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Melioidosis in Australia
Abstract & Commentary
Synopsis: Melioidosis is endemic in parts of Australia that may be visited by tourists.
Source: Melioidosis—Australia (Northern Territory). ProMED-Mail Archives. March 22, 2004.
Allen Cheng reported that, as of March 20, 15 patients with melioidosis had been seen at the Royal Darwin Hospital during the 2003-2004 rainy season. The Royal Darwin is the referral center for the "Top End" region of the Northern Territory of Australia.
Comment by Stan Deresinski, MD, FACP
Melioidosis, first described in homeless morphine addicts in Rangoon in 1932, is caused by the soil and water organism Burkholderia pseudomallei. It is endemic in tropical areas, particularly in Southeast Asia. Cases are also seen in Africa, India, the Middle East, the South Pacific, and northern Australia.1 Isolated cases have occurred in tropical areas of the Western Hemisphere, as well as in Hawaii and Georgia. Infection is believed to be acquired by inhalation of contaminated dust, ingestion of water containing the organism, and by contact with contaminated soil. The latter is facilitated by the presence of abrasions or more severe breaks in epidermal continuity. Person-to-person transmission by contact with body fluids is described, including 2 cases of sexual transmission.
Melioidosis in Australia is not restricted to the Northern Territory, also being reported from Queensland in association with heavy rains. Between November 1, 2001, and October 31, 2002, 47 cases were identified in the Northern Territory and Queensland. While the average annual incidence per 100,000 population was 58 overall, it was 25.5 among indigenous Australians.2 Eighty-seven percent of cases occurred during the wet season. The mortality rate was 21%. In an earlier series of 252 cases in northern Australia over 10 years, 46% of patients were bacteremic, and the overall mortality was 19%.3
The incubation period may be as short as 2 days and as long as years. This means that patients may present after many years in a nonendemic area. After the Vietnam war, this knowledge led to concern of a "ticking time bomb" of disease emerging in veterans well after the war. Fortunately, this event never materialized to any extent.
Infection may be inapparent. Clinical disease may result from an acute localized infection, such as a local cutaneous infection at the site of inoculation, which may, however, lead to bacteremia. Pulmonary infection may range from a relatively mild bronchitis to severe progressive pneumonia, and acute bloodstream infection may present as septic shock. Chronic infection may affect any body organ. One-third of affected Thai children present with acute uppurative parotitis.
B pseudomallei grows readily on a number of media. It may be suspected when an oxidase-positive Gram-negative bacillus is found to be resistant to gentamicin and colistin but susceptible to amoxicillin/clavulanate—a quite unusual antibiotic susceptibility pattern.
Patient with comorbidities such as diabetes mellitus and chronic lung disease are at increased risk of infection. An adult with cystic fibrosis who had returned from vacation in northern Australia was recently seen by the Infectious Disease Service at Stanford with an exacerbation of pulmonary infection due to B pseudomallei. The association with cystic fibrosis has previously been reported a number of times. The combination may be lethal.
A variety of antimicrobials have been used in the treat ment of melioidosis. A randomized trial in Thailand involving 214 culture-confirmed cases found no difference in mortality between patients randomized to either ceftazidime or imipenem, although failure after 48 hours of therapy was observed more frequently in the cephalosporin recipients.4 Meropenem is used at the Royal Darwin Hospital where, in fact, all patients admitted to their ICU with sepsis during the wet season receive this carbapenem as initial therapy until culture results exclude melioidosis. This same group has also reported that adjunctive therapy with G-CSF improved survival in a cohort analysis with comparison to a historical control.5
1. White NJ. Melioidosis. Lancet. 2003;361:1715-1722.
2. Cheng AC, et al. Melioidosis in northern Australia, 2001-02. Commun Dis Intell. 2003;27:272-277.
3. Currie BJ, et al. Endemic melioidosis in tropical northern Australia: A 10-year prospective study and review of the literature. Clin Infect Dis. 2000;31:981-986.
4. Simpson AJ, et al. Comparison of imipenem and ceftazidime as therapy for severe melioidosis. Clin Infect Dis. 1999;29:381-387.
5. Cheng AC, et al. Adjunctive granulocyte colony-stimulating factor for treatment of septic shock due to melioidosis. Clin Infect Dis. 2004;38:32-37.
Stan Deresinski, MD, FACP Clinical Professor of Medicine, Stanford; Associate Chief of Infectious Diseases, Santa Clara Valley Medical Center, is Editor of Infectious Disease Alert.