5-week-old male Yorkshire cross, (Sus scrofa domestics).Three days before submission, the piglet became listless, developed a head tilt, ataxia, hind limb paresis and was circling. The piglet was treated with oral meloxicam and subcutaneous ceftiofur. On the day of submission, the piglet was recumbent with generalized muscle tremors. Additional piglets in this litter were less severely affected; however, one additional piglet from this litter was submitted for necropsy 2 days later with a similar clinical history.
There are small, multifocal, perivascular white to tan plaques on the surface of the cerebral cortex.Â The lateral ventricles are moderately dilated and contain light yellow, clear fluid.
Brain: Within the parenchyma and surrounding vessels around the ventricle, there are low to moderate numbers of lymphocytes, macrophages, plasma cells, neutrophils and few eosinophils.Â Low numbers of neutrophils, lymphocytes, plasma cells and macrophages infiltrate the ependymal layer, which is disorganized, as well as the underlying parenchyma.Â The parenchyma surrounding the ventricle is edematous, and blood vessels with perivascular cuffs are lined by plump endothelial cells.Â The leptomeninges multifocally contain few to low numbers of lymphocytes, fewer macrophages and rare eosinophils and neutrophils.Â The ventricular lumen contains aggregates of fibrin, moderate numbers of neutrophils and macrophages, few multinucleated giant cells and rare eosinophils.Â Occasionally admixed with inflammatory cells and fibrin are Gram-positive cocci that are multifocally arranged in short chains.
Brain: Meningoencephalitis and ventriculitis, neutrophilic, lymphohistiocytic and eosinophilic to pyogranulomatous, subacute, multifocally extensive, moderate, with intralesional gram-positive cocci.
The cause for the neurologic signs was a meningoencephalitis that was localized primarily around and within the ventricles and choroid plexus.Â Multifocally within the ventricles, there were occasional clusters of intralesional gram-positive cocci arranged in short chains.Â Aerobic bacterial culture of the brain yielded Streptococcus sues, confirming suspicion of a streptococcal infection.Â The distribution of the inflammation was similar to what is described in association with this bacterium,(13) although the presence of multinucleated giant cells and eosinophils has not been reported within cases of streptococcal meningoencephalitis.Â This may speculatively have been due to an unusual serotype of the bacterium or an unidentified co-infection.Â The lesions in the other piglet submitted from this group the following week were similar.Â
Streptococcus suis is a gram-positive, facultative anaerobic, Î±-hemolytic streptococcus belonging to Lancefield group D.(3,11) More than 30 serotypes have been identified, and most infections in pigs in most countries are caused by serotype 2.(3) Disease is mainly seen in weanlings and growing pigs, with incidence peaking at weaning, and may include septicemia, serositis, meningitis, polyarthritis, pneumonia, abortions, abscesses and endocarditis.(3,11)
Outbreaks of S.Â suis generally have low morbidity and mortality ranging from 0-20%, depending on treatment.(11) Carriers are significant factors in disease transmission, and outbreaks may occur in closed herds.(11) Stress can predispose to infection, and concurrent infections increase morbidity.(11)
Cerebrum, lateral ventricle: Ventriculitis and paraventriculitis, fibrinosuppurative, granulomatous and eosinophilic, with mild to moderate meningitis and intra-ventricular and intra-neutrophilic gram-positive cocci.
Streptococcus species are catalase-negative, opportunistic pathogens affecting multiple organ systems in various species.Â They are generally categorized on the basis of their hemolytic pattern on blood agar as Î±, Î² or Î³ (non)-hemolytic.Â Î±- and Î³-hemolytic streptococci are often normal inhabitants of the upper respiratory and lower urinary tracts, as well as the skin and gastrointestinal tract, while pathogenic species are usually Î²-hemolytic.Â Streptococcus species can be further designated into Lancefield groups A-V (excluding I and J) based on their cell wall polysaccharides.(5) S.Â suis, considered one of the most important bacterial pathogens of swine, has several important virulence factors, including its capsular polysaccharide and virulence-related proteins such as muramidase-released protein, extracellular protein factor and hemolysin.Â Hemolysin (or suilysin), is thought to enhance bacterial invasion and lysis of host cells.Â Suilysin is expressed by many strains of S.Â suis and has been associated with high virulence.(14)
There are several Streptococcus species of veterinary importance in addition to S.Â suis.Â S.Â canis infection in neonatal and adult dogs (and less commonly cats) has been associated with pneumonia, abortion, septicemia, endocarditis, necrotizing fasciitis, keratitis, lower urinary tract infections, cholangiohepatitis, prostatic abscesses, mastitis, arthritis and meningoencephalitis.(5) S.Â equi subsp.Â equi causes equine strangles, a contagious infection of the upper respiratory tract and local lymph nodes;(12) it has also been linked with immune mediated vasculitis and purpura hemorrhagic a.(7) S.Â equi subs.Â zooepidemicus and S.Â equisimilis are associated with equine reproductive disease, but have also been isolated from the lung, liver, brain, kidney and joints.(8,12) S.Â equi subs.Â zooepidemicus also causes bursitis or fistulous withers in horses,(7) and was implicated in an outbreak of acute hemorrhagic pneumonia in more than 1,000 shelter dogs in California.(2) S.Â agalactiae (and less commonly S.Â dysgalactiae and S.Â uberis) are important causes of bovine mastitis.(9) S.Â iniae is a significant aquatic pathogen of tilapia and other reef fish, which causes necrosis, inflammation and vasculitis.(4) Furthermore, several species of Streptococcus are zoonotic, including S.Â can is,(5) S.Â equip sub.Â zooepidemicus,(12) S.Â iniae(4) and S.Â suis.(11,14)
Conference participants outlined several potential causes for the gross and histologic lesions associated with S.Â suis in swine.Â The fibrinous polyserositis often noted grossly at necropsy(11) could also occur secondary to Hemophilus parasuis or Mycoplasma hyorhinus infection.(1) Ruleouts for the microscopic lesions of meningoencephalitis and ventriculitis include salt toxicity, edema disease and postweaning multisystemic wasting syndrome (PMWS).Â Salt toxicity is characterized by cortical laminar necrosis/malacia with eosinophilic meningoencephalitis.(7) Shiga-toxin producing E.Â coli (STEC), the etiologic agent of porcine edema disease, induces fibrinoid vascular change and necrotizing vasculitis with subsequent edema in various tissues, including the brain.(6) Cerebellar spongiosis, necrotizing vasculitis, edema and hemorrhage are occasionally described in conjunction with porcine circovirus type 2 and PMWS.(10) However, as noted by the contributor, the ventricular localization and fibrinosuppurative character of the lesions in this case are fairly specific for S.Â suis.(11)
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