Difference between revisions of "Lamb Dysentery"

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==Description==
 
==Description==
−
 
+
Clastridiurre perfringens type A causes
−
* [[:Category:Enteropathogenic and Enterotoxaemic Clostridia|''Clostridium perfringens'']] causes very severe acute haemorrhagic enteritis.
+
enterotoxemia, or yellow lamb disease,
−
** Usually affects young farm animals
+
which occurs primarily in the western US
−
*** May also be seen in pets.
+
(McGowan et al., 1958). Depression, anemia,
−
* Type B [[:Category:Enteropathogenic and Enterotoxaemic Clostridia|''Clostridium perfringens'']] infection of lambs leads to '''lamb dysentery'''.
+
icterus and hemoglobinuria, are followed
−
 
+
by death after a clinical course of
−
* Lamb dysentery is usually seen in lambs under 2 weeks of age.
+
6-12 h, and large numbers of C. perfringen.
−
** Related to being kept in a cold, dirty environment, with build-up of infection during the lambing season.
+
s are found in intestinal contents. A
−
* Lambs may produce bloodstained [[Diarrhoea|diarrhoea]] before death, but they often die before this effect is apparent.
+
similar condition occurs in goats (Russell,
−
* Diagnosed by culturing contents of gut.
+
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
 +
from cases of dysentery in newborn
 +
lambs (table II) and hemorrhagic enteritis
 +
in goats (Frank, 1956). Disease is more
 +
common in the UK, South Africa and the
 +
Middle East than in the US (Timoney et
 +
al., 1988). In lambs, inappetence, abdominal
 +
pain and bloody diarrhea are followed
 +
by recumbency and coma. Lesions consist
 +
primarily of hemorrhagic enteritis,
 +
with evidence of enterotoxemia (Frank,
 +
1956). Chronic disease in older lambs
 +
(’pine’) is characterized by chronic
 +
abdominal pain without diarrhea. Pathogenesis
 +
of type B infections may be due to
 +
additive or synergistic effects of a, p and
 +
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.)

Revision as of 15:32, 24 August 2010

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 from cases of dysentery in newborn lambs (table II) and hemorrhagic enteritis in goats (Frank, 1956). Disease is more common in the UK, South Africa and the Middle East than in the US (Timoney et al., 1988). In lambs, inappetence, abdominal pain and bloody diarrhea are followed by recumbency and coma. Lesions consist primarily of hemorrhagic enteritis, with evidence of enterotoxemia (Frank, 1956). Chronic disease in older lambs (’pine’) is characterized by chronic abdominal pain without diarrhea. Pathogenesis of type B infections may be due to additive or synergistic effects of a, p and 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.) Lamb dysentery: type B in lambs up to 3 wk of age

Signalment

Diagnosis

Clincal Signs

Lamb dysentery is an acute disease of lambs <3 wk old. Many may die before signs are seen, but some newborn lambs stop nursing, become listless, and remain recumbent. A fetid, blood-tinged diarrhea is common, and death usually occurs within a few days

Laboratory Tests

Pathology

Hemorrhagic enteritis with ulceration of the mucosa is the major lesion in all species. Grossly, the affected portion of the intestine is deep blue-purple and appears at first glance to be an infarction associated with mesenteric torsion. Smears of intestinal contents can be examined for large numbers of gram-positive, rod-shaped bacteria, and filtrates made for detection of toxin and subsequent identification by neutralization with specific antiserum

  • The gut is blown and distended with foamy ,bloody contents.
  • Sometimes ulceration with perforation and fibrinousperitonitis is seen.
  • Focal or diffuse congestion and haemorrhage
  • Coagulative necrosis of villi.
  • Oedema.
  • Haemorrhage.
  • Influx of inflammatory cells in the lamina propria and submucosa.

Treatment

Treatment is usually ineffective because of the severity of the disease, but if available, specific hyperimmune serum is indicated, and oral administration of antibiotics may be helpful. The disease is best controlled by vaccination of the pregnant dam during the last third of pregnancy: initially, 2 vaccinations 1 mo apart, and annually thereafter. When outbreaks occur in newborn animals from unvaccinated dams, antiserum should be administered immediately after birth.

Prognosis

Treatment is usually ineffective because of the severity of the disease

Links

References

  1. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
  2. The Center for Food Security and Public Health, Iowa State University (2004) Animal Disease Factsheet: Epsilon toxin of Clostridium Perfringens.
  3. Songer, J G (1998) Clostridial diseases of small ruminants. Veterinary Research, 29, 219-232.
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