JPC SYSTEMIC PATHOLOGY
SIGNALMENT (JPC # 2132377): A foal
HISTORY: This foal died acutely.
HISTOPATHOLOGIC DESCRIPTION: Kidney: Multifocally and randomly, centered on and effacing glomeruli within the cortex, are numerous 250-500um microabscesses that occasionally extend into the adjacent interstitium, tubules and vessels, as well as into the medulla. Microabscesses are composed of abundant eosinophilic cellular and karyorrhectic debris (necrosis) admixed with numerous degenerate and nondegenerate neutrophils, fewer macrophages, lymphocytes, plasma cells, fibrin, hemorrhage, edema and large colonies of basophilic, 1x2um coccobacilli. Renal tubules are multifocally, mildly ectatic and renal tubular epithelium has one or more of the following changes: degeneration characterized by swollen and vacuolated cytoplasm, necrosis characterized by hypereosinophilic cytoplasm and shrunken pyknotic nuclei; tubule lumina contain variable amounts of debris and proteinaceous fluid. Multifocally, blood vessels are lined by moderately hypertrophied (reactive) endothelial cells and the interstitium is congested with multifocal areas of hemorrhage. Diffusely, the capsule is expanded up to 500um by fibrin, edema, hemorrhage and small numbers of lymphocytes, plasma cells, fewer macrophages and rare neutrophils.
MORPHOLOGIC DIAGNOSIS: Kidney: Nephritis, embolic, suppurative, subacute, multifocal, moderate, with large colonies of coccobacilli and tubular degeneration and necrosis Thoroughbred, equine
ETIOLOGIC DIAGNOSIS: Renal Actinobacillosis
CAUSE: Actinobacillus equuli
CONDITION: Sleepy foal disease; septicemia of foals; navel-ill; joint-ill
- Gram negative, nonsporulating coccobacilli that causes an acute, highly fatal septicemia of newborn foals
- Two subspecies based on RTX toxin genotype (Aqx – equuli toxin): A. equuli subsp haemolyticus contains this RTX and A. equuli subsp equuli does not
- The higher isolation rates of equuli subsp equuli over A. equuli subsp haemolyticus from septicemic cases indicates other virulence factors play a major role in the pathogenesis
- Most common cause of embolic suppurative nephritis of foals
- Worldwide distribution with high mortality, decreasing incidence
- Normal inhabitant of the adult horse respiratory, alimentary and genitourinary tracts
- Transmission can occur in utero or at partuition, but postnatal infection is most common (likely via the umbilicus)
- Bacilli may persist as an endogenous non-symptomatic focus and cause successive abortions in mares
- Bacteremia results in showers of septic emboli that frequently lodge in small capillaries, particularly in the glomerular tufts
- Causes multiple microabscesses throughout the renal cortex; necrosis often obliterates the glomeruli; microabscesses in other organs and polyarthritis
- Prematurity, failure of passive transfer, dam malnutrition, unsanitary birthing conditions, and environmental stress can be predisposing factors to septicemia and death
- equuli is present in the oral and alimentary cavity of healthy animals and also as an opportunist in pathological tissues, i.e. verminous thrombosis (Strongyles)
- Aqx (RTX-type toxin) – ApxI is most potent
- At low concentrations, toxin interferes with macrophage and neutrophil function by triggering degranulation
- At higher concentrations, toxin is cytolytic for macrophages, erythrocytes, neutrophils and alveolar epithelial cells
- LPS endotoxin damages endothelium causing a vasculitis and thrombosis
TYPICAL CLINICAL FINDINGS:
- Fever, prostration and diarrhea
- Inability to stand and/or nurse
- Swollen, hot, and painful joints
- Most infected foals die within the first three days after birth
- Clinical Pathology
- Leukopenia with a severe left shift
- Hyperfibrinogenemia (if infected in utero)
- Low plasma IgG
TYPICAL GROSS FINDINGS:
- Acute death: No lesions
- 1-2 days: Severe enteritis
- 3-4 days:
- Kidney: Multiple cortical green-yellow foci, of up to 3 mm diameter that contain a droplet of pus, and are uniformly distributed; medulla may contain hemorrhages, but usually no foci
- Joints: Fibrinopurulent polyarthritis and polysynovitis
- Viscera: Multiple small (up to 3 mm) abscesses
- Hemorrhagic pneumonia
- Peritonitis and pleuritis
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Kidney: Multiple microabscesses within the cortex (glomerular and intertubular capillaries) with bacterial colonies and variable numbers of neutrophils that may efface glomerular architecture; hemorrhage within the medulla
- Joints: Fibrinopurulent polyarthritis and polysynovitis
- Lungs: Multifocal microabscesses in the interstitium in association with small vessels
- Vessels: Inflammation and presence of large bacterial colonies
ADDITIONAL DIAGNOSTIC TESTS:
- Bacterial isolation (synovial fluid culture is often negative even in infection)
- Failure of passive transfer
Acute septicemia/synovitis/arthritis (due to failure of passive transfer):
- Escherichia coli
- Rhodococcus equi
Embolic suppurative nephritis:
- Horse: Actinobacillus equuli
- Pig: Erysipelothrix rhusiopathiae; Streptococcus ; Corynebacterium sp.
- Cattle: Trueperella pyogenes from valvular endocarditis
- Sheep and goats: Corynebacterium pseudotuberculosis
- Dogs: Prototheca zopfii
Disease-causing Actinobacillus sp.:
- Actinobacillus equuli: Septicemia in foals (occasionally in pigs and calves; rarely adult horses)
- Actinobacillus suis: Septicemia in piglets and fibrinous pericarditis in horses
- Actinobacillus lignieresii: Wooden tongue in cattle
- Actinobacillus seminis: Epididymitis and polyarthritis in lambs
- Actinobacillus capsulatus: Arthritis in laboratory rabbits
- Actinobacillus pleuropneumoniae: Porcine contagious pleuropneumonia
- Actinobacillus salpingitis: Salpingitis and peritonitis in chickens
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