Introduction
As a key aquaculture species in Nigeria, Clarias gariepinus faces disease threats in its production. We studied the pathogenesis and pathology of an Aeromonas hydrophila isolate from a natural outbreak by experimentally infecting adult Clarias gariepinus.
Methods
Aeromonas hydrophila isolated from the dorsal kidney of a dead Clarias gariepinus during a disease outbreak was further propagated in tryptone soy broth. In total, 1 ml of an overnight broth culture of A. hydrophila (1.4x 108 CFU/mL) was inoculated intraperitoneally into adult Clarias gariepinus (n=50). A control group of 10 adult Clarias gariepinus was inoculated with 1 ml sterile saline intraperitoneally. Analyses included haematology, serum protein chemistry, postmortem, histopathology, immunohistochemistry, descriptive (Frequency tables) and inferential statistics (independent t-test).
Results
Aeromonas hydrophila induced a severe, fulminating disease and mortality in experimentally infected fish. Pathology revealed the liver, kidney, and gills to be the primary targets with infected fish exhibiting hepatic vacuolar degeneration, acute nephritis, hyperplasia and fusion of gill secondary lamellae, widespread haemorrhages, and ascites. Key haematological and serum chemistry findings included leukocytosis (WBC 14766.06±2560/µL vs. control 12840.00±199.69/µL), thrombocytopenia (PLT 145151.56±29006.60/µL vs. control 234900.00±47146.23/µL) and hypoalbuminemia (ALB 1.36±0.35 g/dl vs. control 1.85±0.81 g/dl) at 24 hours post-infection in adults. The leukocytosis persisted at day 18; however, hyperglobulinemia was detected (GLB 5.07±0.26g/dl vs. control 4.80±0.35g/dl). Immunohistochemistry confirmed widespread tissue tropism with intense staining for A. hydrophila antigens in the skin and kidneys.
Conclusion
The haematological profile of A. hydrophila at 24 hours is one of acute inflammatory response with marked thrombocytopenia, probably secondary to disseminated intravascular coagulation. The widespread haemorrhages observed could be linked to this pathophysiology. The key findings in the subacute to chronic phase suggest persistent inflammation or immune response. These results demonstrate a complex host–pathogen interaction where A. hydrophila employs cytotoxic virulence factors to cause significant tissue damage and haematological dysregulation.
