Epidemic meningococcal meningitis in central Australia, 1987–1991

Abstract

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.

Australia's century of meningococcal disease: development and the changing ecology of an accidental pathogen

“…Nationwide epidemics occurred during the two World Wars as part of the pandemics associated with military mobilisation and social disruption 30 , 31 . The only other epidemics since then have been restricted almost entirely to Indigenous people in Central Australia 32 , 33 …”

“…Routine surveillance for MD, as for other notifiable diseases, underestimates disease incidence. However, the consistent secular trends in routine surveillance and mortality data, as well as data from laboratory‐based 9 ‐ 11 and incidence studies 33 (Dr Rob Condon, formerly Infectious Disease Epidemiologist, Telethon Institute for Child Health Research, Perth, WA, personal communication) in the latter part of the last century, provide compelling evidence of the change in epidemiology since the late 1980s. The trends resemble those of other industrialised countries 26 , 31 , 34 , 35 , 37 …”

“…The first, the 1971–1973 epidemic in Central Australia (encompassing adjacent regions of the Northern Territory, South Australia and Western Australia), 32 was concurrent with epidemics caused by clonal subgroup I of SGA in Africa and the Middle East, and with sporadic disease in many other countries, 23 , 25 including an outbreak among Native Americans 38 . The second, the 1987–1991 epidemic in Central Australia, 33 was also caused by this clonal subgroup; 23 the same strain was responsible for the 1985–1987 epidemic in Auckland, NZ, with very high attack rates among Polynesian and Māori children 26 , 39 . SGA‐MD has not recurred in Central Australia since the epidemic ended in 1991.…”

“…The replacement of SGA by SGB and SGC as the major pathogens of MD in industrialised countries reflects microbial co‐adaptation as we modify the ways we live, behave and mix with each other across the globe. This changing ecology led to a shift away from periodic epidemics, except in vulnerable subgroups such as Australian Aboriginals and New Zealand Māori 32 , 33 , 39 , 45 . Poverty, crowded households and neighbourhoods, and reduced access to health services represent socially constructed faultlines along which epidemics may erupt 26 , 32 , 33 , 36 , 38 , 48 .…”

“…This changing ecology led to a shift away from periodic epidemics, except in vulnerable subgroups such as Australian Aboriginals and New Zealand Māori 32 , 33 , 39 , 45 . Poverty, crowded households and neighbourhoods, and reduced access to health services represent socially constructed faultlines along which epidemics may erupt 26 , 32 , 33 , 36 , 38 , 48 . While the demise of epidemic SGA‐MD can be attributed to improved living conditions, 26 the societal determinants of the current hypersporadic phase, in addition to factors related to poverty and crowding, are unclear.…”