- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- swine dysentery
International Common Names
- English: swine dysentery, brachyspira hyodysenteriae, in pigs
Local Common Names
- USA: black scours; bloody scours
Pathogen/sTop of page
OverviewTop of page
Swine dysentery (SD) is a contagious diarrhoeic disease in pigs characterized by mucohaemorrhagic colitis and caused by strongly haemolytic spirochetes of the genus Brachyspira. The disease was originally described 80 years ago and is prevalent in most pig-rearing countries. For example, in the UK the disease was the second most commonly diagnosed enteric disease of pigs in 1995 (Taylor, 1995). Affected herds often suffer devastating production losses (Windsor and Simmons, 1981).
Swine dysentery was first described in 1921 in Indiana, USA by Whiting et al. (1921) as a bloody diarrhoea with necrotic haemorrhagic inflammation of the mucosa of the stomach and the large intestine. The disease has since been reported from most pig-rearing areas worldwide. The first observation in Europe dates from Italy in 1935 (Duthie, 1966). Swine dysentery was reported from Australia in 1938 (McLennan et al., 1938), The Netherlands in 1953 (Ulsen, 1953), Britain in 1957 (Birrel, 1957) and in Scandinavia in 1960 (Ronéus, 1960).
The disease appeared to increase in prevalence and severity with increasing intensification of pig industries and increasing trade in live pigs in the late 1960s. This stimulated the scientific community to investigate the then nebulous causes of SD. The true etiological factor was determined when Taylor and Alexander (1971) were able to provoke swine dysentery in pigs inoculated with a large spirochete.
A similar study was simultaneously performed by Harris et al. (1972a), who induced signs and lesions of dysentery in both specific pathogen-free (SPF) pigs inoculated with a large spirochete in combination with vibrio-like organisms, and in SPF pigs inoculated solely with the spirochete. The spirochete was named Treponema (T.) hyodysenteriae. Strain B78 was selected as the type strain of the new species.
Twenty years later, experiments capitalizing on advances in molecular biology, including DNA–DNA reassociation, sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS–PAGE) profiles of whole-cell proteins and analysis of 16S rRNA sequence data from strains of T. hyodysenteriae, all indicated that the organism was only distantly related to T. pallidum, the reference species of the genus Treponema (Stanton et al., 1991). Consequently, the genus name was changed, first to Serpula (Stanton et al., 1991) and then to Serpulina (Stanton, 1992).
The current designation of the classical etiological agent of SD, Brachyspira hyodysenteriae (Ochiai et al., 1997), was established when DNA-DNA reassociation experiments showed that the genuses Brachyspira and Serpulina should be designated to one genus, Brachyspira. According to taxonomic rules, the genus name Brachyspira (Hovind-Hougen et al., 1982) was selected because it had been proposed 11 years prior to Serpulina (Stanton, 1992). Recently, other Brachyspira spp. not identified as B. hyodysenteriae by laboratory methods have been associated with mucohemorrhagic diarrhoea in pigs including the proposed novel species “Brachyspira suanatina” (Råsbäck et al., 2007) and “Brachyspira hampsonii” (Chander et al., 2012). Experimental inoculation studies have confirmed the pathogenicity of these spirochetes through the induction of clinical disease and/or lesions indistinguishable from those associated with B. hyodysenteriae infection in mice (Burrough et al., 2012a) and susceptible pigs (Råsbäck et al., 2007; Burrough et al., 2012b; Rubin et al., 2013a). Accordingly, it has been recently concluded that the definition of SD be extended to include mucohemorrhagic colitis caused by any strongly haemolytic Brachyspira spp. (Hampson, 2014).
Taxonomy of Brachyspira hyodysenteriae
Brachyspira hyodysenteriae belongs to the genus Brachyspira (Fellström, 1996). Five officially recognized porcine species of Brachyspira have been described: B. hyodysenteriae; B. innocens (Kinyon and Harris, 1979); B.pilosicoli (Trott et al., 1996); Brachyspira intermedia (Stanton et al., 1997); and B. murdochii (Stanton et al., 1997). The genus Brachyspira is included in the order Spirochaetales, which is divided into three families Spirocaetaceae, Brachyspiraceae and Leptospiraceae. The family Spirocaetaceae contains the genera Borrelia, Brevinema, Cristispira, Spirochaeta, Spironema and Treponema, the family Brachyspiraceae contains the genus Brachyspira (Serpulina), and the family Leptospiracea contains the genera, Leptonema and Leptospira (Paster and Dewhirst, 2000). These organisms have morphological features in common which distinguish them from other bacteria. Spirochetes are unicellular, flexible and helical with one or more complete turns. Transmission electron microscopy has revealed that spirochetes have a coiled or wavy protoplasmatic cylinder, an outer sheath or tunica that envelops the whole organism, and unique organelles, called axial filaments (flagellae), which are inserted at each end of the cell and lie between the tunica and the cytoplasmatic membrane (Turner, 1976).
Host AnimalsTop of page
Hosts/Species AffectedTop of page
All domesticated pigs are probably susceptible to infection with B. hyodysenteriae and no breed disposition has been reported. Poor hygiene, cold temperatures, overcrowding, transportation and mixing of new stock may be predisposing factors (Griffin and Hutchings, 1980; Harris, 1984). Diet and immunological factors may also influence the clinical expression of SD. Clinical disease is mainly seen in growing, finishing or young adult stock.
Wild rodents are recognized as potential carriers of Brachyspira spp. (Joens and Kinyon, 1982) and are an important potential source of inter-farm and intra-farm spread. Numerous Brachyspira spp., including B. hyodysenteriae, have been recovered from rodents on pig farms (Backhans et al., 2010). The potential importance of waterfowl as a source of spirochete transmission between farms is supported by the recent isolation of “B. suanatina” in the faeces of mallard ducks in Sweden (Råsbäck et al., 2007) and “B. hampsonii” isolation from the faeces of migratory birds including lesser snow geese in Canada (Rubin et al., 2013b) and mallard ducks and graylag geese in Spain (Martínez-Lobo et al., 2013).
Systems AffectedTop of page
DistributionTop of page
Swine dysentery is a common disease worldwide (Roncalli and Leaning, 1976; Hampson et al., 1997; Hampson, 2000). However, very limited accurate information is available regarding the current prevalence of SD in different countries. Studies performed in the UK and Denmark have suggested a general SD prevalence of around 10% of herds (Møller et al., 1998; Thomson et al., 1998; Pearce, 1999) based on culture. A serological survey in the US indicated that 11% of swine herds had been exposed to B. hyodysenteriae (Mapother, 1993). An overall decline in the prevalence of the disease in the US probably occurred during the 1990s, due to the establishment of high health status herds and changes in management practices. Since the latter part of 2006, a re-emergence of SD has occurred in the United States and Canada (Burrough, 2013); however, the precise factors underlying this re-emergence are poorly understood and may include changes in feeding practices and other factors. The disease is likely to be present in most major pig producing countries outside Europe, the US and Australia, but is probably being controlled by the use of antimicrobial drugs (Hampson, 2000).
Distribution TableTop 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.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Burundi||Absent, No presence record(s)|
|Cabo Verde||Absent, No presence record(s)|
|Central African Republic||Absent, No presence record(s)|
|Congo, Democratic Republic of the||Absent, No presence record(s)|
|Côte d'Ivoire||Absent, No presence record(s)|
|Djibouti||Absent, No presence record(s)|
|Egypt||Absent, No presence record(s)|
|Eritrea||Absent, No presence record(s)|
|Eswatini||Absent, No presence record(s)|
|Ghana||Absent, No presence record(s)|
|Guinea||Absent, No presence record(s)|
|Libya||Absent, No presence record(s)|
|Madagascar||Absent, No presence record(s)|
|Mauritius||Absent, No presence record(s)|
|Sudan||Absent, No presence record(s)|
|Togo||Absent, No presence record(s)|
|Tunisia||Absent, No presence record(s)|
|Uganda||Absent, No presence record(s)|
|Zimbabwe||Absent, No presence record(s)|
|Bahrain||Absent, No presence record(s)|
|Bhutan||Absent, No presence record(s)|
|China||Present||Present based on regional distribution.|
|Georgia||Absent, No presence record(s)|
|India||Absent, No presence record(s)|
|Indonesia||Absent, No presence record(s)|
|Kazakhstan||Absent, No presence record(s)|
|Kuwait||Absent, No presence record(s)|
|-Peninsular Malaysia||Absent, No presence record(s)|
|-Sabah||Absent, No presence record(s)|
|Mongolia||Absent, No presence record(s)|
|North Korea||Absent, No presence record(s)|
|Oman||Absent, No presence record(s)|
|Philippines||Absent, No presence record(s)|
|Singapore||Absent, No presence record(s)|
|Sri Lanka||Absent, No presence record(s)|
|Syria||Absent, No presence record(s)|
|Taiwan||Absent, No presence record(s)|
|Thailand||Absent, No presence record(s)|
|United Arab Emirates||Absent, No presence record(s)|
|Uzbekistan||Absent, No presence record(s)|
|Belarus||Absent, No presence record(s)|
|Czechia||Absent, No presence record(s)|
|Estonia||Absent, No presence record(s)|
|Liechtenstein||Absent, No presence record(s)|
|North Macedonia||Absent, No presence record(s)|
|Portugal||Absent, No presence record(s)|
|Romania||Absent, No presence record(s)|
|Slovakia||Absent, No presence record(s)|
|Slovenia||Absent, No presence record(s)|
|Spain||Absent, No presence record(s)|
|Barbados||Absent, No presence record(s)|
|Bermuda||Absent, No presence record(s)|
|British Virgin Islands||Absent, No presence record(s)|
|Cayman Islands||Absent, No presence record(s)|
|Curaçao||Absent, No presence record(s)|
|Dominica||Absent, No presence record(s)|
|Guatemala||Absent, No presence record(s)|
|Haiti||Absent, No presence record(s)|
|Honduras||Absent, No presence record(s)|
|Jamaica||Absent, No presence record(s)|
|Mexico||Absent, No presence record(s)|
|Nicaragua||Absent, No presence record(s)|
|Panama||Absent, No presence record(s)|
|Saint Kitts and Nevis||Absent, No presence record(s)|
|Saint Vincent and the Grenadines||Absent, No presence record(s)|
|-Western Australia||Present, Widespread|
|French Polynesia||Absent, No presence record(s)|
|Samoa||Absent, No presence record(s)|
|Vanuatu||Absent, No presence record(s)|
|Bolivia||Absent, No presence record(s)|
|Brazil||Absent, No presence record(s)|
|-Rio Grande do Sul||Present|
|Chile||Absent, No presence record(s)|
|Colombia||Absent, No presence record(s)|
|Ecuador||Absent, No presence record(s)|
|Falkland Islands||Absent, No presence record(s)|
|Guyana||Absent, No presence record(s)|
|Uruguay||Absent, No presence record(s)|
PathologyTop of page
Lesions are limited to the large intestine. Early lesions are first noted in the centrifugal and centripetal coils near the apex of the colon. Over time the changes may extend to the whole colon, and beginning day 4 may also affect the caecum. In some instances the whole large intestine may become involved. Typical changes in the acute stage of SD include hyperemia and oedema of the walls and mesentery of the large intestine. The mesenteric lymph nodes may be swollen, and colonic submucosal glands are often more prominent than normal. Mucus, and fibrin containing flecks of blood usually cover the mucosa. As the disease progresses, mucosal lesions may become more severe with increased fibrin exudation, and may form thick, mucofibrinous pseudomembranes. Once the lesions become chronic, the mucosa may take on the appearance of having marked superficial necrosis (Harris and Lysons, 1992).
Microscopically, the damage to the colonic mucosa and submucosa is characterized by superficial necrosis, eroded epithelium, oedema, leukocytic infiltration and hyperplasia of goblet cells. In acute SD, the mucus bilayer in the spiral colon is significantly altered with a reduction in sulphated mucins, decreased expression of mucin 4, and increased expression of mucin 5AC (Wilberts et al., 2014a). As the disease progresses, clumps of epithelial cells may detach from the lamina propria, resulting in exposure of capillaries followed by focal areas of haemorrhage. Large spirochetes are found in the lumen, within crypts and in the lamina propria and are readily visible by silver staining; however, this method is nonspecific and pathogenic spirochetes can be identified to the species level using in situ hybridization with oligonucleotide probes targeting B. hyodysenteriae (Boye et al., 1998) and “B. hampsonii” (Burrough et al., 2013). Using transmission electron microscopy (TEM), B. hyodysenteriae cells can be visualized invading epithelial cells, goblet cells and the lamina propria (Harris and Lysons, 1992).
DiagnosisTop of page
The first clinical evidence of disease is usually soft, yellow to grey faeces, but the most consistent sign of SD is a blood stained, mucoid diarrhoea. As the disease progresses, appearance of white mucofibrinous strands in the stools is almost pathognomonic. Other signs may include an arched back, suggesting abdominal pain, and accompanying anorexia and fever. Swine dysentery is a severe diarrhoeal disease with high mortality in typical cases that are not treated. However, severity may vary, and the use of antibacterials as growth promoters may suppress clinical signs. If the disease is not treated, prolonged diarrhoea may lead to severe dehydration, followed by death. A SD diagnosis may be further indicated by typical findings at necropsy (see Pathology).
Infection with Lawsonia intracellularis, Brachyspira pilosicoli, Trichuris suis or salmonellosis may induce clinical signs that resemble SD.
Bacterial culture and biochemical tests have traditionally been the most common methods used for detection of B. hyodysenteriae, and for differentiation from other species of intestinal porcine spirochetes. The organisms grow well on blood agar plates. Inclusion of antibiotics in the growth media, for example, a combination of spectinomycin, vancomycin and colistin, reduces the growth of other colonic microorganisms and allows the b-haemolytic colonies of B. hyodysenteriae to be identified (Fellström and Gunnarsson, 1995; Jensen, 1997). Porcine intestinal spirochetes can be classified into a scheme according to their biochemical properties (see Table; after Fellström et al., 1999). On a genetic basis, the groups roughly correspond to the hitherto officially recognized species of the genus Brachyspira isolated from pigs (Pettersson et al., 1996), i.e. B. hyodysenteriae (group I), Brachyspira intermedia (group II), B. murdochii (group IIIa), B. innocens (group IIIbc) and B. pilosicoli (group IV). In the biochemical classification, Brachyspira spp. associated with swine dysentery are characterized by strong b-haemolysis and belong to group I (see Table); however, the variability in indole reactivity between SD-associated spirochetes suggests modification of this table may be necessary (i.e. group Ia and Ib) should these putative novel species gain official recognition and require clinical differentiation.
Differentiation of porcine Brachyspira species by biochemical reactions
1Ind = Indole production
2Hipp = Hippurate hydrolysis
3a-gal = alpha-galactosidase activity
4ß-glu = beta-glucosidase activity
* = variable indole reactivity has been reported for B. hyodysenteriae; however, “B. suanatina” isolates are indole positive and “B. hampsonii” isolates are indole negative.
In addition to culture, other techniques for diagnosis of B. hyodysenteriae infections have been developed, including serology and polymerase chain reaction (PCR). Serological tests have shown a lack of sensitivity and/or specificity when used in the field, and are not suited for the reliable detection of individual carrier pigs (Hampson, 2000). Recent studies have suggested that screening ELISAs run on meat juices may be useful in detecting herds infected with B. hyodysenteriae (Song et al., 2012). A number of PCR systems with high specificity have been described (Elder et al., 1994; Leser et al., 1997; Atyeo and Hampson, 1998; Atyeo et al., 1998); however, these were often of limited practical use due to sensitivity issues when applied directly to faecal samples. A duplex assay specifically designed to detect B. hyodysenteriae and B. pilosicoli in pig faeces (La et al., 2003) was adopted by many diagnostic laboratories due to ease of use and rapid turnaround of results relative to selective culture; however, this and other species-based PCR assays may fail to detect novel and/or atypical isolates and should therefore be used with caution.
From a diagnostic standpoint, culture remains a highly sensitive method for detecting Brachyspira spp.; however, it is less specific than PCR and requires additional biochemical or molecular testing for speciation. In many veterinary diagnostic laboratories, cultured spirochetes can be speciated at the molecular level by a variety of PCR assays and/or nox gene sequencing as well as at the protein level using matrix-assisted laser desorption ionization time-of-flight mass spectrometry (Calderaro et al., 2013; Warneke et al., 2014).
Subspecies differentiation of Brachyspira spp. may be achieved by the use of multilocus enzyme electrophoresis (MEE; Lymbery et al., 1990), restriction endonuclease analysis (REA; Combs et al., 1989), restriction fragment length polymorphism (RFLP) analysis (Duhamel et al., 1992; Jensen and Stanton, 1993; Rohde et al., 2002), and pulsed field gel electrophoresis (PFGE; Atyeo and Hampson, 1998; Fellström et al., 1999).
A specific humoral immune response to outer membrane antigens of B. hyodysenteriae is induced following infection (Wannemuehler et al., 1988). Clinical disease is associated with the development of specific IgG, IgA and IgM antibodies in serum, and local production of IgA in gut mucosal tissues. Joens et al. (1984) suggested that the antibody secreted in the colon is the mechanism by which the recovered pig is protected against re-exposure to SD. Mucosal infection stimulates the production of memory cells, but humoral immunity alone is probably not responsible for the onset of a protective response to B. hyodysenteriae (Rees et al., 1989). Cell mediated immunity also may be important in protection against SD (Jenkins et al., 1982; Kennedy et al., 1992; Waters et al., 1999a). Repeated infection provides varying degrees of protection (Olson, 1974; Joens et al., 1979; Adachi et al., 1984; Rees et al., 1989).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Pigs:All Stages||Sign|
|Digestive Signs / Bloody stools, faeces, haematochezia||Pigs:All Stages||Diagnosis|
|Digestive Signs / Dark colour stools, faeces||Sign|
|Digestive Signs / Diarrhoea||Pigs:All Stages||Diagnosis|
|Digestive Signs / Melena or occult blood in faeces, stools||Sign|
|Digestive Signs / Mucous, mucoid stools, faeces||Pigs:All Stages||Diagnosis|
|General Signs / Dehydration||Pigs:All Stages|
|General Signs / Fever, pyrexia, hyperthermia||Pigs:All Stages||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Sign|
|General Signs / Kyphosis, arched back||Pigs:All Stages||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig,Pigs:Gilt||Sign|
|General Signs / Sudden death, found dead||Pigs:All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Pigs:All Stages||Sign|
|Pain / Discomfort Signs / Colic, abdominal pain||Pigs:All Stages||Sign|
Disease CourseTop of page
Many details of the pathogenesis of SD are still not understood. Infection occurs by ingestion of faecal material. The organism is protected from stomach acid by mucus in the dysenteric faeces (Taylor, 1995). Once ingested it invades the mucus and crypts of the mucosa in the large intestine and penetrates colonic enterocytes and goblet cells (Taylor and Blakemore, 1971). Early lesions can be observed before penetration, and therefore, penetration of cells is probably not a precondition for the initiation of SD (Wilcock and Olander, 1979; Albassam et al., 1985). Systemically, the disease is characterized by dehydration, acidosis and hyperkalemia, followed in severe cases by death.
Argenzio et al. (1980) demonstrated that the fluid losses in SD are exclusively the result of failure of the colon to reabsorb the endogenous secretions, due to a failure of the epithelial transport mechanisms to actively transport sodium and chloride from lumen to blood. Extensive fluid losses and ion imbalance occur with the disease, but B. hyodysenteriae does not invade the body nor produce a septicemic state (Kinyon et al., 1980).
Studies in gnotobiotic/germ-free pigs have indicated that B. hyodysenteriae is able to colonize the large intestine without the support of other microorganisms (Harris et al., 1972b; Meyer et al., 1974; Brandenburg et al., 1977; Whipp et al., 1982). However, several reports suggest that other colonic anaerobes act as supporting organisms (Harris et al., 1978; Whipp et al., 1982; Siba et al., 1994). Flagella and motility are probably involved in the colonization process (Kennedy and Yancey, 1996). The organism moves effectively at high speed by chemotaxis through viscous material such as mucin (Kennedy et al., 1988; Milner and Sellwood, 1994). Mutant strains of B. hyodysenteriae (Rosey et al., 1995; Kennedy et al., 1997), deprived of a flagellar gene, have been reported to be less virulent or avirulent in swine, which suggests that motility is an important virulence factor. Whether attachment is an important feature in the disease has not been conclusively demonstrated (Harris and Lysons, 1992).
It has been speculated (Savage, 1980) that an important virulence mechanism for pathogens of the intestinal tract could be their ability to utilize oxygen in order to colonize aerated environments such as the oxygen-respiring epithelial surfaces of the porcine large intestine. Stanton (1989) demonstrated that B. hyodysenteriae can metabolize substantial amounts of oxygen. Further mutants of B. hyodysenteriae strain B204 that have an inactivated NADH oxidase gene, and therefore a reduced ability to utilize oxygen, have been shown to be less virulent than the parent strain B204 (Stanton et al., 2000).
Interaction between B. hyodysenteriae and a fermentative bacterial flora in the colon and caecum has been suggested by Siba et al. (1994) and Pluske et al. (1996) to be involved in development of SD. Pigs fed a highly fermentative diet based on wheat and dehulled lupin seeds all developed SD in a challenge trial with B. hyodysenteriae, while pigs similarly challenged, but fed a diet based on boiled rice and animal protein were spared. The mean pH of caecal content in pigs before challenge for pigs fed the fermentative diet was 5.4, and 6.5 for pigs on the rice-based diet. Later studies (Durmic et al., 1998; Pluske et al., 1998) have further identified that high levels of non-starch polysaccharides, and starch which is not digested in the small intestine, are involved in the onset of SD. However, another similar study could not confirm the relationship between fermentable carbohydrates and the incidence of SD (Lindecrona et al., 2000).
Prohászka and Lukács (1984) demonstrated a pH-dependent antibacterial effect, attributed to the presence of volatile fatty acids (VFAs), in the contents of the large intestine of pigs. In vitro, a low pH <6.0) resulted in loss of motility of B. hyodysenteriae. They suggested that a diet based on maize silage is protective against SD because of the resulting acidic environment in the gut lumen of pigs.
Whether the synergism observed between B. hyodysenteriae and other anaerobes facilitates colonization or expression of pathogenicity (or both) has not been clearly demonstrated. Beckmann (1992) reported a CAMP-like phenomenon in Brachyspira isolates, when the isolates were streaked onto an isolate of Staphylococcus aureus. Whether such synergistic reactions could occur in vivo and if so, whether they might be of importance for pathogenicity is not known. An outer membrane Brachyspira protease may contribute to intestinal damage (Muniappa and Duhamel, 1997). Epithelial necrosis and vascular leakage late in the disease create conditions favouring overgrowth by opportunistic bacteria, which may be a contributing factor in pathogenesis (Albassam et al., 1985).
There is a close correlation between strong ß-haemolytic activity and pathogenicity among Brachyspira strains (Burrough et al., 2012b). However, the exact role played by the haemolysins is not known and the actual causes of the initial damage are not understood. The purified haemolysin (Kent et al., 1988) of B. hyodysenteriae has proved cytotoxic for a number of cell types, both in vitro and in vivo (Lysons et al., 1991; Hutto and Wannemuehler, 1999). Lysons et al. (1991) demonstrated damage to epithelial cells in ligated ileal and colonic loops of germ-free pigs injected with the haemolysin. The lesions, characterized by swelling and shedding of cells with disrupted organelles, were similar to those observed as early changes following injection of pig colonic loops with cultures of B. hyodysenteriae (Kang and Olander, 1990).
The importance of the haemolysin as a virulence factor has been emphasized by experimental infections in mice and pigs (ter Huurne et al., 1992a, b; Hyatt et al., 1994). These workers used recombinant DNA-techniques to produce mutants of B. hyodysenteriae deprived of the haemolysin tlyA gene. The mutants did not cause dysentery, but still produced mild lesions. From these experiments it seems reasonable to conclude that the haemolysin is an important factor in the pathogenesis of SD, though other factors may also be involved. However, reports of avirulent field isolates of B. hyodysenteriae have been published (Burrows and Lemcke, 1981; Lysons et al., 1982; Lee et al., 1993) and extended laboratory passages can produce strains that remain strongly b-haemolytic, but are no longer pathogenic for pigs (Hudson et al., 1974; Kinyon et al., 1977; Jensen and Stanton, 1993). On the other hand, potentiated pathogenicity by in vivo passages of B. hyodysenteriae in susceptible pigs has been demonstrated (Amtsberg et al., 1984; Blaha et al., 1984).
Other toxins may also be involved in causing lesions of SD (Baum and Joens, 1979; Nuessen et al., 1983; Greer and Wannemuehler, 1989a, b; Nibbelink et al., 1997) that may help provoke inflammatory lesions following infection with B. hyodysenteriae. However, Whipp et al. (1978) and Wilcock and Olander (1979) were unable to demonstrate toxic activity either with cell-free derivates of broth cultures or with sonically disrupted whole cultures of B. hyodysenteriae. Schmall et al. (1983) observed no increase above normal values of cyclic adenosine monosulphate (cAMP) and cyclic guanosine monophosphate (cGMP) in colonic mucosa of dysenteric pigs, suggesting that neither enterotoxin nor prostaglandins are involved in causing the diarrhoea.
EpidemiologyTop of page
Swine dysentery is caused by proliferation of strongly haemolytic Brachyspira spp. Infection occurs by ingestion of faecal material. The disease is usually introduced into a herd by carrier pigs, for example, animals that have recovered from a previous infection (Windsor and Simmons, 1981). Such pigs may continue to shed the infectious agent for months, without manifesting clinical signs (Songer et al., 1978; Fisher and Olander, 1981). In addition, B. hyodysenteriae has the ability to survive in pig faeces for up to 48 days (Chia and Taylor, 1978).
Although the infectious agent has only been demonstrated to occur as a natural infection in pigs and rheas (Jensen et al., 1996), wild rodents may be carriers of B. hyodysenteriae (Joens and Kinyon, 1982; Backhans et al., 2010) and waterfowl may also be a source of Brachyspira transmission between farms (Rubin et al., 2013b; Martínez-Lobo et al., 2013).
Brachyspira hyodysenteriae is recombinant with an epidemic population structure (Trott et al., 1997). As a consequence, it is unusal for more than one strain of B. hyodysenteriae to be present in a piggery (Fellström et al., 1999).
Impact: EconomicTop of page
Reduced production due to impaired growth, mortality, costs of medication and treatments, increased inputs for preventive measures and restrictions on movement of stocks may cause considerable economic losses. In Australia, losses resulting from reduced production and deaths was estimated to be 2.5% of annual gross national pig production (Hampson, 1991). Wood and Lysons (1988) estimated the cost due to decreased production in an infected herd in the USA to be US $12.60 per pig sold. In another infected herd in the USA, the costs of medication were estimated to be US $8.30 per pig marketed, and after eradication, medication costs were reduced to US $0.08 per pig marketed (Walter and Kinyon, 1990). Duhamel and Joens (1994) estimated the total national annual losses due to SD in the USA at US $115.2 million.
Zoonoses and Food SafetyTop of page
At present there is no evidence that swine dysentery occurs as a zoonotic disease. Consequently, it is unlikely that SD possesses any kind of threat to humans.
Disease TreatmentTop of page
A variety of antibacterials, such as tylosin, nitroimidazoles (dinitroimidazole, metronidazole, ronidazole), lincomycin, virginiamycin, tiamulin, olaquindox and carbadox, have been used successfully over the years in the treatment and prevention of SD. Although most of these drugs still may have some clinical effect, development of resistance for B. hyodysenteriae to several of those substances has been reported. Furthermore, the pharmacokinetic properties of olaquindox and carbadox make these antibacterials unsuitable for the treatment of SD (Graaf et al., 1988; Spierenburg et al., 1988), in spite of low minimum inhibitory concentrations (MICs) in vitro. Moreover, nitroimidazoles are no longer available in the EU and the USA. A number of reports indicate that pleuromutilins (tiamulin, valnemulin) are the only antimicrobials available with acceptable MICs in relation to pharmacokinetic properties for the treatment of Brachyspira (Rønne and Szancer, 1990; Binek et al., 1994; Buller and Hampson, 1994; Cizek et al., 1996; Fellström et al., 1996; Molnár, 1996; Karlsson and Franklin, 2000). Valnemulin sometimes produces adverse reactions (depression, ataxia, weakness, anorexia) when used in Danish and Swedish Landrace breeds and crosses.
Buller and Hampson (1994) claimed that having only one suitable substance for treatment of SD presents a potential threat to the pig industry. They suggested that the use of antimicrobials must be restricted to specific therapy. Accordingly, it is concerning that recent reports have shown tiamulin resistance in strains of B. hyodysenteriae from Spain (Hidalgo et al., 2011) and another report revealed a gradual rise in tiamulin MICs over time (Pringle et al., 2012). These resistant strains may be somewhat regional as a recent report of tiamulin susceptibility in Polish isolates showed no resistance (Zmudzki et al., 2012). Both the proposed novel Brachyspira spp. associated with SD appear similarly amenable to antimicrobial therapy as isolates of “B. suanatina” have been reported as susceptible to tiamulin, lincomycin, and valnemulin (Råsbäck et al., 2007) and North American isolates of “B. hampsonii” have been reported as sensitive to tiamulin, valnemulin, and carbadox (Mirajkar and Gebhart, 2013). Isolates of “B. hampsonii” from European waterfowl have also been reported as susceptible to tiamulin (Martínez-Lobo et al., 2013). Tiamulin water medication appears highly effective in resolving SD as the additional of tiamulin at 60 ppm in the water resolved clinical disease within 24 hours and eliminated spirochete shedding within 72 hours in pigs experimentally infected with either B. hyodysenteriae or “B. hampsonii” (Wilberts et al., 2014b).
The observation of resistant strains of B. hyodysenteriae underscores the importance of MIC testing of clinical isolates prior to treatment. Furthermore, these findings, and the limited number of efficacious antimicrobials available to treat SD, suggest that alternative means of controlling SD must be developed, such as all in-all out procedures, availability of SD-free stock, and eradication of strongly haemolytic Brachyspira spp. from affected herds.
Prevention and ControlTop of page
Immunization and Vaccines
Repeated infection provides protection in varying degrees. Vaccination has not been shown to offer any advantages over efficient treatment and control measures. Different approaches have been used in the development of vaccines. Most have involved the use of killed whole-cell preparations (Fernie et al., 1983; Diego et al., 1995; Waters et al., 1999b). Subunit vaccines and live vaccines have also been described (Wannemuehler et al., 1990; Lysons et al., 1986). All methods used have been shown to be only partly effective. A reverse vaccinology approach was used to identify B. hyodysenteriae proteins for use as recombinant vaccine components and revealed multiple potential immunogens that may prove useful (Song et al., 2009). No commercial vaccine against B. hyodysenteriae is currently available; however, autogenous bacterin vaccines have been used with some success.
Eradication of the infectious agent should always be considered in infected herds. If producers choose to 'live' with the disease rather than to try and eradicate it, all in-all out production combined with careful cleaning and disinfecting routines are the most important factors in the control of SD. Rodent control is also essential as wild rodents can serve as a source of spread within and between farms. To avoid introduction of SD and other diseases into herds, purchased animals should always be kept in quarantine for at least 3 weeks. If the SD status of such animals is unknown, treatment with pleuromutilins (tiamulin, valnemulin) should be performed.
ReferencesTop of page
Achacha M, Mittal KR, 1995. Production and characterization of monoclonal antibodies against Serpulina hyodysenteriae and S. innocens and their use in serotyping. Journal of Clinical Microbiology, 33(9):2519-2521; [31 Ref.].
Adachi Y, Hara M, Hirano K, 1994. Biological properties of Serpulina hyodysenteriae and Serpulina innocens like organism with plasmid DNAs. Proceedings: The 13th International Pig Veterinary Society Congress, Bangkok, Thailand, 26-30 June 1994., 147; 7 ref.
Adachi Y, Tanaka T, Watase H, 1984. A relationship between the outbreak of swine dysentery and the antibody response to Treponema hyodysenteriae. Proceedings of the 8th International Pig Veterinary Society Congress., 182; 1 ref.
Albassam MA, Olander HJ, Thacker HL, Turek JJ, 1985. Ultrastructural characterization of colonic lesions in pigs inoculated with Treponema hyodysenteriae. Canadian Journal of Comparative Medicine, 49(4):384-390; 19 ref.
Alversammer R, 1993. Bacteriological and epidemiological studies on the occurrence of Serpulina hyodysenteriae in pig breeding herds of Upper Austria. Wiener Tierärztliche Monatsschrift, 80(4):124; [Abstract of disseration].
Amtsberg G, Meier C, Kirpal G, Merkt M, Bisping W, 1984. Occurrence of Treponema in swine. 2. Characterization of Treponema strains by haemolytic and serological properties, indole formation and virulence. Berliner und Münchener Tierärztliche Wochenschrift, 97(5):171-176; 23 ref.
Argenzio RA, Whipp SC, Glock RD, 1980. Pathophysiology of swine dysentery: Colonic transport and permeability studies. Journal of Infectious Diseases, 142:676-684.
Atyeo RF, Hampson DJ, 1998. Pulsed field gel electrophoresis analysis of Serpulina hyodysenteriae isolates. Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, UK, p 130.
Atyeo RF, Oxberry SL, Combs BG, Hampson DJ, 1998. Development and evaluation of polymerase chain reaction tests as an aid to diagnosis of swine dysentery and intestinal spirochaetosis. Letters in Applied Microbiology, 26(2):126-130; 21 ref.
Backhans A, Johansson K, Fellström C, 2010. Phenotypic and molecular characterization of Brachyspira spp. isolated from wild rodents. Environmental Microbiology Reports, 2(6):720-727.
Barcellos DESN, Mathiesen MR, de Uzeda M, Duhamel G, 2000. The identification and prevalence of spirochetes in relation to feed medication in Brazilian pig herds. Proceedings of the 16th International Pig Veterinary Society Congress, Melbourne, Australia, p 10.
Baum DH, Joens LA, 1979. Partial purification of a specific antigen of Treponema hyodysenteriae. Infection and Immunity, 26:1211-1223.
Bellgard MI, Wanchanthuek P, La T, Ryan K, Moolhuijzen P, Albertyn Z, Shaban B, Motro Y, Dunn DS, Schibeci D, Hunter A, Barrero R, Phillips ND, Hampson DJ, 2009. Genome sequence of the pathogenic intestinal spirochete Brachyspira hyodysenteriae reveals adaptations to its lifestyle in the porcine large intestine. PLos One, No.March:e4641. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004641
Binek M, Szynkiewicz Z, Jakubowski T, 1994. Dynamics of susceptibility of Serpulina hyodysenteriae to different chemotherapeutics in-vitro. Proceedings of the 13th International Pig Veterinary Society Congress, Bangkok, Thailand, p 203.
Birrel J, 1957. Infection by Vibrio as a cause of disease in pigs. Veterinary Record, 69:947-950.
Boye M, Jensen TK, Møller K, Leser TD, Jorsal SE, 1998. Specific detection of the genus Serpulina, S. hyodysenteriae and S. pilosicoli in porcine intestines by fluorescent rRNA in situ hybridization. Molecular and Cellular Probes, 12(5):323-330.
Brandenburg AC, Miniats OP, Geissinger HD, Ewert E, 1977. Swine dysentery: inoculation of gnotobiotic pigs with Treponema hyodysenteriae and Vibrio coli and a peptostreptococcus. Canadian Journal of Comparative Medicine, 41:294-301.
Burrough E, Strait E, Kinyon J, Bower L, Madson D, Schwartz K, Frana T, Songer JG, 2012. Comparison of atypical Brachyspira spp. clinical isolates and classic strains in a mouse model of swine dysentery. Veterinary Microbiology, 160(3/4):387-394. http://www.sciencedirect.com/science/journal/03781135
Burrough ER, 2013. Swine dysentery - re-emergence in the United States and Canada. In: Proceedings of the 6th International Conference on Colonic Spirochaetal Infections in Animals and Humans, Guildford, UK, 5-6 September 2013, 55-56.
Burrough ER, Strait EL, Kinyon JM, Bower LP, Madson DM, Wilberts BL, Schwartz KJ, Frana TS, Songer JG, 2012. Comparative virulence of clinical Brachyspira spp. isolates in inoculated pigs. Journal of Veterinary Diagnostic Investigation, 24(6):1025-1034. http://vdi.sagepub.com/content/24/6/1025.abstract
Burrough ER, Wilberts BL, Bower LP, Jergens AE, Schwartz KJ, 2013. Fluorescent in situ hybridization for detection of "Brachyspira hampsonii" in porcine colonic tissues. Journal of Veterinary Diagnostic Investigation, 25(3):407-412. http://vdi.sagepub.com/content/25/3/407.short
Burrows, MR, Lemcke RM, 1981. Identification of Treponema hyodysenteriae by a rapid slide agglutination test. Veterinary Record, 108:187-189.
Calderaro A, Dettori G, Grillo R, Plaisant P, Amalfitano G, Chezzi C, 1998. Search for bacteriophages spontaneously occurring in cultures of haemolytic intestinal spirochaetes of human and animal origin. Journal of Basic Microbiology, 38(5/6):313-322; 21 ref.
Calderaro A, Piccolo G, Montecchini S, Buttrini M, Gorrini C, Rossi S, Arcangeletti MC, Conto FDe, Medici MC, Chezzi C, 2013. MALDI-TOF MS analysis of human and animal Brachyspira species and benefits of database extension. Journal of Proteomics, 78:273-280.
Chander Y, Primus A, Oliveira S, Gebhart CJ, 2012. Phenotypic and molecular characterization of a novel strongly hemolytic Brachyspira species, provisionally designated "Brachyspira hampsonii". Journal of Veterinary Diagnostic Investigation, 24(5):903-910. http://vdi.sagepub.com/content/24/5/903.abstract
Chia SP, Taylor DJ, 1978. Factors affecting the survival of Treponema hyodysenteriae in dysenteric pig faeces. Veterinary Record, 103(4):68-70.
Cizek A, Smola J, Mádr P, 1996. In vitro activity of six anti-dysenteric drugs on Serpulina hyodysenteriae and S. pilosicoli strains in the Czech republic. Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, England, p 135.
Combs BG, Hampson DJ, Harders SJ, 1992. Typing of Australian isolates of Treponema hyodysenteriae by serology and by DNA restriction endonuclease analysis. Veterinary Microbiology, 31(2-3):273-285; 23 ref.
Diego R, Lanza I, Carvajal A, Rubio P, Cármenes P, 1995. Serpulina hyodysenteriae challenge of fattening pigs vaccinated with an adjuvanted bivalent bacterin against swine dysentery. Vaccine, 13(7):663-667; 27 ref.
Duhamel GE, Joens LA, 1994. Laboratory Procedures for Diagnosis of Swine Dysentery. American Association of Veterinary Laboratory Diagnosticians, Inc., Madison, Wisconsin, USA.
Duhamel GE, Ramantham RJ, Bernard RJ, Newman MC, Erickson ED, 1992. Application of restriction fragment length polymorhism typing to epidemiological tracing of Serpulina hyodysenteriae. Proceedings of the 12th International Pig Veterinary Society Congress, the Hague, Netherlands, p 276.
Durmic Z, Pethick DW, Pluske JR, Hampson DJ, 1998. Changes in bacterial populations in the colon of pigs fed different sources of dietary fibre, and the development of swine dysentery after experimental infection. Journal of Applied Microbiology, 85(3):574-582; 32 ref.
Duthie IF, 1966. Swine dysentery. Rivista di Suinicoltura, 7:61-64.
Elder RO, Duhamel GE, Schafer RW, Mathiesen MR, Ramanathan M, 1994. Rapid detection of Serpulina hyodysenteriae in diagnostic specimens by PCR. Journal of Clinical Microbiology, 32(6):1497-1502; 40 ref.
Fellström C, 1996. Phenotypic classification, detection and phylogeny of Serpulina infections in swine. Doctorial thesis. Swedish University of Agricultural Sciences, Uppsala, Sweden.
Fellström C, Gunnarsson A, Holmström G, Franklin A, 1996. In vitro activity of 7 antibacterials against 4 phenotypical variants of Serpulina species. Proceedings of the 14th International Pig Veterinary Society Congress, Bologna, Italy, p 292.
Fellström C, Karlsson M, Pettersson B, Zimmerman U, Gunnarsson A, Aspan A, 1999. Emended descriptions of indole negative and indole positive isolates of Brachyspira (Serpulina) hyodysenteriae. Veterinary Microbiology, 70(3/4):225-238; 28 ref.
Fellström F, Melin L, Wierup M, Gunnarsson A, 1998. Isolation of Serpulina species in Swedish pig herds with diarrhoea. Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, England, p 59.
Fernie DS, Ripley PH, Walker PD, 1983. Swine dysentery: protection against experimental challenge following single dose parental immunisation with inactivated Treponema hyodysenteriae. Research in Veterinary Science, 35:217-221.
Fisher LF, Olander HJ, 1981. Shedding of Treponema hyodysenteriae, transmission of disease, and agglutinin response of pigs convalescent from swine dysentery. American Journal of Veterinary Research, 42:450-455.
Flø H, Bergsjø B, 2000. The prevalence of Brachyspira in Norwegian pig herds. Proceedings of the 16th Congress of the International Pig Veterinary Society, Melbourne, Australia, p 46.
Gabe JD, Chang RJ, Slomiany R, Andrews WH, McCaman MT, 1995. Isolation of extracytoplasmic proteins from Serpulina hyodysenteriae B204 and molecular cloning of the flaB1 gene encoding a 38-kilodalton flagellar protein. Infection and Immunity, 63(1):142-148; 38 ref.
Gabe JD, Dragon E, Chang RayJen, McCaman MT, 1998. Identification of a linked set of genes in Serpulina hyodysenteriae (B204) predicted to encode closely related 39-kilodalton extracytoplasmic proteins. Journal of Bacteriology, 180(2):444-448; 26 ref.
Graaf GJ de, Jager LP, Baars AJ, Spierenburg TJ, 1988. Some pharmacokinetic observations of carbadox medication in pigs. Veterinary Quaterly, 10:34-41.
Greer JM, Wannemuehler MJ, 1989a. Comparison of the biochemical responses produced by lipopolysaccaride and endotoxin of Treponema hyodysenteriae and Treponema innocens. Infection and Immunity, 57:717-723.
Greer JM, Wannemuehler MJ, 1989b. Pathogenesis of Treponema hyodysenteriae: Induction of interleukin-1 and tumor necrosis factor by a treponema butanol/water extract (endotoxine). Microbial Pathogenesis, 7:279-288.
Griffin RM, Hutchings DA, 1980. Swine dysentery: observation on the frequency of latent infection. Veterinary Record, 107:559.
Hampson DJ, 2000. The Serpulina story. Proceedings of the 16th Congress of the International Pig Veterinary Society, Melbourne, Australia, pp 1-5.
Hampson DJ, 2014. Brachyspiral colitis: An evolving problem. In: Proceedings of the 23rd Congress of the International Pig Veterinary Society, Cancun, Mexico, 8-11 June 2014, 40-46.
Hampson DJ, Atyeo RF, Combs BG, 1997. Swine dysentery. Intestinal spirochaetes in domestic animals and humans., 175-209; many ref.
Hampson DJ, Mhoma JRL, Combs BG, Buddle JR, 1989. Proposed revisions to the serological typing system for Treponema hyodysenteriae. Epidemiology and Infection, 102:75-84.
Harel J, Bélanger M, Forget C, Jacques M, 1994. Characterization of Serpulina hyodysenteriae isolates of serotypes 8 and 9 from Quebec by restriction endonuclease fingerprinting and ribotyping. Canadian Journal of Veterinary Research, 58(4):302-305; 22 ref.
Harris DL, 1984. The epidemiology of swine dysentery as it relates to the eradication of the disease. Compendium on Continuing Education for the Practicing Veterinarian, 6(2):S83-S88; 25 ref.
Harris DL, Alexander TJL, Whipp SC, Robinson IM, Glock RD, Matthews PJ, 1978. Swine dysentery: Studies of gnotobiotic pigs inoculated with Treponema hyodysenteria, Bacteroides vulgatus and Fusobacterium necrophorum. Journal of the American Veterinary Association, 172:468-471.
Harris DL, Glock RD, Christensen CR, Kinyon JM, 1972a. Swine dysentery. I. Inoculation of pigs with Treponema hyodysenteriae (new species) and reproduction of the disease. Veterinary Medicine/Small Animal Clinician, 67:61-64.
Harris DL, Glock RD, Meyer RC, 1972b. Inoculation of specific pathogen-free and germ-free pigs with Treponema hyodysenteriae and Vibrio coli. Annual Meeting of the American Society for Microbiology, Philadelphia. Pa, April 23-28, abstract, p 118.
Harris DL, Lysons RJ, 1992. Swine dysentery. In: Leman AD, Straw BE, Mengeling WL, D'Allaire SD, Taylor DJ (ed.), Diseases of Swine, 7th ed. Iowa State University Press, Ames, 599-616.
Hidalgo Â, Carvajal A, Vester B, Pringle M, Naharro G, Rubio P, 2011. Trends towards lower antimicrobial susceptibility and characterization of acquired resistance among clinical isolates of Brachyspira hyodysenteriae in Spain. Antimicrobial Agents and Chemotherapy, 55(7):3330-3337. http://aac.asm.org/cgi/content/abstract/55/7/3330
Hovind-Hougen K, Birch-Andersen A, Henrik-Nielsen R, Orholm M, Pedersen JO, Teglbjærg PS, Thayson EH, 1982. Intestinal spirochetosis: Morphological characterization of the spirochete Brachyspira aalborgi gen. nov., sp. nov.. Journal of Clinical Microbiology, 16:1127-1136.
Hudson MJ, Alexander TJL, Lysons RJ, Wellstead PD, 1974. Swine dysentery: failure of an attenuated strain of spirochaete, given orally, to protect pigs against subsequent challenge. British Veterinary Journal, 130:37-40.
Humphrey SB, Stanton TB, Jensen NS, Zuerner RL, 1997. Purification and characterization of VSH-1, a generalized transducing bacteriophage of Serpulina hyodysenteriae. Journal of Bacteriology, 179(2):323-329; 35 ref.
Hunter D, Saunders CN, 1977. Diagnosis of swine dysentery using an absorbed fluorecent antiserum. Veterinary Record, 101:303-304.
Hutto DL, Wannemuehler MJ, 1999. A comparison of the morphologic effects of Serpulina hyodysenteriae or its beta-hemolysin on the murin cecal mucosa. Veterinary Pathology, 36(5):412-422.
Huurne AAHMter, Houten Mvan, Koopman MBH, Zeijst BAMvan der, Gaastra W, 1992. Characterization of Dutch porcine Serpulina (Treponema) isolates by restriction endonuclease analysis and DNA hybridization. Journal of General Microbiology, 138(9):1929-1934; 33 ref.
Huurne AAHMter, Houten Mvan, Muir S, Kusters JG, Zeijst BAMvan der, Gaastra W, 1992. Inactivation of a Serpula (Treponema) hyodysenteriae hemolysin gene by homologous recombination: importance of this hemolysin in pathogenesis of S. hyodysenteriae in mice. FEMS Microbiology Letters, 92(1):109-113; 18 ref.
Hyatt DR, Huurne AHMter, Zeijst BAMvan der, Jones LA, 1994. Reduced virulence of Serpulina hyodysenteriae hemolysin-negative mutants in pigs and their potential to protect pigs against challenge with a virulent strain. Infection and Immunity, 62(6):2244-2248; 19 ref.
Jenkins EM, Mohammad A, Klesius PH, 1982. Evaluation of cell-mediated immune respons. Proceedings of the 7th International Pig Veterinary Society Congress, Mexico City, Mexico, p 41.
Jensen NS, 1997. Detection, identification and subspecific differentiation of intestinal spirochaetes. Intestinal spirochaetes in domestic animals and humans [ed. by Hampson, D. J.\Stanton, T. B. (Editors)]. Wallingford, UK: CAB INTERNATIONAL, 323-341.
Jensen NS, Stanton TB, 1993. Comparison of Serpulina hyodysenteriae B78, the type strain of the species, with other S. hyodysenteriae strains using enteropathogenicity studies and restriction fragment length polymorphism analysis. Veterinary Microbiology, 36(3/4):221-231; 31 ref.
Joens LA, DeYoung DW, Cramer JC, Glock RD, 1984. The immune response of the porcine colon to swine dysentery. Proceedings of the 8th International Pig Veterinary Society Congress., 187; 5 ref.
Joens LA, Harris DL, Baum DH, 1979. Immunity to swine dysentery in recovered pigs. American Journal of Veterinary Research, 40:1352-1354.
Joens LA, Harris DL, Kinyon JM, Baum DH, 1978. Immunofluorescent studies on Treponema hyodysenteriae. Proceedings of the 5th International Pig Veterinary Society Congress, Zagreb, Yugoslavia, M.2.
Joens LA, Kinyon JM, 1982. Isolation of Treponema hyodysenteriae from wild rodents. Journal of Clinical Microbiology, 15:994-997.
Kang B, Olander HJ, 1990. Scanning electron microscopy of the colon inoculated with Treponema hyodysenteriae in colonic loops of swine. Proceedings, International Pig Veterinary Society, 11th Congress, July 1-5, 1990, Lausanne, Switzerland., 117; 8 ref.
Karlsson M, Fellström C, Heltander M, Johansson K-E, Franklin A, 1999. Genetic basis of macrolide and lincosamide resistance in Brachyspira (Serpulina) hyodysenteriae. FEMS Microbiology Letters, 172:255-260.
Karlsson M, Franklin A, 2000. Antimicrobial susceptibility testing of Swedish Brachyspira hyodysenteriae isolates by broth dilution procedure. In: Proceedings of the Pig Veterinary Society Congress, Melbourne, Australia, p 123.
Kennedy MJ, Rosey EL, Yancey RJ, 1997. Characterization of flaA and flaB mutants of Serpulina hyodysenteriae: both flagellin subunits, FlaA and FlaB, are necessary for full motility and intestinal colonization. FEMS Microbiology Letters, 153(1):119-128; 18 ref.
Kennedy MJ, Rosnick DK, Ulrich RG, Yancey RJ Jr. , 1992. Identification and immunological characterisation of the major immunogenic antigens of serotypes 1 and 2 of Serpulina hyodysenteriae. In: Proceedings of the International Pig Veterinary Congress, The Hague, Netherlands, p 185.
Kent KA, Lemcke RM, Lysons RJ, 1988. Production, purification and molecular weight determination of the haemolysin of Treponema hyodysenteriae. Journal of Medical Microbiology, 27:215-224.
Kinyon JM, Harris DL, 1979. Treponema innocens, a new species of intestinal bacteria, and emended description of the type strain of Treponema hyodysenteriae. International Journal of Systematic Bacteriology, 29:102-109.
Kinyon JM, Harris DL, Glock RD, 1977. Enteropathogenicity of various isolates of Treponema hyodysenteriae. Infection and Immunity, 15:638-646.
Kinyon JM, Harris DL, Glock RD, 1980. Isolation of Treponema hyodysenteriae from experimentally infected pigs at various intervals post-inoculation. Proceedings of the 6th International Pig Veterinary Society Congress, Copenhagen, Denmark, p 232.
Koopman MBH, Baats E, Leeuw OSde, Zeijst BAMvan der, Kusters JG, 1993. Molecular analysis of a flagellar core protein gene of Serpulina (Treponema) hyodysenteriae.. Journal of General Microbiology, 139(8):1701-1706; 44 ref.
Koopman MBH, Leeuw OSde, Zeijst BAMvan der, Kusters JG, 1992. Cloning and DNA sequence analysis of a Serpulina (Treponema) hyodysenteriae gene encoding a periplasmic flagellar sheath protein. Infection and Immunity, 60(7):2920-2925; 34 ref.
Kramomtong I, Neramitmansook W, Whipp SC, Joens LA, Limawongpranee S, 1996. Comparison of ELISA and selective culture in the diagnosis of swine dysentry in Thailand. Veterinary Record, 138(14):332-333; 4 ref.
La T, Phillips ND, Hampson DJ, 2003. Development of a duplex PCR assay for detection of Brachyspira hyodysenteriae and Brachyspira pilosicoli in pig feces. Journal of Clinical Microbiology, 41(7):3372-3375.
Lemcke RM, Burrows MR, 1981. A comparative study of spirochaetes from the porcine alimentary tract. Journal of Hygiene Cambridge, 86:173-182.
Leser TD, Moller K, Jensen TK, Jorsal SE, 1997. Specific detection of Serpulina hyodysenteriae and potentially pathogenic weakly haemolytic porcine intestinal spirochaetes by polymerase chain reaction targeting 23S rDNA. Molecular and Cellular Probes, 11:363-372.
Lindecrona RH, Jensen BB, Jensen TK, Leser TD, Møller K, 2000. The influence of diet on the development of swine dysentery. Proceedings of the 16th Congress of the International Pig Veterinary Society 2000, Melbourne, Australia, p 7.
Lymbery AJ, Hampson DJ, Hopkins RM, Combs B, Mhoma JRL, 1990. Multilocus enzyme electrophoresis for identification and typing of Treponema hyodysenteriae and related spirochaetes. Veterinary Microbiology, 22(1):89-99; 29 ref.
Lysons RJ, Burrows MR, Debney TG, Bew J, 1986. Vaccination against swine dysentery - an effective novel method. Proceedings of the 9th International Pig Veterinary Society Congress, Barcelona, Spain, p 180.
Lysons RJ, Kent KA, Bland AP, Sellwood R, Robinson WF, Frost AJ, 1991. A cytotoxic haemolysin from Treponema hyodysenteriae - a probable virulence determinant in swine dysentery. Journal of Medical Microbiology, 34(2):97-102; 14 ref.
Lysons RJ, Lemcke RM, Bew R, Burrows MR, Alexander TJR, 1982. An avirulent strain of Treponema hyodysenteriae isolated from herds free of swine dysentery. Proceedings of the 7th International Pig Veterinary Society Congress, Mexico City, Mexico, p 40.
Mapother ME, 1993. An estimate of the prevalence of swine dysentery in US swine herds during 1989-1991. Survey, National Animal Health Monitoring System, National Veterinary Services Laboratory, United States Department of Agriculture, Washington DC.
Mapother ME, Jones LA, 1985. New serotypes of Treponema hyodysenteriae. Journal of Clinical Microbiology, 22:161-164.
Martínez-Lobo FJ, Hidalgo Â, García M, Argüello H, Naharro G, Carvajal A, Rubio P, 2013. First identification of "Brachyspira hampsonii" in wild European waterfowl. PLoS ONE, 8(12):e82626. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0082626
McLennan CG, MacIndoe RHF, McKenna DT, 1938. A condition of unknown aetiology affecting pigs. Australian Veterinary Journal, 14:245-246.
Meyer RC, Simon J, Byerly CS, 1974. The etiology of swine dysentery. I. Oral inoculation of germ-free swine with Treponema hyodysenteriae and Vibrio coli. Veterinary Pathology, 11:515-526.
Mhoma JRL, Hampson DJ, Robertson ID, 1992. A serological survey to determine the prevalence of infection with Treponema hyodysenteriae in Western Australia. Australian Veterinary Journal, 69(4):81-84; 17 ref.
Milner JA, Sellwood R, 1994. Chemotactic response to mucin by Serpulina hyodysenteriae and other porcine spirochetes: potential role in intestinal colonization. Infection and Immunity, 62(9):4095-4099; 38 ref.
Mirajkar NS, Gebhart CJ, 2013. Antimicrobial susceptibility patterns of Brachyspira species in U.S. swine herds. In: 6th International Conference on Colonic Spirochaetal Infections in Animals and Humans, Guildford, UK, 5-6 September 2013, 53.
Møller K, Jensen TK, Jorsal SE, Leser TD, Carstensen B, 1998. Detection of Lawsonia intracellularis, Serpulina hyodysenteriae, weakly beta-haemolytic intestinal spirochaetes, Salmonella enterica, and haemolytic Escherichia coli from swine herds with and without diarrhoea among growing pigs. Veterinary Microbiology, 62(1):59-72; 28 ref.
Nibbelink SK, Sacco RE, Wannemuehler MJ, 1997. Pathogenicity of Serpulina hyodysenteriae: in vivo induction of tumor necrosis factor and interleukin-6 by a serpulinal butanol/water extract (endotoxin). Microbial Pathogenesis, 23(3):181-187; 20 ref.
Nuessen ME, Joens LA, Glock RD, 1983. Involvement of a lipopolysaccharide in the pathogenesis of Treponema hyodysenteriae. Journal of Immunology, 131:997-999.
Ochiai S, Adachi Y, Mori K, 1997. Unification of the genera Serpulina and Brachyspira, and proposals of Brachyspira hyodysenteriae comb. nov., Brachyspira innocens comb. nov. and Brachyspira pilosicoli comb. nov. Microbiology and Immunology, 41(6):445-452; 26 ref.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
Okuma S, Okamura Y, Cuypers P, 1992. A comparison of the therapeutic effects of lincomycin and injectable tiamulin against swine dysentery. Proceedings of the 11th International Pig Veterinary Society Congress, the Hague, the Netherlands, p 284.
Olson LD, 1974. Clinical and pathological observations on the experimental passage of swine dysentery. Canadian Journal of Comparative Medicine, 38:7-13.
Paster BJ, Dewhirst FE, 2000. Phylogenic foundation of Spirochetes. Journal of Molecular Microbiology and Biotechnology, 2(4):341-344.
Pettersson B, Fellström C, Andersson A, Uhlén M, Gunnarsson A, Johansson KE, 1996. The phylogeny of intestinal porcine spirochetes (Serpulina species) based on sequence analysis of the 16S rRNA gene. Journal of Bacteriology, 178(14):4189-4199; 63 ref.
Pluske JR, Durmic Z, Pethick DW, Mullan BP, Hampson DJ, 1998. Confirmation of the role of rapidly fermentable carbohydrates in the expression of swine dysentery in pigs after experimental infection. Journal of Nutrition, 128(10):1737-1744; 26 ref.
Pluske JR, Siba PM, Pethick DW, Mullan BP, Hampson DJ, 1996. Reduced incidence of swine dysentery in pigs fed diets that were selected or processed to have reduced fermentation in the large intestine. Proceedings of the 14th International Pig Veterinary Society Congress, Bologna, Italy, p 282.
Pringle M, Landén A, Unnerstad HE, Molander B, Bengtsson B, 2012. Antimicrobial susceptibility of porcine Brachyspira hyodysenteriae and Brachyspira pilosicoli isolated in Sweden between 1990 and 2010. Acta Veterinaria Scandinavica, 54(54):(21 September 2012). http://www.actavetscand.com/content/54/1/54
Prohászka L, Lukács K, 1984. Influence of the diet on the antibacterial effect of volatile fatty acids and on the development of swine dysentery. Zentralblatt für Veterinärmedizin, B, 31(10):779-785; 9 ref.
Rasbäck T, Jansson DS, Johansson KE, Fellström C, 2007. A novel enteropathogenic, strongly haemolytic spirochaete isolated from pig and mallard, provisionally designated 'Brachyspira suanatina' sp. nov. Environmental Microbiology, 9(4):983-991. http://www.blackwell-synergy.com/loi/emi
Ritchie AE, Brown LN, 1971. An agent possibly associated with swine dysentery. Veterinary Record, 89:608-609.
Ritchie AE, Robinson IM, Joens LA, Kinyon JM, 1978. A bacteriophage for Treponema hyodysenteriae. Veterinary Record, 102:34-35.
Rohde J, Rothkamp A, Gerlach GF, 2002. Differentiation of porcine Brachyspira species by a novel nox PCR-based restriction fragment length polymorphism analysis. Journal of Clinical Microbiology, 40(7):2598-2600.
Roncalli RA, Leaning WHD, 1976. Geographical distribution of swine dysentery. Proceedings of the the 4th International Pig Veterinary Society Congress, Ames, USA, p 17.
Ronéus, O, 1960. Swine dysentery: A new form of enteritis in Sweden. Nordisk Veterinaermedicin, 12:648-657.
Rosey EL, Kennedy MJ, Petrella DK, Ulrich RG, Yancey RJJr, 1995. Inactivation of Serpulina hyodysenteriae flaA1 and flaB1 periplasmic flagellar genes by electroporation-mediated allelic exchange. Journal of Bacteriology, 177(20):5959-5970; 62 ref.
Rubin JE, Costa MO, Hill JE, Kittrell HE, Fernando C, Huang YanYun, O'Connor B, Harding JCS, 2013. Reproduction of mucohaemorrhagic diarrhea and colitis indistinguishable from swine dysentery following experimental inoculation with "Brachyspira hampsonii" strain 30446. PLoS ONE, 8(2):e57146. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057146
Rubin JE, Harms NJ, Fernando C, Soos C, Detmer SE, Harding JCS, Hill JE, 2013. Isolation and characterization of Brachyspira spp. including "Brachyspira hampsonii" from lesser snow geese (Chen caerulescens caerulescens) in the Canadian arctic. Microbial Ecology, 66(4):813-822. http://rd.springer.com/article/10.1007/s00248-013-0273-5
Rønne H, Szancer J, 1990. In vitro susceptibility of Danish field isolates of Treponema hyodysenteriae to chemoterapeutics in swine dysentery (SD) therapy. Proceedings of the 11th International Pig Veterinary Society Congress, Lousanne, Switzerland, p 126.
Savage DC, 1980. Colonization by and survival of pathogenic bacteria on intestinal mucosal surfaces. In: Bitton G, Marshall KC (ed.), Adsorption of microorganisms to surfaces. John Wiley and Sons, Inc, New York, 175-206.
Schmall LM, Argenzio RA, Whipps SC, 1983. Pathophysiologic features of swine dysentery: Cyclic nucleotide-independent production of diarrhea. American Journal of Veterinary Research, 44:1309-1316.
Siba PM, Pethick DW, Hampson DJ, 1994. Dietary control of swine dysentery. Proceedings: The 13th International Pig Veterinary Society Congress, Bangkok, Thailand, 26-30 June 1994., 149; 4 ref.
Song Yong, Frey B, Hampson DJ, 2012. The use of ELISAs for monitoring exposure of pig herds to Brachyspira hyodysenteriae. BMC Veterinary Research, 8(6):(17 January 2012). http://www.biomedcentral.com/content/pdf/1746-6148-8-6.pdf
Song Yong, La T, Phillips ND, Bellgard MI, Hampson DJ, 2009. A reverse vaccinology approach to swine dysentery vaccine development. Veterinary Microbiology, 137(1/2):111-119. http://www.sciencedirect.com/science/journal/03781135
Songer JG, Glock RD, Schwartz KJ, Harris DL, 1978. Isolation of Treponema hyodysenteriae from sources other than swine. Journal of the American Veterinary Association, 172:464-466.
Spierenburg T, van Lenthe H, de Graaf G, Jager LP, 1988. Liquid chromatographic determination of olaquindox in medicated feeds and in contents of porcine gastrointestinal tract. Journal-Association of Official Analytical Research Workers, 71:1106-1109.
Stanton TB, 1989. Glucose metabolism and NADH recycling by Treponema hyodysenteriae, the agent of swine dysentery. Applied and Environmental Microbiology, 55:2365-2371.
Stanton TB, Fournié-Amazouz E, Postic D, Trott DJ, Grimont PAD, Baranton G, Hampson DJ, Saint Girons I, 1997. Recognition of two new species of intestinal spirochetes: Serpulina intermedia sp. nov. and Serpulina murdochii sp. nov. International Journal of Systematic Bacteriology, 47(4):1007-1012; 42 ref.
Stanton TB, Jensen NB, Casey TA, Tordoff LA, Dewhirst FE, Paster BJ, 1991. Reclassification of Treponema hyodysenteriae and Treponema innocens in a new genus, Serpula gen. nov., as Serpula hyodysenteriae comb. nov. and Serpula innocens comb. nov. International Journal of Systematic Bacteriology, 41:50-58.
Stanton TB, Jensen NS, 1993. Purification and characterization of NADH oxidase from Serpulina hyodysenteriae. Journal of Bacteriology, 175(10):2980-2987; 45 ref.
Stanton TB, Jensen NS, Bosworth BT, Kunkle RA, 2000. Evaluation of the virulence of rhea S. hyodysenteriae strains for swine. NADC First International Virtual Conference, http://www.nadc.ars.usda.gov/virtconf/subpost/posters/I00006m.htm.
Stanton TB, Jensen NS, Sellwood R, 1995. NADH oxidase (nox) gene of Sepulina hyodysenteriae. In: Abstracts of the 95th General Meeting of the American Society for Microbiology. American Society for Microbiology, Washington , D.C., Abstr. D-9, p 250.
Stanton TB, Rosey EL, Kennedy MJ, Jensen NS, Bosworth BT, 1999. Isolation, oxygen sensitivity, and virulence of NADH oxidase mutants of the anaerobic spirochete Brachyspira (Serpulina) hyodysenteriae, etiologic agent of swine dysentery. Applied and Environmental Microbiology, 65(11):5028-5034; 50 ref.
Stanton TD, 1992. Proposal to change the genus designation Serpula to Serpulina gen. nov. containing the species Serpulina hyodysenteriae comb. nov. and Serpulina innocens comb. nov. International Journal of Systematic Bacteriology, 42(1):189-190; 23 ref.
Taylor DJ, Alexander TJL, 1971. The production of dysentery in swine by feeding cultures containing a spirochaete. British Veterinary Journal, 127:58-61.
Taylor DJ, Blakemore WF, 1971. Spirochaetal invasion of the colonic epithelium in swine dysentery. Research in Veterinary Science, 12:177-179.
ter Huurne AAHM, 1993. Swine dysentery: pathogenesis and vaccine development. Dissertation. Utrecht, The Netherlands.
Thomas W, Sellwood R, 1993. Molecular cloning, expression, and DNA sequence analysis of the gene that encodes the 16-kilodalton outer membrane lipoprotein of Serpulina hyodysenteriae. Infection and Immunity, 61(3):1136-1140; 36 ref.
Trott DJ, Stanton TB, Jensen NS, Duhamel GE, Johnson JL, Hampson DJ, 1996. Serpulina pilosicoli sp. nov., the agent of porcine intestinal spirochetosis. International Journal of Systematic Bacteriology, 46(1):206-215; 41 ref.
Turner LH, 1976. Classification of spirochaetes in general and of the genus Leptospira in particular. In: Johnson, R. C. (ed.). The biology of parasitic spirochetes. Academic press, Inc., New York, San Francisco, London, 95-106.
Ulsen, van FW, 1953. Gastro-enteritis bij varkens. Komt Vibrio-dysenterie in Nederland voor? Tijdschrift voor Diergeneeskunde, 78:560-568.
Waldmann K-H, Wendt M, Amtsberg G, 2000. Untersuchungen zur Brachyspira-Diagnostik und Behandlungsstrategie bei der Schweinendysenterie. Deutche tierärtzliche Wochenschrift, 107:486-489.
Walter DH, Kinyon JM, 1990. Recent MIC determination of six antimicrobials for Treponema hyodysenteriae in the United States; use of tiamulin to eliminate swine dysentery from two farrow to finish herds. Proceedings, International Pig Veterinary Society, 11th Congress, July 1-5, 1990, Lausanne, Switzerland., 129; 15 ref.
Wannemuehler MJ, Ostle AG, Nibbelink SK, Coyle DC, Welter CJ, 1990. Pathogenesis of swine dysentery: preparation of a protective vaccine. Proceedings, International Pig Veterinary Society, 11th Congress, July 1-5, 1990, Lausanne, Switzerland., 124; 12 ref.
Warneke HL, Kinyon JM, Bower LP, Burrough ER, Frana TS, 2014. Matrix-assisted laser desorption ionization time-of-flight mass spectrometry for rapid identification of Brachyspira species isolated from swine, including the newly described "Brachyspira hampsonii". Journal of Veterinary Diagnostic Investigation, 26(5):635-639.
Waters WR, Pesch BA, Hontecillas R, Sacco RE, Zuckermann FA, Wannemuehler MJ, 1999. Cellular immune responses of pigs induced by vaccination with either a whole cell sonicate or pepsin-digested Brachyspira (Serpulina) hyodysenteriae bacterin. Vaccine, 18(7/8):711-719; 26 ref.
Waters WR, Sacco RE, Dorn AD, Hontecillas R, Zuckermann FA, Wannemuehler MJ, 1999. Systemic and mucosal immune responses of pigs to parenteral immunization with a pepsin-digested Serpulina hyodysenteriae bacterin. Veterinary Immunology and Immunopathology, 69(1):75-87; 15 ref.
Whipp SC, Harris DL, Kinyon JM, Songer J, Glock RD, 1978. Enteropathogenicity testing of Treponema hyodysenteriae in ligated colonic loops of swine. American Journal of Veterinary Research, 39:1293-1396.
Whipp SC, Pohlenz J, Robinson IM, Harris DL, 1982. Pathogenicity of Treponema hyodysenteriae in uncontaminated gnotobiotic pigs. Abstracts of papers presented at the 63rd Annual Meeting of the Conference of Research Workers in Animal Disease, 8-9 November 1982., 45; [Abstract 249; Library: BL 0566.5464].
Whiting RA, Doyle LP, Spray RS, 1921. Swine dysentery. Purdue University Agriculture Experiment Station Bulletin, 257:3-15.
Wilberts BL, Arruda PH, Kinyon JM, Madson DM, Frana TS, Burrough ER, 2014. Comparison of lesion severity, distribution, and colonic mucin expression in pigs with acute swine dysentery following oral inoculation with "Brachyspira hampsonii" or Brachyspira hyodysenteriae. Veterinary Pathology, online first, DOI: 10.1177/0300985813516646
Wilberts BL, Arruda PH, Warneke HL, Erlandson KR, Hammer JM, Burrough ER, 2014. Cessation of clinical spirochete shedding after tiamulin treatment in pigs experimentally infected with "B. hampsonii". Research in Veterinary Science, online first, DOI: 10.1016/j.rvsc.2014.08.004
Wilcock BP, Olander HJ, 1979. Studies on the pathogeneseis of swine dysentery. II. Search for a cytotoxin in spirochetal broth cultures and colon content. Veterinary Pathology, 16:567-573.
Windsor RS, Simmons JR, 1981. Investigation in the spread of swine dysentery in 25 herds in East Anglia and assessment of its economic significance in five herds. Veterinary Record, 109:482-484.
Zmudzki J, Szczotka A, Nowak A, Strzelecka H, Grzesiak A, Pejsak Z, 2012. Antimicrobial susceptibility of Brachyspira hyodysenteriae isolated from 21 Polish farms. Polish Journal of Veterinary Sciences, 15(2):259-265. http://www.uwm.edu.pl/pjvsci/content.html
Zuerner RL, Stanton TB, 1994. Physical and genetic map of the Serpulina hyodysenteriae B78 chromosome. Journal of Bacteriology, 176:1087-1092.
Barcellos DESN, Mathiesen MR, de Uzeda M, Duhamel G, 2000. The identification and prevalence of spirochetes in relation to feed medication in Brazilian pig herds. [Proceedings of the 16th International Pig Veterinary Society Congress, Melbourne, Australia], 10.
CABI, Undated. CABI Compendium: Status inferred from regional distribution. Wallingford, UK: CABI
CABI, Undated a. CABI Compendium: Status as determined by CABI editor. Wallingford, UK: CABI
Cizek A, Smola J, Mádr P, 1996. In vitro activity of six anti-dysenteric drugs on Serpulina hyodysenteriae and S. pilosicoli strains in the Czech republic. [Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, England], 135.
Fellström F, Melin L, Wierup M, Gunnarsson A, 1998. Isolation of Serpulina species in Swedish pig herds with diarrhoea. [Proceedings of the 15th International Pig Veterinary Society Congress, Birmingham, England], 59.
Fossi M, 1996. The diagnostics of Serpulina bacteria and an analysis of colonic spirochaetes isolated from pigs in Finland during 1993-1995. (Serpulina-suvun bakteereiden diagnostiikka seka sioista vuosina 1993-1995 eristettyjen Serpulina-suvun bakteereiden tarkastelua.). Suomen Eläinlääkärilehti. 102 (10), 551-557.
Hampson D J, Atyeo R F, Combs B G, 1997. Swine dysentery. In: Intestinal spirochaetes in domestic animals and humans. [ed. by Hampson D J, Stanton T B (Editors)]. Wallingford, UK: CAB INTERNATIONAL. 175-209.
Hampson DJ, 2000. The Serpulina story. [Proceedings of the 16th Congress of the International Pig Veterinary Society, Melbourne, Australia], 1-5.
Harel J, Bélanger M, Forget C, Jacques M, 1994. Characterization of Serpulina hyodysenteriae isolates of serotypes 8 and 9 from Quebec by restriction endonuclease fingerprinting and ribotyping. Canadian Journal of Veterinary Research. 58 (4), 302-305.
Kramomtong I, Neramitmansook W, Whipp S C, Joens L A, Limawongpranee S, 1996. Comparison of ELISA and selective culture in the diagnosis of swine dysentry in Thailand. Veterinary Record. 138 (14), 332-333.
Mapother ME, 1993. An estimate of the prevalence of swine dysentery in US swine herds during 1989-1991., Washington DC, Survey National Animal Health Monitoring System, National Veterinary Services Laboratory, United States Department of Agriculture.
Mhoma J R L, Hampson D J, Robertson I D, 1992. A serological survey to determine the prevalence of infection with Treponema hyodysenteriae in Western Australia. Australian Veterinary Journal. 69 (4), 81-84. DOI:10.1111/j.1751-0813.1992.tb15555.x
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (dataset for 2004)., Paris, France: Office International des Epizooties.
Waldmann KH, Wendt M, Amtsberg G, 2000. (Untersuchungen zur Brachyspira-Diagnostik und Behandlungsstrategie bei der Schweinendysenterie). In: Deutche tierärtzliche Wochenschrift, 107 486-489.
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