Disease and Epidemiology

Swine dysentery is a severe mucohemorrhagic diarrheal disease characterized by extensive inflammation and epithelial necrosis of the large intestine (Figure 29-1). Pigs of any age may be affected, although disease is uncommon in neonates and is seen primarily in grower/finisher pigs. Bloody diarrhea can be fatal if not treated, or may become chronic, with dehydration and emaciation and pseudomembrane formation in the cecum, colon, and rectum. Less acute disease manifests as weight loss and mild diarrhea. Economic losses result mainly from growth retardation, medication costs, and mortality.

FIGURE 29-1 Mucohemorrhagic colonic lesion typical of swine dysentery.

(Courtesy J. Glenn Songer.)

The causative agent of swine dysentery, now known as B. hyodysenteriae (formerly Treponema hyodysenteriae, Serpula hyodysenteriae, and Serpulina hyodysenteriae) was identified and characterized in the early 1970s. Nine serotypes of B. hyodysenteriae are based on differences in lipopolysaccharide (LPS) antigens.

Infection with B. hyodysenteriae is by the fecal-oral route. Reservoir hosts for B. hyodysenteriae include pigs and wild rodents, but farm dogs can also spread the infection by way of coprophagia and subsequent excretion. Recovered, asymptomatic pigs can excrete B. hyodysenteriae in feces for 3 months or more. Environmental survival of B. hyodysenteriae is usually short lived (24-48 hours).

Swine dysentery is a relatively common disease in some major pig-producing countries, but is now relatively uncommon in the United States. When a naive herd is first exposed, disease may appear in only a few pigs, but as environmental accumulations of the organism are increasingly refreshed from diseased and asymptomatic carrier pigs, larger numbers of pigs are affected. The characteristics of an outbreak are influenced by the types of contact with infectious material allowed by the particular management system and housing type. Endemic swine dysentery can manifest a spectrum of severity ranging from mild and transient to severe and occasionally fatal. Disease can be inapparent because of specific medication schemes.

Pathogenesis

Brachyspira hyodysenteriae has two bundles of 7 to 13 periplasmic flagella, which make the organism highly motile in mucus and facilitate colonization of colonic crypts (Figure 29-2) and other mucus-covered enterocytes. Flagella are composed of three antigenically related core polypeptides and two sheath polypeptides. Flagellar mutants are avirulent in swine, suggesting that motility is an important virulence factor.

FIGURE 29-2 Brachyspira hyodysenteriae in colonic crypts (fluorescent antibody stain).

(Courtesy Lynn A. Joens.)

Neither specific nor nonspecific adherence to enterocytes has been demonstrated in vivo. Brachyspira hyodysenteriae and B. innocens adhere equally well in vitro to cultured intestinal and epithelial cells. Thus a role for adhesion in virulence of B. hyodysenteriae remains unproven.

Brachyspira hyodysenteriae is found in epithelial cells in pigs with swine dysentery, but dogma has been that invasion is not an obligate part of pathogenesis. Furthermore, invasion of colonic enterocytes in vitro has not been demonstrated. The organism may invade goblet cells and disseminate to enteroabsorptive cells. Tight junctions between colonic enterocytes may be weakened in response to B. hyodysenteriae infection.

The pathology observed in acute cases of swine dysentery suggests involvement of one or more cytotoxins, possibly in the form of the widely observed β-hemolysin. Lesions similar to those in natural cases develop in intestinal loops exposed to purified hemolysin. Three distinct hemolysin genes, tlyA, tlyB, and tlyC, have been cloned and sequenced. Each gene is present as a single-copy chromosomal locus. Recombinant proteins are hemolytic and cytotoxic, but by an unknown mechanism; tlyA-minus mutants display decreased hemolysis in vitro and are attenuated in mice and in pigs. LPS, however, is of uncertain importance in pathogenesis, in that biological activity of LPS from B. hyodysenteriae differs little from that of B. innocens.

Protease may also contribute to virulence of B. hyodysenteriae. Damage to and detachment of epithelial cell monolayers are partially abrogated by serine protease inhibitors, although only a minority of strains produce demonstrable protease activity.

Dysentery cannot be produced in gnotobiotic pigs with pure cultures of B. hyodysenteriae, and the organism may require interaction with members of the normal flora (e.g., Fusobacterium necrophorum, Bacteroides vulgatus, and B. fragilis).

Diagnosis

Diagnosis of swine dysentery is based, in the first instance, on compatible clinical signs. However, signs may be similar in other types of enteritis (e.g., salmonellosis, colonic spirochetosis, and proliferative enteropathy), so demonstration of B. hyodysenteriae in lesions is the basis for a presumptive diagnosis of swine dysentery.

Mucosal scrapings from affected large intestine, rectal swabs, or feces should be subjected to direct examination and bacteriologic culture. Wet mounts can be examined by darkfield or phase contrast microscopy, and fixed smears should be Gram stained (using carbol fuchsin as the counterstain) and examined by brightfield microscopy. Staining with dilute carbol fuchsin, Victoria blue 4-R, or silver impregnation is also useful; the last is commonly used to demonstrate organisms in tissue. Fluorescent antibody techniques have been described. Demonstration of three to five spirochetes per high-power field is significant (Figure 29-3).

FIGURE 29-3 Brachyspira hyodysenteriae (Victoria blue 4R-stained smear from colon).

(Courtesy D.L. Harris.)

Brachyspira hyodysenteriae (and other members of the genus) grow slowly and are nutritionally fastidious. Specimens are plated onto selective blood agar (containing colistin, vancomycin, and spectinomycin, or spectinomycin alone). Plates incubated at 42° C in an anaerobic environment containing hydrogen and carbon dioxide are examined at 48-hour intervals for up to 10 days. Key features in identification of B. hyodysenteriae are colonial morphology, degree of β-hemolysis, production of indole, and hippurate hydrolysis. Brachyspira hyodysenteriae produces small, translucent colonies with a zone of clear hemolysis after approximately 48 hours’ incubation. Incorporation of 1% sodium RNA into media enhances growth, but also accentuates the difference in hemolysis between B. hyodysenteriae and B. innocens, the latter being weakly β-hemolytic. Brachyspira hyodysenteriae is indole positive and hippurate negative (Table 29-2).

TABLE 29-2 Characteristic Features of Members of the Genus Brachyspira

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