A waterborne outbreak of giardiasis which occurred 5 years after another in the same town in Canada was investigated. Sera from residents defined as cases or non-cases were tested by enzyme-linked immunosorbent assay (ELISA) and compared with sera from symptomatic and asymptomatic control groups. The outbreak-associated Giardia isolate was retrieved from contaminated drinking water and antigen from this strain was used in the serological investigation. Up to 84% of cases were identified by ELISA. More cases were identified by elevated immunoglobulin (Ig) G than by either elevated anti-Giardia IgA or IgM levels. Residents of the community infected during the first outbreak were significantly less likely to have been reinfected during the second outbreak. This is the first report of a second waterborne outbreak occurring in a community and results of the investigations are consistent with an acquired, protective immunity lasting at least 5 years.

On commercial pig farms which used antimicrobial agents, there was a higher level of antimicrobial resistance in the E. coli and Enterococcus spp cultured from the faeces of pigs compared with an organic farm which used no antibiotics. Overall levels of antibiotic resistance in the indicator bacteria isolated from conventional pig farms in this study were similar to those reported for indicator bacteria from pigs in Europe.

Intraabdominal abscesses were induced in mice by intraperitoneal inoculation of Bacteroides fragilis and Escherichia coli plus bran as the abscess-potentiating agent. Sixor seven-day-old abscesses were mechanically disaggregated in buffer, and the cells obtained were fractionated on discontinuous Percoll density gradients. Neutrophil populations of different density, each approximately 90% pure, were isolated. When the abscess-derived neutrophils were subsequently incubated with normal serum in vitro under aerobic conditions, the viability of the gram-negative bacteria that had been phagocytosed within the abscess did not change significantly. This anergy to intracellular bacteria (on subsequent incubation in vitro under optimal conditions for phagocytic killing) was also found for neutrophils that had been obtained from abscesses induced by a mixture that included Proteus mirabilis plus B. fragilis and from those induced by E. coli plus P. mirabilis. While unable to significantly kill intracellular organisms that had been phagocytosed in vivo, the abscessderived neutrophils could engulf and kill organisms to which they were exposed in vitro. Neutrophils from abscesses induced by P. mirabilis only plus bran killed that organism introduced in vitro significantly more effectively than the organisms that had been engulfed in vivo. In contrast, neutrophils from abscesses induced by the gram-positive organism Staphylococcus aureus plus bran were able to kill their intracellular organisms on subsequent incubation in vitro as effectively as they could kill added S. aureus. Neutrophils isolated from the peripheral blood and from induced peritoneal exudates of abscess-bearing mice were able to phagocytose and kill organisms in vitro with greater efficiency than abscess-derived neutrophils. The mechanism whereby neutrophils from abscesses induced by the gram-positive organism S. aureus can kill the organisms phagocytosed in vivo on subsequent in vitro incubation, in contrast to the relative anergy to their intracellular organisms displayed by neutrophils derived from abscesses induced by combinations of gram-negative bacteria, is not known.

The use of residual clinical DNA samples from the Cobas 4800 CT/NG test proved an efficient and effective method for performing AMR genotyping. These data also show for the first time the presence of gonococci with a mosaic penA sequence in New Zealand. Overall, the results further highlight the potential of molecular methods to aid N. gonorrhoeae AMR surveillance, particularly for regions where gonococcal culture is no longer performed.

Bacteroides fragilis and Escherichia coli are synergistic in the production of intraabdominal abscesses. However, these bacteria initiate abscess formation only when inoculated with an agent such as autoclaved colonic contents (ACC) or bran (a fiber analogue). The mechanism of action of the abscess-potentiating agent was studied. Opsonins in normal mouse serum were determined for phagocytic killing by murine neutrophils of B. fragilis and E. coli. Opsonization required fixation of complement by the alternative pathway. ACC (0.2 mg/ml) and bran (1.0 mg/ml) inhibited phagocytic killing of Proteus mirabilis in the presence of normal but not immune serum. Assay of the alternative pathway of complement activation indicated that both bacterial components and abscess-potentiating agents in an abscess-inducing mixture activated complement. These findings suggest that abscess-potentiating agents inhibit opsonization and therefore the subsequent phagocytic killing of bacteria in the nonimmune host.