EVALUATION OF PROCEDURES FOR THE DIAGNOSIS OF BRUCELLA OVIS INFECTION IN RAMS

Procedures for the diagnosis of Br. ovis infection in rams were evaluated by examining 10 rams artificially infected by preputial inoculation. Observations were undertaken at weekly intervals for 1 year to follow changes in clinical, bacteriological and serological findings. Clinical lesions were detected in 1 ram 3 weeks after inoculation and in all rams by 8 weeks; lesions were undetectable in 3 rams at the completion of the trial. The presence of inflammatory cells in semen samples was the earliest indication of infection being demonstrated in 2 rams at 2 weeks and in all rams by 8 weeks; subsequently 86% of samples were positive. Br. ovis was detected in semen smears from 3 rams at 4 weeks but only once in all rams (at 27 weeks); overall 52% of semen smears were positive from 4 weeks onwards. Br. ovis was cultured from semen of 5 rams after 4 weeks and from all rams at 5 weeks; thereafter 97% of samples were positive. All rams developed significant titres to the CFT between 2 and 9 weeks; thereafter the CFT was a reliable indication of infection in 6 rams, highly suggestive in 3 and unreliable in one. By 8–10 weeks all rams developed significant titres to the IHA which were then maintained in all rams for the remainder of the trial.     

EXPERIMENTAL ENCEPHALOMYOCARDITIS VIRUS INFECTION IN CALVES

Nine calves, were inoculated intravenously with the Innisfail strain of encephalomyocarditis (EMC) virus. Apart from a mild fever, no obvious clinical signs were noted. A low titre viraemia was demonstrated in all 5 calves from which blood was collected, and EMC virus was recovered from the myocardium of 3 of 6 calves at 2, 3 and 6 days after inoculation. Virus was not recovered from the central nervous system. No excretion of EMC virus in urine or faeces was detected in 3 calves. Histopathological lesions were present in brain tissue from only 1 calf, destroyed 14 days after inoculation, and in the heart muscle from another calf, destroyed 7 days after inoculation. Macroscopic lesions were not seen in these organs. Both neutralising and haemagglutination-inhibiting antibodies were produced within one week of infection, reached a peak in 3–4 weeks and persisted undiminished until 9 weeks after inoculation. By nitration on Sephadex G 200, it was shown that the early response was due to IgM type antibodies, and these were replaced by IgG antibody. One calf was inoculated intracerebrally with EMC virus. It developed a flaccid posterior paralysis and was destroyed 6 days later. Virus was recovered from the brain and spinal cord, but no significant histopathological lesions were detected in brain or spinal cord from this calf.     

EXPERIMENTAL SALMONELLA ANATUM INFECTION IN HORSES

SUMMARY Salmonella anatum was given orally to 8 horses on 11 occasions in doses ranging from 9.5 × 10⁶ to 8.8 × 10¹¹ organisms. Four distinct syndromes were induced based upon clinical, laboratory and pathological findings: (1) asymptomatic; (2) moderate clinical signs with or without changes in faecal consistency; (3) fever, depression, anorexia with unstructured or diarrhoeic faeces; and (4) septicaemia with or without diarrhoea, and peripheral circulatory failure. All animals excreted the organism. The peak temperature preceded the onset of diarrhoea by 1 or 2 days. Changes in faecal consistency were associated with direct isolation of the organism. The degree of neutropaenia increased with the dosage. Blood cultures were unsatisfactory, only 1 of 33 samples being positive. The serological responses were not significant although one animal displayed a significant seroconversion consistent with the clinical reaction. Indomethacin was not of value in moderating intestinal fluid secretion in one animal. The distribution and quantitation of positive cultures at autopsy closely reflected the type of syndrome induced. The invasiveness of the organism was confirmed by frequent direct recoveries from intestinal wall and draining lymph node samples. S. anatum appears to be of similar pathogenicity to S. typhimurium in the horse, at least under experimental conditions.