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PubMed2005

Clinical presentation of melioidosis in Queensland, Australia.

A retrospective study was performed on culture-positive patients (n = 57) with melioidosis presenting to the Townsville Hospital to define the epidemiology of the disease in Queensland, Australia. Mortality was 25% (n = 14) with a 9% (n = 5) relapse rate. At presentation, primary organs involved included the lungs (58%; n = 33), genitourinary system (11%; n = 6), skin and soft tissue (9%; n = 5), bone and joints (4%; n = 2), central nervous system (4%; n = 2), mycotic aneurysm (2%; n = 1) and peritonitis (2%; n = 1). No focus of infection could be identified in 12% of cases (n = 7). There was no significant difference in the clinical presentation of melioidosis in Queensland compared with the Northern Territory. Regional trends in the clinical presentation of melioidosis in Australia compared with Southeast Asia were confirmed. Risk factors for disease included diabetes (42%), excess alcohol consumption (42%), chronic lung disease (26%), immunosuppressive drug use (12%), renal disease (11%), malignancy (7%) and autoimmune disease (5%). No risk factors were identifiable in 18% of cases. The presence of multiple risk factors for melioidosis was not significantly associated with increased mortality (P > 0.05).

Adolescent↗
PubMed2000

Melioidosis as an emerging global problem.

There is remarkably little known about the incidence of melioidosis outside a few countries (Thailand, Australia, Singapore and Malaysia). Presumably it is widespread in tropical south east Asia. Elsewhere there are tantalising glimpses of the tip of what may be a large iceberg. Since a specific diagnosis of melioidosis requires awareness on the part of clinicians, and the existence of a laboratory capable of isolating and identifying Burkholderia pseudomallei, a luxury not available in most rural tropical areas, the size of this iceberg is likely to remain unknown for the foreseeable future. There is mounting evidence that the disease is endemic in the Indian sub-continent and the Caribbean, and there have been unsubstantiated reports of recent cases in South Africa and the Middle East. It is unclear whether melioidosis has really spread to such areas relatively recently, or has been there but unrecognised for a long time. Almost all cases diagnosed in temperate climates have been imported from the tropics, with the exception of a unique outbreak which occurred in France in the mid-1970s. With increasing world wide travel of both humans and other animals, the potential exists for melioidosis to spread to new and fertile pastures.

Burkholderia pseudomallei↗
PubMed2000

Recent advances in the treatment of severe melioidosis.

For the last decade, high-dose intravenous ceftazidime has been the drug of choice for the treatment of severe melioidosis, after ceftazidime was shown to be superior to the 'conventional' four-drug regimen (chloramphenicol, doxycycline and trimethoprim-sulphamethoxazole) in a randomised trial. Combination ceftazidime-trimethoprim-sulphamethoxazole was compared with the conventional regimen in a separate trial with similar results, but we still do not know whether such combination therapy is needed in melioidosis. Co-amoxiclav (amoxycillin-clavulanate) has been shown to be effective but was associated with a higher rate of treatment failure than ceftazidime. Two further treatment trials in acute melioidosis have recently been conducted in Thailand. In the first of these, high-dose intravenous imipenem was compared with ceftazidime and the results suggest that the two regimens possess similar efficacy. Cefoperazone-sulbactam has been compared with ceftazidime-trimethoprim-sulphamethoxazole in a small number of patients, and further results are awaited. Relapses of melioidosis should be treated in a similar manner to primary infections.

Anti-Bacterial Agents↗
PubMedDate not supplied

A proposed scoring system for predicting mortality in melioidosis.

Melioidosis, due to infection with the environmental organism Burkholderia pseudomallei, continues to be associated with high mortality despite improvements in antibiotic therapy. Using simple clinical findings and baseline laboratory tests available at the time of admission, we attempted to define those patients with acute melioidosis who were at higher risk of death. Using data, collected prospectively from the period October 1989 to June 2002, from patients with acute culture-confirmed melioidosis presenting at the Royal Darwin Hospital, Darwin, Australia, a number of variables were selected that were easily available at the time of admission and reflected organ dysfunction. Mortality was predicted in univariate logistic and multivariate models by the presence of pneumonia, age at diagnosis, serum urea, serum bilirubin, lymphocyte count, and serum bicarbonate. A score was assigned from 0 to 2, based on the degree of abnormality. A melioidosis score was formed from the sum of these scores, with a maximum score of 11. A score of < or = 3 (n = 140) was associated with a mortality of 8.6%, whereas a score of > or = 4 (n = 112) was associated with a mortality of 44.6%. Although this scoring system requires external validation, it may help identify a suitable target group of patients for intensive intervention such as early admission to an intensive care unit, the early use of meropenem, and goal-directed resuscitation therapies.

Female↗
PubMed1991

Parapharyngeal space melioidosis in a diabetic.

Pseudomonas pseudomallei, a gram negative organism causing melioidosis, is found in tropical and subtropical regions. It may manifest as a pulmonary lesion, osteomyelitis, soft tissue abscesses, abscesses in various organs or in septicaemic form. Melioidosis of the parapharyngeal space has not been reported so far. A case of melioidosis of the parapharyngeal space which was successfully treated by drainage and prolonged antibiotic therapy is reported here. Melioidosis should be suspected in severe forms of deep neck space infection, especially if the patient comes from an endemic area.

Adult↗
PubMed2004

Preliminary report on the northern Australian melioidosis environmental surveillance project.

An environmental surveillance programme was developed to determine whether water supplies could be a source of Burkholderia pseudomallei as noted during previous melioidosis outbreak investigations. Water supplies to communities in the three northern Australian jurisdictions (Western Australia, Northern Territory and Queensland) were sampled periodically during 2001 and 2002. Water and soil samples were collected from communities known to have had recent culture-positive melioidosis cases and nearby communities where no cases had been diagnosed. Clinical isolates of B. pseudomallei obtained from northern Australian patients during 2001 and 2002 were compared with the environmental B. pseudomallei isolates by ribotyping and pulsed-field gel electrophoresis. B. pseudomallei was isolated from 11 distinct locations, all in the Northern Territory, seven of which were associated with culture-positive melioidosis cases (>1 case at three locations). Water was implicated as a possible environmental source of melioidosis in six locations. A variety of free-living amoebae including Acanthamoeba and Hartmannella spp. that are potential hosts to B. pseudomallei were recovered from environmental specimens. Culturable B. pseudomallei was not found to be widely dispersed in the environments sampled.

Animals↗
PubMed1999

An exotic pulmonary infection in Thailand: melioidosis.

Melioidosis is an infectious disease from Burkholderia pseudomallei and is confined in specific geographic areas such as Southeast Asia. Its highest prevalence in Thailand is in the north-eastern part. Most infected patients had worked paddy fields or had underlying diseases such as diabetes mellitus. Melioidosis can manifest clinically, with either disseminated or localized features. In the disseminated form patients developed an acute and progressive course with septicaemia. In contrast, patients with the localized form usually presented with prolonged fever, and symptoms of one or more organ involvement, in particular the lung and the liver. Definite diagnosis of melioidosis is made by an isolation of Burkholderia pseudomallei from a variety of clinical specimens. Treatment of choice for the septicaemic patients is an initial combination of ceftrazidime and trimethoprime-sulfamethoxazole, followed by trimethoprime-sulfamethoxazole for up to 6-12 months depending on the result of clinical specimen culture. Treatment for the localized form requires simultaneous antibiotic therapy and surgical drainage. However, optimum duration of antibiotic therapy remains unknown so further research is required. Melioidosis is an important disease in terms of mortality rate and it requires rapid diagnosis and treatment. To prevent recurrence, it is necessary to continue oral doxycycline or trimethoprime-sulfamethoxazole for 6-12 months.

Anti-Bacterial Agents↗
PubMed2003

Adjunctive granulocyte colony-stimulating factor for treatment of septic shock due to melioidosis.

Melioidosis, caused by the intracellular pathogen Burkholderia pseudomallei, is endemic in northern Australia and Southeast Asia. Risk factors for this infection have also been associated with functional neutrophil defects. Because of this, granulocyte colony-stimulating factor (G-CSF) was adopted for use in patients with septic shock due to melioidosis in December 1998. We compared the mortality rates from before and after the introduction of G-CSF therapy at the Royal Darwin Hospital (Darwin, Australia) during the period of 1989-2002. The mortality rate decreased from 95% to 10% after the introduction of G-CSF. Risk factors, the duration of illness before presentation, and the severity of illness were similar in both groups. A smaller decrease in mortality among patients in the intensive care unit who did not have melioidosis was observed, suggesting that other changes in management did not account for the magnitude of the benefit seen. We conclude that G-CSF may have contributed to the reduction in the mortality rate among patients with septic shock due to melioidosis.

Adolescent↗
PubMed1999

A comparison of chloramphenicol, trimethoprim-sulfamethoxazole, and doxycycline with doxycycline alone as maintenance therapy for melioidosis.

A prospective, open, randomized, comparative treatment trial was conducted to compare the therapeutic efficacy of the conventional four-drug combination (chloramphenicol, trimethoprim-sulfamethoxazole, and doxycycline) with that of doxycycline alone in oral maintenance treatment of melioidosis. Adult Thai patients with culture-confirmed melioidosis were randomized to receive treatment with either regimen for a minimum of 12 weeks, usually following intravenous treatment of severe disease. The main outcome measure was culture-confirmed relapse. One hundred sixteen patients were enrolled; 109 had culture-confirmed melioidosis, and 87 were considered evaluable (43 had received doxycycline). Culture-confirmed relapse occurred in one patient randomized to the conventional regimen and in 11 (25.6%) randomized to the doxycycline regimen (P = .009), and treatment failed for 8 (18.2%) versus 20 (46.5%), respectively (P = .009). Adverse effects occurred in 26% of patients overall. Doxycycline alone cannot be recommended for a first-line regimen of oral maintenance treatment of melioidosis.

Adolescent↗
PubMed1994

Ceftazidime vs. amoxicillin/clavulanate in the treatment of severe melioidosis.

An open, paired, randomized, controlled trial of high-dose parenteral ceftazidime (120 mg/[kg.d]) vs. amoxicillin/clavulanate (160 mg/[kg.d]) for the treatment of severe melioidosis was conducted in Ubon Ratchatani in northeastern Thailand. Of 379 patients enrolled in the study, 212 (56%) had culture-proven melioidosis; 106 patients were in each treatment group. The overall mortality rate (47%) was similar for both treatment groups. However, 4 of 75 surviving patients in the ceftazidime group compared with 16 of 69 surviving patients in the amoxicillin/clavulanate group were switched to the alternate regimen because of an unsatisfactory clinical response after > or = 72 hours of treatment (P = .004). The overall therapeutic failure rate (i.e., treatment failure or death due to uncontrolled melioidosis) was significantly higher for the amoxicillin/clavulanate group than for the ceftazidime group (P = .02). Clinical and bacteriologic responses for successfully treated patients were similar in both groups, and both treatments were well tolerated. Parenteral amoxicillin/clavulanate is a safe and effective initial treatment, but parenteral ceftazidime remains the treatment of choice for severe melioidosis.

Adolescent↗
PubMed2005

Extreme weather events and environmental contamination are associated with case-clusters of melioidosis in the Northern Territory of Australia.

BACKGROUND: Melioidosis, the infection due to the environmental organism Burkholderia pseudomallei, is endemic to northern Australia and South East Asia. It is associated with exposure to mud and pooled surface water, but environmental determinants of this disease are poorly understood. We defined case-clusters in northern Australia, determined their contribution to the observed rate of melioidosis, and explored clinical features and associated environmental factors. METHODS: Using geographical information systems data, we examined clustering of melioidosis cases in time and geographical space in the Top End of the Northern Territory of Australia between 1990 and 2002 using a scan statistic. DNA macrorestriction analysis, resolved by pulsed field gel electrophoresis, was performed on isolates from patients. RESULTS: We defined five case-clusters involving 27 patients that occurred within 7-28 days and/or a radius of 100-300 km. Clustered cases were associated with extreme weather events or environmental contamination; no difference in the clinical pattern of disease was noted from other patients not involved in clusters. Isolates from patients linked to environmental contamination were caused by isolates with similar DNA macrorestriction patterns, but isolates from patients linked to severe weather events had more diverse DNA macrorestriction patterns. CONCLUSION: Case-clusters of melioidosis where isolates exhibit diverse DNA macrorestriction patterns in our region are linked to extreme weather events and outbreaks where isolates are predominantly of the same DNA macrorestriction pattern are linked with contamination of an environmental source.

Burkholderia pseudomallei↗
PubMed1989

Enzyme-linked immunosorbent assay for the diagnosis of clinical and subclinical melioidosis.

An enzyme-linked immunosorbent assay (ELISA) for the detection of specific IgG and IgM antibody to Pseudomonas pseudomallei was developed. The IgG-ELISA was compared with the indirect fluorescence assay for IgG antibody (IgG-IFA) and the indirect hemagglutination (IHA) test in studies with serum specimens from persons from endemic areas for melioidosis and from persons from nonendemic areas of Australia. The sensitivity and specificity of the IgG-ELISA were 90% and 99%, respectively, comparable to those obtained with the IgG-IFA. The IgG-ELISA was more sensitive than the IHA test (74%) and was more suitable than the IgG-IFA as a serologic screening test for melioidosis. The IgM-ELISA was compared with the IgM-IFA as a marker of disease stage in patients with melioidosis. There was good diagnostic agreement between the tests; 92% of patients with active disease gave IgM-ELISA titers greater than or equal to 1:5,120 and 93% of patients with subclinical melioidosis had IgM-ELISA titers less than or equal to 1:1,280. Of the overlap group of patients with a borderline IgM-ELISA titer of 1:2,560, approximately 33% were clinical cases. An uncommon disease stage consisting of a self-limited, short-term, flu-like, pyrexial illness accompanied by elevated serum IgM-ELISA titers (greater than or equal to 1:5,120) was seen in a small number of patients residing in endemic Australia.

Adolescent↗
PubMed1992

Tumor necrosis factor in septicemic melioidosis.

Plasma concentrations of the cytokine tumor necrosis factor (TNF) were measured serially in 91 patients suspected of having septicemic melioidosis. This was confirmed in 55. TNF was detectable in admission plasma (TNF0) in 3 of 15 survivors of septicemic melioidosis and 21 of 26 fatal cases (P less than .001). The median (range) TNF0 concentration in melioidosis patients who died was 96 (1-4774) pg/ml, and the median time to death was 25 (5-672) h. TNF0 was inversely correlated with the lowest mean arterial pressure in the succeeding 12 h (Spearman's rank correlation coefficient = .67, 2P less than .001). Three patterns of TNF plasma concentrations were evident: relatively constant values between 100 and 500 pg/ml (n = 7), high admission concentrations (greater than 1000 pg/ml) associated with early death (n = 4), and an apparent pulse release after treatment, with peak values greater than 1000 pg/ml, which then declined with a mean (SD) apparent half-time of 131 (50) min (n = 8). Further studies are necessary to determine whether TNF contributes to lethality in melioidosis.

Adolescent↗
PubMed2003

A comparison of antibiotic regimens in the treatment of acute melioidosis in a mouse model.

Melioidosis is caused by the Gram-negative bacillus Burkholderia pseudomallei. Most clinical reports of disease are from south-east Asia and northern Australia. The organism is intrinsically resistant to most commonly available antibiotics. Standard therapy includes ceftazidime either alone or in combination with co-trimoxazole. The clinical advantage in adding co-trimoxazole has never been determined; nor has the activity of newer, fourth-generation cephalosporins, such as cefepime, been studied in the treatment of this condition. BALB/c mice have been shown to represent an animal model of melioidosis. This animal model was used in this study to compare the efficacy of ceftazidime and cefepime alone or with co-trimoxazole, in the therapy of melioidosis. Antibiotic levels in the mice were determined by HPLC, and dosing was modified to keep plasma antibiotic levels at or above the MIC for the organism-antibiotic combination for a significant part of a 12 h period. Bacterial load, as determined by splenic counts, showed that ceftazidime in combination with co-trimoxazole was the most effective therapeutic option. The animal model described in this study can be used as a preliminary evaluation of therapeutic options for melioidosis.

Acute Disease↗
PubMed2004

Outcomes of patients with melioidosis treated with meropenem.

Melioidosis, an infection due to Burkholderia pseudomallei, is endemic in southeast Asia and northern Australia. We reviewed our experience with meropenem in the treatment of severe melioidosis in 63 patients over a 6-year period. Outcomes were similar to those of ceftazidime-treated patients (n = 153) despite a deliberate selection bias to more-unwell patients receiving meropenem. The mortality among meropenem-treated patients was 19%. One patient had a possible drug fever associated with the use of meropenem. We conclude that meropenem (1 g or 25 mg/kg every 8 h intravenously for >/=14 days) is an alternative to ceftazidime and imipenem in the treatment of melioidosis. The use of meropenem may be associated with improved outcomes in patients with severe sepsis associated with melioidosis.

Adolescent↗
PubMed1961

Complement fixation test in experimental clinical and subclinical melioidosis.

Nigg, Clara (University of California, Berkeley), and Margaret M. Johnston. Complement fixation test in experimental clinical and subclinical melioidosis. J. Bacteriol. 82:159-168. 1961.-Soluble stable antigens prepared from Pseudomonas pseudomallei gave 4+ complement fixation reactions in a dilution of 1 to 8,000 when tested with specific rabbit antiserum diluted 1 to 10,000. The complement fixation reaction was positive in 100% of experimentally infected rabbits 9 to 11 days postinfection. Infected guinea pigs and monkeys showed similar results. Monkeys inoculated with very small infecting doses of P. pseudomallei developed positive complement fixation reactions in the absence of clinical manifestation of infection. An anamnestic complement-fixing antibody response could be induced in such monkeys, after the titer had dropped to approximately the preinfection level, by inoculating very small doses of viable P. pseudomallei or larger doses of killed melioidosis vaccine. The complement fixation test described appeared to be both sensitive and specific, and should be of value in human melioidosis which cannot be diagnosed on the basis of clinical manifestations alone. It is suggested that subclinical infections may play a role in the epidemiology of human meliodosis. The potential application of the complement fixation test to serological surveys in areas where melioidosis occurs endemically is discussed.

Animals↗
PubMed1981

Relationship and significance of specific immunoglobulin M antibody response in clinical and subclinical melioidosis.

Thirty-six hospitalized patients with circulating antibody to pseudomonas pseudomallei were classified as having either clinical or subclinical melioidosis after full clinical examinations and supplementary radiological and culture investigations. Qualitative estimations of immunoglobulin M (IgM) antibody response were determined by complement fixation, indirect hemagglutination, and immunofluorescence, and the estimations were correlated with the clinical findings in each patient. An attempt was made to appraise the importance of IgM antibody, as determined by each test, in establishing the diagnosis of clinical melioidosis. Results obtained from serological tests were of no value in differentiating between active and latent infections. However, the IgM-immunofluorescent test appeared to be relevant to the diagnosis of clinical melioidosis, since the presence and absence of IgM-immunofluorescent antibody bore a close relation to clinical and subclinical disease, respectively. Surveillance studies indicated that the IgM-immunofluorescent test may be of value in monitoring the activity and treatment of the infection, since the results of the test were generally negative 3 to 6 months after administration of chemotherapy appropriate for melioidosis.

Antibodies, Bacterial↗
PubMed1993

Identification of specific antigens of Pseudomonas pseudomallei and evaluation of their efficacies for diagnosis of melioidosis.

Current methods for the diagnosis of melioidosis are based on bacteriological culture. A number of serological tests currently available lack specificity and sensitivity. This is largely due to the use of crude antigens which results in a significant cross-reactivity with sera from individuals infected with other bacteria. In this study five different antigens were prepared and evaluated for their potential usefulness in diagnosis of melioidosis. These included a 19.5-kDa antigen which was previously shown to be specific by Western blotting (immunoblotting), a crude cell extract, a veronal extract, a 39.0-kDa antigen, and an immunoaffinity-purified antigen. All antigens were used for detecting antibody in sera from patients with septicemic melioidosis by indirect enzyme-linked immunosorbent assay. The results were compared with those obtained with sera from patients with other bacterial infections and normal sera from areas where the infection is and is not endemic. The 19.5-kDa antigen exhibited the most satisfactory results, with 92% sensitivity, 91% specificity, 81% positive predictive value, and 96% negative predictive value based on a background obtained with normal sera from the area where the infection is nonendemic. These values were 82% sensitivity, 96% specificity, 94% positive predictive value, and 87% negative predictive value based on results with normal sera from the area where the infection is endemic. Results from this study showed that the 19.5-kDa antigen was potentially useful in the diagnosis of melioidosis and deserves further investigation.

Antibodies, Bacterial↗