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Seven alligators were submitted to the Tifton Veterinary Diagnostic and Investigational Laboratory for necropsy during two epizootics in the fall of 2001 and 2002. The alligators were raised in temperature-controlled [...]

Primers were used to amplify a 561-bp region of the 16S rRNA gene of Ehrlichia phagocytophila from Ixodes scapularis ticks and small mammals collected in Rhode Island and Connecticut. DNA [...]

The article presents a research on the myxozoan parasite Henneguya ictaluri that caused the proliferative gill disease (PGD) in channel catfish Ictalarus punctatus. It notes that the extensive gill damage was caused by prolonged exposure of channel catfish to the actinospore stage of the parasite, resulting to reduced production and significant mortality in commercial operations. Findings showed that increases in parasite load correlated with percent mortality in sentinel fish, as did increases in mean actinospore concentrations. It is believed that both applications are more rapid than current protocols for assessing the PGD status of a catfish pond and identified actinospore levels that correlate to both high and low risk of fish loss.

Primers were used to amplify a 561-bp region of the 16S rRNA gene of Ehrlichia phagocytophila from Ixodes scapularis ticks and small mammals collected in Rhode Island and Connecticut. DNA sequences for all 50 E. phagocytophila-positive samples collected from 1996 through 1998 in southwestern Connecticut were identical to the sequence reported for E. phagocytophila DNA from confirmed human cases. In contrast, the sequences from 92 of 123 E. phagocytophila-positive Rhode Island samples collected from 1996 through 1999 included several variants differing by 1-2 nucleotides from that in the agent infecting humans. While 11.9% of 67 E. phagocytophila-positive ticks collected during 1997 in Rhode Island harbored ehrlichiae with sequences identical to that of the human agent, 79.1% had a variant sequence not previously described. The low incidence of human ehrlichiosis in Rhode Island may in part result from interference by these variant ehrlichiae with maintenance and transmission of the true agent of human disease. [ABSTRACT FROM AUTHOR]

Presents information on the piscirickettsia salmonis, which is the first of the previously unrecognized rickettsial pathogens of fish to be fully characterized. Reference to the impact of rickettsial pathogens in fish becoming more apparent since the recognition of P. Salmonsin in 1989.

Proliferative gill disease (PGD) in channel catfish Ictalurus punctatus is caused by the myxozoan parasite Henneguya ictaluri. There is no effective treatment for PGD, and mortalities can exceed 50% in severe outbreaks. One approach to controlling losses would be to utilize a less susceptible ictalurid species in pond culture; alternatively, one could identify the traits that convey resistance and exploit them in a selective breeding program. Challenge studies have found less severe inflammatory responses in the gill tissue of blue catfish I. furcatus and fewer mortalities than in channel catfish. However, it remains unclear whether infection and subsequent plasmodial development progress the same way in the two species. To investigate this, we compared the dynamics of H. ictaluri infection in blue catfish, channel catfish, and channel catfish x blue catfish hybrids in continuous long-term (5-7-d) and short-term (24-h) pond challenges. After long-term challenge, 66.2% of the channel catfish and 63.6% of the hybrid catfish developed characteristic PGD lesions, compared with 3.7% of the blue catfish. Quantitative polymerase chain reaction analysis detected H. ictaluri in larger percentages of channel and hybrid catfish than blue catfish (98.7% and 95.7% versus 45.9%), with significantly greater parasite DNA equivalents in channel and hybrid catfish than blue catfish. Similar findings were obtained in the short-term exposures. Histologically, channel and hybrid catfish developed severe PGD accompanied by large numbers of developing plasmodia. While mild PGD was observed in some blue catfish, the progression of lesions lagged behind that in channel and hybrid catfish. Most importantly, developing plasmodia were not observed in blue catfish, and parasite DNA was not detected 14 d after removal from the source of infection. Our findings indicate that the resistance of blue catfish to H. ictaluri infection can be overcome by large numbers of infective actinospores but that infection appears to be eliminated before plasmodial development occurs.

This report details findings of an investigation into complaints by commercial fingerling producers of low-grade mortalities, poor reproductive success, emaciation, skin lesions, and severely arched backs among broodstock of channel catfish Ictalurus punctatus. Gross lesions involved the jaw, fin bases, and vertebral column. Jaw and fin lesions consisted of small hemorrhagic ulcers and exudate-filled tracts that communicated with underlying joints and destroyed their articular surfaces. Spinal changes, recognized grossly by severe arching of the proximal vertebral column, resulted from the collapse and displacement of vertebral bodies, causing compression of the spinal cord. Affected vertebrae were lysed by pyogranulomatous inflammation that infiltrated into adjacent muscle and the spinal canal. A Streptococcus-like organism was visualized in exudate and isolated repeatedly from lesions, but only once from the kidney of a single fish. Preliminary analysis of a 16S ribosomal DNA sequence showed a close relationship to S. iniae, S. parauberis, and S. canis. Koch's postulates were fulfilled after challenge with and reisolation of the agent from identical lesions that appeared at fin bases at 2 weeks postinjection. Historical evidence and gross and microscopic findings imply the presence of a pathogen of low virulence that is capable of producing severe localized infections after a brief period of septicemia. The disease presents as a chronic debilitating syndrome that is sufficient to inhibit mobility, feeding, and reproductive activity in affected fish. Complete biochemical and molecular characterization of the bacterium (published elsewhere) has established the agent as a novel species, S. ictaluri.

Tilapia are cultured worldwide and are increasing in popularity among aquaculturalists in the United States; however, data regarding normal health parameters are limited. Few hematologic and plasma biochemical values of clinically normal tilapia have been reported, but these data may be key for identifying and managing disease issues in recirculating systems. Therefore, blood was collected from clinically normal hybrid tilapia (Oreochromis aureus x Oreochromis nilotica) housed in recirculating systems for the purpose of establishing normal hematologic and plasma biochemical reference ranges. Using standard clinical techniques the following hematologic values were determined: packed cell volume, plasma protein, leukocyte counts, leukocyte differentials, and thrombocyte counts. Additionally, the following plasma biochemical values were determined: albumin, total protein, globulins, albumin/globulin ratio, aspartate aminotransferase, alkaline phosphatase, glucose, uric acid, calcium, phosphorus, magnesium, sodium, potassium, chloride, urea nitrogen, and creatinine. The condition of the sample was also noted (lipemic, hemolysis, and icterus). The reference ranges reported in this study can be used in the management of cultured tilapia in recirculating systems.

In 1994, tilapia (Oreochromis mossambicus and Sarotherodon melanotheron) in wild and farmed populations on Oahu, Hawaii, USA, began to die of an unknown disease that was similar but not identical to piscirickettsiosis in salmonids. Only tilapia were affected. Diseased tilapia often swam erratically and had trouble staying at depth. Scattered cutaneous haemorrhage and exophthalmia were often noted. In many cases, fish were found dead with no clinical signs. Gills exhibited epithelial hyperplasia with severe multifocal consolidation of secondary lamellae. Multiple granulomas were observed in the gills, spleen, kidney, choroid gland and testes, but not in the liver. Tilapia mortalities occurred only during the cooler months (October to April) of the year and were not recorded during the warmer months (May to September). The mortalities declined with each successive year, after the 1994 outbreak, and currently losses are sporadic. Oxytetracycline-medicated feed reduced mortality. Cytologic examination of blood smears revealed moderate to large numbers of Gram-negative, pleomorphic, intracellular bacteria in rare circulating monocytes. Histologically, some predilection for nervous tissue and brain was observed. When viewed with transmission electron microscopy, pleomorphic coccoid bacteria, measuring 0.56 +/- 0.14 x 0.7 +/- 0.20 microm, occurred free in the cytoplasm and within phagolysosomes. The organisms had a double cell wall, no defined nucleus and variable electron-dense and -lucent areas. Unlike Piscirickettsia salmonis, the agent of piscirickettsiosis, the Hawaiian tilapia Piscirickettsia-like organism (HTPLO) does not form craterform lesions in the liver and is active above 20 degrees C. HTPLO can be transmitted horizontally by cohabitation, and cold stress induces the syndrome in juvenile tilapia from farms where the disease is endemic.