Burkholderia pseudomallei infections
Don't need the entire report?
Generate a print friendly version containing only the sections you need.Generate report
IdentityTop of page
Preferred Scientific Name
- Burkholderia pseudomallei infections
International Common Names
- English: melioidosis; melioidosis, burkholderia pseudomallei- exotic; Whitmore's disease
OverviewTop of page
Burkholderia spp. are aerobic, Gram-negative rods, straight or slightly curved, 1-5 by 0.5-1 µm, motile (with the exception of B. mallei) by means of one or more polar flagella. They grow on MacConkey agar and appear as non-fermenters.
Taxonomically they originally comprised Group II of five Pseudomonas rRNA homology groups but the group was re-assigned to new genus in the early 1990s (Yabuuchi et al., 1992). The genus Burkholderia now contains seven species, the best known of which in terms of human or animal disease are: B. cepacia, a nosocomial human pathogen associated with contaminated disinfectants, equipment and medications; B. mallei, the agent of glanders; and B. pseudomallei, the agent of melioidosis. As judged by DNA hybridization studies, high GC content, serological cross-reactivity and phage specificity, B. mallei and B. pseudomallei are closely related. However, there are significant differences in the diseases they cause.
The first description of B. pseudomallei in 1912 followed its isolation from a case in a human in Burma initially thought to be glanders (Whitmore, 1913). The name 'melioidosis', from the Greek and its Latin derivation malleus (severe disease), was applied in 1921 (Stanton and Fletcher, 1921; Howe et al., 1971). It became recognized as a serious disease in domestic animals in endemic areas.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Bos indicus (zebu)|
|Bos taurus (cattle)||Domesticated host||Cattle & Buffaloes: All Stages|
|Camelus dromedarius (dromedary camel)||Domesticated host||Other: All Stages|
|Canis familiaris (dogs)||Domesticated host||Other: All Stages|
|Capra hircus (goats)||Domesticated host, Experimental settings||Sheep & Goats: All Stages|
|Equus caballus (horses)||Domesticated host, Experimental settings||Other: All Stages|
|Felis catus (cat)||Domesticated host||Other: All Stages|
|Gallus gallus domesticus (chickens)||Domesticated host, Experimental settings||Poultry: All Stages|
|Ovis aries (sheep)||Domesticated host, Experimental settings||Sheep & Goats: All Stages|
|Sus scrofa (pigs)||Domesticated host, Experimental settings||Pigs: All Stages|
Hosts/Species AffectedTop of page
In contrast to glanders, the susceptibility of equines to melioidosis is relatively low, whereas a range of other species, including domestic animals (cattle, sheep, goats, pigs, camels, cats and dogs) and other wild or zoo animals and birds (crocodiles, deer, dolphins, kangaroos, koalas, monkeys and rodents) can contract the disease (Groves, 1979; Sanwong et al., 1989; Ladds et al., 1990; Wernery et al., 1997; Blue et al., 1998; Ellis and Titball, 1999; Choy et al., 2000).
Systems AffectedTop of page multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of poultry
multisystemic diseases of small ruminants
DistributionTop of page
Melioidosis is a tropical disease. Most cases occur between latitudes 20°N and 20°S (Blue et al., 1998; Choy et al., 2000). B. pseudomallei occurs as a normal inhabitant of soil and water in South-East Asia, northern Australia, parts of Africa and of south and central America and the Caribbean (Redfearn et al., 1966; Howe et al., 1971; Groves, 1979; Dance, 1991; Dance, 1998). The terrain of flooded, low-lying plains appears to favour the organism. One survey of soil and surface waters in Malaysia found it in 14-33% of samples from rice fields, but in only 1-3% of samples from forests (Strauss et al., 1969). In Thailand, it was found in 68-78% of rice fields (Nachiangmai et al., 1985). Occasional cases or outbreaks have occurred in Europe through importation (Dance, 1991; Dance et al., 1992).
The ecology of B. pseudomallei is poorly understood. It is thought to persist in deeper clay layers during the dry season, rising to the surface soils after the annual rains (Thomas et al., 1979).
In addition to the countries listed in the table, B. pseudomallei has also been found present in the soil in the following countries; however, cases were not actually reported.
Saudi Arabia (Barbour et al., 1997)
Vietnam (Dance, 1991)
Burkina Faso (Dance, 1991)
Chad (Dance, 1991)
Cote d'Ivoire (Dance, 1991)
Madagascar (Dance, 1991; Ellis and Titball, 1999)
Niger (Dance, 1991)
Reunion (Dance, 1991)
South Africa (van der Lugt and Henton, 1995)
El Salvador (Dance, 1991)
Guadeloupe (Dance DAB, Plymouth Public Health Laboratory, personal communication)
Martinique (Dance DAB, Plymouth Public Health Laboratory, personal communication)
Mexico (Dance, 1991)
Panama (Dance, 1991)
Puerto Rico (Dance DAB, Plymouth Public Health Laboratory, personal communication)
Brazil (Dance, 1991)
Ecuador (Dance DAB, Plymouth Public Health Laboratory, personal communication)
Peru (Dance, 1991)
France (Ellis and Titball, 1991)
Fiji (Dance DAB, Plymouth Public Health Laboratory, personal communication)
Guam (Dance DAB, Plymouth Public Health Laboratory, personal communication)
New Caledonia (OIE)
Papua New Guinea (Dance DAB, Plymouth Public Health Laboratory, personal communication)
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
PathologyTop of page
Post-mortem findings in horses are usually confined to the respiratory tract with inflammation of the respiratory mucosa and multiple pulmonary abscesses.
In sheep and goats at post-mortem, lesions include polyarthritis, visceral abscesses, particularly of the lungs and spleen, ulceration of the nasal mucosa and meningoencephalitis.
In experimentally infected goats at necropsy (Thomas et al., 1988), fibrous adhesions were present in the thoracic and abdominal cavities of one-third of the animals and visceral abscesses were found (one to several, with a tendency to coalesce in the lungs).
In experimentally infected pigs (Thomas et al., 1990b), visible nodules at post-mortem were largely confined to the inoculation sites in the trachea, lungs and spleens. In natural infections, abscesses may be found in the bronchial, gastrohepatic and mediastinal lymph nodes and liver as well (King-Tiong et al., 1991; Choy et al., 2000). Lesions (microabscesses or lymphocytic infiltration) are also occasionally found in the central nervous system (Choy et al., 2000).
In military dogs in Vietnam, post-mortem lesions consisted of multiple abscesses mainly of the skin, lungs, liver and epididymis (Groves, 1979). A narrow red halo around each focal lesion is described as characteristic of B. pseudomallei infection in dogs (Benirschke et al., 1978).
Multiple abscesses of the lung and liver, with subcutaneous abscesses at the site of surgical interventions and osteomyelitis were recorded in experimentally infected subhuman primates (Groves, 1979). In a natural outbreak of melioidosis in cynamolgus monkeys imported into Britain from the Philippines, the main organ involved was the spleen with liver, skin and subcutaneous tissues frequently affected (Dance et al., 1992).
Guinea pigs typically have multiple visceral abscesses and bilateral orchitis at death from B. pseudomallei infection. Laboratory mice infected intraperitoneally showed purulent pneumonia, liver abscesses, karrorrhexis of hepatocytes and meningoencephalitis (Veljanov et al., 1996). Different mouse strains produced similar inflammatory responses with predominance of granulocytes at the early stage of infection and subsequent increase of macrophages. The major observable differences between the different mouse strains lay in the degree of macrophage response, which correlated with the rate of clearance of the infecting organisms from the visceral organs (Veljanov et al., 1996) and reflected the relative susceptibilities of the different mouse strains (Leakey et al., 1998).
Histopathological changes in experimentally infected mice consisted of purulent pneumonia, haemhorragic necrotic damage of the liver, meningoencephalitis and lymphomalacia in the spleen. Hyperaemia was observed in intra-alveolar capillaries of the lung on day 1 and the bronchial walls became infiltrated with neutrophils with karryorrhexia by day 3. The alveoli and bronchi were filled with leukocytes and serous exudate. By day 7, small abscess formation with necrotic areas had formed around the bronchi and peribronchial blood vessels. Meningoencephalitis with infiltration of the cerebral membranes was observed (Veljanov et al., 1996).
Histologically, the abscess exudate in pigs was seen as a caseated mass of inflammatory cells with neutrophils discernible only on the periphery. Many of the neutrophils were necrotic. A narrow zone of macrophages surrounded by fibrous tissue comprised the capsule (King-Tiong et al., 1991).
In dogs, histology showed the focal lesions to have a central zone of necrosis with intense neutrophilic infiltration and an outer rim of haemorrhage. Non-specific changes in the lung included alveolar oedema and septal infiltration by a mixed-cell population (Benirschke et al., 1978).
The histopathological picture in human melioidosis has been described and reviewed by Wong et al. (1995).
DiagnosisTop of page
The clinical symptoms of melioidosis are vague, rendering definitive diagnosis dependent on isolation and identification of B. pseudomallei from blood culture, nasal or oral discharges or any site of infection. Although relatively simple and economical to do, it takes 3 to 4 days and requires experienced personnel, particularly in the interpretation of the results (Sirisinha et al., 2000).
Complement fixation, indirect haemagglutination and fluorescent antibody tests based on sterile culture filtrates as antigen are the long-standing immunological diagnostic tools (Thomas et al., 1990b), though cross-reactivity with other Gram-negative organisms was always a problem. Diagnosis using these methods must be based on rising titres to distinguish relevant antibodies from cross-reacting ones or persisting antibodies from earlier or subclinical infections (Groves, 1979). According to Sirisinha et al. (2000), complement fixation is not used much today and various antigens have now been identified (though yet to be fully evaluated) as specific for B. pseudomallei. Diagnostic ELISA and DNA probe and PCR systems designed to detect specific antigens have also been described, with increasing numbers of reports on molecular methods in recent literature, but again none of these have been fully evaluated in the field and culture remains the diagnostic method of choice (Dance, 1991; Ellis and Titball, 1999; Sirisinha et al., 2000).
For differential purposes, caseous lymphadenitis and nasal actinobacillus infections in sheep, and glanders and strangles in horses should be considered. Other causes of abscesses in pyaemic pigs are Actinomyces pyogenes and Streptococci species (King-Tiong et al., 1991).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Sign|
|Cardiovascular Signs / Weak pulse, small pulse||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Other:All Stages||Sign|
|Digestive Signs / Diarrhoea||Other:All Stages||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Dehydration||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Other:All Stages||Sign|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Forelimb weakness, paresis, paralysis front leg||Sign|
|General Signs / Generalized lameness or stiffness, limping||Other:All Stages||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Other:All Stages||Sign|
|General Signs / Head, face, ears, jaw weakness, droop, paresis, paralysis||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Hypothermia, low temperature||Sign|
|General Signs / Icterus, jaundice||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Other:All Stages||Sign|
|General Signs / Mammary gland swelling, mass, hypertrophy udder, gynecomastia||Sign|
|General Signs / Opisthotonus||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Swelling mass penis, prepuce, testes, scrotum||Sign|
|General Signs / Swelling skin or subcutaneous, mass, lump, nodule||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness of one hindlimb, paresis paralysis rear leg||Sign|
|General Signs / Weight loss||Other:All Stages||Sign|
|Nervous Signs / Circling||Other:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Nervous Signs / Excitement, delirium, mania||Sign|
|Nervous Signs / Head tilt||Sign|
|Nervous Signs / Hyperesthesia, irritable, hyperactive||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Nervous Signs / Tremor||Sign|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Nystagmus||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Other:All Stages||Diagnosis|
|Pain / Discomfort Signs / Pain on external abdominal pressure||Sign|
|Pain / Discomfort Signs / Pain, testes||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Reproductive Signs / Mastitis, abnormal milk||Other:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Other:All Stages||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Other:All Stages||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Purulent nasal discharge||Other:All Stages||Diagnosis|
|Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair||Sign|
|Skin / Integumentary Signs / Moist skin, hair or feathers||Sign|
|Skin / Integumentary Signs / Skin fistula, sinus||Sign|
|Skin / Integumentary Signs / Warm skin, hot, heat||Sign|
|Urinary Signs / Enlarged, distended, urinary bladder||Other:All Stages||Sign|
Disease CourseTop of page
The disease manifestations can range from acute to chronic with subclinical infection being common. Infection can be associated with single or multiple abscesses, with lungs, spleen and liver most often affected. Incubation periods for naturally occurring animal melioidosis are unknown. Latent infections may be common (Groves, 1979). Central nervous system (CNS) involvement is often observed (Choy et al., 2000). B. pseudomallei is said to have a predilection for the CNS, possibly gaining access through the cranial nerves (Thomas et al., 1988).
Clinical signs commonly reported in horses include fever, anorexia, dyspnoea, mild cough and occasionally purulent discharge (Groves, 1979). Sometimes intestinal symptoms or lymphangitis are seen and meningoencephalitis has been recorded (Blood et al., 1983). Affected horses may survive several months, becoming debilitated and emaciated (Blood et al., 1983). Signs in sheep and goats consist of weakness and recumbency with death occurring in a few days. In goats a more chronic course with abscessation may occur. Lameness and other neurological signs are sometimes observed. Nasal and ocular discharges and mastitis are typically reported. In goats, fatal disease is more common in the young animal (Groves, 1979). Aortic aneurysm appears to be common in goats and abortion has been reported (Choy et al., 2000). Two forms are recognized in pigs (Thomas et al., 1990b): an epizootic form, mainly acute with fever and anorexia, discharges from nose and mouth, respiratory symptoms and/or posterior paresis, diarrhoea occasionally and deaths occurring in the young animals, and the more common sporadic, mainly chronic form, usually only diagnosed at slaughter and characterized by cervical lymphadenitis (Groves, 1979; Thomas et al., 1990b; Radostits et al., 2000). Bovines appear to be relatively resistant to the disease, although splenic and liver abscesses, joint and CNS infections have been reported. A case of bovine abortion is on record (Das and Paranjape, 1986). Despite their high exposure in rice fields, cases in water buffaloes are not reported (Groves, 1979). Infected military dogs in Vietnam exhibited fever, dermal abscesses, epididymitis and palpable testicular enlargement, lameness and swelling in the legs (Benirschke et al., 1978; Groves, 1979). Guinea pigs and hamsters are highly susceptible to B. pseudomallei infection. Relatively large doses cause death from septicaemia in 24-48 h; there may be milky discharges from the eyes and nose. Small doses result in a local necrotic lesion that becomes ulcerative with enlargement and suppuration of lymph nodes. Death ensues at about 3 weeks with abscesses in the organs. The lungs may be filled with nodules that may have coalesced and the peritoneal surface may show small disseminated nodules. Distension of the bladder is notable in guinea pigs and rabbits (Minett, 1959). Susceptibility of mice varies with strain of animal (Veljanov et al., 1996; Leakey et al., 1998).
In experimentally infected sheep, high fever with anorexia, lameness and a thick yellow exudate from the nose and eyes were observed. Some animals showed signs of CNS involvement. The infection was generally fatal (Radostits et al., 2000). In goats, subcutaneous administration of 500 to 500,000 bacilli showed temperature rises up to 41.5°C in 24-48 h with anorexia, wasting, lameness/paresis and abscessation at the site of injection (Thomas et al., 1988). Undulating fever continued until they were killed at 1 to 5 months. One pregnant animal aborted; another gave birth to twins, one of which was stillborn, whereas the other was normal. Mastitis was apparent in both dams. Seven goats given low doses (90 bacilli) showed no clinical signs. At necropsy, these were culture negative and had no gross lesions. Animals with clinical signs had fibrous lesions in the thoracic and abdominal cavities and abscesses 0.1 to 3 cm in diameter, single to multiple, were present in the organs. B. pseudomallei could normally be isolated from these. The spleen, lungs and prescapular lymph nodes were the major sites of isolation. Faecal and urine samples taken throughout the trial were culture negative.
Early experimental infections in equines were reviewed by Minett (1959) with results ranging from transient and local abscesses which healed, to nasal discharges and enlarged and necrotic, but culture-negative lymph glands at slaughter some months later to death at 8 to 20 days with local suppuration and lesions in the lung, spleen and lymph glands.
Both the acute and chronic forms were demonstrated in pigs infected with 5 x 108 bacilli administered by intratracheal injection (Thomas et al., 1990b). The major clinical signs were initial fever, marked neutrophilia and, in the acute cases, respiratory distress. There were no signs of nasal and ocular discharge, paresis or diarrhoea.
In experimentally infected chickens, the infection took a generalized subacute course. Inflammatory necrotic changes were found in the viscera and brain at 3 and 15 days. The organism was isolated from the yolk sac at 15 and 30 days (Vesselinova et al., 1996).
EpidemiologyTop of page
Most cases of melioidosis occur during the monsoon or wet seasons; this is believed to be associated with increased numbers of B. pseudomallei in the wet soil and water runoffs (Blue et al., 1998). The incidence of the disease does not always correlate with the frequency of occurrence with which the bacterium can be found in the soil. The nature of the environment (soil and water composition and climate), the virulence of the local strains, the contact conditions between animal and bacterium (type of farming), the condition of the animals and the local laboratory capabilities may all influence the real or reported incidence of the disease in any one location (Dance, 1991).
Infection appears to result from contaminated environmental sources, although the actual exposure source is rarely identified. Unlike glanders, an animal reservoir has not been identified (Blue et al., 1998). Wild rodents were once suspected of being part of the infection cycle (Groves, 1979), but this was never substantiated. Environmental contamination of soil by an infected animal can occur in non-endemic regions. One theory is that it was not always endemic in Australia but was introduced there in the 1940s (Groves, 1979). B. pseudomallei is well able to survive in the environment (Minett, 1959). Direct animal-to-animal spread is unusual. Faecal spread in horses was reported on one occasion and intrauterine transmission has been recorded in goats and pigs (Thomas et al., 1988, 1990a).
Modern molecular techniques, such as pulsed-field gel electrophoresis, are beginning to be applied to epidemiological studies of melioidosis (Choy et al., 2000).
Zoonoses and Food SafetyTop of page
As indicated under Epidemiology, melioidosis is usually contracted from the environment by both humans and animals. B. pseudomallei has been isolated from both mastitic and normal goat’s milk (Thomas et al., 1988). Although there have been no reports of human cases of melioidosis from drinking infected milk, this does suggest a public health risk exists (Thomas et al., 1988) and sensible public health measures include pasteurization of commercially sold milk and condemnation of infected carcasses in the slaughterhouse (Choy et al., 2000). Overall, however, transmission from animals to humans is only a minor contribution to the human disease (Blue et al., 1998).
Disease TreatmentTop of page
B. pseudomallei infections can occur in humans, so incidences of melioidosis in animals have public health implications. Formal treatment policies for infection may not exist, even in countries with well-established veterinary and public health services. Nontheless, consultation with medical and veterinary authorities as to the extent of local regulations is advised before embarking on a treatment programme.
B. pseudomallei is intrinsically resistant to many antibiotics, including aminoglycosides, macrolides, early ß-lactams and most cephalosporins (Walsh and Wuthiekanun, 1996). It is susceptible to amoxyclav, ceftazimidine, the carbapenems, chloramphenicol, doxycycline and co-trimoxazole. A number of these are not marketed as veterinary products. Reports of resistance to chloramphenicol and tetracyclines can be found (King-Tiong et al., 1991; van der Lugt and Henton, 1995). Early diagnosis and appropriate chemotherapy are needed for successful management and, because of the tendency to latent infection, treatment may need to be prolonged. Consequently, decisions on treatment for animals, which may become expensive, prolonged and then unsuccessful (Choy et al., 2000), depend on the situation. For pets, it may be appropriate to follow treatment regimes similar to those used for humans, with ceftazimidine and carbapenems the drugs of choice. Alternatively, tetracyclines, possibly in combination with chloramphenicol or sulfadiazine, possibly in combination with trimethoprim (co-trimazine) may be used. Chloromycetin (chloramphenicol) has been used effectively in horses (Radostits et al., 2000), although they rapidly metabolise the drug.
With the potential difficulties of successful treatment and the absence of vaccines, control is best approached by avoiding conditions conducive to infection. Excessive contact with wet soil and surface water in endemic areas during periods of heavy rain should be avoided (Groves, 1979). Use of wooden slats, concrete floors or paved floors, chlorination of water supplies, including water to drinking troughs (Choy et al., 2000) and elimination of infected animals with disinfection of premises (Radostits et al., 2000) have been recommended. Adequate chlorination will eliminate B. pseudomallei (Choy et al., 2000), but in line with pseudomonads in general, it may survive in antiseptics/disinfectants that are common in the household or in veterinary practice (Choy et al., 2000).
ReferencesTop of page
Ashdown LR, 1979. An improved screening technique for isolation of Pseudomonas pseudomallei from clinical specimens. Pathology, 11:293-297.
Ashdown LR, 1992. Melioidosis and safety in the clinical laboratory. Journal of Hospital Infection, 21:301-306.
Ashdown LR, 1992. Rapid differentiation of Pseudomonas pseudomallei from Pseudomonas cepacia. Letters in Applied Microbiology, 14:203-205.
Ashdown LR; Koehler JM, 1990. Production of hemolysin and other extracellualar enzyme by clinical isolates of Pseudomonas pseudomallei. Journal of Clinical Microbiology, 28:2331-2334.
Barbour EK; Nabbut NH; Hamadeh SK; Al-Nakhli HM, 1997. Bacterial identity and characteristics in healthy and unhealthy respiratory tracts of sheep and calves. Veterinary Research Communications, 21(6):421-430; 28 ref.
Benirschke K; GHarner FM; Jones TC, eds. , 1978. Pathology of Laboratory Animals. New York, USA: Springer-Verlag.
Blood DC; Radostits OM; Henderson JA; Arundel JH; Gay CC, 1983. Veterinary medicine. A textbook of the diseases of cattle, sheep, pigs goats and horses. Veterinary medicine. A textbook of the diseases of cattle, sheep, pigs goats and horses., Edition 6:xv + 1310pp.; [210 x 296 x 47 mm].
Blue S; Pombo DJ; Woods ML, 1998. Glanders and melioidosis. In: Palmer SR, Soulsby L, Simpson DIH, eds. Zoonoses. Biology, Clinical Practice, and Public Health Control. Oxford, UK: Oxford University Press, 105-113.
Conigliaro S; Baigún R; Luna F, 1999. First isolation of Pseudomonas pseudomallei from cattle in Argentina (communication). Veterinaria Argentina, 16(154):285-288; 5 ref.
Cowan ST, 1974. Cowan and Steel's Manual for the Identification of Medical Bacteria, edition 2. London, UK: Cambridge University Press.
Dance DAB, 1991. Melioidosis: the tip of the iceberg? Clinical Microbiological Reviews, 4:52-60.
Dance DAB, 1998. Melioidosis and Glanders. In: Collier L, Balows A, Sussman M, eds. Topley and Wilson's Microbiology and Microbial Infections, edition 9, Vol. 3, Bacterial Infections. London, UK: Arnold, 919-929.
Dance DAB; King C; Aucken H; Knott CD; West PG; Pitt TL, 1992. An outbreak of melioidosis in imported monkeys in Britain. Veterinary Record, 130:525-529.
Dance DAB; Wuthiekanun V; Naigowit P; White NJ, 1989. Identification of Pseudomonas pseudomallei in clinical practice: use of simple screening tests and API 20NE. Journal of Clinical Pathology, 42:645-648.
Egan AM; Gordon DL, 1996. Burkholderia pseudomallei activates complementand is ingested but not killed by polymorphonuclear leukocytes. Infection and Immunity, 12:4952-4959.
Ellis JF; Titball RW, 1999. Burkholderia pseudomallei: medical, veterinary and environmental aspects. Infectious Disease Review, 1:174-181.
Garrity GM; Winters M; Searles DB, 2001. Taxonomic outline of the procaryotic genera. Bergey's Manual of Systematic Bacteriology, edition 2, Release 1.0, April 2001. New York, USA: www.cme.msu.edu/bergeys/.
Gilligan PH; Whittier S, 1991. Burkholderia, Stenotrophomonas, Ralstonia, Brevundimonas, Comamonas, and Acidovorax. In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of Clinical Microbiology, edition 7. Washington, DC, USA: ASM Press, 526-538.
Groves MG, 1979. Melioidosis. In: Steele JH, ed. CRC Handbook Series in Zoonoses, Vol. 1. Boca Raton, Florida, USA: CRC Press, 465-472.
Howe C; Sampath A; Spotnitz M, 1971. The pseudomallei group: a review. Journal of Infectious Diseases, 124:598-606.
Indriana J; Hirst RG, 1992. Antigenic differences between strains of Pseudomonas pseudomallei. Penyakit Hewan, 24:93-102.
Kanai K; Kondo E, 1994. Recent advances in biomedical sciences of Burkholderia psudomallei. Japanese Journal of Medical Science and Biology, 47:1-45.
Kenny DJ; Russell P; Rogers D; Eley SM; Titball RW, 1999. In vitro susceptibilities of Burkholderia pseudomallei in comparison to thos of other pathogenic Burkholderia spp. Antimicrobial Agents and Chemotherapy, 43:2773-2775.
King-Tiong C; Sin-Bin C; Singh D, 1991. Pyaemia in pigs. British Veterinary Journal, 147:256-269.
Leakey AK; Ulett GC; Hirst RG, 1998. BALB/c and C57BI/6 mice infected with Burkholderia pseudomallei provide contrasting animal models for the acute and chronic forms of human melioidosis. Microbial Pathogenesis, 24:269-275.
Minett FC, 1959. Glanders (and melioidosis). In: Stableforth AW, Galloway IA, eds. Infectious Diseases of Animals. Diseases due to Bacteria, Vol. 1. London, UK: Butterworths Scientific Publications, 296-318.
Nachiangmai N; Patamasucon P; Tipayamonthein B; Kongpon A; Nakaviroj S, 1985. Pseudomonas pseudomallei in southern Thailand. Southeast Asian Journal of Tropical Medicine and Public Health, 16:83-87.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
Perry MB; MacLean LL; Schollaardt T; Bryan LE; Ho M, 1995. Structural characterization of the lipopolysaccharide O antigens of Burkholderia pseudomallei. Infection and Immunity, 63:3348-3352.
Pitt TL, 1990. Pseudomonas.. Topley & Wilson's Principles of bacteriology, virology and immunity. Volume 2. Systematic bacteriology., 255-273; many ref.
Rapaport FT; Millar JW; Ruch J, 1961. Endotoxic properties of Pseudomonas pseudomallei. Archives of Pathology, 71:429-436.
Reckseidler SL; DeShazer D; Sokol PA; Woods DE, 2001. Detection of bacterial viulence genes by subtractive hybridizaton: identification of capsular polysaccharide of Burkholderia pseudomallei as a major virulence determinant. Infection and Immunity, 69:34-44.
Redfearn MS; Palleroni NJ; Stanier RY, 1966. A comparative study of Pseudomonas pseudomallei and Bacillus mallei. Journal of General Microbiology, 43:293-313.
Sanwong K; Methapivat S; Tharavichitkul P; Khantawa B, 1989. Melioidosis in Fea's barking deer (Muntiacus feae). Thai Journal of Veterinary Medicine, 19:97-102.
Sirisinha S; Anuntagool N; Dharakul T; Ekpo P; Wongratanacheewin S; Naigowit P; Petchclai B; Thamlikitkul V; Suputtamongkol Y, 2000. Recent developments in laboratory diagnosis of meliodosis. Acta Tropica, 74:235-245.
Stanton AT; Fletcher W, 1921. Melioidosis, a new disease of the tropics. Transactions of the 4th Congress of the Far Eastern Association for Tropical Medicine, 2:196-198.
Strauss JM; Groves MG; Mariappan M; Ellison DW, 1969. Melioidosis in Malaysia. II. Distribution of Pseudomonas pseudomallei in soil and surface water. American Journal of Tropical Medicine and Hygiene, 18:698-702.
Thomas AD, 1983. Evaluation of the API 20E and Microbact 24E systems for the identification of Pseudomonas pseudomallei. Veterinary Microbiology, 8:611-615.
Thomas AD; Forbes-Faulkner J; Parker M, 1979. Isolation of Pseudomonas pseudomallei from clay layers at defined depths. American Journal of Epidemiology, 110:515-521.
Thomas AD; Forbes-Faulkner JC; D'Arcy TL; Norton JH; Hoffmann D, 1990. Experimental infection of normal and immunosuppressed pigs with Pseudomonas pseudomallei.. Australian Veterinary Journal, 67(2):43-46; 27 ref.
Thomas AD; Forbes-Faulkner JC; Norton JH; Trueman KF, 1988. Clinical and pathological observations on goats experimentally infected with Pseudomonas pseudomallei.. Australian Veterinary Journal, 65(2):43-46; 22 ref.
Thomas AD; Spinks GA; D'Arcy TL; Hoffmann D, 1990. Evaluation of a modified complement fixation test and an indirect hemagglutination test for the serodiagnosis of melioidosis in pigs. Journal of Clinical Microbiology, 28(8):1874-1875; 19 ref.
Veljanov D; Vesselinova A; Nikolova S; Najdenski H; Kussovski V; Markova N, 1996. Experimental melioidosis in inbred mouse strains. Zentralblatt fur Bacteriol., 283:351-359.
Walsh AL; Wuthiekanun MD; Smith Y; Suputtamongko Y; White NJ, 1995. Selective broth for the isolation of Pseudomonas pseudomallei from clinical samples. Transactions of the Royal Society of Tropical Medicine and Hygiene, 89:124.
Walsh AL; Wuthiekanun V, 1996. The laboratory diagnosis of melioidosis. British Journal of Biomedical Science 53:249-253.
Wernery R; Kinne J; Haydn-Evans J; Ul-Haq A, 1997. Melioidosis in a seven year old camel, a new disease in the United Arab Emirates (UAE). Journal of Camel Practice and Research, 4(2):141-143; 5 ref.
Whitmore A, 1913. An account of glanders-like disease occurring in Rangoon. Journal of Hygiene, 13:1-34.
Wong KT; Puthucheary SDF; Vadivelu J, 1995. The histopathology of human melioidosis. Histopathology, 26:51-55.
Woods DE; DeShazer D; Moore RA; Brett PJ; Burtnick MN; Reckseidler SL; Senkiw MD, 1999. Current studies on the pathogenesis of melioidosis. Microbes and Infection, 2:157-162.
Yabuuchi E; Kosako Y; Oyaizu H; Yano I; Hotta H; Hashimoto Y; Ezaki T; Arakawa M, 1992. Proposal of Burkholderia gen. nov. and transfer of seven species of the genus Pseudomonas homology group II to the new genus, with the type species Burkholderia cepacia (Paleroni and Holmes 1981) comb. nov. Microbiology and Immunology, 36:1251-1275.
Yahya MD; Chui Lik SY, 1995. Suppression of delayed-type hypersensitivity in mice by Burkholderia pseudomallei. Malaysian Applied Biology, 24:105-107.
Yang H; Kooi CD; Sokol PA, 1993. Ability of Pseudomonas pseudomallei malleobactin to acquire transferrin-bound, lactoferrin-bound, and cell-derived iron. Infection and Immunity, 61:656-662.
CABI, Undated. CABI Compendium: Status as determined by CABI editor. Wallingford, UK: CABI
Conigliaro S, Baigún R, Luna F, 1999. First isolation of Pseudomonas pseudomallei from cattle in Argentina (communication). (Primer aislamiento en Argentina de Pseudomonas pseudomallei en bovinos (comunicación).). Veterinaria Argentina. 16 (154), 285-288.
Ellis JF, Titball RW, 1999. Burkholderia pseudomallei: medical, veterinary and environmental aspects. In: Infectious Disease Review, 1 174-181.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
Wernery R, Kinne J, Haydn-Evans J, Ul-Haq A, 1997. Melioidosis in a seven year old camel, a new disease in the United Arab Emirates (UAE). In: Journal of Camel Practice and Research [Proceedings of the International Conference on Camelids: science and productivity, held at Eilat (Israel) December 15-19, 1996.], 4 (2) 141-143.
Distribution MapsTop of page
Unsupported Web Browser:
One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/