Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


Rhodococcus equi infections



Rhodococcus equi infections


  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Rhodococcus equi infections
  • Pathogens
  • Rhodococcus equi
  • Overview
  • Rhodococcus equi (previously Corynebacterium equi) is a Gram-positive coccobacillus belonging to the nocardioform actinomycete group (

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Preferred Scientific Name

  • Rhodococcus equi infections

International Common Names

  • English: lymphadenitis; lymphadenitis in cattle; lymphadenitis in pigs; mastitis; ovine pneumonia


Top of page Rhodococcus equi


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Rhodococcus equi (previously Corynebacterium equi) is a Gram-positive coccobacillus belonging to the nocardioform actinomycete group (Goodfellow et al., 1982). It is a soil-dwelling bacterium that causes pulmonary and extrapulmonary pyogranulomatous infections in a variety of animal species and humans (reviewed by Vázquez-Boland et al., 2013). R. equi is an important cause of disease in foals, primarily those between 1 and 6 months of age (Ellenberger and Genetzky, 1986).

R. equi was first isolated by Magnusson (1923) from cases of foal pneumonia in Sweden. Since then it has been isolated throughout the world from a variety of lesions in a number of different species including pigs, cattle, buffalo, sheep and goats (Barton and Hughes, 1980), but clinical disease is much rarer in these species. It has been suggested that it is an opportunistic pathogen (Barton and Hughes, 1980). R. equi infection is of significance in pigs and cattle, as it can produce lymph node lesions (lymphadenitis) in these species that are difficult to distinguish from those of tuberculosis at postmortem inspection (McKenzie and Donald, 1979; Dvorská et al., 1999; Ocepek and Zdovoc, 2000; Flynn et al., 2001). Misdiagnosis can have serious consequences for the fate of the carcass and of the disease status of the farm from which the animal originated.

R. equi was first isolated from tuberculosis-like lesions of pigs in the 1930s (McCarter et al., 1935; Holth and Amundsen, 1936). Karlson et al. (1940) and Feldman et al. (1940) subsequently reported the isolation of R. equi from the lymph nodes of healthy pigs. The bacterium has since been isolated from the mandibular and submaxillary lymph nodes of pigs with and without tuberculosis-like lesions (Barton and Hughes, 1980; Rao et al., 1982; Takai and Tsubaki, 1985; Takai et al., 1986b; Katsumi et al., 1991; Madarame et al. 1998), but the causative role of R. equi in granulomatous lymphadenitis remains unclear (Takai et al., 1996). In some cases, Mycobacterium spp. and R. equi have been recovered together (Dvorská et al., 1999; Ocepek and Zdovc, 2000). R. equi has occasionally been associated with serious clinical disease in pigs, including one outbreak of oral abscesses and one of pneumonia (Thal and Rutquist, 1959; Rao et al., 1982). R. equi has also been isolated from wild boars (Makrai et al., 2008; Ribeiro et al., 2011; Sakai et al., 2012).

As in pigs, reports of R. equi infection in cattle have mainly been associated with lymph node lesions (Woolcock and Rudduck, 1973; McKenzie and Donald, 1979; Dürrling, 1991; Soedarmanto et al., 1997). In a recent study, the prevalence among 3.3 million cattle examined postmortem was 0.008% (Flynn et al., 2001). There have also been occasional reports of pyometra (Craig and Davis, 1940) and mastitis (Natarajan and Nilakantan, 1974; Garg and Kapoor, 1986; Wani et al., 2003) in cattle associated with R. equi and the bacterium has been isolated from buffaloes in India with mastitis (Rahman and Baxi 1983a,b), vaginal discharge (Rajagopalan and Gopalakrishnan, 1938) and pneumonia (Singh, 1982).

R. equi was isolated from abscesses of goats in the 1970s (Natarajan and Nilakantan, 1974; Whitford and Jones, 1974), but until recently was considered to be a rare cause of disease in this species. R. equi has now emerged as a relatively common cause of disseminated abscesses and mortality in goats (Guerrault et al., 1984; Diteko et al., 1988; Moraal et al., 1990; Ojo et al., 1993; Fitzgerald et al., 1994; Tkachuk-Saad et al., 1998; Davis et al., 1999; Jeckel et al., 2011). Lesions have been observed in the lungs, liver, spleen and lymph nodes. Osteomyelitis due to R. equi infection has also been reported (Carrigan et al., 1988; Kabongo et al., 2005).

R. equi infections in sheep are very rare. There have been reports of pneumonia (Roberts, 1957; Addo and Dennis, 1977), abortion (Dennis and Bamford, 1966), and bronchopneumonia.

Host Animals

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Animal nameContextLife stageSystem
Bos grunniens (yaks)Domesticated host
Bos indicus (zebu)Domesticated hostCattle & Buffaloes: All Stages
Bos taurus (cattle)Domesticated host
Bubalus bubalis (Asian water buffalo)Domesticated hostCattle & Buffaloes: All Stages
Capra hircus (goats)Domesticated hostSheep & Goats: All Stages
Equus caballus (horses)Domesticated hostOther: Juvenile
Lama glama (llamas)Domesticated host, Wild host
Ovis aries (sheep)Domesticated hostSheep & Goats: All Stages
Sus scrofa (pigs)Domesticated hostPigs: All Stages
wild boarWild host

Hosts/Species Affected

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R. equi infections are common in foals, but adult horses develop resistance, and rarely show clinical signs of infection (Barton and Hughes, 1980). Infections have been reported sporadically in other species including pigs, cattle, sheep, goats, cats, humans, crocodilians, koalas, buffalo (Barton and Hughes, 1980), dogs (Cantor et al., 1998) and llamas (Hong and Donahue, 1995). Young animals and those with an immunological deficiency seem to be particularly vulnerable to infection (Barton and Hughes, 1980).

Species-specific tropism of R. equi for horses, pigs and cattle appears to be determined by host-adapted virulence plasmid types (Vázquez-Boland et al., 2013).

Systems Affected

Top of page blood and circulatory system diseases of large ruminants
blood and circulatory system diseases of pigs
blood and circulatory system diseases of small ruminants
digestive diseases of large ruminants
digestive diseases of pigs
digestive diseases of small ruminants
mammary gland diseases of large ruminants
multisystemic diseases of large ruminants
multisystemic diseases of pigs
multisystemic diseases of small ruminants
respiratory diseases of large ruminants
respiratory diseases of pigs
respiratory diseases of small ruminants


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In its principal host, the foal, R. equi causes disease on a worldwide basis. Infections in foals are usually sporadic, but the disease is endemic on some farms (Barton and Hughes, 1980). In other animals, such as pigs, cattle, sheep and goats, clinical disease is rare but widespread.

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


IndiaPresentRahman and Baxi, 1983a; Rahman and Baxi, 1983b; Moitra, 1972; Rao et al., 1982; Wani et al., 2003
-HaryanaPresentGarg and Kapoor, 1986
-Uttar PradeshPresentNatarajan and Nilakantan, 1974; Singh, 1982
JapanPresentTakai and Tsubaki, 1985; Takai et al., 1996; Fukunaga et al., 1999; Sakai et al., 2012
ThailandPresentPoolkhet et al., 2010


BotswanaPresentDiteko et al., 1988
KenyaPresentNeave, 1951
NigeriaPresentAddo and Dennis, 1977
South AfricaPresentKabongo et al., 2005
-Canary IslandsPresentRodriguez et al., 2000

North America

CanadaPresentPresent based on regional distribution.
-OntarioPresentPrescott and Zubaidy, 1979; Tkachuk-Saad et al., 1998
USAPresentFeldman et al., 1940; Karlson et al., 1940; Karlson and Thoen, 1971
-MichiganPresentFitzgerald et al., 1994; Davis et al., 1999
-TexasPresentWhitford and Jones, 1974

Central America and Caribbean

Trinidad and TobagoPresentOjo et al., 1993

South America

BrazilPresentRibeiro et al., 2011
-CearaPresentAlmeida et al., 1986
-Rio Grande do SulPresentOliveira et al., 1995


Czech RepublicPresentDvorská et al., 1999
DenmarkPresentBendixen and Jepsen, 1938
FrancePresentGuerrault et al., 1984
GermanyPresentSoedarmanto et al., 1997
HungaryPresentMakrai et al., 2005; Makrai et al., 2008
IrelandPresentFlynn et al., 2001
NetherlandsPresentMoraal et al., 1990
NorwayPresentHolth and Amundsen, 1936
Russian FederationLazovskaya et al., 2010
SloveniaPresentOcepek and Zdovc, 2000; Pate et al., 2004
SpainPresentPresent based on regional distribution.
SwedenPresentMagnusson, 1940; Thal and Rutqvist, 1959
UKPresentCraig and Davis, 1940; Roberts and Hamilton, 1968; Jeckel et al., 2011


AustraliaPresentRoberts, 1957; Dennis and Bamford, 1966; Woolcock and Rudduck, 1973
-New South WalesPresentCarrigan et al., 1988
-QueenslandPresentMcKenzie and Donald, 1979; Mutimer and Woolcock, 1980; Rogers et al., 1980
-Western AustraliaPresentLloyd and Peet, 1979


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The lesions of R. equi infection are abscesses and granulomas. In cattle, R. equi sometimes occurs in localized lesions that cannot be easily differentiated from tuberculous processes either macroscopically or histologically (McKenzie and Donald, 1979; Rogers et al., 1980). Granulomata resembling tuberculosis have been seen in mesenteric lymph nodes; typically these lesions take the form of coagulation necrosis surrounded by a mixed cellular reaction of plasma cells, fibroblasts, macrophages, epithelioid cells, neutrophils and eosinophils with the occasional Langhans-type giant cell (Woolcock and Rudduck, 1973; McKenzie and Donald, 1979). There is usually mineralization. Flynn et al. (2001) detected lymph node lesions in 6719 cattle, from a total of 3.3 million examined postmortem in abattoirs in the Irish Republic. A total of 1122 of the lesions were cultured for R. equi because the histological findings were difficult to interpret or were suggestive of R. equi infection. R. equi was isolated from 264 lesions, giving a prevalence of 0.008% in the 3.3 million cattle examined. Almost all of the R. equi granulomas were confined to a single lymph node, and were present predominantly in the retropharyngeal, bronchial and mediastinal lymph nodes.

Similarly in pigs, it is not possible to differentiate the gross lesions of R. equi-induced lymphadenitis from those caused by Mycobacterium spp. (Dvorská et al. 1999; Ocepek and Zdovc, 2000). Affected submandibular and cervical nodes are enlarged, containing multiple yellow-tan foci, often in a subcapsular location. Caseation and calcification of these foci sometimes occur (Taylor, 1999).

In goats, postmortem examinations have revealed granulomatous or caseous abscesses in the liver, lungs, lymph nodes and spleen (Whitford and Jones, 1974; Carrigan et al., 1988; Tkachuk-Saad et al., 1998; Davis et al., 1999;). Pulmonary oedema, purulent pneumonia and fibrionopurulent pleuritis have also been recorded (Whitford and Jones, 1974). Carrigan et al. (1988) found osteomyelitis during postmortem examination of an R. equi-infected goat.

In sheep, infection with R. equi has been associated with purulent pneumonia and pleurisy with abscesses in the bronchial lymph glands (Roberts, 1957).


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Clinical signs of R. equi infection are rare in animals other than horses and diagnosis is usually at postmortem. Gross lesions of R. equi-induced lymphadenitis and those caused by Mycobacterium spp. are very similar (McKenzie and Donald, 1979; Dürrling, 1991; Dvorská et al., 1999). Definitive diagnosis cannot be made on histopathological examination alone, but heavy neutrophil infiltration of necrotic areas is sometimes a distinguishing feature (McKenzie and Donald, 1979). Clumps of intracellular cocci may be detected in the histology slice, but ultimately the diagnosis must be made on bacteriological culture of the fresh material. In sheep and goats, abscesses may be indistinguishable from lesions due to Corynebacterium pseudotuberculosis (Addo and Dennis, 1977).

Isolation of R. equi from clinical samples is easily achieved by aerobic culture on routine media at 37°C, although optimum temperature is 28-30°C. R. equi is identifiable after 2 days of culture. Selective media, such as that developed by Woolcock et al. (1979) are required for faecal isolation.

In foals, a combination of tracheal aspiration and bacterial isolation is the most valuable method for routine diagnosis of R. equi pneumonia. Radiography, serodiagnosis and faecal culture were shown to be valuable, but limited, diagnostic methods (Anzai et al., 1997). PCR tests are being developed for rapid diagnosis of R. equi infection and for use in epidemiological studies (Sellon et al. 1997; Sellon et al. 2001).

The majority of R. equi infections occur in young animals with immature immune responses. In horses, animals older than 6 months show signs of immunizing exposures to R. equi and are relatively resistant (Barton and Hughes, 1980). Humoral and cellular components of the immune system are involved in the clearance of R. equi (Hines et al., 1997). Both appear to be involved in enabling macrophages to kill infecting organisms. The rarity of reports in species other than horses suggests that most animals are resistant to infection unless predisposed by some immunosuppressive factor such as stress, illness or iatrogenic drug immunosuppression, as has been noted in humans receiving immunosuppressive therapy (Berg et al., 1977).

List of Symptoms/Signs

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SignLife StagesType
Digestive Signs / Diarrhoea Sheep & Goats:All Stages Sign
General Signs / Fever, pyrexia, hyperthermia Pigs:All Stages Sign
General Signs / Head, face, ears, jaw, nose, nasal, swelling, mass Pigs:Piglet Sign
General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes Cattle & Buffaloes:All Stages,Pigs:All Stages,Sheep & Goats:All Stages Sign
General Signs / Neck swelling, mass cervical region Pigs:Piglet Sign
General Signs / Sudden death, found dead Sheep & Goats:All Stages Sign
General Signs / Weight loss Pigs:All Stages,Sheep & Goats:All Stages Sign
Reproductive Signs / Mastitis, abnormal milk Cattle & Buffaloes:Cow Sign
Respiratory Signs / Purulent nasal discharge Sheep & Goats:All Stages Sign

Disease Course

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R. equi enters the host by ingestion or inhalation and is spread via the bloodstream. In foals, infection leads to severe, suppurative bronchopneumonia with suppurative lymphadenitis of regional nodes and, in approximately 50% of animals, to necrotizing enterocolitis (Yager, 1987). Infections can be subacute, with foals dying within days of showing respiratory distress, or chronic, with pneumonia and unthriftiness progressing for weeks (Ellenberger and Genetzky, 1986).

In cattle and pigs, the primary targets of R. equi are the lymphoid organs, and the organism has been associated with lymphadenitis (Katsumi et al., 1991; Soedarmanto et al., 1997; Flynn et al., 2001). Lymphadenitis causes no significant clinical signs. R. equi can also be isolated from normal lymph nodes (Mutimer and Woolcock, 1980; Takai et al., 1986b; Katsumi et al., 1991; Madarame et al., 1998; Flynn et al., 2001) and its pathogenic role in pigs has been questioned (Madarame et al., 1998). After exposure of piglets to an aerosol of 107R. equi for seven consecutive days, the only clinical evidence of disease was elevated temperature (Zink and Yager, 1987). Intravenous and intramuscular inoculation of pigs produced no clinical signs other than transient fever and weight loss (Madarame et al., 1998). However, an acute outbreak of R. equi infection, resulting in oedematous swelling of the face, snout and neck has been reported in piglets (Rao et al. 1982).

R. equi is emerging as a relatively common cause of disseminated abscesses in goats (Guerrault et al., 1984; Diteko et al., 1988; Moraal et al., 1990; Ojo et al., 1993; Tkachuk-Saad et al., 1998; Davis et al., 1999) and infection may be fatal in some cases (Fitzgerald et al. 1994). Clinical signs reported by Carrigan et al. (1988) include lethargy, abdominal pain, and green watery diarrhoea. R. equi was reported by Roberts (1957) as the cause of purulent pneumonia and pleurisy with abscesses in the bronchial lymph glands of a sheep from Western Australia. The flock had about 0.5% deaths each year from a wasting disease characterized by nasal discharge. R. equi has also been associated with abortion (Dennis and Bamford, 1966) and bronchopneumonia (Addo and Dennis, 1977), but reports are very rare.

R. equi is a facultative intracellular bacterium and its ability to persist in macrophages forms the core of its pathogenesis (Hondalus, 1997). Its ability to replicate within the macrophage correlates with the possession of a large plasmid and expression of plasmid-encoded virulence associated proteins (Vap). Isolates of R. equi from pneumonic foals typically contain large, 85 or 90 kb plasmids encoding virulence-associated protein A (VapA), a highly immunogenic 15-17 kDa surface lipoprotein. Giguere et al. (1999) showed that the 85 kb plasmid of R. equi is essential for intracellular replication within mouse macrophages and for development of disease in the foal. R. equi strains of intermediate virulence for mice possess a 20 kDa protein designated virulence associated protein B (VapB) and a virulence plasmid of 79-100 kb, and can be recovered from the submaxillary lymph nodes of pigs (Takai et al., 1996; Fukunaga et al., 1999) and the environment of pig farms (Fukunaga et al., 1999). Takai et al. (2000) showed that R. equi strains possessing VapB are less virulent in foals than strains possessing VapA. In a study of R. equi isolates from the lymph nodes of cattle, the 15-17 and 20 kDa antigens, associated with virulence and intermediate virulence, respectively, were not detected (Flynn et al., 2001). In addition to the virulence associated proteins, the pathogenesis of R. equi infection is also thought to involve the granulomagenic activity related to lipids and cell wall structures (Takai et al., 1995).


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R. equi is a soil organism that is ingested by many herbivores and is widespread in their environment (Barton and Hughes, 1980; Takai and Tsubaki, 1985; Prescott, 1991). It has been isolated from the faeces of cattle, goats, horses, pigs, poultry and sheep (Carman and Hodges, 1987). Environmental distribution of R. equi favours soils enriched with herbivore manure (Barton and Hughes, 1984; Prescott, 1991). Simple organic acids in faeces of herbivores, especially acetate and propionate, appear to be important for supporting its growth (Hughes and Sulaiman, 1987). The organism is robust and can survive in soil for at least a year and withstand drying and direct sunlight (Ellenberger and Genetzky, 1986). It multiplies progressively as temperatures rise (Prescott, 1987).

Compared with horses, little is known of the epidemiology of natural R. equi infections in livestock. R. equi infection is likely to be acquired from the environment (Woolcock et al., 1980). The normal mode of exposure in foals is ingestion (Takai et al., 1986a) and a similar situation probably occurs in other animals. Although R. equi may reach the lungs of foals after intestinal infection, pneumonic disease is usually the result of direct respiratory infection (Prescott et al., 1980). Aerosol infection via dust of paddocks is a major route of foal infections (Benoit et al., 2000). Foals are also an important source of airborne virulent R. equi as they breathe off high concentrations in exhaled air (Muscatello et al., 2007).

Pigs are extremely resistant to experimental infection. Early studies suggested that pigs are resistant to R. equi given by the oral and nasal routes (Cotchin, 1943; Thal and Rutqvist, 1959), although the organism has been recovered from the cervical and submaxillary lymph nodes of inoculated pigs (Karlson et al., 1940). Cotchin (1943) found that pigs are resistant to intravenous inoculation with R. equi, whereas Thal and Rutqvist (1959) produced local abscesses with regional lymphadenitis after subcutaneous injection of the bacterium. Zink and Yager (1987) showed that R. equi is cleared very slowly from the lungs of pigs after aerosol exposure, but clinical signs and pathological lesions of pneumonia were minimal despite exposure to 107 organisms on 7 consecutive days. Pneumonia has, however, been introduced by intratracheal inoculation of fluid inocula (Thal and Rutqvist, 1959).

There are very few reports of experimental infections in other species. Sheep and cattle have been shown to be refractory to experimental infection (Rajagopalan and Gopalikrishnan, 1938). McKenzie et al. (1981) produced granulomas at the sites of inoculation in cattle inoculated intratracheally, subcutaneously and into a prescapular lymph node, but no lung infections were produced. Magnusson (1923) produced a small local abscess in a goat by subcutaneous inoculation.

Impact: Economic

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The economic losses due to R. equi infections in pigs, cattle, sheep and goats are insignificant due to the rarity of clinical disease. Some losses may accrue from condemnation at slaughter, but there are no studies that indicate the extent of this loss.

Zoonoses and Food Safety

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The first report of lesions in man associated with R. equi was by Golub et al. (1967), although there are some indications that it had been isolated previously (Barton and Hughes, 1980). Recently, R. equi has emerged as an important pulmonary pathogen among immunosuppressed patients, especially those with human immunodeficiency virus (HIV) infection (Harvey and Sunstrum, 1991; Lasky et al., 1991; Prescott, 1991; Drancourt et al., 1992; Gradon et al., 1992). The route of infection in human cases remains obscure (Takai et al., 1996). Contact with farm animals and manure has been reported in some of the human cases (Drancourt et al., 1992; Harvey and Sunstrum, 1991; Lasky et al., 1991). Others may have acquired infection from contact with soil or wild bird manure (Prescott, 1991). Takai et al. (1996) found two plasmids in pig isolates that were the same size as those in human isolates. They speculate that some human cases may be of porcine origin.

Disease Treatment

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R. equi infections are rarely diagnosed antemortem. In foals, therapy requires long-term administration of antibiotics. This is usually not feasible for livestock on economic grounds. Rifampin in combination with erythromycin is effective in the treatment of foals. These expensive drugs can be given orally. They penetrate the phagocytic cells where R. equi are found, and are not toxic when used over prolonged periods. Most R. equi isolates are susceptible to rifampin and erythromycin, but some resistance has been reported (Kenney et al., 1994; Takai et al., 1997).

Prevention and Control

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There are few incentives to institute control measures in species other than horses. Vaccines have been developed for horses (Becu et al., 1997), but their use in other species is not warranted. Even in horses the sporadic nature of the disease in most situations makes the usefulness of vaccines doubtful (Barton and Hughes, 1980). Administration of hyperimmune plasma to foals has been shown to be useful for prevention of R. equi infections on endemic farms (Becu et al., 1997; Higuchi et al., 1999). As the growth of R. equi is promoted in herbivore faeces, sanitary measures aimed at reducing focal areas of faecal contamination in the environment should lessen the risk for R. equi infection (Hughes and Sulaiman, 1987).


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