JPC SYSTEMIC PATHOLOGY

CARDIOVASCULAR SYSTEM

APRIL 2022

C-B02

 

Signalment (JPC #1482029):  5-month-old guinea pig

 

HISTORY:   This animal died following a brief period of depression and anorexia.  

 

SLIDE A: HISTOPATHOLOGIC DESCRIPTION:  Heart: The epicardium is diffusely replaced by an adherent, variably thick (up to 1mm) mat of pale eosinophilic, homogenous to fibrillar material (fibrin) that contains numerous enmeshed viable and degenerate heterophils, moderate numbers of erythrocytes (hemorrhage), eosinophilic cellular and karyorrhectic debris (necrosis), and fewer scattered lymphocytes, plasma cells, and macrophages. The mat multifocally extends into the subjacent myocardium where it separates, surrounds, and replaces cardiomyocytes that are often shrunken (atrophy) or rarely swollen with vacuolated sarcoplasm and loss of cross striations (degeneration). In these areas, there is increased clear space (edema). Subjacent to this infiltrate are reactive fibroblasts separated by minimal amounts of loose fibrous connective tissue and many perpendicular, evenly spaced, small caliber blood vessels lined by hypertrophic endothelium (granulation tissue).  Multifocally, vessel lumina are partially to completely occluded by adherent fibrinocellular thrombi that contain enmeshed heterophils, macrophages, and fewer lymphocytes and plasma cells, and endothelial cells are often hypertrophic. There is focal mild chondrous metaplasia within the tunica media of the proximal ascending aorta.

 

SLIDE B:  Heart (Brown & Brenn stain): The fibrinous mat contains abundant scattered extracellular and intraheterophilic Gram-positive diplococci.

 

MORPHOLOGIC DIAGNOSIS:  Heart: Epicarditis, fibrinosuppurative, chronic-active, diffuse, severe, with mild subepicardial myocarditis, fibrin thrombi, and abundant extracellular and intraheterophilic Gram-positive diplococci, guinea pig, rodent.

 

ETIOLOGY:  Streptococcus pneumoniae

 

ETIOLOGIC DIAGNOSIS:  Diplococcal (pneumococcal) epicarditis

 

GENERAL DISCUSSION:

• Gram-positive, 1-2 µm, heavily encapsulated, alpha-hemolytic cocci in pairs (diplococci) and short chains; capsular polysaccharide types 4 and 19 most frequently isolated from guinea pigs
• S. pneumoniae is common inhabitant of upper respiratory tract of clinically normal guinea pigs, rabbits, horses, cattle, monkeys, rats, dogs, cats, and humans, and is an important cause of bacterial pneumonia and meningitis in humans 
• Serotypes isolated from guinea pigs are identical to human isolates, however interspecies transmission has not been proven to date
• Infection in guinea pigs is most often associated with the lower respiratory tract; extra-pulmonary lesions are rare in the absence of pneumonia
• Additional disease syndromes include fibrinopurulent bronchopneumonia; bacteremia; fibrinopurulent polyserositis; suppurative inflammation of the middle or inner ear, joints, peritoneum, lungs, heart, kidneys; and panophthalmitis

 

PATHOGENESIS:

• Transmission: Aerosol and direct contact
• Predisposing factors: Stress (e.g. transportation), pregnancy, poor husbandry, inadequate nutrition (hypovitaminosis C), poor climate control, waning passive immunity, immunosuppression, concurrent viral infection
• Virulence factors:  

• S. pneumoniae does not produce exotoxins
• Cell wall proteins mediate attachment and invasion of mucosal membranes
• A thick protective polysaccharide capsule resists phagocytosis
• Many pneumococci can activate alternate complement pathway which may be important in early tissue changes

• Extrapulmonary lesions occur with bacteremia

 

TYPICAL CLINICAL FINDINGS:

• Up to 50% of infected guinea pigs may be subclinical carriers
• Epizootics occur most often during winter months
• Young animals and pregnant sows are most at risk
• Signs of disease include ruffled coat, anorexia, dyspnea, inactivity, nasal and ocular discharge, vestibular signs (if middle ear infection), stillbirth, abortion, torticollis; death is often the only sign

 

TYPICAL GROSS FINDINGS:

• Fibrinopurulent polyserositis (e.g. pericarditis, pleuritis, peritonitis, periorchitis), meningitis, metritis

• Lesions may be confined to the meninges in some fatal cases

• Consolidation of affected lung lobe(s) (“lobar pneumonia”): dark red to dull tan, relatively firm, non-resilient
• Upper respiratory exudate, purulent otitis interna/media, abscessed lymph nodes

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Heart lesions: May have bacteria (diplococci), endocardium is typically not affected 

• Mild: Fibrinous epicardial tags, neutrophilic and lymphocytic infiltration around epicardial vessels
• Severe: Thick epicardial mats of fibrin and debris infiltrated by abundant neutrophils, lymphocytes, and plasma cells; fibrin thrombi
• Chronic: Epicardial granulation tissue, hemosiderosis, hemorrhage, adhesions

• Pulmonary lesions: Acute bronchopneumonia with fibrinous exudate and neutrophilic infiltration, thrombosis in acute cases
• Additional lesions: Fibrinopurulent polyserositis (pleuritis, peritonitis, pericarditis, perihepatitis), fibrinopurulent meningitis, splenitis, lymphadenitis, endometritis, suppurative embolic lesions (e.g. liver, spleen, kidney, ovary), suppurative arthritis and osteomyelitis, centrilobular hepatic necrosis, otitis media

 

ADDITIONAL DIAGNOSTIC TESTS:

• Gram stain on direct smears of exudate or histologic sections
• Culture of nasal passage wash

 

DIFFERENTIAL DIAGNOSIS:

Pericarditis in the guinea pig:  

• S. equi subsp. zooepidemicus (also causes bilateral suppurative lymphadenitis of the cervical lymph nodes, see H-B02, “cervical lymphadenitis” or “lumps”)
• Salmonella spp.
• Klebsiella pneumoniae (see P-B13)
• Pasteurella multocida 

 

Respiratory infection in the guinea pig:  

 

COMPARATIVE PATHOLOGY:

• Bacterial endocarditis: Often valvular; acute valvular endocarditis can be caused by many bacterial species, including Streptococcus sp., Staphyloccus sp, Escherichia coli, and more species-specific bacteria, e.g. Trueperella pyogenes (most common cause in cattle), Erysipelothrix rhusiopathiae (most commonly isolated in pigs), Actinobacillus equuli (horse), Bartonella spp. (dogs, cats), 
• Fibrinous pericarditis: caused by hematogenous spread of the following agents; chronicity in cattle and pigs can lead to constrictive pericarditis with compensatory myocardial hypertrophy and heart failure

• Cattle: Pasteurella multocida, Clostridium chauvoei, Mycoplasma mycoides subsp. mycoides, and as a component of neonatal coliform infections
• Swine: P. multocida, Mycoplasma hyopneumoniae or as part of Glasser’s disease (Glaeserella parasuis, similar to disease due to Streptococcus suis and Mycoplasma hyorhinus)
• Sheep: P. multocida
• Equine: Mycoplasma felis or Streptococcus spp.

• Meningitis/leptomeningitis (see N-B08): In many animal species, meningitis is most commonly caused by hematogenous dissemination of bacteria like E. coli and Streptococcus sp.; Streptococcus pneumoniae is the most common cause of bacterial meningitis in nonhuman primates, and is also reported in guinea pigs, rabbits, horses, cattle, rats, dogs, and cats
• Bronchopneumonia (see P-B07):  Streptococcus pneumoniae is a major cause of bronchopneumonia in nonhuman primates especially secondary to viral infection (e.g. human metapneumovirus, parainfluenza-3, and human respiratory syncytial virus in gorillas and chimpanzees), and can be carried subclinically on the nasopharyngeal mucosa; it also causes pneumonia in rats, guinea pigs, hamsters, ferrets, mink, and foals; pleuritis with bronchopneumonia is common; the bacteria may cause acute primary disease but it is also an important secondary invader; bronchopneumonia may be followed by development of lesions in other organs (e.g. arthritis, meningitis)
• Polyserositis in ducks and other waterfowl:  Reimerella anatipestifer, a Gram-negative bacillus, causes septicemia in waterfowl resulting in exudative and fibrinous polyserositis, sinusitis, bronchopneumonia, and myocarditis; bacteria may be found extracellularly or in macrophages
• In a retrospective study of streptococcal infections in 54 baboons, the most common isolate in the lungs and air sacs was Streptococcus pneumoniae; 16 baboons had staphylococcal meningitis and half of these had concurrent lower respiratory disease (Davis, Vet Pathol. 2020)

 

REFERENCES:

1. Barthold SW, Griffey SM, Percy DH. Pathology of Laboratory Rodents & Rabbits. 4th ed. Ames, IA: Blackwell Publishing Ltd; 2016:144-145,186,230.
2. Davis KL, Gonzalez O, Kumar S, Dick EJ, Jr. Pathology Associated With Streptococcus spp. Infection in Baboons (Papio spp.). Vet Pathol. 2020;57: 714-722.
3. Fenton H, McManamon R, Howerth EW. Anseriformes, Ciconiiformes, Charadriiformes, and Gruiformes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. San Diego, CA: Elsevier; 2018: 708.
4. Gal A, Castillo-Alcala F. Cardiovascular System, Pericardial Cavity, and Lymphatic Vessels, In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:677-678.
5. Lowenstine LJ, McManamon R, Terio KA.  Apes.  In: Terio KA, McAloose D, St. Leger J, eds.  Pathology of Wildlife and Zoo Animals.  San Diego, CA: Elsevier; 2018:387, 392.
6. Lowenstine LJ, Osborn KG. Respiratory Diseases of Nonhuman Primates. In: Abee CR et al, eds.  Nonhuman Primates in Biomedical Research, Volume 2: Diseases. San Diego, CA: Academic Press; 2012:452-453.
7. Matz-Rensing K, Lowenstine LJ.  New world and old world monkeys.  In: Terio KA, McAloose D, St. Leger J, eds.  Pathology of Wildlife and Zoo Animals.  San Diego, CA: Elsevier; 2018:363, 364.
8. Miller AD, Porter BF. Nervous system. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 7^th ed. St. Louis, MO: Mosby Elsevier; 2022: 924-925.
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, MO: Elsevier; 2016:25-28.
10. Simmons J, Gibson S. Bacterial and Mycotic Diseases of Nonhuman Primates. In: Abee CR et al, eds.  Nonhuman Primates in Biomedical Research, Volume 2: Diseases. San Diego, CA: Academic Press; 2012:107-109. 

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