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Burkholderia pseudomallei (also known as Pseudomonas pseudomallei) is a Gram-negative,
bipolar, aerobic, motile rod-shaped bacterium.[2] It is a soil-dwelling bacterium endemic in
tropical and subtropical regions worldwide, particularly in Thailand and
northern Australia.[3] It infects humans and animals and causes
the disease melioidosis. It is
also capable of infecting plants.[4]
B. pseudomallei measures 2–5 μm in length and 0.4–0.8 μm in
diameter and is capable of self-propulsion using flagella. The
bacteria can grow in a number of artificial nutrient environments, especially betaine- and arginine-containing
ones.
In
vitro, optimal proliferation temperature is reported around
40 °C in neutral or slightly acidic environments (pH 6.8–7.0). The majority of strains are
capable of fermentation of sugars without gas formation (most importantly, glucose and galactose; older
cultures are reported to also metabolize maltose and starch).
Bacteria produce both exo- and endotoxins. The
role of the toxins identified in the process of melioidosis symptom development
has not been fully elucidated.[5]
B. pseudomallei is susceptible to numerous disinfectants, including benzalkonium
chloride, iodine, mercuric chloride, potassium
permanganate, 1% sodium
hypochlorite, 70% ethanol, 2% glutaraldehyde, and to a lesser extent, phenolic
preparations.[29] B. pseudomallei is effectively killed by the commercial
disinfectants, Perasafe and Virkon.[30] The microorganism can also be destroyed by
heating to above 74 °C for 10 min or by ultraviolet irradiation.[31] B. pseudomallei is not reliably disinfected by chlorine.[32][33]
B. pseudomallei infection in humans is called melioidosis; its mortality is 20 to 50% even with treatment.[22]
The antibiotic of choice is ceftazidime.[22] While various antibiotics are active in vitro (e.g., chloramphenicol, doxycycline, co-trimoxazole), they
have been proven to be inferior in
vivo for the treatment of
acute melioidosis.[34] Disc diffusion tests are unreliable when
looking for co-trimoxazole resistance in B. pseudomallei (they greatly overestimate resistance)
and Etests or agar
dilution tests
should be used in preference.[35][36] The actions of co-trimoxazole and
doxycycline are antagonistic, which suggests these two drugs ought not to be
used together.[37]
The organism is intrinsically
resistant to gentamicin[38] and colistin, and
this fact is helpful in the identification of the organism.[39] Kanamycin is used to kill B. pseudomallei in the laboratory, but the
concentrations used are much higher than those achievable in humans.[40]
B. pseudomallei is an opportunistic pathogen. An
environmental organism, it has no requirement to pass through an animal host to
replicate. From the point of view of the bacterium, human infection is an
developmental "dead end".[41]
Strains which cause disease in
humans differ from those causing disease in other animals, by possessing
certain genomic
islands.[42] It may have the ability to cause disease in
humans because of DNA it has acquired from other microorganisms.[42] Its mutation rate is also high, and the
organism continues to evolve even after infecting a host.[43]
B. pseudomallei is able to invade cells (it is an
intracellular pathogen).[44] It is able to polymerise actin, and
to spread from cell to cell, causing cell fusion and the formation of
multinucleated giant cells.[45] It possesses a uniquely fusogenic type-6
secretion system that is required for cell-cell spread and virulence in mammalian
hosts.[46] The bacterium also expresses a toxin called
lethal factor 1.[47] B. pseudomallei is one of the first Proteobacteria to be
identified as containing an active type-6 secretion system. it is also the only
organism identified that contains up to six different type-6 secretion systems.[48]
B. pseudomallei is intrinsically resistant to a large
number of antimicrobial agents by virtue of its efflux
pump mechanism.
This mediates resistance to aminoglycosides (AmrAB-OprA), tetracyclines, fluoroquinolones, and macrolides (BpeAB-OprB).[49]
