JPC SYSTEMIC PATHOLOGY
MUSCULOSKELETAL SYSTEM
APRIL 2022
M-P02

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 and randomly replacing 20% of 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 and multinucleated giant cells (foreign body and Langhans types), further surrounded by fewer eosinophils, lymphocytes, and plasma cells, and further surrounded by a thin rim of concentric rings of reactive fibroblasts and fibrous connective tissue. There are also many multifocal, random, markedly hypertrophied myocytes that have abundant eosinophilic, fibrillar cytoplasm and multiple large, disorganized, vesiculate nuclei (nurse cells) that contain cross sections of nematode larvae within intrasarcoplasmic 75-150 um diameter cysts with a 10 um thick, eosinophilic, hyalinized cyst wall.  Larvae are 25-30 um in diameter with a thin, eosinophilic cuticle, coelomyarian-polymyarian musculature, bilateral hypodermal bands, a cluster of basophilic cells that surround an esophagus (stichosome), an intestinal tract, and a developing gonad.  Occasionally, 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 

 

GENERAL DISCUSSION:

• Trichinellosis is a zoonotic disease (humans are dead-end hosts) 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
• Aphasmid Nematode; 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
• nativa: 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

 

LIFE CYCLE:

• 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 intestinal crypts 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 grow and enlarge in the host cells, become coiled, and modify 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
• Degenerate 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

 

DIFFERENTIAL DIAGNOSIS: 

• 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

 

COMPARATIVE PATHOLOGY: 

• Report of wild European mustelids being infected likely from domesticated swine (Oltean, J Wildl Dis, 2014)
• 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 can calcify and be seen grossly; seen in active muscles; focal inflammation consisting of eosinophils, neutrophils, and lymphocytes
• Red foxes and golden jackals: spiralis and T. britovi

 

REFERENCES:

1. Cooper BJ, Valentine BA. Muscle and Tendon. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. St. Louis: Elsevier; 2016:237-238.
2. Dmitric M, Vidanovic D, Vaskovic N, et al. TRICHINELLA INFECTIONS IN RED FOXES (VULPES VULPES) AND GOLDEN JACKALS (CANIS AUREUS) IN SIX DISTRICTS OF SERBIA. J Zoo Wildl Med. 2017;48(3):703-707.
3. Gardiner CH, Poynton SL. An Atlas of Metazoan Parasites in Animal Tissues. Washington, DC: Armed Forces Institute of Pathology; 2009:3, 13, 40-42.
4. Keel, MK, Terio, KA, McAloose, D. Canidae, Ursidae, Ailuridae In: Terio K, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals, San Diego, CA: Elsevier 2018: 249-250.
5. Larter NC, Elkin BT, Forbes LB, Wagner B, Allaire Trichinella Surveillance in Black Bears (Ursus americanus) from the Dehcho Region, Northwest Territories, Canada, 2002–15. J Wildl Dis. 2017;53(2):405-407.
6. Martinez MAJ, Gasper DJ, del Carmen Carmona Mucino M, Terio KA. Suidae and Tayassuidae. In: Terio K, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals, San Diego, CA: Elsevier 2018: 221.
7. McAdam AJ, Milner DA, Sharpe AH. Infectious diseases. In: Kumar V, Abbas AK, Aster JC, eds. Robbins and Cotran Pathologic Basis of Disease. 10th ed. Philadelphia, PA: Saunders Elsevier; 2021:396-397.
8. Oltean M, Kalmar Z, Kiss BJ, et al. European mustelids occupying pristine wetlands in the Danube Delta are infected with Trichinella likely derived from domesticated swine. J Wildl Dis. 2014;50(4):972-975.
9. Robinson WF, Robinson NA. Cardiovascular system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 3. 6th ed. St. Louis: Elsevier; 2016:44.
10. Valentine BA. Skeletal muscle. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7^th St. Louis, MO: Elsevier; 2022: 427, 1011, 1028.

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