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Characterization of Histopathological and Ultrastructural Changes in Channel Catfish Experimentally Infected with
Hossam Abdelhamed1, Iman Ibrahim1,2, Wes Baumgartner3
1Department of Basic Sciences, College of Veterinary Medicine, Mississippi State University, StarkvilleMS, United States.
Insights
Highly virulent Aeromonas hydrophila (vAh) rapidly caused severe tissue damage and inflammation in channel catfish organs. This study details the histopathological and ultrastructural changes following vAh infection in fish.
Area of Science:
- Aquatic Animal Health
- Fish Pathology
- Bacterial Disease Research
Background:
- Motile Aeromonas septicemia, caused by Aeromonas hydrophila (vAh), is a significant epizootic in channel catfish.
- The pathology of vAh-induced disease in channel catfish requires further investigation.
Purpose of the Study:
- To investigate the histopathological and ultrastructural alterations in channel catfish challenged with virulent Aeromonas hydrophila (vAh).
Main Methods:
- Channel catfish fingerlings were exposed to vAh (strain ML09-119) via bath challenge.
- Fish were sampled at various time points (1-48 hours post-challenge) for light microscopy and transmission electron microscopy (TEM).
Main Results:
- Early lesions (spleen, stomach) observed at 1 hour post-challenge (HPC); widespread organ damage (intestine, gills, kidney, liver) by 24-48 HPC.
- TEM revealed extensive tissue destruction, bacterial outer membrane vesicle secretion, and bacterial presence in phagosomes.
- Unique findings include degranulated eosinophilic granular cells and dendritic cell-like (DC-like) cells in necrotic intestinal epithelium.
Conclusions:
- Virulent Aeromonas hydrophila rapidly proliferates and disseminates throughout channel catfish organs post-infection.
- The study provides critical insights into the pathogenesis of vAh in channel catfish.
Abstract:
A highly virulent clonal population of Aeromonas hydrophila (vAh) has been the cause of recent motile Aeromonas septicemia epizootic in channel catfish (Ictalurus punctatus) farms in the Southeastern United States. The pathology of the disease caused by vAh has not been studied well yet. Thus, our aim was to determine histopathological and ultrastructural changes in channel catfish following vAh challenge. To accomplish this, catfish fingerlings were challenged with vAh (strain ML09-119) by bath. Six fish per each time point were collected at 1, 3, 5, 6, 24, and 48 h for light microscopy, and six fish were collected at 48 h for transmission electron microscopy (TEM). The first pathological lesions were detected in the spleen and stomach at 1 h post-challenge (HPC) while intestine, gills, kidney, and liver lesions were observed at 24 and 48 HPC. Histopathological examination revealed degenerative changes, necrosis, extensive edema, and inflammation in internal organs. The TEM showed severe tissue destruction with multiple bacterial cells secreting outer membrane vesicles, especially in spleen and gills and far number in the stomach. Degenerated bacterial cells were observed in the intestinal lumen and the phagosomes of phagocytic kidney cells. We identified, for the first time, degranulate eosinophilic granular cells, and dendritic cells like (DC-like) cells in the necrotic intestinal epithelium. These findings suggest that vAh rapidly proliferated and spread through the catfish organs following bath challenge.
