Introduction
Erysipelas is a bacterial disease caused by Erysipelothrix rhusiopathiae, which could potentially occur in all vertebrate species. The disease of greatest prevalence and economic importance is swine erysipelas. The acute, sub-acute, and chronic forms of swine erysipelas may occur in sequence or separately. Mortality can range between 0-100%, with death occurring up to 6 days after the first signs of illness. Pigs are the most commonly affected species; however, cases have been reported in birds, sheep, fish, and reptiles (Imada et al., Reference IMADA, TAKASE, KIKUMA, IWAMARU, AKACHI and HAYAKAWA2004; Erikkson et al., 2009; Wang et al., Reference WANG, CHANG and RILEY2010).
Erysipelas in birds is generally an acute, fulminating infection. It is a septicaemic disease; however the chronic form occasionally occurs after acute outbreaks. Erysipelas is of primary importance in turkeys, although outbreaks sometimes occur in other birds species. Outbreaks usually occur suddenly, with a few birds being found dead initially, followed by increasing levels of mortality on subsequent days. Mortality may range from <1% to 50%. (Bailie et al., Reference BAILIE, BURY, BICKNELL and KNUDTSON1970; Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978; Boerner et al., Reference BOERNER, NEVIS, HINCKLEY, WEBER and FRASCA2004; Opriessnig et al., Reference OPRIESSNIG, VANCE and HALBUR2005) The regulation of this disease is important because E. rhusiopathiae may cause serious economic losses to farmers. Infection due to E. rhusiopathiae in humans is occupationally related, and principally occurs as a result of contact with sick animals, their products or wastes, or contaminated soil/bedding. Three forms of human disease have been recognised: (1) a localised cutaneous lesion form, termed ‘erysipeloid’; (2) a generalised cutaneous form, and (3) a septicaemic form, often associated with endocarditis. Erysipeloid is the most common form of infection in humans, and while it has been suggested that the incidence of human infection might be declining due to technological advances in the animal industry, infection continues to occur in certain environments (Mutalib et al., Reference MUTALIB, KING and McDONOUGH1993; Reference MUTALIB, KEIRS and AUSTIN1995; Veraldi et al., Reference VERALDI, GIRGENTI, DASSONI and GIANOTTI2009; Wang et al., Reference WANG, CHANG and RILEY2010).
Etiology
Erysipelothrix rhusiopathiae is a gram-positive bacillus that is resistant to environmental factors, and does not produce endospores. This bacterium may occur as a pathogen or commensal organism in many species of wild and domestic mammals, in addition to birds and fish (Bricker and Saif, Reference BRICKER and SAIF1997; Wang et al., Reference WANG, CHANG and RILEY2010). The bacteria was first isolated in 1876 by Koch from the blood of mice with symptoms of septicaemia, hence the original name Erysipelothrix murisepticemia. The pathogen was later isolated from a variety of vertebrate species, and was called, among others names, Erysipelothrix insidiosa (Trevisan 1885), Bacillus rhusiopathiae suis (Kitt 1893), Bacterium rhusiopathiae (Migula 1900), Erysipelothrix porci (Rosenbach 1909), and Erysipelothrix erysipeloides (Rosenbach 1909). In the published literature, 36 different names have been recorded for Erysipelothrix spp. and the present name of Erysipelothrix rhusiopathiae was accepted in 1966. The name of the bacteria was created from Greek words erysipelas (rose, red skin), trix (hair), rhusius (reddening), and pathus (disease). The comparison with hair originated from a specific image of the bacterium on a slide that presented the rough colonies from chronic form of the disease. On this slide, long filiform cells that resemble hair are visible (Woodbine, Reference WOODBINE1950). The cell morphology of E. rhusiopathiae is variable. The mentioned rough form of the colony (R) was isolated on blood agar from animal tissues with the chronic form of the disease. Colonies of the rough form are about 1-2 mm in size, have irregular edges, and are flat and dry (Bricker and Saif, Reference BRICKER and SAIF1997). Bacterial cells may be arranged in small chains that form long threads. Such cell morphology also occurs in the older colonies of the smooth form. The rough form grows well at a temperature of 37°C and on media with a pH of 7. Smooth colonies (S) are small, with a diameter of 0.3-1.5 mm, and are round with a slightly convex surface. These colonies tend to grow from the acute form of the disease, forming small colonies with a zone of alpha haemolysis. Staining shows that the bacteria are gram-positive, short, slightly bent bacilli. The smooth form grows well at a temperature of 33°C, and on media with a pH of 7.6-8.2 (Wang et al., Reference WANG, CHANG and RILEY2010).
The genus Erysipelothrix includes E. tonsillarum, however this species is considered non-pathogenic, which has been confirmed with the experimental intracutaneous infection of swine that had been previously subjected to immune-suppressive medicines (Harada et al., Reference HARADA, MURAMATSU, SUZUKI, TAMURA, SAWADA and TAKAHASHI2011). In addition, chickens that were inoculated with the strain E. tonsillarum did not show any symptoms of disease (Takahashi et al., Reference TAKAHASHI, TAKAGI, YAMAOKA, OHISHI, NORIMATSU, TAMURA and NAKAMURA1994). There was only one case where E. tonsillarum have been isolated from a dog with endocarditis (Takahashi et al., Reference TAKAHASHI, TAMURA, YOSHIMURA, NAGAMINE, KIJIMA, NAKAMURA and DEVRISE1993). Erysipelothrix sp. strains are classified based on serological properties, which are determined by a heat-stable antigen, namely, the peptydoglycan of the cell wall. Serotypes 1, 2, 4, 5, 6, 8, 9, 11, 12, 15, 16, 17, 19, 21, and N belong to the species E. rhusiopathiae, while serotypes 3, 7, 10, 14, 20, and 22 belong to the species E. tonsillarum. Due to a slight homology in the DNA of E. rhusiopathiae and E. tonsillarum, some authors differentiate Erysipelothrix sp. as strain 1 (serotype 13) and Erysipelothrix sp. as strain 2, (serotype 18) (Bricker and Saif, Reference BRICKER and SAIF1997; Takeshi et al., Reference TAKESHI, MAKINO and IKEDA1999; Bender et al., Reference BENDER, KINYON, KARIYAWASAM, HALBUR and OPRIESSNIG2009). The serotypes recorded in birds to date include 1, 2, 4, 5, 6, 8, 15, 16, and 21. In swine, the serotypes that most frequently cause the disease are serotypes 1, 2, and 21, while in sheep and goats, the most frequent serotypes are 1, 2, 5, 15, and 21 (Takahashi et al., Reference TAKAHASHI, FUJISAWA, TAMURA, SUZUKI, MURAMATSU, SAWADA, BENNO and MITSUOKA1992; Imada et al., Reference IMADA, TAKASE, KIKUMA, IWAMARU, AKACHI and HAYAKAWA2004; Eriksson et al., Reference ERIKSSON, JANSSON, JOHANSSON, BAVERUD, CHIRICO and ASPAN2009). Chooromoney et al. (Reference CHOOROMONEY, HAMPSON, EAMENS and TURNER1994) analysed the different strains using multilocus enzyme electrophoresis (MEE), and established that serotyping was not related to the epidemiological properties of the strains. The apathogenicity of E. tonsillarum probably results from the lack of an ability to produce neuraminidase, which is the enzyme responsible for the decomposition of sialic acid, leading to cell damage. The amount of enzyme that is produced increases at the moment that the bacterium proliferates. Strains of lower virulence tend to produce less of the enzyme (Wang et al., Reference WANG, CHANG, MEE and RILEY2005; Reference WANG, CHANG and RILEY2010; Harada et al., Reference HARADA, MURAMATSU, SUZUKI, TAMURA, SAWADA and TAKAHASHI2011). Coagulase and hialuronidase are additional factors of virulence, as these enzymes facilitate the penetration of host cells. It is suspected that different bird species exhibit different levels of sensitivity to E. rhusiopathiae infection (Bailie et al., Reference BAILIE, BURY, BICKNELL and KNUDTSON1970; Dhillon et al., Reference DHILLON, WINTERFIELD, THACKER and RICHARDSON1980; Bricker and Saif, Reference BRICKER and SAIF1997; Hollifield et al., Reference HOLLIFIELD, COOPER and CHARLTON2000; Derakhshanfar et al., Reference DERAKHSHANFAR, GHANBARPOUR and YAZDANI2004; Gartrell et al., Reference GARTRELL, ALLEY, MACK, DONALD, MCINNES and JANSEN2005).
Source of infection
Infections with E. rhusiopathiae occur through damaged skin or mucous membranes, and infection per os (orally) has been confirmed experimentally. The dosage required to cause death in turkeys ranged from 104 to 106 cells of the bacterium given subcutaneously or per os. Mortality of turkeys occurred at 44-120 hours after exposure to the disease. Symptoms occurred later and mortality was lower when administering the infection per os (Bricker and Saif, Reference BRICKER and SAIF1997). The amount of the bacteria in the blood, when the first symptoms of the disease were documented, ranged from 107 to 108/ml (Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978).
Broiler chickens infected intramuscularly with a dosage of 6.2 x 108 – 1.3 x 109 of the bacterium exhibited typical symptoms of the disease, including depression, asthenia, fluffing of the feathers, and the lowering of the wings. The infection resulted in 25% mortality in infected birds (Takahashi et al., Reference TAKAHASHI, TAKAGI, YAMAOKA, OHISHI, NORIMATSU, TAMURA and NAKAMURA1994). In the case of laying hens, symptoms occurred 2-5 days after initial infection. Many authors suggest that, among different age classes of hens, older birds are significantly more sensitive to infection. In field cases of the disease, the highest mortality occurred in hens during the period of egg laying, with 31% mortality of the flock being recorded at the end of the production cycle and 6.5% mortality being recorded in the 34th week of life. For birds up to the 20th week of life (point of lay), death only occurred occasionally. Mortality is probably related to the high burden of the organism, which leads to a decline in bird immunity. Despite the infective dosage of the pathogen being unknown in field cases, certain authors reported an exacerbation in the course of the disease in older birds (Mazaheri et al., Reference MAZAHERI, LIERZ and HAFEZ2005; Reference MAZAHERI, PHILIPP, BONSACK and VOSS2006; Brannstrom et al., Reference BRANNSTROM, HANSSON and CHIRICO2010; Kurian et al., Reference KURIAN, NEUMANN, HALL and MARKS2012). A clear decrease in age-related sensitivity to infection has not been observed in turkeys (Bricker and Saif, Reference BRICKER and SAIF1997).
Milne et al. (Reference MILNE, WINDSOR, ROGERSON and PENNYCOT1997) suggested that pheasants are the least sensitive bird species to the infection, reporting that E. rhusiopathiae only weakly expressed pathological symptoms and internal body changes in pheasants compared to turkeys. Another example of the disease, resembling E. rhusiopathiae was observed by Brickford et al. (Reference BRICKFORD, CORSTVET and ROSENWALD1978) in turkeys. In this instance, post mortems showed the presence of numerous ecchymosis in muscles and parenchymatous organs.
Opinions differ with respect to the level of sensitivity of waterfowl to infections with E. rhusiopathiae. According to Janowska et al. (Reference JANOWSKA, KRASNODĘBSKA-DEPTA and BIESZKE1978), incidence is higher in ducks compared to geese, which indicates that geese have lower sensitivity to infection with E. rhusiopathiae. However, personal observations indicate that the incidence of this disease in geese causes significant economic losses due to high mortality, and it seems that younger geese are more sensitive to infection (Bailie et al., Reference BAILIE, BURY, BICKNELL and KNUDTSON1970). Dhillon et al. (Reference DHILLON, WINTERFIELD, THACKER and RICHARDSON1980) observed a similar percentage of deaths in farmed ducks. The course of the disease probably depends on level of exposure to the infective agents.
The source of infection with E. rhusiopathiae depends on the poultry husbandry system. Birds are more exposed to infection when they are in contact with the external environment, such as on domestic or ecological farms, in aviaries or with access to an outdoor run. This is due to the increased possibility of contact with carriers, such as wild fowl, rodents, and insects (Morgan et al., Reference MORGAN, BRITT, COCKRILL and EITEN1994; Mazaheri et al., Reference MAZAHERI, PHILIPP, BONSACK and VOSS2006; Eriksson et al., Reference ERIKSSON, JANSSON, JOHANSSON, BAVERUD, CHIRICO and ASPAN2009). Contact with the soil is an important infection vector, as Erysipelothrix may survive in soil for several months. The bacterium primarily enters the soil via the faeces of sick animals. Herds of swine and sheep kept in the vicinity are most frequently mentioned as a source of infection (Bailie et al., Reference BAILIE, BURY, BICKNELL and KNUDTSON1970; Janowska et al., Reference JANOWSKA, KRASNODĘBSKA-DEPTA and BIESZKE1978). In addition, fish and badly prepared fishmeal may be a source of Erysipelothrix (Panigrahy and Hall, Reference PANIGRAHY and HALL1977; Boerner et al., Reference BOERNER, NEVIS, HINCKLEY, WEBER and FRASCA2004). Turkeys and geese are most commonly exposed to this infection, with the exposure of geese being related with access to runs and significant contact with the surrounding environment. The spread of the disease is supported by the occurrence of cannibalism in flocks of turkeys.
Poultry that are housed in closures with a limited possibility of contact with other birds are least exposed to infection. Outbreaks of E. rhusiopathiae may occur in laying hens kept in cages in the event of infestation with the mite Dermansyssus gallinae. This parasite may carry both viruses and bacteria, including E. rhusiopathiae, which has been confirmed by the results from tests of Erysipelothrix isolates obtained from hens, in which D. gallinae was documented on the same farm. Tests using molecular biology techniques indicated that the isolates are identical (Eriksson et al., Reference ERIKSSON, JANSSON, JOHANSSON, BAVERUD, CHIRICO and ASPAN2009). Despite the fact that it is not possible to cause the experimental infection of hens during blood taking by infected parasites, it is likely that Erysipelothrix is one of several bacteria that are carried by D. gallinae (Brannstrom et al., Reference BRANNSTROM, HANSSON and CHIRICO2010).
Hen eggs were excluded as a potential source of the infection. It was suspected that in the event of bacteremia, the pathogen might be delivered to the oocyte and the egg. This phenomenon may lead to the higher mortality of embryos, carrier-state, or development of the disease in chicks. Eggs laid and incubated from hens with confirmed E. rhusiopathiae exhibited no increase in embryonic mortality, despite the lack of disinfection of shells that could have allowed infection. Furthermore, the hatchling chicks from infected hens did not show any symptoms of the disease. Erysipelothrix rhusiopathiae has not been isolated from cultured eggs, dead embryos, or chicks killed on the 10th and 20th day of life (Mazaheri et al., Reference MAZAHERI, PHILIPP, BONSACK and VOSS2006). Hence, it can be concluded that the health of the progeny is not directly affected by E. rhusiopathiae in infected flocks of parent stock.
Clinical symptoms
Erysipelas usually has an acute course in birds. Despite the fact that the disease does not occur in the form of an epidemic, and is rather subject to repeat endemics in a given area, its outbreak may bring about significant losses. In the case of turkey flocks, the disease tends to occur suddenly, and has the course in the form of sepsis. Symptoms that occur just before death include unsteady walking and a lack of coordinated movement (Janowska et al., Reference JANOWSKA, KRASNODĘBSKA-DEPTA and BIESZKE1978; Gunning and Morton, Reference GUNNING and MORTON1988). In general, before the first deaths occur, irregularities in the flock are not visible. Sometimes limited or uncharacteristic symptoms occur, such as the fluffing of the feathers or a decline in feed consumption (Takahashi et al., Reference TAKAHASHI, TAKAGI, YAMAOKA, OHISHI, NORIMATSU, TAMURA and NAKAMURA1994).
Erysipelothrix rhusiopahiae may cause spots to appear on the skin of birds. Significant dark red crusty patches on the back of laying hens kept in cages have been observed (Mutalib et al., Reference MUTALIB, KING and McDONOUGH1993). The snood (head area) of turkeys may appear pale with oedema (swelling), along with dark rough patches on the head (Milne et al., Reference MILNE, WINDSOR, ROGERSON and PENNYCOT1997; Derakhshanfar et al., Reference DERAKHSHANFAR, GHANBARPOUR and YAZDANI2004). After experimental subcutaneous infection, the affected area exhibited oedema after several hours, with the skin of the birds becoming blue, with small amounts of serum-fibrinous effusion. Necrosis of the skin and hypoderma was observed (Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978; Derakhshanfar et al., Reference DERAKHSHANFAR, GHANBARPOUR and YAZDANI2004). In addition, the reddening of the skin of the toes in 2-to-4-day-old turkeys after toe-trimming has been observed. The toe joints were oedematous; however, no effusion was observed in any of the turkeys, although cultures prepared from the surface of the joint indicated the presence of E. rhusiopahiae (Hollifield et al., Reference HOLLIFIELD, COOPER and CHARLTON2000). Arthritis is a characteristic in the chronic form of the disease. The chronic form occurs most frequently in turkeys that have been vaccinated against erysipelas. In addition to changes in the joints, endocarditis may be present (Bricker and Saif, Reference BRICKER and SAIF1997).
Excluding the case of natural infection in hens with E. rhusiopahiae, clear symptoms of the disease may not be observed. Problems tend to occur suddenly, with farmers first suspecting that the flock has been poisoned (Mutalib et al., Reference MUTALIB, KING and McDONOUGH1993; Milne et al., Reference MILNE, WINDSOR, ROGERSON and PENNYCOT1997). However, egg production clearly declines during the production period of flocks. In the case of experimental infection symptoms appear around the third day after inoculation, including a decline in appetite, asthenia, and paleness of the cap occurred. The disease usually lasts about three weeks in hen flocks (Bricker and Saif, Reference BRICKER and SAIF1997; Brannstrom et al., Reference BRANNSTROM, HANSSON and CHIRICO2010)
Erysipelothrix rhusiopahiae is able to cause cellulitis, which can be an economic cost in terms of exclusion at slaughter, and has been confirmed experimentally in broiler chickens. The generation of clear necrosis changes, with oedema and infiltration of heterophils, can be observed in birds that survive longer than 24 hours from the moment of infection. In birds that die within 24 hours as a result of sepsis in the histological preparation, a slight infiltration of inflammatory cells is normally observed (Derakhshanfar et al., Reference DERAKHSHANFAR, GHANBARPOUR and YAZDANI2004).
Autopsy and anatomical-pathological changes
From the moment that natural cases of erysipelas occurs in birds, symptoms indicate the presence of generalised sepsis (Bricker and Saif, Reference BRICKER and SAIF1997). In all species of birds for which cases of erysipelas have been described so far, autopsy indicated similar internal anatomical changes. Most frequently, dead birds were in good condition and correctly muscled, although ecchymosis may be visible in the subcutaneous fat and muscles of the thighs (Mutalib et al., Reference MUTALIB, KING and McDONOUGH1993; Gartrell et al., Reference GARTRELL, ALLEY, MACK, DONALD, MCINNES and JANSEN2005). The internal organs become engorged, swollen, and congested, including the liver, spleen and kidneys. Often, greyish-yellow points of necrosis the size of a pin head occur in the liver (Panigrahy and Hall, Reference PANIGRAHY and HALL1977; Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978; Gunning and Morton, Reference GUNNING and MORTON1988; Morgan et al., Reference MORGAN, BRITT, COCKRILL and EITEN1994; Takahashi et al., Reference TAKAHASHI, TAKAGI, YAMAOKA, OHISHI, NORIMATSU, TAMURA and NAKAMURA1994), and hepatic mottling and sub-capsular ecchymosis may be present (Panigrahy and Hall, Reference PANIGRAHY and HALL1977; Milne et al., Reference MILNE, WINDSOR, ROGERSON and PENNYCOT1997; Gartrell et al., Reference GARTRELL, ALLEY, MACK, DONALD, MCINNES and JANSEN2005). Ecchymosis is also visible in the pericardial fat and on the cardiac muscle (Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978; Janowska et al., Reference JANOWSKA, KRASNODĘBSKA-DEPTA and BIESZKE1978) and sometimes it is possible to observe fluid in the pericardial sac. Points of necrosis may be found in the spleen (Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978). The lungs are usually engorged with a little ecchymosis in the parenchyma (Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978; Boerner et al., Reference BOERNER, NEVIS, HINCKLEY, WEBER and FRASCA2004).
The intestines become congested, with various levels of inflammation occurring, ranging from catarrh to haemorrhagic inflammation; however, it is not a pathognomic symptom (Panigrahy and Hall, Reference PANIGRAHY and HALL1977; Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978; Janowska et al., Reference JANOWSKA, KRASNODĘBSKA-DEPTA and BIESZKE1978; Gartrell et al., Reference GARTRELL, ALLEY, MACK, DONALD, MCINNES and JANSEN2005; Opriessnig et al., Reference OPRIESSNIG, VANCE and HALBUR2005). Ecchymosis is usually observed on the surface of the pancreas (Bailie et al., Reference BAILIE, BURY, BICKNELL and KNUDTSON1970). The kidneys become oedematous, and both may become congested (Takahashi et al., Reference TAKAHASHI, TAKAGI, YAMAOKA, OHISHI, NORIMATSU, TAMURA and NAKAMURA1994) and pale (Pettit et al., Reference PETTIT, GOUGH and TRUSCOTT1976; Brickford et al., Reference BRICKFORD, CORSTVET and ROSENWALD1978). Changes in the reproductive system were not observed (Mutalib et al., Reference MUTALIB, KING and McDONOUGH1993; Reference MUTALIB, KEIRS and AUSTIN1995). The chronic form is characterised by oedema of the joints. After the joints have been cut, effusion can be visible (Panigrahy and Hall, Reference PANIGRAHY and HALL1977; Hollifield et al., Reference HOLLIFIELD, COOPER and CHARLTON2000).
When conducting histopathological testing of parenchymatous organs, vascular changes predominate. Conglomerates of bacteria surrounded by thrombocytes are visible in the capillaries and smaller arterial and venous vessels. Points of necrosis related to infarctions regarding large vessels are rarely observed, with degenerative changes of parenchymatous organs being more likely to be observed. The destruction of the parenchymatous cells of organs in the acute form of the disease is clearly visible in the liver, spleen, and kidneys.
Atrophy of the lymphatic tissue, often leading to a complete lack of lymphocytes, may be observed in the spleen. In extreme cases, the pulp of the spleen is completely destroyed, with only a vascular layer and hypertrophic reticular cells remaining. Ecchymosis and oedema of the cells are particularly visible in the heart and lungs. Infiltration of the mononuclear cells in the endocardium and pericardial sac usually occurs several days after the onset of infection. Infiltration of inflammatory cells in the synovium is observed in the joints.
Immunisation of birds
The only species of poultry for which vaccines against erysipelas have been registered are turkeys. The most frequently used vaccines are based on bacterial cells that have been inactivated with formalin (Bricker and Saif, Reference BRICKER and SAIF1997). Tests have confirmed that vaccines applied widely in swine husbandry are also effective on turkeys (Adler and Nilson, Reference ADLER and NILSON1952; Bricker and Saif, Reference BRICKER and SAIF1988). In Poland, research on the effectiveness of the vaccines against erysipelas for turkeys was carried out by Krasnodębska-Depta and Janowska (Reference KRASNODĘBSKA-DEPTA and JANOWSKA1980) and Krasnodębska-Depta and Koncicki (Reference KRASNODĘBSKA-DEPTA and KONCICKI1988). These researchers established that a double intravenous administration of both life vaccines and inactivated vaccines gave full protection of turkeys against infection with Erysipelothrix sp. In addition, the administration of vaccines for application per os obtained a satisfactory level of protection. However, the double administration of the vaccine with drinking water resulted in lower level of antibodies compared to injection (Krasnodębska-Depta and Koncicki, Reference KRASNODĘBSKA-DEPTA and KONCICKI1988). Bricker and Saif (Reference BRICKER and SAIF1988) assessed the application of the vaccine against erysipelas administered per os, and found that an appropriate level of protection may be obtained only after a double administration of the vaccine has been given at an appropriate dosage. The minimal dosage (administered twice to birds to fully protect them) is 4 x 109 bacteria.
The vaccination of bird species for which the vaccine was not registered has produced satisfactory results. One example is emus, which were vaccinated subcutaneously in the fourth and eighth week of life with the dosage recommended for turkeys (0.5 ml/ bird), with the subsequent experimental infection with E. rhusiopathiae producing no symptoms of the disease (Swan and Lindsey, Reference SWAN and LINDSEY1998). In vaccinated flocks of emu, erysipelas caused by the strain belonging to serotype 21 occurred. Despite the fact that the applied vaccine contained both serotypes 1 and 2, which tend to be isolated from cases of erysipelas in swine, the birds showed full immunity to infection with E. rhusiopahiae after infection. The existence of cross-immunity among individual serotypes of E. rhusiopahiae has been indicated through observations from mice, swine, and dolphins (Takahashi et al., Reference TAKAHASHI, TAKAGI, SAWADA and SETO1984; Sawada and Takahashi Reference SAWADA and TAKAHASI1987; Redhead et al., Reference REDHEAD, PUGH, JENSEN and HOUGHTON1998; Lacave et al., Reference LACAVE, COX, HERMANS, DEVRIESE and GODDEERIS2001). Mutalib et al. (Reference MUTALIB, KING and McDONOUGH1993) has suggested the effectiveness of vaccines in flocks of laying hens.
Our own observations in geese indicate the possibility of the safe application of vaccines developed for swine and turkeys in flocks threatened by the occurrence of erysipelas (data not published).
Treatment
It has been assumed that E. rhusiopahiae is mainly sensitive to penicillin, but it also responds to cephalosporins, tetracyclines, quinolines, clindamycin, erythromycin, and piperacillin. It is resistant to vancomycin, chloromycetin, gentamycin, polymyxin B, streptomycin, and sulphametaxasol. The selected medicines for treatment include penicillins and cephalosporins (Veraldi et al., Reference VERALDI, GIRGENTI, DASSONI and GIANOTTI2009), with penicillins being most frequently used in animals.
Conclusions
Erysipelas is likely to occur in a wide range of avian hosts. In most species, the disease occurs as a septicaemia, characterised by ecchymosis on the surface of the heart and pancreas, and internal organs become enlarged, including the liver, spleen, and kidneys. Chronic erysipelas may appear in both urticarial and endocardial forms. The internal anatomical changes can prove useful for diagnosis; however, full diagnosis must be based on microbiological examination of organ samples (liver, heart, and joints). The isolation and identification of E. rhusiopathiae is necessary for definitive diagnosis, and the antibiotic of choice for treating E. rhusiopathiae is penicillin.
