNS

 

COMPARATIVE PATHOLOGY:

 

Sarcocystis sp.	Intermediate hosts	Definitive hosts
S. cruzi	Cattle	Dog, wild canids
S. bovifelis	Cattle	Cat
S. hominis	Cattle	Human/Primate
S. gigantea	Sheep	Cat
S. tenella	Sheep	Dog
S. capracanis	Goat	Dog
S. miescheriana	Swine	Dog
S. porcifelis	Swine	Cat
S. porchihominis	Swine	Human
S. bertrami	Horse	Dog
S. fayeri	Horse	Dog
S. neurona	Birds/Horses*	Opossum
S. lindemanni	Human	Unknown
S. hemionilatrantis	Deer	Dog
S. cervi	Deer	Unknown
S. muris	Mouse	Cat
S. cuniculi	Rabbit	Cat
S. falcatula	Birds	Virginia Opossum

*Horses an accidental host - causes protozoal myeloencephalitis (N-P01)

 

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