Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide


eperythrozoonosis in pigs



eperythrozoonosis in pigs


  • Last modified
  • 03 January 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • eperythrozoonosis in pigs
  • Overview
  • Eperythrozoonosis is a sub-acute or chronic disease of pigs. The name 'eperythrozoon' is derived from the Greek prefix epi- meaning on; the Greek adjective erythrus meaning red and the Greek noun ...

  • 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

Preferred Scientific Name

  • eperythrozoonosis in pigs

International Common Names

  • English: eperythrozoonosis, eperythrozoon suis, in swine


Top of page

Eperythrozoonosis is a sub-acute or chronic disease of pigs. The name 'eperythrozoon' is derived from the Greek prefix epi- meaning on; the Greek adjective erythrus meaning red and the Greek noun zoon meaning animal.

From 1932 a disease of swine characterised by ictero-anaemia was reported in the USA (Kinsley, 1932; Doyle, 1932). Early reports referred to the possibility that this disease was associated with a protozoal infection or was a Ricketsia-like or Anaplasmosis-like disease.

The aetiological agent was reported to be Eperythrozoon suis by Splitter and Williamson (1950). Splitter (1950a) also described Eperythrozoon parvum which he reported to be non-pathogenic in pigs. E. suis has now been reclassified as Mycoplasma suis (Anon, 2002). According to Zachary and Basgall (1985) and Liebich and Heinritzi (1992), it is likely that Mycoplasma (Eperythrozoon) suis and E. parvum are in fact simply different forms of one organism. This supposition is supported by the fact that there have been no reports of E. parvum infection in recent years.

While most natural infection with M. suis is subclinical, several disease syndromes associated with M. suis infection in pigs are now well recognised and it is now considered that porcine eperythrozoonosis (PE) causes economic loss (Hoelzle, 2008; Ritzmann et al., 2009). M. suis infection in pigs has long been associated with the production of cold auto-agglutinins and extra-vascular haemolysis (Zachary and Basgall, 1985) but recent research has now shown that warm auto-agglutinins are also involved (Felder et al., 2010) and that the immunopathology of PE is still yet to be fully understood (Hoelzle, 2008).

In pigs in which the haemolysis becomes de-compensated, anaemia and sometimes jaundice occur.  M. suis also metabolises glucose and heavy infection may cause hypoglycaemia (Smith et al., 1990). Predisposing factors in outbreaks of M. suis infection are unclear although this is influenced by the virulence of the strain of M. suis, the susceptibility of the pigs and their immunocompetence and there is also evidence that certain virus infections may predispose to the development of clinical disease (Vide infra). Splenectomy is reported to induce clinical disease in infected pigs and infection of splenectomised pigs also causes PE (Splitter 1950b). Use of immunosuppressive drugs is also reported to cause disease in infected pigs and such treatment of pigs affected with chronic PE will increase the number of bacteria present in the blood stream (Yuan et al., 2007). Routine diagnosis of M. suis infection was initially limited to direct microscopy on blood smears but infection can now be detected using gene-based techniques such as polymerase chain reaction (PCR) and serology. The diagnosis of clinical disease (PE) associated with M. suis infection is however still problematical and treatment and control is not simple. M. suis is still reported to be unculturable. Commercially available vaccines have not yet been produced.

Possible Eperythrozoon infection in humans has been reported since 1929 (Schuffner, 1929) but it remains unclear if M. suis is a zoonosis.

Hosts/Species Affected

Top of page

Infection with M. suis and eperythrozoonosis associated with M. suis infection have been reported in domesticated pigs and infection has also been reported in wild pigs (Hoelzle et al., 2010). It is likely that this also occurs in feral pigs. Mice are also susceptible to experimental infection with M. suis (Yu et al., 2008) as are rats (Gong et al., 2010) but it is not clear if this also occurs naturally nor if M. suis infection can be maintained in mice, rats or other rodents. Bacteria with a similar morphology to haemotrophic mycoplasmas have also been reported in humans for many years (the first report being in 1929 (Schuffner, 1929)). M. suis infection has also been reported in humans on the basis of PCR (Yuan et al., 2009) although the authors comment that additional research is needed to assess the possibility of interspecies transmission.

The lack of diagnosed infection and disease in feral pigs and wild boar may be, in part at least, due to problems of collecting blood samples from feral pigs and wild boar and also due to difficulties of studying disease in these animals.


Top of page

Porcine eperythrozoonosis (PE) is not reportable to the World Organisation for Animal Health (OIE). Until recent years, reports of M. suis infection of swine were solely based on the detection of forms consistent with M. suis in stained blood smears by light microscopy which is not straightforward. However, gene-based tests and serological tests for M. suis infection are now becoming more widely available and as a result M. suis infection is now increasingly reported from countries around the world although infection is still not reported from some major pig producing countries.

In many countries where M. suis infection is recognised, the incidence and prevalence of M. suis infection and PE are unknown but where serology is available the detected herd prevalence is often at least 20-40%.

In Great Britain (GB), direct microscopy on samples from 47/178 herds indicated 26.4% herd prevalence (Gresham, 1998). Sero-surveillance in the USA using indirect haemagglutination assay (IHA) indicated wide (16-40 percent) herd prevalence (Gwaltney, 1995).  Grimm et al. (2008) reported that M. suis infection was detected by PCR in 33.3-48% of herds in different parts of Germany and that the within herd prevalence ranged from 25-46.2% with an average of 34.2%. Wu et al. (2006) reported that PE is now present in all Chinese provinces except Tibet.

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


ChinaPresentMa et al., 2003; Wu et al., 2006
-GansuPresentXin et al., 1995
-LiaoningPresentBa et al., 2009
-ShaanxiPresentChang and Wang, 2000
Korea, DPRPresentJeon, 1971
TaiwanPresentHsu et al., 1992
ThailandPresentVayuchote et al., 1991


GhanaPresentPermin et al., 1999
KenyaPresentBarnett, 1963
NigeriaPresentDipeolu et al., 1982
South AfricaPresentJANSEN, 1952

North America

CanadaPresentPresent based on regional distribution.
-AlbertaPresentAyroud, 1994
-OntarioPresentWilson et al., 1988
-QuebecPresentBeaudin et al., 2000
MexicoPresentTalavera Santos, 1977
USAPresentPresent based on regional distribution.
-AlabamaPresentAdams et al., 1959
-CaliforniaPresentSplitter, 1950b
-GeorgiaPresentSplitter, 1950b
-IllinoisPresentSplitter, 1950b; Kinsley, 1932
-IndianaPresentSplitter, 1950b; DOYLE, 1932
-IowaPresentSplitter, 1950b; KINSLEY and RAY, 1934
-KansasPresentSplitter, 1950b; DICKE, 1934
-MissouriPresentSplitter, 1950b; KINSLEY and RAY, 1934
-NebraskaPresentSplitter, 1950b
-New YorkPresentBIBERSTEIN et al., 1956
-North DakotaPresentSplitter, 1950b
-OhioPresentSplitter, 1950b
-South DakotaPresentSplitter, 1950b; KINSLEY and RAY, 1934
-WisconsinPresentSplitter, 1950b

Central America and Caribbean

CubaPresentCruz et al., 1985

South America

ArgentinaPresentMachuca et al., 1999
BrazilPresentLopes et al., 1982
-Minas GeraisPresentBoretti et al., 1987


AustriaPresentReigler, 1990
BelgiumPresentBusser et al., 2008
CroatiaPresentModric et al., 1987
DenmarkPresentMadsen, 1986
FrancePresentSolignac et al., 1996
GermanyPresentKorn and Mussgay, 1968
HungaryPresentKántás and Andó, 1987
ItalyPresentVezzoli et al., 2003
NetherlandsPresentUilenberg et al., 1981
PolandPresentPejsak, 1995
PortugalPresentPerestrelo-Vieira et al., 1997
SerbiaPresentPotkonjak et al., 2009
SwitzerlandPresentHeinritzi et al., 1990
UKPresentJENNINGS and SEAMER, 1956; Gresham et al., 1994


Top of page


The pathogenesis of porcine eperythrozoonosis is still incompletely understood but this is now improving with use of genetic techniques such as PCR.  Until recently, it was considered that M. suis simply causes disease by alteration of the erythrocyte membrane leading to the production of cold auto-agglutinins which are antibodies of the IgM class usually to determinants on the erythrocyte membrane (Zachary and Basgall, 1985); according to Hoffmann et al. (1981), the (pathological) process in porcine eperythrozoonosis should be classified as an acquired auto-immune haemolytic anaemia due to ‘cold’ antibodies. With developments in laboratory techniques it is however now considered that immunoglobulin G class antibodies are also involved (Felder et al., 2010).

Hoelzle (2008) has provided an eloquent review on recent advances in M. suis; this includes a review of the immunology and immunopathology of M. suis infection although it is apparent that this has still yet to be fully understood.

In respect of the pathology of PE it is however important to note that cold auto-agglutinins cause agglutination of erythrocytes which are removed by erythrocyte phagocytosis and destruction by the mononuclear phagocyte system in the liver, spleen and bone marrow. In addition erythrocyte agglutination leading to obstruction to blood flow may, in part, be a cause for cyanosis of the extremities as occurs in some cases of PE and this may be seen for example as cyanosis and necrosis of the margins of the ears.

The process of extravascular haemolysis occurs in the majority of haemolytic anaemias in animals and humans. This is in contrast to ‘intravascular’ haemolysis where red cell lysis occurs within the vascular tree. Pospichil and Hoffmann (1982) reported that ‘intravascular’ haemolysis was not a feature of pigs experimentally infected with M. suis

Felder et al. (2011) have also reported that eryptosis (programmed cell death of erythrocytes characterised by cell shrinkage, micro-vesiculation and phosphatidylserine exposure on the outer membrane) also has a role in the pathogenesis of anaemia caused by M. suis and other haemotrophic mycoplasmas.

Anaemia occurs if haemolysis is decompensated in pigs infected with M. suis. This is common in acutely affected pigs. Jaundice may occur if haemolysis is severe and this is due to an elevated plasma concentration of unconjugated bilirubin and total bilirubin. In experimental PE, hypoglycaemia may be detected reflecting the consumption of glucose by eperythrozoa (Smith et al., 1990) and lactacidosis also occurs due to impaired pulmonary gaseous exchange (Heintritzi et al., 1990). In naturally occurring PE, anorexia and loss of bodyweight is common; while hypoglycaemia does occur in some cases of PE, and while this is common in severely affected pigs (Gwaltney and Oberst, 1994), hypoglycaemia alone is not a useful indicator of the disease process and this may also just reflect reduced feed intake.

M. suis suppresses T-lymphocyte function (Zachary and Smith, 1985) which leads to increased susceptibility to bacterial infections which commonly occur in the respiratory and alimentary tracts (Gwaltney, 1995).

If death does not occur following infection with M. suis, growth depression and reduced reproductive performance (see clinical signs) may be observed (Hoelzle, 2008). Mortality may be increased where secondary infections occur.


The macroscopic and microscopic pathological features of uncomplicated acute disease reflect the anaemia and erythrocyte agglutination that occur in affected pigs. According to Smith (1992) the severity of anaemia may vary with the degree of bacteraemia, the virulence of the organism and the physical and nutritional status of the pig. Anaemia and serous effusions in the body cavities are commonly identified. The blood is thin and watery and, as in normal pigs, clots rapidly on exposure to air. In pigs affected with eperythrozoonosis, blood collected into tubes containing anti-coagulant will show fine-grained microagglutination when the sample is cooled. This microagglutination reduces significantly when the blood sample is warmed to 37°C. According to Heinritzi (1999) this is specific for eperythrozoonosis. Jaundice is not uncommon and may be severe but is an inconsistent finding. The carcase musculature including the heart is pale and in more chronic cases the heart may appear dilated and thin walled. The liver is often yellow-brown in colour and is sometimes enlarged. The bile is strongly coloured. Splenomegaly is an occasional finding. The lymph nodes generally may be enlarged and oedematous.

Chronic disease is often complicated by secondary bacterial infections, however such pigs are usually ill-thriven and severe anaemia may be present. According to Spencer (1940), the histopathological features of uncomplicated PE are splenic reticuloendothelial hyperplasia and haemosiderosis and hepatic congestion, centrilobular degeneration, haemosiderosis and mononuclear cell infiltration of the portal tracts. Bone marrow erythropoietic activity is increased (Hoffman et al., 1981).


Top of page

Clinical signs

Natural infection of pigs with M. suis is usually clinically inapparent and ictero-anaemia, which is characteristic of PE, is an inconsistent finding. The clinical syndromes that have been associated with M. suis infection are very variable both in terms of morbidity and mortality and all ages of pigs may be affected. Acute and chronic disease syndromes have been reported in association with M. suis infection.

The major acute presentation is ictero-anaemia in weaned and growing swine.  Morbidity and mortality are variable but may reach 60 percent and 90 percent respectively in affected pigs. 

Clinical signs in acutely affected pigs occur at about 7 days (range 3-20 days) post-infection and include lethargy, mild pyrexia (41-42°C), anorexia and ictero-anaemia. Jaundice and anaemia may be difficult to detect clinically and jaundice is not a constant finding. Generalised pallor and also pallor of the mucous membranes can occur but this can be difficult to assess in pigs in poorly lit buildings. Jaundice is often more clearly identified in natural rather than artificial light. Cyanosis of the extremities (especially the ears) may occur.  Necrosis of the margins of the ears occurs if disease is prolonged. Clinically apparent anaemia is usually severe and death often occurs within several days in affected pigs.

Sub-acute and more chronically affected pigs exhibit mild pyrexia and slight reduction in appetite. Anaemia is rarely clinically apparent in these pigs and mortality from uncomplicated chronic disease is low although secondary bacterial infections of the respiratory and alimentary tracts may complicate the clinical presentation in affected pigs. 

Chronic M. suis infection has also been associated with various disease syndromes (Henry, 1979; Gwaltney, 1995). These syndromes have all been diagnosed by association of the presence of the organism with the appropriate clinical disease: 


  1. Increased susceptibility to bacterial infections of the enteric and respiratory systems.
  2. Ill-thrift and reduced tolerance to stress.
  3. Chronic low-grade anaemia.
  4. Poor growth rate in growing and finishing pigs.
  5. Reproductive failure - delayed and irregular oestrus, early embryonic death, abortions and stillbirths.
  6. Reduced birth weight, anaemia, weakness and stillbirth in newborn pigs.

M. suis infection may be associated with outbreaks of the mastitis, metritis and agalactia (MMA) syndrome. Hoelzle (2008) reported clinical signs in some sows after farrowing.  Clinical signs have also been reported in sows at weaning and this may also affect conception rates (Messick, 2004). 

In these presentations morbidity is variable but may be high. Piglet mortality may be more than 50 percent in affected piglets. 


Differential diagnosis

The prime differential diagnosis of ictero-anaemia in pigs is leptospirosis and in countries where Leptospira pomona is present, this infection is the most likely alternative aetiology. The diagnosis of jaundice in pigs includes possible haemolytic, hepatogenous and obstructive causes. Haemolytic and haematogenous jaundice occurs in porcine leptospirosis. Hepatogenous jaundice is not common in pigs, but this is an inconsistent finding in outbreaks of post weaning multi-systemic wasting syndrome and this may also occur as a result of toxicity due to materials such as phenolic compounds. Obstructive jaundice is an uncommon finding in pigs and may occur for example due to heavy infestation with Ascaris suum.

The differential diagnosis of anaemia in pigs includes possible dys-haemopoietic, haemolytic or haemorrhagic causes. Without iron supplementation, dys-haemopoietic anaemia due to iron deficiency is common in piglets reared indoors. Copper deficiency may also lead to dys-haemopoietic anaemia particularly where a dietary excess of other divalent cations such as zinc is present. In major pig-producing countries in temperate climates, leptospirosis is a common cause of haemolytic anaemia. Blood loss or haemorrhagic anaemia in pigs commonly occurs due to lesions of the gastrointestinal tract and may be due to gastric ulceration, Hyostrongylus rubidus infestation, ileal haemorrhage associated with Lawsonia intracellularis infection or dysentery associated with Brachyspira hyodysenteriae infection.

In the live pig, the differentiation of these different types of jaundice and anaemia can be achieved by the laboratory examination of blood samples. In pig herds, this is best achieved by the clinical and pathological examination of a number of pigs; this should include haematological and biochemical tests to enable characterisation of the anaemia and jaundice present.

There are many differential diagnoses for chronic PE. The prime differential diagnoses will be limited by the main presenting sign. The reader is referred to standard texts for further information.

A diagnosis of acute or chronic PE requires a detailed investigation which should include an accurate history and the collection of clinical, pathological, haematological and biochemical data from the herd. Where available, specific direct tests and serological examinations for M. suis should be carried out to prove the presence of M. suis infection in the herd and particularly in the affected pigs.

It is important to note that M. suis infection is common and is often subclinical, and also that many of the disease syndromes that have been associated with M. suis infection have also been reported to occur with alternative infectious and non-infectious causes. It is therefore important to establish an accurate diagnosis of PE before controls for M. suis infection are put in place.


Laboratory diagnosis (pathogen detection, isolation and serology)

The laboratory diagnosis of PE is problematical and cannot be based solely on the detection of M. suis infection. Subclinical infection is common (Splitter and Williamson, 1950) and none of the recognised clinical presentations are pathognomonic.

Only in acute post-weaning disease are the clinical and gross pathological changes of ictero-anaemia combined with a pathological finding of splenomegaly relatively specific.  Nonetheless, in outbreaks of both acute and chronic disease, haematological tests, bilirubin estimation, direct tests for M. suis and serology can be useful aids to diagnosis.

According to Heinritzi (1999) a significant reduction of fine-grained microagglutination when a cooled anti-coagulated blood sample is warmed to 37°C is specific for eperythrozoonosis.

Similarly to other haemotrophic mycoplasmas, M. suis has not been cultivated in vitro. Nonaka et al (1996) reported that M. suis can be maintained in vitro for up to 72 hours and mouse models have been described. These procedures are not of significant benefit in the routine diagnosis of porcine eperythrozoonosis but may be of use in the development of diagnostic tests and the evaluation of therapeutic compounds.

M. suis can be detected in stained blood smears (for example using Romanowsky type stains) and using acridine-orange stain and fluorescence microscopy (Krier and Gothe, 1976). Various forms may be seen including dots or cocci, rods or bacilli, discs and rings.  It is only the ring-form which is characteristic.  While fluorescence microscopy enables easier differentiation of M. suis from background staining, this method too is not specific for M. suis as other nuclear material from the pig is also stained.

Identifying M. suis in blood films/smears is not straightforward. To detect M. suis it is important that blood films are correctly stained. If the blood film is too lightly stained or if the pH of the solutions used is incorrect, M. suis infection may not be identified (Splitter, 1950b). In addition, M. suis is extremely delicate and quickly deteriorates when removed from the host. This occurs as rapidly as 15-30 minutes after sampling. According to Nonaka et al. (1996) eperythrozoa deteriorate faster in the presence of ethylene-diamine tetra-acetic acid (EDTA) as compared to lithium-heparin anticoagulant. The early stage of this deterioration is shrinkage of the ring form into a coccoid structure. It is impossible to reliably distinguish these structures from artefacts such as stain deposit and some nuclear remnants such as Howell-Jolly bodies. In these cases, the diagnosis may easily be missed. According to Gwaltney, (1995) in cases where M. suis is present on less than 50% of the erythrocytes in a blood smear, the diagnosis is often overlooked.

To reduce the deterioration of M. suis, and erythrocyte agglutination due to cooling of the sample, the blood smears/films should be prepared immediately from freshly collected samples of blood and using slides warmed to blood heat. These samples should preferably be taken from peripheral rather than central blood samples; a drop of blood taken from an ear vein is suitable. The use of anticoagulants in the preparation of these smears should be avoided. If an anticoagulant has to be used, lithium-heparin is that of choice. The blood films should be air-dried and fixed in absolute methanol straight-away unless they are to be stained immediately.

Very few, if any, organisms should be found in smears from normal pigs and if the animal is clinically and otherwise haematologically normal, any M. suis found is likely to represent sub-clinical infection.

According to Splitter (1950b), in experimentally infected splenectomised pigs, peak bacteraemia occurs at about 7-14 days post infection and at this time, all the erythrocytes in a blood smear may be found to be infected with one or more M. suis. Peak bacteraemia occurs before anaemia is clinically detectable. The level of bacteraemia then declines rapidly and at four weeks post-infection, less than 5-10 percent of erythrocytes may be found to be infected with M. suis.

It is very difficult to identify M. suis in blood smears from pigs which have been treated with tetracycline antibiotics. Tetracyclines are now widely used in pigs for the treatment and control of various infections in pigs; particularly those affecting the reproductive and respiratory systems. As such this may mask the diagnosis of M. suis infection.

Although clinically apparent anaemia and jaundice is often not present until at least three to four weeks post-infection, anaemia is detectable on the basis of haematological tests from about seven days post-infection (Splitter, 1950b). Haemoglobin, erythrocyte counts and haematocrit fall significantly for about seven days. Splitter reported that haemoglobin concentrations declined to 2-4g/dl, erythrocyte counts reached 1 - 2 x106 / ml3 and packed cell volume was 4-7%. In splenectomised pigs recurrent bouts of infection and anaemia occurred. Splitter also reported that in experimentally infected pigs, spontaneous agglutination of erythrocytes was commonly observed and an increased erythrocyte sedimentation rate may occur. A marked leucocytosis was observed in some cases.

In naturally infected pigs the anaemia may be very variable but is sometimes severe and may persist for several weeks. While macrocytosis, polychromasia, reticulocytosis, anisocytosis, rouleaux formation, an increased erythrocyte sedimentation rate, thrombocytopenia and leucocytosis may occur, the anaemia is often normocytic and normochromic which is not specific. A macrocytic hypochromic anaemia may normally be anticipated with a severe chronic haemolytic process.

In natural eperythrozooosis, secondary bacterial infections which commonly occur in the alimentary and respiratory tracts, often complicate the haematological and biochemical test results.

Jaundice may occur if haemolysis is severe. This is due to an elevated plasma concentration of unconjugated bilirubin and total bilirubin (> 7 µmol/l). Jaundice does not occur in all acutely affected pigs but when this occurs it may be pronounced.  An elevated unconjugated fraction is consistent with a haemolytic cause.

In experimental eperythrozoonosis, hypoglycaemia may be detected reflecting the consumption of glucose by eperythrozoa (Smith et al., 1990). In natural PE, anorexia and loss of bodyweight is common and hypoglycaemia alone is not a useful indicator of the disease process.

Molecular methods (DNA hybridisation and polymerase chain reaction (PCR) based on the detection of the 16s RNA gene of  M. suis have been described for some years (Oberst et al., 1990; Gwaltney et al., 1993a,b;  Oberst et al., 1993; Messick et al., 1999; Hoezle et al., 2003). These tests have been refined and a LightCycler real-time PCR for the quantitative detection of M. suis has been described (Hoelzle et al., 2007a). Ha et al. (2005) have also reported the development of in-situ hybridisation for the detection of M. suis in formalin-fixed paraffin wax-embedded tissues from experimentally infected pigs. These molecular test methods can detect the presence of M. suis at various stages of acute and chronic eperythrozoonosis. While these methods hold promise for overcoming the low sensitivity of diagnosing M. suis infection by light microscopy and serology, they have not yet been developed for routine diagnostic use in many countries.

The serological tests previously described for the detection of M. suis infection include the complement fixation test (CFT) (Splitter, 1958), indirect haemagglutination (IHA) test (Smith and Rahn, 1975), and enzyme-linked immunosorbent assay (ELISA) (Hsu et al., 1992). The IHA is more sensitive than the CFT (Smith and Rahn, 1975), and the ELISA is more sensitive again (Hsu et al., 1992). These tests were all based on using relatively crude and variable antigens of M. suis collected from blood of experimentally infected pigs and were directed at IgM antibodies; as a result these tests proved to be of limited diagnostic value particularly in individual swine.

Hoezle et al. (2006) have however now reported the identification of M. suis specific antigens for use in an ELISA of greater specificity and Hoezle et al. (2007b) have now also reported use of recombinant antigens produced in Escherichia coli for use in an ELISA which they describe as highly specific, sensitive and reliable. The authors report that a positive result in this test can be correlated with haematological changes of clinical and aetiological significance. This holds great promise for wider use and understanding of the significance of M. suis infection and PE.

List of Symptoms/Signs

Top of page
SignLife StagesType
Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate Sign
Cardiovascular Signs / Weak pulse, small pulse Sign
Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed Sign
Digestive Signs / Diarrhoea Sign
General Signs / Ataxia, incoordination, staggering, falling Sign
General Signs / Cyanosis, blue skin or membranes Diagnosis
General Signs / Exercise intolerance, tires easily Sign
General Signs / Fever, pyrexia, hyperthermia Sign
General Signs / Generalized weakness, paresis, paralysis Sign
General Signs / Hypothermia, low temperature Sign
General Signs / Icterus, jaundice Diagnosis
General Signs / Lack of growth or weight gain, retarded, stunted growth Sign
General Signs / Pale mucous membranes or skin, anemia Diagnosis
General Signs / Reluctant to move, refusal to move Sign
General Signs / Trembling, shivering, fasciculations, chilling Sign
General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift Sign
General Signs / Weight loss Sign
Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless Sign
Reproductive Signs / Abnormal length estrus cycle, long, short, irregular interestrus period Sign
Reproductive Signs / Abortion or weak newborns, stillbirth Sign
Reproductive Signs / Agalactia, decreased, absent milk production Sign
Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus Sign
Reproductive Signs / Edema of mammary gland, udder Sign
Reproductive Signs / Female infertility, repeat breeder Sign
Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs Sign
Respiratory Signs / Coughing, coughs Sign
Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping Sign
Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea Sign
Skin / Integumentary Signs / Cold skin, cool ears, extremities Sign
Skin / Integumentary Signs / Rough hair coat, dull, standing on end Sign
Skin / Integumentary Signs / Skin edema Sign
Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene Sign
Urinary Signs / Haemoglobinuria or myoglobinuria Sign
Urinary Signs / Red or brown urine, pink Sign


Top of page

Horizontal and vertical transmission of infection from carrier animals occurs but the precise means of natural transmission of infection is unknown. Splitter (1950b) showed that experimental transmission of infection can be achieved by inoculation of blood from infected pigs. This can be achieved by subcutaneous, intravenous, intraperitoneal and oral inoculation. Infection can be spread naturally on farms on blood-contaminated needles and surgical instruments and snares and by ingestion of blood from infected pigs (Heinritzti, 1992). According to Heinritzi (1999) infection may be transmitted by boars at service if penile haemorrhage occurs. Mechanical transmission by arthropod vectors also occurs; Heinritzi (1992) reported experimental transmission of M. suis by the pig louse (Haematopinus suis). Prullage et al. (1993) reported experimental transmission of M. suis by the stable fly (Stomoxys calcitrans) and the yellow fever mosquito (Aedes aegypti).  According to Neimark et al. (2001), Eperythrozoon species have been shown to be transmitted by various blood-feeding arthropods including ticks, lice, fleas, flies and mosquitoes. Smith (1992) reported that field experience has indicated that in addition to other control measures such as medication, mange control is also required for effective control of PE.

Early reports (Quinn, 1938; Spencer, 1940) of outbreaks of PE, described an increased incidence of disease in the Summer months, this was thought to be due to increased activity of arthropod vectors at that time of year. Smith (1992) commented that infection can occur at any time of year since many pigs are now kept indoors and because of the possibility for iatrogenic transmission of infection. In GB, Gresham and Rogers (1995) reported that although an increased incidence of disease was noted in the Summer and Autumn, disease was also observed throughout the Winter and Spring and that disease was also identified in herds recorded as free of louse infestation. This indicated that although arthropod activity may cause an increased incidence of disease during the Summer months, the activity of lice alone is not essential for the spread of infection and disease.

Berrier and Gouge (1954) reported vertical (trans-placental) transmission of M. suis from carrier sows to their piglets.

The factors which predispose to the development of eperythrozoonosis in an infected pig have not been clearly identified. Smith (1992) stated that historically PE has been a disease associated with stress. Experimentally eperythrozoonosis can be induced by infection of splenectomised pigs (Splitter 1950b) and using immunosuppressive drugs such as dexamethazone (Yuan et al., 2009), but according to Heinritzi (1999) other stress factors (such as inappropriate management) may be required before disease occurs in such pigs.

There is also considerable anecdotal evidence that outbreaks of PE occurred after certain virus infections have been introduced into pig herds. In the USA, outbreaks of PE have been observed after outbreaks of disease associated with classical swine fever (CSF) virus infection and following the use of live CSF vaccines (before CSF was eradicated) (Quinn, 1938; Spencer 1940; Splitter and Williamson 1950).

In the UK, Gresham (1996) reported that PE was commonly identified in pig herds after outbreaks of porcine reproductive and respiratory syndrome virus (PRRSV) and swine influenza virus (SIV) infection. The chronology of the appearance of PRRSV in the UK in 1991, SIV strain H1195852 in 1992 and SIV strain H1N2 in 1994 coupled with the identification of M. suis infection and PE in the United Kingdom (UK) in 1993 indicated that PRRSV and SIV infections were possibly significant predisposing factors in the development of PE in the UK.

Solignac et al. (1996) have also commented that in France, in some herds the immunosuppressive effects of PRRSV may predispose to the development of eperythrozoonosis. Gresham (1996) commented that these observations, coupled with that of Riley (1964) that murine eperythrozoonosis associated with E. coccoides infection may be predisposed by lactic dehydrogenase virus (LDHV) infection, does suggest that viral infection is probably a significant cause for the development of eperythrozoonosis in swine. LDHV and PRRSV are both arteriviruses. 

Impact: Economic

Top of page

While the effects of clinically apparent ictero-anaemia in weaned pigs can be quantified, this is an inconsistent presentation in outbreaks of PE. The majority of M. suis infection in pigs is sub-clinical or chronic (Hoelzle, 2008). Clinical signs associated with chronic PE include anaemia, mild jaundice and poor growth in newborn pigs, reduced growth rates in growing and fattening pigs and reduced reproductive performance in sows. It is also suspected that immune suppression due to M. suis infection predisposes to secondary infections; these are often associated with enteric and respiratory disease (Zachary and Smith, 1985). Mortality due to PE is normally low (less than one percent according to Heinritzi (1999)) but some authors, for example Wu et al. (2006), record higher levels of mortality associated with PE. The true economic significance of PE is still unknown but it is likely that the syndromes associated with chronic PE cause a significant level of economic loss (Hoelzle, 2008). Wu et al., (2006) recorded that PE caused serious economic losses in infected herds. The limited understanding of the significance of PE is in part due to the limitations of the available diagnostic tests and also due to the poor understanding of the less overt production losses (reduced reproductive performance and reduced growth rates) due to chronic disease.

It remains important to note however that M. suis infection in pigs is commonly subclinical and that there is a risk that the significance of M. suis infection may be overestimated when this is detected.

Zoonoses and Food Safety

Top of page

There have been a number of reports of possible Eperythrozoon infection in humans since 1929 (Schuffner, 1929). Most of these reports have been made on the basis of observation of eperythrozoon-like bodies in stained blood films. According to Kreier and Ristic (1984) some of these reports have been of doubtful validity.

In recent years there have been a number of reports of possible Eperythrozoon infection in humans (for example, Puntaric et al. (1986), Tai et al. (1991), Feng et al. (1992), Shang (1994 and 1995), Shang et al. (1996 and 1997), Yang et al. (2000)). The report from Yang et al. (2000) provides results of light microscopy and electron microscopy and states that Eperythrozoon spp. infection was identified in blood samples from 35.35% of 1529 people. The prevalence of this infection in humans was reported to be more common in the Summer and Autumn and was also more common (115/257 (55.3%)) in groups of people such as farmers and veterinarians who had close contact with livestock (such as pigs, sheep, cattle or chickens) or in those people who had contact with wild animals. Yang et al. (2000) reported that vertical transmission occurred and 8/44 mothers and 8/44 neonates showed clinical signs of haemolytic jaundice. Severe infection was reported in 8/44 (18.2%) neonates, 2/43 (4.7%) of 1- to 7-year-old children and 11/541 (2%) of 7- to 70-year-old people. This condition was reported to be responsive to treatment with erythromycin or tetracycline antibiotics.

Speciation of the Eperythrozoon infection has not been reported in the publications mentioned above. Specifically human infection with M. suis was not reported. In 2009, Yuan et al. reported the detection of positive PCR results for M. suis in samples from swine farm workers in Shanghai. The authors commented that although their results indicated a close phylogenetic relationship between isolates of mycoplasma from pigs and humans, additional research is needed to assess the possibility of interspecies transmission.

Collectively these reports indicate that zoonotic infection by haemotrophic Mycoplasma spp. infection may occur but this is not known for certain. It is not known if M. suis is a zoonosis nor if this may be transmitted from pigs to humans by direct contact or by arthropod vectors.

It is also not known if consumption of pig products from pigs infected with M. suis represents a food-safety risk. The survival of M. suis in pig products is not known.  Because M. suis is (so far) uncultivable and is difficult to maintain in vitro, this suggests that the survival of M. suis in pig products is likely to be of a very short duration. There is very little information in the literature of the viability of M. suis after exposure to heat. Eperythrozoa generally are very fragile organisms and most are killed within minutes by drying. Seamer (1960) reported that eperythrozoa were not detected in blood samples (from infected pigs) which were exposed to 56°C for 20 minutes. Gong et al. (2010) have reported that M. suis can be maintained at -20oC for 835 days and at 4oC for 205 days. Collectively this information indicates that M. suis will be inactivated by cooking but not necessarily by freezing.

Disease Treatment

Top of page

In countries where arsenilic acid is available, this is widely used for the treatment and control of eperythrozoonosis in swine. In many countries, and including European Union Member States, arsenical compounds are not licensed for use in food producing animals. An additional problem, as indicated by Smith (1992), is that in some countries, if PE is not a listed indication for these compounds, even if arsenical compounds are licensed for use in pigs, feed mills may be unable to incorporate these compounds for this purpose. In such cases on-farm mixing of these drugs may be required. Oxytetracycline and chlortetracycline are the commonly used alternative medications.

Withdrawal times are not given in the table below as the disease syndromes associated with PE are not listed indications for the use of these compounds in most countries around the world. Piglets and chronically anaemic pigs should also be treated with 200 mg iron dextran /piglet. 




Dosage and  administration 

Life stages

Adverse effects

Drug resistance


Long acting oxytetracycline 20mg/kg by intramuscular injection of sows at 5-6 days pre-farrowing

New-born piglets

Injection reactions

Not recorded


Dual-dose long acting oxytetracycline 20mg/kg by intramuscular injection. Three injections at 7, 14 and 21 days of age.

Weaned pigs

Injection reactions


In-water medication with oytetracycline or chlortetracycline to achieve 20mg/kg.



Tetracycline compounds

In-feed medication (in the nursery ration) with  oxytetracycline or chlortetracycline to achieve 20mg/kg.

Growing pigs


Not recorded

Organic arsenical compounds

In-feed medication with  Arsanilic acid 45-90 g/tonne.

Growing pigs

Arsenic toxicity


In-feed medication of sows with oytetracycline or chlortetracycline 800g/tonne for 4 weeks and repeat 4 weeks later.

Adults and growing pigs


Arsanilic acid

85gm/tonne in feed (42g/tonne in the lactation ration)  (approximately 250mg/sow per day) for 1 month.

Adult pigs

Arsenic toxicity



Effective treatment of M. suis infection requires an understanding of the pathogenesis of eperythrozoonosis and recognition that, as immunity to M. suis infection is short lived, recrudescence may occur. The response to treatment of established and often complicated disease in affected pigs is therefore often poor.

Treatment regimes using tetracycline antibiotics and/or organic arsenical compounds in laboratory and field studies, have been described. Early field reports (Kinsley (1932) and Spencer (1940)) described the use of intravenous and in-feed arsenical compounds for the treatment of affected pigs. Splitter (1950c) reported the use of intravenous neoarsphenamine in the treatment of experimental eperythrozoonsis in swine. Splitter commented that to be beneficial, treatment had to be carried out early in the disease process and that treatment would be of little value if this was delayed until peak bacteraemia and severe haematological changes occurred. Splitter and Castro (1957) described the use of oxytetracyline in the treatment of experimental eperythrozoonsis in swine.

Smith (1992) described various in-feed and in-water treatment regimes using arsanilic acid, sodium arsanilate and oxytetracycline and also injectable oxytetracycline. Smith pointed out that while these arsenical compounds are used in some countries as feed additives in pigs for growth promotion and increasing feed conversion efficiency and for the treatment of swine dysentery, these arsenical compounds and tetracycline antibiotics have not been listed in the US Feed Additive Compendium for treatment of M. suis infection or eperythrozoonosis. As such, for example in the USA, where these compounds are used for the treatment of M. suis infection or eperythrozoonosis, the prescribing veterinarian assumes legal responsibility.

Splitter (1950c) reported that treatment using neoarsphenamine in the anticipation of peak bacteraemia and before the appearance of icteroanaemia is often the most effective treatment in outbreaks of acute eperythrozoonosis. Similarly Gresham and Rogers (1995) reported that prophylactic treatment using tetracycline antibiotics in the same way was the most effective treatment in outbreaks of acute eperythrozoonosis. The use of oxytetracycline or chlortetracycline (20mg/kg liveweight for a minimum of four to five days) was described. These authors also commented that in such cases it is essential to achieve an adequate therapeutic dose rate and that in all cases, an assessment of a response to treatment must be considered in the light of the accuracy of the diagnosis.

Although the treatment of affected pigs with tetracycline antibiotics or arsenical compounds will reduce the level of infection and mitigate disease, it is not thought that the elimination of infection is possible (Gwaltney, 1995).

According to Smith (1992) natural outbreaks of eperythrozoonosis cannot be controlled unless lice and mange are also controlled in the affected herd.

Prevention and Control

Top of page

M. suis infection is recorded as present in many countries around the world. In the countries where it is recorded, it is widely prevalent. Although Gwaltney (1995) and Hoezle et al. (2003) advocated the possibility of eradicating M. suis infection by the removal of infected carrier animals which had been detected by PCR no reports of attempted eradication by, for example medicated early weaning, have been found.

Effective prevention and control of PE requires an understanding of the pathogenesis of PE and recognition that the clinical presentation of PE may be very variable and also that immunity to M. suis infection is short lived.

Where possible, reducing the effects of likely predisposing factors such as PRRSV, CSFV and SIV infections and other stress factors is logical. In countries where these diseases are present, available vaccines may be used. The potential for the spread of infection in blood on equipment such as needles and snares should be reduced between adult pigs and between litters or groups of growing pigs by sterilising equipment contaminated with blood. Where possible, the control of ectoparasites (particularly lice), and flies and mosquitoes, if present, has been advocated as a necessary adjunct to this.

Control of predisposing viral infection and the use of tetracycline antibiotics are the main-stay of M. suis control in most pig herds affected with PE. To be effective, therapeutic concentrations of tetracycline antibiotics must be given prior to the onset of clinical signs at the time of presumed peak bacteraemia.

There are no licensed vaccines available for the control of M. suis infection in the European Community and there are no published reports of the availability of such vaccines in other countries.

Hoelzle et al. (2009) reported that vaccination of pigs with recombinant M. suis adhesin protein (MSG1) elicited a strong immune response but failed to induce protection against challenge with M. suis infection.                         


Top of page

Adams EW; Lyles DI; Cockrell KO, 1959. Eperythrozoonosis in a herd of purebred Landrace pigs. Journal of the American Veterinary Medical Association, 135:226-228.

Anon, 2002. Notification that new names and new combinations have appeared in volume 52, part 2, of the IJSEM. International Journal of Systematic and Evolutionary Microbiology, 52:691-692.

Ayroud M, 1994. First confirmed case in Alberta of eperythrozoonosis in swine. Canadian Veterinary journal, 35(4):200

Ba CaiFeng; Li JiuChun; Feng HuiQuan; Zhao Wei, 2009. Establishment and clinical application of a new PCR diagnostic method of Mycoplasma suis. Journal of Liaoning Medical University, 30(2):125-127.

Barnett SF, 1963. Eperythrozoon parvum in pigs in Kenya. Bull. Epizoot. Dis. Afr, 11:185-195.

Beaudin S; Chabot R; Desnoyers M, 2000. A case of eperythrozoonosis on a pig farm in Quebec. (Cas d'épérythrozoonose dans un élevage porcin du Québec.) Médecin Vétérinaire du Québec [La vaccination.], 30(1):39-40.

Berrier HH; Gouge RE, 1954. Eperythrozoonosis transmitted in-utero from carrier sows to their piglets. Journal of the American Veterinary Medical Association, 124:98-100.

BIBERSTEIN EL; BARR LM; LARROW LL; ROBERTS SJ, 1956. Eperythrozoonosis of swine in New York State. Cornell Veterinarian, 46:288-297.

Boretti LP; Lima JD; Leite RC; Modena CM, 1987. Survey of parasites and diseases of pigs in the Mata de Ponte Nova area of Minas Gerais. (Diagnostico sanitario em suinos na micro-região homogenea Mata de Ponte Nova, Minas Gerais.) Arquivo Brasileiro de Medicina Veterinária e Zootecnia, 39(2):213-222.

Busser EVde; Mateusen B; Vicca J; Hoelzle LE; Haesebrouck F; Maes D, 2008. Mycoplasma suis infection in suckling pigs on a Belgian farm. Vlaams Diergeneeskundig Tijdschrift, 77(3):182-186. HTTP://VDT.UGENT.BE

Chang YongCheng; Wang WeiMing, 2000. Diagnosis and treatment of eperythrozoonosis in piglets. Chinese Journal of Veterinary Medicine, 26(9):22.

Cruz E; Delgado L; López R; Polanco H; Lombillo RD; Rodríguez ON, 1985. Organ pathology in experimental porcine eperythrozoonosis. (Morfopatologia organica de la eperitrozoonosis porcina experimental.) Revista de Salud Animal, 7(1):59-66.

DICKE WE, 1934. Anaplasmosis-Like Disease in Swine. Veterinary Medicine, 29:288.

Dipeolu OO; Majaro OM; Akinboade OA; Nwufor KJ, 1982. Studies on the blood parasites of pigs in Ibadan, Nigeria. Veterinary Parasitology, 10(1):87-90.

DOYLE LP, 1932. A Rickettsia-Like or Anaplasmosis-Like Disease in Swine. Journal of the American Veterinary Medical Association, 81:668-671.

Felder KM; Hoelzle K; Heinritzi K; Ritzmann M; Hoelzle LE, 2010. Antibodies to actin in autoimmune haemolytic anaemia. BMC Veterinary Research, 6(18):(30 March 2010).

Felder KM; Hoelzle K; Ritzmann M; Kilchling T; Schiele D; Heinritzi K; Groebel K; Hoelzle LE, 2011. Hemotrophic mycoplasmas induce programmed cell death in red blood cells. Cellular Physiology and Biochemistry, 27(5):557-564.

Feng LM; Pan HZ; Fang F, 1992. Human eperythrozoonosis. Chinese Journal of Haematology, 13:320-322.

Gong DaChun; Jiang Tao; Wan ChunYun; Yang LanLing, 2010. Observation on several biological characteristics of Eperythrozoon. Chinese Journal of Zoonoses, 26(2):183-185.

Gresham ACJ, 1996. Eperythrozoon suis infection in pigs. The Pig Journal, 37:20-28.

Gresham ACJ, 1998. Eperythrozoon suis infection in pigs in England and Wales. Prevalence and possible factors predisposing to eperythrozoonosis. In: Proceedings of the 15th International Meeting of the Pig Veterinary Society, Birmingham, UK, 3. 407.

Gresham ACJ; Rogers JP, 1995. An update on Eperythrozoon suis. The Pig Journal, 36:212-215.

Gresham ACJ; Rogers JP; Tribe HA; Phipps LP, 1994. Eperythrozoon infection in weaned pigs. Veterinary Record, 134:71-72.

Grimm J; Ritzmann M; Heinritzi K; Wittenbrink MM; Hoelzle K; Hoelzle LE, 2008. Investigation of the distribution of Mycoplasma suis in Germany by real-time PCR. (Untersuchungen zur Prävalenz von Mycoplasma suis in Deutschland mittels real-time Polymerasekettenreaktion.) Tierärztliche Umschau, 63(1):21-25.

Groebel K; Hoelzle K; Wittenbrink MM; Ziegler U; Hoelzle LE, 2009. Mycoplasma suis invades porcine erythrocytes. Infection and Immunity, 77(2):576-584.

Guimaraes AMS; Santos AP; Sanmiguel P; Walter T; Timenetsky J; Messick JB, 2011. Complete genome sequence of Mycoplasma suis and insights into its biology and adaption to an erythrocyte niche. PLoS ONE, No.May:e19574.

Gwaltney SM, 1995. Eperythrozoon suis infections in pigs: clinical syndromes and diagnosis. Swine Health and Production, 3(1):25-27.

Gwaltney SM; Hays MP; Oberst RD, 1993. Detection of Eperythrozoon suis using the polymerase chain reaction. Journal of Veterinary Diagnostic Investigation, 5(1):40-46.

Gwaltney SM; Oberst RD, 1994. Comparison of an improved polymerase chain reaction protocol and the indirect hemagglutination assay in the detection of Eperythrozoon suis infection. Journal of Veterinary Diagnostic Investigation, 6(3):321-325.

Gwaltney SM; Willard LH; Oberst RD, 1993. In situ hybridizations of Eperythrozoon suis visualized by electron microscopy. Veterinary Microbiology, 36(1/2):99-112.

Ha SK; Jung K; Choi C; Ha Y; Song HC; Lim JH; Kim SH; Chae C, 2005. Development of in-situ hybridization for the detection of Mycoplasma haemosuis (Eperythrozoon suis) in formalin-fixed, paraffin wax-embedded tissues from experimentally infected splenectomized pigs. Journal of Comparative Pathology, 133(4):294-297.

Heinritzi K, 1992. Studies on the transmission of Eperythrozoon suis. Tierärztliche Umschau, 47(8):588.599; 27 ref.

Heinritzi K, 1999. Eperythrozoonosis. In: Diseases of Swine, 8th Edition [ed. by Leman, A. D.]. Ames, Iowa: Iowa State University Press, 413-418.

Heinritzi K; Plank G; Peteranderl W; Sandner N, 1990. Acid-base balance and carbohydrate metabolism in Eperythrozoon suis infected pigs. (Untersuchungen zum Säure-Basen-Haushalt und Kohlenhydratstoffwechsel bei der Infektion mit Eperythrozoon suis.) Journal of Veterinary Medicine. Series B, 37(6):412-417.

Henry SC, 1979. Clinical observations on eperythrozoonosis. Journal of the American Veterinary Medical Association [Swine.], 174(6):601-603.

Heon Y; Jang H; Park KS, 1992. Isolation of Eperythrozoon suis from slaughtered pigs in Korea. Research Reports of the Rural Development Administration, Veterinary, 34(1):7-14.

Hoelzle K; Doser S; Ritzmann M; Heinritzi K; Palzer A; Elicker S; Kramer M; Felder KM; Hoelzle LE, 2009. Vaccination with the Mycoplasma suis recombinant adhesion protein MSG1 elicits a strong immune response but fails to induce protection in pigs. Vaccine, 27(39):5376-5382.

Hoelzle K; Engels M; Kramer MM; Wittenbrink MM; Dieckmann SM; Hoelzle LE, 2010. Occurrence of Mycoplasma suis in wild boars (Sus scrofa L.). Veterinary Microbiology, 143(2/4):405-409.

Hoelzle K; Grimm J; Ritzmann M; Heinritzi K; Torgerson P; Hamburger A; Wittenbrink MM; Hoelzle LE, 2007. Use of recombinant antigens to detect antibodies against Mycoplasma suis, with correlation of serological results to hematological findings. Clinical and Vaccine Immunology, 14(12):1616-1622.

Hoelzle LE, 2008. Haemotrophic mycoplasmas: recent advances in Mycoplasma suis. Veterinary Microbiology, 130(3/4):215-226.

Hoelzle LE; Adelt D; Hoelzle K; Heinritzi K; Wittenbrink MM, 2003. Development of a diagnostic PCR assay based on novel DNA sequences for the detection of Mycoplasma suis (Eperythrozoon suis) in porcine blood. Veterinary Microbiology, 93(3):185-196.

Hoelzle LE; Helbling M; Hoelzle K; Ritzmann M; Heinritzi K; Wittenbrink MM, 2007. First LightCycler real-time PCR assay for the quantitative detection of Mycoplasma suis in clinical samples. Journal of Microbiological Methods, 70(2):346-354.

Hoelzle LE; Hoelzle K; Ritzmann M; Heinritzi K; Wittenbrink MM, 2006. Mycoplasma suis antigens recognized during humoral immune response in experimentally infected pigs. Clinical and Vaccine Immunology, 13(1):116-122.

Hoffmann R; Schmid DO; Hoffmann-Fezer G, 1981. Erythrocyte antibodies in porcine eperythrozoonosis. Veterinary Immunology and Immunopathology, 2(2):111-119.

Hsu FS, 1988. Clinical diseases and pathological morphologies of Eperythrozoon suis concurrent Salmonella choleraesuis infection in a large intensive swine herd. In: Proceedings, 10th International Pig Veterinary Society, August 14-17 1988. São Paulo, Brazil: International Pig Veterinary Society, Brazilian Section, 260.

Hsu FS; Liu MC; Chou SM; Zachary JF; Smith AR, 1992. Evaluation of an enzyme-linked immunosorbent assay for detection of Eperythrozoon suis antibodies in swine. American Journal of Veterinary Research, 53(3):352-354.

JANSEN BC, 1952. The occurrence of Eperythrozoon parvum Splitter, 1950 in South African swine. Onderstepoort Journal of Veterinary Research, 25(4):5-6 pp.

JENNINGS AR; SEAMER J, 1956. A new blood parasite in British pigs. Nature, 178:153-154.

Jeon Y, 1971. [Morphological study and experimental production of porcine eperythrozoonosis.]. Research Reports of the Office of Rural Development, Korea. Veterinary Series, 14:35-40.

Kántás K; Andó P, 1987. Eperythrozoonosis in swine in Hungary. (Eperythrozoonosis sertesben Magyarorszagon.) Magyar Âllatorvosok Lapja, 42(11):673-676.

KINSLEY AT; RAY JD, 1934. Anaplasmosis-Like Disease in Swine. Journal of the American Veterinary Medical Association, 84:891-892.

Kinsley, 1932. Protozoon like body in blood of swine. Veterinary Medicine, 27:196.

Korn G; Mussgay M, 1968. Eperythrozoon infection in a pig. Differentiation from swine fever. Zentralblatt fur Veterinarmedizin, 15B:617-630.

Kreier JP; Gothe R, 1976. Aegyptianellosis, eperythrozoonosis, grahamellosis and haemobartonellosis. Veterinary Parasitology, 2(1):83-95.

Kreier JP; Ristic M, 1984. Eperythrozoon. In: Bergey's Manual of Systematic Bacteriology, volume 1 [ed. by Kreig, N. R.]. Baltimore, USA: Williams and Wilkins, 725-726.

Li YueMei; Xing Ying; Zhang ShouFa; Xue ShuJiang; Zheng XiuHong; LüZhou, 2010. Comparative analysis of nucleotide sequence 16S rRNA of Eperythrozoon suis of three provinces in Northeast. Journal of China Agricultural University, 15(2):59-63.

Liebich H; Heinritzi K, 1992. Light and electron microscopic studies of Eperythrozoon suis. (Licht- und elektronen mikroscopische untersuchungen an Eperythrozoon suis.) Tierarztliche Praxis, 20(3):270-274.

Liu Bing; Zhang ShouFa; Yu LongZheng; Jia LiJun; Tian Ye, 2007. Establishment of experimental animal model with Eperythrozoon suis. Veterinary Science in China, 37(1):12-15.

Liu Cao; Wang ZhenYong; Yang DuBao; Lei LiuZhen; Gao YuanYuan; Chen TianTian; Xia JunFeng; Zhu Hui, 2010. Selection of effective immunomodulators for eperythrozoonosis. Journal of Northwest A & F University - Natural Science Edition, 38(5):13-16, 21.

Lopes CWG; Rezende HEBde; Massard CL; Faccini HL, 1982. Eperythrozoonosis in pigs in the state of Rio de Janeiro. (Eperitrozoonose em suinos no estado do Rio de Janeiro.) Revista Brasileira de Medicina Veterinaria, 5:26-29.

Ma HaiLi; Huang MeiSheng; Ren JiaYan; Zheng MingXue; Li HongQuan, 2003. Haematological characteristics of pigs with natural infection of Eperythrozoon suis. Chinese Journal of Veterinary Science, 23(3):247-249.

Machuca MA; Quiroga MA; Armocida AD; Arauz S; Idiart JR; Stornelli MA; Perfumo CJ, 1999. Swine eperythrozoonosis: description of an outbreak in the province of Buenos Aires. (Eperitrozoonosis porcina: descripción de un brote en la provincia de Buenos Aires.) Revista de Medicina Veterinaria (Buenos Aires), 80(6):470-474.

Madsen M, 1986. Eperythrozoonosis in swine - an overlooked disease? Nordisk Veterinaermedicin, 38(2):57-67.

Messick JB, 2004. Hemotrophic mycoplasmas (hemoplasmas): a review and new insights into pathogenic potential. Veterinary Clinical Pathology, 33(1):2-13.

Messick JB; Cooper SK; Huntley M, 1999. Development and evaluation of a polymerase chain reaction assay using the 16 S rRNA gene for detection of Eperythrozoon suis infection. Journal of Veterinary Diagnostic Investigation, 11(3):229-236.

Messick JB; Santos AP; Guimaraes AMS, 2011. Complete genome sequences of two hemotropic mycoplasmas, Mycoplasma haemofelis strain Ohio2 and Mycoplasma suis strain Illinois. Journal of Bacteriology, 193(8):2068-2069.

Modric Z; Dzakula N; Stojiljkovic D; Culjak K; Grabarevic Z; Milas Z; Bedrica L, 1987. First appearance of Eperythrozoon infection in swine in Yugoslavia. (Prvi nalaz eperitrozoonoze u svinja u Jugoslaviji.) Veterinarski Glasnik, 41(3/4):233-238.

Neimark H; Johansson KE; Rikihisa Y; Tully JG, 2001. Proposal to transfer some members of the genera Haemobartonella and Eperythrozoon to the genus Mycoplasma with descriptions of 'Candidatus Mycoplasma haemofelis', 'Candidatus Mycopl. International Journal of Systematic and Evolutionary Microbiology, 51(3):891-899.

Neimark H; Johansson KE; Rikihisa Y; Tully JG, 2002. Revision of haemotrophic Mycoplasma species names. International Journal of Systematic and Evolutionary Microbiology, 52(2):683.

Nonaka N; Thacker BJ; Schillhorn van Veen TW; Bull RW, 1996. In vitro maintenance of Eperythrozoon suis. Veterinary Parasitology, 61(3/4):181-199.

Oberst RD; Gwaltney SM; Hays MP; Morgan S; Stair EL, 1993. Experimental infections and natural outbreaks of eperythrozoonosis in pigs identified by PCR-DNA hybridizations. Journal of Veterinary Diagnostic Investigation, 5(3):351-358.

Oberst RD; Hall SM; Schoneweis DA, 1990. Detection of Eperythrozoon suis DNA from swine blood by whole organism DNA hybridizations. Veterinary Microbiology, 24(2):127-134.

Oehlerking J; Kube M; Felder KM; Matter D; Wittenbrink MM; Schwarzenbach S; Kramer MM; Hoelzle K; Hoelzle LE, 2011. Complete genome sequence of the hemotrophic Mycoplasma suis strain KI3806. Journal of Bacteriology, 193(9):2369-2370.

Pejsak Z, 1995. Eperythrozoon suis infection in pigs. (Eperytrozoonoza.) Medycyna Weterynaryjna, 51(2):84-86.

Perestrelo-Vieira R; Heinritzi K; Perestrelo-Vieira H; Sobestiansky J; Abreu-Lopes JA, 1997. First diagnosis of Eperythrozoon suis in Portugal. (Primeiro diagnóstico de Eperythrozoon suis em Portugal.) Revista Portuguesa de Ciências Veterinárias, 92(521):14-19.

Pereyra NB; Perez AM; Messick JB; Cane FD; Guglielmone AA, 2011. Estimation of the sensitibity and specificity of two Mycoplasma suis diagnostic tests in Argentina using a Bayesian model. Archivos de Medicina Veterinaria, 43(2):117-125.

Pereyra NB; Sarradell JE; Cane FD; Francois SE; Pidone CL; Comba ER; Rodríguez F; Guglielmone AA, 2006. Detection of Mycoplasma suis in clinical cases with postweaning multisystemic wasting syndrome in swine. (Detección de Mycoplasma suis en casos clínicos de síndrome del desmedro multisistémico posdestete en porcinos.) Revista Argentina de Microbiología, 38(3):130-133.

Permin A; Yelifari L; Bloch P; Steenhard N; Hansen NP; Nansen P, 1999. Parasites in cross-bred pigs in the Upper East Region of Ghana. Veterinary Parasitology, 87(1):63-71; 17 ref.

Portiansky EL; Quiroga MA; Machuca MA; Perfumo CJ, 2004. Mycoplasma suis in naturally infected pigs: an ultrastructural and morphometric study. Pesquisa Veterinária Brasileira, 24(1):1-5.

Pospischil A; Hoffmann R, 1982. Eperythrozoon suis in naturally infected pigs: a light and electron microscopic study. Veterinary Pathology, 19(6):651-657.

Potkonjak A; Lako B; Milicevic V; Savic B; Ivetic V; Jakic-Dimic D; Stevancevic O; Toholj B, 2009. PCR-diagnostics of swine infection caused by Mycoplasma suis. (PCR-dijagnostika infekcije kod svinja koju izaziva Mycoplasma suis.) Veterinarski Glasnik, 63(5/6):353-358.

Prullage JB; Williams RE; Gaafar SM, 1993. On the transmissibility of Eperythrozoon suis by Stomoxys calcitrans and Aedes aegypti. Veterinary Parasitology, 50(1-2):125-135; 34 ref.

Puntaric V; Borcic D; Vukelic D(et al), 1986. .

Quinn AH, 1938. A herd condition of swine characterised by icterus and anaemia. Journal of the American Veterinary Medical Association, 93:327-328.

Reigler E, 1990. Serological survey for Eperythrozoon suis infection of pigs in Austria. Wiener Tierarztliche Monatsschrift, 77(8):272-273.

Riley V, 1964. Synergism between a lactate dehydrogenase-elevating virus and Eperythrozoon coccoides. American Association for the Advancement of Science. Science, 146:921-923.

Ritzmann M; Grimm J; Heinritzi K; Hoelzle K; Hoelzle LE, 2009. Prevalence of Mycoplasma suis in slaughter pigs, with correlation of PCR results to hematological findings. Veterinary Microbiology, 133(1/2):84-91.

Schmidt P; Kaspers B; Jüngling A; Heinritzi K; Lösch U, 1992. Isolation of cold agglutinins in Eperythrozoon suis-infected pigs. Veterinary Immunology and Immunopathology, 31(1-2):195-201.

Schuffner WAP, 1929. Unusual finding in the blood of a young patient with anaemia. Pseudoleucaemia infantum (Von Jaksch-Hayem's anaemia). Nederland Tijdschrift Voor Geneeskunde, 2:3778-3780.

Seamer J, 1960. Studies with Eperythrozoon parvum Splitter, 1950. Parasitology, 50:67-80.

Shang DQ, 1994. Advances in the study of eperythrozoonosis. Chinese Journal of Epidemiology, 15:234-240.

Shang DQ, 1995. An epidemiological investigation of Eperythrozoon infection in human and animals. A Collaborative Research Group on Eperythrozoonosis. Chinese Journal of Epidemiology, 16:143-146.

Shang DQ; Li LY; Lu ZG, 1997. An epidemiological investigation of Eperythrozoon infection in human and animals (III). Chinese Journal of Epidemiology, 18:150-152.

Shang DQ; Li LY; Pei B, 1996. An epidemiological investigation of Eperythrozoon infection in human and animals (II). Chinese Journal of Epidemiology, 17:221-224.

Smith AR, 1992. Eperythrozoonosis. Chapter 37. In: Diseases of Swine, 7th Edition [ed. by Leman, A. D.]. Ames, Iowa, USA: Iowa State University Press, 470-474.

Smith AR; Rahn T, 1975. An indirect haemagglutionation test for the diagnosis of Eperythrozoon suis infection in swine. American Journal of Veterinary Research, 39:1319-1321.

Smith JE; Cipriano JE; Hall SM, 1990. In vitro and In vivo glucose consumption in swine eperythrozoonosis. Journal of Veterinary Medicine. Series B, 37(8):587-592.

Smola J; Celer V; Molínková D, 2008. Infection of piglets and stillborn fetuses with Mycoplasma haemosuis findings. (Infekce selat a martve rozených fetu s prukazem Mycoplasma haemosuis.) Veterinárství, 58(10):626-629.

Solignac T; Nicolas Y; Fourchon P, 1996. Eperythrozoonosis in pigs: identification in French herd. (L'épérythrozoonose dans l'espèce porcine: mise en évidence dans des élevages français.) Revue de Médecine Vétérinaire, 147(2):131-138.

SPENCER R, 1940. Anaplasmosis-Like Disease of Swine. Veterinary Medicine, 35:294-295.

SPLITTER EJ, 1950. Eperythrozoon suis n.sp. and Eperythrozoon parvum n. sp., two new blood parasites of swine. Science III. 513-516.

Splitter EJ, 1950. Eperythrozoon suis, the etiologic agent of ictero-anaemia or an anaplasmosis-like disease in swine. American Journal of Veterinary Research, 11:324-330.

SPLITTER EJ, 1950. Neoarsphenamine in acute eperythrozoonosis of swine. Journal of the American Veterinary Medical Association, 117:371-373.

SPLITTER EJ, 1958. The complement-fixation test in diagnosis of eperythrozoonosis in swine. Journal of the American Veterinary Medical Association, 132:47-49.

SPLITTER EJ; CASTRO ER, 1957. Antibiotic therapy in acute eperythrozoonosis of swine. Journal of the American Veterinary Medical Association, 131:293-294.

SPLITTER EJ; WILLIAMSON RL, 1950. Eperythrozoonosis In swine. A preliminary report. Journal of the American Veterinary Medical Association, 116:360-364.

Tai XZ; Yang DX, 1991. Human eperythrozoonosis. Chinese Inner Mongolian Medical Journal, 11:122.

Talavera Santos HJ, 1977. Eperythrozoon suis in blood of swines kept for slaughtering at the Irapuato, Gto. slaughter house Mexico. Master of Veterinary Science thesis. Mexico City, Mexico: Universidad Nacional Autonoma de Mexico, 102 pp.

Uilenberg G; Zeeuwen AA; Ruijter Tde, 1981. Eperythrozoon parvum (Rickettsiales) in swine in the Netherlands. Tijdschrift voor diergeneeskunde, 106(9):456.

Vayuchote C; Trongwongsa L; Chompoochan T; Siriwan C, 1991. Occurrence of eperythrozoonosis in weaning pigs. Thai Journal of Veterinary Medicine, 21(3):139-147.

Vezzoli F; Gualdi V; Luini M; Arioli E; Botti S; Recordati C, 2003. Anaemia and mortality in piglets infected with Mycoplasma suis [Eperythrozoon suis]. (Anemia e mortalita' da Mycoplasma suis (Eperythrozoon suis) in suinetti sotto-scrofa.) In: Atti della Societa Italianà di Patologia ed Allevamento dei Suini 2003 XXIX Meeting Annuale, Salsomaggiore Terme, Italy. Parma, Italy: Società Italiana di Patologia ed Allevamento dei Suini, 355-363.

Wilson MR; Dewey C; Friendship R; Conlon J, 1988. "Eperythrozoa", hemoglobin, and stillbirth. In: Proceedings, 10th International Pig Veterinary Society, August 14-17 1988. São Paulo, Brazil: International Pig Veterinary Society, Brazilian Section, 261.

Wu JianSan; Yu JianMin; Song CuiPing; Sun ShengJun; Wang ZhiLiang, 2006. Porcine eperythrozoonosis in China. Annals of the New York Academy of Sciences [Impact of Emerging Zoonotic Diseases and Animal Health: 8th Biennial Conference of the Society for Tropical Veterinary Medicine, Hanoi, Vietnam, 26 June-1 July 2005.], 1081:280-285.

Xin ShiKun; Li MingRui; Xue ZhiQing; Yan YongQi; Fu Zhong; Zhen XiRong; Li MeiGan; Liu FuTing; Sun YanLin; Yan XueLiang; Niu ZhangGui, 1995. Epidemiological investigation of the first outbreak of eperythrozoonosis in pigs in Zhangye Region, Gansu, China. Chinese Journal of Veterinary Medicine, 21(3):31.

Yang DianXiang; Tai XiuZheng; Qiu Ying; Yun Sheng, 2000. Prevalence of Eperythrozoon spp. infection and congenital eperythrozoonosis in humans in Inner Mongolia, China. Epidemiology and Infection, 125(2):421-426.

Yu Fei; Hua XiuGuo; Cui Li; Yuan CongLi; Yang ZhiBiao, 2008. Establishment of a mouse model with Eperythrozoon suis and haematological changes. Journal of Shanghai Jiaotong University - Agricultural Science, 26(1):42-45.

Yuan C; Yang Z; Zhu J; Cui L; Hua X, 2007. Effect of an immunosuppressor (dexamethasone) on Eperythrozoon infection. Veterinary Research Communications, 31(6):661-664.

Yuan CL; Liang AB; Yao CB; Yang ZB; Zhu JG; Cui Li; Yu Fei; Zhu NY; Yang XW; Hua XG, 2009. Prevalence of Mycoplasma suis (Eperythrozoon suis) infection in swine and swine-farm workers in Shanghai, China. American Journal of Veterinary Research, 70(7):890-894.

Zachary JF; Basgall EJ, 1985. Erythrocyte membrane alterations associated with the attachment and replication of Eperythrozoon suis: a light and electron microscopic study. Veterinary Pathology, 22(2):164-170.

Zachary JF; Smith AR, 1985. Experimental porcine eperythrozoonosis: T-lymphocyte suppression and misdirected immune responses. American Journal of Veterinary Research, 46(4):821-830.

Distribution Maps

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