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Following a statewide outbreak of legionellosis due to Legionella longbeachae serogroup 1 in South Australia in 1988 and 1989, studies were performed to find a source of the organism. A number of water and soil samples with and without acid decontamination were examined for L. longbeachae by using a selective medium containing vancomycin, aztreonam, and pimafucin. There were no isolations of L. longbeachae from water samples. Organisms resembling L. longbeachae were isolated from a number of samples of potting mixes and from soil surrounding plants in pots collected from the homes of four patients. The organisms were found to persist for 7 months in two potting mixes stored at room temperature. Legionellae were isolated with difficulty from potting mixes which were allowed to dry out. Identification of isolates as L. longbeachae serogroup 1 was confirmed by quantitative DNA hybridization and serological tests. Restriction-fragment-length-polymorphism studies showed minor differences between patient and environmental isolates but differentiated these readily from L. longbeachae serogroup 2 and other antigenically related legionellae. The isolation of L. longbeachae from some potting mixes and the prolonged survival of the organisms in this medium suggest that soil rather than water is the natural habitat of this species and may be the source of human infections.

isolated from a small number of samples of uncomposted pine sawdusts, but it is not known whether sawdust was the source of some of the legionellae found in potting soils. Legionella spp. persisted for periods ranging from 3 to 10 months in a potting soil held at temperatures between-20 and 35°C. Isolates of L. longbeachae serogroup 1 from soil did not grow at 43°C, a temperature which was also lethal for this species in soil. Most Legionella spp. isolated from potting and natural soils belonged to one distinct group according to analysis of ubiquinones and were serologically related to several known species in this group. A small number of potting

SUMMARYThe relationship between maturation of the small intestine and change in mucosal immune activity was examined in the DA rat during the weaning period from 12 to 30 days. Two stages ofjejunal maturation were observed: an initial stage of morphological development and crypt proliferation (days 12 to 22), followed by a period of stabilisation (days 24 to 30). By day 22 of the initial phase, villi increased principally in width but not in length, crypt length increased, and crypt cell production rate increased from 0 5 (day 12) to 11.1 (day 22) cells/crypt/hour. Various measures of mucosal immune activity showed a biphasic response. Up to days 20 to 22, the weight of the mesenteric lymph node increased seven-fold (p<0.0001), counts of jejunal eosinophils and goblet cells increased 3-(p<0l0001) and 19-fold (p<0-0001) respectively, and mean serum rat mucosal mast cell protease II, released from mucosal mast cells, increased from 24 (day 12) to 313 (day 22) ng/ ml (p<0O0001). After day 22, mesenteric lymph node weight stabilised, eosinophil count stabilised and goblet cells decreased, serum rat mucosal mast cell protease II decreased three-fold (p<00001), and mean jejunal count of intraepithelial lymphocytes increased from 26 (day 22) to 54 (day 24) cells per mm of muscularis mucosae (p<0O0001), before stabilising. These results demonstrated a close association between maturation of the small intestine and change in activity of the mucosal immune system.The small intestine in the rat undergoes a process of development and maturation that is associated with weaning; its weight increases from 15 days of age; and this is associated with lengthening of intestinal crypts and with increased cell proliferation.' Interestingly, suckling and germ free animals have fewer intestinal lymphoid cells than adult animals, and their intestinal crypts are smaller and less active in proliferation.`i As cell mediated responses cause crypt lengthening and increased crypt cell production rate (CCPR) in enteropathies,' it is possible that the effect of bacterial flora on mucosal morphology and epithelial cell proliferation is mediated by antigen driven activation of local T cells. There have been no studies, however, to relate mucosal immune activity to change in bacterial flora and gut maturation during weaning.

Investigations of the etiology of diarrhea in patients in South Australia and the Northern Territory showed that Campylobacter spp. other than Campylobacterjjejuni and C. coli were common in children. Campylobacters which were hippurate positive, nitrate negative, and susceptible to cephalothin and polymyxins were shown to be closely related to C. jejuni by DNA studies. Thermotolerant catalase-negative campylobacters were also isolated. These were H2S negative and biochemically resembled the catalase-negative or weak strains found in dogs in Sweden. DNA studies showed these campylobacters to be distinct from C. sputorum subsp. sputorum and to form a homogeneous group distinct from the enteropathogenic catalase-positive campylobacters. Preliminary studies suggest that these campylobacters are related to the Swedish catalase-negative or weak strains.