A commercial red tilapia farm was diagnosed with Streptococcus agalactiae infection using histopathology, microbiology and immunohistochemistry. One hundred fish were randomly taken from different weight/age groups including broodstock, market fish (larger than 150 g), on-growing fish between 20 and 150 g, juveniles and larvae. Fish were clinically examined, anaesthetised and necropsied. Samples were taken from brain, liver, spleen, eyes and kidney for microbiology. All organs were processed for histopathology and an indirect immunoperoxidase test (IIP). Organs from wild fish and birds found in close proximity to the farm were also sampled for microbiology and IIP. The prevalence of lesions or infection found by IIP, histopathology and microbiology was 16%, 29% and 7% respectively. Clinical disease, lesions or infection were not seen in larvae or juveniles. By contrast, infection and disease were found in fish larger than 20 g, suggesting that the condition was linked to the intensive culture conditions of broodstock, on-growing and market fish. S. agalactiae was not found in wild fish, or in birds, by microbiology and IIP.

Streptococcus agalactiae causes a severe systemic disease in fish, and the routes of entry are still ill-defined. To address this issue, two groups of 33 red tilapia Oreochromis spp. each of 10 g were orally infected with S. agalactiae (n = 30), and by immersion (n = 30), six individuals were control-uninfected fish. Three tilapias were killed at each time point from 30 min to 96 h post-inoculation (pi); controls were killed at 96 h. Samples from most tissues were examined by haematoxylin-eosin (H&E), indirect immunoperoxidase (IPI) and periodic acid-Schiff; only intestine from fish infected by gavage was evaluated by transmission electron microscopy. The results of both experiments suggest that the main entry site of S. agalactiae in tilapia is the gastrointestinal epithelium; mucus seems to play an important defensive role, and environmental conditions may be an important predisposing factor for the infection.

The distribution of antigen and pathological changes induced by an experimental infection with Aeromonas hydrophila strain KJ99, and its extracellular products, were studied in two species of fish. The microorganism was disseminated systemically and the haemodynamic and tissue changes were similar to those observed in septicaemia of mammals. Intussusception, degeneration and necrosis of the nervous plexus and muscular layers of the gastrointestinal tract were common findings.

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The histological lesions caused by Edwardsiella tarda in a variety of fish species, including tilapia, have been well characterized. There are apparent differences in the type of inflammatory response manifested by these different species, which may be due to the fish species itself, the phase of infection, or the virulence factors produced by different strains of E. tarda. In catfish, systemic abscesses involving muscles of the flank or caudal peduncle are the most common lesions. By contrast, infection in tilapia and red sea bream is more likely to be associated with granulomatous inflammation. Necrotic meningitis, encephalitis, and vasculitis with fibrinoid necrosis of the blood vessels walls, as well as the formation of a plaque-like structure in the brain, are described in the current study. The presence of E. tarda was confirmed by microbiological isolation and a positive nested polymerase chain reaction in paraffin wax-embedded tilapia tissues.

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Abstract. Rickettsial organisms are well-known fish pathogens in both natural and culture environments. This study reports an outbreak of disease in red tilapia larvae caused by piscirickettsia-like organisms (PLOs), which lasted from June until October 2009. Severe mortality was recorded almost exclusively in larvae and postlarvae aged 1-22 days old. Although clinical or gross findings were not evident in diseased fish, histopathology revealed severe necrosis of the epidermis and gill epithelium, with concomitant changes in the underlying skeletal muscle as being the most relevant microscopic lesions. Although PLOs were visible with the routine hematoxylin eosin technique, they were better observed with Giemsa and toluidine blue stains. Transmission electron microscopy revealed that the bacterium was located within the cytoplasm and phagolysosoma-like structures of epithelial cells from the gills and the skin. The bacteria measured 0.9 6 0.2 mm 3 2.1 6 0.6 mm and had a double cell membrane (the outer one having undulating projections), with variable electron-dense and electron-lucent areas. Ultrastructurally, abundant myelin figures surrounded the microorganisms within host cell cytoplasm. Results indicated that Piscirickettsia-like organisms can cause massive epithelial cell damage associated with concomitant alteration of the electrolyte balance.