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