Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


brucellosis (Brucella suis)



brucellosis (Brucella suis)


  • Last modified
  • 27 June 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • brucellosis (Brucella suis)
  • Overview
  • The causative organism of Brucellosis was first described by Bruce, 1887, and was recovered from the spleens of soldiers serving on the Island of Malta, who had died from an undulant fever, known locally as Malta feve...

  • There are no pictures available for this datasheet

    If you can supply pictures for this datasheet please contact:

    CAB International
    OX10 8DE
  • Distribution map More information

Don't need the entire report?

Generate a print friendly version containing only the sections you need.

Generate report


Top of page


Top of page

Preferred Scientific Name

  • brucellosis (Brucella suis)

International Common Names

  • English: Brucella suis infections; brucellosis; brucellosis in pigs, swine brucella infection; brucellosis, porcine; brucellosis, swine; porcine brucellosis; swine brucellosis


Top of page

The causative organism of Brucellosis was first described by Bruce, 1887, and was recovered from the spleens of soldiers serving on the Island of Malta, who had died from an undulant fever, known locally as Malta fever. Bruce published this work in 1893, in which he formally named the organism Micrococcus melitensis. The subsequent link between Micrococcus melitensis and an indistinguishable bacterium recovered from aborting cattle, then referred to as Bacillus abortus (Bang, 1897), saw the formation of the genus Brucella (Evans, 1918; Meyer and Shaw, 1920). Since the formation of the genus, other species have been added and in 1914 an organism resembling Brucella abortus, but which was far more virulent, was recovered from an aborted piglet (Traum, 1914). Similar isolates were subsequently identified and Brucella suis was included in the genus Brucella in 1929 (Huddleson, 1929). Following a survey of wildlife in America, a new Brucella spp. was isolated from the desert wood rat (Neotoma lepida Thomas) (Stoenner and Lackman, 1957). The inclusion of the atypical rough B. ovis and B. canis species in the genus was more controversial. B. ovis was accepted some years after its original isolation (Buddle and Boyes, 1953; Buddle, 1956). B. canis was accepted more readily (Carmichael and Bruner, 1968). In recent years a number of new Brucella species associated with diverse mammalian hosts have been described though none appear to be significant pathogens impacting man when compared with a number of the classically described species (Whatmore 2009; Whatmore et al., 2014).

B. abortus, B. melitensis and B. suis are divided into 8, 3 and 5 biovars, respectively. The principal hosts for B.melitensis are goats and sheep; for B.abortus cattle; for B.neotomae desert wood rats; for B. ovis sheep; and for B.canis dogs. The most common host for B. suis biovars 1 and 3 are pigs, and these biovars are worldwide in distribution. B. suis biovar 2 occurs in Europe where the hosts are pigs and the European hare (Lepus capinensis) which can form a reservoir for outbreaks in both wild and domestic pigs (Bendtsen et al., 1954). The disease in pigs caused by this biovar differs slightly from that caused by biovars 1 and 3 in that milliary brucellosis of the uterus is a feature and unlike them it does not appear to be pathogenic for man. B. suis biovar 4 is enzootic in reindeer and caribou (Rangifer spp.) in Arctic regions which, although it causes many cases of human brucellosis, is apparently not pathogenic for pigs. B. suis biovar 5 causes murine brucellosis (Alton et al., 1988) but is genetically distinct from other biovars (Whatmore et al., 2007; Wattam et al., 2014) and has rarely been reported since initial description.

Brucella suis is the only recognised Brucella species to cause systemic or generalised infection leading to reproductive failure in pigs. Pigs can be infected with other Brucella species, but a characteristic of the infection is almost invariably a symptomless, self-limiting localised infection of lymph nodes regional to the point of entry.

Infection in animals principally causes reproductive losses due to abortion and post-infection sterility. The evidence suggests that whilst many swine would normally recover naturally from B. suis infection, a core of chronically infected swine serve as a constant reservoir for infection. The condition of the stock may also suffer, although infected animals often appear asymptomatic. Since the only reliable way to contain the disease is slaughter there will inevitably be stock losses. Therefore the necessary control measures introduce an additional expense. In addition, the economic implications of brucellosis in farm staff should not be overlooked. Early reports placed this factor above the consequences of swine infection, with worker efficiency markedly reduced for over 2 years following diagnosis, despite treatment (Hoerlein et al., 1954). Although the situation is less protracted with the judicious combination of antibiotics (rifampicin and doxycycline or streptomycin and doxycycline) the chance of relapse is still present (Montejo et al., 1993). The more general implications of human brucellosis caused by B. suis in consumers increases the overall cost of the disease.

The predominant route of transmission is via oral or ocular contact with discharges from infected animals (Crawford et al., 1990). However, it should be noted that since porcine brucellosis is a disease that principally concerns reproduction, and where the causative agent can be transmitted sexually, the disease has implications for artificial insemination practices where the disease could be transmitted without direct contact with an infected animal. The success of the venereal route of transmission is dependent upon the species and strain involved, although there is known to be a role for embryo transfer in the spread of animal brucellosis (Yantzis and Kastanidou, 1990).

Since infections with B. suis are seen in both domesticated and wild swine, in endemic regions the risk of infection in domestic pigs is greatest when farming practices allow the two populations to mix. In addition, because the symptoms of porcine brucellosis are not always overt there is a risk of introducing the disease into a Brucella-free herd through the importation or introduction of an infected pig. The Brucella-free herd is likely to consist of a naive population that will be highly susceptible to infection with B. suis. This puts great emphasis on diagnostic procedures as part of an ongoing screening program to identify infected animals. In regions where there is neither the infrastructure nor the funds available to support such a scheme, controlling the disease poses a major challenge.

It is important to note that B. suis is a Hazard Group 3 pathogen readily transmissible to humans and requires, for safe culture and identification, containment level III facilities and staff experienced with the organism. There have been many reports of laboratory acquired Brucella infections (Miller et al., 1987; Martin-Mazuelos et al., 1994; Fiori et al., 2000).

This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. For further information on this disease from OIE, see the website:

Host Animals

Top of page
Animal nameContextLife stageSystem
Sus scrofa (pigs)Domesticated host, Wild hostPigs: All Stages

Hosts/Species Affected

Top of page

Hosts other than pigs

The most common host for B. suis biovars 1 and 3 are pigs, and these biovars are worldwide in distribution (Díaz Aparicio, 2013). In some regions, infection is maintained in populations of wild boar and feral pigs that can serve as reservoirs if there is contact with domestic pigs reared outdoors. Infection of cattle can occur, and although the disease is self-limiting, excretion of organisms can occur in the milk leading to human disease (Corbel, 1997). Infection of horses (Cook and Kingston, 1988; Cohen et al., 1992; Cvetnic et al., 2005) and dogs (Neiland, 1975; Barr et al., 1986; Ramamoorthy et al, 2011) has been reported, but again infection appears generally self-limiting.

B. suis biovar 2 occurs widely in Europe where the hosts are pigs and hare (Lepus capensis, L. europaeus) which can form a reservoir for occasional and sporadic outbreaks in pigs (Godfroid & Kasbohrer, 2002). These episodes are of increasing importance with the increase in outdoor pig rearing. In hares, the disease is characterized by chronic granulomata in liver, spleen and genitalia (Sterba, 1982). The disease in pigs caused by this biovar differs slightly from that caused by biovars 1 and 3 in that milliary brucellosis of the uterus is a feature and unlike them it does not appear to be pathogenic for man with the exception of the occasional case in immunocompromised individuals (Garin-Bastuji et al., 2006; Díaz Aparicio, 2013). Cases of infection of cattle with B. suis biovar 2 have been reported with increasing frequency (Fretin et al, 2013; Szulowski et al., 2013).

B. suis biovar 4 is enzootic in reindeer and caribou (Rangifer spp.) in Arctic regions of Europe and North America; although it causes many cases of human brucellosis it is apparently not pathogenic for pigs. B. suis biovar 5 is associated with murine brucellosis but has been rarely reported and little studied since initial description in the former Soviet Union. The placement of this biovar within B. suis has been questioned historically but recent whole genome based studies have confirmed that this biovar represents a very early branching group of the B. suis lineage (Wattam et al., 2014).

Systems Affected

Top of page bone, foot diseases and lameness in pigs
mammary gland diseases of pigs
multisystemic diseases of pigs
nervous system diseases of pigs
reproductive diseases of pigs


Top of page

For current information on disease incidence, see OIE's WAHID Interface.

Although porcine infections due to B. abortus, B. melitensis and B. microti (Ronai et al., 2015) have been reported, the overwhelming majority of porcine brucellosis is caused by B. suis biovars 1, 2 or 3. By far the most widespread of these is biovar 1, which is found particularly in the United States, Latin America, South China, many islands of the Pacific, and in Australia (Alton, 1991; Robson et al., 1993; Díaz Aparicio, 2013; Pederson et al., 2014). There is also a low prevalence reported in many mainland European countries (Alton, 1991).

Biovar 3 has a more restricted distribution than biovar 1, and is found principally in North America and South China (Corbel, 1988; Pederson et al., 2014).

Biovar 2 is not as pathogenic as biovars 1 and 3, but nevertheless causes disease in domestic and wild swine (Vizcaino et al., 1976; Teyssou et al., 1989; Godfroid et al., 1994). Biovar 2 appears to be widely distributed in mainland Europe from Scandinavia to the Balkans (Garin-Bastuji et al., 2000; Godfroid and Kasbohrer, 2002; Al Dahouk et al., 2005; Cvetnic et al., 2009). The maintenance of biovar 2 in the wild swine population may be related to its relatively low pathogenicity, which may enable the organism to persist as a sub-clinical infection. Swine from which B. suis biovar 2 has been isolated rarely seroconvert in the standard serum agglutination test (Godfroid et al., 1994). Consequently, biovar 2 infections are more likely to go undetected by clinical or serological indicators. In addition, infection may be perpetuated through contact with the unusual natural reservoir of this biovar (i.e. European hare).

Distribution Table

Top 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.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes


AfghanistanNo information availableOIE, 2009
ArmeniaPresentOIE, 2009
AzerbaijanDisease not reportedNULLOIE, 2000a; OIE, 2009
BahrainDisease never reportedOIE, 2009
BangladeshDisease not reportedOIE, 2009
BhutanNo information availableOIE, 2009
Brunei DarussalamDisease not reportedOIE Handistatus, 2005
CambodiaNo information availableOIE, 2009
ChinaRestricted distributionOIE, 2009
-Hong KongNo information availableOIE, 2009
Georgia (Republic of)Last reported1995OIE Handistatus, 2005
IndiaNo information availableOIE, 2009
IndonesiaDisease not reportedOIE, 2009
IranDisease never reportedOIE, 2009
IraqNo information availableOIE, 2009
IsraelDisease never reportedOIE, 2009
JapanDisease never reportedNULLOIE, 2000a; OIE, 2009
JordanNo information availableOIE, 2009
KazakhstanDisease not reportedOIE, 2009
Korea, DPRDisease not reportedOIE Handistatus, 2005
Korea, Republic ofPresentNULLOIE, 2000a; OIE, 2009
KuwaitDisease never reportedOIE, 2009
KyrgyzstanRestricted distributionNULLOIE, 2000a; OIE, 2009
LaosDisease not reportedOIE, 2009
LebanonDisease not reportedOIE, 2009
MalaysiaDisease not reportedOIE, 2009
-Peninsular MalaysiaDisease not reportedOIE Handistatus, 2005
-SabahDisease never reportedOIE Handistatus, 2005
-SarawakDisease never reportedOIE Handistatus, 2005
MongoliaNo information availableOIE, 2009
MyanmarDisease never reportedNULLOIE, 2000a; OIE, 2009
NepalNo information availableOIE, 2009
OmanDisease never reportedOIE, 2009
PakistanNo information availableOIE, 2009
PhilippinesNo information availableOIE, 2009
QatarNo information availableOIE, 2009
Saudi ArabiaDisease never reportedOIE, 2009
SingaporeDisease not reported1989OIE, 2000a; OIE, 2009
Sri LankaDisease not reported1998OIE, 2000a; OIE, 2009
SyriaDisease never reportedOIE, 2009
TaiwanDisease never reportedOIE Handistatus, 2005
TajikistanDisease not reportedOIE, 2009
ThailandNo information availableOIE, 2009
TurkeyNo information availableOIE, 2009
TurkmenistanDisease not reportedOIE Handistatus, 2005
United Arab EmiratesNo information availableOIE, 2009
UzbekistanLast reported1995OIE, 2000a; OIE Handistatus, 2005
VietnamNo information availableOIE, 2009
YemenNo information availableOIE, 2009


AlgeriaNo information availableOIE, 2009
AngolaNo information availableOIE, 2009
BeninDisease not reportedOIE, 2009
BotswanaDisease never reportedOIE, 2009
Burkina FasoNo information availableOIE, 2009
BurundiNo information availableOIE Handistatus, 2005
CameroonNo information availableOIE Handistatus, 2005
Cape VerdeDisease never reportedOIE Handistatus, 2005
Central African RepublicDisease not reportedOIE Handistatus, 2005
ChadNo information availableOIE, 2009
CongoNo information availableOIE, 2009
Congo Democratic RepublicDisease not reportedOIE Handistatus, 2005
Côte d'IvoireReported present or known to be presentOIE Handistatus, 2005
DjiboutiDisease never reportedOIE, 2009
EgyptNo information availableOIE, 2009
EritreaNo information availableOIE, 2009
EthiopiaNo information availableOIE, 2009
GabonNo information availableOIE, 2009
GambiaNo information availableOIE, 2009
GhanaDisease not reportedOIE, 2009
GuineaNo information availableOIE, 2009
Guinea-BissauNo information availableOIE, 2009
KenyaDisease not reportedOIE, 2009
LesothoNo information availableOIE, 2009
LibyaDisease never reportedOIE Handistatus, 2005
MadagascarDisease never reportedOIE, 2009
MalawiDisease never reportedOIE, 2009
MaliNo information availableOIE, 2009
MauritiusDisease not reportedOIE, 2009
MoroccoNo information availableOIE, 2009
MozambiqueNo information availableOIE, 2009
NamibiaDisease not reportedOIE, 2009
NigeriaNo information availableOIE, 2009
RéunionDisease never reportedOIE Handistatus, 2005
RwandaRestricted distributionOIE, 2009
Sao Tome and PrincipeNo information availableOIE Handistatus, 2005
SenegalNo information availableOIE, 2009
SeychellesNo information availableOIE Handistatus, 2005
SomaliaDisease not reportedOIE Handistatus, 2005
South AfricaDisease never reportedOIE, 2009
SudanDisease never reportedOIE, 2009
SwazilandDisease never reportedOIE, 2009
TanzaniaDisease not reportedOIE, 2009
TogoNo information availableOIE, 2009
TunisiaDisease not reportedOIE, 2009
UgandaAbsent, reported but not confirmedNULLOIE, 2000a; OIE, 2009
ZambiaNo information availableOIE, 2009
ZimbabweDisease not reportedOIE, 2009

North America

BermudaDisease not reportedOIE Handistatus, 2005
CanadaDisease never reportedOIE, 2009
GreenlandDisease never reportedOIE, 2009
MexicoDisease not reportedNULLOIE, 2000a; OIE, 2009
USARestricted distributionOIE, 2009

Central America and Caribbean

BarbadosDisease never reportedOIE Handistatus, 2005
BelizeDisease never reportedOIE, 2009
British Virgin IslandsDisease never reportedOIE Handistatus, 2005
Cayman IslandsDisease not reportedOIE Handistatus, 2005
Costa RicaNo information availableOIE, 2009
CubaPresentNULLOIE, 2000a; OIE, 2009
CuraçaoDisease not reportedOIE Handistatus, 2005
DominicaDisease not reportedOIE Handistatus, 2005
Dominican RepublicNo information availableNULLOIE, 2000a; OIE, 2009
El SalvadorDisease not reportedOIE, 2009
GuadeloupeNo information availableOIE, 2009
GuatemalaDisease never reportedOIE, 2009
HaitiNo information availableOIE, 2009
HondurasNo information availableOIE, 2009
JamaicaDisease never reportedOIE, 2009
MartiniqueDisease not reportedOIE, 2009
NicaraguaDisease not reportedOIE, 2009
PanamaNo information availableNULLOIE, 2000a; OIE, 2009
Saint Kitts and NevisNo information availableOIE Handistatus, 2005
Saint Vincent and the GrenadinesDisease never reportedOIE Handistatus, 2005
Trinidad and TobagoDisease never reportedOIE Handistatus, 2005

South America

ArgentinaPresentNULLOIE, 2000a; OIE, 2009
BoliviaDisease not reported20080515OIE, 2000a; OIE, 2009
BrazilDisease not reportedOIE, 2009
ChileDisease not reported1987OIE, 2000a; OIE, 2009
ColombiaDisease not reportedOIE, 2009
EcuadorDisease not reportedOIE, 2009
Falkland IslandsDisease never reportedOIE Handistatus, 2005
French GuianaNo information availableOIE, 2009
GuyanaDisease not reportedOIE Handistatus, 2005
ParaguayDisease not reportedOIE Handistatus, 2005
PeruDisease not reportedOIE, 2009
UruguayPresentNULLOIE, 2000a; OIE, 2009
VenezuelaNo information availableNULLOIE, 2000a; OIE, 2009


AlbaniaNo information availableOIE, 2009
AndorraDisease not reportedOIE Handistatus, 2005
AustriaDisease not reported2004OIE, 2000a; OIE, 2009
BelarusDisease never reportedOIE, 2009
BelgiumDisease not reportedNULLOIE, 2000a; OIE, 2009
Bosnia-HercegovinaDisease not reportedOIE Handistatus, 2005
BulgariaDisease not reportedOIE, 2009
CroatiaPresentNULLOIE, 2000a; OIE, 2009
CyprusDisease not reportedOIE, 2009
Czech RepublicPresentNULLOIE, 2000a; OIE, 2009
DenmarkDisease not reported2002OIE, 2000a; OIE, 2009
EstoniaDisease not reported1988OIE, 2000a; OIE, 2009
FinlandDisease never reportedOIE, 2009
FranceRestricted distributionNULLOIE, 2000a; OIE, 2009
GermanyPresentNULLOIE, 2000a; OIE, 2009
GreeceDisease not reported2001OIE, 2000a; OIE, 2009
HungaryDisease not reported2005OIE, 2000a; OIE, 2009
IcelandDisease never reportedOIE, 2009
IrelandDisease never reportedOIE, 2009
Isle of Man (UK)Disease never reportedOIE Handistatus, 2005
ItalyRestricted distributionOIE, 2009
JerseyDisease never reportedOIE Handistatus, 2005
LatviaDisease not reported199402OIE, 2000a; OIE, 2009
LiechtensteinDisease not reportedOIE, 2009
LithuaniaDisease not reported1992OIE, 2000a; OIE, 2009
LuxembourgDisease not reportedOIE, 2009
MacedoniaAbsent, reported but not confirmedOIE, 2009
MaltaDisease never reportedOIE, 2009
MoldovaLast reported2002OIE, 2000a; OIE Handistatus, 2005
MontenegroDisease not reportedOIE, 2009
NetherlandsDisease not reported1973OIE, 2000a; OIE, 2009
NorwayDisease never reportedOIE, 2009
PolandDisease not reportedOIE, 2009
PortugalPresentNULLOIE, 2000a; OIE, 2009
RomaniaPresentNULLOIE, 2000a; OIE, 2009
Russian FederationDisease not reportedOIE, 2009
SerbiaDisease not reportedOIE, 2009
SlovakiaDisease not reported1992OIE, 2000a; OIE, 2009
SloveniaDisease not reportedNULLOIE, 2000a; OIE, 2009
SpainDisease not reportedOIE, 2009
SwedenDisease not reported1957OIE, 2000a; OIE, 2009
SwitzerlandDisease not reportedOIE, 2009
UKDisease never reportedOIE, 2009
-Northern IrelandDisease never reportedOIE Handistatus, 2005
UkraineDisease not reported20080620OIE, 2000a; OIE, 2009
Yugoslavia (former)No information availableOIE, 2000a; OIE Handistatus, 2005
Yugoslavia (Serbia and Montenegro)Last reported2003OIE Handistatus, 2005


AustraliaDisease not reported2004OIE, 2000a; OIE, 2009
French PolynesiaPresentNULLOIE, 2000a; OIE, 2009
New CaledoniaDisease never reportedOIE, 2009
New ZealandDisease never reportedOIE, 2009
SamoaDisease never reportedOIE Handistatus, 2005
VanuatuDisease not reportedOIE Handistatus, 2005
Wallis and Futuna IslandsReported present or known to be presentOIE, 2000a; OIE Handistatus, 2005


Top of page

Macroscopic pathologic changes produced by B. suis in pigs are quite variable. Enough abscess formation may occur in affected organs to result in necrosis and desquamation of a significant proportion of the mucous membrane. Generally, the histopathological changes consist of uterine glands filled with leukocytes, cellular infiltration of the endometrial stroma, and hyperplasia of periglandular connective tissue. Diffuse suppurative inflammation is usually present in affected placentas. There also may be considerable necrosis of epithelium and diffuse hyperplasia of fibrous connective tissue.

Focal microscopic granulomatous lesions are frequently observed in livers of pigs with brucellosis, particularly during bacteraemic phases of the disease. These foci frequently are necrotic areas infiltrated with lymphocytes, macrophages, neutrophils, and giant cells, with sheets of histocytic and epithelioid cells with a central zone of caseous or coagulative necrosis. The lesions are usually partially or completely enclosed by a fibrous capsule. The necrotic portions of the granulomas are heavily infiltrated with neutrophils and liquefaction and mineralisation may occur (Enright, 1990). These lesions are not specific for brucellosis, since similar hepatic lesions are associated with other bacterial infections.

Microscopic lesions of bones are sometimes caused by B. suis infection. These occur both in vertebrae and in long bones. The lesions are most frequently located adjacent to the epiphyseal cartilage and usually consist of caseous centres surrounded by a zone of macrophages and leukocytes and often by an outer zone of fibrous connective tissue.

Focal areas of chronic lymphocytic and macrocytic inflammation or focal abscesses are found infrequently in kidneys, spleen, brain, ovaries, adrenal glands, lungs, and other tissues of infected pigs (Deyoe, 1968).


Top of page

One of the most important aids to diagnosis is a detailed herd history of the occurrence of abortions and genital discharge. Good records of clinical manifestations, movement of animals, additions to the herd, breeding records, and illnesses in persons working with the pigs provide invaluable information necessary to arrive at a diagnosis of brucellosis. Accurate epidemiological information is an essential supplement to laboratory tests.

Detection of Brucella

The isolation of Brucellae by direct culture is possibly the most accurate and the most sensitive method to diagnose porcine brucellosis, but often it is not feasible because of inadequate or unavailable laboratory facilities and trained personnel (Deyoe, 1969). B. suis can readily be grown on standard Brucella media in the absence of added CO2 and the techniques are fully described by Alton et al (1988). It has been noted however that biovar 2 isolates may be more sensitive to selective media (OIE, 2012). Definitive identification to species and biovar level is traditionally carried out by phage typing and biochemical tests usually performed in specialised laboratories. Bacteriological cultures from small samples of lymph nodes from carcasses have been sufficient in the past to reveal as many positives as serological diagnosis (Rogers et al., 1989; Alton, 1990).This is a very practical survey strategy, as virtually all the produce of the industry passes through abattoirs and sampling may be performed without damage to the carcass. Vaginal swabs or products of abortion, semen samples or castrated testicles, the contents of swollen joints and blood samples are also suitable sample materials for culture.

Direct detection of B. suis antigen in tissues of infected pigs has been attempted primarily using fluorescent antibody (FA) techniques. The general conclusion has been that Brucellae are seldom detectable in lymph node impression smears with FA procedures because of the relatively low numbers of organisms typically present (Deyoe, 1972). Nevertheless, FA tests could probably be useful for examining aborted materials, since large numbers of B. suis are present in such specimens. In recent years, molecular approaches have increasingly been applied to detect and characterise Brucella. PCR, based on species specific markers such as IS711, has been applied in research studies and for confirmation post cultural isolation but has yet to find widespread use in diagnostic laboratories particularly when applied directly to field material (Whatmore and Gopaul, 2012; Hansel et al, 2015). Based on data showing that IS711 PCR can detect Brucella in serologically negative blood and is more sensitive than culture when applied to lymph nodes, it has been suggested to have value as a complementary tool in brucellosis surveillance programs and confirmation of diagnosis in difficult cases (Hinic et al., 2009). A number of different molecular typing tools have been developed in the last decade that can characterise B. suis to the species (Bruceladder multiplex PCR, SNP typing), biovar (SNP typing) or sub-biovar level (multilocus sequence typing and multilocus variable number of tandem repeat typing (Garcia-Yoldi et al., 2007; Whatmore et al., 2007; Gopaul et al., 2008; Fretin et al., 2008; Lopez-Goni et al., 2011). These tools are increasingly useful to understand both global and local epidemiology and to track the transmission and spread of strains (Escobar et al., 2013; Duvnjak et al., 2015). It is likely that whole genome sequencing will be an increasing important epidemiological tool in the future having already been used for epidemiological traceback of human B. suis infection (Quance et al., 2016).

Serological Tests

Although serological procedures are generally the most practical and most common means of diagnosis in pigs, the results obtained are far from perfect. Surveys in market pigs have shown that as many as 18% of normal pigs may react at 1:25 level in plate agglutination tests (Deyoe, 1969). Pigs exposed to a minimal infective dose of B. suis generally have a prolonged incubation period before significant quantities of antibody is detectable. The various stages of disease found in an infected group of pigs ensure that some individual infected pigs will have no detectable Brucella antibody. Moreover, some strains of B. suis apparently do not stimulate antibody production as well as others (Deyoe, 1967). Therefore, current serological tests are not effective for the diagnosis of individual pigs but, as stressed in the OIE manual, must be regarded as herd tests.

Serological tests commonly used to detect antibodies against Brucella may be grouped as agglutination tests, buffered Brucella antigen tests, immunodiffusion tests, complement fixation tests, and ELISA (MacMillan, 1990). Many of these were developed for diagnosis of bovine brucellosis and have been adapted for testing pig sera (Alton et al., 1988). Whole-cell antigens from B. abortus strains 1119-3 and S99 are commonly used because they have the same or very similar surface lipopolysaccharide complex as smooth B. suis. The standardized antigens are produced and distributed by the Animal and Plant Health Inspection Service (APHIS) of the USDA, or the Animal and Plant Health Agency, Weybridge, UK, and are equally useful for diagnosis of both bovine and porcine brucellosis. The major antigen involved in all the serological tests currently available is the smooth lipopolysaccharide (LPS) and serological diagnosis is complicated by the presence of epitopes that cross-react with those in the corresponding LPS of other bacteria notably Yersinia enterocolitica serotype O:9 (Jungersen et al., 2006). Y. enterocolitica O:9 has been isolated from many herds with cross-reacting pigs where, despite extensive investigation, B. suis could not be recovered (Wrathall et al., 1993). Further, experimental studies have shown that infection with organisms from several other genera can also produce antibodies that react in diagnostic tests for brucellosis (see Corbel, 1985).

The original test methods for the diagnosis of porcine brucellosis were tube and plate agglutination procedures. Interpretation of results were based on the finding that most infected pigs herds contained one or more animals with >100 international units (IU) of agglutination. It is now known that serum agglutination tests (SAT), although sensitive, are not sufficiently specific to be reliable diagnostic tools when used alone. Some of the inaccuracies can be overcome in situations where frequent and repeated testing is practicable and the trend of antibody titres can be determined.

Buffered Brucella antigen tests use stained Brucella antigen buffered at pH 3.65. Reducing the pH of antigen-serum mixtures reduced non-specific agglutination whilst not affecting agglutination caused by serum from infected animals. The buffered Brucella antigen became the basis of the brucellosis card test and similar procedures such as buffered plate antigen and Rose-Bengal tests (RBT). These tests are the most practical method of diagnosis for porcine brucellosis at present and are possibly still the preferred method for large-scale surveillance testing.

Today the indirect (i) and competitive (c) ELISA formats, the Rose Bengal test, complement fixation test (CFT) and the more recently developed fluorescence polarisation assay (FPA) are prescribed tests for international trade, with RBT or ELISA recommended as screening tests, FPA as a screening or confirmatory test and CFT as a complementary test. It has been suggested that sensitivities and specificities of RBT, ELISAs and the FPA are broadly similar though with somewhat reduced sensitivity for the FPA (Paulo et al., 2000). Field evaluations comparing performance of RBT, FPA, iELISA and cELISA in French Polynesia showed cELISA to be most sensitive and cELISA and RBT most specific (Praud et al., 2013) and similar studies in France confirmed cELISA as the most specific and sensitive test (Praud et al., 2012). In older pigs use of FPA or cELISA may reduce cross-reactivity issues, though this requires confirmation outside an experimental infection scenario (Jungersen et al., 2006). Sensitivity levels may be low for the CFT reflecting pro-complementary activity in swine sera and non-specific antibody, likely IgM, that can reduce the specificity of conventional tests notably the SAT (OIEl, 2012). Various groups in Europe have examined the potential of using rough LPS preparations as antigens to address the problem of false positive reactions in pigs with the use of gel immunodiffusion tests (Dieste-Pérez et al., 2015b) or iELISA (McGiven et al., 2012) explored as possible tools to address this issue.


Cellular Immunity

Lymphocyte transformation tests have been used on a limited scale to measure cell-mediated immune responses in infected pigs (Kaneene et al., 1978). There was high correlation between recovery of B. suis from tissues and detectable lymphocyte stimulation responses, but the complexity of the method probably eliminates it from routine diagnostic use. Tests based on the detection of porcine γ-interferon (Por γ-IFN) after the stimulation of blood cells with Brucella antigens have been explored but protocols need full standardisation and validation before routine use can be considered.

Tests for delayed hypersensitivity, using intradermal injection of Brucella allergens (e.g. Brucellin), have been studied with field trials showing good sensitivity (Dieste-Pérez et al., 2014). In the face of cross-reactions caused by Y. enterocolitica O:9, the use of such tests are perhaps the most specific method of pen-side diagnosis as false positive serological reactors give negative results in the skin test (Dieste-Pérez et al., 2014). However, the difficulties in application make it inappropriate for most surveillance and testing programmes. Nevertheless, skin tests are used frequently for diagnosis of brucellosis of pigs in many countries, particularly in Eastern Europe.

List of Symptoms/Signs

Top of page
SignLife StagesType
General Signs / Fever, pyrexia, hyperthermia Pigs:All Stages Sign
General Signs / Forelimb lameness, stiffness, limping fore leg Sign
General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area Sign
General Signs / Hindlimb lameness, stiffness, limping hind leg Sign
General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes Pigs:All Stages Sign
General Signs / Paraparesis, weakness, paralysis both hind limbs Pigs:All Stages Sign
General Signs / Swelling mass penis, prepuce, testes, scrotum Pigs:Boar Diagnosis
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Pigs:All Stages Sign
Pain / Discomfort Signs / Forelimb pain, front leg Sign
Pain / Discomfort Signs / Hindlimb pain, hind leg Sign
Pain / Discomfort Signs / Pain, testes Pigs:All Stages Sign
Reproductive Signs / Abnormal size testes / scrotum Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Pigs:Gilt,Pigs:Sow Diagnosis
Reproductive Signs / Female infertility, repeat breeder Sign
Reproductive Signs / Foul smelling discharge, vulvar, vaginal Pigs:Gilt,Pigs:Sow Diagnosis
Reproductive Signs / Heat on palpation scrotum, testes Pigs:Boar Diagnosis
Reproductive Signs / Lack of libido or erection Sign
Reproductive Signs / Male infertility Pigs:Boar Diagnosis
Reproductive Signs / Mucous discharge, vulvar, vaginal Pigs:Gilt,Pigs:Sow Diagnosis
Reproductive Signs / Purulent discharge, vulvar, vaginal Pigs:Gilt,Pigs:Sow Diagnosis
Reproductive Signs / Purulent or mucoid discharge, cervix or uterus Pigs:Gilt,Pigs:Sow Diagnosis
Reproductive Signs / Retained placenta, fetal membranes Pigs:Gilt,Pigs:Sow Diagnosis

Disease Course

Top of page

The clinical presentation of B. suis infection in a herd varies considerably. The majority of affected herds may have no obvious signs of brucellosis recognisable by the herd owner. The classic manifestations of pig brucellosis are abortion, infertility, orchitis, posterior paralysis, and lameness. Infected pigs often fail to show any persistent or undulating pyrexia. Clinical signs may be transient and death is a rare occurrence.

Abortions may occur at any time during gestation and are influenced more by the time of exposure than by the time of gestation. The rate of abortion is highest in sows or gilts exposed via the genital tract at the time of breeding (Deyoe and Manthei, 1969). Abortions have been observed as early as 17 days following natural insemination by boars disseminating B. suis in the semen. Early abortions are usually overlooked under field conditions, and the first indication is a large percentage of sows or gilts showing signs of oestrus 30-45 days after the service that resulted in conception. Little or no vaginal discharge is observed with early abortions. Abortions that occur during the middle or late stages of gestation are usually associated with females that acquire infection after pregnancy has advanced past 35 or 40 days. Placentas from aborting sows are hyperemic and edematous with yellowish purulent miliary nodules (Olsen and Palmer, 2014). The persistence of genital infection in females varies considerably.

A small percentage of sows have been shown to shed B. suis in vaginal discharges for as long as 30 months. However, the majority has ceased shedding organisms within 30 days. A clinically apparent abnormal vaginal exudate is seldom observed in sows that have uterine infection except just prior to and for a short time after abortions. The majority of female pigs eventually recover from genital infection.

When genital infection in sows persists only a short time after abortion, parturition, or breeding to an infected boar and the sows are permitted 2 or 3 oestrous cycles of sexual rest, subsequent conception rates and reproductive capacity are usually very good.

Genital infection tends to be more persistent in boars than in sows. Some infected boars do not develop a localised genital infection. However, boars that do develop genital infection seldom recover from it. Pathologic changes in the male accessory glands or testes are generally more extensive and irreversible than in the uterus. Infertility and lack of sexual drive may occur in infected boars and is frequently associated with testicular involvement. More commonly, however, boars have infection in accessory genital glands and as a result disseminate large numbers of B. suis in their semen (Lord et al., 1998). These boars do not necessarily have reduced fertility (Vandeplassche et al., 1967). In most circumstances, clinically apparent lesions of B. suis biovar 1, 2, or 3 infection in boars are seldom encountered.

Clinical evidence of brucellosis in suckling and weaning pigs is usually spondylitis associated with posterior paralysis (occasionally observed in any age of pigs).

The symptoms with greatest economic significance in porcine brucellosis are abortion (at all stages of gestation), infertility, orchitis, posterior paralysis and lameness. However, the most common clinical signs of swine brucellosis are pyrexia, anorexia and depression between 2 to 9 days post infection, but these symptoms do not last longer than 2 days (Deyoe, 1967). During the later stages of infection there may be further indications, with some animals showing a loss of weight and condition, polydypsia, malaise and a reluctance to stand. However, these are seen in a minority of pigs, and in most swine the infection progresses asymptomatically (Alton, 1991). Bacteraemia generally appears soon after infection and before diagnostically significant agglutinins appear. Organisms may be recovered from the blood for an average of 5 weeks, after which isolation is infrequent and spasmodic. However, there is a great variation in the duration of bacteraemia, with periods as short as one week or as long as 34 months recorded in individual swine. At post mortem the most likely site for the isolation of the organism are the lymph nodes, in particular those local to the entry site of the infection, especially those in the region of the head, neck and genital organs. Under experimental conditions bacteria can be recovered from liver, spleen, lungs, thymus and tonsils. Lymph nodes are the most reliable sample for recovery for up to 8 weeks post infection, after which no tissues were culture positive (Deyoe, 1967). In chronically infected swine Brucella have been recovered from bone marrow and joint fluids.


Top of page

In pigs the most important routes of infection are through the alimentary and genital tracts, and the gregarious habits of pigs and peculiarities of the disease strongly suggest that the alimentary tract is the most common primary portal of entry. Most B. suis infection is transmitted to susceptible animals through direct association, and usually through ingestion of food contaminated with discharges from infected pigs. Suckling piglets are infected frequently by nursing dams, and when breeding pigs are confined together, by the consumption of aborted foetal materials. Pigs of all ages are susceptible. Brucellosis as a venereal disease may be transmitted when pigs and sows are mated with infected boars or artificially inseminated with semen containing B. suis. Experimentally, pigs may be infected via conjunctival or intranasal routes with suspensions of B. suis.

Other than infected domestic pigs, only the European hare and feral pigs have been established as significant potential reservoirs of B. suis (Davis, 1990). The European hare was identified as a natural host for B. suis biovar 2 as early as 1954 (Bendsten et al., 1954), and is still incriminated for periodic outbreaks in European pigs. Feral pigs in the south-eastern United States, and to a much lesser extent elsewhere (Drew et al., 1992) have been discovered to have a high rate of serological reactors, with isolation of B. suis biovar 1 from some animals (Wood et al., 1976; Becker et al., 1978; Pederson et al., 2014). In the state of Florida, groups with high incidences of brucellosis have been found in some populations (Leek et al., 1993). The epidemiological importance of feral pigs in the maintenance of porcine brucellosis depends largely on the degree of contact between wild and domestic pigs, and the prevention of contact between these populations would make feral pigs more of a threat to public health than to the pig industry (Nettles, 1991). The vaccination of feral populations using dosed baits, possibly with strain RB51, has been shown to be a feasible option to be considered in certain situations in the future (Fletcher et al., 1990; Enright, 1995). There have been numerous instances of B. suis infection or seropositivity for brucellosis in rodents or carnivorous species in areas where brucellosis in domesticated pigs has occurred. However, general indications are that these species acquired infection from the pigs and are terminal hosts. Without exceptions, epidemiological investigation of new outbreaks has revealed the source of infection as other domesticated pigs.

Experimental studies have shown that pigs can be infected with B. suis biovar 4. However, there has been no evidence that these organisms invade the genital tract, are transmissible between pigs, or localise in any tissues other than lymph nodes draining the site of infection.

Pigs infected with B. suis biovars 1, 2, or 3 can serve as sources of infection for other domesticated animal species. B. suis infection can occur naturally in horses, cattle and dogs. Although the most common Brucella infection in horses is B. abortus, fistulous withers and other syndromes have been recorded as B. suis infections when horses were associated with infected pigs. Cattle are rarely infected with B. suis, but when it does occur, the characteristic infection is mastitis, and Brucellae are excreted in the milk presenting a potentially serious human health risk (OIE, 2012).

Impact: Economic

Top of page

Figures are not available concerning the global economic significance of porcine brucellosis (McDermott et al., 2013). However, given the extensive distribution of the causative agent and its impact on reproductive success these are believed to be substantial. Infected herds typically have low-grade loss of productivity for as long as the infection is present. When first infected, effects may be more pronounced. In many countries the disease is absent or of such low incidence that it is not economically important. However, it is important to ensure absence of B. suis when pigs or pig products are traded, especially internationally and the occurrence of false positive reactions can be a hindrance to trade between B. suis free countries.

Zoonoses and Food Safety

Top of page

Public Health

Porcine brucellosis has important public health implications. B. suis was formerly found in many cases of human brucellosis (Fox and Kaufmann, 1977). The public health hazard caused by porcine brucellosis is of proportionately greater significance than the risk from bovine brucellosis, primarily because B. suis (biovars 1 and 3) appears to have a much higher degree of pathogenicity for humans than B. abortus. There also tend to be higher numbers of B. suis organisms in the tissues, providing a greater exposure to persons who come in contact with infected pigs. As pigs do not produce dairy produce, the incidence of B. suis in man is almost entirely occupational: farmers, veterinarians and abattoir workers. Interestingly, although the infection of cattle with B. suis biovars infectious for humans is rare, Cooke and Noble (1984), working in Australia, reported several cases that were probably contracted as a result of contact with feral pigs. Persistent excretion in bovine milk may give rise to human epidemics (Borts et al., 1943). B. suis infection of a ram has been reported by Paolicchi et al. (1993) who suggest that this may represent a public health hazard. 

Disease Treatment

Top of page

There has long been a generalised opinion that animal brucellosis should not be treated with antibiotics and thus information on potential antibiotic treatment for swine brucellosis is scanty and incomplete (Dieste-Pérez et al., 2015a). Oxytetracycline treatment, given orally for 90 days, has been reported to minimise impact of swine brucellosis (Olsen et al., 2012) however abortion rates and pathogen spread increased after treatment cessation (Dieste-Pérez et al., 2015a). There has been recent interest in the use of new generation antibiotics with improved tissue penetration and high performance pharmacokinetics leading to studies suggesting efficacy of an oxytetracycline/tildipirosin (a macrolide derivative which is taken up by the inflammatory cells within which Brucellae survive) combination with small scale studies in sows suggesting this treatment cleared B. suis (Dieste-Pérez et al., 2015a). Although depopulation of infected holdings is likely to remain the preferred way to handle outbreaks, these studies suggest antibiotic therapy may be feasible in carefully controlled circumstances.

Prevention and Control

Top of page

Experiences in control of porcine brucellosis in countries such as the USA and Australia indicate that eradication of the disease from pigs is desirable and feasible. One significant factor facilitating control has been the tendency for pig production to become more specialised and less a part of diversified farming operations. Consequently, the occurrence of reproductive disease in pigs has become proportionately more important, confinement systems and closed herds have eliminated many opportunities for inter-farm spread of disease, and larger units have eliminated the "community boar" in most instances. Another important instrument in control of pig brucellosis has been the establishment and maintenance of validated brucellosis-free herds, particularly pure-bred herds or those selling breeding stock via a pyramid system. Implementation of effective surveillance programs such as market pig identification and testing have been instrumental in locating and eliminating large numbers of infected herds. Finally, it has been found that whenever recommended procedures to eradicate brucellosis from an individual herd or an enzootic area are conscientiously followed, there is very seldom any recurrence of the disease in that locality (Spencer and Mattison, 1975).

There are three acceptable alternative plans recommended for use when pig herds are found to be, or suspected of being, infected with B. suis. Plan 1 consists of depopulation of the entire herd, which is by far the most successful and the most economical in the long run. Plan 2 is a procedure designed to salvage irreplaceable bloodlines and basically consists of marketing the adult pigs for slaughter and retaining weaning pigs for breeding stock, a plan that is not always successful and necessitates considerable isolation and re-testing requirements. Plan 3 consists of removing only serological reactors and re-testing the herd as many times as necessary. This latter procedure is rarely successful if the herd is actually infected but is the plan of choice if it contains only a single reactor or if a very low proportion of animals are reactors and there is reasonable doubt that brucellosis exists. There are currently no effective vaccines validated for use in pig herds and antibiotic treatment, although possible, is seldom feasible. Numerous attempts have been made to develop a vaccine to immunise pigs against B. suis. Only one product has found any acceptance for field use, this is B. suis strain 2 vaccine (S2) which has been used extensively in China (Dequi et al., 2002). To date, it does not appear to have been used elsewhere in pigs and it is recommended that before S2 vaccine is accepted for use in countries outside China, its safety and immunogenicity should be thoroughly investigated under the conditions pertaining in each country.


Top of page

Al-Dahouk S, Nöckler K, Tomaso H, Splettstoesser WD, Jungersen G, Riber U, Petry T, Hoffmann D, Scholz HC, Hensel A, Neubauer H, 2005. Seroprevalence of brucellosis, tularemia, and yersiniosis in wild boars (Sus scrofa) from North-Eastern Germany. Journal of Veterinary Medicine. Series B, 52(10):444-455.

Alton GG, 1990. Brucella melitensis.. Animal brucellosis., 383-409; 154 ref.

Alton GG, 1991. Porcine brucellosis as a world problem. Networking in brucellosis research. Report of the United Nations University Brucellosis Research Network., 217-231; 39 ref.

Alton GG, Jones LM, Angus RD, Verger JM, 1988. Techniques for the brucellosis laboratory. Techniques for the brucellosis laboratory., 190 pp.; many ref.

Bang B, 1897. The etiology of epizootic abortion. Journal of Comparative Pathology and Therapeutics, 10:125.

Barr SC, Eilts BE, Roy AF, Miller R, 1986. Brucella suis biotype 1 infection in a dog. Journal of the American Veterinary Medical Association, 189(6):686-687; 9 ref.

Becker HN, Belden RC, Breault T, Burridge MJ, Frankenberger WB, Nicoletti P, 1978. Brucellosis in feral swine in Florida. J. Am. Vet. Med. Assoc., 173:1181-1182.

Bendtsen H, Christiansen M, Thomsen A, 1954. Brucella enzootics in swine herds in Denmark - presumably with hare as a source of infection. Nord. Vet. Med., 6:11-21.

Borts IH, Harris DM, Joynt MF, Jennings JR, Jordan CF, 1943. A milk borne epidemic of brucellosis caused by the porcine biotype of Brucella, (Brucella suis) in a raw milk supply. J. Am. Vet. Med. Assoc., 121:319.

Boschiroli ML, Ouahrani-Bettache S, Foulongne V, Michaux-Charachon S, Bourg G, Allardet-Servent A, Cazevieille C, Liautard JP, Ramuz M, O'Callaghan D, 2002. The Brucella suis virB operon is induced intracellularly in macrophages. Proceedings of the National Academy of Sciences of the United States of America, 99(3):1544-1549.

Bruce D, 1887. Note on the discovery of a microorganism in Malta Fever. Practitioner, 39:161-170.

Bruce D, 1893. Sur une nouvelle forme de fievre. Ann. Inst. Pasteur Paris, 7:289.

Buddle MB, 1956. Studies on B. ovis (n. sp.) a case of genital disease of sheep in New Zealand and Australia. Journal of Hygiene, 54:351.

Buddle MB, Boyes BW, 1953. A Brucella mutant causing genital disease in sheep in New Zealand. State Veterinary Journal, 29:145.

Carmichael LE, Bruner DW, 1968. Characteristics of newly recognised species of Brucella responsible for canine abortions. Cornell Veterinarian, 48:579.

Cohen ND, Carter GK, McMullan WC, 1992. Fistulous withers in horses: 24 cases (1984-1990). Journal of the American Veterinary Medical Association, 201(1):121-124; 32 ref.

Cook DR, Kingston GC, 1988. Isolation of Brucella suis biotype 1 from a horse. Australian Veterinary Journal, 65(5):162-163; 15 ref.

Cook DR, Noble JW, 1984. Isolation of Brucella suis from cattle. Australian Veterinary Journal, 61(8):263-264; 12 ref.

Corbel MJ, 1985. Recent advances in the study of Brucella antigens and their serological cross-reactions. Veterinary Bulletin, 55(12):927-942.

Corbel MJ, 1988. Brucellosis. In: Laing JA, Morgan WJB, Wagner WC, eds. Fertility and Infertility. Bailliere, Tindall, 189-221.

Corbel MJ, 1997. Brucellosis: An overview. Emerging Infectious Diseases, Apr-Jun, 3(2):213-221.

Crawford RP, Adams LG, Richardson BE, 1990. Effect of dose of Brucella abortus strain 19 in yearling heifers on the relative risk of developing brucellosis from challenge exposure with strain 2308. American Journal of Veterinary Research, 51(11):1837-1840; 20 ref.

Cvetnic Z, Spicic S, Curic S, Jukic B, Lojkic M, Albert D, Thiébaud M, Garin-Bastuji B, 2005. Isolation of Brucella suis biovar 3 from horses in Croatia. Veterinary Record, 156(18):584-585.

Cvetnic Z, Spicic S, Toncic J, Majnaric D, Benic M, Albert D, Thiébaud M, Garin-Bastuji, 2009. Brucella suis infection in domestic pigs and wild boar in Croatia. Revue Scientifique et Technique - Office International des Épizooties, 28(3):1057-1067.

Davis DS, 1990. Brucellosis in wildlife. Animal brucellosis., 321-334; 129 ref.

Deyoe BL, 1967. Pathogenesis of three strains of Brucella suis in swine. American Journal of Veterinary Research, 28:951-957.

Deyoe BL, 1968. Histopathologic changes in male swine with experimental brucellosis. American Journal of Veterinary Research, 29:1215-1220.

Deyoe BL, 1969. Diagnostic tests for swine brucellosis. Proceedings of 53rd Annual Meeting Livestock Conservation, 20-22.

Deyoe BL, 1972. Research findings applicable to eradication of swine brucellosis. Proceedings of the Annual Meeting US Animal Health Association, 76:108-114.

Deyoe BL, Manthei CA, 1969. Swine brucellosis. In: Proceedings 1967 Symposium On Factors Producing Embryonic Abnormalities, Death and Abortion in Swine. ARS 91-73:54-60.

Díaz Aparicio E, 2013. Epidemiology of brucellosis in domestic animals caused by Brucella melitensis, Brucella suis and Brucella abortus. Revue Scientifique et Technique - Office International des Épizooties, 32(1):43-51 (Es), 53-60 (En).

Dieste-Pérez L, Blasco JM, Miguel MJde, Marín CM, Barberán M, Conde-Álvarez R, Moriyón I, Muñoz PM, 2014. Performance of skin tests with allergens from B. melitensis B115 and rough B. abortus mutants for diagnosing swine brucellosis. Veterinary Microbiology, 168(1):161-168.

Dieste-Pérez L, Blasco JM, Miguel MJde, Moriyón I, Muñoz PM, 2015. Diagnostic performance of serological tests for swine brucellosis in the presence of false positive serological reactions. Journal of Microbiological Methods, 111:57-63.

Dieste-Pérez L, Fraile L, Miguel MJde, Barberán M, Blasco JM, Muñoz PM, 2015. Studies on a suitable antibiotic therapy for treating swine brucellosis. Journal of Veterinary Pharmacology and Therapeutics, 38(4):357-364.

Drew ML, Jessup DA, Burr AA, Franti CE, 1992. Serological survey for brucellosis in feral swine, wild ruminants, and black bear of California, 1977 to 1989. Journal of Wildlife Diseases, 28(3):355-363; 21 ref.

Duvnjak S, Racic I, Spicic S, Zdelar-Tuk M, Reil I, Cvetnic Z, 2015. Characterisation of Brucella suis isolates from southeast Europe by multi-locus variable-number tandem repeat analysis. Veterinary Microbiology, 180(1/2):146-150.

Enright F, 1995. Update on research with RB51 strain of Brucella abortus. Proceedings of the Annual Meeting of the United States Animal Health Association, 99:647-648.

Enright FM, 1990. The pathogenesis and pathobiology of Brucella infection in domestic animals. Animal brucellosis., 301-320; 55 ref.

Escobar GI, Jacob NR, López G, Ayala SM, Whatmore AM, Lucero NE, 2013. Human brucellosis at a pig slaughterhouse. Comparative Immunology, Microbiology & Infectious Diseases, 36(6):575-580.

Evans AC, 1918. Further studies on Bacterium abortus and related bacteria II. A comparison Bacterium abortus and Bacterium brochisepticus with the organism which causes Malta Fever. Journal of Infectious Diseases, 22:580.

Figueiredo Pde, Ficht TA, Rice-Ficht A, Rossetti CA, Adams LG, 2015. Pathogenesis and immunobiology of brucellosis : review of Brucella-host interactions. American Journal of Pathology, 185(6):1505-1517.

Fiori PL, Mastrandrea S, Rappelli P, Cappuccinelli P, 2000. Brucella abortus infection acquired in microbiology laboratories. Journal of Clinical Microbiology, 38(5):2005-2006.

Fletcher WO, Creekmore TE, Smith MS, Nettles VF, 1990. A field trial to determine the feasibility of delivering oral vaccines to wild swine. Journal of Wildlife Diseases, 26(4):503-510; 43 ref.

Fox MD, Kaufmann AF, 1977. Brucellosis in the United States, 1965-1974. Journal of Infectious Diseases, 136:312-316.

Fretin D, Mori M, Czaplicki G, Quinet C, Maquet B, Godfroid J, Saegerman C, 2013. .

Fretin D, Whatmore AM, Al-Dahouk S, Neubauer H, Garin-Bastuji B, Albert D, Hessche Mvan, Ménart M, Godfroid J, Walravens K, Wattiau P, 2008. Brucella suis identification and biovar typing by real-time PCR. Veterinary Microbiology, 131(3/4):376-385.

García-Yoldi D, Fleche Ple, Miguel MJde, Muñoz PM, Blasco JM, Cvetnic Z, Marín CM, Vergnaud G, López-Goñi I, 2007. Comparison of multiple-locus variable-number tandem-repeat analysis with other PCR-based methods for typing Brucella suis isolates. Journal of Clinical Microbiology, 45(12):4070-4072.

Garin-Bastuji B, Hars J, Calvez D, Thiébaud M, Artois M, 2000. Brucellosis of domestic pigs. Re-emergence of Brucella suis biovar 2 in France. (Brucellose du porc domestique et du sanglier sauvage due a Brucella suis biovar 2 en France.) Épidémiologie et Santé Animale, No. 38:1-5.

Garin-Bastuji B, Vaillant V, Albert D, Tourrand B, Danjean M, Lagier A, Rispal P, Benquet B, Maurin M, Valk HDe, Mailles A, 2006. Is brucellosis due to the biovar 2 of Brucella suis an emerging zoonosis in France? Two case reports in wild boar and hare hunters. In: Proceedings of the International Society of Chemotherapy Disease Management Meeting, 1st International Meeting on Treatment of Human Brucellosis, Ioannina, Greece, 7-10 November 2006.

Godfroid J, Käsbohrer A, 2002. Brucellosis in the European Union and Norway at the turn of the twenty-first century. Veterinary Microbiology, 90(1/4):135-145.

Godfroid J, Michel P, Uytterhaegen, De Smedt C, Rasseneur F, Boelaert F, Saegerman C, Patigny X, 1994. Brucellose enzootique a Brucella suis biotype 2 chez le sanglier (sus scrofa) en Belgique. Ann. Med. Vet, 138:263-268.

Gopaul KK, Koylass MS, Smith CJ, Whatmore AM, 2008. Rapid identification of Brucella isolates to the species level by real time PCR based single nucleotide polymorphism (SNP) analysis. BMC Microbiology, 8(86):(02 June 2008).

Hinic V, Brodard I, Thomann A, Holub M, Miserez R, Abril C, 2009. IS711-based real-time PCR assay as a tool for detection of Brucella spp. in wild boars and comparison with bacterial isolation and serology. BMC Veterinary Research, 5(22):(28 May 2009).

Hoerlein AB, Hubbard ED, Leith TS, Biester HE, 1954. Swine Brucellosis. Vet. Med. Res. Inst., Iowa State Coll.

Huddleston IF, 1929. The differentiation of the species in the genus Brucella. Michigan State College of Agriculture Experiment Station Technical Bulletin No. 100, East Lansing, Michigan.

Hänsel C, Mertens K, Elschner MC, Melzer F, 2015. Novel real-time PCR detection assay for Brucella suis. Veterinary Record Open, 2(1):e000084.

Jungersen G, Sørensen V, Giese SB, Stack JA, Riber U, 2006. Differentiation between serological responses to Brucella suis and Yersinia enterocolitica serotype O:9 after natural or experimental infection in pigs. Epidemiology and Infection, 134(2):347-357.

Kaneene JM, Anderson RK, Johnson DW, Angus RD, Muscoplate CC, Pietz DE, Vanderwagon LC, Sloane EE, 1978. Cell-mediated immune responses in swine from a herd infected with Brucella suis. American Journal of Veterinary Research, 39:1607-1611.

Leek MLvan der, Becker HN, Humphrey P, Adams CL, Belden RC, Frankenberger WB, Nicoletti PL, 1993. Prevalence of Brucella sp. antibodies in feral swine in Florida. Journal of Wildlife Diseases, 29(3):410-415; 16 ref.

López-Goñi I, García-Yoldi D, Marín CM, Miguel MJde, Barquero-Calvo E, Guzmán-Verri C, Albert D, Garin-Bastuji B, 2012. New Bruce-ladder multiplex PCR assay for the biovar typing of Brucella suis and the discrimination of Brucella suis and Brucella canis. Veterinary Microbiology, 154(1/2):152-155.

Lord VR, Cherwonogrodzky JW, Schurig GG, Lord RD, Marcano MJ, Meléndez GE, 1998. Venezuelan field trials of vaccines against brucellosis in swine. American Journal of Veterinary Research, 59(5):546-551.

Luchsinger DW, Anderson RK, Werring DF, 1965. A swine brucellosis epizootic. J. Am. Vet. Med. Assoc., 147:632-636.

MacMillan A, 1990. Conventional serological tests. Animal brucellosis., 153-197; 206 ref.

Martin-Mazuelos E, Nogales MC, Florez C, Gomez-Mateos JM, Lozano F, Sanchez A, 1994. Outbreak of Brucella melitensis among microbiology laboratory workers. Journal of Clinical Microbiology, 32(8):2035-2036.

McDermott J, Grace D, Zinsstag J, 2013. Economics of brucellosis impact and control in low-income countries. Revue Scientifique et Technique - Office International des Épizooties, 32(1):249-261.

McGiven JA, Nicola A, Commander NJ, Duncombe L, Taylor AV, Villari S, Dainty A, Thirlwall R, Bouzelmat N, Perrett LL, Brew SD, Stack JA, 2012. An evaluation of the capability of existing and novel serodiagnostic methods for porcine brucellosis to reduce false positive serological reactions. Veterinary Microbiology, 160(3/4):378-386.

Meyer KF, Shaw EB, 1920. A comparison of the morphological, cultural and biochemical characteristics of B. abortus and B. melitensis. Journal of Infectious Diseases, 27:173.

Miller CD, Songer JR, Sullvan JF, 1987. A twenty-five year review of laboratory-acquired human infections at the National Animal Disease Centre. Am. Ind. Hyg. Assoc. J., 48(3):271-275.

Montejo JM, Alberola I, Glez-Zarate P, Alvarez A, Alonso J, 1993. Open, randomized therapeutic trial of six antimicrobial regimes in he treatment of human brucellosis. Clinical Infectious Diseases, 16(5):671-676.

Neiland KA, 1975. Further observations on rangiferine brucellosis in Alaskan carnivores. Journal of Wildlife Diseases, 11(1):45-53.

Nettles VF, 1991. Short- and long-term strategies for resolving problems of pseudorabies and swine brucellosis in feral swine. Proceedings - Annual Meeting of the United States Animal Health Association, 95:551-556.

O'Callaghan D, Cazevieille C, Allardet-Servent A, Boschiroli ML, Bourg G, Foulongne V, Frutos P, Kulakov Y, Ramuz M, 1999. A homologue of the Agrobacterium tumefaciens VirB and Bordetella pertussis Ptl type IV secretion systems is essential for intracellular survival of Brucella suis. Molecular Microbiology, 33(6):1210-1220.

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.

OIE, 2000. The Manual of Standards for Diagnostic Tests and Vaccines. Paris, France: Office International Des Epizooties.

OIE, 2001. World Animal Health in 2000. Parts 1 and 2. Paris, France: Office International Des Epizooties.

OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health.

OIE, 2012. Porcine brucellosis, chapter 2.8.5. In: Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. Paris, France: World Organisation for Animal Health.

Olsen SC, Garin-Bastuji B, Blasco JM, Nicola AM, Samartino L, 2012. Brucellosis. In: Diseases of Swine, 10th Edition [ed. by Zimmerman, J. J. \Karriker, L. A. \Ramirez, A. \Schwartz, K. J. \Stevenson, G. W.]., USA: Wiley Blackwell, 697-708.

Olsen SC, Palmer MV, 2014. Advancement of knowledge of Brucella over the past 50 years. Veterinary Pathology, 51(6):1076-1089.

Paolicchi FA, Terzolo HR, Campero CM, 1993. Isolation of Brucella suis from the semen of a ram. Veterinary Record, 132(3):67; 10 ref.

Paulo PS, Vigliocco AM, Ramondino RF, Marticorena D, Bissi E, Briones G, Gorchs C, Gall D, Nielsen K, 2000. Evaluation of primary binding assays for presumptive serodiagnosis of swine brucellosis in Argentina. Clinical and Diagnostic Laboratory Immunology, 7(5):828-831.

Pedersen K, Quance CR, Robbe-Austerman S, Piaggio AJ, Bevins SN, Goldstein SM, Gaston WD, Deliberto TJ, 2014. Identification of Brucella suis from feral swine in selected states in the USA. Journal of Wildlife Diseases, 50(2):171-179.

Poester FP, Samartino LE, Santos RL, 2013. Pathogenesis and pathobiology of brucellosis in livestock. Revue Scientifique et Technique - Office International des Épizooties, 32(1):105-115.

Praud A, Gimenez O, Zanella G, Dufour B, Pozzi N, Antras V, Meyer L, Garin-Bastuji B, 2012. Estimation of sensitivity and specificity of five serological tests for the diagnosis of porcine brucellosis. Preventive Veterinary Medicine, 104(1/2):94-100.

Praud A, Gimenez O, Zanella G, Pozzi N, Antras V, Meyer L, Garin-Bastuji B, 2013. Evaluation of five serological tests for the diagnosis of porcine brucellosis in French Polynesia. Tropical Animal Health and Production, 45(4):931-933.

Quance C, Robbe-Austerman S, Stuber T, Brignole T, DeBess EE, Boyd L, LeaMaster B, Tiller R, Draper J, Humphrey S, Erdman MM, 2016. Identification of source of Brucella suis infection in human by using whole-genome sequencing, United States and Tonga. Emerging Infectious Diseases, 22(1):79-82.

Ramamoorthy S, Woldemeskel M, Ligett A, Snider R, Cobb R, Rajeev S, 2011. Brucella suis infection in dogs, Georgia, USA. Emerging Infectious Diseases, 17(12):2386-2387.

Robson JM, Harrison MW, Wood RN, Tilse MH, McKay AB, Brodribb, TR, 1993. Brucellosis: re-emerging and changing epidemiology in Queensland. Med. J. Aust., 159(3):153-158.

Rogers RJ, Cook DR, Kettlerer PJ, Baldock FC, Blackall PJ, Stewart RW, 1989. An evaluation of three serological tests for antibody to Brucella suis in pigs. Australian Veterinary Journal, 66:77-80.

Rónai Z, Kreizinger Z, Dán Á, Drees K, Foster JT, Bányai K, Marton S, Szeredi L, Jánosi S, Gyuranecz M, 2015. First isolation and characterization of Brucella microti from wild boar. BMC Veterinary Research, 11(147):(11 July 2015).

Shang DeQiu, Xiao DongLou, Yin JiMing, 2002. Epidemiology and control of brucellosis in China. Veterinary Microbiology, 90(1/4):165-182.

Spencer PL, Mattison JR, 1975. Pike County, Illinois, swine brucellosis project. Proceedings of the Annual Meeting of the US Animal Health Association, 79:86-91.

Sterba F, 1982. Pathological changes in brucellosis in hares. Veterinarni Medicina, 27(7):437-438.

Stoenner HG, Lackman DB, 1957. A new species of Brucella isolated from the desert wood rat, Neotoma lepida Thomas. American Journal of Veterinary Research, 69:947.

Szulowski K, Iwaniak W, Weiner M, Zotnicka J, 2013. Brucella suis biovar 2 isolations from cattle in Poland. Annals of Agricultural and Environmental Medicine, 20(4):672-675.

Teyssou R, Morvan J, Leleu JP, Roumegou P, Goullin B, Carteron B, 1989. A case of brucellosis in man due to Brucella suis biovar 2. Médecine et Maladies Infectieuses, 19(3):160-161; 6 ref.

Traum J, 1914. Report to the chief of the Bureau of Animal Industry, US Department of Agriculture, Washington, 30.

Vandeplassche M, Herman J, Spincemaille J, Bouters R, Dekeyser P, Brone E, 1967. Brucella suis infection and infertility in swine. Meded Veeartsenijsch Rijksuniv Gent, 11:1-40.

Vizcaino LL, Perez MG, Garcia AM, 1976. Suplemento Cientifico del Boletin Informativo Consejo General de Colegios Veterinarios de Espana, 206:37-42.

Wattam AR, Foster JT, Mane SP, Beckstrom-Sternberg SM, Beckstrom-Sternberg JM, Dickerman AW, Keim P, Pearson T, Shukla M, Ward DV, Williams KP, Sobral BW, Tsolis RM, Whatmore AM, O'Callaghan D, 2014. Comparative phylogenomics and evolution of the Brucellae reveal a path to virulence. Journal of Bacteriology, 196(5):920-930.

Whatmore AM, 2009. Current understanding of the genetic diversity of Brucella, an expanding genus of zoonotic pathogens. Infection, Genetics and Evolution, 9(6):1168-1184.

Whatmore AM, Davison N, Cloeckaert A, Al Dahouk S, Zygmunt MS, Brew SD, Perrett LL, Koylass MS, Vergnaud G, Quance C, Scholz HC, Dick Jr EJ, Hubbard G, Schlabritz-Loutsevitch NE, 2014. Brucella papionis sp. nov., isolated from baboons (Papio spp.). International Journal of Systematic and Evolutionary Microbiology, 64(12):4120-4128.

Whatmore AM, Gopaul, KK, 2012. Recent advances in molecular approaches to Brucella diagnostics and epidemiology. In: Brucella: Molecular Microbiology and Genomics [ed. by Lopez-Goni, I. \O'Callaghan, D.]. Norwich, UK: Caister Academic Press, 57-88.

Whatmore, AM, Perrett LL, MacMillan AP, 2007. Characterisation of the genetic diversity of Brucella by multilocus sequencing. BMC Microbiology, 7:34.

Wood GW, Hendricks JB, Goodman DE, 1976. Brucellosis in feral swine. Journal of Wildlife Diseases, 12:579-582.

Wrathall AE, Broughton ES, Gill KPW, Goldsmith GP, 1993. Serological reactions to Brucella species in British pigs. Veterinary Record, 132(18):449-454; 21 ref.

Yantzis D, Kastanidou C, 1990. Isolation of Brucella suis in fetuses. First case in Greece. Deltion tes Elle^macron~nike^macron~s Kte^macron~niatrike^macron~s Etaireias = Bulletin of the Hellenic Veterinary Medical Society, 41(2):100-106; 27 ref.


Top of page

04/02/16 Updated by:

Dr Adrian Whatmore, Animal and Plant Health Agency, Woodham Lane, Addlestone, Surrey, KT15 3NB, UK.

Distribution Maps

Top of page
You can pan and zoom the map
Save map