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J. Fish Biol.

(1974) 6, 197-208
The effects of environmental stress on outbreaks of
infectious diseases of fishes*
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.
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 intro-
duction 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 under-
stand 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.
I t 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.
I t 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.
198 S . F . SK I ESZK O
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.
I n 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, 1972) 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 tem-
perature 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
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. I n 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 con-
trolled by lowering temperature to 15" C or less (Wood, 1968). Infectious haemato-
poietic 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). I n 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). I t 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.
Oxygen is essential for respiration, but nitrogen is biologically inert. Both are
dissolved in water and both are involved in fish diseases if present i n 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). I n 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. I n 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 super-
saturation 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. SNI ESZKO
sapidissirnu (Wilson) in San J oaquin 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
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 dis-
tribution 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
Peritoneal cavity
In order of predominance
Pseudonzonas Pseudomonas
Aeromonas Aeromonas
Myxobacteria Pseudomonas
Pseudomonas Aeronwnas
Coryneforms Questionables (?)
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. I n 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. I n 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 fresh-
water lakes '. This worker noticed frequent outbreaks of columnaris disease i n
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
made bacteriological examination of the skin surface, gills, and organs of healthy
and diseased fishes collected from lakes, impoundments and hatcheries. This in-
formation is so revealing that the tables are included (Tables I and 11).
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. I n 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,
Sampling site Rainbow trout Minnows
Skin slime
Peritoneal cavity
In order of predominance
Myxobacteria (Columnaris) Pseudomonas
Pseudomonas A eromoms
Myxobacteria (Columnaris) Aeromonas
Aeromonas liqucfaciens Pseudomonas
Corynebacterium Corynebacterium
Corynebacteriuni Sterile (?)
Sterile Sterile
Pseudomonas Sterile (?)
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 con-
tained 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
202 S . F. SNI ESZKO
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
(over 20 cmSL) 35 15
(5-20 cmSL)
Landing-May to
(Million kg) 0.35 0.35
1969 1970 1971
1 0
15 7
3 6
3 10
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. I n 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 distri-
bution 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 hk e Apopka in Florida (Shotts et al., 1972)
were carried out independently, and very likely without knowledge of each others
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.
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
* 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. SNI ESZKO
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.
Fishes are used now as important test animals for assaying water pollution. I n
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. Enlong
range assays, stress caused by the tested substance may increase likelihood of out-
breaks 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 J une 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 septi-
cemia caused by a bacterium which was named Pastcurella piscicida (J anssen &
Surgalla, 1968). Since that time this bacterium has been isolated in several fish
disease outbreaks on the Atlantic Coast, Gulf of Mexico, and in J apan (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. I t 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 & J ones,
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 con-
centrations of carbaryl and 2,4-D for several months, showed invasion of the central
nervous system by an undetermined myxosporidan parasite. The incidence of in-
fection 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), J apan, 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. I n 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 . SNI ESZKO
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
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. J r. (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.
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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. l n 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 of 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 lique-
faciens 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.
J anssen, W. A. & Surgalla, M. J. (1968). Morphology, physiology, and serology of a
Pasteurella species pathogenic for white perch (Roccus americanus). J. Bact. 96,
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