In the epidemiology of bovine viral diarrhoea (BVD), immunotolerant – persistently infected animals (IPI) appear to be major sources of contamination. These animals produce large quantities of replicating virus and have therefore been proposed as being responsible for generating antigenic variability. However, limited studies have failed to detect antigenic or genetic changes in viruses isolated at different times from IPI. An hypothesis is that the immunotolerance of IPI against their homologous strain is accompanied by immune elimination of antigenic variants. The presence of an IPI in a herd could therefore limit antigenic variation, eventually leading to the existence of herd specific strains. To verify this hypothesis we characterized, against a panel of monoclonal antibodies, 37 BVD virus strains isolated from IPI of 12 herds in Eastern Belgium. Intra-herd antigenic variation was compared to inter-herd variation. Antigenic variation within herds was found to be surprisingly high but, nevertheless, significantly lower than variation between herds.

Pseudomonas aeruginosa is not generally considered a cause of infectious diarrhoea. However, it was the predominant organism isolated from the faeces of 23 unrelated, hospital outpatients investigated in the course of a year for persistent (>1 week duration) diarrhoea. To investigate the possible aetiological role of P. aeruginosa, these patient histories were reviewed and a selection of their faecal isolates were investigated in vitro (n[ges ]10) and in vivo (n=2) for virulence. The patients had a mean age of 60 years, were receiving antibiotics and/or had an underlying illness. Extensive microbiological investigations identified no other potential or recognized enteropathogen in the faeces of 20 of these patients. More than 40% of the isolates tested were able to adhere to HEp-2 cells and exhibited twitching motility (type IV pili), properties indicative of their ability to colonize the human intestine. Cytotoxic activity was demonstrated in bacterium-free cell supernatants of over 80% of isolates; supernatants of four isolates tested in infant mice were weakly enterotoxigenic. Two isolates intragastrically inoculated into clindamycin pre-treated rats established persistent infections and induced signs and symptoms of enteritis. Overall these findings suggest that P. aeruginosa can cause diarrhoea particularly in immunodeficient individuals.

Two groups of pigs were infected with a recent Italian isolate of swine vesicular disease virus (SVDV). Blood, nasal swabs and faeces were collected for up to 6 months after exposure to infection and animals were killed at regular intervals to obtain tissues post-mortem. These samples were examined for virus by conventional means and for viral RNA (vRNA) by reverse transcription-nested polymerase chain reaction (RT-nPCR). Virus was identified intermittently from both clinically and subclinically infected animals in nasal swabs, faeces and tonsillar tissue by either virus isolation or RT-nPCR up to 63 days post infection (dpi). Between 63 and 119 dpi virus was not detected in the secretions, excretions or tissues of any pigs. Following mixing of the two groups of animals at 119 dpi, SVDV was again identified in faeces for up to 7 days suggesting that the stress of mixing reactivated the excretion of virus in pigs from which the agent could no longer be identified. Minor antigenic changes were identified between the parental virus and isolates recovered late in the course of infection. Altered antigenicity corresponded with deduced amino acid substitutions identified from differences in nucleotide sequence between early and late isolates. This investigation demonstrates that SVDV and vRNA can be present in pigs for considerably longer after exposure to infection than has previously been recognized and provides preliminary evidence for a carrier state in swine vesicular disease.

A set of 723 diagnostic sera from human patients, submitted for the microscopic agglutination test (MAT) for antibodies to a group of 6 leptospiral serovars, was also tested by MAT for antibodies to the recently-discovered Leptospira fainei serovar hurstbridge. MAT titres of [ges ]128 to serovar hurstbridge were detected in 13·4% of these sera, and titres of [ges ]512 in 7·2%. In contrast, none of 62 sera obtained from a control population of laboratory staff gave titres of [ges ]128. The difference between the number of titres of [ges ]128 given by the two groups of sera was highly significant (P<0·01). The titres observed may have been due to cross-reactions with other leptospiral serovars, but this could not be demonstrated. An alternative explanation is that serovar hurstbridge is present in the human population.

This study sought to determine whether the decline in prevalence of hepatitis A virus (HAV) antibodies detected in Israel in 1977, 1984, and 1987 has continued. The anti-HAV antibody prevalence of a systematic sample of 578 male and female recruits inducted into the Israel Defence Force in 1996 was 38·4%. The reduction in antibody prevalence from 1977 (64%) was highly significant (P<0·001). There was a smaller decrease rate in recruits of European, North American, Australian and South African origin than from elsewhere. A ‘strategy’ that uses active immunization against hepatitis A (inactivated vaccine, instead of gamma globulin) should be considered, particularly in high risk groups such as field units during military service.

To investigate to what extent wild passerine birds are carriers of Chlamydia psittaci, 312 faecal samples from 18 bird species were collected. Using the PCR technique and subsequent DNA sequencing, C. psittaci DNA was demonstrated in faecal samples from 9 (2·9%) birds of 6 different species. Sera from 65 bird-ringers, highly exposed to wild birds, were tested by microimmunofluorescence assay for the occurrence of IgG and IgM antibodies to C. psittaci. No such antibodies were found. This results indicate that a significant proportion of wild passerine birds are carriers of C. psittaci, but rarely infectious to humans.