What is Clostridium perfringens?(Association with Aspergillus?

(Quinn and Markey – Concise Review of Veterinary Microbiology p. 37-38)

 Large, spore-forming
 Gram-positive rods
 Anaerobic
 Present in soil, alimentary tract of animals, and in feces
 Enteropathogenic and enterotoxemia-producing clostridia
o

(Songer and Post – Veterinary Microbiology p. 345 - 352)

 C. perfringens causes myonecrosis and gas gangrene
 Humans are typically affected by Type A strains
 Are divided based on type of toxin produced


 Type A:
o More common in beef and dairy calves
o Infection can originate from contaminated colostrum or method of administration
 Ingestion of icy colostrum in large amounts is associated with disease
o Symptoms in ruminants:
 Bloating
 Affected animals die quickly
 Hemorrhagic gastroenteritis
 Abomasum is dilated and has thickened emphysematous walls/folds
 Severe necrosis
 Gas bubbles can be observed in mucosa/submucosa
 Type B:
o Can be associated with hemorrhagic enteritis in goats, calves, and foals
o Type B strains proliferate in the gut and lead to enterotoxemia, followed by hemorrhage and
ulceration of the small intestine
o Symptoms include: appetite loss, severe abdominal pain, bloody diarrhea, recumbency, and
eventually death
 Type C:
o Neonates are typically infected with Type C strains because they can proliferate easily
without a well established normal intestinal flora
o Sudden dietary changes that affect the flora can lead to Type C proliferation
o Symptoms in piglets:
 Diarrhea
 Dysentery
 Blood and necrotic debris in feces
 Jejunal mucosal necrosis
o Symptoms in neonatal calves, lambs, and goats:
 Hemorrhagic necrotic enteritis
 Enterotoxemia
 Possible nervous signs:
 Tetany
  Opisthotonos
o Damage to gastrointestinal mucosa often due to poor quality feed usually precedes Type C
proliferation in abomasum and small intestine
 Type D:
o Causes enterotoxemia in sheep of all ages except neonates
o Common in suckling lambs 3-10 weeks old, and in feedlot animals
o Excess dietary starch in small intestine facilitates growth of Type D strains and production of
E-toxin
o E-toxin mediates its own absorption, leading to toxemia with little evidence of enteritis
o Symptoms:
 Affects on central nervous system (CNS)
 Opisthotonos
 Convulsions
 Agonal struggling
 Affected sheep display blindness, head pressing, and anorexia
 "Pulpy kidney" is common name for Type D enterotoxemia
 Due to rapid postmortem autolysis in toxin-damaged tissue
o Rare disease in adult cattle, deer, domesticated camels, and horses
 Type E:
o Associated with enterotoxemia of lambs, calves, and rabbits
o Distinguishable from other strains by their production of I-toxin
o Pathogenesis is not well known
o Enterotoxin gene, cpe, can be detected by PCR in most Type E isolates
 Pathogenesis:
o Alpha-toxin (CPA) is a multifunctional phospholipase that is produced in varying amounts by
all animals
 A-toxin hydrolyzes cell membrane phospholipids, which leads to hemolysis, necrosis,
and lethality
 Plays a dominant role in myonecrosis
 May also play role in enterotoxemia because large amounts are found in feces of
affected animals
 CPA alone causes only milk enteritis and villous edema, with minimal damage to
epithelium and blood vessels
 If CPA is in circulation, it can cause:
 Intravascular hemolysis
 Capillary damage
 Inflammation
 Platelet aggregation
 Shock
 Cardiac effects
 Eventually death
o Beta-toxin (CPB) is responsible for mucosal necrosis and possibly CNS signs
 IV administration causes increased blood pressure, decreased heart rate, and possible
ECG disturbances suggestive of atrioventricular block (AV)
 In pigs:
 CPB acts in jejunum under conditions of decreased proteolytic activity due to
neonatal pancreatic secretion deficiency or ingestion of protease inhibitors in
colostrum
  Damage to microvilli, mitochondria, and terminal capillaries --> Adhesion of C.
perfringens to jejunal mucosa --> Widespread mucosal necrosis with bacterial
invasion, toxin production, epithelial cell death, and desquamation
o Epsilon-prototoxin is converted to Epsilon-toxin (ETX) by proteolytic cleavage
 Small amount of ETX in gut of normal animals is most likely innocuous