Clostridium Flashcards
What is the causative agent of tetanus?
Clostridium tetani – best known anaerobic spore-forming bacillus.
Describe the morphology of Clostridium tetani.
Straight slender rod (0.4–0.6 µm x 2–5 µm), found singly in tissues and culture.
Describe the spores of Clostridium tetani.
Formed after 24–48 hours at the rod’s end; appear like a badminton racket or drumstick. Gram-variable, with peritrichous flagella.
What do Clostridium tetani colonies look like in deep agar?
Fluffy, cottony spheres with a brush-like effect in gelatin.
How resistant is Clostridium tetani to sporicidal agents?
Highly resistant; spores killed by boiling for 15 minutes (most strains).
How many serotypes does Clostridium tetani have, and what antigen?
9 serotypes; glycopeptide antigen.
Where is Clostridium tetani commonly found?
Soil and horse manure.
What toxins does Clostridium tetani produce?
Tetanospasmin, tetanolysin, and a peripherally active non-spasmogenic toxin.
What toxin is responsible for the symptoms of tetanus?
Tetanospasmin.
What does tetanolysin cause?
Local tissue necrosis favorable for bacterial multiplication.
Describe the structure of tetanospasmin.
Two subunits: heavy and light chains, non-toxic when separated.
What destroys tetanospasmin?
Gastric juices.
What does tetanospasmin bind to in the body?
Gangliosides bound to cerebrosides.
Why are antibodies ineffective against tetanospasmin?
The toxin’s binding is difficult to reverse.
What neurotransmitter does tetanospasmin inhibit?
Glycine.
What is glycine’s function in the spinal cord?
An inhibitory neurotransmitter.
What is the effect of tetanospasmin on the nervous system?
Inhibition of protein synthesis in the brain, leading to paralysis.
How does tetanospasmin travel in the body?
Along motor and sensory nerves.
What is ascending tetanus?
Spreads upward in opposite limbs and trunk muscles.
What is descending tetanus?
Common in humans and horses; affects facial/jaw muscles, causing lockjaw (risus sardonicus).
What are portals of entry for Clostridium tetani?
Nail wounds (horses), castration/docking (lambs), calving, dehorning, nose ringing (cattle).
Which animals have natural immunity to C. tetani?
Birds.
Which species do not have antitoxins against C. tetani?
Horses, dogs, pigs, and humans.
Which animals have neutralizing antibodies against C. tetani?
Sheep and goats.
What provides protection for 2–3 weeks against C. tetani?
Hyperimmunized serum from horses (1,500 units).
Describe the C. tetani vaccine.
0.4% formalin, precipitated with aluminum potassium sulfate, suspended in saline.
What is the vaccination schedule for horses?
Toxoids at 6–8 week intervals, followed by booster at 6–12 months.
What is the treatment for C. tetani?
Antitoxin ASAP (100,000–200,000 units IV/intracisternal) and large penicillin doses.
What is Clostridium botulinum known for?
Potent neurotoxin causing botulism.
What is botulism?
Disease with flaccid paralysis leading to respiratory failure and death.
What are the 3 forms of C. botulinum infection?
Intoxication, wound infection, and infant botulism.
Where was C. botulinum first discovered?
Belgium, in imperfectly smoked ham.
What is infant botulism?
Intestinal colonization type of botulism.
Describe C. botulinum spores.
Oval, centric or eccentric.
What is a major metabolic product of C. botulinum?
Acetic acid.
What is the characteristic of non-proteolytic C. botulinum types?
They acidify but do not coagulate milk.
What is the characteristic of proteolytic C. botulinum types?
They slowly curdle milk and partially digest/darken the curd.
How many serotypes and toxin types does C. botulinum have?
6 serotypes and 7 toxin types.
What disease does C. botulinum type A cause in humans and mink?
Botulism.
What disease does C. botulinum type A cause in cattle and horses?
Forage poisoning.
What disease does C. botulinum type A cause in chickens?
Limberneck.
What disease does C. botulinum type B cause in foals?
Shaker foal syndrome.
What disease does C. botulinum type C cause in ducks?
Limberneck and Western duck disease.
What disease does C. botulinum type D cause in cattle?
Lamsiekte.
What does the botulinum toxin complex consist of?
Toxin molecules and a hemagglutinin moiety.
What enzyme activates toxins of non-proteolytic strains?
Trypsin.
What causes a depraved appetite for decaying carcasses?
Aphosphorosis.
What is Lamsiekte?
Lameness associated with phosphorus deficiency.
What is toxicoinfectious botulism?
Toxin produced in necrotic body areas (e.g., foals).
What is shaker foal syndrome?
Characterized by dysphagia, tremors, weakness, recumbency, and death.
Which nerves does botulinum toxin affect?
Cholinergic nerves of the peripheral nervous system.
What kind of antitoxin is used for birds (but not universally practiced)?
Homologous antitoxin.
Why is polyvalent antitoxin ineffective after toxin binds?
It cannot neutralize toxins already bound to nerve membranes.
What condition is caused by Clostridium perfringens type A?
Yellow lamb disease.
What condition is caused by C. perfringens type B?
Lamb dysentery and hemorrhagic enteritis in sheep/goats.
What condition is caused by C. perfringens type C?
Necrotic enteritis and “Struck” in sheep.
What condition is caused by C. perfringens type D?
Enterotoxemia (overeating disease, pulpy kidney disease).
What condition is caused by C. perfringens type E?
Enterotoxemia in lambs and calves.
What conditions are caused by Clostridium hemolyticum?
Red water disease, hemorrhagic disease, infectious icterohemoglobinuria.
What diseases are caused by Clostridium novyi?
Big head in rams, black disease (necrotic hepatitis in sheep).
What does Clostridium chauvoei cause?
Blackleg, black quarter, quarter evil, symptomatic anthrax.
What does Clostridium septicum cause?
Malignant edema, braxy or bradsot.
What does Clostridium colinum cause?
Ulcerative enteritis (quail disease).
What does Clostridium spiroforme cause?
Iota enterotoxemia in rabbits.
What does Clostridium difficile cause?
Enterotoxemia in hamsters.
What does Clostridium villosum cause?
Subcutaneous abscesses in cats.
Describe C. perfringens morphology.
Oval spores, pleomorphic cells in old cultures, non-flagellated, with capsules in tissue.
What are the five types of C. perfringens?
Types A to E.
What is the hemolytic pattern of C. perfringens?
Inner zone: complete hemolysis; outer zone: incomplete.
What enzymatic activity does C. perfringens have?
Lecithinase (phospholipase C), stormy fermentation of litmus milk.
What are the four major toxins of C. perfringens?
Alpha (phospholipase), beta, epsilon, and iota.
What is the most common cause of necrotizing myositis in horses?
Clostridium perfringens.
Where is C. perfringens commonly found?
Ubiquitous in nature, normal intestinal flora.
What is the function of alpha toxin in C. perfringens?
Causes intravascular hemolysis and capillary damage.
What does beta toxin of type B C. perfringens do?
Causes hemorrhagic zones and ulcerations.
How is type C beta toxin affected by the digestive system?
It is labile and denatured by intestinal enzymes.
What damage does type C beta toxin cause?
Necrosis of the abomasum and small intestine mucosa.
What is associated with C. perfringens type D?
Pulpy kidney disease, overeating disease.
What is unique about epsilon toxin?
Requires trypsin/chymotrypsin for activation; enhances intestinal absorption.
What effect does activated epsilon toxin have on blood pressure?
Increases it.
What is caused by type E C. perfringens?
Hemorrhagic, necrotic enteritis in calves.
Describe Clostridium hemolyticum.
Closely related to C. novyi type D; motile; subterminal oval spores causing bulging.
What cultural requirement is essential for C. hemolyticum?
Tryptophan under good anaerobic conditions.
What toxins are involved in C. hemolyticum and C. novyi type B?
Beta and alpha toxins, respectively.
Where does C. hemolyticum produce toxins?
In the liver.
What provides a microenvironment for spore germination in C. hemolyticum?
Migration of liver flukes.
What does beta toxin (phospholipase C) cause?
Intravascular hemolysis and capillary damage.
What color is urine during hemoglobinuria?
Dark red or port-colored, clear but foamy.
During hemoglobinuria, how much hemoglobin is destroyed?
40–50%.
What causes RBC death in clostridial disease?
Anoxemia due to hemoglobin destruction.
What are the three types of Clostridium novyi?
Types A, B, and C.
What are the growth requirements of C. novyi?
Strict anaerobic conditions, requires reduced cysteine.
Where is C. novyi found, and what does it cause?
Soil and herbivore intestines; causes gas gangrene via contaminated wounds.
What enzymes are elevated in C. novyi infections?
Lactic dehydrogenase and glutamic-oxaloacetic transaminase.
What is “Black disease”?
Necrotic hepatitis in sheep caused by C. novyi.
What parasite facilitates C. novyi infections?
Fasciola hepatica (liver fluke).
What does FAT stand for in diagnostics?
Fluorescent Antibody Technique.
Describe Clostridium chauvoei spores.
Oval, excentric, swell rods into lemon shapes.
What antigens and toxins does C. chauvoei produce?
Flagellar, somatic, and spore antigens; alpha toxin, hyaluronidase, and DNase.
What does C. chauvoei cause?
Myonecrosis—necrotizing and spreading tissue damage.
What does infected tissue with C. chauvoei look like?
Reddish-brown to black, crepitant, spongy, and dry when cut.
What is Clostridium septicum also known as?
Ghon-Sachs bacillus or malignant edema bacillus.
Describe the growth of C. septicum.
Grows well anaerobically on all media, with excentric oval spores.
Where is C. septicum commonly found, and how does it infect lambs?
Soil and intestinal tract; infects via wounds, umbilicus, or abomasal lining.
