The term "spinal diarrhea" refers to the colitis of pigs during growth and development, which is associated with hemolytic intestine infection, but is distinct from infection with Treponema hydor? Sensiforme? (swine). 1980, 1992). Recent studies have shown (Taylor et al., 1980) that the pathogen is a particular species of spirochete. The current official name is the colonic hairy spirochaete or Serpulina pilosicoli? (Trott et al., 1996e). ?Spilosicoli? was previously known in the literature as Anguillina coli? (Lee et al., 1993), Serpulina coli? (Duhamel et al., 1993a), and Group IV hemolytic enteroheptal spirochetes (Fellstrm and Gunnarsson, 1994). Colonic pilosima spirochete infections are characterized by mild to moderate blind colitis and lead to drainage-like or mucous-like faeces that reduce weight loss and slow growth. The most prominent histological feature of this disease is the large number of intestinal spirochetes whose cells connect at one end to the surface of the colon epithelium. This characteristic adsorption is also found in humans (Lee and Hampson, 1994), primates (Duhamel et al., 1996), dogs (Duhamel et al., 1995b), chickens (McLaren et al., 1997), and ducks (Trott et al., 1996a). . The phenomenon that the gut spirochete adsorbs on human colonic epithelium on one end before it is classified as colonic pilosima and it is recognized as the cause of diarrhea in pigs and other hosts is called %2634; gut spirochete%2634 (Harland and Lee, 1967). Therefore, when the name of the colonic pilosima is still used, we are still accustomed to using %2634; pig gut spirochete% 2634; (PIS) instead of %2634; spirochete diarrhea %2634; to describe the pig disease it causes (Trott et al. 1996). In North America, the disease is also known as %2634; porcine <RTI ID=0.0>colonosporosis</RTI> %2634; (Girard et al., 1995), but %2634 will be used in the remainder of this chapter; pig enterobacterosis %2634;. Taylor and Coworkers (1980) first described PIS. They attacked experimental pigs with a weak beta-hemolytic strain of the intestinal hemotoxin (P??43/6/78?), resulting in colitis with hemorrhage. Mucoid diarrhea. This strain was initially considered to be a non-invasive spirochete, but is now considered to be a typical strain of the colonic hairy spirochaete. This disease has been used? Spiloscicoli? Many other strains replicate successfully in pigs (Andrews and Hoffman, 1982; Thompson et al., 1996; Trott et al., 1996). PIS is now considered to be a major cause of porcine colitis in pigs, especially after intensive production has been used to control other major bowel diseases such as salmonellosis and swine dysentery (Duhamel, 1996). Despite the presence of non-infectious, diet-induced colitis (Wood, 1991), the UK reported %2634; non-specific colitis% 2634; at least part of it appears to be caused by the colonic pilosyposis. PIS has been reported in most swine countries, including the United Kingdom (Taylor et al., 1980), Canada (Girard and Higgi??ns, 1989; Girard et al., 1995; Jacques et al., 1989; Spearman et al., 1988), Australia ( Hampson, 1991; Hampson and Trott, 1995), USA (Duhamel et al., 1993; Ramanathan et al., 1993), Sweden (Fellstrm et al., 1996), and Denmark (Möller et al., 1996). Many studies on PIS have been carried out in recent years. Many important aspects of the disease are still unclear, including pathogenicity, host immunity, and detailed epidemiology. The pathogenic colonic spirochetes are named after the histological appearance of PIS. One end of the spirochete is adsorbed on the colon epithelium, just as the hair covers the surface of the colon (?Serpullina pilosicoli? Latin means %2634; Small hairy colony of snakes %2634 ;) (Trott et al., 1996). The colonic pilosima spirochetes have a characteristic spirochete morphology that looks similar to other species of Serpulina, usually shorter (6 to 10 μm long) and finer (0 to 25 to 0? 30 μm wide), with less surface plastic flagella (4 to 7 per end), with a sharp tip (Figure 40-1). These differences can only be seen under the electron microscope, but with phase contrast microscopy, the cells appear to be smaller than other species of S. virescens. The culture conditions for the colonic pilosima and the T. hyodysenteriae are the same, except for After 6 days of incubation in order to observe hemolysis, antibiotics (rifampicin and spiramycin) are also needed to isolate T. hyodysenteriae and inhibit the growth of sensitive microorganisms (Trott et al., 1996d), which can hydrolyze casein in the pancreatic enzyme. Soy agar grows into small stripe colonies with weak beta-hemolysis. Olson (1996) reported that when the T. hyodysenteriae was isolated, the initial inoculation of the agar cut into pieces may help to obtain the colonic piliform psoriasis isolate without other microbial contamination. The classification of swine intestinal gyrocystis is a rapidly developing field (Hampson and Stanton, 1997), in addition to harmless Treponema (?S?innocens?) and colonic pilosiligal? Two new species with weak beta-hemolytic properties: intermediate Treponema (?S?intennedia?) and Serpulina murdochii? (Stanton et al., 1997). The above four hemolysed enterococci have similar patterns on blood agar and can only be distinguished from one another by biochemical and genotyping techniques. The harmless Treponema, Treponema pallidum and SS?murdochii? are not pathogenic in normal pigs and are generally considered to be non-pathogenic (Hudson and Alexander, 1976; Kinyon et al., 1977; Lee et al., 1993). However, strains of Treponema pallidum have been found to be pathogens of commercial chickens (Mclaren et al., 1997). When inoculated in isolated porcine colon loops, this strain can cause lesions (Binek et al., 1984), but rarely in the field. Diarrhea in pigs (Fellstrm and Gunnarsson, 1995). In addition, some insecure Treponema strains isolated from diarrhea pigs were also found to cause pig diarrhea and pathological changes when inoculated to the gilts (Neef et al., 1994). Colitis and diarrhea caused by intermediate Treponema have been referred to as %2634; spirochetic colitis%2634; (Hampson and Trott, 1995; Taylor and Trott, 1997). Little is known about this disease, and it is rarely encountered. It is only mentioned briefly as a differential diagnosis. Epidemiology The details of the epidemiology of the PIS have not been fully understood. It is thought that infection by the feces/mouth route has led to the introduction of infected pigs that are susceptible to disease in non-immune pigs. SPF pigs without swine dysentery can artificially infect the disease (Atyeo et al., 1996c). Like the previously discovered T. hyodysenteriae (Chia and Taylor, 1978), this microorganism can survive in feces for a long time. Using culture techniques, different pig farm infection rates ranged from 5% (Atyeo et al., 1996c) to 37.5% (Duhamel, 1996). However, these data are often inhibited by the simultaneous use of antibiotics, the age of the pigs examined, the extent of the culture tests, and the degree of microbial contamination in other faeces to inhibit the growth of the spirochete. In Sweden, out of 8 pigs with diarrheal symptoms, 6 pigs were isolated from the colon pilosima pilosicoli; 11 colonies without diarrhea had only one colony of pilosima pneumoniae isolated (Fellstrm et al., 1996). ). Pigs of different growth stages can isolate the colonic pilosima pilosicoli, but the weaning pigs and growing pigs have the most infections, and the incidence is more serious. There are no specific serological tests that can be used to detect serum titers in infected pigs. The outbreak of infection with T. hyodysenteriae in pigs is usually caused by a single strain. The colon is a genotypically diverse species (Atyeo et al., 1996a; Lee and Hampson, 1994), and from a single More than one type of strain can often be isolated in ring pigs (Atyeo et al., 1996c). The presence of multiple strains in the herd can help explain the phenomenon of repeated attacks of PIS in rehabilitation herds or the use of antibiotics in herds. Unlike the T. hyodysenteriae, the colonic pilosima is present in a wide range of animal species (Atyeo et al., 1996a). In all these types of hosts, the typical clinical symptoms and pathologies associated with PIS are found, including humans. Isolated isolates from pigs, dogs and humans have a genetically close relationship (Lee and Hampson, 1994), but the evidence has shown that only infection can occur between dogs and humans (Trott et al., 1996b). In addition, human colonic strains of the genus Helicobacter pylori can cause morbidity when inoculated on common pigs (Trott et al., 1996c), so that potential cross-infection between humans and pigs cannot be ignored because of the distribution of colonic pilosiliform organisms. It is immunosuppressive or living in developing countries, and healthy pig workers do not appear to be infected from pigs infected with PIS. Other host species, particularly birds, may represent the persistent source of infection in pigs. Although rodents have been found to be carrier of T. hyodysenteriae and may be a spirochete that produces weak β-hemolysis, all other rodent-originated strains we identified are SS?murdochii? Disease type (Trott et al., 1996a). Despite this, the P43?6/78? strain has been found to be able to reproduce in experimentally infected mice, indicating that the mouse is a potential carrier (Sacco et al., 1996). Pathogenesis: The pathogenesis of PIS is not yet fully understood, but it has several important differences from swine dysentery. Colonic hairy worms do not adsorb pathogens in the intestinal mucosa of pigs in the same way as pathogenic strains of T. hyodysenteriae. Previously (Milner and Sellwood, 1994), a large number of spirochetes are commonly found at the time of infection, with one end of the bacteria attached to the epithelial surface of the cecum and colon. In addition, PIS associated with colitis is much lighter than swine dysentery and only occurs early in the disease. After bacterial infection from the oral cavity, colon mucosal epithelium colonized, 2 to 7 days after inoculation can be detected in feces cotton swabs; but the incubation period can also be up to 20 days. In the early stage of infection, a large number of colonic pilosigma organisms adsorbed to the surface of blind and colonic epithelial cells, resulting in the disappearance of microvilli and disruption of peripheral endoplasmic reticulum function. Adhesion occurs only at the tip of the microvilli of mature intestinal epithelial cells, and spirochetes do not adhere to immature cells in the intestinal crypts (Trott et al., 1995). Degeneration of epithelial cells results in accelerated mitosis of acinar cells. Foams elongate, forming immature epithelial tissue containing mucous cells or columnar cells. The necrotic changes in the epithelium are mainly small adhesive nodules on the mucosal surface. Colonic P. pallidum has now been found in dilated intestinal follicles (Trott et al., 1996c), goblet cells (Thompson et al., 1996), lamina propria, and it invades through tight junctions between epithelial cells. Colonic piliform spirochetes appear in the crypts and lamina propria and are associated with neutrophil aggregation (crypt abscesses) and edematous colitis, accompanied by mucosal, lamina propria, and sometimes muscular neutrophils. Lymphocyte infiltration (Duhamel, 1996). Both infiltrating phenomena that occur simultaneously with the adsorption of spirochetes into epithelial cells or appear alone have been observed. A large number of colon pouchworms reproduce on the damaged mucosal surface. Colonic hairy spirochaetes have been isolated from the blood of clinically symptomatic or immunosuppressed patients (Trott et al., 1997). Although systemic spirochete bacteremia has not been directly observed in pigs, its presence cannot be ruled out. Some animals are often found to have died of certain lesions, presumably mucosal hemorrhagic colitis caused by the colonic pilosima pallidum. To date, there have been no reports of attempting to culture blood from such animals with a suitable medium for the isolation of the colonic hairy spirochetes. Colonization, local invasion, and subsequent colitis in the epithelium cause the cecal and colon contents to increase in moisture, and produce more mucus, and sometimes clots. The resulting epithelial lesions and immature epithelium can lead to a decrease in the surface area of ​​the colon, a decrease in the absorption of volatile fatty acids, a decrease in feed conversion and a reduction in weight gain (Duhamel, 1996). The host immune mechanism directly against the colonic pilosima is still unclear. In experimentally infected pigs, circulating antibodies exist, but the immune response has not yet been fully investigated (Taylor et al., 1980). Sigil pigs (Neef et al., 1994), old chickens (Adachi and Minato, 1986; Duhamel et al., 1995a; Trott et al., 1995) and mice (Sacco et al., 1996) have been successfully used as models for experimental infections. In the case of artificially infected normal pigs, only a small proportion (33%) of the infected pigs were infected (Trott et al., 1996c). Adachi et al. (1982) infected pigs (most likely the colonic pilosima spp.) with a micro-hemococci, and found that pigs with high titer of complement-binding antibodies had the least amount of bacteria excreted from the feces.
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