Line 1: |
Line 1: |
| ==Description== | | ==Description== |
− | Clastridiurre perfringens type A causes
| + | |
− | enterotoxemia, or yellow lamb disease,
| |
− | which occurs primarily in the western US
| |
− | (McGowan et al., 1958). Depression, anemia,
| |
− | icterus and hemoglobinuria, are followed
| |
− | by death after a clinical course of
| |
− | 6-12 h, and large numbers of C. perfringen.
| |
− | s are found in intestinal contents. A
| |
− | similar condition occurs in goats (Russell,
| |
− | 1970), and type A probably also causes
| |
− | tympany, sometimes accompanied by
| |
− | hemorrhagic, necrotic abomasitis in calves.
| |
− | Gram-positive bacilli are demonstrable on
| |
− | the mucosa and in the submucosa and a
| |
− | toxin is found in intestinal contents
| |
− | (Roeder et al., 1988). Intravascular hemolysis,
| |
− | capillary endothelial damage, platelet
| |
− | aggregation, shock and cardiac effects in
| |
− | natural infections are predictable systemic
| |
− | actions of a hemolytic toxin (Stevens et
| |
− | al., 1988; Timoney et a]., 1988). Chymotrypsin
| |
− | resistance of a toxin from
| |
− | enterotoxemia isolates may allow accumulation
| |
− | in the gut and entry to circulation
| |
− | (Ginter et al., 1995).
| |
| C. pgheernfrsi type B is frequently isolated | | C. pgheernfrsi type B is frequently isolated |
| from cases of dysentery in newborn | | from cases of dysentery in newborn |
Line 41: |
Line 17: |
| of type B infections may be due to | | of type B infections may be due to |
| additive or synergistic effects of a, p and | | additive or synergistic effects of a, p and |
− | c toxins. | + | c toxins |
− | Neonates of most species are highly
| |
− | susceptible to infection by C. perfringen.s
| |
− | type C (MacKinnon, 1989) (table ll), and
| |
− | colonization in advance of normal intestinal
| |
− | flora or alteration of flora by dietary
| |
− | changes are significant factors in pathogenesis
| |
− | (Timoney et al., 1988). In lambs,
| |
− | type C infection resembles lamb dysentery,
| |
− | and may be accompanied by nervous
| |
− | signs, including tetany and opisthotonus.
| |
− | Peracute death, occasionally without other
| |
− | clinical signs, is not uncommon, but the
| |
− | clinical course may also extend to several
| |
− | days. Young ewes and other adult sheep
| |
− | can also develop type C enterotoxemia, a
| |
− | condition known as ’struck’, in which the
| |
− | clinical disease occurs so rapidly that it
| |
− | often suggests that the animal has been
| |
− | struck by lightning. Mucosal damage, perhaps
| |
− | caused by poor quality feed, facilitates
| |
− | abomasal and small intestinal multiplication
| |
− | of organisms, with resulting
| |
− | mucosal necrosis. Fluid accumulation in
| |
− | the peritoneum and thoracic cavity suggest
| |
− | toxemia, and enteric lesions, dysentery
| |
− | and diarrhea are often absent (Sterne
| |
− | and Thomson, 1963). Similarities of cpb,
| |
− | the (3 toxin gene, to the genes for staphylococcal
| |
− | a and y toxins and leukocidin
| |
− | (Hunter et al., 1993), strengthen suggestions
| |
− | that (3 toxin may affect the CNS
| |
− | (Jolivet-Reynaud et al., 1986; McDonel,
| |
− | 1986). However, hemorrhagic enterotoxemia
| |
− | has not been reproduced in lambs by
| |
− | inoculation with cell-free culture supernatant
| |
− | fluid (Niilo, 1986).
| |
− | Enterotoxemia (’overeating’) in sheep
| |
− | of all ages except newborns is caused by
| |
− | C. perfrivgetes type D (table II) (Timoney
| |
− | et al., 1988). Lambs 3-10 weeks old, suckling
| |
− | heavily lactating ewes, are commonly
| |
− | affected, as are feedlot animals up to 100
| |
− | months of age. Upsets in the gut flora, following
| |
− | sudden changes to a rich diet, continuous
| |
− | feeding of concentrates (Popoff,
| |
− | 1984), and the presence of excess dietary
| |
− | starch in the small intestine are often
| |
− | involved. e toxin facilitates its own absorption
| |
− | (Niilo, 1993), resulting in toxemia
| |
− | with little or no enteritis. Some animals
| |
− | display dullness, retraction of the head,
| |
− | opisthotonus and convulsions (Niilo, 1993;
| |
− | Popoff, 1984), but sudden death is common.
| |
− | Degeneration and necrosis in the
| |
− | CNS is typical (Buxton and Morgan,
| |
− | 1976), and focal encephalomalacia is a
| |
− | chronic neurological manifestation of nonfatal
| |
− | disease (Griner, 1961; Buxton and
| |
− | Morgan, 1976). The extent of incoordination
| |
− | and convulsions is directly related to
| |
− | the severity of lesions (Griner, 1961). Peritoneal
| |
− | and pericardial effusions are typical
| |
− | in sheep, and glycosuria is pathognomonic
| |
− | (Gardner, 1973; Niilo, 1993). The common
| |
− | name ’pulpy kidney’ derives from
| |
− | the post mortem autolysis of hyperemic,
| |
− | toxin-damaged tissue.
| |
− | Goats develop catarrhal, fibrinous, or
| |
− | hemorrhagic enterocolitis. The condition
| |
− | is often chronic, and pulpy kidney is
| |
− | absent (von Rotz et al., 1984; Blackwell
| |
− | and Butler, 1992).
| |
− | C. perfringens type E is an apparently
| |
− | uncommon cause of enterotoxemia of
| |
− | lambs (table II), and recent isolates have
| |
− | been obtained from calves with hemorrhagic
| |
− | enteritis, in the western and midwestern
| |
− | US (Meer and Songer, 1997).
| |
− | However, type E remains of uncertain
| |
− | overall importance in animal disease.
| |
− | An increasing body of evidence suggests
| |
− | a role for enterotoxigenic strains,
| |
− | particularly of type A, in the etiology of
| |
− | diarrheal conditions in several animal
| |
− | species (Estrada-Correa and Taylor, 1989;
| |
− | Niilo, 1993). In one study, CPE production
| |
− | was observed in 12 % of isolates from cattle,
| |
− | sheep and chickens with enteritis
| |
− | (Niilo, 1978), and in another, genotyping
| |
− | revealed that about 5 % of isolates are
| |
− | enterotoxigenic, with most of these being
| |
− | type A (Songer and Meer, 1996; Meer and
| |
− | Songer, 1997).
| |
− | CPE is weakly immunogenic when
| |
− | administered via the intestinal tract. Disease
| |
− | gives rise to serum antibodies in
| |
− | sheep and other domestic species, but antibodies
| |
− | produced following parenteral inoculation
| |
− | are not protective (Niilo and Cho,
| |
− | 1985; Estrada-Correa and Taylor, 1989).
| |
− | The best target for immunoprophylaxis
| |
− | may be the toxin’s membrane binding
| |
− | event (Hanna et al., 1989; Mietzner et al.,
| |
− | 1992).
| |
− | Immunoprophylaxis is a control measure
| |
− | of paramount importance, due to the
| |
− | rapid and frequently fatal course of disease
| |
− | caused by the various types of C. perfringens.
| |
− | Lambs born to ewes vaccinated
| |
− | against types B, C or D are protected
| |
− | against dysentery (Smith and Matsuoka,
| |
− | 1959; Kennedy et al., 1977; Odendaal et
| |
− | al., 1989), and may be immunized at 3
| |
− | days of age (Kennedy et al., 1977). Enterocolitis,
| |
− | but not toxemia, may occur in
| |
− | vaccinated goats (Blackwell et al., 1991;
| |
− | Blackwell and Butler, 1992).
| |
| | | |
| Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals. Types B and C both produce the highly necrotizing and lethal β toxin that is responsible for severe intestinal damage. This toxin is sensitive to proteolytic enzymes, and disease is associated with inhibition of proteolysis in the intestine. Sow colostrum, which contains a trypsin inhibitor, has been suggested as a factor in the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats. The diseases are listed below, categorized as to cause and host. C perfringens also has been associated with hemorrhagic enteritis in dogs. (See also intestinal diseases in horses, Intestinal Diseases in Horses and Foals: Introduction.) | | Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals. Types B and C both produce the highly necrotizing and lethal β toxin that is responsible for severe intestinal damage. This toxin is sensitive to proteolytic enzymes, and disease is associated with inhibition of proteolysis in the intestine. Sow colostrum, which contains a trypsin inhibitor, has been suggested as a factor in the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats. The diseases are listed below, categorized as to cause and host. C perfringens also has been associated with hemorrhagic enteritis in dogs. (See also intestinal diseases in horses, Intestinal Diseases in Horses and Foals: Introduction.) |