JPC SYSTEMIC PATHOLOGY
CARDIOVASCULAR SYSTEM
April 2019
C-M07

Signalment (JPC Accession #2307591):  13-year-old female owl monkey (Aotus sp.)

HISTORY:  This monkey was found moribund at the bottom of the cage. 

HISTOPATHOLOGIC DESCRIPTION: 

Slide A 

Heart, left ventricle:  Multifocally, affecting approximately 40% of the myocardium, predominately the papillary muscles, inner aspect of the myocardium and endocardium, there is moderate to marked loss of cardiomyocytes with replacement by hypertrophied fibroblasts and fibrous connective tissue (fibrosis).  Remaining myocytes are variably sized and exhibit the following changes: increased diameter (hypertrophy); shrunken, individualized, and surrounded by fibrous connective tissue (atrophy); contain pale granular or vacuolated sarcoplasm (degeneration); or are shrunken with hypereosinophilic sarcoplasm, loss of cross striations and pyknotic nuclei (necrosis).  Multifocally, within the epicardium, the subepicardial connective tissue and myocardium, there are low numbers of lymphocytes, plasma cells, macrophages, and rare neutrophils, ectatic lymphatics (edema), and scattered small foci of hemorrhage.  Many myocytes contain variable amounts of golden-brown perinuclear pigment (lipofuscin). 

Slide B

Lung:  Multifocally, approximately 80% of alveoli are variably filled with mildly increased numbers of macrophages with foamy cytoplasm or intra-cytoplasmic hemosiderin pigment (“heart failure cells”) and few extravasated erythrocytes.  Multifocally alveolar septa are thickened up to 50um by congestion, macrophages, eosinophilic finely beaded material (fibrin) and edema.   

Lymph node, site not specified:  Diffusely, subcapsular and medullary sinuses contain many erythrocytes (draining hemorrhage) and increased numbers of macrophages that exhibit erythrophagocytosis and hemosiderosis.

Trachea:  No significant lesions.

Slide C

Liver: Affecting approximately 70% of the liver parenchyma, there is diffuse, marked centrilobular to midzonal necrosis and hemorrhage with variable retention of architecture. Hepatocytes within affected areas are lost and replaced by, or individualized and widely separated by hemorrhage and fibrin with minimal necrotic debris. There is marked dilation of sinusoids with congestion.  Remaining hepatocytes contain few to many variably sized, clear discrete vacuoles (lipid-type vacuolar change/degeneration) and/or fine brown granules in their cytoplasm (lipofuscin, bile, hemosiderin, or copper).  There are bile plugs within canaculi (cholestasis) and Kupffer cells within sinusoids which contain brown granular intracytoplasmic pigment (bile or hemosiderin). Multifocally portal areas contain ectatic lymphatics filled with an eosinophilic proteinaceous material (edema).

MORPHOLOGIC DIAGNOSIS:

  1. Heart, left ventricle: Myocardial loss and atrophy, multifocal to coalescing, marked, with fibrosis, owl monkey (Aotus), non-human primate.
  2. Lung: Alveolar histiocytosis, diffuse, moderate, with hemosiderosis, congestion and edema.
  3. Lymph node, site not specified: Draining hemorrhage, diffuse, moderate, with erythrophagocytosis and hemosiderosis
  4. Liver: Necrosis, centrilobular to midzonal, diffuse, severe, with hemorrhage, hemosiderosis, congestion, edema and lipid-type vacuolar degeneration (chronic passive congestion).

CONDITION:  Aotus cardiomyopathy

GENERAL DISCUSSION:

PATHOGENESIS:

TYPICAL CLINICAL FINDINGS:

TYPICAL GROSS FINDINGS:

TYPICAL LIGHT MICROSCOPIC FINDINGS:

ADDITIONAL DIAGNOSTIC TESTS: 

DIFFERENTIAL DIAGNOSIS:

COMPARATIVE PATHOLOGY:

 REFERENCES:

  1. Chilton J, Wilcox A, Lammey M, Meyer D. Characterization of a cardiorenal-like syndrome in aged chimpanzees (Pan troglodytes). Vet Pathol. 2016;53(2):417-424.
  2. Gozalo AS, Chavera A, Montoya EJ, Takano J, Weller RE. Relationship of creatine kinase, aspartate aminotransferase, lactate dehydrogenase, and proteinuria to cardiomyopathy in the owl monkey (Aotus vociferans). J Med Primatol. 2008;37 Suppl 1:29-38.
  3. Juan-Salles C, Soto S, Garner MM, Montesinos A, Ardiaca M. Congestive heart failure in 6 African grey parrots (Psittacus erithacus). Vet Pathol. 2011; 48(3):691-7.
  4. Lowenstein LJ, McManamon R, Terio KA. Comparative pathology of great apes: bonobos, chimpanzees, gorillas, and orangutans. Vet Pathol. 2016;53(2):250-76.
  5. Rajendra RS, Brady AG, Parks VL, Massey CV, Gibson SV, Abee CR. The normal and abnormal owl monkey (Aotus) heart: looking at cardiomyopathy changes with echocardiography and electrocardiography. J Med Primatol. 2010; 39:143-150.
  6. Reader, JR, Canfield DR, et al. Left Ventricular Hypertrophy in rhesus macaques (Macaca mulatta) at the California National Primate Research Center (1992-2014).  Comp Med. 2016;66(2):162-9.
  7. Rishniw MR, Schiavetta AM, Johnson TO: Cardiomyopathy in captive owl monkeys. Comp Med. 2005;55:162-168.
  8. Robinson WF, Robinson NA. Cardiovascular system. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. 3. 6th ed. St. Louis, MO: Elsevier; 2016:46-49.
  9. Sassevlle VG, Hotchkiss CE, Levesque PC, Mankowski JL. Hematopoietic, cardiovascular, lymphoid, and mononuclear phagocyte systems of nonhuman primates. In: Abee CR, Mansfield K, Tardiff S, Morris T, eds. Nonhuman Primates in Biomedical Research Vol 2: Diseases. 2nd ed. Waltham, MA: Elsevier; 2012:372.
  10. Simmons HA. Age-associated pathology in rhesus macaques (Macaca mulatta). Vet Pathol. 2016;53(2):399-416.
  11. Weller RE. Infectious and noninfectious diseases in owl monkeys. In: Baer JF, Weller RE, Kakoma I, eds. Aotus: The Owl Monkey. San Diego, CA: Academic Press; 1994: 193-195.


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