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Burkholderia pseudomallei infections

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Datasheet

Burkholderia pseudomallei infections

Summary

  • Last modified
  • 20 November 2019
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Burkholderia pseudomallei infections
  • Overview
  • 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...

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    Compendia
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    OX10 8DE
    UK
    compend@cabi.org
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Identity

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Preferred Scientific Name

  • Burkholderia pseudomallei infections

International Common Names

  • English: melioidosis; melioidosis, burkholderia pseudomallei- exotic; Whitmore's disease

Overview

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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 Animals

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Animal nameContextLife stageSystem
Bos indicus (zebu)
Bos taurus (cattle)Domesticated hostCattle & Buffaloes: All Stages
Camelus dromedarius (dromedary camel)Domesticated hostOther: All Stages
Canis familiaris (dogs)Domesticated hostOther: All Stages
Capra hircus (goats)Domesticated host, Experimental settingsSheep & Goats: All Stages
Equus caballus (horses)Domesticated host, Experimental settingsOther: All Stages
Felis catus (cat)Domesticated hostOther: All Stages
Gallus gallus domesticus (chickens)Domesticated host, Experimental settingsPoultry: All Stages
Ovis aries (sheep)Domesticated host, Experimental settingsSheep & Goats: All Stages
Sus scrofa (pigs)Domesticated host, Experimental settingsPigs: All Stages

Hosts/Species Affected

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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 Affected

Top of page multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of poultry
multisystemic diseases of small ruminants

Distribution

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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 Table

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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
Continent/Country/Region Distribution Last Reported Origin First Reported Invasive Reference Notes

Africa

AlgeriaAbsent, No presence record(s)OIE Handistatus (2005)
BotswanaAbsent, No presence record(s)OIE Handistatus (2005)
BurundiAbsent, No presence record(s)OIE Handistatus (2005)
Cabo VerdeAbsent, No presence record(s)OIE Handistatus (2005)
CameroonAbsent, No presence record(s)OIE Handistatus (2005)
Central African RepublicAbsent, No presence record(s)OIE Handistatus (2005)
Congo, Democratic Republic of theAbsent, No presence record(s)OIE Handistatus (2005)
Côte d'IvoireAbsent, No presence record(s)OIE Handistatus (2005)
DjiboutiAbsent, No presence record(s)OIE Handistatus (2005)
EritreaAbsent, No presence record(s)OIE Handistatus (2005)
EthiopiaAbsent, No presence record(s)OIE Handistatus (2005)
GuineaAbsent, No presence record(s)OIE Handistatus (2005)
MadagascarAbsent, No presence record(s)OIE Handistatus (2005)
MauritiusAbsent, No presence record(s)OIE Handistatus (2005)
NamibiaAbsent, No presence record(s)OIE Handistatus (2005)
São Tomé and PríncipeAbsent, No presence record(s)OIE Handistatus (2005)
SudanAbsent, No presence record(s)OIE Handistatus (2005)
TogoAbsent, No presence record(s)OIE Handistatus (2005)
TunisiaAbsent, No presence record(s)OIE Handistatus (2005)
UgandaAbsent, No presence record(s)OIE Handistatus (2005)
ZimbabweAbsent, No presence record(s)OIE Handistatus (2005)

Asia

BahrainAbsent, No presence record(s)OIE Handistatus (2005)
BangladeshAbsent, No presence record(s)Dance (1991)
BhutanAbsent, No presence record(s)OIE Handistatus (2005)
CambodiaAbsent, No presence record(s)Dance (1991)
ChinaPresentDance (1991)
-FujianPresentDance (1991)
-GuangdongPresentDance (1991)
-GuangxiPresentDance (1991)
-HainanPresentDance (1991)
GeorgiaAbsent, No presence record(s)OIE Handistatus (2005)
Hong KongAbsent, No presence record(s)Dance (1991); Ellis and Titball (1999); OIE Handistatus (2005)
IndiaPresentDas and Paranjape (1986); Dance (1991)
IndonesiaAbsent, No presence record(s)Dance (1991); Indriana and Hirst (1992); Ellis and Titball (1999); OIE Handistatus (2005)
JordanAbsent, No presence record(s)OIE Handistatus (2005)
KazakhstanAbsent, No presence record(s)OIE Handistatus (2005)
KuwaitAbsent, No presence record(s)OIE Handistatus (2005)
LaosPresentDance (1991)
MalaysiaPresentDance (1991)
-Peninsular MalaysiaPresent, Serological evidence and/or isolation of the agentOIE Handistatus (2005)
-SabahPresentOIE Handistatus (2005)
-SarawakPresent, Serological evidence and/or isolation of the agentOIE Handistatus (2005)
MongoliaAbsent, No presence record(s)OIE Handistatus (2005)
North KoreaAbsent, No presence record(s)OIE Handistatus (2005)
OmanAbsent, No presence record(s)OIE Handistatus (2005)
PakistanAbsent, No presence record(s)Dance (1991)
PhilippinesAbsent, No presence record(s)Dance (1991); OIE Handistatus (2005)
SingaporePresent1994Chiew King-Tiong et al. (1991); Dance (1991)
South KoreaAbsent, No presence record(s)OIE Handistatus (2005)
Sri LankaAbsent, No presence record(s)Dance (1991); OIE Handistatus (2005)
SyriaAbsent, No presence record(s)OIE Handistatus (2005)
TaiwanAbsent, No presence record(s)Dance (1991); OIE Handistatus (2005)
ThailandPresentDance (1991); OIE Handistatus (2005)
TurkmenistanAbsent, No presence record(s)OIE Handistatus (2005)
United Arab EmiratesAbsent, No presence record(s)Wernery et al. (1997); OIE Handistatus (2005)
VietnamAbsent, No presence record(s)OIE Handistatus (2005)

Europe

AustriaAbsent, No presence record(s)OIE Handistatus (2005)
BelarusAbsent, No presence record(s)OIE Handistatus (2005)
BulgariaAbsent, No presence record(s)OIE Handistatus (2005)
CroatiaAbsent, No presence record(s)OIE Handistatus (2005)
CyprusAbsent, No presence record(s)OIE Handistatus (2005)
CzechiaAbsent, No presence record(s)OIE Handistatus (2005)
EstoniaAbsent, No presence record(s)OIE Handistatus (2005)
FinlandAbsent, No presence record(s)OIE Handistatus (2005)
FranceAbsent, No presence record(s)OIE Handistatus (2005)
GermanyAbsent, No presence record(s)OIE Handistatus (2005)
GreeceAbsent, No presence record(s)OIE Handistatus (2005)
HungaryAbsent, No presence record(s)OIE Handistatus (2005)
IcelandAbsent, No presence record(s)OIE Handistatus (2005)
IrelandAbsent, No presence record(s)OIE Handistatus (2005)
Isle of ManAbsent, No presence record(s)OIE Handistatus (2005)
JerseyAbsent, No presence record(s)OIE Handistatus (2005)
LatviaAbsent, No presence record(s)OIE Handistatus (2005)
LiechtensteinAbsent, No presence record(s)OIE Handistatus (2005)
LithuaniaAbsent, No presence record(s)OIE Handistatus (2005)
LuxembourgAbsent, No presence record(s)OIE Handistatus (2005)
MaltaAbsent, No presence record(s)OIE Handistatus (2005)
MoldovaAbsent, No presence record(s)OIE Handistatus (2005)
NetherlandsAbsent, No presence record(s)OIE Handistatus (2005)
North MacedoniaAbsent, No presence record(s)OIE Handistatus (2005)
NorwayAbsent, No presence record(s)OIE Handistatus (2005)
PortugalAbsent, No presence record(s)OIE Handistatus (2005)
RomaniaAbsent, No presence record(s)OIE Handistatus (2005)
SlovakiaAbsent, No presence record(s)OIE Handistatus (2005)
SloveniaAbsent, No presence record(s)OIE Handistatus (2005)
SpainAbsent, No presence record(s)OIE Handistatus (2005)
SwedenAbsent, No presence record(s)OIE Handistatus (2005)
SwitzerlandAbsent, No presence record(s)OIE Handistatus (2005)
UkraineAbsent, No presence record(s)OIE Handistatus (2005)
United KingdomAbsent, No presence record(s)OIE Handistatus (2005)
-Northern IrelandAbsent, No presence record(s)OIE Handistatus (2005)

North America

ArubaPresentDance (1991)
BarbadosAbsent, No presence record(s)OIE Handistatus (2005)
BermudaAbsent, No presence record(s)OIE Handistatus (2005)
British Virgin IslandsAbsent, No presence record(s)OIE Handistatus (2005)
CanadaAbsent, No presence record(s)OIE Handistatus (2005)
Cayman IslandsAbsent, No presence record(s)OIE Handistatus (2005)
CubaAbsent, No presence record(s)OIE Handistatus (2005)
CuraçaoAbsent, No presence record(s)OIE Handistatus (2005)
DominicaAbsent, No presence record(s)OIE Handistatus (2005)
Dominican RepublicAbsent, No presence record(s)OIE Handistatus (2005)
El SalvadorAbsent, No presence record(s)OIE Handistatus (2005)
GuadeloupeAbsent, No presence record(s)OIE Handistatus (2005)
GuatemalaAbsent, No presence record(s)OIE Handistatus (2005)
HaitiAbsent, No presence record(s)OIE Handistatus (2005)
HondurasAbsent, No presence record(s)OIE Handistatus (2005)
JamaicaAbsent, No presence record(s)OIE Handistatus (2005)
NicaraguaAbsent, No presence record(s)OIE Handistatus (2005)
Saint Kitts and NevisAbsent, No presence record(s)OIE Handistatus (2005)
Saint Vincent and the GrenadinesAbsent, No presence record(s)OIE Handistatus (2005)
Trinidad and TobagoAbsent, No presence record(s)OIE Handistatus (2005)

Oceania

AustraliaPresentDance (1991); OIE Handistatus (2005)
-Northern TerritoryPresentChoy et al. (2000)
-QueenslandPresentChoy et al. (2000)
-Western AustraliaPresentChoy et al. (2000)
French PolynesiaAbsent, No presence record(s)OIE Handistatus (2005)
New CaledoniaPresentOIE Handistatus (2005)
New ZealandAbsent, No presence record(s)OIE Handistatus (2005)
VanuatuAbsent, No presence record(s)OIE Handistatus (2005)

South America

ArgentinaAbsent, No presence record(s)Conigliaro et al. (1999); OIE Handistatus (2005)
BoliviaAbsent, No presence record(s)OIE Handistatus (2005)
BrazilAbsent, No presence record(s)OIE Handistatus (2005)
ChileAbsent, No presence record(s)OIE Handistatus (2005)
ColombiaAbsent, No presence record(s)OIE Handistatus (2005)
EcuadorAbsent, No presence record(s)OIE Handistatus (2005)
Falkland IslandsAbsent, No presence record(s)OIE Handistatus (2005)
GuyanaAbsent, No presence record(s)OIE Handistatus (2005)
PeruAbsent, No presence record(s)OIE Handistatus (2005)
UruguayAbsent, No presence record(s)OIE Handistatus (2005)
VenezuelaAbsent, No presence record(s)OIE Handistatus (2005)

Pathology

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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).

Diagnosis

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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/Signs

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SignLife StagesType
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 Course

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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).

Epidemiology

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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 Safety

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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 Treatment

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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).

References

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Distribution References

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Chiew King-Tiong, Chua Sin-Bin, Dalawara Singh, 1991. Pyaemia in pigs. British Veterinary Journal. 147 (3), 256-269. DOI:10.1016/0007-1935(91)90050-W

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Ellis JF, Titball RW, 1999. Burkholderia pseudomallei: medical, veterinary and environmental aspects. In: Infectious Disease Review, 1 174-181.

Indriana J, Hirst R G, 1992. Antigenic differences between strains of Pseudomonas pseudomallei. Penyakit Hewan. 24 (44), 93-102.

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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.

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