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Campylobacter fetus subsp. fetus infection can occur in female sheep, causing infertility or abortion. Despite extensive research on the effect of these bacteria on female fertility, little research has been done on the influence of C. fetus subsp. fetus on the male factor. Our objective was to examine the influence of C. fetus subsp. fetus on ram sperm. Motility index, percentage of live spermatozoa, mean alphat value (an indication of the chromatin stability of the sperm cell) and percentage of sperm cells expressing the FAS receptor were measured in sperm incubated in the presence or absence of C. fetus subsp. fetus. The motility index and viability of sperm incubated with the bacteria were lower than those of untreated sperm samples after 5 h. In bacteria-incubated sperm cells, the percentage expressing FAS receptor was already significantly elevated at 15 min. Bacteria-incubated sperm showed a greater prevalence of morphological damage. The bacteria were attached to tail and acrosome regions, and the sperm damage was concentrated in both the motility and chromatin regions. Bacteria-infected sperm cells showed a decrease in motility, increase in early acrosome reaction and chromatin damage. Similar effects were induced by incubation of the sperm with supernatants from C. fetus subsp. fetus cultures. Thus this study demonstrates that C. fetus subsp. fetus has a detrimental effect on the quality of ram sperm.

Studies were performed on a cytotoxin (CT) from human strains of Campylobacter jejuni isolated in Malaysia. CT was detected by cytopathic effect (CPE) on HeLa cells at titres from 8 to 32, in culture filtrates from 14 (48%) of 29 human isolates. The CPE correlated well with a quantitative 51Cr-release assay where a specific release of 54-68% was noted. CT production was lost after 5-7 subcultures. CT activity was also detected in 5 (26%) of 19 faecal filtrates from which CT-producing isolates were subsequently obtained. The mol. wt of CT was estimated by Sephadex G-50 chromatography to be greater than 30,000. In a suckling-mouse assay, CT consistently failed to demonstrate fluid accumulation after intragastric inoculation of culture filtrate. The Removable Intestinal Tie Adult Rabbit Diarrhoea (RITARD) assay was also used. Rabbits given CT-producing strains of C. jejuni developed bacteraemia and severe watery mucus-containing diarrhoea for the duration of the experiment with death of some animals. Rabbits given CT non-producing strains had less severe disease and none died. Rabbits given partially-purified CT had diarrhoea for 3 days but none died.

Pregnant guinea pigs were used to compare the virulence of four human isolates of Campylobacter fetus ss. fetus and four of C. jejuni on the basis of their ability to cause abortion and bacteraemia. Of the four strains of C. fetus ss. fetus two produced abortion readily after intramuscular injection. The four C. jejuni isolates were, however, of comparatively low virulence and no differences between them were demonstrated. Some of the isolates differed in their ability to survive in vitro in human and guinea-pig serum. It is suggested that campylobacters vary in their virulence for man and that this may influence the outcome of infections. Guinea pigs may prove useful in studying the pathogenesis of systemic campylobacter infections.

The serotypes of strains of Campylobacter jejuni isolated from patients attending the International Center for Diarrhoeal Disease Research, Bangladesh (ICDDR, B), Dhaka, and from animals were ascertained by Penner and Hennessy's (1980) serotyping scheme. Of 102 isolates from man, 74% were typable and serotypes 53, 15 and 22 predominated. Of 26 isolates from animals, 65% were typable and serotypes 15 and 53 occurred frequently. The diarrhoeal illnesses associated with different serotypes were similar. In one-third of cases other enteropathogens were present. C. jejuni was isolated from 7% of patients tested in a 4% sampling system during 1983, and the prevalent serotypes appeared in most months. It is concluded that C. jejuni is a common enteropathogen in Bangladesh, that a few serotypes predominate among isolates from both man and animals, and that serotype does not determine clinical symptoms.

The roles of macrophages and the complement system as potential host defence mechanisms in mice against campylobacter infection were studied in vivo, by depleting the murine serum-complement or the phagocytic cells. Macrophage-depletion was performed by intraperitoneal (i.p.) injection of silica dust, Liquoid or dextran sulphate. During 5 days after infection, such mice showed a significant increase in mortality, compared with controls. In contrast, mice that were previously decomplemented by i.p. injection of Cobra Venom Factor showed no significant increase in mortality. The results with combined macrophage depletion and decomplementation did not differ from those with macrophage depletion alone. These experiments suggest that macrophages seem to be more important than complement in the defence of mice against experimental campylobacter infection.

Axenic and monoxenic C3H mice were used to develop an animal model for enteroinvasiveness and translocation of Campylobacter jejuni. After oral administration of 10(7)-10(8) viable cells of C. jejuni on day 0 (D0), bacterial colonisation was followed quantitatively during 23 days by counting free luminal bacteria and tissue-associated bacteria in the duodenum, ileum and colon. The kinetics of bacterial colonisation were the same in axenic and monoxenic mice; bacteria were more numerous in distal than in proximal intestinal segments. Electronmicroscope studies of axenic infected mice showed C. jejuni free in the intestinal lumen on D2 and D7, and adhering to microvilli or included in enterocyte vacuoles in the colon on D2 without inflammatory reaction; C. jejuni was isolated from mesenteric lymph nodes until D23, but from blood, spleen, liver and bile until D1 only. In monoxenic infected mice, C. jejuni was found from D1 to D4 in mesenteric lymph nodes and Peyer's patches, whereas the associated bacterium (Clostridium perenne) was never cultured from any organs. On the basis of our observations in this gnotobiotic model, C. jejuni appears to be an enteroinvasive bacterium with a particular affinity for lymphoid organs.

Intraperitoneal injection of Campylobacter fetus ss. jejuni into HAM/1CR mice was lethal, but viable counts of bacteria from whole body homogenates, organs and blood indicated that death was not due to sustained bacterial multiplication. Heat-killed organisms (5 X 10(9) cfu) injected into 7-day-old mice caused death within 24 h and this was shown to be due to endotoxin. Both ferric iron and heterologous lipopolysaccharide enhanced virulence; the LD50 was lowered from 1.8 X 10(9) cfu to 2.7 X 10(7) cfu when both were used. Three-day-old or adult animals survived challenge with Campylobacter fetus without clinical symptoms when challenged orally or by intravenous or intraperitoneal routes.

Ligated ileal loops in rats of the Charles-Foster strain, weighing 200-250 g and aged 7-8 months, provided a sensitive and reproducible means of testing the enterotoxigenicity of Campylobacter jejuni. All of 16 chicken isolates caused fluid accumulation comparable to that produced by toxigenic Vibrio cholerae O1, strain 569B. However, 11 of the isolates required one to three consecutive passages through the rat gut before doing so. The amount of fluid produced increased after each passage. Of three culture media tested, brucella broth of pH 6.7 supported the highest degree of enterotoxigenesis. Filtrates of cultures of all 16 chicken isolates in this medium were as effective as viable C. jejuni in producing fluid in ileal loops. The enterotoxin was neutralised completely by cholera antitoxin diluted 1 in 160, indicating its close immunobiological relationship to cholera toxin.