A morbillivirus has been isolated and added to an increasing list of emerging viral diseases. This virus caused an outbreak of fatal respiratory disease in horses and humans. Genetic analyses show it to be only distantly related to the classic morbilliviruses rinderpest, measles, and canine distemper. When seen by electron microscopy, viruses had 10- and 18-nanometer surface projections that gave them a "double-fringed" appearance. The virus induced syncytia that developed in the endothelium of blood vessels, particularly the lungs.

The epidemiology of melioidosis was investigated in 8 intensive piggery units which used water from the same river in south eastern Queensland. In 3 consecutive years cases of disease followed heavy rainfall and flooding. Although Pseudomonas pseudomallei was not isolated from water or soil samples the water supply was suspected as the source of infection. Affected pigs were detected at slaughter by the presence of abscesses most commonly in the bronchial lymph nodes (40%) and spleen (34%). One hundred and fifty nine cases were observed at slaughter from a total of 17,397 animals at risk. Infection by inhalation of water aerosols derived from nipple drinkers, hose sprays and a water misting cooler was considered to be responsible for the bronchial lymph node lesions. These outbreaks occurred outside the area in which melioidosis is generally regarded as being endemic.

Laboratory examinations of equine morbillivirus included experimental reproductions of the disease caused by the virus by transmission of mixed lung and spleen taken from two field equine cases into two horses and by inoculating tissue culture virus into a further two horses. The most distinctive gross lesions of the diseases that developed in three of the horses was that of pulmonary edema characterized by gelatinous distension of subpleural lymphatics. Histologically, the lesions in the lungs were those of serofibrinous alveolar edema, alveolar macrophages, hemorrhage, thrombosis of capillaries, and syncytial cells. Clearly defined vascular lesions in three horses that became clinically affected within 8 days of inoculation of virus included intramural hemorrhage, edema, and necrosis and syncytial cells in the endothelium of pulmonary vessels (approximately 40-70 microm in diameter). Vascular lesions accompanied by parenchymal degeneration were also seen in the heart, kidney, brain, spleen, lymph node, and stomach. A fourth horse, which survived for 12 days, had detectable lesions only in the lungs, which were more chronic than those in the other three horses, a greater degree of cellular infiltration, and fewer well-defined vascular lesions. Sections stained by an indirect immunocytochemical method showed equine morbillivirus antigen was present in the vascular lesions and along alveolar walls. When endothelial cells were examined by electron microscope, cytoplasmic virus inclusion bodies containing filamentous structures were seen that reacted to an immunogold test to equine morbillivirus antigen. The presence of the syncytia in the small blood vessels in the lungs and other organs was interpreted as an important characteristic of the disease and consistent with a reaction to a morbillivirus.

This paper reviews the laboratory diagnosis of Leptospira hardjo infection in cattle. Two genotypes of L hardjo, Hardjoprajitno and Hardjobovis, have been identified in cattle, but only Hardjobovis has been isolated in Australia. There are problems with diagnosis and control of bovine leptospirosis. Infection is usually subclinical and the serological titres vary greatly in peak and duration. Leptospires may be excreted in urine for up to 18 months. Low microscopic agglutination test titres may be significant in unvaccinated herds as indicators of endemic infection. Vaccines differ in their composition, and their efficacy is difficult to evaluate. The serological response after vaccination is difficult to differentiate from the response after infection. Pregnant cows that become infected may abort, but this is usually after the serological response has peaked. Therefore, paired serum samples are of little use in diagnosing abortion caused by L hardjo. Fluorescent antibody techniques are more sensitive than dark field microscopy for detection of leptospires in urine and tissue samples. Techniques for culture have improved but are still difficult to perform and take 3 months or longer for results to be known. DNA probes and polymerase chain reaction tests are very sensitive and specific, quick to perform, and can be used on fluid and tissue samples.

Two cases of lnortalities in cultured red claw Materials and methods. Since 1989, sick or dead red crayfish Cherax quadricarinatus associated with systemic Vibno mimicus infections are described. In these cases, V rnirnicus appears to have been an opportunistic pathogen following stress caused by either overcrowding or mismanagement and poor water quality. Humans consuming raw or improperly cooked infected crayfish could be at risk of contracting gastrointestinal disease.