Objectives To describe an epidemic of dengue type 3 that occurred in far north Queensland in 1997–1999 and its influence on the further development of dengue prevention and control strategies. Design Epidemiological and laboratory investigation of cases, entomological surveys and phylogenetic analysis of dengue virus isolates. Main outcome measures Numbers and characteristics of confirmed cases; Breteau Index (BI; number of containers breeding Aeries aegypti per 100 premises); effect of control measures on mosquito populations; genetic homology of epidemic virus with other dengue virus isolates. Results The epidemic lasted 70 weeks and comprised 498 confirmed cases in three towns (Cairns, Port Douglas and Mossman); 101 patients (20%) were admitted to hospital. Median interval between symptom onset and notification was seven days (range, 0–53 days), and cumulative duration of viraemia of public health significance was 2072 days, Bls in affected areas were high, particularly in Mossman (45) and Port Douglas (31). Control measures significantly reduced mosquito populations (assessed as number of ovitraps containing Ae. aegypti eggs and mean number of eggs per trap [P < 0.05 for both]). However, transmission persisted in several foci, in part due to undetected waterfilled containers breeding Ae. aegypti. The epidemic virus belonged to serotype 3; phylogenetic analysis suggested it was imported from Thailand. Conclusions The epidemic had greater morbidity than other recent Queensland epidemics of dengue and was harder to control, necessitating substantial revision of the Dengue Fever Management Plan for North Queensland. The epidemic's severity supports the hypothesis that dengue viruses from South East Asia are more virulent than others.

Seven cases of Salmonella meningitis have occurred in infants in Far North Queensland since 1982. The mean age of onset was 2.8 months, and at least five of the cases were caused by Salmonella virchow. Five of the cases had significant complications during the acute illness: all required prolonged (median 34 days) inpatient management, and four developed permanent neurological sequelae. S. virchow is the serovar most frequently isolated from infants in Far North Queensland. The source of S. virchow infections in these infants remains uncertain, but transmission may occur through cross-infection and person-to-person transmission in the home.

Although a relatively low proportion of the children had adequate antibody levels against hepatitis B the clinical significance of this observation is uncertain. Further studies are needed to determine whether fully vaccinated Torres Strait Island children have been adequately protected and whether they require a booster dose of hepatitis B vaccine. A substantial proportion of fully vaccinated Aboriginal and Torres Strait Island children are inadequately protected against poliomyelitis, and therefore any such child with acute flaccid paralysis should be investigated fully for poliomyelitis. Vaccinated Aboriginal and Torres Strait Island children are well protected against measles, as are other Australian children.

Objective To describe an outbreak of meningococcal meningitis and the impact of rifampicin chemoprophylaxis on secondary attack rates among Aboriginal people in central Australia. Design Prospective study of patients admitted to hospital between September 1987 and May 1991. Setting The Alice Springs Health Region of the Northern Territory and the Anangu Pitjantjatjara Lands of South Australia, covering a population of 13 228 Aboriginal people. Subjects Patients admitted to the Alice Springs Hospital with clinical signs or autopsy findings of meningococcal disease. Rifampicin chemoprophylaxis was given to close contacts of all cases. Mencevax AC vaccine was offered to children aged 1 to 15 years In the Region. Main outcome measures Blood or cerebrospinal fluid (CSF) with Neisseria meningitidis, or a positive result of latex agglutination testing on CSF. Positive Isolates were serogrouped. Results Seventy‐seven cases of meningococcal disease were diagnosed in Aboriginal people over four years compared with one to two cases per year previously; of these, 60 were definite, 7 probable and 10 suspected cases. Seventy‐six subjects had meningitis, of whom one also had the clinical features of meningococcal septicaemia; one other subject had positive blood cultures with a mild febrile illness without features of meningitis. The annual attack rate of meningococcal disease in the Aboriginal population was 1.6/1000. The relative risk for secondary cases was estimated to be between 0.3 (95% confidence Interval [Cl], 0.09–0.92) and 0.5 (95% Cl, 0.15–1.53). The annual attack rate In the non‐Aboriginal population was 0.04/1000. Conclusions The epidemic closely resembled those In sub‐Saharan Africa, and in socloeconomlcally marginalised groups in developed countries. The relative risk for secondary cases was lower than generally reported, and was attributed to chemoprophylaxis for close contacts and the mass vaccination program for children. Until there are major improvements in living conditions, infectious diseases such as those transmitted by airborne droplets will continue to occur In Aboriginal communities.