The Effects of Environmental Stress on Outbreaks of Infectious Diseases of Fishes

J. Fish Biol. (1974) 6, 197-208

The effects of environmental stress on outbreaks of infectious diseases of fishes*

S. F. SNIESZKO Eastern Fish Disease Laboratory, Leetown, Route No. 1 , Box 17A, Kearneysviile,

West Virginia 25430, U.S.A.

(Received 28 September 1973)

Infectious diseases of fishes occur when susceptible fishes are exposed to virulent pathogens under certain environmental stress conditions. Very little research has been carried out to show the effect of pollution on outbreaks of infectious diseases of fishes. Therefore, examples taken from the literature were selected and reviewed to show the coincidence of infectious diseases with stress caused by temperature, eutrophication, sewage, metabolic products of fishes, industrial pollution, and pesticides.

I. INTRODUCTION There is voluminous literature on fish kills and fish pathology caused by various pollutants, but much less information is available on the effects of toxic substances in the environment and the incidence of infectious diseases of fishes. In the introduction to the symposium entitled Diseases of Fishes, Mawdesley-Thomas (19724 said: ' . . . disease, per se, is not an entity or an end in itself. Disease is the end result of an interaction between a noxious stimulus and a biological system and to understand disease is to understand all aspects of the biology of the species '. In attempting to discuss the role of environmental stress on outbreaks of infectious diseases of fishes, particularly those of bacterial etiology, one has to consider the relationship between the ' noxious stimulus ' and outbreaks of disease.

It is well known, from epidemiology, that an infectious agent causes a disease of the host if environmental conditions are right. The influence of each subset is variable-disease breaks out only if there is a sufficient relationship between them (Fig. 1). The chemical and physical characteristics of water are variable and affected by natural factors and the noxious effects of human activities, called pollution. The inland aquatic environment and coastal areas are more affected than the open seas. In consequence, fishes in these areas are exposed to frequent stresses. If the occurrence of stress coincides with the presence of pathogenic micro-organisms it is logical to assume that outbreaks of diseases are more likely to take place. Most of the present evidence is based on the coincidence of stress with outbreaks of infectious diseases. It is generally accepted that stress is a very important factor in outbreaks of infectious diseases of fishes (Wedemeyer, 1970; Meyer, 1970).

* Keynote report. Environmental Protection Agency Workshop: Pathlogic Effects of Chemicals on Aquatic Organisms. Pensacola, Florida. 8 May 1973.

197

198 S . F . S K I E S Z K O

II. TEMPERATURE Significant modifications of water temperature are brought about by human

activities and are called ‘ thermal pollution ’. Thcre is justification for including temperature in this presentation because it affects the rate of metabolism, immuno- logic response, reproduction, amount of oxygen dissolved in water, biological oxygen demand, toxicity of pollutants, and growth of fish pathogens and parasites. Tem- perature has a particularly significant influence on diseases of fishes in areas where there is a wide amplitude in daily and seasonal temperature changes (Meyer, 1970). Fish culturists have long recognized that increased mortalities of cultured carp occur in spring. During the winter months fish feed little, or not at all, their tissue reserves are depleted, and the dissolved oxygen is often low in frozen-over bodies of water. Soviet investigators, as reviewed by Snieszko (1 972), have carried out observations on overwintering of fishes in impoundments. Haematological observations made on carp wintering in bodies of water, covered with ice, and having three levels of dissolved oxygen, showed that at 3.7 parts/106 of oxygen haematological parameters remained normal, at 2.5-2.6 parts/l06 carp were compensating with increased Iiaematopoicsis

FIG. 1 . An overt infectious disease occurs when a susceptible host is exposed to a virulent pathogen under proper environmental conditions.

during the winter, at 1.8-1-9 parts/106 there wac a breakdown of compensation before the end of winter and by spring carp became extremely anaemic. In addition to stress caused by overwintering, the development of reproductive cells during late winter and early spring causes additional drain on the resources of the fishes body. In areas with cold winters the greatest losses of carp and other fishes occur in the spring from infections caused by Aeronfonas liqzaefariens (Schaperclaus, 1954), spring viraemia of carp (Fijan, 19’72) and other not yet sufficiently described diseases.

Rychlicki & Zarnecki (1957) found that if haiidling of fish in spring was eliminated losses caused by A . Ziquefaciens and spring kiraemia were greatly reduced. In Israel, where there is a short and mild winter, the spring epidemics among carp are insigni- ficant (Sarig, 1971). Some of the most important observations on the eflect of temperature on the systemic presence of bacteria in fish tissues and immuric response were reviewed by Bisset (1947) and Cushing (1971). With temperature a few degrees above freezing, bacteria were usually present in fish tissues. When the tempcrature was increased fish either became diseased and died, or bacteria disappeared from the

EFFECTS OF ENVIRONMENTAL STRESS ON I?U'FECTIOUS DISEASES OF FISHES 199

tissues. Apparently at low temperature the cellular and humoral defense were not active and the temperature was too low for bacteria to multiply and cause an acute disease. When the temperature approached optimum for fish, bacteria were eliminated in normal fishes, but were causing fatal diseases in fishes debilitated by winter (Liebmann et al., 1960).

Temperature also has selective influence on the types of diseases. In salmonid fishes of the Pacific coast, Cytophaga psychrophilin causes cold water disease at temperatures of 5-10' C. This disease can be controlled by increasing temperature to between 10 and 15" C. At temperatures above 15" C, preferably 20" C or higher, another myxobacterium, Chondrococcus cohimnaris is recognized as an important pathogen of salmonids. Disease caused by Chondrococcus columnaris can be controlled by lowering temperature to 15" C or less (Wood, 1968). Infectious haematopoietic necrosis (IHN), a viral disease of sockeye salmon, Uncorhyncus nerka (Walbaum), which was first observed in California, usually occurs at 8-10' C. It can be controlled by increasing the temperature shortly after infection to 18-20" C, or prevented by rearing fish at 15" C. The virus apparently disappears in infected fish maintained for several days at 18-20" C and recurrence takes place only if fishes are reinfected (Amend, 1970).

Changes in temperature are important in outbreaks or reduction of fish diseases. Temperature affects the response of fishes to an invasion by pathogens. This subject was reviewed by Meycr in 1970 and more recently by Roberts (1973). In coryne- bacterial disease, called Dee or kidney disease, false diphtherial membranes develop on viscera at temperatures below 9" C. At temperatures above 10" C membranes are absent but necrotic lesions appear instead (Smith, 1964). Roberts & Mace, Scotland, observed that at temperatures below 10" C hyperplasia affects the Mal- phigian cells of the epidermis, fins, and caudal peduncle in plaice, Pleuronectes platessa (L.) (Roberts, 1973). It was believed that the cold water myxobacteria, such as Cytophaga psychophila invade this proliferating tissue resulting in peduncle disease and fin rot. These few examples show that a change in water temperature may affect the occurrence of outbreaks of bacterial and viral diseases, if the potential pathogens are present.

III. DEFICIENCY AND EXCESS OF OXYGEN AND NITROGEN Oxygen is essential for respiration, but nitrogen is biologically inert. Both are

dissolved in water and both are involved in fish diseases if present in too low or too high concentrations. Supersaturation of water with oxygen, but particularly with nitrogen, combined with changes of atmospheric pressure and temperature often results in gas embolisms called gas bubble disease (Rucker, 1972). In the Columbia River, with high dams, turbulence and pressure created in turbines and spillways, gas bubble disease is chronic. Tt is estimated that more than 50% of the fishes may be lost due to gas embolisms. In borderline cases lesions caused by gas blisters in gills and skin invite microbial invasion. The most recent case of gas bubble disease occurred on 9 April 1973 below the efluent from the Rocky Point power plant in Massachusetts (Smithsonian Institution, Center for short-lived phenomena. No. 1624, 4 May 1973). Increase of the water temperature by about 15" C caused gas supersaturation and resulted in heavy loss of menhaden due to gas bubble disease.

Depletion of oxygen was believed to be the stress factor which resulted in heavy mortalities of threadfin shad Dorosoma petense (Giinther) and American shad, Alosa

200 S . F . S N I E S Z K O

sapidissirnu (Wilson) in San Joaquin River in California (Haley et a!., 1967). Water, heavily polluted by cannery effluent, contained only 1.2 to 2-6 parts/106 of dissolved oxygen. Diseased fishes displayed signs of bacterial infection and A . Ziquefaciens was isolated from moribund fishes. In this outbreak, oxygen deficiency was combined with abundance of bacteria as shown by highly increased biological oxygen demand (B.O.D.).

IV. EUTROPHICATION In eutrophic waters there are frequent and wide fluctuations in dissolved oxygen

and pH. Fishes are exposed to these and other stresses. Numerous potential fish pathogens, for example Pseudomorics, Aeromonas and myxobacteria, are also present in such waters. The physiological stresses on fishes caused by eutrophication were reviewed by Fry (1969). He believes that reduction of the oxygen content of water ' is the most pressing source of stress for fishes in an eutrophic lake and that almost all other stresses are incidental to, or aggravated by, that primary one '. Interesting quantitative studies on the relationship of eutrophication to the presence and distribution of aquatic bacteria in two English lakes were reported by Collins (1970).

TABLE I. The predominant genera of bacteria containing fish pathogenic species isolated from healthy freshwater fishes (modified after Collins, 1970)

Sampling site Rainbow trout Minnows

Skin slime

Gills

Liver

Kidney Heart Peritoneal cavity

In order of predominance Pseudonzonas Pseudomonas Aeromonas Aeromonas Myxobacteria Myxobacteria Pseudomonas Pseudomonas Aeronwnas Coryneforms Questionables (?) Flavobacteria Sterile Sterile Sterile Sterile Pseudomonas, etc. Sterile (?)

She observed the effect of eutrophication on the increase of types of bacteria which include fish pathogens, incidence of diseases, and the presence of these bacteria in the organs of healthy and diseased fishcs. In an oligotrophic lake the number of bacteria were smaller and their distribution was more uniform than in an eutrophic one. Rains caused washing of bacteria and nutrients from agricultural lands. The presence of aquatic birds, and their droppings, resulted in increased numbers of bacteria. Myxobacteria and flavobacteria were absent in the English lake district for many years. In lakes receiving enrichment from farmland and sewage these yellow pig- mented bacteria became numerous. Collins says that myxobacteria ' appear to be exceedingly good bacterial indicators of the steadily increasing enrichment of freshwater lakes '. This worker noticed frequent outbreaks of columnaris disease in eutrophic lakes. This increase in myxobacteria is reaching a stage when columnaris disease can be expected to be present in English lakes all the year round. Collins

EFFECTS OF ENVIRONMENTAL STRESS ON INFECTIOUS DISEASES OF FISHES 201

made bacteriological examination of the skin surface, gills, and organs of healthy and diseased fishes collected from lakes, impoundments and hatcheries. This information is so revealing that the tables are included (Tables I and 11).

V. SEWAGE It is very difficult to define precisely the importance of each separate stress factor

when fishes are observed in nature. Stresses occur as complexes and their effects are additive or synergistic. Sewage may contain domestic wastes and numerous chemicals. Sewage can be treated in various ways. The purpose of the trcatrnent of sewage is to oxidize organic waste and to eliminate as many pathogenic and faecal bacteria as possible. According to Heuschmann-Brunner (1970) domestic sewage contains a predominance of faecal bacteria. In the treated sewage the number of coliforms is reduced, but replaced by Aeromonas which multiply in the slime lining the pipes carrying the sewage. While coliforms grow best at human body temperature, Aero- monas also grows well at 2 to 20" C. Schubert (1963) related the quantity of Aeromonas

TABLE 11. The predominant genera of bacteria containing fish pathogenic species isolated from diseased freshwater fishes (modified after Collins,

1970)

Sampling site Rainbow trout Minnows

Skin slime

Gills

Liver

Kidney Heart Peritoneal cavity

In order of predominance Myxobacteria (Columnaris) Pseudomonas Pseudomonas A eromoms Myxobacteria (Columnaris) Aeromonas Aeromonas liqucfaciens Pseudomonas Pseudomonas Corynebacterium Corynebacterium Columnaris Corynebacteriuni Sterile (?) Sterile Sterile Pseudomonas Sterile (?) Aeromonus

in open waters to the degree of organic pollution. In a test stream, he found 21 000 to 33 000 Aeromonas and 500 to 700 coliforms per ml of water. Sewer effluent contained 1 to 20 millions of Aeromnnas per ml. Schubert concluded that Aeromonas is important in self-purification of water and that it can be used in the evaluation of organic pollution of water. Aeromonns is also pathogenic for freshwater, coldblooded vertebrates and even occasionally for people. Aeromonas liquefaciens (punctata, hydrophila) is the most common bacterial fish pathogen of freshwater fishes. Its abundance in water inhabited by fishes depends on the organic load of water. There- fore sewage, fish feed, and fish excrements all contribute to the multiplication of Aeromonas and increased biological oxygen demand. It is important to recognize these factars in outbreaks of bacterial fish diseases. During a four month period Vezina and Derochers (1971) examined 450 perch, Perm flavescens (Mitchill) from four lakes in Canada. A . liquefaciens was present in the internal organs of 78 fishes (17%).

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The effect of sewage pollution on marine fishes has been studied in California and in the vicinity of New York City. Near Los Angeles, Young (1964) found that within the polluted area fish had exophthalmus, open external sores; and bottom fishes, such as flatfishes, had numerous epitheliomas and papillomas. Mahoney et al. (1973) studied the summer outbreaks of fin rot in estuarine fishes in the New York Bight area. Affected fishes were found up to 15 miles from shore (Table 111). Necrosis started on dorsal and caudal fins of flounders. In bluefish and striped bass the caudal fin was eroded with some fish becoming completely tailless. In fishes experimentally exposed to the polluted water skin haemorrhages, opaqueness of eyes and blindness were observed. In terminal stages there was an accumulation of fluid in the body cavity and internal haemorrhages. Aeromonas, Pseudonzonas and Vibrio were isolated from the diseased fishes. All strains isolated from marine fishes were halophilic. Mummichog experimentally exposed to infection with bacteria isolated from diseased fishes in the New York Bight area developed typical fin rot and many have died (Table IV).

TABLE 111. Percentage of diseased fishes among principal species collected in the Raritan River, Lower, and Sandy Hook Bay area, July-August, 1967-71

(Mahoney et al., 1973)*

Fish 1967 1968

Bluefish 70 25 Summer flounder 40 45 Winter flounder 25 55 Weakfish

(over 20 cm SL) 35 15 Weakfish

(5-20 cm SL) Landing-May to

September (Million kg) 0.35 0.35

Year 1969 1970 1971

5 40

2

15

60

0.24

1 0 15 7 3 6

3 10

0.20

Most recent observations were made on Lake Apopka, in central Florida, polluted by sewage and waste from citrus groves and processing plants (Shotts et al., 1972). All fishes and amphibians, except the most resistant species, disappeared from this lake before 1971. In the spring of 1971 even the most resistant species of fishes, turtles and alligators started to die with signs of bacterial septicemia. Examination showed that the main cause of disease was A. liquefaciens. ' The widespread distribution and prevalence of Aeromonas spp. among the inhabitants and water of Lake Apopka were quite surprising, as was the general lack of coliforms and other sewage- related microorgunisms. Recovery of almost pure cultures of Aeromonas spp. from the effluent of the sewage-treatment and citrus-processing plants suggested a re1 a t ' ion- ship to the heavy concentration of Aeronzonas in the lake '.

Research results of Collins in England (1 970), Heuschmann-Brunner in Germany (1970), and the recent observations on h k e Apopka in Florida (Shotts et al., 1972) were carried out independently, and very likely without knowledge of each others

EFFECTS OF ENVIRONMENTAL STRESS ON INFECTIOUS DISEASES OF FlSHES 203

work. All observations made in England, Germany, and the United States show that pollution of lakes or estuarine water with sewage results in greatly increased numbers of Aeromonas. This in turn increases the incidence of diseases of aquatic animals in which Aeromonas plays an important role. When one adds stresses caused by low dissolved oxygen, high temperature, and pollution by chemicals, including pesticides, the picture becomes very complicated by the abundance of factors which are con- ducive to outbreaks of infectious diseases of aquatic animals.

VI. METABOLIC PRODUCTS OF FISHES Pungent odours during low tide at the seashore were noticed long before pollution

caused by human activities became significant. Marine animals also metabolize and produce waste. The pungent smell of the seashore, so much appreciated by the summer visitors, is the smell of decomposing waste. As long as the amount of waste is moderate these odours are part of nature's life cycle. Enormous deposits of guano (bird faeces) found on the arid shores in Chile are greatly valued as fertilizer. Where- ever there is a fish hatchery, a fish farm, fresh or salt water, there is also waste created

TABLE IV. Inducement of caudal fin necrosis in mummichog by experimental superficial infection by the isolated assumed to be pathogenic bacteria (Mahoney et al., 1973)"

Type of bacterium No. fish No. fish with No. mortalities inoculated fin necrosis within 15 days

Aeromonas sp. 10 Pseudomonas sp. 10 Vibrio sp. 10 Vibrio sp. (virulent) 5 Enterics 10 Cytophaga (?) 5 Medium alone (control) 10

10 10 10 5 0 0 0

* Condensed.

by fishes. This waste can be used as valuable fertilizer. Every fish culturist knows that crowding results in diseases, and the danger of disease outbreaks is proportional to crowding. Crowding also leads to accumulation of ammonia and increased oxygen demand, the two most common limiting factors in fish culture. The most frequent bacterial diseases caused by crowding are fin rot, columnaris, gill disease, and septicemia caused by Aeromonas in freshwater and Yibrio in saltwater. Enteric bacteria, as Edwardsiella, are now becoming increasingly important as pondfish culture is intensified (Meyer & Bullock, 1973).

The study of detrimental effects of pollution produced by fishes and exerted on fishes is a new field of research. Burrows (1964) and Burrows & Combs (1968) have shown, in their pioneering research, that the incidence of gill disease in hatchery raised salmonids was affected by the rate and pattern flow of water. These authors also have directed attention to the damaging effect of metabolic unionized ammonia on gills of fishes. In a recent paper, Larmoyeux & Piper (1973) further documented this relationship using rainbow trout as experimental fish. Trout were evenly distri- buted among seven tanks arranged in tandem in duplicate. As water flowed through

204 S . F . S N I E S Z K O

these tanks the dissolved oxygen was reduced from 7.7 to 3.3 parts/106 and ammonia increased from 0.1 to 0.8 parts/lOO. In tanks four through to seven the increased load of ammonia resulted in swelling and even fusing of gill lamellae, and the fillamentous bacteria associated with bacterial gill disease became abundant. Haematocrits in trout in the last four tanks were also higher due to haematological compensation stimulated by low dissolved oxygen. Downing & Merkens (1955) reported that the toxicity of ammonia is increased by the decrease in dissolved oxygen. When fish from the stressed tanks were returned to normal conditions the visible signs of stress and pathology disappeared (Smith & Piper, 1973). Meyer & Kramer (1973) used rainbow trout for observation on the rate of metabolism in crowded conditions. They noted that trout kept in lower tanks utilized less oxygen and grew more slowly. It is not clear if the reduced respiration was caused by epithelial proliferation, or if lower oxygen consumption was the physiological effect of dissolved ammonia. These are challenging questions to be answered. Microscopical examination of gills of these experimental trout showed that trout in the lower tanks suffered from myxobacterial gill disease. Fromm (1970) has shown that the presence of unionized ammonia in water hinders excretion of ammonia through the gills in trout. Dissolved ammonia is significantly less toxic for goldfish which excretes urea instead of ammonia.

VJJI. INDUSTRIAL POLLUTION Fishes are used now as important test animals for assaying water pollution. In

short-term tests for acute chemical pollution the role of communicable diseases is not important since tests are completed before infection and disease can develop. En long range assays, stress caused by the tested substance may increase likelihood of outbreaks of infectious diseases. I am not aware of any research carried out explicitly to determine the effect of specific pollutants on outbreaks of specific infectious diseases of fishes. The wide use of fishes in assaying chemical pollution presents an excellent opportunity for such studies. Up to this time, most of the reports on the effect of pollution in outbreaks of infectious diseases were based more on circumstantial evidence than experiments made for this purpose (Mawdesley-Thomas, 1972b). The Chesapeake Bay is highly polluted by every type of waste. Some of this waste is nutritious and causes eutrophication with the increase of bacteria and algae and critical deficiencies of oxygen. Fish kills occur frequently in summer.

From June to September 1963, there were tremendous mortalities among white perch, Morone americana (Gmelin), and lesser kill among striped bass, M. saxatilis (Walbaum) (Snieszko et al., 1964). Millions of fishes were washed out on beaches and the cost of removal was high. The epidemic started at the mouth of the Potomac, it progressed along the western shore of the bay close to Baltimore, crossed the bay to the eastern shore and then southward. The ultimate cause of death was a septicemia caused by a bacterium which was named Pastcurella piscicida (Janssen & Surgalla, 1968). Since that time this bacterium has been isolated in several fish disease outbreaks on the Atlantic Coast, Gulf of Mexico, and in Japan (Simidu & Egusa, 1972; Kusuda & Miura, 1972; Kusuda & Yamaoka, 1972). Another epidemic among white perch in the Chesapeake Bay occurred in summer of 1965. This time the diseased and moribund fishes were dying from a disease caused by C. colurnnaris. Marine biologists believed that, in both cases, the fish mortalities were caused by pollution and that Pastewella piscicida and C. columnaris were opportunists taking


advantage of this occasion. Other investigators were able to reproduce identical diseases of white perch with pure cultures of these bacteria. It seems that these epidemics were excellent examples of a combined effect of bacteria, susceptible hosts, and environmental stress. There is no need to discuss in detail the pathology caused in fishes by the galaxy of chemicals which find their way to water and cause diseases or kills. Salts of zinc, copper and other metals cause coagulation and precipitation of mucus and cytological damage to the gills (Burton et al., 1972; Starr & Jones, 1957; Skidmore, 1970). Coagulation results in reduced gas exchange at the gills, tissue hypoxia and death. When the effect of metal salts is not sufficient to cause fatal hypoxia, the partial hypoxia and gill lesions reduce the resistance and open portals of entry for pathogenic bacteria which may cause diseases if the environmental stress reaches sufficient levels.

An extremely convincing observation on the effect of river pollution by zinc and copper on fish mortalities attributed to A . liquefaciens was described by Pippy & Hare (1969). These outbreaks occurred in August of 1967 and 1968 in the Miramichi River in New Brunswick, Canada, following a surge of copper and zinc pollution at the time when temperature was high and the water was low. The victims were the grilse of Atlantic salmon returning from the sea. Moribund fishes were infected with A. liquefaciens. Test fishes inoculated with the isolated cultures also died. The lesions in naturally diseased salmon consisted of fin rot, external ulcerations, and muscular petechiae. The Irish Sea, near Scotland, is heavily polluted by industrial and domestic waste. In the spring of 1971 plaice, Pleuronectes platessa (L.) and dab, Limanda Iimanda (L.) fishes which spent at least one winter deep in the water, showed lesions similar to that observed by Mahoney et al. (1973) in the New York Bight. They consisted of fin damage, epidermal ulcers, and even lymphocystis. Perkins et al. (1972) who observed this condition, suspect PCB (polychlorinated biphenyls). Bacteriological examination was not made.

Gardner (1973) found that the so-called ‘ crazy ’ or ‘ spinning ’ menhaden Brevoorfia tyrannus (Larrobe) collected from heated effluent at Millstone Point in Connecticut displayed foci of inflammation, increase in eosinophils, popeye, and eye haemorrhages which are characteristic in some infectious diseases of fishes. Heat stress often results in outbreaks of bacterial diseases, and the omnipresence of Vibrio anguillariim in coastal waters is well established but bacteriological examination of diseased fishes was not made in this case. Butler (1969) reported that test fish exposed to low concentrations of carbaryl and 2,4-D for several months, showed invasion of the central nervous system by an undetermined myxosporidan parasite. The incidence of infection with this parasite was much lower in the unexposed controls.

Butler (1969) also observed an opposite effect. Oysters in the Gulf Coast area are often infected with a fungus. Test oysters exposed to common pesticides were free of the fungus parasite. This is similar to the effect of the herbicide ‘ Diquat’ which, according to Wood (1968), is used for effective control of bacterial gill disease and external infections caused by C. columnaris. Shimada (1972), Japan, observed that guppies and trout given food containing DDT showed pathological changes in the intestines, spleen, adrenal and thyroid glands. The author believes that DDT was the primary cause of a secondary bacterial invasion of the lesions. In experiments on the effect of Mirex, a pesticide used for control of the fire ant, Van Valin et al. (1968) observed that goldfish, but not bluegills, from earthen ponds developed granulomas containing acid-fast bacteria. The incidence of these lesions was much greater in

206 S . F . S N I E S Z K O

goldfish exposed to Mirex than in controls. It is important to note that this occurred only in earthen ponds. The first observation of mycobacteriosis in carp held in earthen ponds was made in France by Bataillon et al. (1897). One has to remember that soil and plants contain an abundance of mycobacteria and similar acid-fast organisms.

VUCI. PESTICIDES Couch (1973) found that in flowing sea water, 95% of spot, Leiosfonius xantlzurus

(Lac6p;de), exposed for up to 30 days to Arachlor, a PCB, developed fin rot similar to that observed by Mahoney et al. (1973) in the New York Bight. There was no fin rot in the controls. Microbiological examination of the affected fish was not made. Treatment with sulfamerazine and aureomycin (mode of administration not given) had no visible beneficial effect. Couch did not intend to study the effect of these chemicals on the presence of infectious diseases in fishes. The fact that chemicals often caused pathological changes in the liver brings to my mind the previously discussed paper by Collins (1970) where a greater incidence of bacteria in the liver of fishes living in the polluted lakes than in the oligotrophic lakes was found. We believe that the aggravating effect of stress, from various types of pollution, causes a high incidence of infectious diseases in fishes. Unfortunately, this belief, which I also intuitively share, is not as yet adequately documented.

This brings me to a thought on the evolution of science in general and this can be graphically presented by a hyperbola. When one goes away from the focus, the hyperbola covers larger and larger areas, similar to the geometric growth of science in 10 year periods. The hyperbola contacts the assymptotes in the infinity. Similarly, science is growing faster and faster and may answer all questions in the infinity.

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water temperature. J. Fish. Res. Bd Can. 27, 265-270. Bataillon, Dubard et Terre* (1897). Un nouveau type de tuberculose. C.r. hebd. Seanc.

Acnd. Sci., Paris 4, 446-449. Bisset, K. A. (1947). Bacterial infection and immunity in lower vertebrates and invertebrates.

J. Hyg., Camb. 45, 128-135. Burrows, R. E. (1964). Effects of accumulated excretory products on hatchery-reared

salmonids. Res. Rep. U.S. Fish. Wildl. Sew. 66, 12. Burrows, R. E. & Combs, B. D. (1968). Controlled environments for salmon propagation.

Progve Fish Cult. 30, 123-136. Burton, D. T., Jones, A. H. & Cairns, J. Jr. (1972). Acute zinc toxicity to rainbow trout

(Sulmo gnirdneri) : confirmation of the hypothesis that death is related to tissue hypoxia. J. Fish. Res. Bd Can. 29, 1463-1466.

Butler, P. A. (1969). The sub-lethal effects of pesticide pollution. In Environmental Health Sciences Series No. 1 , The Biologicnl Impact of Pesticides in the Etzvironnzent (Ed. Gillett, J. W.), pp. 87-89. Corvallis: Oregon State University.

Collins, V. G. (1970). Recent studies of bacterial pathogens of freshwater fish. Wat. Treat. Exam. 19, 3-31.

Couch, J. A. (1974). Histopathologic effects of pesticides and related chemicals on the livers of fishes. In Symposium on Fish Pathology (Eds Ribelin, W. E. & Migaki, G.). Madison: University of Wisconsin Press.

Cushing, J. E. (1971). Immunology of fish. ln Fish Physiology (Eds Hoar, W. S. & Randal, D. J.), pp. 465-500. New York: Academic Press.

* Initials of authors not given.


Downing, K. & Merkens, J. C. (1955). The influence of dissolved oxygen concentrations on the toxicity of un-ionized ammonia to rainbow trout (Salmo gairdneri, Richardson). Ann. appl. Biol. 43, 243-246.

Fijan, N. N. (1972). lnfectious dropsy in carp-a disease complex. In Diseuses of Fish (Ed. Mawdesley-Thomas, L. E.), pp. 39-51. London: Academic Press.

Fromni, P. 0. (1970). Toxic action o f water soluble pollutants on freshwater fish. Water Pollut. Res. Control Series 18050, 56.

Fry, F. E. J. (1969). Some possible physiological stresses induced by eutrophication. In Eutrophication: Causes, Consequences, Correctives, pp. 53 1-536. Washington : National Academy of Science.

Gardner, G. R. (1974). Chemically induced lesions in estuarine or marine teleosts. In Symposium on FishPathology (Eds Ribelin, W. E. & Migaki, G.). Madison: University of Wisconsin Press.

Haley, R., Davis, S. P. & Hyde, J. M. (1967). Environmental stress and Aeromonas liquefaciens in American and threadfin shad mortalities. Prugve Fish Cult. 29, 193.

Heuschmann-Brunner, G. (1970). Die Aeromonaden in der Hydrobiologie. 2. Wusser Abwasser Forschung (WAF) 3 ,4041.

Janssen, W. A. & Surgalla, M. J. (1968). Morphology, physiology, and serology of a Pasteurella species pathogenic for white perch (Roccus americanus). J. Bact. 96, 1606-1610.

Kusuda, R. & Miura, W. (1972). Characteristics of a Pasteurella sp. pathogenic for pond- cultured Ayu. Fish Pathology 7 (I), 51-57.

Kusuda, R. & Yamaoka, M. (1972). Etiological studies on bacterial pseudotuberculosis in cultured yellowtail with Pasteurella piscicida as the causative agent-1. On the morphological and biochemical properties. Bull. Jap. Sue. wienf. Fish. 38, 1325-1 332.

Larmoyeux, J. D. &Piper, R. G. (1973). Effects of water reuse on rainbow trout in hatcheries. Pr0gi.e Fish Cult. 35, 2-8.

Liebmann, H., OfThaus, K. & Riedmiiller, S. (1960). Elektrophoretische Blutuntersuchungen bei normalen und bauchwassersuchtkranken Karpfen. Schweiz. 2. Hydrol. 21,

Mahoney, J. B., Midlige, F. H. & Deuel, D. G . (1973). A fin rot disease of marine and euryhaline fishes in the New York Bight. Trans. Ain. Fish. SOC. 102, 596-605.

Mawdesley-Thomas, L. E. (Ed.) (19720). Diseases of Fish, p. 11. London: Academic Press. Mawdesley-Thomas, L. E. (1972b). Research into fish diseases. Nature, Lond. 235, 17-19. Meyer, F. L. & Kramer, R. H. (1973). EfTects of hatchery water reuse on rainbow trout

metabolism. Progve Fish Cult. 35, 9-10. Meyer, F. P. (1970). Seasonal fluctuations in the incidence of disease on fish farms. Am.

Fish. Soc. Symp. Special Publication 5, 21-29. Meyer, F. P. & Bullock, G. L. (1973). A new pathogen of channel catfish (Zctaluru~punc~uatus).

Appl. Microbiol. 25, 155-156. Perkins, E. J., Gilchist, J. R. S. & Abbott, 0. J. (1972). Incidence of epidermal lesions in

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Documents

The Effects of Environmental Stress on Outbreaks of Infectious Diseases of Fishes