JPC SYSTEMIC PATHOLOGY
Musculoskeletal System
April 2019
M-P01

Signalment (JPC #2209517):  Dog

HISTORY:  This dog had muscle weakness.

HISTOPATHOLOGIC DESCRIPTION:  Skeletal muscle: Multifocally effacing and replacing myofibers are discrete aggregates of neutrophils, macrophages, and fewer lymphocytes and plasma cells (pyogranulomas) with frequent intrahistiocytic 3-4um spherical protozoal merozoites.  Multifocally, separating and compressing myocytes are multilamellar mucopolysaccharide cysts (“onion skin cysts”) that are up to 200 um in diameter and are centered on a macrophage with abundant foamy to granular cytoplasm and a single nucleus with a prominent nucleolus, surrounded by concentric lamellations of amphophilic, mucinous material, further surrounded by 1-3 layers of spindle cells. Macrophages within the cysts occasionally contain a round to oval 6-10um eosinophilic protozoal trophozoite. Rarely within the center of the cyst, there is a 75um meront containing numerous 4-5 um diameter merozoites. Diffusely there is marked atrophy and loss of myofibers, while remaining myofibers variably exhibit either pale swollen and vacuolated sarcoplasm (degeneration),  or hypereosinophilic fragmented sarcoplasm with loss cross of cross strations (necrosis) or basophililc sarcoplasm with multiple central nuclei (regeneration). Multifocally are rare multinucleated, misshapen regenerative myocytes (muscle giant cells) within affected muscle bundles (abortive regeneration). The perimysium and endomysium are expanded up to 50 um by abundant fibrosis and edema, with few scattered macrophages, neutrophils, lymphocytes and plasma cells.

MORPHOLOGIC DIAGNOSIS:  Skeletal muscle:  Myositis, pyogranulomatous, diffuse, marked, with myocyte degeneration, necrosis, regeneration, and atrophy, fibrosis, and numerous mucopolysaccharide (onion skin) protozoal cysts and merozoites, breed unspecified, canine.

ETIOLOGIC DIAGNOSIS:  Hepatozoon myositis

CAUSE:  Hepatozoon americanum

CONDITION:  American canine hepatozoonosis

GENERAL DISCUSSION:

PATHOGENESIS

Transmitted via ingestion of the definitive host (Amblyomma maculatum); predation with ingestion of cystozoites from infected host tissues; NOT transmitted via tick bite

LIFE CYCLE

TYPICAL CLINICAL FINDINGS

TYPICAL GROSS FINDINGS

TYPICAL LIGHT MICROSCOPIC FINDINGS

ULTRASTRUCTURE

ADDITIONAL DIAGNOSTIC TESTS

DIFFERENTIAL DIAGNOSIS:

COMPARATIVE PATHOLOGY:

REFERENCES:

  1. Baneth G. Perspectives on canine and feline hepatozoonosis. Vet Parasitol. 2011;181:3-11.
  2. Cooper BJ, Valentine BA. Muscle and tendon. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. Louis, MO: Elsevier; 2016:240.
  3. Craig LE, Dittmer KE, Thompson KG. Bones and joints. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. Louis, MO: Elsevier; 2016:94,98.
  4. Cummings CA, Panciera RJ, Kocan KM, Mathew JS, Ewing SA. Characterization of stages of Hepatozoon americanum and parasitized canine host cells. Vet Pathol. 2005;42(6):788-796.
  5. Macintire DK, Vincent-Johnson NA, Potter M. Hepatozoon americanum In: Greene C, ed. Infectious Diseases of the Dog and Cat. 4th ed. St Louis MO: Elsevier Saunders; 2012: 757-763.
  6. Valli VEO, Kiupel M, Bienzle D. Hematopoietic system. In: Maxie MG, Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. Philadelphia, PA: Elsevier; 2016:110-111.


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