12 Observations on Vibriosis in Cultured Flatfish

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76 R. H Richards

Gross lesions and clinical signs also varied with the species of fish, age and tempe

rature, but could be broadly classified as follows:

1 Peracute Death often occurred with no visible gross changes except for a dark

ening of colouration. n young 0+ turbot, peri-orbital oedema and gut oedema with

copious quantites of peritoneal fluid were also found. This resulted in gross abdominaldistension and typical white circlets of tissue surrounding the eye. Skin lesions were

absent. Following a peracute outbreak, an acute syndrome often developed.

2 Acute Two main classes of lesion were generally found. In both cases fish were

inappetant, dark in colour and lethargic. Erosions of the jaw area were frequently

found as a primary lesion in turbot of all age-classes. Cytophaga spp. organisms were

usually present in such areas in large numbers, as well as a range of other bacteria in

cluding a variety of Vibrio spp. The large numbers of Cytophaga often led to a dis-

tinct yellow or orange colouration of the lesion. Further lesion development then

principally involved either skin and superficial musculature, or internal organs.

Skin lesions usually commenced with an increased quantity of mucus and dis-

tinct haemorrhages in a number of areas, but principally involving the fins. In more

long-standing cases, sloughing of areas of skin associated with haemorrhage was often

seen. Gross internal lesions were seldom seen and lesions progressed more rapidly at

higher temperatures. Fish were also affected with Vibrio spp. infections without

marked skin lesions. In these cases haemorrhages were evident in many of the internal

organs, the gut was often inflamed and contained a thick mucus, and quantities of

straw-coloured or blood-stained ascitic fluid were found. The gills were usually pale

in colour.

3 Chronic Chronic skin lesions were generally deep ulcers with marked haemorrhage and fibrin deposition. On occasion, ulceration penetrated through the abdominal

wall, leading to protrusion of the viscera through the fistula. In Dover sole, areas of

dark-coloured necrotic skin developed very rapidly, forming the condition now

commonly referred to as black patch disease. In systemic cases, peritoneal fluid still

remained and fish often showed peritoneal adhesions. Gills were again pale in colour

and chronic infections of the eye often led to evulsion of orbital contents.

Histopathology

1 Peracute In juvenile turbot, there was a pronounced submucosal oedema of the

gut with congestion and occasional haemorrhage, but the epithelium appeared normal.

Muscular layers were variably affected with oedematous change (Fig. 1 a). Oedema of

the choroid and the muscular and fibrous tissues surrounding the orbit was also pre

sent with spongiotic changes in overlying epidermis. This process extended around ner

ve trunks where it was often associated with an inflammatory response. Retinal oedema

led to retinal detachment at the junction between the neural layers and the pigment

epithelium.

The atrium of the heart showed myofibrillar necrosis with sloughing of the atrial

endothelium. Liver showed areas of focal necrosis (Fig. 1 b) and varying degrees of

fatty degeneration, but the latter change was also variably present in apparently healthy

fish and thought to be associated with dietary imbalance. Haematopoietic tissue was



Observations on Vibriosis in Cultured Flatfish

Fig. 1 a Gut oedema. and E x125. Note submucosal and muscle oedema. b Liver. and E

x320. Extensive focal necrosis. c Integument. and E x50. Note sloughing epidermis (u owed).

extensive hypodermal bacterial infection b) and muscular inflammatory response m). d Kidney.

Perl s stain x125. Note iron deposits in melanomacrophage centres (a owed)



Observations on Vibriosis in Cultured Flatfish 79

Reduction of temperature was occasionally beneficial but care must be taken not

to reduce feeding response.

iscussion

The aetiology of vibriosis in marine flatfish is complex. Outbreaks often occur following

netting of wild 0+ stock and subsequent transfer to ongrowing facilities. Skin lesions

caused during netting allow entry of a variety of pathogenic organisms and strains of

V anguillarum and other ibrio species readily proliferate in such areas. Particularly

pathogenic strains of V anguillarum have always caused systemic vibriosis and strains

with different temperature optima have been isolated. t has recently been found that

initial isolation of some pathogenic strains of ibrio anguillarum depends upon the

presence of blood in the isolation medium (Horne, personal communication 1979).

The strains involved are probably opportunist invaders, the type of bacteria present

depending on the skin (or gut) flora, which is generally a reflection of the bacteriolo

gical status of the environment (Evelyn and McDermott, 1961; Horsley, 1973). Trans

fer of fish from one locality to another may expose them to new strains of bacteria to

which they have little immunity, although there is evidence that amongst the genus

ibrio there may be homologous plasmids responsible for pathogenicity (Crosa et aI.,

1977). As fish are fed on marine offals, there is also the likelihood of introducing

quantities of a variety of ibrio spp. via the food, suspected as a cause of ibriosis

in freshwater farming systems.A number of species and strains of ibrio are apparently involved in causing

disease in flatfish. t has been suggested that the marine vibrios form a spectrum of

organisms with heterogeneous properties rather than a number of well-defined species

(Baross et aI. 1978) but the isolation of types from diseased turbot serologically iden

tical with strain 1669 affecting sahnonids in the Pacific Northwest (Novotny, personal

communication) demonstrates a widespread occurrence and an apparent lack of host

specificity, although for instance the haemolysins produced may show a variation in

effect between species (McArdle, 1973).

t the farm in question, heated effluent from a power station is mixed with

ambient sea water to produce higher mean temperatures suitable for increased growth.Unfortunately, pump failures occasionally lead to rapid temperature fluctuations, and

under such conditions outbreaks of vibriosis rapidly develop. Chlorination is used to

control pollution in piping systems. t low levels this is advantageous in controlling

populations of bacteria and other pathogens. On occasion, however, flushes of chlorine

of higher concentration pass through the farm and these have led to gill and skin da

mage resulting in outbreaks of disease.

Traumatic damage occurs during netting and the nature of the tank surface may

also be responsible for early damage to the jaw area which often precedes a clinical

outbreak. The reduction in the incidence of black patch disease by the provision of

sand may be due to the removal of excess mucus and bacteria from the skin surface.

Healing certainly improves considerably when excessive mucus and dead tissue are re

moved, as in the treatment of sahnonid bacterial gill disease (Cawley, 1976).



80 R. H. Richards

Vibriosis in marine flatfish has been described on a number of occasions but with

the exception of reports from Britain Anderson and Conroy, 1968; Horne et aI., 1977)

most reports have been concerned with wild fish e.g. Levin et al., 1972). The peracute

syndrome in juvenile turbot was essentially as previously described by Horne et a1 in

1977 with the exception of marked gut oedema seen since that date. Such a syndromehas so far only been noted in juvenile turbot. The oedema is thought to result from

cardiac failure and perhaps an effect on capillary permeability rather than through re-

nal failure Horne et al., 1977). Except for the work of Horne et a1 1977) only an

acute to chronic condition involving skin ulceration with the development of anaemia

has been described. Although no haematological measurements were made in the pre-

sent work, evidence of damage to haematopoietic tissue and accumulation of iron de-

posits predominantly in the spleen [similar to those described by Agius 1979)] suggests

anaemia with compensatory haematopoiesis in the more chronic condition. Skin

lesions were similar to those described by Hodgkiss and Shewan 1950), Anderson and

Conroy 1970), Levin et al. 1972), and McArdle 1973). Inflammatory response des-

cribed by Levin et a1 1972) consisted principally of lymphocyte infiltration. The res-

ponse in the present work was more pronounced at higher temperature and was of

mixed cell-type.

Healing of skin wounds would appear to depend on the absence of necrotic ma-

terial and bacteria and the effects of temperature. Many vibrio strains are more active

at higher temperatures Le. 15 0-20 0c) and a reduction in temperature, though re-

ducing the speed of healing, markedly inhibits proliferation of such strains. t is for

this reason that a temperature reduction often aids recovery, though strains active at

lower temperature have been found, parallelling fmdings in the USA Harrell et al.,

1976; Sawyer, personal communication 1976).

Death in vibrio outbreaks is thought to result from toxic damage to parenchymal

organs Umbreit and Tripp, 1975) or through anaemia Tanaka, 1974). t also seems

extremely likely that death from osmotic imbalance such as occurs in Sapro egniIJ in-

fections in salmonids Richards and Pickering, 1979) is a common sequel to extensive

ulceration and loss of skin surface.

Vibriosis may be controlled by careful husbandry practice, prompt and rational

use of antibiotics and perhaps, in future, through vaccination programmes.

References

Agius C 1979) The role of melano-macrophage centres in iron storage in normal and diseased fish.

J Fish Dis 2:337-343

Anderson JlW, Conroy DA 1968) The significance of disease in preliminary attempts to raise

flatfish and salmonids in sea water. Bull OffInt Epiz 69 7-8):1129-1137

Anderson JlW, Conroy DA 1970) Vibrio disease in marine fishes. In: Snieszko SF ed) A sym

posium on diseases of fishes and shellfishes. American Fisheries Society. Spec Publ No 5,

Washington DC

Bagge J, Bagge 0 1956) Vibrio nguillllrum as the cause of ulcer disease in torsk Gadus call1lrills

Linne) Danish). Nord Veterinaermed 8:481-492

Baross JA, Liston J, Morita RY 1978) Ecological relationship between V. p r hoemolyticus and

agar digesting vibrios as evidenced by bacteriophage susceptibility patterns. Appl Environ

MicrobioI36:500-505

12 Observations on Vibriosis in Cultured Flatfish

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