JPC SYSTEMIC PATHOLOGY
Signalment (ACVP 75-34): 1-year-old pig
HISTORY: Clinical signs consisted of lameness, especially of the hind legs, anorexia, weight loss, malaise and rough hair coat.
HISTOPATHOLOGIC DESCRIPTION: Skeletal muscle: Multifocally replacing myocytes are numerous granulomas composed of a central area of necrotic, often mineralized cellular debris and degenerate nematode larvae surrounded by moderate numbers of epithelioid macrophages, foreign body and Langhans type multinucleated giant macrophages, further surrounded by fewer eosinophils, lymphocytes, plasma cells and concentric rings of reactive fibroblasts and fibrous connective tissue. Multifocally hypertrophied myocytes with abundant eosinophilic fibrillar cytoplasm and multiple large, disorganized, vesiculate nuclei (nurse cells) contain intrasarcoplasmic 75-150 um diameter cysts with a 10 um thick, eosinophilic, hyalinzed wall that contains cross sections of nematode larvae. Larvae are 25-30 um in diameter with a thin, eosinophilic cuticle, coelomyarian and polymyarian musculature, bilateral hypodermal bands, a cluster of basophilic cells that surround an esophagus (stichosome), musculature, intestinal tract and developing gonad. Occasionally, encysted larvae are surrounded by moderate numbers of previously described inflammatory cells; other involved myocytes contain only debris from remnants of nematode larvae and mineral. Occasionally, adjacent myofibers are shrunken and brightly eosinophilic (atrophy) or are replaced by fibrous connective tissue.
MORPHOLOGIC DIAGNOSIS: Skeletal muscle: Granulomas, eosinophilic, multifocal, moderate, with hypertrophied myocytes (nurse cells) with intra-sarcoplasmic, encysted aphasmid larvae, pig, porcine.
ETIOLOGIC DIAGNOSIS: Trichinella myositis
CAUSE: Trichinella spiralis
CONDITION: Trichinosis, Trichinellosis
- Aphasmid Nematode; humans are dead-end hosts
- Trichinellosis is a zoonotic disease and involves animal-to-animal transmission through consumption of infected muscle; there is a wide range of hosts, but infection is usually maintained in carnivore or scavenger species; horses, birds and other species may become infected if fed infected animal tissue
- Five species and eight genotypes of Trichinella produce disease:
- spiralis: Temperate regions; pigs, rodents, red foxes, golden jackals, man (zoonotic potential); moderately resistant to freezing; most prevalent strain
- native: Artic; polar bears, bears, aquatic mammals; resistant to long-term freezing
- nelsoni: Eastern and southern Africa; central and eastern Europe and middle Asia; wild carnivores, pigs
- T. pseudospiralis: Northeastern Europe; raccoons, cats, mice and birds; fails to encyst in muscle; no nurse cell formation
- brivoti: Europe, Eurasia, Africa; carnivores, red foxes, golden jackals, pigs
- Ingestion of encysted larvae in muscle > stomach digestive secretions excyst L1 > migrate to duodenum/jejunum and molt to L4 > adults emerge and mate > ovoviviparous females penetrate crypts of Lieberkuhn and deposit larvae in lymphatics > L1 disseminate via lymphatic and blood throughout body and invade any host tissue, but remain immature and unencapsulated outside of skeletal muscle (i.e. invade cardiac muscle but do not encyst; cause myocarditis) > encyst in skeletal muscle fibers, especially diaphragm, limbs, tongue, periocular, masticatory and intercostal muscles
- Larvae grows and enlarges in the host cells, becomes coiled, and modifies the host cell into nurse cells (enlarged nuclei, loss of myofibrils, thickened basement membrane) by forming a collagenous capsule that protects the larvae from the host’s immune system and anthelmintic therapy
- Life cycle perpetuated when another mammal consumes infected muscle
TYPICAL CLINICAL FINDINGS:
- Most often asymptomatic
TYPICAL GROSS FINDINGS:
- Multifocal pale areas in skeletal muscle; preferential involvement of respiratory and masticatory muscles
- Larvae usually not visible grossly unless mineralized
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Larvae lie within a bulging hyalinized segment (capsule) of a hypertrophied, multinucleated muscle fiber (nurse cell); they may be encircled by low numbers of eosinophils and later by lymphocytes, plasma cells and macrophages; inflammation variable depending on level of degeneration of encysted muscle fiber
- Degenerative larvae are exposed to the immune system resulting in a more intense eosinophilic inflammatory response (Th2 response; production of IL-4, IL-5, IL-10, and IL-13)
- Muscle fibers adjacent to encysted larvae may show degenerative and regenerative changes
- Encapsulating muscle may form mineral deposits
- Nematode features: Hypodermal bacillary bands, stichosome (long chain of large glandular cells/stichocytes)
- Patchy severe interstitial myocarditis with multinucleated giant cell macrophages and eosinophils, but no encysted larvae in cardiac muscle
ADDITIONAL DIAGNOSTIC TESTS:
- Skeletal muscle biopsy
- Meat inspection “trichinoscopes”
- PCR: Very sensitive; can detect one larva
- ELISA: High specificity, but lag time between infected and detectable level
- Ancylostoma and Toxocara spp. larvae can enter skeletal muscle and remain dormant (larval migrans), but do not form “nurse cells” in myofibers
- Sarcocystis and other protozoans encysted in muscle
- Cysticercus (larval form) encysted in muscle
- Gongylonema found in the lingual mucosa of pigs who graze grass
- Recent report of European mustelids being infected likely from domesticated swine
- Polar bears; bears (black): native
- Humans are susceptible to infection after ingestion of undercooked meat of pigs, bears, and aquatic mammals (polar bear and walrus)
- Pigs; spiralis; major economic importance in porcine industry; show no clinical signs; encysted larvae not typically observed on gross examination but dead larvae cant calcify and be seen; seen in active muscles; focal inflammation consisting of eosinophils, neutrophils, and lymphocytes
- Red foxes and golden jackals: spiralis and T. britovi
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