JPC SYSTEMIC PATHOLOGY
Signalment (JPC#2023960): Unknown breed, age and gender puppy
HISTORY: This puppy was euthanized following a 5-day illness characterized by inability to walk. The puppy remained alert throughout the course of the disease.
HISTOPATHOLOGIC DESCRIPTION: Cerebrum: Multifocally, predominately within the white matter and extending into the adjacent gray matter, are areas of rarefaction and spongiosis that progress to complete loss of the neuroparenchyma (necrosis) with replacement by moderate numbers of gitter cells, eosinophils, lymphocytes, plasma cells, fewer neutrophils and reactive astrocytes. Within affected areas there are few cross and tangential sections of nematode larvae. The larvae are 50 um diameter with a 5 um thick cuticle, lateral chords, lateral alae, coelomyarian-polymyarian musculature, pseudocoelom, and an intestine lined by many uninucleate columnar epithelial cells with a brush border. Adjacent to necrotic areas, there are scattered dilated myelin sheaths that contain swollen axons (spheroids),Virchow-Robin space is expanded up to 5-6 cell layers thick by moderate numbers of lymphocytes, plasma cells, and fewer eosinophils (perivascular cuffing), which often obscure the vessel wall, and vessels are lined by hypertrophied endothelium. Multifocally within the meninges and choroid plexus there are a few scattered macrophages, neutrophils, and eosinophils. The ventricle is mildly dilated (hydrocephalus).
MORPHOLOGIC DIAGNOSIS: Cerebrum: Encephalitis, necrotizing, granulomatous and eosinophilic, multifocal, moderate with astrogliosis, spheroids and few nematode larvae, breed unspecified, canine.
ETIOLOGIC DIAGNOSIS: Cerebral baylisascariasis
CAUSE: Baylisascaris procyonis
· Common roundworm parasite in the small intestine of raccoons (definitive host)
· Shown to produce neural larval migrans (cerebrospinal nemotodiasis) or other visceral larval migrans in many species of birds and mammals
· Phylum Nematoda, Family Ascarididae
· B. procyonis eggs may remain infective for years; migration of larvae in aberrant hosts is similar to larvae of Toxocara canis (visceral larva migrans)
· Larvae molt and grow as they migrate (unlike Toxocara larvae) through tissues increasing in size from 300 um to 1500-1900 um causing mechanical damage and inciting severe inflammatory reactions
o Adult female worms in small intestine produce eggs > shed in feces > young raccoons ingest eggs containing infective second stage larvae > hatch in small intestine, penetrate the wall to develop and later reenter the intestinal lumen to mature
· Aberrant hosts:
o Accidental ingestion of infective eggs from an environment contaminated by raccoon feces > larvae penetrate intestinal wall > portal circulation to liver and then lungs > enter pulmonary veins, gaining access to left heart and systemic arterial circulation > distributed throughout body but especially to head and anterior body (brain and eyes) > usually become encapsulated in eosinophilic granulomas but small percentage migrate through brain
· Ingesting encysted larvae in the tissues of aberrant hosts (i.e. small rodents)
TYPICAL CLINICAL FINDINGS:
· Neurologic signs: Behavioral changes, ataxia, tremors, circling, head pressing, recumbency and paddling, followed by coma and death
· Ocular disease: Unilateral vision loss and photophobia related to inflammatory reactions from the larval migration, usually involving retina
· Clinical pathology: Eosinophilic pleocytosis of cerebral spinal fluid with peripheral eosinophilia
TYPICAL GROSS FINDINGS:
· Often no significant gross lesions
· Non-specific multifocal granulomatous inflammation may be present anywhere in the body with or without the presence of larval parasites
· Nematode larval migration can appear as linear or serpentine tracts of necrosis and/or hemorrhage
· Migration can result in vascular occlusion and infarction
· In raccoons, the intestines may contain high numbers of robust ascarids, similar to ascarid infections in other species
TYPICAL LIGHT MICROSCOPIC FINDINGS:
· Granulomatous and eosinophilic inflammation with extensive tracts of necrosis and microcavitation in the neural tissue, predominantly in the white matter of brain and spinal cord
· Migration can result in endothelial injury, vasculitis and thrombosis
· Perivascular aggregates of macrophages, lymphocytes, plasma cells and eosinophils are usually present
· Nematode larvae: 50-70 um diameter with lateral alae, lateral chords, and intestine lined by many uninucleate columnar cells with a brush border
ADDITIONAL DIAGNOSTIC TESTS:
· Diagnosis usually made on history, clinical findings, and serological testing
· Specific diagnosis made by morphologic identification of larvae recovered from tissues or in histopathologic sections
For histologic findings:
· Other Baylisascaris species:
o B. melis (badgers), B. columnaris (skunks), B. laevis (woodchuck), B. schroederi (pandas), B. devosi (fishers and martens), and B. transfuga (bears) are all potentially capable of causing similar lesions if enough eggs are ingested
· Toxocara canis: Larvae are much smaller than Baylisascaris sp because T. canis larvae do not grow during migration
Other causes of cerebrospinal nematodiasis:
· Parelaphostrongylus tenuis: Definitive host is the white-tailed deer; larvae migrate develop in the dorsal horns of the spinal cord at all levels and then migrate into the meningeal spaces; some penetrate dural veins and sinuses and mature; larvae cause a reaction in red deer, elk moose and sheep
· Parastrongylus (Angiostrongylus) cantonensis:Definitive host is the rat – metastrongyle lungworm; dogs aberrant migration causes an ascending paralysis, randomly distributed granulomatous lesions in the brain and cord (more severe in the spinal cord) and rarely degenerate parasites are located in the granulomas
· Elaphostrongylus rangiferi and panticola (reindeer)
· Elaeophora schneideri: Develops in meningeal arteries of various cervids, sheep and goats
· Setaria digitata: Normally found in the peritoneal cavity of buffalo; larvae can wander in the brain and spinal cord in sheep, goats, horses and camels causing lumbar paralysis in Asia
· Halicephalobus gingivalis: Granulomatous and eosinophilic meningoencephalitis, myelitis, polyradiculoneuritis
· Gurltia paralysans: Spinal veins of cats
· Angiostrongylus vasorum: Hemorrhagic malacia in brains of dogs
· Stephanurus dentatus: Spinal canal and encyst on the meninges in pigs
- Bowman DD. Georgi"s Parasitology for Veterinarians. 10th ed. Philadelphia, PA: WB Saunders Company; 2014: 207.
- Gardiner CH, Fayer R, Dubey JP. An Atlas of Protozoan Parasites in Animal Tissues, 2nd ed. Washington, DC: Armed Forces Institute of Pathology; 1998:19-21.
- Kazacos KR. Baylisascaris procyonis and related species. In: Samuel WM, Pybus MJ, Kocan AA, eds. Parasitic Diseases of Wild Mammals. 2nd ed. Ames IA: Iowa State University Press; 2001:301-335.
- Miller AD, Zachary JF. Nervous system. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby Elsevier; 2017: 846.
- Percy DH, Barthold SW, Griffey SM. Pathology of Laboratory Rodents and Rabbits. 4th ed. Ames, IA: Blackwell Publishing; 2016: 237, 300-301.
- Santiago SD, Uzal FA, Giannitti F, Shivaprasad HL. Cerebrospinal nematodiasis outbreak in an urban outdoor aviary of cockatiels (Nymphicus hollandicus) in southern California. J Vet Diagn Invest. 2012;24(5): 994-999.
- Summers BA, Cummings JF, de Lahunta A. Veterinary Neuropathology. St. Louis, MO: Mosby Yearbook; 1995:160-162.