A prospective population-based study was conducted in Australia and New Zealand during 1994-1997 to elucidate the epidemiology of cryptococcosis due to Cryptococcus neoformans var. neoformans (CNVN) and C. neoformans var. gattii (CNVG) and to relate clinical manifestations to host immune status and cryptococcal variety. The mean annual incidence per 10(6) population was 6.6 in Australia and 2.2 in New Zealand. Of 312 episodes, CNVN caused 265 (85%; 98% of the episodes in immunocompromised hosts) and CNVG caused 47 (15%; 44% of the episodes in immunocompetent hosts). The incidence of AIDS-associated cases in Australia declined annually (P<.001). Aborigines in rural or semirural locations (P<.001) and immunocompetent males (P<.001) were at increased risk of CNVG infection. Cryptococcomas in lung or brain were more common in immunocompetent hosts (P< or =.03) in whom there was an association only between lung cryptococcomas and CNVG. An AIDS-associated genetic profile of CNVN serotype A was confirmed by random amplification of polymorphic DNA analysis. Resistance to antifungal drugs was uncommon. The epidemiology of CNVN infection has changed substantially. Clinical manifestations of disease are influenced more strongly by host immune status than by cryptococcal variety.

A population-based register of cases of cryptococcosis in patients treated in Victoria, Australia, over a 10-year period was established for studying the epidemiologic and clinical features of infection with Cryptococcus neoformans and its two varieties, gattii and neoformans. One hundred thirty-three cases of cryptococcosis were entered on the register; the incidence was 3.0 cases per 1 million population per year, a rate that increased to 5.0 cases per 1 million population per year over the decade as a result of the AIDS epidemic. There was a distinct association between immune status and C. neoformans variety: all C. neoformans variety gattii infections occurred in healthy hosts and 90% of C. neoformans variety neoformans infections occurred in immunosuppressed hosts. Meningitis was the commonest manifestation, with focal CNS and pulmonary lesions occurring primarily in healthy hosts with C. neoformans variety gattii infection; isolation of C. neoformans from blood and urine was associated with immunosuppression and C. neoformans variety neoformans infection. The mortality among patients with C. neoformans variety neoformans infection was high, while none of those patients with C. neoformans variety gattii died but often had neurological sequelae that required surgery and prolonged therapy. These findings appear to be related to variety-specific interactions between host and parasite and warrant further epidemiologic and immunologic study.

The association between Campylobacter jejuni infection and Guillain-Barr6 syndrome was investigated serologically in a retrospective study of 56 patients admitted to this hospital over four years. Evidence of preceding C jejuni infection was found in 21 (38%) of these patients, indicating that C jejuni was the most common single identifiable pathogen precipitating the disease. Among those patients who had presented with preceding diarrhoea the serum antibody response was similar to that in uncomplicated C jejuni enteritis. Patients with serological evidence of preceding C jejuni infection manifested a significantly more severe form of the disease. In cerebrospinal fluid the predominant specific antibody class was IgG, and this was closely related to the serum titres of specific IgG. IgA and IgM specific antibodies were found only in the cerebrospinal fluid of patients with recent C jejuni infection.These findings support the possibility that humoral immune factors are responsible for the neural damage and demyelination seen in Guillain-Barre syndrome.

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