Burkholderia pseudomallei and Burkholderia mallei : Melioidosis and Glanders


Revised August 10, 2021

The genus Burkholderia is currently composed of many species, but only three are notable pathogens for humans or animals: the former B. cepacia complex (described in Chapter 220 ), B. pseudomallei (the agent of melioidosis), and B. mallei (the agent of equine glanders). All three are aerobic, nonsporulating, straight or slightly curved gram-negative bacilli that were formerly placed in the genus Pseudomonas.

Melioidosis

Melioidosis is a disease of humans and animals; it has enormous clinical diversity, spanning asymptomatic infection, localized skin ulcers or abscesses, chronic pneumonia mimicking tuberculosis, and fulminant septic shock with abscesses in multiple internal organs. Most disease is from recent infection, but latency with subsequent activation is well recognized and can occur decades after exposure. Most cases are reported from Southeast Asia and northern Australia, but melioidosis is increasingly being recognized in other tropical and subtropical locations and in people infected in an endemic region who return or travel to Europe and the United States ( Fig. 221.1 ). More recent modeling suggested that melioidosis is greatly underdiagnosed in most of the 45 countries in which it is known to be endemic and predicted that it may be present in a further 34 countries where it has not yet been reported. The modeling estimated 165,000 infections and 89,000 deaths worldwide annually. Targeted surveillance and support for improved regional microbiology facilities are needed to determine the accuracy of these predictions. The causative bacterium, B. pseudomallei, is also considered a potential biological warfare agent.

FIG. 221.1, Known global distribution of melioidosis.

History

In 1912 Whitmore and Krishnaswami described cases of a newly recognized septicemic disease in morphine addicts in Rangoon, Burma. Fatal cases were characterized by widespread caseous consolidation of the lung and abscesses in liver, spleen, kidney, and subcutaneous tissues. The bacillus isolated from tissues was similar to that causing glanders (B. mallei) but was motile. Whitmore and Krishnaswami noted the clinical similarity to glanders, and Stanton and Fletcher subsequently proposed the name melioidosis, derived from the Greek melis (distemper of asses). Various names were used for the causative bacterium, including Bacillus whitmori and, for many years, Pseudomonas pseudomallei. In 1992 seven Pseudomonas spp. were moved to a new genus, Burkholderia. B. cepacia is the type species in the genus, which includes the organisms causing melioidosis (B. pseudomallei) and glanders (B. mallei).

Etiology

B. pseudomallei is a small, gram-negative, oxidase-positive, motile, aerobic bacillus with occasional polar flagella. On staining, a bipolar “safety pin” pattern is seen. The organism is easily recovered on standard culture medium and must be distinguished from the closely related soil saprophytes B. thailandensis, B. oklahomensis, and B. humptydooensis, as well as from Pseudomonas stutzeri and other Pseudomonas species.

The organism is present in soil and surface water in endemic regions. Humans and animals are infected by percutaneous inoculation, inhalation, aspiration, or ingestion. Occasional laboratory-acquired infections are described, but person-to-person spread and zoonotic infection are very uncommon.

Epidemiology

After the initial account in Burma, melioidosis was documented in humans and animals in Malaysia and Singapore from 1913, in Vietnam from 1925, and in Indonesia from 1929. Thailand has reported the largest number of cases, with an estimated 2000 to 3000 cases of melioidosis each year. Melioidosis is also common in Malaysia and Singapore. Other countries in the region where melioidosis is recognized in humans and animals include China (especially Hong Kong), Taiwan, Brunei, Vietnam, Cambodia, and Laos. Melioidosis is also likely to occur in the Philippines. Melioidosis has been increasingly recognized in India, although reports that some of the “plague” scares of 1994 may have been cases of melioidosis have been disproved. Cases have been reported from Sri Lanka, Bangladesh, and Pakistan. Despite the early documentation of melioidosis in Burma and Indonesia, more recent cases were not reported from Indonesia until after the 2004 Asian tsunami. Cases of melioidosis have also been documented from Papua New Guinea, Fiji, and New Caledonia, but the extent of endemicity in the Pacific Islands remains to be defined.

Cases of melioidosis are increasingly being documented from outside the classic endemic region of Southeast Asia, Australasia, the Indian subcontinent, and China. These include sporadic human or animal cases or environmental isolates of B. pseudomallei from the Middle East, Africa, the Caribbean, and Central and South America. Regional endemicity of the disease in Puerto Rico has been documented. Although some of these reports are from incorrect species diagnosis, others are confirmed, making the endemic limitations of melioidosis very unclear. Sporadic cases and occasional case clusters have recently occurred in Brazil and elsewhere in the Americas. Despite more recent cases from Madagascar and Malawi, the true extent and magnitude of the presence of B. pseudomallei in Africa remain entirely unknown. Global warming may result in expansion of the endemic boundaries of melioidosis. A global phylogeny study has supported the origin of B. pseudomallei to be Australia, with subsequent spread to Southeast Asia and then to Africa. Spread from Africa to the Americas was calculated to have been much more recent, potentially linked to the times of the slave trade.

The two locations where melioidosis is arguably the most important bacterial pathogen for humans are some northeast provinces in Thailand and the Top End of the Northern Territory of Australia. In northeast Thailand, 20% of community-acquired septicemic cases are caused by melioidosis, which accounts for 39% of fatal septicemias and 36% of fatal community-acquired pneumonias. In the Top End of the Northern Territory, melioidosis has been the most common cause of fatal community-acquired bacteremic pneumonia.

In addition to endemic melioidosis, there are several documented situations where melioidosis became established in nontropical locations. In France in the 1970s cases of melioidosis occurred in animals in a Paris zoo, with spread to other zoos and equestrian clubs. In addition to fatal animal and human cases, there was extensive soil contamination persisting for some years. B. pseudomallei is considered likely to have been introduced by importation of infected animals. A cluster of cases occurred over a 25-year period in southwestern Western Australia (31° S) involving animal cases and one human infection in a farmer. Ribotyping of the farm animal and human isolates and one isolate from the soil showed identical patterns. This supported the suggestion of clonal introduction of B. pseudomallei, probably via an infected animal, with environmental contamination, local dissemination, and persistence. In 2017, further cases in animals with the same B. pseudomallei genotype were again documented in that location following a storm with near record rainfall. This was 26 years after the previous case and demonstrates more than 50 years of persistence of B. pseudomallei in this temperate region.

Melioidosis was an important cause of morbidity and mortality in foreign troops fighting in Southeast Asia. Dance noted that at least 100 cases occurred among French forces in Indochina between 1948 and 1954. By 1973, 343 cases had been reported in American troops fighting in Vietnam. Concerns of reactivation of latent infection in soldiers returning from Vietnam, with estimates from serology studies of approximately 225,000 potential cases, resulted in melioidosis being called the “Vietnamese time bomb.” However, although occasional cases of reactivation of B. pseudomallei still occur in Vietnam veterans, it is rare compared with the numbers of troops exposed.

Update: Melioidosis Acquired in the USA

Transmission

Fig. 221.2 summarizes the natural history of infection with B. pseudomallei. Studies from Malaysia, Thailand, and Australia have found that the organism is more common in cleared, irrigated sites such as rice paddies and farms. It has been suggested that the increase in melioidosis cases in Thailand may be partly due to the increased number of bacteria in such environments and partly due to increased exposure to bacteria resulting from changes in behaviors such as farming techniques. In Australia, B. pseudomallei has been found most commonly in clay soils to a depth of 25 to 45 cm, and it has been proposed that the bacteria move to the surface with the rising water table during the wet season. Exposure to mud in an endurance challenge (10-km or 21-km obstacle course including river crossing and mud crawl) has been associated with melioidosis in the Northern Territory of Australia. An alternative explanation for the variable bacterial presence found is that during times of stress such as in prolonged dry seasons, B. pseudomallei may persist in soil in a viable but nonculturable state. Differential gene activation may allow such environmental bacteria to respond and adapt to different environmental conditions. This possibility is also relevant to the pathogenicity, latency, and reactivation of infection with B. pseudomallei in humans. Melioidosis endemic locations may vary in their specific ecologic niches for B. pseudomallei. B. pseudomallei colonizes and thrives in the rhizosphere and aerial parts of native and imported grasses in northern Australia, raising implications for global epidemiology and potential dispersal. The role of biofilms in the persistence of B. pseudomallei in the environment as well as in animal and human hosts requires further study.

FIG. 221.2, Natural history of infection with Burkholderia pseudomallei .

In most endemic regions, there is a close association between melioidosis and rainfall. In northeast Thailand and northern Australia, 75% and 81% of cases, respectively, have occurred in the wet season. In a study of cases in Singapore, increased incidence was associated with humidity and rainfall. Although early animal studies showed infection with B. pseudomallei through oral or nasal exposure and from ingestion, more recent reviews have considered that most human cases are from percutaneous inoculation of B. pseudomallei after exposure to muddy soils or surface water in endemic locations. Ingestion and sexual transmission have been suggested as unusual modes of transmission of B. pseudomallei. Nevertheless, a more recent study from Thailand raised the possibility that ingestion of water contaminated with B. pseudomallei may be a more common infecting event than previously thought, especially in endemic regions with unchlorinated water supplies. Presentations of melioidosis pneumonia after presumptive inoculating skin injuries have been documented in patients with soil-contaminated burns and are common in tropical Australia. This suggests hematogenous spread to the lung rather than inhalation or spread from the upper respiratory tract. However, under certain epidemiologic conditions, the inhalation route may predominate, as suggested for soldiers exposed to dusts raised by helicopter rotor blades in Vietnam. Melioidosis after near drowning is well documented, with the probable infecting event being aspiration. Intensity of rainfall is an independent predictor of melioidosis manifesting as pneumonia and of a fatal outcome, suggesting that heavy monsoonal rainfall and winds may result in a shift toward inhalation as the mode of infection with B. pseudomallei. At the present time the overall proportion of melioidosis cases resulting from inhalation rather than percutaneous inoculation remains uncertain. Several outbreaks of melioidosis in Australia have been linked to contamination of potable water with B. pseudomallei. The water supplies involved were unchlorinated, or the chlorination was below standard. The contamination of the water supply has been attributed to soil disturbance during excavations. Drinking water was also identified as a likely source of infections in the more recent study from Thailand.

The incubation period for melioidosis is influenced by inoculating dose, mode of infection, host risk factors, and probably differential virulence of infecting B. pseudomallei strains. Onset of melioidosis within 24 hours has been seen in presumed aspiration after near drowning and, in some cases, after severe weather events. In 25 cases of acute melioidosis in which a clear incubation period could be determined between the inoculating injury and the onset of symptoms, the incubation period was 1 to 21 days (mean, 9 days), which is consistent with a series of nosocomial cases from Thailand in which the incubation period was 3 to 16 days (mean, 9.5 days).

In a review of 72 published cases in travelers, 73% acquired the infection in Southeast Asia, most commonly Thailand, and 19% were infected in Central America. In this review and a separate review of 82 published cases, traveling during heavy rains or floods and adventure travel were common. Most patients presented with sepsis, pneumonia, or abscesses. Onset of illness was an average of 23 days after return (range, 1–360 days).

Pathogenesis

Serology studies have shown that most infections with B. pseudomallei are asymptomatic. In northeast Thailand, most of the rural population is seropositive by indirect hemagglutination (IHA), with most seroconversion occurring between 6 months and 4 years of age. Although melioidosis occurs in all age groups, severe clinical disease, such as septicemic pneumonia, is seen mostly in patients with risk factors such as diabetes, renal disease, and hazardous alcohol use.

In addition to infection by inhalation, bacterial load on exposure (inoculating dose) and virulence of the infecting strain of B. pseudomallei are likely to influence the severity of disease. However, it has been noted that despite the large bacterial load in severely ill patients with septicemic pulmonary melioidosis, person-to-person transmission is extremely unusual. This, together with the rarity of fulminant melioidosis in healthy people, supports the primary importance of host risk factors for development of melioidosis. Furthermore, although it is clear from laboratory studies of isolates of B. pseudomallei from animals, humans, and the environment that virulence differs among B. pseudomallei isolates, the importance of this variation in virulence in determining clinical aspects of melioidosis remains uncertain. Molecular typing that shows clonality of isolates in animal and human clusters has revealed that the same outbreak strain can cause different clinical presentations, with host factors being most important in determining the severity of disease. Whole-genome sequencing and subsequent molecular studies have shown that B. pseudomallei has two chromosomes, with a complex accessory genome that includes multiple genomic islands that are variably present in different strains and have a great propensity for horizontal gene transfer. Further studies are required to unravel the global phylogeny and evolutionary history of B. pseudomallei and related species and to determine which genes or gene clusters may be critical for pathogenesis and disease presentation and outcome. Bacterial genome-wide association studies have begun to show presence or absence of specific genes linked to neurologic and cutaneous melioidosis.

B. pseudomallei is a facultative intracellular pathogen that can invade and replicate inside various cells including polymorphonuclear leukocytes and macrophages and some epithelial cell lines. Resistance to human serum (conferred by lipopolysaccharide [LPS]) and the ability of B. pseudomallei to survive intracellularly (conferred in part by capsular polysaccharide) appear to be critical in the pathogenesis of melioidosis. Type III and type VI secretion systems in B. pseudomallei have also been found to be important in cell invasion and intracellular survival. Quorum sensing may play an important role in many aspects of virulence of B. pseudomallei including cell invasion, cytotoxicity, and antimicrobial resistance. Other putative virulence factor candidates include flagella; type IV pili and other adhesins; a siderophore; and secreted proteins such as hemolysin, lipases, and proteases. Burkholderia lethal factor 1 is similar to Escherichia coli cytotoxic necrotizing factor 1 and interferes with initiation of translation, leading to alteration of the actin cytoskeleton and ultimately cell death.

Intracellular survival of B. pseudomallei in human and animal hosts is likely to explain the ability for latency. After internalization, B. pseudomallei escapes from endocytic vacuoles into the cell cytoplasm, and induction of actin polymerization at one bacterial pole leads to membrane protrusions, with cell-to-cell spread involving these actin tails. An additional survival factor for B. pseudomallei is the ability for phenotypic switching with a change in colony morphology resulting in changes in the expression of putative virulence factors such as biofilm and flagella.

A number of studies have shown elevated levels of various endogenous inflammatory mediators and cytokines to be associated with severity and outcomes of melioidosis. Nevertheless, whether these elevated cytokines are a cause or result of severe disease is not established. In Thailand, there was an association of severe melioidosis with tumor necrosis factor-α (TNF-α) gene allele 2, which is linked to higher constitutive and inducible production of TNF-α. However, in a mouse model of melioidosis, neutralization of TNF-α or interleukin-12 increased susceptibility to infection in vivo, and interferon-γ (IFN-γ) was found to be important for survival, with mice treated with monoclonal anti–IFN-γ dying more quickly. A role for Toll-like receptors in the innate immune response in melioidosis has been proposed. Therefore there are important host protective mechanisms against B. pseudomallei in cytokine responses as well as potentially detrimental ones, with the timing of cytokine release and the balance between proinflammatory and antiinflammatory responses likely to determine the severity of disease and outcome of infection. The extent to which host polymorphisms in immune response contribute compared with differences in organism virulence, infecting dose of B. pseudomallei, and defined host risk factors such as diabetes remains to be clarified. Nevertheless, the predominant association with fatal melioidosis is the presence of defined patient risk factors.

Although a vigorous cell-mediated immune response may protect against disease progression, there is no definitive evidence for the development of immunity from melioidosis after natural exposure to B. pseudomallei . Moreover, reinfection can occur with a different strain of B. pseudomallei after successful treatment of melioidosis.

Table 221.1 summarizes the risk factors for melioidosis. The most important risk factors are diabetes, hazardous alcohol use, and renal disease. In Thailand, the adjusted odds ratios for diabetes and renal disease (chronic renal impairment or renal or ureteric calculi) in cases of melioidosis versus control subjects were 12.9 (95% confidence interval [CI], 5.1–37.2) and 2.9 (95% CI, 1.7–5.0), respectively. Other risk factors for melioidosis include chronic lung disease (including cystic fibrosis), thalassemia (odds ratio in Thailand, 10.2; 95% CI, 3.5–30.8), malignancies, steroid therapy, iron overload, and tuberculosis. Severe disease and fatalities are uncommon in patients without risk factors in whom infection is diagnosed early and early treatment is administered, with only two deaths in 106 patients without risk factors in one study. Risk factors are less common in children than in adults. A study from Sabah, Malaysia, demonstrated the importance of iron overload in thalassemia as a risk factor for melioidosis in children, with no cases after introduction of regular iron chelation therapy.

TABLE 221.1
Risk Factors for Melioidosis
RISK FACTOR a THAILAND (% OF CASES) b AUSTRALIA (% OF CASES) c
Diabetes 23–60 37
Alcohol excess 12 39
Renal disease 20–27 10
Chronic lung disease NR 27
Thalassemia 7 0
No risk factors 24–36 20
NR, Not reported.

a Not listed: malignancy, steroid therapy, iron overload, cardiac failure.

b Thailand data from Punyagupta S. Melioidosis: review of 686 cases and presentation of a new clinical classification. In: Punyagupta S, Sirisanthana T, Stapatayavong B, eds. Melioidosis . Bangkok: Bangkok Medical; 1989:217–229; Chaowagul W, White NJ, Dance DA, et al. Melioidosis: a major cause of community-acquired septicemia in northeastern Thailand. J Infect Dis . 1989;159:890–899; Suputtamongkol Y, Chaowagul W, Chetchotisakd P, et al. Risk factors for melioidosis and bacteremic melioidosis. Clin Infect Dis . 1999;29:408–413; and Limmathurotsakul D, Chaowagul W, Chierakul W, et al. Risk factors for recurrent melioidosis in northeast Thailand. Clin Infect Dis . 2006;43:979–986.

c Australia data from Currie BJ, Fisher DA, Howard DM, et al. Endemic melioidosis in tropical northern Australia: a 10-year prospective study and review of the literature. Clin Infect Dis. 2000;31:981–986.

Evidence suggests that the predisposition to melioidosis in patients with diabetes, hazardous alcohol use, or chronic renal disease may reflect impairment of innate immune function, especially neutrophil and other phagocytic cell functions such as mobilization, delivery, adherence, ingestion, and killing. Melioidosis has also been described in chronic granulomatous disease.

Clinical Manifestations

The earliest descriptions of melioidosis documented the fulminant end of the clinical spectrum, with abscesses throughout both lungs and in many organs. At the other end of the spectrum are asymptomatic infections and localized skin ulcers or abscesses without systemic illness. Howe and colleagues classified melioidosis as acute, subacute, and chronic. The Infectious Disease Association of Thailand summarized 345 cases in these categories, as follows :

  • 1

    Multifocal infection with septicemia (45% of cases, 87% mortality)

  • 2

    Localized infection with septicemia (12% of cases, 17% mortality)

  • 3

    Localized infection (42% of cases, 9% mortality)

  • 4

    Transient bacteremia (0.3%)

Bacteremia and overall mortality rates, respectively, have been reported as 60% and 44% in Thailand, 55% and 14% in Australia, and 43% and 39% in Singapore.

Table 221.2 summarizes the clinical manifestations in patients with melioidosis in northern Australia. Pneumonia is the most common clinical manifestation in patients with melioidosis in all studies, accounting for about half of cases. Secondary pneumonia after another primary presentation occurs in about 10% of cases. Acute melioidosis pneumonia has a spectrum from fulminant septic shock (mortality up to 90%) ( Figs. 221.3 to 221.6 ) to mild undifferentiated pneumonia, which can be acute or subacute in nature, with little mortality. Septicemic patients present acutely unwell with high fevers and prostration and often little initial cough or pleuritic pain. On chest radiographs, diffuse nodular infiltrates often develop throughout both lungs, and they coalesce, cavitate, and progress rapidly, consistent with the caseous necrosis and multiple metastatic abscess formation seen at autopsy. Nonsepticemic patients with pneumonia and some patients with septicemic pneumonia have a more predominant cough, with productive sputum and dyspnea, and their chest radiographs show discrete but progressive consolidation in one or more lobes ( Fig. 221.7 ). In endemic regions, acute pneumonia with upper lobe consolidation warrants consideration of melioidosis, although lower lobe infiltrates are also common.

TABLE 221.2
Clinical Presentations and Outcomes of Melioidosis in Northern Australia
From Currie BJ, Ward L, Cheng AC. The epidemiology and clinical spectrum of melioidosis: 540 cases from the 20-year Darwin prospective study. PLoS Negl Trop Dis . 2010;4:e900.
TOTAL BACTEREMIC NONBACTEREMIC
Number Deaths (Mortality) Number Deaths (Mortality) Number Deaths (Mortality)
Septic shock present 116 (21%) 58 (50%) 103 48 (47%) 13 10 (77%)
Pneumonia 88 43 (49%) 78 35 (45%) 10 a 8 (80%)
No evident focus 13 8 (62%) 12 7 (58%) 1 b 1 (100%)
Genitourinary 10 5 (50%) 9 4 (44%) 1 c 1 (100%)
Osteomyelitis/septic arthritis 4 2 (50%) 4 2 (50%) 0 0 (0%)
Soft tissue abscess 1 0 (0%) 0 0 1 0 (0%)
Not septic shock 424 (79%) 19 (4%) 195 13 (7%) 229 6 (3%)
Pneumonia 190 12 (6%) 89 9 (10%) 101 3 (3%)
Skin infection 68 0 (0%) 1 0 (0%) 67 0 (0%)
Genitourinary 66 2 (3%) 41 2 (5%) 25 0 (0%)
No evident focus 52 2 (4%) 47 2 (4%) 5 0 (0%)
Soft tissue abscess 18 0 (0%) 4 0 (0%) 14 0 (0%)
Osteomyelitis/septic arthritis 16 0 (0%) 10 0 (0%) 6 0 (0%)
Neurologic 14 3 (21%) 3 0 (0%) 11 3 (27%)
Total 540 77 (14%) 298 (55%) 61 (20%) 242 (45%) 16 (7%)

a Seven blood cultures not done; three blood cultures negative.

b Culture was positive for Burkholderia pseudomallei only from rectal swab, although fatal septic shock.

c Blood culture not done.

FIG. 221.3, Multiple pustules in a 46-year-old diabetic man with fatal septicemic melioidosis.

FIG. 221.4, Chest radiograph of patient in Fig. 221.3 showing multiple pulmonary abscesses.

FIG. 221.5, Computed tomography scan of the chest of a 26-year-old woman with fatal melioidosis showing large pulmonary abscess.

FIG. 221.6, Multiple lung abscesses seen at autopsy of a patient with acute melioidosis pneumonia.

FIG. 221.7, Extensive left upper lobe consolidation in a 54-year-old man with fatal melioidosis pneumonia.

In 11% of cases in northern Australia, patients present with chronic melioidosis, defined as illness with symptoms for longer than 2 months’ duration on presentation. Many of these patients have features mimicking tuberculosis, with fevers, weight loss, productive cough (sometimes with hemoptysis), and classic upper lobe infiltrates, with or without cavitation on chest radiographs ( Fig. 221.8 ). In these patients, disease can be remitting and relapsing over many years, sometimes with an initial misdiagnosis of tuberculosis. Although acute deterioration with septicemia may occur, mortality in this group is low.

FIG. 221.8, Radiograph of a 62-year-old man with nonfatal chronic melioidosis showing right upper lobe cavitation.

Previously it was thought that a colonization state did not exist for B. pseudomallei, with presence in sputum or the throat always reflecting disease. However, it has more recently become evident that B. pseudomallei can both colonize airways and cause disease in patients with cystic fibrosis (CF) and bronchiectasis. The similarity to infection with B. cepacia complex in CF is concerning, given the association of B. cepacia complex with more rapid deterioration in lung function. Furthermore, likely transmission of B. pseudomallei between two siblings with CF has been reported. Patients with CF traveling to locations where melioidosis is endemic should be warned of the risk of melioidosis, which should be considered if they become sick after returning.

It is common for patients to present with skin ulcers or abscesses ( Figs. 221.9 and 221.10 ). Occasionally a patient presents with septic arthritis or osteomyelitis, or one of these conditions can develop after the patient has presented with another primary diagnosis, usually pneumonia ( Fig. 221.11 ). Also well recognized, regardless of the clinical presentation, are abscesses in internal organs, especially spleen, kidney, prostate, and liver ( Figs. 221.12 to 221.16 ). Where available, abdominopelvic computed tomography (CT) scanning is useful in all patients with melioidosis to detect internal abscesses, with ultrasound an alternative for children and women of childbearing age to avoid radiation.

FIG. 221.9, Cutaneous melioidosis seen on the right forearm of a 50-year-old man.

FIG. 221.10, Cutaneous melioidosis of the right thigh in an 11-year-old boy.

FIG. 221.11, Radiograph of a 43-year-old man showing large lucent areas in proximal tibia.

FIG. 221.12, Right psoas abscess in a 17-year-old girl with melioidosis.

FIG. 221.13, The patient in Fig. 221.12 developed an L3 osteomyelitis 6 weeks later.

FIG. 221.14, Computed tomography scan of a 60-year-old diabetic patient showing splenic abscesses.

FIG. 221.15, Abscesses seen at splenectomy performed on the patient in Fig. 221.14 .

FIG. 221.16, Melioidosis orchitis and scrotal ulcer in a 49-year-old man.

Three differences have been noted between Thailand and tropical Australia. First, suppurative parotitis accounts for 40% of melioidosis in children in Thailand but is very rare in Australia. Second, prostatic melioidosis is well recognized but uncommon except in Australia, where routine abdominopelvic CT scanning of all patients with melioidosis has shown prostatic abscesses to be present in 18% of all male patients with melioidosis ( Fig. 221.17 ). Some prostatic abscesses were incidental in patients presenting with pneumonia or septicemia, but a primary genitourinary presentation was common with fevers, abdominal discomfort, dysuria, and sometimes diarrhea and urinary retention. Third, neurologic melioidosis accounts for about 4% of cases in northern Australia, with the distinctive clinical features being brainstem encephalitis, often with cranial nerve palsies (especially the seventh nerve), together with peripheral motor weakness or occasionally just flaccid paraparesis alone. CT scan is often normal, but dramatic changes are seen on magnetic resonance imaging, most notably a diffusely increased T2-weighted signal in the midbrain, brainstem, and spinal cord ( Fig. 221.18 ). Direct bacterial invasion of the brain and spinal cord occurs melioidosis encephalomyelitis. Neurologic melioidosis is occasionally seen outside Australia, although mostly as macroscopic brain abscesses.

FIG. 221.17, Melioidosis prostatic abscesses in a 31-year-old man who presented with fever and urinary retention.

FIG. 221.18, Melioidosis encephalomyelitis in a 24-year-old man.

Unusual foci of melioidosis infection described in case reports or case series include mycotic aneurysms, lymphadenitis resembling tuberculosis, mediastinal masses, pericardial collections, and adrenal abscesses.

It has long been recognized that B. pseudomallei, similar to tuberculosis, has the potential for reactivation from a latent focus, usually in the lung—hence the concern of the “Vietnamese time bomb” in returned soldiers. The longest latency period from exposure to B. pseudomallei in an endemic region to onset of melioidosis in a nonendemic region was previously documented as being 62 years. Importantly, this case was refuted by recent genotyping, which showed a sequence type not linked to Southeast Asia, the presumptive location of infection in the case report. Cases of reactivated B. pseudomallei appear to be very uncommon, accounting for only 4% of cases in northern Australia. The vast majority of cases of melioidosis occur in the monsoonal wet seasons of the various endemic regions, supporting the concept that in endemic areas most patients with melioidosis have recent infections that appear with acute illness. Reactivation of melioidosis has been associated with influenza, other bacterial infections, and development of known melioidosis risk factors such as diabetes. What proportion of asymptomatic seropositive people actually have latent infection with the potential for reactivation is unknown.

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