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In Papua New Guinea cryptococcal meningitis occurs predominantly in immunocompetent patients in whom Cryptococcus neoformans var, gattii is implicated in 95% of cases. Ocular complications are common. We have reviewed ophthalmic findings in 82 immunocompetent patients and have attempted to identify those features of the disease that predict an unfavourable visual outcome. Visual loss occurred in 52.6% of survivors and was associated with optic atrophy following optic disc swelling in 60.9%. Progression of disc swelling to optic atrophy was predicted by the presence of an abducens palsy (P = 0.049) and cerebrospinal fluid (CSF) cryptococcal antigen titres > 1:1024 (P = 0.036). Raised intracranial pressure (defined as opening CSF pressure > or = 300 mm on admission) was not associated with visual loss. Vision deteriorated in 17.3% of patients despite anticryptococcal therapy and in 3.7% it followed curative therapy. The high rate of visual loss in immunocompetent patients with C. neoformans var. gattii infection contrasts with others' experience of immunosuppressed patients with C. neoformans var. neoformans infection, in whom visual loss was rare. This difference may reflect immune mediated optic nerve dysfunction in C. neoformans var. gattii meningitis caused by either compression due to arachnoid adhesions or oedema and inflammatory cell-mediated damage.

An outbreak of acute methyl alcohol intoxication occurred in Port Moresby, Papua New Guinea, in March 1977. Twenty-eight young men attended a drinking party and drank methyl alcohol. The amount consumed by each individual ranged from an equivalent of 60--600 ml of pure methanol. Three had prior ethanol ingestion. All 28 became ill 8--36 hours after drinking and were hospitalized. The most commonly observed clinical syndromes were: acute metabolic acidosis, severe visual impairment and acute pancreatitis. Four died within 72 hours after admission to the hospital. All had severe metabolic acidosis and visual impairment and three pancreatitis. Of 24 who recovered, 16 showed no residual complications, six had bi-lateral visual impairment and two had difficulty in speech as well as visual impairment. A three month follow-up examination showed no change in the findings. Coma, seizures and prolonged acidosis were poor prognostic signs. The estimated amount of consumed methanol and the rapidity of the appearance of signs of toxicity following methanol ingestion did not seem to influence the outcome of poisoning. The treatment of acute methyl alcohol intoxication in centres where dialysis is not available is discussed.

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