JPC SYSTEMIC PATHOLOGY
Signalment (JPC# POLA-1): Guinea pig
HISTOPATHOLOGIC DESCRIPTION: Cerebrum at the level of the hippocampus and thalamus: Multifocally filling the third ventricle and obscuring ependymal cells as well as expanding the leptomeninges up to 20 um is a dense cellular infiltrate composed of numerous macrophages, lymphocytes, and heterophils admixed with fibrin and proteinaceous fluid (edema). These inflammatory cells often transmurally infiltrate or obscure vessel walls. Multifocally vessels within the leptomeninges and underlying neuropil are congested and often exhibit hypertrophied (reactive) endothelium. The periventricular gray matter around the third ventricle is characterized by increased numbers of glial cells (gliosis), infiltration by rare heterophils, increased pallor of the neuropil (edema), and multifocal vacuolation of the neuropil (spongiosis).
MORPHOLOGIC DIAGNOSIS: Cerebrum: Meningitis, ependymitis, and ventriculitis, fibrinous, heterophilic, and lymphohistiocytic, subacute, multifocal, moderate, guinea pig, Cavia porcellus.
ETIOLOGIC DIAGNOSIS: Streptococcal meningitis
CAUSE: Streptococcus pneumoniae
ETIOLOGY SYNONYMS: Pneumonococcus pneumoniae, Diplococcus pneumoniae
· Important streptococcal (Gram positive) pathogens in guinea pigs:
· S. equi subsp. zooepidemicus (H-B02; beta-hemolytic; Lancefield group B): Cervical lymphadenitis (“lumps”)
· S. pneumoniae (encapsulated diplococci; alpha-hemolytic, do not lyse erythrocytes): Pneumonia and/or meningitis
· Capsular polysaccharide type 19 and type 4 cause disease in guinea pigs; serotypes identical to human isolates- interspecies transmission possible (not proven)
· Normal guinea pigs and nonhuman primates can carry S. pneumoniae in upper respiratory tract asymptomatically
· +/- S. pyogenes (beta-hemolytic, Lancefield group A): Hemorrhagic septicemia (adults in a single colony); necrohemorrhagic and fibrinopurulent pneumonia, metritis, hemopericardium/thorax
· Epizootics typically occur in winter; young animals/pregnant sows at risk
· Other predisposing factors: Changes in temperature, poor husbandry, experimental procedures, inadequate nutrition
· Aerosol transmission > colonizes nasopharynx > ear or lung infection > bacteremia > invades CNS > meningitis
· Virulence factors:
· Polysaccharide capsule is antiphagocytic by forming a hydrophilic gel, which shields from antibodies and complement proteins (don’t produce toxins)
· Several serotypes produce tissue damage by activation of the alternative complement pathway> this may stimulate early tissue changes
TYPICAL CLINICAL FINDINGS:
· Weakness, ataxia, lethargy, anorexia, muscle tremors, flaccid paralysis, clonic seizures, constricted pupils, delayed light reflexes, nystagmus, torticollis
· Dyspnea, nasal/ocular discharge
· Abortion, stillbirth
· Sudden death
TYPICAL GROSS FINDINGS:
· Opaque/hyperemic meninges, accumulation of grayish-yellow fibrinopurulent exudate
· Fibrinopurulent pleuritis, pericarditis, peritonitis, conjunctivitis, lung consolidation with abscessation and hemorrhage, and otitis media
TYPICAL LIGHT MICROSCOPIC FINDINGS:
· Diffuse fibrinous exudate, Gram positive paired cocci, heterophilic, lympoplasmacytic, histiocytic inflammation
· Fibrinopurulent meningitis
· Acute bronchopneumonia with fibrin and polymorphonuclear cell infiltration; elongated/fusiform infiltrating cells forming palisading patterns in airways and alveoli
· +/- Thrombosis of pulmonary vessels in acute cases
· Splenitis, metritis, ovarian abscessation, hepatic necrosis, lymphadenitis
· Suppurative arthritis and osteomyelitis reported in guinea pigs with borderline vitamin C deficiency (M-M07)
ADDITIONAL DIAGNOSTIC TESTS:
· Gram stain
· Culture - isolation of bacteria
· For histologic finding of meningitis in guinea pigs:
· Bordetella bronchiseptica (P-B09): Gram-negative; typically causes suppurative bronchopneumonia but may see meningitis if septicemic
· Streptococcus zooepidemicus (H-B02): Gram positive; typically causes suppurative lymphadenitis but meningitis may be seen if septicemic
· Lymphocytic choriomeningitis (N-V18, arenavirus): Rare; lymphocytic inflammation of the meninges, ependyma, and choroid plexus
· Nonhuman primates: The most common cause of fibrinopurulent meningitis/meningoencephalitis in NHPs is S. pneumoniae; also causes fibrinous pleuropneumonia (P-B07), septicemia, polyserositis, conjuncitivitis/panophthalmitis, peritonitis, sudden death
· Stress, viral infection, and waning neonatal passive immunity predispose infection
· Differential diagnosis for meningitis in non-human primates: Bacillus anthracis (anthrax): Necrohemorrhagic meningitis (“Cardinal’s cap”)
· Neonates: Neonatal bacterial suppurative meningitis (NBSM): Two causes of NBSM are streptococci and E. coli; most common in ruminants and pigs; initial portal of entry may be oral, intrauterine, umbilical, or surgical; steptococcal NBSM in calves, lambs, and piglets (but not foals) frequently manifests with a combination of polyarthritis, purulent leptomeningitis, choroiditis, and (in calves only) endophthalmitis
· In piglets up to 3 weeks of age, S. suis types 1 & 2 are causes of NBSM (also called Streptococcal chorio-meningo-ependymitis)
· S. pneumoniae usually produces fulminant septicemia in calves
· Rat: Outbreaks rare in well-managed facilities; organism carried in nasoturbinates and tympanic bullae of normal rats; typically opportunistic/2o invader; as in guinea pigs, some serotypes isolated from sick rats are the same as those from human cases (zoonotic hazard)
· Fibrinopurulent polyserositis, pleuropneumonia, pericarditis, peritonitis, meningitis, rhinitis, and otitis media +/- embolic suppurative lesions in liver, spleen, kidney
· Hamster: S. pneumonia has been associated with upper respiratory disease, otitis and bronchopneumonia
· Otters: S. lutetiensis sp. nov. causes a fatal meningoencephalitis and infective endocarditis in northern sea otters; S. phocae has been reported to cause meningoencephalitis in Southern sea otters
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