March 2017



Slide A

Signalment (JPC # 1856158): A 14-week-old dog




HISTOPATHOLOGIC DESCRIPTION: Cerebellum with choroid plexus and leptomeninges: Focally, the leptomeninges are expanded up to 1 mm by multiple sections of larval nematodes (which are occasionally degenerate) that are surrounded by an inflammatory infiltrate composed of numerous epithelioid macrophages, moderate numbers of viable and degenerate eosinophils, fewer lymphocytes, plasma cells, reactive fibroblasts, collagen bundles, neutrophils, minimal eosinophilic and karyorrhectic debris (necrosis) and hemorrhage. Larval nematodes are 125 μm in diameter with a 5 to 8 μm wide eosinophilic, hyalinized, smooth cuticle lined by coelomyarian-polymyarian musculature. The pseudocoelom contains an intestinal tract lined by few multinucleated cells with a vague brush border, paired excretory glands and lateral chords. Larvae often contain a developing gonad. Multifocally, the remaining, less affected meninges are mildly expanded by macrophages, plasma cells, and lymphocytes. There is focal loss of the cerebellar molecular, Purkinje cell, and granular cell layers (necrosis) with replacement by numerous gitter cells, plasma cells, edema and hemorrhage.

MORPHOLOGIC DIAGNOSIS: Cerebellum; leptomeninges: Meningoencephalitis, granulomatous and eosinophilic, multifocal, moderate, with necrosis and larval metastrongyles, etiology consistent with Parastrongylus sp., breed unspecified, canine.


Slide B

Signalment (JPC # 1562195): A rat


HISTORY: This rat was from Southeast Asia.


HISTOPATHOLOGIC DESCRIPTION: Brain, cerebrum and cerebellum: Multifocally, the leptomeninges are expanded up to 0.5 mm with multiple cross and tangential sections of larval nematodes admixed with numerous eosinophils, neutrophils, fewer macrophages, multinucleated giant cells, lymphocytes, plasma cells, minimal eosinophilic and karyorrhectic debris (necrosis) and hemorrhage. Focally, there is also a cross section of a larval nematode adhered to the ependyma of the fourth ventricle. Larval nematodes are 125 μm in diameter with a 5 to 8 μm wide eosinophilic, hyalinized, smooth cuticle lined by coelomyarian-polymyarian musculature. The pseudocoelom contains an intestine lined by few multinucleated cells with a vague brush border, paired excretory glands and lateral chords. Larvae often contain a developing gonad. Within the adjacent cerebrum, hippocampus and cerebellum, there are multiple, focally extensive areas of rarefaction characterized by loss of white and gray matter (necrosis), spongiosis, occasional neuronal necrosis, gemistocytic astrocytes, reactive microglial cells, moderate numbers of gitter cells and rare lymphocytes and plasma cells. In addition, there are few aggregates of neutrophils within the areas of necrosis in the hippocampus. Focally within the ventral calvarium, the bone is thinned and irregular with few osteoclasts within Howships lacunae (osteolysis).


MORPHOLOGIC DIAGNOSIS: Brain, cerebrum and cerebellum; leptomeninges: Meningitis, granulomatous and eosinophilic, multifocal, moderate, with larval metastrongyles, and multifocal gray matter and neuronal necrosis and gliosis, etiology consistent with Parastrongylus sp., breed unspecified rat, rodent.


ETIOLOGICAL DIAGNOSIS: Meningeal parastrongylosis


CAUSE: Parastrongylus cantonensis


ETIOLOGY SYNONYMS: Previously called Angiostrongylus cantonensis


      A common, neurotropic, metastrongylid lungworm of rats found in Australia, South Pacific, Southeast Asia, the Caribbean and southern United States (Louisiana, Mississippi, Florida)


      Rats are the natural host

o   Life cycle completion suspected in captive Geoffreys tamarin

      Intermediate hosts are gastropods (snails, slugs), giant African snail

      Paratenic hosts (substitute intermediate or transport) are crabs and frogs

      Aberrant hosts

o   Dogs

o   Humans: The most common cause of eosinophilic meningoencephalitis



      Natural infections in rats usually cause little disease

      In aberrant hosts, spectrum of disease varies with strain of parasite, severity of infection and host response

      Signs in aberrant hosts are due to inflammation associated with parasites, migration of larval nematodes in neural parenchyma and thrombosis and occlusion of vessels leading to infarction

      In immunosuppressed individuals, parasites may migrate back to the lungs, causing fatal pulmonary edema and pneumonia; proliferative endarteritis may occur



      Natural host: Adult parasite in pulmonary arteries lays eggs > migrate and lodge in alveolar capillaries > larvae hatch in about 6 days > tracheal-intestinal route to exterior > L1 larvae penetrate intermediate host and develop to L3 > ingestion of intermediate or paratenic host by definitive or aberrant host > migration of gastrointestinal tract to the brain, kidney and muscle > additional molts in CNS to L5 > migrate to the subarachnoid space for two weeks > young adults invade cerebral vein > heart and pulmonary arteries to complete maturation




o   Paraparesis, paraplegia, ataxia, urinary and fecal incontinence and tail paralysis

o   Extreme pain during lumbar palpation or manipulation

o   CSF: Eosinophilic pleocytosis


      Minor infections: Asymptomatic

      Heavy infections: Weakness, ataxia, circling, paraplegia, upper respiratory disease, coma or death

      May be lethal in other rat species (Ryukuu Islands tree rat; Diplothrix legata)



      Brain: Meningeal congestion

      Lungs: Mottled, atelectatic, consolidated, pleural adhesions

      Rat lung: Adult nematodes within pulmonary arteries



      Molting larvae in brain produce a mild to severe inflammatory reaction

      Eosinophilic to granulomatous meningoencephalitis in aberrant hosts

      Immature adults: Smooth, 3 to 5 μm diameter cuticle, coelomyarian-polymyarian somatic musculature, four accessory hypodermal chords, intestine composed of few, large multinucleate cells



      Fecal examination for eggs or larvae



      Other causes of cerebrospinal nematodiasis in animals:

      Setaria digitata: Filarid parasite of peritoneal cavity of cattle in Far East; causes cerebrospinal nematodiasis in aberrant infections of sheep, goats and horses

     Parelaphostrongylus tenuis: Parasite inhabits subdural space and venous sinuses of white-tailed deer with little disease; infection in aberrant species (moose, elk, caribou, sheep, llama and horse) causes destructive lesions in brain due to migrating parasites

     Halicephalobus gingivalis (H. deletrix): Saprophytic filarid nematode causing encephalitis and inflammation of multiple tissues in horses and man

     Other nematodes: Baylisascaris procyonis (various species), Strongylus vulgaris in horses (migrating larvae), Draschia megastoma (horses), Toxocara sp., Dirofilaria immitis (adult nematode) in dogs and cats, Meningonema peruzzi and Dipetalonema perstans in monkeys

      Other causes of verminous encephalomyelitis:

      Coenurus cerebralis, various Cysticerci sp., Echinococcus sp., Troglotrema sp., Oestrus ovis, Hypoderma bovis and Cuterebra sp. (Feline ischemic encephalopathy)



      Nonhuman primates: Eosinophilic meningitis or meningoencephalitis

      Horses: Two reported cases in foals by a CNS angiostrongylid

      Dogs and wild carnivores: Angiostrongylus (Parastrongylus) vasorum, pulmonary artery and right ventricle; causes obstruction, endarteritis and thrombosis




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10.  Strait K, Else JG, Eberhard ML. Parasitic diseases of nonhuman primates. In: Abee CR, Mansfield K, Tardif S, et al., eds. Nonhuman Primates in Biomedical Research: Diseases. Vol 2. 2nd ed. London, UK: Elsevier; 2012:235-236.

11.  Summers BA, Cummings JF, de Lahunta A. Inflammatory diseases of the central nervous system. In: Summer BA, Cumming JF, de Lahunta A, eds. Veterinary Neuropathology. St. Louis, MO: Mosby-Year Book; 1995:162.

12.  Tanabe M, Kelly R, de Lahunta A, et al. Verminous encephalitis in a horse produced by nematodes in the family Protostrongylidae. Vet Pathol. 2007;44(1):119-122.

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