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词条 Melioidosis
释义

  1. Signs and symptoms

     Acute  Chronic  Latent 

  2. Cause

     Bacteria  Transmission 

  3. Pathogenesis

  4. Diagnosis

  5. Prevention

     Postexposure prophylaxis  Vaccination 

  6. Treatment

     Intensive phase  Eradication phase  Surgical treatment  Others 

  7. Prognosis

  8. Biological warfare potential

  9. Epidemiology

  10. History

  11. Synonyms

  12. References

  13. External links

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| caption = Burkholderia pseudomallei
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Melioidosis is an infectious disease caused by a Gram-negative bacterium, Burkholderia pseudomallei, found in soil and water. It is of public health importance in endemic areas, particularly in northeast Thailand, Vietnam, and northern Australia. It exists in acute and chronic forms. Signs and symptoms may include pain in chest, bones, or joints; cough; skin infections, lung nodules, and pneumonia.

B. pseudomallei was previously classed as part of the genus Pseudomonas; until 1992, it was known as Pseudomonas pseudomallei. It is phylogenetically related closely to Burkholderia mallei which causes glanders, an infection primarily of horses, donkeys, and mules. The name melioidosis is derived from the Greek melis (μηλις) meaning "a distemper of asses" with the suffixes -oid meaning "similar to" and -osis meaning "a condition", that is, a condition similar to glanders.[1]

Signs and symptoms

Acute

The mean incubation period of acute melioidosis was 9 days (range 1–21 days).[2] Symptoms usually appear 2 to 4 weeks after exposure. Those affected are presented with symptoms of sepsis (predominantly fever) with or without pneumonia, or localised abscess or other focus of infection. The presence of non-specific signs and symptoms has caused meliodosis to be nicknamed as "the great mimicker".[3]

The clinical manifestation of the disease can range from simple skin changes to severe organ involvement. Among the commonest organs affected are: liver, spleen, lungs, prostate, and kidneys. Bacteremia can occur in 40 to 60% of the people while septic shock occurs in 20% of the cases. Pneumonia is present in 50% of the cases.[3] The risk factors of getting meliodosis are diabetes mellitus or occupation or seasonal exposure to the disease in question. The disease should be considered in anyone who has fever and staying in endemic areas and those who has abscesses in liver, spleen, prostate, or parotid gland with pneumonia.[3] 1% to 5% of those infected could develop encephalomyelitis or brain abscess, 40 to 60% of them could develop myocarditis or mycotic aneurysm, 14 to 28% of the cases could develop acute pyelonephritis, kidney abscess or prostatic abscesses, 0 to 30% would develop neck or parotid gland abscess, 10 to 33% would develop liver, spleen, or paraintestinal abscesses and 4 to 14% of the cases could develop septic arthritis and osteomyelitis.[3] Specifically in Australia, up to 20% of the males can get prostatic abscess. In Thailand, 30% of the infected children can get parotid abscess.[3]

Chronic

Chronic melioidosis is usually defined by a duration of symptoms greater than two months and occurs in about 10% of patients.[3] The clinical presentation of chronic melioidosis is protean and includes such presentations as chronic skin infections, chronic lung nodule, and pneumonia. In particular, chronic melioidosis closely mimics tuberculosis, and has sometimes been called "Vietnamese tuberculosis".[4][5][6]

Latent

In latent infection, immunocompetent people have the ability to clear out the infection without showing any symptoms. However, less than 5% of all meliodosis cases has activation after a period of latency.[3] Patients with latent melioidosis may be symptom-free for decades; the longest period between presumed exposure and clinical presentation is 62 years.[7]

The potential for prolonged incubation was recognized in US servicemen involved in the Vietnam War, and was referred to as the "Vietnam time-bomb". A wide spectrum of severity exists; in chronic presentations, symptoms may last months, but fulminant infection, particularly associated with near-drowning, may present with severe symptoms over hours.

Cause

Bacteria

Meliodosis is caused by gram negative, opportunistic, facultative, intracellular, motile saprophyte bacteria named Burkholderia pseudomallei.[8] In animals, another similar organism named Burkholderia mallei is the causing agent which results in a disease named glanders.[8] B pseudomallei is highly adaptable to various host environments, thus it has a survival advantage in the human body.[8]

The genome of B. pseudomallei consists of two replicons: chromosome 1 which encodes for housekeeping function of the bacteria such as cell wall synthesis, mobility, and metabolism, and chromosome 2 which encodes for functions that allow the bacteria to adapt to various environments. Horizontal gene transfer between two bacteria causes highly variable genome in B. pseudomallei. Australia has been suggested as the early reservoir for B. psudomallei because of high genetic variability of the bacteria found in this region. The bacteria isolates from Africa, Central and South America seems to have a common ancestor originated from 17th to 19th century.[8]

Transmission

Infection can enter through wounds, inhalation, and ingestion.[8] Patients with melioidosis usually have risk factors for disease, such as diabetes, thalassemia, hazardous alcohol use, or kidney disease, and frequently give a history of occupational or recreational exposure to mud or pooled surface water.[9]

Pathogenesis

The bacteria has the ability to infect various types of cells and to evade human immune response.[8] When skin is broken, B pseudomallei first enters and replicates in the epithelial cells of the broken skin. The bacteria then can infect both phagocytes and non-phagocytes in the blood stream. The bacteria enters these cells through endocytosis inside an endocytic vesicle.[8] B pseudomallei has multiple secretory systems and can be transported across cellular membranes, aiding invasion into a host cell.[8] B. pseudomallei uses Type III secretion system (T3SS) system effector proteins for invasion into a cell. T3SS is a molecular syringe that injects effector proteins into host cells. The effector proteins rearrange the host cytoskeleton to facilitate invasion.The cell entry is aided by flagella, LPS, type IV pilin, and adhesion proteins BoaA and BoaB. The T3SS effector protein bopA helps to disrupt endocytic vesicle and thus avoid the bacteria from being digested by lysosomes inside the cell. The bacteria then replicates inside the cytoplasm of the cell. The bacteria are also able to withstand high oxidative stress in an endocytic vesicle by creating an acidic environment. Once inside cytoplasm, BimA autotransporter proteins protein helps escape the bacteria from phagosome. Premature killing of macrophage can also cause the evasion of B. pseudomallei from being digested. Besides, the delayed degradation of infected neutrophils ingested by macrophages also causes the bacteria to proliferate inside the host cells.[8] CD4 T cells and cytotoxic CD8 T cells are important to keep meliodosis at bay. Reduction of these cells is associated with higher risk of death.[8] Although activation of coagulation cascade is helpful in containing meliodosis infection, overactivation coagulation cascade can cause disseminated intravascular coagulation (DIC).[8]

Meliodosis infection induces humoral immunity through the release of interferon gamma (IFN) and cell-mediated immunity.[8] In the host, Protease-activated receptor-1 (PAR-1) expressed on the surface of endothelial cells, platelets, and monocytes helps B. pseudomallei invasion.[8] However, macrophages activated by IFN has improved killing of B. pseudomallei via the production of inducible nitric oxide synthase (NOS).[8] Human Toll-like receptor (TLRs) such as TLR2, TLR4, TLR 5 recognizes the pathogen-associated molecular pattern (PAMPs) of the bacteria such as LPS and flagella, thus initiating immune response against the bacteria. As a result, Interleukin 1 beta (IL-1β) and Interleukin 18 (IL-18) are produced.[8] Neutrophils, dendritic cells, B cell and T cells activate the human complement membrane attack complex (MAC) but the complement activity is hampered by external capsule and lipopolysaccharide (LPS) of the bacteria. These two features of the bacteria are also resistant to lysosomal degradation, thus enabling the survival of the bacteria in human phagocytes.[8] Once B. pseudomallei escaped from the lysosomal destruction, it enters the cytosol of the cell. Meanwhile, inside the human cell, Pattern recognition receptors of the cytosol namely NOD-like receptors detects the Damage-associated molecular pattern (DAMP)s of the bacteria. As a result, inflammasomes which contains Caspase 1 are released to digest the bacteria. Activation of Caspase 1 enables the pyroptosis of the bacteria and increases the production of Interleukin 1 beta (IL-1β) and Interleukin 18 (IL-18). IL-18 increases IFN production throughn natural killer cells while IL-1beta reduces the IFN production. Thus, reduction in IFN gamma contributes to the persistence of the bacteria intra-cellularly.[8] However, HIV infection is not a risk factor for meliodosis. Although macrophages show deregulated cytokine response in individuals with HIV infection, bacterial internalization and intracellular killing are still effective.[8]

The bacteria then proceeds to spread from cell to cell. The bacteria rearrange the host cell cytoskeleton using Bim A to allow the latter to form a membranous protusions that extends into neighbouring cells. The bacteria then travel into another cell using actin. The action of these bacteria causes the fusion of the adjacent cells which leads to the formation of multinucleated giant cells (MNGCs). When MNGCs lyse, they form plaques (a central clear area with a ring of fused cells). These plaques then provide shelter for the bacteria for further replication or latent infection. With the help of Bim A autotrasporter protein, the bacteria are able to travel through nerve roots in the spinal cord and brain, thus leading to encephalomyelitis (inflammation of the brain and spinal cord).[8]

Besides spreading from cell to cell, the bacteria can also spread through blood stream, causing sepsis. The bacteria can survive in antigen presenting cells and dendritic cells. Thus, these cells acts as vehicles that transport the bacteria into the lymphatic system, causing widespread dissemination of the bacteria in the human body.[8]

B. pseudomallei can remain latent in the human body from 19 to 29 years until it is reactivated duringhuman immunosuppression or stress response. The mechanism of latent infection remains unclear as of 2018. Amongst mechanisms suggested are: residing in the nucleus of the cell to prevent being digested, entering a stage of slower growth rate, antibiotic resistance, and genetic adaption to the host environment.[8] Granulomas (containing neutrophils, macrophages, lymphocytes, and multinucleated giant cells) formed at the infection site in meliodosis has been associated with latent infection in human body.[8]

Diagnosis

A definitive diagnosis is made by culturing the organism from any clinical sample, because the organism is never part of the normal human flora.

A definite history of contact with soil may not be elicited, as melioidosis can be dormant for many years before manifesting.[10] Attention should be paid to a history of travel to endemic areas in returned travellers. Some authors recommend considering possibility of melioidosis in every febrile patient with a history of traveling to and/or staying at endemic areas.

Bacterial culture is the definitive diagnosis of melidosis. It is important not misinterpret the bacterial growth as Pseudomonas or Bacillus spp. B. pseudomallei is never part of human flora. Therefore, any growth of the bacteria should be regarded as diagnostic of meliodosis. Blood culture is the most important sample for culture because the bacteria are usually found in blood. Other samples such as throat, rectal swabs, pus from abscesses, and sputum can also be used for culture. Blood cultures can be positive in 50 to 60% of the cases. For those strongly suspected of meliodosis but with initial negative culture, repeated cultures can be taken because the culture can become positive subsequently. The agar plates should be incubated and inspected daily for four days. B. pseudomallei can be grown on sheep blood agar, MacConkey agar, and Ashdown agar (containing gentamicin). On agar plates, B. pseudomallei will be seen as creamy, non-haemolytic, with shape similar to a rod on Day 2 of incubation. On Day 4 of incubation, the colonies will appear dry and wrinkled.[8]

Latex agglutination is useful in screening for suspected B. pseudomallei colonies.[8] Molecular methods such as 16srDNA and polymerase chain reaction (PCR) can be used to detect B. pseudomallei bacteria.[8]

Ashdown's medium, a selective medium containing gentamicin, may be required for cultures taken from nonsterile sites. Burkholderia cepacia medium may be a useful alternative selective medium in nonendemic areas, where Ashdown's is not available.[11] A new medium derived from Ashdown, known as Francis medium, may help differentiate B. pseudomallei from B. cepacia and may help in the early diagnosis of melioidosis,[12] but has not yet been extensively clinically validated.

B. pseudomallei can be observed under microscopy. The organism is described as gram negative rod shaped bacterium with bipolar staining similar to safety pin appearance. However, light microscopy is both not [[Sensitivity and specificity


|specific]] and not sensitive. Immunofluorescent microscopy approaches 100% in specificity and while achieved less than 50% sensitivity. A lateral flow immunoassay has been developed but not extensively evaluated.[8]Serological tests such as indirect haemagglutination test has been used to detect the presence of antibodies against B. pseudomallei. However, the test suffered from poor sensitivity and specificity because those staying in meliodosis endemic areas usually shows high background antibody titres.[8] A commercial ELISA kit for melioidosis appears to perform well.[13] but no ELISA test has yet been clinically validated as a diagnostic tool.[14]

It is not possible to make the diagnosis on imaging studies alone (X-rays and scans),[15] but imaging is routinely performed to assess the full extent of disease.[16] Imaging of the abdomen using CT scans or ultrasound is recommended routinely, as abscesses may not be clinically apparent and may coexist with disease elsewhere. Australian authorities suggest imaging of the prostate specifically due to the high incidence of prostatic abscesses in northern Australian patients. A chest X-ray is also considered routine, with other investigations as clinically indicated. The presence of honeycomb abscesses in the liver is considered characteristic, but is not diagnostic.[15][16]

The differential diagnosis is extensive; melioidosis may mimic many other infections, including tuberculosis.[4]

Prevention

Person-to-person transmission is exceedingly unusual;[52][53][54] and patients with melioidosis should not be considered contagious. Lab workers should handle B. pseudomallei under BSL-3 isolation conditions,[17] as laboratory-acquired melioidosis has been described. There are also several cases of hospital-acquired infection of meliodosis. Therefore, healthcare providers are still recommended to practice hand hygiene and universal precautions.[8]

Large scale water chlorination has been successful in Australia. In middle to low income countries, water should be boiled before consumption. In high income countries, water could be treated with ultraviolet light for those at risk of contracting melidosis. Those who are high risk of contact with the bacteria should wear protective gear (such as boots and gloves) during work. Those who are staying in endemic areas should avoid direct contact with soil, and outdoor exposure to heavy rain, or dust clouds. Bottled water or boiled water are preferred as drinking water.[8]

Postexposure prophylaxis

After exposure to B. pseudomallei (particularly following a laboratory accident), treatment with co-trimoxazole is recommended. Alternatively, co-amoxiclav and doxycycline can be used for those who is intolerant co-trimoxazole. In view of possibility of severe side effects caused by co-trimoxazole, only high risk individuals will receive such treatments. Low risk individuals would receive frequent monitoring instead.[8]

Vaccination

{{Further|Burkholderia_pseudomallei#Vaccine_candidates}}

Several vaccine candidates are being researched; but as of 2018, there is no vaccine approved for public use.[8] There is a fear that when a vaccine is licensed, financial constraints will make the vaccination an unrealistic factor for many countries that are suffering from high rates of melioidosis.[18]

Treatment

The treatment of melioidosis is divided into two stages, an intravenous intensive phase and an eradication phase to prevent recurrence. The choice of antibiotics depends upon the suscepbility of the bacteria to various types of antibiotics. B. pesudomallei are generally susecptible to ceftazidime, meropenem, imipenem, and co-amoxiclav. These drugs are designed to kill the bacteria. B. pseudomallei is also susceptible to doyxcycline, chloramphenicol, and co-trimoxazole. These drugs are designed to inhibit the growth of the bacteria. However, the bacteria is resistant to penicillin, ampicillin, 1st and 2nd generation cephalosporin, gentamicin, streptomycin, tobramycin, macrolides, and polymyxins.[8] On the other hand, B. pseudomallei isolates from the region of Sarawak, Malaysia are susceptible to gentamicin.[8]

Intensive phase

Intravenous ceftazidime is the current drug of choice for treatment of acute melioidosis and should be administered 10 to 14 days after getting the infection.[19][20][21] Meropenem,[22] imipenem[2] and the cefoperazone-sulbactam combination (Sulperazone)[23] are also effective.[24] Intravenous amoxicillin-clavulanate (co-amoxiclav) may be used if none of the above four drugs is available, but it produces inferior outcomes.[25] Intravenous antibiotics are given for a minimum of 10 to 14 days, and are not usually stopped until the patient's temperature has returned to normal for more than 48 hours. Even with appropriate antibiotic therapy, fevers often persist for weeks or months, and patients may continue to develop new lesions even while on appropriate treatment. The median fever clearance time in melioidosis is 10 days:[25] and failure of the fever to clear is not a reason to alter treatment.

Meropenem is the preferred antibiotic therapy for neurological meliodosis. Co-trimoxazole is recommended for neurological melidosis, osteomyelitis, septic arthritis, skin and gastrointestinal infection, and deeply seated abscess.[8] For deep seated infections such as abscesses of internal organs, osteomyelitis, septic arthritis, and neurological meliodosis, the duration of antibiotics given should be longer (up to 4 to 8 weeks). The time taken for fever to be resolved can be more than 10 days in those with deep seated infection.[8] The dosage for intravenous ceftazidime is 2g 6 hourly in adults (50 mg/kg up to 2g in children less than 15 years old). The dosage for meropenem is 1g 8 hourly in adults (25 mg/kg up to 1g in children).[8]

Theoretical reasons are given for believing mortality might be lower in patients treated with imipenem: first, less endotoxin is released by dying bacteria during imipenem treatment,[26] and the minimum inhibitory concentration (MIC) for imipenem is lower than for ceftazidime. However, no clinically relevant difference was found in mortality between imipenem and ceftazidime treatments.[2] The MIC of meropenem is higher for B. pseudomallei than for many other organisms, and patients being haemofiltered will need more frequent or higher doses.[27] Intravenous meropenem is routinely used in Australia.[3] Meropenem is the drug of choice for severe meliodosis with septic shock in Australia. Once the clinical condition improved, meropenem can be switched back to ceftazidime.[8]

Moxifloxacin, cefepime, tigecycline, and ertapenem do not appear to be effective in vitro.[28][29] Piperacillin-sulbactam,[28] doripenem and biapenem[29][30] appear to be effective in vitro, but no clinical experience exists on which to recommend their use.

Adjunctive treatment with granulocyte colony-stimulating factor[31] or co-trimoxazole[32][33] were not associated with decreased fatality rates in trials in Thailand.

Eradication phase

Following the treatment of the acute disease, eradication (or maintenance) treatment with co-trimoxazole is the drug of choice which should be used for at least 3 months. For those with neurological meliodosis and osteomyelitis, duration more than 6 months. Co-amoxiclav and doxycycline are drugs of second choice. Co-trimoxazole should not be used in those with glucose-6-phosphate dehydrogenase (G6PD) deficiency as it can cause haemolytic anemia. Other side effects such as rash, hyperkalemia, renal dysfunction, and gastrointestinal symptoms should prompt the reduction of co-trimoxazole doses.[8] Chloramphenicol is no longer routinely recommended for this purpose. Co-amoxiclav is an alternative for those patients who are unable to take co-trimoxazole and doxycycline (e.g., pregnant women and children under the age of 12),[34][35] but is not as effective. Single agent treatment with a fluoroquinolone (e.g., ciprofloxacin)[36][37] or doxycycline[38] for the oral maintenance phase is ineffective.[39]

In Australia, co-trimoxazole is used in children and could also be used in pregnant mothers after the first 12 weeks of pregnancy. Meanwhile, in Thailand, co-amoxiclave is the drug of choice for children and pregnancy women. However, the co-amoxiclav dosing is problematic and B. pseudomallei can easily acquire resistance when this drug is used.[8] The dosing regimen for co-trimoxazole (trimethoprim/sulfamethoxazole) in eradication phase is 6/30 mg/kg, up to maximum 240/1200 mg in children, 240/1200 mg in adults weighing 40 to 60 kg, and 320/1600 mg in adults weighing more than 60 kg, taken orally every 12 hours. In children, co-trimoxazole is taken together with folic acid (0.1 mg/kg up to 5mg in children). There are also cases where melidosis is successfully treated with co-trimoxazole for 3 months without going through intensive therapy provided that there is only skin manifestations without involvement of internal organs or sepsis.[8]

Surgical treatment

Surgical drainage is indicated for single, large abscess in the liver, muscle, and prostate. However, for multiple abscesses in the liver, spleen, and kidney, surgical drainage may not be possible or necessary. For septic arthritis, arthrotomy washout and drainage is required. Surgical debridement may be necessary for surgical debridement. For those with mycotic aneurysm, urgent surgery is required for prosthetic vascular grafts. Life-long therapy with co-trimoxazole may be needed for those with prosthetic vascular grafts. Other abscesses rarely need to be drained because majority of them can resolve with antibiotic treatment.[8]

Others

Immunomodulating therapies such as granulocyte colony-stimulating factor (G-CSF), Interleukin 7 (IL-7), and anti-PDI (programmed cell death) could be useful in meliodosis treatment. This is because immune function is strongly associated with the pathogenesis of meliodosis.[8]

Prognosis

In resourceful settings, where the disease can be detected and treated early, the risk of death is 10%. Meanwhile, in resource poor settings, the risk of death from the disease is more than 40%.[8]

For those with incomplete treatment, recrudescence can occur. Then, hospital admission is needed for intravenous antibiotics. For those completed treatment successfully, recurrence can also occur due to recrudescence or new meliodosis infection. With better therapies, the recrudescence rate has reduced from 10% to 5%. New infection is now more common than recrudescence.[8] Recurrence occurs in 10 to 20% of patients, but with co-trimoxazole eradication therapy, this can be reduced to 4%.[40] While molecular studies have established the majority of recurrences are due to the original infecting strain, a significant proportion of recurrences (perhaps up to a quarter) in endemic areas may be due to reinfection, particularly after two years.[41] Risk factors include severity of disease (patients with positive blood cultures or multifocal disease have a higher risk of relapse), choice of antibiotic for eradication therapy (doxycycline monotherapy and fluoroquinolone therapy are not as effective), poor compliance with eradication therapy and duration of eradication therapy less than 8 weeks.[39][42]

Underlying medical conditions such as diabetes mellitus, chronic kidney disease, and malignancy can worsens the long term survival and disability of those recovered from infection. The most severe complication of meliodosis is encephalomyelitis. It can cause quadriparesis (muscle weakness in all the limbs) or partial, flaccid paraparesis (muscle weakness of both legs) or foot drop. For those with previous meliodosis associated bone and joint infection, complications such as sinus tract infection, bones and joint deformities with limited range of motion can occur.[8]

Biological warfare potential

Interest in melioidosis has been expressed because it has the potential to be developed as a biological weapon. It is classified by the US Centers for Disease Control (CDC) as a category B,[43] Tier 1 select agent.[8] Another similar bacteria, Burkholderia mallei was used by the Germans in World War I to infect livestocks shipped to Allied countries. Soviet Union reportedly used B. mallei during Soviet–Afghan War in 1982 and 1984.[108] B. pseudomallei, like B. mallei, was studied by both US[44] and Soviet Union as a potential biological warfare agent, but never weaponized.[45]

Epidemiology

Meliodosis is an understudied disease which remained endemic in developing countries. As of 2018, meliodosis is not included in the WHO list of neglected tropical diseases. In 2015, International Meliodosis Society (IMS) was formed to raise awareness regarding the disease.[8] Melioidosis is endemic in parts of southeast Asia (including Thailand,[46] Laos,[47][48][49] Singapore,[50] Brunei,[51] Malaysia, Burma and Vietnam), China,[52] Taiwan[53][54] and northern Australia.[55][56] Flooding can increase its extent, including flooding in central Australia.[57] Multiple cases have also been described in Hong Kong and Brunei[58] India,[59][60][61][62] and sporadic cases in Central and South America,[63][64][65] the Middle East, the Pacific and several African countries.[66][67] Although only one case of melioidosis has ever been reported in Bangladesh,[68] at least five cases have been imported to the UK from that country. Recent news reports indicate B. pseudomallei has been isolated from soil in Bangladesh,[69] but this remains to be verified scientifically. This suggests that melioidosis is endemic to Bangladesh and that a problem of underdiagnosis or under-reporting exists there.[70] most likely due to a lack of adequate laboratory facilities in affected rural areas. A high isolation frequency (percentage of positive soil samples) was found in east Saravan in rural Lao PDR distant from the Mekong River, thought by the investigators to be the highest geometric mean concentration in the world (about 464 (25-10,850 CFU/g soil).[71]

A statistical model indicated that the incidence will be 165,000 cases per year in 2016 (95% confidence interval, 68,000 to 412,000), with 138,000 of those occurring in East and South Asia and the Pacific.[72] In about half of those cases (54% or 89,000), people will die.[8] Northeast Thailand has the highest incidence of melioidosis recorded in the world (an average incidence of 12.7 cases per 100,000 people per year).[73] In Northeast Thailand, 80% of children are positive for antibodies against B. pseudomallei by the age of 4;[74] the figures are lower in other parts of the world.[75][76][77][78] Under-reporting is a prevalent problem because only 1,300 cases were reported worldwide since 2010, which is less than 1% of the projected incidence based on modeling.[8] Besides, lack of laboratory diagnositic capabilities and the lack of disease awareness amongst health care providers also causes underdiagnosis. Even if the culture turns positive for ‘’B. pesudomallei’’, it could discarded as contaminant especially in laboratories in non-endemic areas.[8]

Melioidosis is a recognised disease in animals, including cats,[79] goats, sheep, and horses. Cattle, water buffalo, and crocodiles are considered to be relatively resistant to melioidosis despite their constant exposure to mud.[80] An outbreak at the Paris Zoo in the 1970s ("L’affaire du jardin des plantes") was thought to have originated from an imported panda.[81]

B. pseudomallei is normally found in soil and surface water, and is more abundant at greater than 10 cm from the soil surface.[8] B. pseudomallei can survive in nutrient poor condition such as distilled water, desert, and nutrient depleted soil for more than 16 years.[8] A history of contact with soil or surface water is, therefore, almost invariable in patients with melioidosis;[55] that said, the majority of patients who do have contact with infected soil suffer no ill effects. Even within an area, the distribution of B. pseudomallei within the soil can be extremely patchy,[82][83] and competition with other Burkholderia species has been suggested as a possible reason.[84] Contaminated ground water was implicated in one outbreak in northern Australia.[85] Also implicated are severe weather events such as flooding[86] tsunamis[87] and typhoons.[88][89] Inadequate chlorination of water supply had been associated with B. pseudomallei outbreak in Northern and Western Australia. The bacteria is also found in unchlorinated water supply in rural Thailand. Irrigation fluid contaminated with B pseudomallei is associated with nosocomial wound infection in hospitals.[8]

Based on whole genome sequencing, humans may play a role in moving B. pseudomallei from place to place.[90]

Meliodosis is found in all age groups.[8] For Australia and Thailand, the median age of infection is 50 years; 5 to 10% of the patients are less than 15 years.[8] The single most important risk factor for developing melioidosis is diabetes mellitus, followed by hazardous alcohol use, chronic kidney disease, and chronic lung disease.[166] In all people with meliodosis, greater than 50% of them have diabetes. Diabetes has 12 folds increased risk of meliodosis. Diabetes decreases the ability of macrophages to fight the bacteria and reduced the ability of T helper cell production. Excessive release of Tumor necrosis factor alpha (TNF) and Interleukin 12 by mononuclear cells causes greater risk of septic shock. The Glibenclamide drug taken by diabetes patients can also cause blunting of monocyte’s inflammatory responses.[8]

Other risk factors include thalassaemia, occupation (rice paddy farmers),[91] cystic fibrosis,[92][64], exposure to soil, water, male, age > 45 years, and prolonged steroids/immunosuppresion.[8] However, 8% of the peadiatrics and 20% of the adult with meliodosis have no risk factors.[8] The mode of infection is believed to be through either a break in the skin, or the inhalation of aerosolized B. pseudomallei cells. Person-to-person spread has been described, but is extremely unusual.[92][93][94] Transmission from animals to humans is also rare.[8] HIV infection does not predispose to melioidosis.[95][96][97] Neonatal cases have been reported possibly due to mother-to-child transmission, community acquired infection, or healthcare-associated infection.[8]

The disease is clearly associated with increased rainfall, with the number (and severity) of cases rising following increased precipitation.[50][98][99][100][101][102]

History

Pathologist Alfred Whitmore and assistant Krishnaswami first reported the disease among beggars and morphine addicts at autopsy in Rangoon, present-day Myanmar, in a report published in 1912.[103] Arthur Conan Doyle may have read the 1912 report before writing a short story that involved the fictitious tropical disease "tapanuli fever" in a Sherlock Holmes adventure.[104]The term “meliodosis” was first coined in 1921.[8]They distinguished it from glanders, a disease of humans and animals that is similar in presentation, but caused by a different micro-organism. B. pseudomallei, also known as the Whitmore bacillus, was identified in 1917 in Kuala Lumpur.[105] First human case of meliodosis was reported in Sri Lanka in 1927.[8] In 1932, 83 cases were reported in South and Southeast Asia with 98% mortality.[8] In 1936, first animal (sheep) case of meliodosis was reported in Madagascar, South Africa.[8] In 1937, soil and water are identified as habitat of B pseudomallei.[8] During Vietnam War from 1967 to 1973, 343 American soldiers were reported with meliodosis, with about 50 cases reported to have transmitted through inhalation.[8] First evidence of B. pseudomallei (in soil) in Brazil was reported in 1983.[8]

Prior to 1989, the standard treatment for acute melioidosis was a three-drug combination of chloramphenicol, co-trimoxazole and doxycycline; this regimen is associated with a mortality rate of 80% and is no longer be used unless no other alternatives are available.[20] All three drugs are bacteriostatic (they stop the bacterium from growing, but do not kill it) and the action of co-trimoxazole antagonizes both chloramphenicol and doxycycline.[106] Aerosolised B pseudomallei was first isolated in 1989.[8] In the same year, Ceftazidime had been shown to reduce the risk of death of meliodosis from 74% to 37%. In 1992, the pathogen was formally named B. pseudomallei. In 2002, B. pseudomallei was classified as "Category B agent". Attenuated vaccine was developed on the same year. In 2003, multilocus sequence typing for B. pseudomallei was developed. In 2012, B pseudomallei was classified as "Tier 1 select agent" by CDC. In 2014, co-trimoxazole was established as the oral eradication therapy. In 2015, B pseudomallei DNA was detected in filtered air using quantitative PCR.[8] In 2016, a statistical model was developed to predict the occurrence of global meliodosis per year. In 2017, whole genome sequencing points to Australia as the early reservoir for meliodosis.[8]

Synonyms

  • Pseudoglanders
  • Whitmore's disease (after Captain Alfred Whitmore, who first described the disease)[107]
  • Nightcliff gardener's disease (Nightcliff is a suburb of Darwin, Australia where melioidosis is endemic)[108]
  • Paddy-field disease[109]
  • Morphia injector's septicaemia[110]

References

1. ^{{cite book|vauthors=Stanton AT, Fletcher W |chapter=Melioidosis, a new disease of the tropics|title=Far Eastern Association of Tropical Medicine: Transactions of the Fourth Congress|location=Batavia, Dutch East Indies|publisher=Javasche Boekhandel en Drukkerij|year=1921}}
2. ^1 2 {{cite journal|author1=A J Simpson |author2=Suputtamongkol Y |author3=Smith MD |title=Comparison of imipenem and ceftazidime as therapy for severe melioidosis|journal=Clinical Infectious Diseases|volume=29|issue=2|year=1999|pages=381–387|pmid=10476746|doi=10.1086/520219|display-authors=etal}}
3. ^1 {{cite journal |vauthors=Currie BJ, Fisher DA, Howard DM, et al |title=Endemic melioidosis in tropical northern Australia: a 10-year prospective study and review of the literature|journal=Clinical Infectious Diseases |volume=31|issue=4|year=2000|pages=981–986|pmid=11049780|doi=10.1086/318116}}
4. ^1 {{cite journal|vauthors=Falade OO, Antonarakis ES, Kaul DR, Saint S, Murphy PA |title=Clinical problem-solving. Beware of first impressions|journal=New England Journal of Medicine|year=2008|volume=359|issue=6|pmid=18687644|pages=628–634|doi=10.1056/NEJMcps0708803|pmc=4007002}}
5. ^{{cite journal|last1=Chetchotisakd|first1=P|last2=Anunnatsiri|first2=S|last3=Kiatchoosakun|first3=S|last4=Kularbkaew|first4=C|title=Melioidosis pericarditis mimicking tuberculous pericarditis|journal=Clinical Infectious Diseases|volume=51|issue=5|pages=e46–49|year=2010|pmid=20645861|doi=10.1086/655699}}
6. ^{{cite journal |vauthors=Suntornsut P, Kasemsupat K, Silairatana S, et al |title=Prevalence of Melioidosis in Patients with Suspected Pulmonary Tuberculosis and Sputum Smear Negative for Acid-Fast Bacilli in Northeast Thailand|journal=American Journal of Tropical Medicine and Hygiene|year=2013|volume=89|issue=5|pages=983–985| doi=10.4269/ajtmh.13-0286|pmid=24062474|pmc=3820347}}
7. ^{{cite journal|vauthors=Ngauy V, Lemeshev Y, Sadkowski L, Crawford G | title=Cutaneous Melioidosis in a Man Who Was Taken as a Prisoner of War by the Japanese during World War II|year=2005|journal=Journal of Clinical Microbiology Microb|volume=43|issue=2|pages=970–972|pmid=15695721|doi=10.1128/JCM.43.2.970-972.2005|pmc=548040}}
8. ^1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 70 71 72 73 74 75 {{cite journal |last1=W Joost |first1=Wiersinga |last2=Harjeet |first2=S Virk |last3=Alfredo |first3=G Torres |last4=Bart |first4=J Currie |title=Meliodosis |journal=Nature Reviews Disease Primers |date=1 February 2018 |volume=4 |issue=17107 |pages=17107 |doi=10.1038/nrdp.2017.107|pmid=29388572 }}
9. ^{{cite journal| last=Raja | first=NS |author2=Ahmed MZ |author3=Singh NN |title=Melioidosis: an emerging infectious disease |journal=Journal of Postgraduate Medicine | date=1 April 2005| volume=51 | issue=2 | pages=140–145 | url=http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2005;volume=51;issue=2;spage=140;epage=145;aulast=Raja | pmid=16006713}}
10. ^{{cite journal|vauthors=Ngauy V, Lemeshev Y, Sadkowski L, Crawford G |title=Cutaneous Melioidosis in a Man Who Was Taken as a Prisoner of War by the Japanese during World War II|journal=Journal of Clinical Microbiology|year=2005|volume=43|pmid=15695721|issue=2|pages= 970–972|pmc=548040|doi=10.1128/JCM.43.2.970-972.2005}}
11. ^{{cite journal |vauthors=Peacock SJ, Chieng G, Cheng AC, et al | title = Comparison of Ashdown's Medium, Burkholderia cepacia Medium, and Burkholderia pseudomallei Selective Agar for Clinical Isolation of Burkholderia pseudomallei| journal = Journal of Clinical Microbiology| year = 2005| volume = 43| issue= 10| pages = 5359–5361| pmid = 16208018| doi=10.1128/JCM.43.10.5359-5361.2005| pmc=1248505}}
12. ^{{cite journal | title=An improved selective and differential medium for the isolation of Burkholderia pseudomallei from clinical specimens| journal = Diagnostic Microbiology and Infectious Diseases | volume=55 | issue=2 | pages=95–99|vauthors=Francis A, Aiyar S, Yean C, Naing L, Ravichandran M | doi=10.1016/j.diagmicrobio.2005.11.008 | pmid=16626918 | year=2006 }}
13. ^{{cite journal |vauthors=Limmathurotsakul D, Chantratita N, Teerawattanasook N, et al |title= Enzyme-Linked Immunosorbent Assay for the Diagnosis of Melioidosis: Better Than We Thought|journal=Clinical Infectious Diseases|year=2011|volume=52|issue=8|pages=1024–1028|pmid=21460318|doi=10.1093/cid/cir080|pmc=3070030}}
14. ^{{cite journal|vauthors=Peacock SJ, Cheng AC, Currie BJ, Dance DA|title=The Use of Positive Serological Tests as Evidence of Exposure to Burkholderia pseudomallei|journal=American Journal of Tropical Medicine and Hygiene|year=2011|volume=84|issue=6|pages= 1021–1022|pmid=21633045|doi=10.4269/ajtmh.2011.11-0114a| pmc=3110358}}
15. ^1 {{cite journal|vauthors=Lim KS, Chong VH |title=Radiological manifestations of melioidosis|journal=Clinical Radiology|year=2010|volume=65|issue=1|pmid=20103424|pages=66–72|doi=10.1016/j.crad.2009.08.008}}
16. ^1 {{cite journal|vauthors=Muttarak M, Peh WC, Euathrongchit J, Lin SE, Tan AG, Lerttumnongtum P, Sivasomboon C |title=Spectrum of imaging findings in melioidosis|journal= British Journal of Radiology|year=2008|pmid=19098086|volume=82|issue=978|pages=514–521|doi=10.1259/bjr/15785231}}
17. ^{{cite book|author=Centers for Disease Control and Prevention|title=Biosafety in Microbiological and Biomedical Laboratories|publisher=National Institutes of Health|location=Atlanta, Georgia|year=2009|edition=5th}}
18. ^{{cite journal | author = Cheng AC, Currie BJ | year = 2005 | title = Melioidosis: Epidemiology, Pathophysiology, and Management | journal = Clinical Microbiology Reviews | volume = 18 | issue = 2| pages = 383–416 | doi=10.1128/CMR.18.2.383-416.2005| pmid = 15831829 | pmc = 1082802 }}
19. ^Centers for Disease Control and Prevention. Melioidosis. 2012. Accessed February 27, 2017.
20. ^1 {{cite journal |vauthors=White NJ, Dance DA, Chaowagul W, et al | title = Halving of mortality of severe melioidosis by ceftazidime| journal = Lancet| year = 1989| volume = 2| issue = 8665| pages = 697–701| pmid = 2570956| doi = 10.1016/S0140-6736(89)90768-X}}
21. ^{{cite journal |vauthors=Chierakul W, Anunnatsiri S, Chaowagul W, et al | title = Addition of trimethoprim-sulfamethoxazole to ceftazidime during parenteral treatment of melioidosis is not associated with a long-term outcome benefit| journal = Clinical Infectious Diseases| volume = 45| issue = 4| pages = 521–523| year = 2007| pmid = 17638209| doi = 10.1086/520010}}
22. ^{{cite journal| title = Outcomes of Patients with Melioidosis Treated with Meropenem |vauthors=Cheng AC, Fisher DA, Anstey NM, et al | journal = Antimicrob Agents Chemother| year = 2004| pages = 1763–65| volume = 48| issue = 5| doi = 10.1128/AAC.48.5.1763-1765.2004| pmid = 15105132| pmc = 400582}}
23. ^{{cite journal|vauthors=Chetchotisakd P, Porramatikul S, Mootsikapun P, Anunnatsiri S, Thinkhamrop B | title = Randomized, double-blind, controlled study of cefoperazone-sulbactam plus cotrimoxazole versus ceftazidime plus cotrimoxazole for the treatment of severe melioidosis| journal = Clinical Infectious Diseases| year = 2001| volume = 33| pages = 29–33| pmid = 11389491|doi=10.1086/320878| issue = 1}}
24. ^{{cite journal|vauthors=Dance DA, Wuthiekanun V, White NJ, Chaowagul W |title=Antibiotic resistance in Pseudomonas pseudomallei|journal=Lancet|year=1988|volume=1|issue=8592|pages=994–995|pmid=2896855|doi=10.1016/S0140-6736(88)91810-7}}
25. ^1 {{cite journal |vauthors=Suputtamongkol Y, Rajchanuwong A, Chaowagul W, et al | title=Ceftazidime vs. amoxicillin/clavulanate in the treatment of severe melioidosis | journal=Clinical Infectious Diseases | year=1994 | volume=19 | pages=846–853 | pmid=7893868 | issue=5 | doi=10.1093/clinids/19.5.846}}
26. ^{{cite journal|title=Differential antibiotic-induced endotoxin release in severe melioidosis|journal=Journal of Infectious Diseases|volume=181|issue=3|pages=1014–1019|doi=10.1086/315306|pmid=10720525|year=2000|last1=Simpson|first1=A. J. H.|last2=Opal|first2=S. M.|last3=Angus|first3=B. J.|last4=Prins|first4=J. M.|last5=Palardy|first5=J. E.|last6=Parejo|first6=N. A.|last7=Chaowagul|first7=W.|last8=White|first8=N. J.}}
27. ^{{Cite journal | doi = 10.1128/AAC.01582-09 | title = Meropenem Dosing in Critically Ill Patients with Sepsis Receiving High-Volume Continuous Venovenous Hemofiltration | year = 2010 | last1 = Bilgrami | first1 = I. | last2 = Roberts | first2 = J. A. | last3 = Wallis | first3 = S. C. | last4 = Thomas | first4 = J. | pmc = 2897321 | last5 = Davis | first5 = J. | last6 = Fowler | first6 = S. | last7 = Goldrick | first7 = P. B. | last8 = Lipman | first8 = J. | journal = Antimicrobial Agents and Chemotherapy | volume = 54 | pages = 2974–2978 | pmid = 20479205 | issue = 7}}
28. ^1 {{cite journal|journal=Infection|date=February 2008|doi=10.1007/s15010-008-7324-8|author1=Shih H-I |author2=Chuang Y-C |author3=Cheung BM-H |title=Sporadic and outbreak cases of melioidosis in southern Taiwan: clinical features and antimicrobial susceptibility|volume=37|issue=1|pages=9–15|pmid=18854938|display-authors=etal}}
29. ^1 {{cite journal|journal=International Journal of Antimicrobia Agents|year=2011|volume=37|issue=6|pages=547–549| title = Comparative in vitro susceptibility of Burkholderia pseudomallei to doripenem, ertapenem, tigecycline and moxifloxacin|vauthors=Harris P, Engler C, Norton R |doi=10.1016/j.ijantimicag.2011.02.001|pmid=21481571}}
30. ^{{cite journal|journal=International Journal of Antimicrobia Agents|year=2010|title=In vitro activity of biapenem against Burkholderia pseudomallei|vauthors=Thamlikitkul V, Trakulsomboon S |pmid=20188524|doi=10.1016/j.ijantimicag.2010.01.002|volume=35|issue=5|pages=514}}
31. ^{{cite journal |vauthors=Cheng AC, Limmathurotsakul D, Chierakul W, et al | title = A randomized controlled trial of granulocyte colony-stimulating factor for the treatment of severe sepsis due to melioidosis in Thailand| journal = Clinical Infectious Diseases| year = 2007| volume = 45| issue = 3| pages = 308–314| pmid = 17599307 |doi=10.1086/519261}}
32. ^{{cite journal |vauthors=Chierakul W, Anunnatsiri S, Short JM, et al | title = Two randomized controlled trials of ceftazidime alone versus ceftazidime in combination with trimethoprim-sulfamethoxazole for the treatment of severe melioidosis| journal = Clinical Infectious Diseases| year = 2005| volume = 41| issue = 8| pages = 1105–1113| pmid = 16163628 |doi=10.1086/444456}}
33. ^{{cite journal|vauthors=Chierakul W, Anunnatsiri S, Chaowagul W, Peacock SJ, Chetchotisakd P, Day NP | title = Addition of trimethoprim-sulfamethoxazole to ceftazidime during parenteral treatment of melioidosis is not associated with a tong-term outcome benefit| journal = Clinical Infectious Diseases| year = 2007 |volume=45| issue = 4| pages = 521–523| pmid = 17638209| doi = 10.1086/520010}}
34. ^{{cite journal | journal=Transactions of the Royal Society of Tropical Medicine and Hygiene| year=1995 | volume=89 | pages=546–549 | title=A prospective comparison of co-amoxiclav and the combination of chloramphenicol, doxycycline, and co-trimoxazole for the oral maintenance treatment of melioidosis |vauthors=Rajchanuvong A, Chaowagul W, Suputtamongkol Y, Smith MD, Dance DA, White NJ | pmid=8560537 | doi=10.1016/0035-9203(95)90104-3 | issue=5}}
35. ^{{cite journal |vauthors=Cheng AC, Chierakul W, Chaowagul W, et al |title=Short Report: Consensus Guidelines for Dosing of Amoxicillin-Clavulanate in Melioidosis|journal=American Journal of Tropical Medicine and Hygiene|volume=78|issue=2|year=2008|pages=208–209|pmid=18256414|pmc=3034162|doi=10.4269/ajtmh.2008.78.208}}
36. ^{{cite journal |vauthors=Chaowagul W, Supputtamongkul Y, Smith MD, White NJ | title=Oral fluoroquinolones for maintenance treatment of melioidosis | journal=Transactions of the Royal Society of Tropical Medicine and Hygiene | year=1997 | volume=91 | pages=599–601 | doi=10.1016/S0035-9203(97)90044-4 | pmid=9463680 | issue=5}}
37. ^{{cite journal| journal = American Journal of Tropical Medicine and Hygiene| date = Jan–Feb 2001| volume = 64| issue = 1–2| pages = 24–27| title = Maintenance therapy of melioidosis with ciprofloxacin plus azithromycin compared with cotrimoxazole plus doxycycline|vauthors=Chetchotisakd P, Chaowagul W, Mootsikapun P, Budhsarawong D, Thinkamrop B | pmid = 11425157| doi=10.4269/ajtmh.2001.64.24}}
38. ^{{cite journal| author = Chaowagul W| title = Clin Infect Dis| volume = 29| issue = 2| date = August 1999| pages = 375–380| pmid = 10476745| doi = 10.1086/520218| last2 = Simpson| first2 = Andrew J. H.| last3 = Suputtamongkol| first3 = Yupin| last4 = Smith| first4 = Michael D.| last5 = Angus| first5 = Brian J.| last6 = White| first6 = Nicholas J.| journal = Clinical Infectious Diseases}}
39. ^1 {{cite journal|author1=Limmathurotsakul D |author2=Chaowagul W |author3=Chierakul Wirongrong |title=Risk factors for recurrent melioidosis in Northeastern Thailand | journal=Clinical Infectious Diseases|year=2006|volume=43|pages=979–986|pmid=16983608|doi=10.1086/507632|issue=8|display-authors=etal}}
40. ^{{cite journal |vauthors=Sarovich DS, Ward L, Price EP, et al |title=Recurrent melioidosis in the Darwin Prospective Melioidosis Study: improving therapies mean that relapse cases are now rare.|journal=Journal of Clinical Microbiology|year=2014|volume=52|issue=2|pages=650–653|doi= 10.1128/JCM.02239-13|pmid=24478504|pmc=3911345}}
41. ^{{cite journal |vauthors=Maharjan B, Chantratita N, Vesaratchavest M, et al | title=Recurrent Melioidosis in Patients in Northeast Thailand Is Frequently Due to Reinfection Rather than Relapse | journal=Journal of Clinical Microbiology | year=2005 | volume=43 | issue=12 | pages=6032–6034 | pmid=16333094 | doi=10.1128/JCM.43.12.6032-6034.2005 | pmc=1317219}}
42. ^{{cite journal |vauthors=Chaowagul W, Suputtamongkol Y, Dance DA, Rajchanuvong A, Pattara-arechachai J, White NJ | year=1993 | title=Relapse in melioidosis: incidence and risk factors | journal=Journal of Infectious Diseases | volume=168 | pages=1181–1185 | pmid=8228352 | issue=5 | doi=10.1093/infdis/168.5.1181}}
43. ^{{cite web |title=Bioterrorism |url=https://www.cdc.gov/melioidosis/bioterrorism/index.html |publisher=Centers for Disease Control and Prevention |accessdate=15 February 2019 |archiveurl=https://web.archive.org/web/20190113052428/https://www.cdc.gov/melioidosis/bioterrorism/index.html |archivedate=13 January 2019|date=2018-11-23 }}
44. ^{{cite book|author=Withers MR (ed.)|title=USAMRIID's Medical Management of Biological Casualties Handbook|edition=8th|publisher=U.S. Army Medical Institute of Infectious Diseases|location=Fort Detrick, Maryland|year=2014|url=http://www.usamriid.army.mil/education/bluebookpdf/USAMRIID%20BlueBook%208th%20Edition%20-%20Sep%202014.pdf|pages=53}}
45. ^1 {{cite journal |last1=Matthew |first1=E. Smith |last2=William |first2=G. Gossman |title=Glanders and Meliodosis |date=27 October 2018 |pmid=28846298 |url=https://www.ncbi.nlm.nih.gov/books/NBK448110/ |accessdate=15 February 2019 |publisher=StatPearls Publishing |id=NBK448110}}
46. ^{{cite journal |author=V Vuddhakul |title=Epidemiology of Burkholderia pseudomallei in Thailand |journal=American Journal of Tropical Medicine and Hygiene |volume=60 |issue=3 |year=1999 |pages=458–461 |display-authors=etal |doi=10.4269/ajtmh.1999.60.458}}
47. ^{{cite journal |journal=Journal of Clinical Microbiology |year=2005 |volume=43 |issue=2 |pages=923–924 |title=Detection of Burkholderia pseudomallei in soil within the Lao People's Democratic Republic |vauthors=Wuthiekanun V, Mayxay M, Chierakul W, Phetsouvanh R, Cheng AC, White NJ, Day NP, Peacock SJ |pmid=15695707 |doi=10.1128/JCM.43.2.923-924.2005 |pmc=548109}}
48. ^{{cite journal |vauthors=Rattanavong S, Wuthiekanun V, Langla S, Amornchai P, Sirisouk J, Phetsouvanh R, Moore CE, Peacock SJ, Buisson Y, Newton PN |title=Randomized Soil Survey of the Distribution of Burkholderia pseudomallei in Rice Fields in Laos |year=2010 |pmid=21075883 |doi=10.1128/AEM.01822-10 |volume=77 |issue=2 |pmc=3020526 |pages=532–536 |journal=Applied and Environmental Microbiology}}
49. ^{{cite journal |vauthors=Vongphayloth K, Rattanavong S, Moore CE, Phetsouvanh R, Wuthiekanun V, Sengdouangphachanh A, Phouminh P, Newton PN, Buisson Y |title=Burkholderia pseudomallei detection in surface water in southern Laos using Moore's swabs. |journal=American Journal of Tropical Medicine and Hygiene |year=2012 |volume=86 |issue=5 |pages=872–877 |pmid=22556090 |doi=10.4269/ajtmh.2012.11-0739 |pmc=3335696}}
50. ^1 {{cite journal |vauthors=Lo TJ, Ang LW, James L, Goh KT |title=Melioidosis in a Tropical City State, Singapore |year=2009 |journal=Emerging Infectious Diseases |volume=15 |issue=10 |pages=1645–1647 |pmid=19861063 |pmc=2866399 |doi=10.3201/eid1510.090246}}
51. ^{{cite journal |vauthors=Kadir KA, Satyavani M, Pande K |title=Melioidosis: Antibiogram of cases in Brunei Darussalam. |journal=Brunei International Medical Journal |date=2014 |volume=10 |issue=1 |pages=19–24 |url=http://www.bimjonline.com/PDF/Bimj%202014%20Volume%2010,%20Issue%201/BIMJ201410119.pdf}}
52. ^{{cite journal |author=Yang S |year=2000 |title=Melioidosis research in China |journal=Acta Tropica |volume=77 |issue=2 |pages=157–165 |doi=10.1016/S0001-706X(00)00139-X}}
53. ^{{cite journal |journal=Emerging Infectious Diseases|year=2007 |volume=13 |issue=6 |pages=896–898 |title=Melioidosis Outbreak after Typhoon, Southern Taiwan |last1=Ko |first1=WC |last2=Cheung |first2=BM |last3=Tang |first3=HJ |last4=Shih |first4=HI |last5=Lau |first5=YJ |last6=Wang |first6=LR |last7=Chuang |first7=YC |pmid=17553230 |pmc=2792857 |doi=10.3201/eid1306.060646}}
54. ^{{cite journal |vauthors=Chen YS, Lin HH, Mu JJ, Chiang CS, Chen CH, Buu LM, Lin YE, Chen YL |title=Distribution of Melioidosis Cases and Viable Burkholderia pseudomallei in Soil: Evidence for Emerging Melioidosis in Taiwan |journal=Journal of Clinical Microbiology |year=2010 |pmid=20147639 |doi=10.1128/JCM.01720-09 |volume=48 |issue=4 |pages=1432–1434 |pmc=2849618}}
55. ^1 {{cite journal |author=White NJ |title=Melioidosis |journal=Lancet |year=2003 |volume=361 |pages=1715–1722 |doi=10.1016/S0140-6736(03)13374-0 |pmid=12767750 |issue=9370}}
56. ^{{cite journal |vauthors=Cheng AC, Currie BJ |title=Melioidosis: Epidemiology, Pathophysiology, and Management |journal=Clinical Microbiology Reviews |year=2005 |volume=18 |pages=383–416 |doi=10.1128/CMR.18.2.383-416.2005 |pmid=15831829 |issue=2 |pmc=1082802}}
57. ^{{Cite web | url=http://www.abc.net.au/news/2017-01-09/melioidosis-risk-spreads-to-central-australia-heavy-rain/8169824 | title=Risk of deadly mud disease spreads to Central Australia| date=2017-01-09}}
58. ^{{cite journal |author=Chong VH |title=Changing spectrum of microbiology of liver abscess: Now Klebsiella, next Burkholderia pseudomallei |journal=Journal of Emerging Medicine |volume=41 |issue=6 |pages=676–677 |year=2010 |pmid=20079999 |doi=10.1016/j.jemermed.2009.10.027}}
59. ^{{cite journal |author=Chugh TD |title=Emerging and re-emerging bacterial diseases in India |journal=Journal of Biosciences |year=2008 |volume=33 |issue=4 |pages=549–555 |pmid=19208980 |doi=10.1007/s12038-008-0073-0}}
60. ^{{cite journal |vauthors=Antony B, Pinto H, Dias M, Shetty AK, Scaria B, Kuruvilla T, Boloor R |title=Spectrum of melioidosis in the suburbs of Mangalore, S West Coast of India |journal=Southeast Asian J Trop Med Public Health |year=2010 |volume=41 |issue=1 |pages=169–74}}
61. ^{{cite journal |title=Tuberculosis mimicked by melioidosis |vauthors=Vidyalakshmi K, Chakrapani M, Shrikala B, Damodar S, Lipika S, Vishal S |journal=International Journal of Tuberculosis and Lung Disease |year=2008 |volume=12 |issue=10 |pages=1209–1215}}
62. ^{{cite journal|authors=Prakash A, Thavaselvam D, Kumar A |title=Isolation, identification and characterization of Burkholderia pseudomallei from soil of coastal region of India. |journal=SpringerPlus |year=2014 |volume=3 |pages=438 |doi=10.1186/2193-1801-3-438 |pmid=25187882|display-authors=etal |pmc=4152474}}
63. ^{{cite journal |vauthors=Inglis TJ, Rolim DB, De Queroz Sousa A |title=Melioidosis in the Americas |journal=American Journal of Tropical Medicine and Hygiene |year=2006 |volume=75 |issue=5 |pages=947–954 |pmid=17123994|doi=10.4269/ajtmh.2006.75.947 }}
64. ^1 {{cite journal |vauthors=O'Sullivan BP, Torres B, Conidi G, et al |title=Burkholderia pseudomallei infection in a child with cystic fibrosis: acquisition in the western hemisphere |journal=Chest |year=2011 |volume=140 |issue=1 |pages=239–242 |pmid=21729895 |doi=10.1378/chest.10-3336}}
65. ^{{cite journal |vauthors=Brilhante RS, Bandeira TJ, Cordeiro RA, et al |journal=Journal of Clinical Microbiology |year=2012 |pmid=22814457 |doi=10.1128/JCM.01577-12 |volume=50 |issue=10 |title=Clinical-epidemiological features of 13 cases of melioidosis in Brazil |pages=3349–3352|pmc=3457459 }}
66. ^{{cite journal |vauthors=Katangwe T, Purcell J, Bar-Zeev N, Denis B, Montgomery J, Alaerts M, Heyderman RS, Dance DA, Kennedy N, Feasey N, Moxon CA |title=Human melioidosis, Malawi, 2011. |journal=Emerging Infectious Diseases |year=2013 |volume=19 |issue=6 |pages=981–984 |doi=10.3201/eid1906.120717 |pmid=23735189 |pmc=3713813}}
67. ^{{cite journal |vauthors = Morosini MI, Quereda C, Gil H, Anda P, Núñez-Murga M, Cantón R, López-Vélez R |title=Melioidosis in traveler from Africa to Spain |journal=Emerging Infectious Diseases |volume=19 |issue=10 |pages=1656–1659 |year=2013 |pmid=24047798 |pmc=3810733 |doi=10.3201/eid1910.121785}}
68. ^{{cite journal |vauthors=Struelens MJ, Mondol G, Bennish M, Dance DA |title=Melioidosis in Bangladesh: a case report |journal=Transactions of the Royal Society of Tropical Medicine and Hygiene |year=1998 |volume=82 |pages=777–778 |doi=10.1016/0035-9203(88)90234-9 |issue=5}}
69. ^{{cite news|first=Akram |last=Hosen |title=Deadly bacteria in Gozipur soil |newspaper=The Daily Star |date=30 Jul 2013 |url=http://www.thedailystar.net/beta2/news/deadly-bacteria-in-gazipur-soil/ |accessdate=30 Aug 2013 |archivedate=2013-07-21 |archiveurl=https://web.archive.org/web/20130721082533/http://www.thedailystar.net/beta2/news/deadly-bacteria-in-gazipur-soil/ |place=Dhaka, Bangladesh |deadurl=yes |df= }}
70. ^{{cite journal |vauthors=Dance DA, Smith MD, Aucken HM, Pitt TL |title=Imported melioidosis in England and Wales |journal=Lancet |year=1999 |volume=353 |issue=9148 |pages=208 |doi=10.1016/S0140-6736(05)77217-2 |pmid=9923882}}
71. ^{{cite journal|title=Burkholderia pseudomallei|journal=Mahout Microbiology Review|date=2013|volume=7|page=4|url=http://www.tropmedres.ac/_asset/file/mahosot-micro-review-eng-no-7.pdf|accessdate=24 April 2016}}
72. ^{{cite journal |last1=Limmathurotsakul |first1=Direk |last2=Golding |first2=Nick |last3=Dance |first3=David A. B. |last4=Messina |first4=Jane P. |last5=Pigott |first5=David M. |last6=Moyes |first6=Catherine L. |last7=Rolim |first7=Dionne B. |last8=Bertherat |first8=Eric |last9=Day |first9=Nicholas P. J. |last10=Peacock |first10=Sharon J. |last11=Hay |first11=Simon I. |title=Predicted global distribution of Burkholderia pseudomallei and burden of melioidosis |journal=Nature Microbiology |date=11 January 2016 |volume=1 |issue=1 |pages=15008 |doi=10.1038/nmicrobiol.2015.8 |pmid=26877885 |pmc=4746747}}
73. ^{{cite journal |vauthors=Limmathurotsakul D, Wongratanacheewin S, Teerawattanasook N |title=Increasing Incidence of Human Melioidosis in Northeast Thailand |journal=American Journal of Tropical Medicine and Hygiene|year=2010 |volume=82 |issue=6 |pmid=20519609 |doi=10.4269/ajtmh.2010.10-0038 |pmc=2877420 |pages=1113–1117}}
74. ^{{cite journal |vauthors=Kanaphun P, Thirawattanasuk N, Suputtamongkol Y, et al |title=Serology and carriage of Pseudomonas pseudomallei: a prospective study in 1000 hospitalized children in northeast Thailand |journal=Journal of Infectious Diseases |year=1993 |volume=167 |issue=1 |pages=230–233 |pmid=7678106 |doi=10.1093/infdis/167.1.230}}
75. ^{{cite journal |vauthors=Vuddhakul V, Tharavichitkul P, Na-Ngam N, et al |title=Epidemiology of Burkholderia pseudomallei in Thailand |journal=American Journal of Tropical Medicine and Hygiene |volume=60 |issue=3 |pages=4584–61 |date=March 1999 |pmid=10466977 |doi=|url=http://www.ajtmh.org/cgi/pmidlookup?view=long&pmid=10466977}}
76. ^{{cite journal |vauthors=Kanai K, Dejsirilert S |title=Pseudomonas pseudomallei and melioidosis, with special reference to the status in Thailand |journal=Japanese Journal of Medical Science and Biology |volume=41 |issue=4 |pages=123–157 |date=August 1988 |pmid=3075004 |doi=10.7883/yoken1952.41.123 |url=}}
77. ^{{cite journal |vauthors=Yang S, Tong S, Mo C, et al |title=Prevalence of human melioidosis on Hainan Island in China |journal=Microbiology and Immunology |volume=42 |issue=9 |pages=651–654 |year=1998 |pmid=9802565 |doi=10.1111/j.1348-0421.1998.tb02335.x |url=}}
78. ^{{cite journal |vauthors=Chen YS, Chen SC, Wu TR, Kao CM, Chen YL |title=Seroprevalence of anti-flagellin antibody against Burkholderia pseudomallei in Taiwan |journal=Japanese Journal of Infectious Diseases |volume=57 |issue=5 |pages=224–225 |date=October 2004 |pmid=15507783 |doi= |url=http://www.nih.go.jp/JJID/57/224.html |deadurl=yes |archiveurl=https://web.archive.org/web/20080619054606/http://www.nih.go.jp/JJID/57/224.html |archivedate=2008-06-19 |df= }}
79. ^{{cite journal |title=Primary ocular melioidosis due to a single genotype of Burkholderia pseudomallei in two cats from Arnhem Land in the Northern Territory of Australia |journal=Journal of Feline Medicine and Surgery |year=2009 |doi=10.1016/j.jfms.2009.02.009 |last1=Parkes |first1=Helen M. |last2=Shilton |first2=Catherine M. |last3=Jerrett |first3=Ian V. |last4=Benedict |first4=Suresh |last5=Spratt |first5=Brian G. |last6=Godoy |first6=Daniel |last7=O'Brien |first7=Carolyn R. |last8=Krockenberger |first8=Mark B. |last9=Mayo |first9=Mark. |last10=Currie |first10=Bart J. |last11=Malik |first11=R |volume=11 |pages=856–863 |pmid=19428280 |issue=10 |display-authors=8}}
80. ^{{cite journal |vauthors=Sprague LD, Neubauer H |title=Melioidosis in Animals: A review on epizootiology, diagnosis and clinical presentation |journal=Journal of Veterinary Medicine. B, Infectious Diseases and Veterinary Public Health |year=2004 |volume=51 |issue=7 |pmid=15525357 |pages=305–320 |doi=10.1111/j.1439-0450.2004.00797.x}}
81. ^{{cite journal |author=Mollaret HH |title="L'affaire du Jardin des plantes" ou comment le mélioïdose fit son apparition en France |journal=Médecine et Maladies Infectieuses |year=1988 |volume=18 |issue=Suppl 4 |pages=643–654 |doi=10.1016/S0399-077X(88)80175-6}}
82. ^{{cite journal |vauthors=Corkeron ML, Norton R, Nelson PN |title=Spatial analysis of melioidosis distribution in a suburban area |journal=Epidemiology and Infection |year=2010 |volume=138 |issue=9 |pages=1346–1352 |pmid=20092666 |doi=10.1017/S0950268809991634}}
83. ^{{cite journal |vauthors=Chantratita N, Wuthiekanun V, Limmathurotsakul D, et al |title=Genetic Diversity and Microevolution of Burkholderia pseudomallei in the Environment |journal=PLoS Neglected Tropical Diseases |volume=2 |issue=2 |pages=e182 |pmid=18299706 |year=2008 |doi=10.1371/journal.pntd.0000182 |pmc=2254201 |editor1-last=Currie |editor1-first=Bart}} {{open access}}
84. ^{{cite journal |author1=Lin HH |author2=Chen YS |author3=Li YC |author4=e al. |title=Burkholderia multivorans acts as an antagonist against the growth of Burkholderia pseudomallei in soil |journal=Microbiology and Immunology |year=2011 |doi=10.1111/j.1348-0421.2011.00365.x |pmid=21752084 |volume=55 |issue=9 |pages=616–624}}
85. ^{{cite journal |vauthors=Inglis TJ, Garrow SC, Henderson M, Clair A, Sampson J, O'Reilly L, Cameron B |title=Burkholderia pseudomallei traced to water treatment plant in Australia |journal=Emerging Infectious Diseases |year=2000 |volume=6 |pages=56–559 |pmid=10653571 |issue=1 |pmc=2627980 |doi=10.3201/eid0601.000110|doi-broken-date=2019-02-20 }}
86. ^{{cite journal |vauthors=Apisarnthanarak A, Khawcharoenporn T, Mundy LM |title=Flood-associated melioidosis in a non-endemic region of Thailand |journal=International Journal of Infectious Diseases |year=2012 |pmid=22421023 |doi=10.1016/j.ijid.2012.01.013 |volume=16 |issue=5 |pages=e409–410}}
87. ^{{cite journal |vauthors=Chierakul W, Winothai W, Wattanawaitunechai C, et al |journal=Clinical Infectious Diseases |year=2005 |volume=41 |issue=7 |pages=982–990 |pmid=16142663 |doi=10.1086/432942 |title=Melioidosis in 6 tsunami survivors in southern Thailand}}
88. ^{{cite journal |vauthors=Ko WC, Cheung BM, Tang HJ, Shih HI, Lau YJ, Wang LR, Chuang YC |title=Melioidosis outbreak after typhoon, southern Taiwan |journal=Emerging Infectious Diseases |year=2007 |volume=13 |issue=6 |pages=896–898 |pmid=17553230 |pmc=2792857 |doi=10.3201/eid1306.060646}}
89. ^{{cite journal |vauthors=Inglis TJ, O'Reilly L, Merritt AJ, Levy A, Heath CH |title=The aftermath of the Western Australian melioidosis outbreak. |journal=American Journal of Tropical Medicine and Hygiene |year=2011 |volume=84 |issue=6 |pages=851–857 |pmid=21633018 |doi=10.4269/ajtmh.2011.10-0480|pmc=3110376 }}
90. ^{{cite journal |vauthors=Baker A, Pearson T, Price EP, et al |title=Molecular Phylogeny of Burkholderia pseudomallei from a Remote Region of Papua New Guinea |journal=PLoS ONE |year=2011 |volume=6 |issue=3 |pages=e18343 |pmid=21483841 |pmc=3069084 |doi=10.1371/journal.pone.0018343}} {{open access}}
91. ^1 {{cite journal |vauthors=Suputtamongkol Y, Chaowagul W, Chetchotisakd P, et al |year=1999 |title=Risk factors for melioiosis and bacteremic melioidosis |journal=Clinical Infectious Diseases |pmid=10476750 |volume=29 |issue=2 |pages=408–413 |doi=10.1086/520223}}
92. ^1 2 {{cite journal |journal=Clinical Infectious Diseases |year=2002 |volume=35 |issue=12 |pages=e138–140 |title=Cystic fibrosis and Burkholderia pseudomallei infection: an emerging problem? |vauthors=Holland DJ, Wesley A, Drinkovic D, Currie BJ |pmid=12471591 |doi=10.1086/344447}}
93. ^1 {{cite journal |author=McCormick J B |title=Human-to-human transmission of Pseudomonas pseudomallei |journal=Annals of Internal Medicine |volume=83 |issue=4 |year=1975 |pages=512–513 |doi=10.7326/0003-4819-83-4-512}}
94. ^1 {{cite journal |vauthors=Kunakorn M, Jayanetra P, Tanphaichitra D |title=Man-to-man transmission of melioidosis |journal=Lancet |year=1991 |volume=337 |issue=8752 |pages=1290–1291 |pmid=1674089 |doi=10.1016/0140-6736(91)92962-2}}
95. ^{{cite journal |vauthors=Phe T, Vlieghe E, Reid T, et al |title=Does HIV status affect the aetiology, bacterial resistance patterns and recommended empiric antibiotic treatment in adult patients with bloodstream infection in Cambodia? |journal=Tropical Medicine and International Health |volume=18 |issue=4 |pages=485–494 |year=2013 |doi=10.1111/tmi.12060 |pmid=23294446}}
96. ^{{cite journal |vauthors=Kanai K, Kurata T, Akksilp S, et al |title=A preliminary survey for human immunodeficient virus (HIV) infections in tuberculosis and melioidosis patients in Ubon Ratchathani, Thailand. |journal=Japanese Journal of Medical Science and Biology |year=1992 |volume=45 |issue=5–6 |pages=247–253 |pmid=1306871 |doi=10.7883/yoken1952.45.247}}
97. ^{{cite journal |vauthors=Chierakul W, Wuthiekanun V, Chaowagul W, et al |title=Short report: disease severity and outcome of melioidosis in HIV coinfected individuals. |journal=American Journal of Tropical Medicine and Hygiene |year=2005 |volume=73 |issue=6 |pages=1165–1166 |pmid=16354832|doi=10.4269/ajtmh.2005.73.1165 }}
98. ^{{cite journal |vauthors=Suputtamongkol Y, Hall AJ, Dance DA, et al |title=The epidemiology of melioidosis in Ubon Ratchatani, Northeast Thailand |journal=International Journal of Epidemiology |volume=23 |year=1994 |pages=1082–1089 |doi=10.1093/ije/23.5.1082 |pmid=7860160 |issue=5}}
99. ^{{cite journal |vauthors=Currie BJ, Jacups SP |title=Intensity of Rainfall and Severity of Melioidosis, Australia |journal=Emerging Infectious Diseases |volume=9 |issue=12 |pages=1538–1542 |date=December 2003 |pmid=14720392 |doi=10.3201/eid0912.020750 |pmc=3034332}}
100. ^{{cite journal |vauthors=Liu Y, Loh JP, Aw LT, Yap EP, Lee MA, Ooi EE |title=Rapid molecular typing of Burkholderia pseudomallei, isolated in an outbreak of melioidosis in Singapore in 2004, based on variable-number tandem repeats |journal=Transactions of the Royal Society of Tropical Medicine and Hygiene |volume=100 |issue=7 |year=2006 |pages=687–692 |pmid=16343569 |doi=10.1016/j.trstmh.2005.08.017}}
101. ^{{cite journal |doi=10.1016/j.jinf.2006.07.007 |title=Melioidosis and rainfall in Kuala Lumpur, Malaysia |journal=Journal of Infection |pmid=16965821 |vauthors=Sam IC, Puthucheary SD |volume=54 |issue=5 |year=2007 |pages=519–520}}
102. ^{{cite journal |last1=Baker |first1=Anthony L. |last2=Ezzahir |first2=Jessica |last3=Gardiner |first3=Christopher |last4=Shipton |first4=Warren |last5=Warner |first5=Jeffrey M. |last6=Wooten |first6=R. Mark |title=Environmental Attributes Influencing the Distribution of Burkholderia pseudomallei in Northern Australia |journal=PLOS ONE |date=23 September 2015 |volume=10 |issue=9 |pages=e0138953 |doi=10.1371/journal.pone.0138953 |pmid=26398904 |pmc=4580599}}
103. ^{{cite journal|last1=Whitmore|first1=A|last2=Krishnaswami|first2=CS|title=An account of the discovery of a hitherto undescribed infectious disease among the population of Rangoon|journal=Indian Medical Gazette|date=1912|volume=47|pages=262–267}}
104. ^{{cite journal|author=Vora SK|title=Sherlock Holmes and a biological weapon|journal=Journal of the Royal Society of Medicine|volume=95|issue=2|pages=101–103|date=February 2002|pmid=11823558|pmc=1279324|doi=10.1258/jrsm.95.2.101|url=http://www.jrsm.org/cgi/pmidlookup?view=long&pmid=11823558}}
105. ^{{cite book|last1=Strong|first1=Richard P|title=Stitt's Diagnosis, Prevention and Treatment of Tropical Diseases|date=1944|publisher=The Blakiston Company|location=Philadelphia|page=732|edition=7th}}
106. ^{{cite journal|vauthors=Dance DA, Wuthiekanun V, Chaowagul W, White NJ |title=Interactions in vitro between agents used to treat melioidosis|journal=Journal of Antimicrobial Chemotherapy|year=1989|volume=24|pages=311–316|pmid=2681117|doi=10.1093/jac/24.3.311|issue=3}}
107. ^{{cite journal|vauthors=Whitmore A, Krishnaswami CS |title=An account of the discovery of a hitherto undescribed infective disease occurring among the population of Rangoon|journal=Indian Medical Gazette|year=1912|volume=92|pages=262–267}}
108. ^{{cite web|url=http://www.abc.net.au/pm/content/2005/s1285014.htm|title=Rise in melioidosis rates in NT|author=Barker A|date=19 June 2005|accessdate=2007-06-24|publisher=Australian Broadcasting Corporation}}
109. ^{{cite journal|author=Orellana C|title=Melioidosis strikes Singapore|journal=Lancet Infect Dis|date=November 2004|volume=4|issue=11|pages=655 |pmid=15534940 |doi=10.1016/S1473-3099(04)01190-9}}
110. ^{{cite journal|author=C S Krishnaswami|title=Morphia injectors' septicaemia|journal=Indian Medical Gazette|volume=52|issue=1917|pages=296–299}}

External links

{{Medical resources
| DiseasesDB = 30833
| ICD10 = {{ICD10|A|24|1|a|20}}-{{ICD10|A|24|4|a|20}}
| ICD9 = {{ICD9|025}}
| ICDO =
| OMIM =
| MedlinePlus =
| eMedicineSubj = emerg
| eMedicineTopic = 884
| MeshID = D008554
}}{{Commons category|Burkholderia pseudomallei}}
  • Resource Center for melioidosis
  • {{CDCDiseaseInfo|melioidosis}}
  • [https://web.archive.org/web/20110824032305/http://patricbrc.org/portal/portal/patric/Taxon?cType=taxon&cId=28450 Burkholderia pseudomallei] genomes and related information at PATRIC, a Bioinformatics Resource Center funded by [https://www.niaid.nih.gov/ NIAID]
  • Monograph on Melioidosis ({{ISBN|978 0 444 53479-8}}); Elsevier Press, 2012, https://espaces.edu.au/melioidosis/melioidosis-a-century-of-observation-and-research
{{Bacterial diseases}}

3 : Bacterium-related cutaneous conditions|Zoonotic bacterial diseases|Biological weapons
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