Trends in Microbiology | Microbe of the Month

Burkholderia pseudomallei
Erica D. Phillips1 and Erin C. Garcia 1,
*
1
University of Kentucky College of Medicine, Lexington, KY 40536, USA

KEY FACTS:
B. pseudomallei was first reported by
Whitmore in 1911 as the causative agent
of a ‘glanders-like’ disease.

Local regulatory guidelines for

B. pseudomallei vary across the globe.
The US Centers for Disease Control and
Prevention categorizes the organism as
a biosafety level 3 (BSL-3) pathogen and
select agent.

Two chromosomes (~4 Mbp and ~3 Mbp)

make up the large B. pseudomallei
genome, which contains numerous
genomic islands.

Environmental factors, such as soil type,

temperature, moisture, pH, salinity, and
nutrient levels influence B. pseudomallei
prevalence in the soil.

Virulence mechanisms include capsule

production, biofilm formation, adherence
to host cells, resistance to reactive
oxygen species, secondary metabolite
Trends in Microbiology production, quorum sensing, and
intracellular survival mediated by
flagellar- and actin-based motility, type 3
secretion, and type 6 secretion.
Burkholderia pseudomallei is a Gram negative, facultative intracellular bacterium that resides in the rhizosphere
of tropical soils. B. pseudomallei causes melioidosis, which is transmitted by cutaneous entry, ingestion, or Colony morphology variants (including
inhalation of contaminated soil or water. Infection with B. pseudomallei can cause a wide array of clinical symp- small-colony variants) differ in gene
toms such as pneumonia, bone, joint, skin, genitourinary, and central nervous system infections, as well as expression, virulence properties, biofilm
parotid abscesses in children. Mammalian virulence is linked to the B. pseudomallei intracellular life cycle, production, and susceptibility to
which begins with attachment and internalization by host cells. B. pseudomallei can infect a wide range of antibiotics.
eukaryotic cells, including macrophages, monocytes, and neutrophils, as well as nonphagocytic cells. Once
internalized, a type 3 secretion system (T3SSBsa ) facilitates B. pseudomallei escape from the phagosome, B. pseudomallei is intrinsically resistant to
and the bacteria replicate in the cytoplasm. Autotransporter protein BimA mediates actin polymerization, multiple classes of antibiotics, including
enabling B. pseudomallei to spread, cell to cell, using actin-based motility. This process, coupled with aminoglycosides, rifamycins, penicillins,
the activity of a type 6 secretion system (T6SS-5), results in host membrane fusion and the formation of cephalosporins, and cationic peptides.
multinucleated giant cells. Capsule polysaccharides also contribute to virulence and evasion of host innate
immunity. Treatment of B. pseudomallei infections is complicated by the organism’s intrinsic resistance B. pseudomallei is metabolically flexible,
to multiple classes of antimicrobials, largely due to an abundance of efflux pumps and reduced outer mem- utilizing numerous carbon sources and
brane permeability. While B. pseudomallei is commonly associated with endemic ‘hotspots’ in southeast encoding the potential to produce a large
Asia and northern Australia, there is increasing evidence that it is likely endemic in a large range of tropical array of secondary metabolites.
and subtropical areas, including regions in Africa, South America, the Middle East, Central America, and
the Caribbean. Soil and climate conditions favorable for B. pseudomallei survival are also found in addi- DISEASE FACTS:
tional areas worldwide. Consequently, it is important for clinical and public health laboratories located out- Comprehensive global modeling
side of high-endemicity areas to be aware of B. pseudomallei, as well as for improved diagnostic and estimated that there were 165 000
reporting methods. melioidosis cases in 2015, resulting in 89
000 deaths worldwide (estimated 54%
mortality rate).

*Correspondence:
erin.garcia@uky.edu (E.C. Garcia).

Trends in Microbiology, January 2024, Vol. 32, No. 1 © 2023 The Author(s). Published by Elsevier Ltd. https://doi.org/10.1016/j.tim.2023.07.008 105
This is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/).
Trends in Microbiology | Microbe of the Month
Diabetes mellitus is the leading risk factor
for melioidosis. Other risk factors include
chronic kidney or lung disease, liver
disease, and heavy alcohol use, but an
estimated ~20% of adult infections
occur in patients who do not have
defined risk factors.

Human-to-human transmission is rare,

and infections are primarily due to
environmental exposure to contaminated
soil or water.

Melioidosis cases are seasonal and

increase during the rainy season.

Typical incubation periods are 1–21 days,

although decades-long latency periods
following exposure have been reported.

Diagnosis is made through culture of

patient samples (blood, sputum, urine,
pus, cerebrospinal fluid), but
misidentification of the organism may
occur, particularly in non-endemic areas.

The initial phase of disease is treated

Trends in Microbiology intensively using intravenous ceftazidime
or carbapenem over 10–14 days. Oral
trimethoprim–sulfamethoxazole is
administered during the subsequent
Acknowledgments eradication phase for at least 3 months
Work in the Garcia laboratory is supported by a grant from the National Institutes of Health (R01AI150767). Figures were created with and is also used prophylactically.
BioRender.com.
Although vaccine development is an
active area of research, currently no
Declaration of interests vaccines are available to prevent
No interests are declared. B. pseudomallei infection.

Literature TAXONOMY AND CLASSIFICATION:

1. Whitmore, A. (1913) An account of a glanders-like disease occurring in Rangoon. J. Hyg. 13, 1–34 KINGDOM: Bacteria
PHYLUM: Pseudomonadota
2. Tuanyok, A. et al. (2008) Genomic islands from five strains of Burkholderia pseudomallei. BMC Genomics 9, 566
(Proteobacteria)
3. Limmathurotsakul, D. et al. (2016) Predicted global distribution of Burkholderia pseudomallei and burden of melioidosis. CLASS: Betaproteobacteria
Nat. Microbiol. 1, 15008 ORDER: Burkholderiales
FAMILY: Burkholderiaceae
4. Gassiep, I. et al. (2020) Human melioidosis. Clin. Microbiol. Rev. 33, e00006–19
GENUS: Burkholderia
5. Wiersinga, W.J. et al. (2018) Melioidosis. Nat. Rev. Dis. Primers 4, 17107 SPECIES: Burkholderia pseudomallei
6. French, C.T. et al. (2020) Virulence from the rhizosphere: ecology and evolution of Burkholderia pseudomallei-complex
species. Curr. Opin. Microbiol. 54, 18–32
7. Rhodes, K.A. and Schweizer, H.P. (2016) Antibiotic resistance in Burkholderia species. Drug Resist. Updat. 28, 82–90
8. Stone, J.K. et al. (2014) Melioidosis: molecular aspects of pathogenesis. Expert Rev. Anti-Infect. Ther. 12, 1487–1499
9. Peacock, S.J. et al. (2008) Management of accidental laboratory exposure to Burkholderia pseudomallei and B. mallei.
Emerg. Infect. Dis. 14, e2
10. Kaestli, M. et al. (2016) The association of melioidosis with climatic factors in Darwin, Australia: a 23-year time-series analysis.
J. Infect. 72, 687–697

106 Trends in Microbiology, January 2024, Vol. 32, No. 1 © 2023 The Author(s). Published by Elsevier Ltd. https://doi.org/10.1016/j.tim.2023.07.008
This is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/).