Many of the ugly, deep lesions associated with pfiesteria-related fish kills in the Chesapeake Bay are caused by a fungus infection, say fish pathologists who have studied the wounds.

The extensive lesions found in scores of dead fish examined by pathologists were caused by a slow-growing fungus species called Aphanomyces, which the pathologists say had to have afflicted the fish for a week or more before the die-offs took place.

“These menhaden lesions are chronic lesions that are caused by a deeply penetrating fungal agent,” said Wolfgang Vogelbein, a pathologist at the Virginia Institute of Marine Science. “It indicates to us that those lesions are older than a few hours or a few days. They’re probably a week or more old.”

Other scientists say that conclusion does not change the basic consensus that pfiesteria and related organisms were responsible for last year’s fish kills in Eastern Shore rivers.

But the findings of Vogelbein and Vicki Blazer, a pathologist with the U.S. Geological Survey’s Leetown Science Center, do raise questions about the relationship between deep lesions and pfiesteria.

It could mean, for example, that pfiesteria in at least some cases began striking fish days or weeks before fish kills were observed. And because the fungus is slow to grow, it is possible that fish with ugly lesions swim elsewhere and are observed in areas where there is no pfiesteria, the pathologists say. That, in turn, could reduce the value of lesions as an indicator of pfiesteria in a particular area.

“It is time to separate the fish kills from the fish lesions,” Blazer said.

Pfiesteria are single-celled organisms with a highly complex life cycle that includes at least 24 different forms, several of which can produce toxins. Laboratory work conducted by JoAnn Burkholder, of North Carolina State University, have shown that fish exposed to high levels of pfiesteria toxins can be stunned and killed.

That can happen without causing any lesions. Burkholder’s work also shows that pfiesteria-produced toxins can erode the skin tissue of the fish.

But pathologists say those lesions, formed quickly by direct exposure to high levels of pfiesteria toxins, are different from the deep lesions observed in many menhaden at the fish kills which, in some cases, penetrate almost entirely through the body of the fish.

What is possible, Vogelbein said, is that low-levels of pfiesteria created an initial opening on the skin that allowed the fungus to invade the fish. If that is the case, though, that means pfiesteria struck the fish at least a week — and perhaps two or three weeks — before the fish kills took place. “If pfiesteria plays a role in the development of these lesions, it is most likely an early role,” Vogelbein said.

Other scientists say such a scenario is entirely possible, especially if the fish remain in the same area.

Robert Magnien, who heads the Maryland Department of Natural Resources’ Tidewater Ecosystem Assessment Division, said recent DNR surveys have shown that schools of menhaden not only remain in the same river — but often stay at the same site in the same river — for weeks at a time, allowing the fish to be subjected to a series of pfiesteria encounters.

“We were able to repeatedly find schools of menhaden in certain areas over a period of a couple of months,” Magnien said. “So there is some suggestion from those findings that at least some of the menhaden may have stayed in fairly local areas for an extended period of time.”

Vogelbein cautioned that more studies are needed to determine whether pfiesteria is, in fact, the triggering mechanism that weakens the fish and makes them susceptible to fungus invasions.

“Pfiesteria may well play a role in the development of those lesions,” Vogelbein said. “However, it must also be recognized that other factors could play a role as initiators of this fungus.” He said it is also possible that the fungus is a primary pathogen that could infect and spread without the presence of pfiesteria. “The jury on that is out,” Vogelbein said.

In Virginia, Vogelbein said all of the roughly 100 menhaden with lesions that he examined had the same fungal infection, yet there have been no pfiesteria-related fish kills confirmed in the state. That means, he said, either pfiesteria was not a factor in the lesions, or the menhaden were exposed to low levels of pfiesteria that did not cause fish kills, or the fish he examined were exposed elsewhere.

But Magnien said the Maryland experience strongly suggests the deep lesions are related to pfiesteria. Surveys around Maryland’s portion of the Bay and tributary areas showed that the vast majority of menhaden with deep lesions in 1997 were found in areas with fish kills.

“It seems to me more than coincidental that the areas that had fish kills, presumably because of the presence of pfiesteria, also were the only ones that had high incidences of lesions,” he said.

Donald Boesch, president of the University of Maryland’s Center for Environmental Science and the chair of the state’s Pfiesteria Technical Advisory Committee, agreed that it was likely that fish with the most severe lesions were exposed to low levels of pfiesteria some time before fish kills took place.

“The pathologists are right — very right — in the sense that when you see a fish with these big open lesions, it means that this is an after-the-fact indicator at best, because it means the exposure took place some time ago, which explains why the lesions would be deeply invaded by fungi,” Boesch said.

And that, he said, is why scientists need to find a better, and quicker, way to identify the presence of pfiesteria in the water.

He said scientists recognized last year that using the presence of lesions was an “imperfect indicator” of pfiesteria because some lesions found during the fish kill on the Pocomoke River clearly “were not the result of an acute event that happened yesterday.”

Boesch noted that rivers have never been closed based on the presence of lesions alone. Past closures have been made as a result of fish kills or when large numbers of fish appeared to be in distress — behaving erratically as though exposed to some toxin. In all past fish closures in Maryland, water samples have subsequently shown the presence of pfiesteria.

But Boesch said any suggestion that there is no link between pfiesteria and lesions is “based on a selective use of evidence, particularly discounting the results of North Carolina investigators that show pfiesteria can induce lesions under experimental conditions.”

Therefore, until a faster way is developed to identify pfiesteria in the water, Boesch said lesions should continue to be considered as one of the indicators of potential trouble areas. “I would hope that the pathological studies are not used to suggest that we shouldn’t act to reduce public exposure to pfiesteria when we see a lot of these lesions,” Boesch said. “I think that’s the wrong approach. We have to be cautionary.”

Meanwhile, Vogelbein and Blazer also say more work needs to be focused on the fungus, noting that the link between it and pfiesteria is only circumstantial. They are puzzled as to why almost 100 percent of the deep lesions each of them have examined are infected by the same fungus species, while a whole host of fungi, bacteria and other organisms can thrive in an open sore.

“Why is it so consistently this pathogen?” Blazer asked. “It just makes sense to me that if you’re immuno suppressing, or causing skin damage, then anything that’s there is going to move in and cause disease. And we’re not seeing that in the menhaden.”

In fact, Vogelbein said, the same lesions have been identified each fall in menhaden taken by VIMS trawl surveys since 1984. And in the mid to late 1980s, the fungus was reported in menhaden along much of the East Coast.

“To clarify the relationships between pfiesteria and this fungal infection, we will need to conduct laboratory-based disease challenge studies,” Vogelbein said, adding that such studies, aimed at learning why and how the fungus infect menhaden, is under way at VIMS.

While pfiesteria is considered a threat to human health, Blazer said the fungus is not because it lives at temperatures several degrees cooler than the human body.