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W. K. Vogelbein

Publications and source records attributed to W. K. Vogelbein.

5 recordsLinked to original sources

Mycobacterial infections in striped bass from Delaware Bay

Eighty striped bass Morone saxatilis were obtained from Delaware Bay using commercial gill nets set adjacent to Woodland Beach (n = 70) and Bowers Beach (n = 10) in December 2003. Fish were examined for gross lesions. Total lengths (TLs) and eviscerated weights were determined to calculate condition factors (K). Portions of spleens were aseptically harvested for bacterial culture, and portions of spleens, kidneys (anterior and posterior), livers, and gonads were obtained for histological examination. The size distribution of the striped bass was relatively homogeneous; the mean TL was about 600 mm for all samples. Mean K exceeded 0.95 in all samples and was not significantly different (P > 0.05) among samples. Significant differences in mycobacterial infection prevalence (P ??? 0.05) were observed among samples; samples obtained at Woodland Beach (WB) on December 10 (53.8%, n = 13) and December 17 (7.1%, n = 42) exhibited the most striking differences in prevalence. Mycobacterial infection intensity ranged from 1 ?? 102 to 1 ?? 107 colony-forming units per gram of spleen. Acanthocephalan infection prevalence and intensity, non-acid-fast bacterial infection prevalence, and fish sex ratio were also significantly different among the samples (P ??? 0.05). Similar to the mycobacterial infections, differences in sex ratio, acanthocephalan infection, and non-acid-fast bacterial infection were observed between the WB samples taken on December 10 and 17. However, no significant associations (P > 0.05) were observed between sex ratio or these infections and mycobacterial infection. The differences in bacterial and parasite infection prevalence and intensity and fish sex ratio in some samples indicate that these fish had a different history and that the epizootiology of mycobacterial infection in striped bass from Delaware Bay may be relatively complex. ?? Copyright by the American Fisheries Society 2007.

Journal of Aquatic Animal Health

Experimental mycobacteriosis in striped bass Morone saxatilis

Striped bass Morone saxatilis were infected intraperitoneally with approximately 10 5 Mycobacterium marinum, M. shottsii sp. nov., or M. gordonae. Infected fish were maintained in a flow-through freshwater system at 18 to 21°C, and were examined histologically and bacteriologically at 2, 4, 6, 8, 17, 26, 36 and 45 wk post-infection (p.i.). M. marinum caused acute peritonitis, followed by extensive granuloma development in the mesenteries, spleen and anterior kidney. Granulomas in these tissues underwent a temporal progression of distinct morphological stages, culminating in well-circumscribed lesions surrounded by normal or healing tissue. Mycobacteria were cultured in high numbers from splenic tissue at all times p.i. Standard Ziehl-Neelsen staining, however, did not demonstrate acid-fast rods in most early inflammatory foci and granulomas. Large numbers of acid-fast rods were present in granulomas beginning at 8 wk p.i. Between 26 and 45 wk p.i., reactivation of disease was observed in some fish, with disintegration of granulomas, renewed inflammation, and elevated splenic bacterial densities approaching 10 9 colony-forming units g -1 . Infection with M. shottsii or M. gordonae did not produce severe pathology. Mild peritonitis was followed by granuloma formation in the mesenteries, but, with 1 exception, granulomas were not observed in the spleen or anterior kidney. M. shottsii and M. gordonae both established persistent infections in the spleen, but were present at densities at least 2 orders of magnitude less than M. marinum at all time points observed. Granulomas in the mesenteries of M. shottsii- and M. gordonae-infected fish resolved over time, and no reactivation of disease was observed.

Diseases of Aquatic Organisms

Infectivity and pathogenicity of the oomycete Aphanomyces invadans in Atlantic menhaden Brevoortia tyrannus

Atlantic menhaden Brevoortia tyrannus develop characteristic skin ulcers in response to infection by the oomycete Aphanomyces invadans . To investigate pathogenicity , we conducted a dose response study. Juvenile menhaden were inoculated subcutaneously with 0, 1, 5, 10, 100, and 500 secondary zoospores per fish and monitored for 37 d post-injection (p.i.). Survival rates declined with increasing zoospore dose, with significantly different survivorship curves for the different doses. Moribund and dead fish exhibited characteristic ulcerous lesions at the injection site starting at 13 d p.i. None of the sham-injected control fish (0 zoospore treatment) died. The LD 50 (lethal dose killing 50% of exposed menhaden ) for inoculated fish was estimated at 9.7 zoospores; however, some fish receiving an estimated single zoospore developed infections that resulted in death. Menhaden were also challenged by aqueous exposure and confirmed that A. invadans was highly pathogenic by this more environmentally realistic route. Fish that were acclimated to culture conditions for 30 d, and presumably free of skin damage, then aqueously exposed to 100 zoospores ml -1 , exhibited 14% lesion prevalence with 11% mortality. Net-handled fish that were similarly infected had a significantly higher lesion prevalence (64%) and mortality (64%). Control fish developed no lesions and did not die. Scanning electron microscopy of fish skin indicated that zoospores adhered to intact epidermis, germinated and penetrated the epithelium with a germ tube. Our results indicate that A. invadans is a primary pathogen of menhaden and is able to cause disease at very low zoospore concentrations.

Diseases of Aquatic Organisms

Induction of skin ulcers in Atlantic menhaden by injection and aqueous exposure to the zoospores of Aphanomyces invadans

The infectivity and role of Aphanomyces invadans in the etiology of skin ulcers in Atlantic menhaden Brevoortia tyrannus were investigated with two laboratory challenges. In the first experiment, Atlantic menhaden received subcutaneous injections with secondary zoospores from one of three cultures of Aphanomyces : WIC (an endemic isolate of A. invadans in Atlantic menhaden from the Wicomico River, Maryland), PA7 (an isolate of A. invadans from striped snakehead Channa striata (also known as chevron snakehead), infected with epizootic ulcerative syndrome from Thailand), and ATCC-62427 (an isolate from Atlantic menhaden from North Carolina). Fish were injected with 1.9 × 10 2 (WIC-low), 1.9 × 10 3 (WIC-high), 5.2 × 10 2 (PA7), or 6.0 × 10 2 (ATCC-62427) zoospores and held in static water at 23.5°C (6‰ salinity) for 21 d. Both low and high doses of WIC caused incipient, granulomatous lesions after 5 d. Fish injected with the high-dose WIC died within 7 d. All fish injected with the low-dose WIC were dead after 10 d. Fish injected with zoospores of PA7 developed lesions after 9 d. Fish injected with the ATCC-62427 isolate or those that received subcutaneous injections of sterile water (controls) did not develop lesions. In the second experiment, fish were bath-exposed with zoospores of the WIC isolate after various trauma-inducing treatments. These treatments consisted of handling fish with a net (net stress, exposed for 2 h to either 70 or 700 zoospores/mL), physically removing a few scales (trauma, exposed for 1 h to 700 zoospores/mL), or acclimating fish with less handling (acclimated, untraumatized, exposed for 5.5 h to 110 zoospores/mL). Unexposed fish served as controls. Mortality ranged from 94% to 100% for net-handled and traumatized fish, with the prevalence of ulcerous lesions ranging from 70% to 79% in net-handled fish. However, mortality was 24% for the “untraumatized” fish and the prevalence of lesions was 32%. Fish injected with or exposed to bath challenges of zoospores developed lesions that were grossly and histologically identical to those observed in naturally infected Atlantic menhaden from several estuaries and rivers along the mid-Atlantic coast of the USA. The deeply penetrating ulcers were characterized by dermatitis, myofibrillar degeneration, and deep, necrotizing granulomatous myositis. Experimentally induced lesions, however, exhibited invasiveness, often involving the kidney. Injected or bath-exposed fish developed incipient granulomas after 5 d, which progressed to overt lesions over 7–9 d. We have here demonstrated that ulcerative skin lesions can be experimentally induced in Atlantic menhaden after exposure to oomycete zoospores of an endemic strain of A. invadans .

Journal of Aquatic Animal Health

Aphanomyces as a cause of ulcerative skin lesions of menhaden from Chesapeake Bay Tributaries

During the summer and fall of 1997, an unusually high prevalence of skin lesions in fishes from Chesapeake Bay tributaries as well as two fish kills in the Pocomoke River stimulated significant public concern. Atlantic menhaden Brevoortia tyrannus were the most frequent target of the acute fish kills and displayed skin lesions that were attributed to the presence of the toxic dinoflagellate Pfiesteria piscicida. Hence, the penetrating skin ulcers so commonly found in this species are now widely viewed by the general public and some scientists as Pfiesteria -related and to be caused by exposure to Pfiesteria toxin. We examined, histologically, 121 menhaden with these ulcers collected from both Maryland and Virginia waters of the Chesapeake Bay in 1997 and 31 from the Pocomoke and Wicomico rivers in 1998. All of the deeply penetrating ulcers, as well as raised lesions (with or without eroded epithelium), were characterized by deeply penetrating fungal hyphae surrounded by chronic, granulomatous inflammation. These lesions had an appearance identical or similar to epizootic ulcerative syndrome (EUS), an ulcerative mycotic syndrome of fishes in other parts of the world caused by the fungal pathogen Aphanomyces invadans. They were also identical to ulcerative mycosis of menhaden previously reported along the Atlantic coast of the USA as associated with Aphanomyces spp. In 1998, using methods for isolation of A. invadans , we were able to culture from affected menhaden an Aphanomyces sp. that by preliminary tests is similar or identical to A. invadans. We believe these findings suggest that factors other than Pfiesteria toxin need to be considered as the cause or initiator of these lesions.

Journal of Aquatic Animal Health