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Burkholderia pseudomallei infections

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Datasheet

Burkholderia pseudomallei infections

Summary

  • Last modified
  • 09 November 2017
  • 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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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.

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).

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.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AzerbaijanNo information availableOIE Handistatus, 2005
BahrainDisease never reportedOIE Handistatus, 2005
BangladeshDisease never reportedDance, 1991
BhutanDisease never reportedOIE Handistatus, 2005
Brunei DarussalamNo information availableDance, 1991; OIE Handistatus, 2005
CambodiaDisease not reportedDance, 1991
ChinaPresentDance, 1991
-FujianPresentDance, 1991
-GuangdongPresentDance, 1991
-GuangxiPresentDance, 1991
-HainanPresentDance, 1991
-Hong KongDisease not reportedDance, 1991; Ellis and Titball, 1999; OIE Handistatus, 2005
Georgia (Republic of)Disease never reportedOIE Handistatus, 2005
IndiaDas and Paranjape, 1986; Dance, 1991
IndonesiaDisease not reportedDance, 1991; Indriana and Hirst, 1992; Ellis and Titball, 1999; OIE Handistatus, 2005
IranNo information availableDance, 1991; Ellis and Titball, 1999; OIE Handistatus, 2005
IraqNo information availableOIE Handistatus, 2005
IsraelNo information availableOIE Handistatus, 2005
JapanNo information availableOIE Handistatus, 2005
JordanDisease not reportedOIE Handistatus, 2005
KazakhstanDisease not reportedOIE Handistatus, 2005
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofDisease not reportedOIE Handistatus, 2005
KuwaitDisease not reportedOIE Handistatus, 2005
LaosPresentDance, 1991
LebanonNo information availableOIE Handistatus, 2005
MalaysiaPresentDance, 1991
-Peninsular MalaysiaSerological evidence and/or isolation of the agentOIE Handistatus, 2005
-SabahReported present or known to be presentOIE Handistatus, 2005
-SarawakSerological evidence and/or isolation of the agentOIE Handistatus, 2005
MongoliaDisease never reportedOIE Handistatus, 2005
MyanmarNo information availableDance, 1991; OIE Handistatus, 2005
NepalNo information availableOIE Handistatus, 2005
OmanDisease not reportedOIE Handistatus, 2005
PakistanDisease not reportedDance, 1991
PhilippinesDisease not reportedDance, 1991; OIE Handistatus, 2005
QatarNo information availableOIE Handistatus, 2005
SingaporeLast reported1994Dance, 1991; King-Tiong et al., 1991; OIE Handistatus, 2005
Sri LankaDisease never reportedDance, 1991; OIE Handistatus, 2005
SyriaDisease not reportedOIE Handistatus, 2005
TaiwanDisease never reportedDance, 1991; OIE Handistatus, 2005
TajikistanNo information availableOIE Handistatus, 2005
ThailandReported present or known to be presentDance, 1991; OIE Handistatus, 2005
TurkeyNo information availableOIE Handistatus, 2005
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesDisease not reportedWernery et al., 1997; OIE Handistatus, 2005
VietnamDisease never reportedOIE Handistatus, 2005
YemenNo information availableOIE Handistatus, 2005

Africa

AlgeriaDisease not reportedOIE Handistatus, 2005
AngolaNo information availableOIE Handistatus, 2005
BeninNo information availableOIE Handistatus, 2005
BotswanaDisease not reportedOIE Handistatus, 2005
Burkina FasoNo information availableOIE Handistatus, 2005
BurundiDisease never reportedOIE Handistatus, 2005
CameroonDisease never reportedOIE Handistatus, 2005
Cape VerdeDisease not reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE Handistatus, 2005
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireDisease not reportedOIE Handistatus, 2005
DjiboutiDisease not reportedOIE Handistatus, 2005
EgyptNo information availableOIE Handistatus, 2005
EritreaDisease not reportedOIE Handistatus, 2005
EthiopiaDisease never reportedOIE Handistatus, 2005
GhanaNo information availableOIE Handistatus, 2005
GuineaDisease never reportedOIE Handistatus, 2005
Guinea-BissauNo information availableOIE Handistatus, 2005
KenyaNo information availableOIE Handistatus, 2005
LibyaNo information availableOIE Handistatus, 2005
MadagascarDisease not reportedOIE Handistatus, 2005
MalawiNo information availableOIE Handistatus, 2005
MaliNo information availableOIE Handistatus, 2005
MauritiusDisease not reportedOIE Handistatus, 2005
MoroccoNo information availableOIE Handistatus, 2005
MozambiqueNo information availableOIE Handistatus, 2005
NamibiaDisease never reportedOIE Handistatus, 2005
NigeriaNo information availableOIE Handistatus, 2005
RéunionNo information availableOIE Handistatus, 2005
RwandaNo information availableOIE Handistatus, 2005
Sao Tome and PrincipeDisease not reportedOIE Handistatus, 2005
SenegalNo information availableOIE Handistatus, 2005
SeychellesNo information availableOIE Handistatus, 2005
SomaliaNo information availableOIE Handistatus, 2005
South AfricaNo information availableOIE Handistatus, 2005
SudanDisease not reportedOIE Handistatus, 2005
SwazilandNo information availableOIE Handistatus, 2005
TanzaniaNo information availableOIE Handistatus, 2005
TogoDisease never reportedOIE Handistatus, 2005
TunisiaDisease not reportedOIE Handistatus, 2005
UgandaDisease not reportedOIE Handistatus, 2005
ZambiaNo information availableOIE Handistatus, 2005
ZimbabweDisease not reportedOIE Handistatus, 2005

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease never reportedOIE Handistatus, 2005
MexicoNo information availableOIE Handistatus, 2005
USANo information availableOIE Handistatus, 2005

Central America and Caribbean

ArubaPresentDance, 1991
BarbadosDisease never reportedOIE Handistatus, 2005
BelizeNo information availableOIE Handistatus, 2005
British Virgin IslandsDisease not reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaNo information availableOIE Handistatus, 2005
CubaDisease not reportedOIE Handistatus, 2005
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicDisease never reportedOIE Handistatus, 2005
El SalvadorDisease never reportedOIE Handistatus, 2005
GuadeloupeDisease never reportedOIE Handistatus, 2005
GuatemalaDisease never reportedOIE Handistatus, 2005
HaitiDisease never reportedOIE Handistatus, 2005
HondurasDisease never reportedOIE Handistatus, 2005
JamaicaDisease never reportedOIE Handistatus, 2005
MartiniqueNo information availableOIE Handistatus, 2005
NicaraguaDisease never reportedOIE Handistatus, 2005
PanamaNo information availableOIE Handistatus, 2005
Saint Kitts and NevisDisease never reportedOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease not reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaDisease never reportedConigliaro et al., 1999; OIE Handistatus, 2005
BoliviaDisease not reportedOIE Handistatus, 2005
BrazilDisease not reportedOIE Handistatus, 2005
ChileDisease never reportedOIE Handistatus, 2005
ColombiaDisease never reportedOIE Handistatus, 2005
EcuadorDisease never reportedOIE Handistatus, 2005
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaNo information availableOIE Handistatus, 2005
GuyanaDisease never reportedOIE Handistatus, 2005
ParaguayNo information availableOIE Handistatus, 2005
PeruDisease never reportedOIE Handistatus, 2005
UruguayDisease never reportedOIE Handistatus, 2005
VenezuelaDisease never reportedOIE Handistatus, 2005

Europe

AndorraNo information availableOIE Handistatus, 2005
AustriaDisease not reportedOIE Handistatus, 2005
BelarusDisease never reportedOIE Handistatus, 2005
BelgiumNo information availableOIE Handistatus, 2005
Bosnia-HercegovinaNo information availableOIE Handistatus, 2005
BulgariaDisease never reportedOIE Handistatus, 2005
CroatiaDisease never reportedOIE Handistatus, 2005
CyprusDisease never reportedOIE Handistatus, 2005
Czech RepublicDisease not reportedOIE Handistatus, 2005
DenmarkNo information availableOIE Handistatus, 2005
EstoniaDisease never reportedOIE Handistatus, 2005
FinlandDisease never reportedOIE Handistatus, 2005
FranceDisease not reportedOIE Handistatus, 2005
GermanyDisease not reportedOIE Handistatus, 2005
GreeceDisease not reportedOIE Handistatus, 2005
HungaryDisease never reportedOIE Handistatus, 2005
IcelandDisease never reportedOIE Handistatus, 2005
IrelandDisease never reportedOIE Handistatus, 2005
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyNo information availableOIE Handistatus, 2005
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease never reportedOIE Handistatus, 2005
LiechtensteinDisease not reportedOIE Handistatus, 2005
LithuaniaDisease not reportedOIE Handistatus, 2005
LuxembourgDisease not reportedOIE Handistatus, 2005
MacedoniaDisease not reportedOIE Handistatus, 2005
MaltaDisease not reportedOIE Handistatus, 2005
MoldovaDisease never reportedOIE Handistatus, 2005
NetherlandsDisease never reportedOIE Handistatus, 2005
NorwayDisease never reportedOIE Handistatus, 2005
PolandNo information availableOIE Handistatus, 2005
PortugalDisease not reportedOIE Handistatus, 2005
RomaniaDisease not reportedOIE Handistatus, 2005
Russian FederationNo information availableOIE Handistatus, 2005
SlovakiaDisease not reportedOIE Handistatus, 2005
SloveniaDisease not reportedOIE Handistatus, 2005
SpainDisease not reportedOIE Handistatus, 2005
SwedenDisease never reportedOIE Handistatus, 2005
SwitzerlandDisease never reportedOIE Handistatus, 2005
UKDisease not reportedOIE Handistatus, 2005
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease never reportedOIE Handistatus, 2005
Yugoslavia (former)No information availableOIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)No information availableOIE Handistatus, 2005

Oceania

AustraliaDance, 1991; OIE Handistatus, 2005
-Australian Northern TerritoryPresentChoy et al., 2000
-QueenslandPresentChoy et al., 2000
-Western AustraliaPresentChoy et al., 2000
French PolynesiaDisease not reportedOIE Handistatus, 2005
New CaledoniaReported present or known to be presentOIE Handistatus, 2005
New ZealandDisease never reportedOIE Handistatus, 2005
SamoaNo information availableOIE Handistatus, 2005
VanuatuDisease never reportedOIE Handistatus, 2005
Wallis and Futuna IslandsNo information availableOIE 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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