D. A. Pass

Investigations into the causes of mortality of the pearl oyster, Pinctada maxima (Jamson), in Western Australia

Abstract An investigation into the cause of high mortality of the pearl oyster, Pinctada maxima , in the north-west of Western Australia was carried out over a 3-year period. Pathological and microbiological investigations revealed that the majority of diseased oysters were infected with marine Vibrio bacteria. One common isolate, Vibrio harveyi , was shown experimentally to induce disease similar to that seen in the field. Pearl oyster mortality during pearling industry operations occurred following transportation of oysters in tanks on carrier boats from collection grounds to oyster lease sites. The number of marine Vibrios in the water of carrier tanks increased rapidly during transportation because of inadequate water circulation and this was believed to be the time when infection occurred. Mortalities were greatest at times when water temperatures were lowest and experiments showed that oysters were most susceptible to disease at these low temperatures. It is postulated that oysters, weakened by exposure to low ambient temperature, come into contact with high concentrations of bacteria during transportation to lease sites at which time bacterial invasion occurs.

Chronic eosinophilic gastroenteritis in the horse.

Four cases of chronic eosinophilic gastroenteritis in horses are described. The disease was manifested clinically by weight loss, malabsorption and diarrhea or soft, formless feces. A chronic inflammatory reaction, with diffuse and focal eosinophilic infiltrates, was present in the esophagus, stomach, small and large intestine, and mesenteric lymph nodes. The cause of the lesion was not determined but was thought to be due to an ingested allergen, as the lesion is indicative of an on-going, immediate hypersensitivity reaction. One horse had generalized acanthosis, hyperkeratosis, and ulcerative coronitis.

Canine Parvoviral Myocarditis: A Morphologic Description of the Natural Disease:

Naturally occurring acute parvoviral myocarditis in puppies 3 to 8 weeks of age was characterised clinically by sudden death or death following a brief period of dyspnoea. Mortality within litters varied from 20% to 100%. The principal lesion was in the myocardium, which in most cases was mottled by pale patches and bands. Moderate to severe pulmonary oedema with marked peribronchial and perivascular oedema was present. In some cases, the wall of the gall bladder was oedematous. Microscopically the ventricular myocardium had myofibre loss, multifocal myofibre necrosis, a mononuclear cell infiltrate of variable intensity and reactive stromal elements. In every case there were Feulgen-positive, amphophilic, intranuclear inclusion bodies in myocardial nuclei. Ultrastructurally the inclusions were composed of dense granular material and particles resembling parvovirions. Pulmonary alveolar septae were thickened by fibroblasts. Peribronchial and perivascular lymphatics were distended with oedema fluid and occasionally erythrocytes. The pulmonary lesions were considered secondary to the myocardial dysfunction. Some of the puppies that survived the acute disease developed ventricular myocardial fibrosis and died in congestive heart failure.

Poisoning of chickens and ducks by pyrrolizidine alkaloids of Heliotropium europaeum.

The disease produced by feeding chickens and ducks a commercial poultry feed containing heliotrine and lasiocarpine, pyrrolizidine alkaloids of Heliotropium europaeum, is described. Illthrift, ascites and degenerative lesions in the liver were the major findings. Similar lesions occurred in chickens fed a diet containing H. europaeum. The source of the alkaloids in commercial poultry feed was probably the seeds of H. europaeum harvested with wheat.

Pathophysiology of Mesocestoides corti infection in the mouse.

Liver histology and serum enzyme and protein changes were studies in two strains of mice showing different initial susceptibilities to infection with Mesocestoides corti. The results show an increase in ALT and AST levels during the period of invasion and proliferation in the liver and a decrease in the levels of these two enzymes following encapsulation of the parasite in the liver and liver regeneration. A progressive loss of albumin was accompanied by increases in the levels of the beta- and gamma-globulins. These changes are discussed in the light of our knowledge of the effects of this parasite upon its host.

BCG-induced inhibition and destruction of Taenia taeniaeformis in mice.

Summary Pretreatment of mice with BCG induced a high level of protection against infection with Taenia taeniaeformis. Protection was manifested both during and after establishment by the parasite suggesting that two separate mechanisms were stimulated by BCG. The first inhibits initial establishment by the parasite and may be antibody mediated. The second is responsible for the destruction of developing strobilocerci in the liver and may require the involvement of cellular defence mechanisms.

Basophilic Enterocolitis in a Horse

phoid tumors are relatively common neoplasms in most domestic animals.’ Those classified as lymphosarcoma are much more frequent than lymphocytic leukemias. This is the first reported case of lymphocytic leukemia in the ferret. A one-year-old male ferret was housed in an outdoor Wire mesh enclosure with a female ferret. The ferrets had been in good health until the male was found dead unexpectedly one morning. On gross examination, the mesenteric lymph nodes, anterior thoracic lymph nodes, and spleen were enlarged. The liver was swollen and pale. Histological examination revealed a marked leukemic infiltration in all organs examined. The tumor cells were pleomorphic round cells with round or indented nuclei containing clumped chromatin and one or more prominent nucleoli. Cytoplasm was scant, and mitotic figures were rare. The architecture of the lymph nodes was effaced and the leukemic cells had invaded the capsule and perinodal fat. The hepatic sinusoids were flooded with tumor cells resulting in extensive atrophy of the hepatic cords. (figs. 1,2) A diagnosis of a welldifferentiated lymphocytic leukemia was made. Serum from this ferret was not available, however, the female ferret housed in the same cage was bled and found to be FeLV negative. References

Investigations of an enteric infection of cockatoos caused by an enterovirus-like agent

An enteric infection in cockatoos associated with a 30nm diameter enterovirus‐like agent seen in faeces and intestinal epithelial cells is described. The disease is characterised by intractable, profuse, mucoid diarrhoea, weight loss, dehydration and death. Lesions in the intestine consist of villous atrophy, villous fusion, enterocyte hyperplasia and, in some cases, chronic inflammation. Affected birds so far examined have concurrent psittacine beak and feather disease.