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Community-acquired Acinetobacter infections - a severe but poorly described problem in tropical regions



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30th June 2011

Acinetobacter is an environmental bacterium which is traditionally thought of as an opportunistic nosocomial pathogen with a tendency to develop resistance to multiple antibiotics. However, community-acquired Acinetobacter infection is an increasingly recognised problem in tropical areas and differs from the more commonly reported nosocomial Acinetobacter in several important aspects. Community-acquired Acinetobacter is generally sensitive to gentamicin, quinolones, ticarcillin and piperacillin and typically causes a rapidly progressive necrotising pneumonia.  The largest previously reported case series of community-associated Acinetobacter infections is 19 patients from Taiwan.

Since 1997, we have been prospectively collecting data on all patients with community-onset Acinetobacter bacteraemia (COAB) admitted to Royal Darwin Hospital (RDH), a 350-bed teaching hospital in tropical northern Australia. From January 1996 until December 2010, 48 patients with clinically significant COAB were admitted to RDH. The mean age was 43 years, 56% were male and 78% were Indigenous Australians. The most important underlying comorbidities were excess alcohol consumption in and chronic lung disease. The majority of cases occurred during the monsoonal wet season.

Because COAB has a high mortality, in 1991, empirical gentamicin was added to ceftriaxone in RDH treatment protocols for all severe pneumonia, and for moderate pneumonia with risk factors for Acinetobacter infection. Following this, and improvements in intensive care management, the mortality rate for community onset bacteraemic Acinetobacter pneumonia fell from 64% (1981-1991) to 11% (1997-2010), p<0.001.

The clinical features, risk factors and outcomes from this cohort will be discussed, as well as the speciation and susceptibility profile of the isolates. The important questions which remain about community-acquired Acinetobacter infections concern the optimal treatment, the environmental reservoir, the pathogenicity, and the molecular epidemiology of these isolates compared with nosocomial isolates.  Data from RDH and elsewhere will be discussed in an attempt to address these questions.

Josh Davis is an Infectious Diseases specialist at Royal Darwin Hospital and a senior research fellow at MSHR. His PhD was completed at Menzies in 2010, and dealt with the epidemiology and pathophysiology of severe sepsis. He has an ongoing interest in severe bacterial infections.