Detailed Research Information

Detailed project information for
Study Plan Number 01078-01

Branch : Fish Health Branch

Study Plan Number : 01078-01

Study Title : Influences of environmental factors, point source pollution and pathogen distribution on fish health issues in the Chesapeake Bay: 1) Menhaden lesions

Starting Date : 06/01/1999

Completion Date : 03/01/2001

Principal Investigator(s) : Blazer, Vicki S.

Primary PI : Blazer, Vicki S.

Telephone Number : (304) 724-4434

Email Address : vicki_blazer@usgs.gov

SIS Number :

Primary Program Element : Fisheries and Aquatic Resources

Second Program Element : Fish and Aquatic Habitats

Status : Completed

Abstract : BACKGROUND
Reports of high incidences of fish with skin lesions in the summer and fall of 1996 and again in 1997 in the Pocomoke River and other tributaries of Chesapeake Bay stimulated a great deal of public and scientific interest. These skin lesions range from small pinpoint hemorrhages to abrasions to deep ulcers. In addition, there were two fish kills involving primarily Atlantic menhaden (Brevoortia tyrannus) in the Pocomoke River in August. These skin lesions as well as the fish kills have been blamed (in the popular press) on the presence of Pfiesteria piscicida (Steidinger et al. 1996) or Pfiesteria-like dinoflagellates.

Worldwide there has been a reported increase in frequency and severity of harmful algal blooms, HABs, (Lassus et al. 1995). Dinoflagellates contribute to these HABs with over 40 species verified as producing toxins (Steidinger 1993). P. piscicida was first observed in 1988 in an experimental tilapia (Tilapia aurea) culture system in North Carolina (Smith et al. 1988; Noga et al. 1993). It is interesting to note that acute mortality occurred with moribund fish showing respiratory distress (shallow, rapid breathing), neurological signs (including hyperexcitability, lack of balance and spinning in the water column) and a cloudiness of the skin (Noga et al. 1993). Ulcerative skin lesions as those attributed to Pfiesteria in the wild were not reported. Subsequently P. piscicida has been implicated as the cause of major estuarine fish kills in the Neuse and Pamlico estuaries (Burkholder et al. 1992; 1995; Noga et al. 1996).

On August 6, 1997, hundreds of dead and dying fish, primarily menhaden were found in the Pocomoke River near Shelltown, MD. The fish kill lasted four days and the state closed a portion of the river from August 7 to 13. Maryland Department of Natural Resources personnel collected moribund fish and 20 were processed for histology. A second fish kill began in Pocomoke Sound on August 26. In this instance, fish with lesions but "low numbers" of dead fish were observed. However, a portion of the river was closed until October 3. Seventeen menhaden collected on Aug. 26 and 4 menhaden collected on Aug. 28 were processed for histology. Kings Creek off the Manokin River was closed on September 10 because a "significant" number of menhaden with "Pfiesteria-like" lesions were observed and four days later a portion of the Chicamacomico River was also closed for the same reason (Hughes et al. 1997). Ten menhaden were collected on Sept. 11 from the Kings Creek area for histologic examination.

In the summer and fall of 1997 we (fish health lab personnel) necropsied and examined histologically: menhaden from the Aug. 26 fish kill in the Pocomoke River and from the King's Creek "fish kill", approximately 120 fish of various species, some with lesions and some without from the Pocomoke, Nanticoke, and Choptank Rivers, and 10 striped bass from Pocomoke and other areas of Chesapeake Bay as well as three from Delaware Bay. In addition, to the ones we collected and processed we have received slides from the MD state pathologist for examination from the Aug. 6 fish kill in the Pocomoke, more fish from the rivers listed above as well as the Chicamacomico.

The majority of the lesions we see in menhaden - those from fish kills as well as those caught sporadically at other sites - are either raised, often grayish-white lesions or ulcerations which may also be grayish-white or have a red margin. Many are on the posterior surface of the fish around the anus but many are elsewhere on the body surface. Very consistently (not always but in 80% + cases) the menhaden lesions consist of a chronic granulomatous reaction around fungal hyphae. These fungal hyphae are evident penetrating into the muscle and elicit a very active inflammatory reaction. This type of reaction is chronic and takes days, probably weeks to develop.

The presence of fish, particularly menhaden, with ulcerated lesions has been used in Maryland waters of the Chesapeake Bay, as an indicator of the presence of the toxic Pfiesteria or Pfiesteria-like dinoflagellates. In some cases, the observation of these lesions has lead to the closing of stretches of certain tributaries for recreational, commercial and research uses. However, the chronic nature of these lesions in migratory fish and the consistent presence of an invasive fungal pathogen raises some questions as to the advisability of using these ulcers as an indicator of toxic dinflagellates. Skin lesions in fish can be caused by a variety of infectious and noninfectious insults. Indeed, Sindermann (1988) states that skin ulcers are one of the most useful biomarkers of polluted or otherwise stressful aquatic environments. Often these lesions are caused by opportunistic, facultative pathogens which infect weakened or stressed hosts. These facultative pathogens may gain entry because of impaired immune or disease resistance factors or because the natural defense mechanisms of the skin are impaired or breached and include bacteria, fungi and parasites.

The skin lesions we observed in menhaden from Chesapeake Bay are similar to those described as ulcerative mycosis in menhaden from North Carolina in the 1980's (Noga and Dykstra 1986; Noga et al. 1988; Dykstra et al. 1989). The fungal pathogen Aphanomyces was reported to be involved with ulcerative mycosis in menhaden by Dykstra et al. (1986). More recently, based on a study examining fish which survived an acute sublethal experimental exposure to P. piscicida, it was suggested that the fungal infections seen in menhaden and other estuarine fish in North Carolina are secondary to exposure of the fish to toxins from Pfiesteria (Noga et al. 1996). However, the same chronic granulomatous reaction around a penetrating fungal hyphae was not demonstrated in these experimental exposures. Indeed, histologic sections from only one fish showed evidence of fungal hyphae, present in necrotic muscle, without an obvious inflammatory reaction. This manifestation is much more consistent with secondary Saprolegnia or other species infection than to the pathogenic Aphanomyces.

Epizootic ulcerative syndrome (EUS), red spot disease (RSD) and mycotic granulomatosis (MG) are cutaneous ulcerative syndromes, characterized histologically by granulomatous dermatitis and myositis associated with invasive non-septate fungal hyphae. The lesions we observed in menhaden from the Chesapeake are also similar or identical to the lesions observed in these diseases. These syndromes have occurred in wild and cultured freshwater and estuarine fish in the Asia-Pacific region since the 1970's (Callinan 1994). They are characterized by the lesions of varied appearance and size, ranging from small hemorrhagic lesions in the early stage to large, deep necrotic ulcers in more advanced cases. Hatai et al. (1977) and Fraser et al. (1992) have proposed Aphanomyces as the primary causative agent for MG and RSD respectively. Roberts et al. (1993) noted that one or more invasive fungi had been implicated in EUS but that "accepting the traditional view that these agents may have a purely secondary role, extensive efforts have been made to determine the nature of the primary agent". Hence, based on the recommendations of the international expert consultation on EUS, held under the auspices of the United Nations in Bangkok in 1986, an interdisciplinary survey on the aspects of this disease were carried out throughout the affected region. A total of 840 cases cases from a wide variety of fish species were studied. In all cases the lesions contained wide, septate, non-sporulating fungal mycelium. In mature lesions, as in most of the wild fish studied, there was a thick layer of chronic inflammation consisting of macrophages and epitheloid cells. Much of the mycelium within these areas appeared dead. In farmed Indian carp from Bangladesh, samples were taken regularly to follow the course of the disease. In this cases, early lesions were observed in which there was an intense acute inflammatory response with massive myofibrillar necrosis. This occured prior to the more mature chronic lesions (Roberts et al. 1993). Pathogenicity of isolates from wild fish was tested by inserting a small piece of mycelium under the dermis of healthy snakeheads (Channa striatus) via an incision on the left shoulder. When the slow-growing, thermolabile strains of Aphanomyces were inserted, there was initially a mild, local inflammatory lesion, followed by severe invasive myonecrosis extending deep into the muscle (within 5 days). At his time a macrophage response was beginning. Within 15-20 days the lesion matured to resemble the typical chronic granulomatous response seen in wild EUS-infected fish. This experiment was carried out at 22 C. When the same infectivity studies are carried out with strains of Achlya, Saprolegnia and fast-growing Aphanomyces there is a local inflammation and a localized foriegn-body-type response and the inoculation site heals. Despite these findings the authors state that an environmental or more likely a viral component to the disease complex is necessary to precipitate invasion of the pathogenic Aphanomyces which is responsible for the tissue damage (Roberts et al. 1993). Conversely, Callinan et al. (1995) suggest the fungus may be the primary infectious agent in both EUS and RSD based on the high rate of recovery from affected fish. These authors compared peptide extracts of representative isolates of EUS and RSD Aphanomyces using SDS-PAGE electrophoresis. This work showed that the EUS and RSD isolates represent strains within a single species and that this species is different than A. cochloides, A. laevis and A. euteiches.

The pathogenic isolate of Aphanomyces was named as a new species, Aphanomyces invaderis, in 1995. This species is a slow-growing, aquatic fungus with wide, aseptate mycelium. It grows best at 24 and 30 C, will grow at 31 C but dies at 37 C (Willoughby et al. 1995).

Outbreaks of EUS and RSD have been correlated with rainfall and temperature. In a study done between 1984 and 1988 in eastern Australia, six outbreaks of RSD in sea mullet (Mugil cephalus) were observed. Each was preceded by several days of heavy rainfall which caused moderate to severe local flooding. Two to five weeks after the rain event locally extensive, necrotizing, granulomatous dermatitis and myositis were observed. Dermal ulcers were most common 4-16 weeks after rain events. It was postulated that environmental factors associated with climatic changes may damage skin and allow the invasive fungi to invade. They found dissolved oxygen (DO) levels fell to < 1 gm/l in the affected tributaries after the rain events (Callinan et al. 1989). Plumb et al. (1976) describe hemorrhagic and necrotic lesions in skin and skeletal muscle of channel catfish (Ictalurus punctatus) exposed to DO concentrations of < 1 mg/l for several days. This lead Callinan et al. (1989) to suggest low DO as a predisposing factor for RSD. In this study significantly more ulcers on the posterior/dorsal subdivisions of the body surface than elsewhere. It was hypothesized that these areas are at the periphery of circulatory fields relatively distant from the heart and hence the most compromised under hypoxic conditions. In the Phillipines EUS was also closely associated with rainfall but not DO (Bondad-Reantaso 1992).

The similarities of the lesions we observe in menhaden and other fish species from the Chesapeake Bay to lesions observed in outbreaks of EUS, RSD and MG certainly raise the possibility that factors other than Pfiesteria or Pfiesteria-like organisms can be involved in the initiation of the ulcers. Is it possible that all the outbreaks of EUS, RSD and MG in both fresh and estuarine waters in wild and cultured fishes in the Asia - Pacific area are initiated by toxic dinoflagellates and investigators in these areas have overlooked that possibility? Or is it more likely that this pathogenic fungi is spreading and a variety of environmental factors which cause skin damage can allow it's entry and subsequent growth within the fish? There is certainly circumstantial evidence that during the two actual fish kills toxic dinoflagellates were involved. It is also possible that survivors would have had enough damage to skin to be susceptible to a variety of secondary infections. And, in fact, we saw a variety of organisms in many of the lesions from other fish. However, if the menhaden lesions were induced by dinoflagellate toxins why weren't there many different organisms observed? We hypothesis that the lesions in the menhaden are there well before the fish are killed by Pfiesteria or other toxic dinoflagellates during a bloom. Is it possible weakened (dead and dying) menhaden with lesions stimulate toxic dinoflagellate blooms? If the primary lesion is caused by a fungal infection, it is important to know what does predispose the fish to the fungal infection, where is the fungus coming from, what environmental factors lead to proliferation of the fungus and does the presence of "sick" fish have anything to do with initiation of dinoflagellate blooms. It is also important to know whether damage to the skin is necessary to initiate the fungal infection and if so, what environmental factors can cause this type of damage. Pfiesteria toxin, low DO, pH changes, net damage, nutritional changes and contaminants all need to be considered. Once we get the fungus in culture we will begin experimental work to answer some of these questions. These are all questions which need to be addressed by both field and laboratory studies.

The striped bass appear to have a different problem. Again chronic lesions are found within the skin as well as the internal organs. The skin lesions we have studied differ from the menhaden skin lesions in that they are generally confined to the epidermis and dermis and do not often penetrate into the muscle. They are composed of focal granulomatous inflammation within which there are acid-fast bacteria. Investigators in VA and MD have isolated species of Mycobacteria - definitive speciation is still pending. In menhaden the internal organs are usually not involved. In striped bass it is not uncommon to have much of the spleen, liver and kidney replaced by granulomas. Again, we feel the relationship between these lesions and toxic dinoflagellates is tenuous at best.

The above preliminary findings suggest that some factor or group of factors is leading to epidermal damage and/or immunosuppression allowing for a variety of organisms to cause disease in various fish species. Hence, we proposed to assess overall fish health in selected tributaries which 1) have and have not been reported to have a high incidence of fish with lesions and 2) which have different land use and water quality. By comparing our findings with existing and ongoing water quality monitoring, toxic chemical evaluation, land use, nutrient input, presence of toxic dinoflagellates and weather, we hope to be able to determine the causes of these lesions and identify any predisposing factors.
OBJECTIVES
1. Characterize the types and causes(s) of lesions from different tributaries of the Chesapeake Bay.

2. Evaluate overall fish health using necropsy-based, physiological, histological and immunological techniques.

3. Map regional distributions of fish lesions from field surveys by FHL, MD DNR, the Cooperative Research Unit and others.

4. Map and/or compile current land use information for the upland and near-stream environment of selected tributaries.

5. Compile and analyze existing information on stream flow and water quality trends, point- and non-point nutrient and toxicant sources, soils, topography and other environmental factors for selected Bay tributaries.

6. Analyze data using GIS and models for correlations among 3-5 above.
HYPOTHESES TO BE TESTED
1). Differences in fish health and fish lesion prevalence observed in selected Chesapeake Bay tributaries can be correlated with water quality/land use differences.

2). Typical "Pfiesteria-like" lesions can be induced without exposure to dinoflagellate toxins in the laboratory.

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Branch :	Fish Health Branch
Study Plan Number :	01078-01
Study Title :	Influences of environmental factors, point source pollution and pathogen distribution on fish health issues in the Chesapeake Bay: 1) Menhaden lesions
Starting Date :	06/01/1999
Completion Date :	03/01/2001
Principal Investigator(s) :	Blazer, Vicki S.
Primary PI :	Blazer, Vicki S.
Telephone Number :	(304) 724-4434
Email Address :	vicki_blazer@usgs.gov
SIS Number :
Primary Program Element :	Fisheries and Aquatic Resources
Second Program Element :	Fish and Aquatic Habitats
Status :	Completed
Abstract :	BACKGROUND Reports of high incidences of fish with skin lesions in the summer and fall of 1996 and again in 1997 in the Pocomoke River and other tributaries of Chesapeake Bay stimulated a great deal of public and scientific interest. These skin lesions range from small pinpoint hemorrhages to abrasions to deep ulcers. In addition, there were two fish kills involving primarily Atlantic menhaden (Brevoortia tyrannus) in the Pocomoke River in August. These skin lesions as well as the fish kills have been blamed (in the popular press) on the presence of Pfiesteria piscicida (Steidinger et al. 1996) or Pfiesteria-like dinoflagellates. Worldwide there has been a reported increase in frequency and severity of harmful algal blooms, HABs, (Lassus et al. 1995). Dinoflagellates contribute to these HABs with over 40 species verified as producing toxins (Steidinger 1993). P. piscicida was first observed in 1988 in an experimental tilapia (Tilapia aurea) culture system in North Carolina (Smith et al. 1988; Noga et al. 1993). It is interesting to note that acute mortality occurred with moribund fish showing respiratory distress (shallow, rapid breathing), neurological signs (including hyperexcitability, lack of balance and spinning in the water column) and a cloudiness of the skin (Noga et al. 1993). Ulcerative skin lesions as those attributed to Pfiesteria in the wild were not reported. Subsequently P. piscicida has been implicated as the cause of major estuarine fish kills in the Neuse and Pamlico estuaries (Burkholder et al. 1992; 1995; Noga et al. 1996). On August 6, 1997, hundreds of dead and dying fish, primarily menhaden were found in the Pocomoke River near Shelltown, MD. The fish kill lasted four days and the state closed a portion of the river from August 7 to 13. Maryland Department of Natural Resources personnel collected moribund fish and 20 were processed for histology. A second fish kill began in Pocomoke Sound on August 26. In this instance, fish with lesions but "low numbers" of dead fish were observed. However, a portion of the river was closed until October 3. Seventeen menhaden collected on Aug. 26 and 4 menhaden collected on Aug. 28 were processed for histology. Kings Creek off the Manokin River was closed on September 10 because a "significant" number of menhaden with "Pfiesteria-like" lesions were observed and four days later a portion of the Chicamacomico River was also closed for the same reason (Hughes et al. 1997). Ten menhaden were collected on Sept. 11 from the Kings Creek area for histologic examination. In the summer and fall of 1997 we (fish health lab personnel) necropsied and examined histologically: menhaden from the Aug. 26 fish kill in the Pocomoke River and from the King's Creek "fish kill", approximately 120 fish of various species, some with lesions and some without from the Pocomoke, Nanticoke, and Choptank Rivers, and 10 striped bass from Pocomoke and other areas of Chesapeake Bay as well as three from Delaware Bay. In addition, to the ones we collected and processed we have received slides from the MD state pathologist for examination from the Aug. 6 fish kill in the Pocomoke, more fish from the rivers listed above as well as the Chicamacomico. The majority of the lesions we see in menhaden - those from fish kills as well as those caught sporadically at other sites - are either raised, often grayish-white lesions or ulcerations which may also be grayish-white or have a red margin. Many are on the posterior surface of the fish around the anus but many are elsewhere on the body surface. Very consistently (not always but in 80% + cases) the menhaden lesions consist of a chronic granulomatous reaction around fungal hyphae. These fungal hyphae are evident penetrating into the muscle and elicit a very active inflammatory reaction. This type of reaction is chronic and takes days, probably weeks to develop. The presence of fish, particularly menhaden, with ulcerated lesions has been used in Maryland waters of the Chesapeake Bay, as an indicator of the presence of the toxic Pfiesteria or Pfiesteria-like dinoflagellates. In some cases, the observation of these lesions has lead to the closing of stretches of certain tributaries for recreational, commercial and research uses. However, the chronic nature of these lesions in migratory fish and the consistent presence of an invasive fungal pathogen raises some questions as to the advisability of using these ulcers as an indicator of toxic dinflagellates. Skin lesions in fish can be caused by a variety of infectious and noninfectious insults. Indeed, Sindermann (1988) states that skin ulcers are one of the most useful biomarkers of polluted or otherwise stressful aquatic environments. Often these lesions are caused by opportunistic, facultative pathogens which infect weakened or stressed hosts. These facultative pathogens may gain entry because of impaired immune or disease resistance factors or because the natural defense mechanisms of the skin are impaired or breached and include bacteria, fungi and parasites. The skin lesions we observed in menhaden from Chesapeake Bay are similar to those described as ulcerative mycosis in menhaden from North Carolina in the 1980's (Noga and Dykstra 1986; Noga et al. 1988; Dykstra et al. 1989). The fungal pathogen Aphanomyces was reported to be involved with ulcerative mycosis in menhaden by Dykstra et al. (1986). More recently, based on a study examining fish which survived an acute sublethal experimental exposure to P. piscicida, it was suggested that the fungal infections seen in menhaden and other estuarine fish in North Carolina are secondary to exposure of the fish to toxins from Pfiesteria (Noga et al. 1996). However, the same chronic granulomatous reaction around a penetrating fungal hyphae was not demonstrated in these experimental exposures. Indeed, histologic sections from only one fish showed evidence of fungal hyphae, present in necrotic muscle, without an obvious inflammatory reaction. This manifestation is much more consistent with secondary Saprolegnia or other species infection than to the pathogenic Aphanomyces. Epizootic ulcerative syndrome (EUS), red spot disease (RSD) and mycotic granulomatosis (MG) are cutaneous ulcerative syndromes, characterized histologically by granulomatous dermatitis and myositis associated with invasive non-septate fungal hyphae. The lesions we observed in menhaden from the Chesapeake are also similar or identical to the lesions observed in these diseases. These syndromes have occurred in wild and cultured freshwater and estuarine fish in the Asia-Pacific region since the 1970's (Callinan 1994). They are characterized by the lesions of varied appearance and size, ranging from small hemorrhagic lesions in the early stage to large, deep necrotic ulcers in more advanced cases. Hatai et al. (1977) and Fraser et al. (1992) have proposed Aphanomyces as the primary causative agent for MG and RSD respectively. Roberts et al. (1993) noted that one or more invasive fungi had been implicated in EUS but that "accepting the traditional view that these agents may have a purely secondary role, extensive efforts have been made to determine the nature of the primary agent". Hence, based on the recommendations of the international expert consultation on EUS, held under the auspices of the United Nations in Bangkok in 1986, an interdisciplinary survey on the aspects of this disease were carried out throughout the affected region. A total of 840 cases cases from a wide variety of fish species were studied. In all cases the lesions contained wide, septate, non-sporulating fungal mycelium. In mature lesions, as in most of the wild fish studied, there was a thick layer of chronic inflammation consisting of macrophages and epitheloid cells. Much of the mycelium within these areas appeared dead. In farmed Indian carp from Bangladesh, samples were taken regularly to follow the course of the disease. In this cases, early lesions were observed in which there was an intense acute inflammatory response with massive myofibrillar necrosis. This occured prior to the more mature chronic lesions (Roberts et al. 1993). Pathogenicity of isolates from wild fish was tested by inserting a small piece of mycelium under the dermis of healthy snakeheads (Channa striatus) via an incision on the left shoulder. When the slow-growing, thermolabile strains of Aphanomyces were inserted, there was initially a mild, local inflammatory lesion, followed by severe invasive myonecrosis extending deep into the muscle (within 5 days). At his time a macrophage response was beginning. Within 15-20 days the lesion matured to resemble the typical chronic granulomatous response seen in wild EUS-infected fish. This experiment was carried out at 22 C. When the same infectivity studies are carried out with strains of Achlya, Saprolegnia and fast-growing Aphanomyces there is a local inflammation and a localized foriegn-body-type response and the inoculation site heals. Despite these findings the authors state that an environmental or more likely a viral component to the disease complex is necessary to precipitate invasion of the pathogenic Aphanomyces which is responsible for the tissue damage (Roberts et al. 1993). Conversely, Callinan et al. (1995) suggest the fungus may be the primary infectious agent in both EUS and RSD based on the high rate of recovery from affected fish. These authors compared peptide extracts of representative isolates of EUS and RSD Aphanomyces using SDS-PAGE electrophoresis. This work showed that the EUS and RSD isolates represent strains within a single species and that this species is different than A. cochloides, A. laevis and A. euteiches. The pathogenic isolate of Aphanomyces was named as a new species, Aphanomyces invaderis, in 1995. This species is a slow-growing, aquatic fungus with wide, aseptate mycelium. It grows best at 24 and 30 C, will grow at 31 C but dies at 37 C (Willoughby et al. 1995). Outbreaks of EUS and RSD have been correlated with rainfall and temperature. In a study done between 1984 and 1988 in eastern Australia, six outbreaks of RSD in sea mullet (Mugil cephalus) were observed. Each was preceded by several days of heavy rainfall which caused moderate to severe local flooding. Two to five weeks after the rain event locally extensive, necrotizing, granulomatous dermatitis and myositis were observed. Dermal ulcers were most common 4-16 weeks after rain events. It was postulated that environmental factors associated with climatic changes may damage skin and allow the invasive fungi to invade. They found dissolved oxygen (DO) levels fell to < 1 gm/l in the affected tributaries after the rain events (Callinan et al. 1989). Plumb et al. (1976) describe hemorrhagic and necrotic lesions in skin and skeletal muscle of channel catfish (Ictalurus punctatus) exposed to DO concentrations of < 1 mg/l for several days. This lead Callinan et al. (1989) to suggest low DO as a predisposing factor for RSD. In this study significantly more ulcers on the posterior/dorsal subdivisions of the body surface than elsewhere. It was hypothesized that these areas are at the periphery of circulatory fields relatively distant from the heart and hence the most compromised under hypoxic conditions. In the Phillipines EUS was also closely associated with rainfall but not DO (Bondad-Reantaso 1992). The similarities of the lesions we observe in menhaden and other fish species from the Chesapeake Bay to lesions observed in outbreaks of EUS, RSD and MG certainly raise the possibility that factors other than Pfiesteria or Pfiesteria-like organisms can be involved in the initiation of the ulcers. Is it possible that all the outbreaks of EUS, RSD and MG in both fresh and estuarine waters in wild and cultured fishes in the Asia - Pacific area are initiated by toxic dinoflagellates and investigators in these areas have overlooked that possibility? Or is it more likely that this pathogenic fungi is spreading and a variety of environmental factors which cause skin damage can allow it's entry and subsequent growth within the fish? There is certainly circumstantial evidence that during the two actual fish kills toxic dinoflagellates were involved. It is also possible that survivors would have had enough damage to skin to be susceptible to a variety of secondary infections. And, in fact, we saw a variety of organisms in many of the lesions from other fish. However, if the menhaden lesions were induced by dinoflagellate toxins why weren't there many different organisms observed? We hypothesis that the lesions in the menhaden are there well before the fish are killed by Pfiesteria or other toxic dinoflagellates during a bloom. Is it possible weakened (dead and dying) menhaden with lesions stimulate toxic dinoflagellate blooms? If the primary lesion is caused by a fungal infection, it is important to know what does predispose the fish to the fungal infection, where is the fungus coming from, what environmental factors lead to proliferation of the fungus and does the presence of "sick" fish have anything to do with initiation of dinoflagellate blooms. It is also important to know whether damage to the skin is necessary to initiate the fungal infection and if so, what environmental factors can cause this type of damage. Pfiesteria toxin, low DO, pH changes, net damage, nutritional changes and contaminants all need to be considered. Once we get the fungus in culture we will begin experimental work to answer some of these questions. These are all questions which need to be addressed by both field and laboratory studies. The striped bass appear to have a different problem. Again chronic lesions are found within the skin as well as the internal organs. The skin lesions we have studied differ from the menhaden skin lesions in that they are generally confined to the epidermis and dermis and do not often penetrate into the muscle. They are composed of focal granulomatous inflammation within which there are acid-fast bacteria. Investigators in VA and MD have isolated species of Mycobacteria - definitive speciation is still pending. In menhaden the internal organs are usually not involved. In striped bass it is not uncommon to have much of the spleen, liver and kidney replaced by granulomas. Again, we feel the relationship between these lesions and toxic dinoflagellates is tenuous at best. The above preliminary findings suggest that some factor or group of factors is leading to epidermal damage and/or immunosuppression allowing for a variety of organisms to cause disease in various fish species. Hence, we proposed to assess overall fish health in selected tributaries which 1) have and have not been reported to have a high incidence of fish with lesions and 2) which have different land use and water quality. By comparing our findings with existing and ongoing water quality monitoring, toxic chemical evaluation, land use, nutrient input, presence of toxic dinoflagellates and weather, we hope to be able to determine the causes of these lesions and identify any predisposing factors. OBJECTIVES 1. Characterize the types and causes(s) of lesions from different tributaries of the Chesapeake Bay. 2. Evaluate overall fish health using necropsy-based, physiological, histological and immunological techniques. 3. Map regional distributions of fish lesions from field surveys by FHL, MD DNR, the Cooperative Research Unit and others. 4. Map and/or compile current land use information for the upland and near-stream environment of selected tributaries. 5. Compile and analyze existing information on stream flow and water quality trends, point- and non-point nutrient and toxicant sources, soils, topography and other environmental factors for selected Bay tributaries. 6. Analyze data using GIS and models for correlations among 3-5 above. HYPOTHESES TO BE TESTED 1). Differences in fish health and fish lesion prevalence observed in selected Chesapeake Bay tributaries can be correlated with water quality/land use differences. 2). Typical "Pfiesteria-like" lesions can be induced without exposure to dinoflagellate toxins in the laboratory.
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U.S. Department of the Interior \|\| U.S. Geological Survey 11700 Leetown Road, Kearneysville, WV 25430, USA URL: http://www.lsc.usgs.gov Maintainer: lsc_webmaster@usgs.gov Last Modified: October 21, 2002 dwn Privacy Policy and Disclaimers \|\| FOIA \|\| Accessibility