JPC SYSTEMIC PATHOLOGY
URINARY SYSTEM
November 2023
U-B08
SIGNALMENT (JPC #2243999): Chinook salmon (Oncorhynchus tshawytscha)
HISTORY: Tissue from a chinook salmon.
HISTOPATHOLOGIC DESCRIPTION: Caudal mesonephric kidney: Multifocally separating and surrounding uriniferous tubules and glomeruli and expanding and replacing hematopoietic tissue are dense aggregates of epithelioid macrophages admixed with fewer lymphocytes, neutrophils, eosinophilic cellular and karyorrhectic debris (lytic necrosis), and rare aggregates of dark basophilic fragmented mineral. Numerous macrophages contain myriad intracytoplasmic, 1-2 µm coccobacilli. Multifocally, the tubular epithelium multifocally exhibits one or more of the following changes: hypertrophy with pale vacuolated cytoplasm (degeneration); shrunken with hypereosinophilic cytoplasm and fragmented pyknotic or karyolytic nuclei (necrosis); or piling up with a high nuclear to cytoplasmic ratio, hyperchromatic nuclei and cytoplasmic basophilia (regeneration). Multifocally, tubule lumina occasionally contain sloughed epithelial cells, necrotic debris, erythrocytes, and macrophages (granular or cellular casts). Diffusely and globally, glomerular capillary basement membranes are expanded up to twice normal width and are eosinophilic and hyalinized (suggestive of membranous glomerulonephropathy). Frequently there is hypertrophy and hyperplasia of the visceral and parietal epithelia of Bowman’s capsule, and occasionally, the visceral epithelium is adhered to Bowman’s capsule (synechia).
Liver: Affecting approximately 90% of the liver, hepatic cord architecture is lost and replaced by extensive multifocal to coalescing areas of eosinophilic cellular and basophilic karyorrhectic debris (lytic necrosis) admixed with neutrophils, macrophages, fibrin, edema, and hemorrhage. There is dissociation of individual hepatocytes, and sinusoids are expanded by fibrin and edema. Numerous macrophages contain myriad intracytoplasmic, 1-2 µm coccobacilli. There are multifocal to coalescing areas of fibrosis and few round to oval poorly defined granulomas.
Heart: There are multifocal to coalescing areas of myofiber degeneration and necrosis throughout the myocardium. Degenerate myofibers are swollen, pale, and vacuolated with loss of normal myofiber architecture. Areas of necrosis are characterized by replacement of myofibers with eosinophilic cellular and karyorrhectic debris (lytic necrosis), abundant fibrin, edema, and hemorrhage. Areas of necrosis also contain many macrophages which often contain abundant intracytoplasmic, 1-2 µm coccobacilli; fewer neutrophils are admixed.
Gill; skin: No significant findings.
MORPHOLOGIC DIAGNOSIS: 1. Caudal mesonephric kidney: Nephritis, interstitial, necrotizing and histiocytic, multifocal to coalescing, severe, with intrahistiocytic coccobacilli, tubular necrosis and regeneration, and membranous glomerulonephropathy, Chinook salmon, piscine.
2. Liver: Hepatitis, necrotizing and histiocytic, multifocal to coalescing, severe, with intrahistiocytic coccobacilli.
3. Heart: Myocarditis, necrotizing and histiocytic, multifocal, moderate, with intrahistiocytic coccobacilli.
ETIOLOGIC DIAGNOSIS: Renibacterial nephritis
CAUSE: Renibacterium salmoninarum
CONDITION: Bacterial kidney disease (BKD), Spawning rash; Dee disease
GENERAL DISCUSSION:
- Renibacterium salmoninarum: Gram-positive, 0.5 x 1.0-2.0 µm, coryneform-like rod-shaped bacteria
- Obligate pathogen of salmonids; important pathogen of cultured salmon but seen in wild populations as well
- Salmon can be affected at any age, but losses most often in 6 to 12-month-old juveniles and pre-spawning adults; infection associated with reduced growth in juveniles
- Pacific salmon species are most susceptible; Atlantic salmon are more resistant
PATHOGENESIS:
- Transmission
- Horizontal via contaminated water, skin abrasions, ingesting, contamination of wire tags (in tagged salmon)
- Vertical transmission via infected eggs
- Intraovum infection before ovulation or infection of ovulated egg by peritoneal fluid both possible
- Demonstrated in both salt water and fresh water
- Disease is chronic but stress (spawning, freshwater to seawater move) may trigger acute disease
TYPICAL CLINICAL FINDINGS:
- Epidemics during declining water temperatures (fall, winter)
- Acute mortality during times of stress
TYPICAL GROSS FINDINGS:
- External signs may be absent
- Dark coloration, exophthalmos, pale gills, abdominal distension, hemorrhages at vent or base of fins, fluid-filled vesicles on the flanks
- Kidney (target organ), spleen, other viscera: White nodular masses
- Pseudo-diphtheritic membrane covering abdominal viscera (usually at temperatures below 50°F)
- Large cavitations in skeletal muscle (less common)
- “Spawning rash” – Dermal infection resulting in vesicles on the flanks that rupture to form small ulcers
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Granulomas: Focal, often large; comprised of macrophages containing phagocytosed bacteria
- Encapsulated in relatively resistant species (Atlantic Salmon)
- Unencapsulated in more susceptible species (Pacific salmon)
- Caseous necrosis with free bacteria in advanced lesions
- Chronic interstitial nephritis
ADDITIONAL DIAGNOSTIC TESTS:
- Tissue smears (Gram stain) for presumptive identification of bacteria
- Histology: Presumptive identification, should be paired with antibody or gene probe for confirmation
- Culture: Slow-growing (3-6 weeks) and requires special medium and temperature control within a narrow range (59°F-64°F)
- Serology: ELISA, fluorescent antibody testing (used in conjunction for screening)
- PCR
DIFFERENTIAL DIAGNOSIS:
- Small gram-positive bacteria that cause pseudokidney disease
- Carnobacterium pisciola (aka Lactobacillus pisciola), Lactococcus piscium, Vagococcus salmoninarum,
- Easily differentiated based on their growth at 86°F on commercially-available media
- Rhodococcus spp.
- Can cause kidney granulomas in Atlantic slamon
- Mycobacerium spp.
- Can cause similar lesions
- Acid-fast positive
- Nocardiosis (N. asteroides, N. seriolae) and fungi (Ichthyophonus hoferi) can also cause granulomas
Reference:
Noga EJ. Fish Disease: Diagnosis and Treatment. 2nd ed. Ames, IA: Wiley Blackwell; 2010: 201-208.
