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Bacteriology and Mycology > Enterotoxigenic clostridium > Flashcards

Enterotoxigenic clostridium Flashcards

1
Q

What is C. perfringens?

A
  • Gram +
  • Spore formin- subterminal
  • Rod shaped
  • With double zone hemolysis
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2
Q

Where is C. perfringes found?

A
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3
Q

What are the types of C. perfringens and what toxins do they produce?

A
  • A* - alpha toxins
  • B - Alpha, Beta, Epsilon toxins
  • C* - Alpha, Beta toxins
  • D* - Alpha, Epsilon toxins
  • E - Alpha, Iota toxins
  • F - Alpha, CP Enterotoxin
  • G* - Alpha, Necrotic enteritis beta-like toxin (NetB)
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4
Q

What is the activity and effects of Alpha toxin in C. perfringens?

A
  • A zinc metallophospholipase
  • Hemolytic and cytotoxic
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5
Q

What is the activity and effects of Beta toxin ot C. perfringens?

A
  • A pore-forming toxin
  • Induces inflammation and necrosis in the intestine
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6
Q

What is the activity and effects of Epsilon toxin of C. perfringens?

A
  • Secreted as a prototoxin and requires activation by pepsin and chymotrpsin in the gut
  • Third most potent clostridial toxin
  • A pore-forming toxin, increases intestinal permeability
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7
Q

What is the activity and effects of Iota toxin ot C. perfringens?

A
  • A binary toxin because it has two polypeptides, named IA and IB
    • IA: ADP-ribosylates of skeletal muscle and nonmuscle actins causing cell death
    • IB: Mediates binding to cells
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8
Q

What is the activity and effects of CPE toxin ot C. perfringens?

A
  • A pore-foring cytotoxin
  • Produced by all types, except B.
  • Induces cell death of enterocytes and fluid secretion
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9
Q

What is the activity and effects of NetB toxin of C. perfringens?

A
  • A pore-forming cytotoxin.
  • Lyses enterocytes
  • Mostimportant toxin involved in avian necrotic enteritis
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10
Q

What other toxins of C. perfringens are there?

A
  • At least 8 other exotoxins
  • Gamma, Delta, Eta, Theta, Kappa, Lambda, Mu, Nu
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11
Q

What is Perfringolysin (PFO)?

A
  • Also called Theta toxin
  • A pore-forming hemolysin
  • Acts synergistically with alpha hemolysin
  • Involved in gas gangrene
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12
Q

What is Enterotoxemia?

A
  • Commonly used term to describe enteritis caused by C. perfringens
  • Implies systemic spread of the toxin produced in the intestines
  • In many instances the toxin effect is confined to the intestines alone
  • Preferred term “Necrotic enteritis”
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13
Q

What diseases do type A Infections of C. perfringens cause?

A
  • Humans - Gas Gangrene in humans and animals
  • Cattle, Goats, Swine, Horse, Dogs, Minks - Necrotic enteritis (Hemorrhagic enteritis or Enterotoxemia)
  • Calves - Abomasal bloat and Ulcers
  • Dairy cows - Hemorrhagic bowel syndrome
  • Sheep - Yellow lamb disease
  • Chicken - Gagrenous Dermatitis
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14
Q

What diseases does a Type B infection of C. perfringes cause?

A
  • Caused by Alpha, Beta, and Epsilon toxins
  • Sheep - Lamb dysentery
    • UK, Middle East, S. Africa
  • Cattle, Goats - Necrotic enterits (Hemorrhagic enteritis or Enterotoxemia)
  • Not common in the US
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15
Q

What diseases are caused by Type C infections of C. perfringens?

A
  • Caused by Alpha and Beta toxins
  • Humans - Necrotic enteritis (Pig bel)
  • Sheep, Goats - Struck (Enterotoxemia) in Britain Necrotic enteritis (Enterotoxemia) in lambs and kids
  • Cattle - Necrotic enteritis (Enterotoxemia) in calves
  • Horses - Necrotic enteritis (Enterotoxemia) in foals
  • Swine - Necrotic enteritis (Endotoxemia) in piglets
  • Most common type in the US
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16
Q

What are Type C infections?

A
  • Alpha Toxin: hemolytic
  • Beta Toxin: Induces inflammation and necrosis in the intestines
  • Most common in newborn (<1 week old)
  • More common in piglets than other animals
  • Acute disease
  • High mortality
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17
Q

What are the clinical signs of Type C infections?

A
  • Depression
  • Hemorrhagic diarrhea
  • Death
  • Lesions: Hemorrhagic inflammation of the jejunum and ileum
    • Necrosis (with gas) of the mucosa and the submucosa
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18
Q

What is the Pathogenesis of Type C infections?

A
  • Generally seen in animals healthy and vigorous
  • Increased feed intake
  • Gut stasis
  • Overgrowth of bacteria and production of toxins
  • Toxin may or may not get absorbed
  • Acute illness and death
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19
Q

What diseases are caused by Type D infections of C. perfringens?

A
  • Sheep - Enterotoxemia (Overeating disease or Pulpy Kidney disease)
  • Cattle, Goats - Necrotic enteritis (Enterotoxemia)
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20
Q

What diseases are caused by Type E infections of C. perfringens?

A
  • Rabbits - Iotaenterotoxemia. Rarely in calves and lambs
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21
Q

What is Epsilon Toxin?

A
  • Third most potent clostridial toxin (Botulinum, Tetanospasmin)
  • Requires activation by trypson or Chymotrypsin
  • Enhances intestinal permeability
  • Rapid absorption of toxin
  • Affects of CNS and other organs
  • Responsible for perivascular edema, foci of necrosis and hemorrhages in the meninges
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22
Q

What diseases are caused by Type F infections of C. perfringens?

A
  • Humans - Foodborne gastroenteritis
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23
Q

What diseases are caused by Type G infections of C. perfringens?

A
  • Chickens - Necrotic enteritis
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24
Q

What is Yellow Lamb Disease?

A
  • Occurs in the spring in CA and OR
  • Nursing lambs
  • Alpha toxin from the intestine enters blood and causes hemolysis
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25
Q

What are the clinical signs of Yellow Lamb Disease?

A
  • Acute onset
  • Anemia
  • Dyspnea
  • Hemoglobinuria
  • icterus
  • Lesion: Generalized icterus, red urine in the bladder, enlarged spleen
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26
Q

What is Abomasal Bloat and Ulcers?

A
  • Neonatal calves, lambs, and goat kids
  • Copper and/or selenium deficiencies may be predisposing factos
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27
Q

What are the clinical signs of Abomasal Bloat and Ulcers?

A
  • Acute onset
  • Anorectic
  • Abdominal bloat
  • discomfort
  • Lesions: Gas, hemorrhage, ulceration
28
Q

How are Abomasal Bloat and Ulcers treated?

A
  • Oral Antibiotics: Tetracyclines, monensin
  • 0.1% formalin in milk replacers
  • Type A toxoid vaccine
29
Q

What is Sarcina ventriculi?

A
  • Anaerobic, Gram positive cocci
  • Ferments carbohydrtes and exhibits vigorous gas production
  • Can survive in acidic pH of abomasum
  • Possible role in Abomasal Bloat?
30
Q

What is Hemorrhagc Bowel Syndrome?

A
  • Relatively new disorder affecting primarily dairy cows
  • Intraluminal hemorrhage or submucosal hematoma in the jejunum
31
Q

What is the Etiology of Hemorrhagic Bowel Syndrome?

A
  • Clostridium perfringens, Type A
  • Aspergillus fumigatus
32
Q

What are the clinical signs of Hemorrhagic Bowel Syndrome?

A
  • Abdominal pain
  • Inappetance
  • Weakness
  • Drop in milk production
  • Scat feces
  • Abdominal distension
  • Death
33
Q
A
34
Q

What is the Etiology of Gangrenous Dermatitis?

A
  • C. perfringens Type A
  • C. septicum with or without S. aureus
35
Q

What are the clinical signs of Gangrenous Dermatitis?

A
  • Depression
  • Incoordination
  • Weakness
  • Inappetence
  • Ataxia
  • Lesions: Skin-edematous with or without gas, and necrotic
36
Q

What is Overeating Disease or Pulpy Kidney Disease

A
  • Occurs in Sheep and goats fed high grain diets
  • Rarely in cattle
  • Grain diets leads to overgrowth of C. perfringens
  • Epsilon Toxin is the major virulence factor
37
Q

What are the Clinical Signs of Overeating/Pulpy Kidney Disease?

A
  • Sudden death
  • Neurological signs often precede death
  • Dullness
  • Blindness
  • Ataxia
  • Convulsions
38
Q

What lesions are seen in Overeating/Pulpy Kidney Disease?

A
  • Hemorrhages and foci of necrosis on the meninges
  • Hemorrhages present on serosal surfces of rumen, abomasum, duodenum, and in the diaphragm and abdominal muscles
  • Kidneys: Hyperemia and degenerative changes
  • Soft and friable (pulpy) because of rapid autolysis
39
Q

What are Type F infections?

A
  • Thrid most prevalent bacterial foodborne illness (~600,000 cases)
  • Virulence factor: C. perfringens enterotoxin
  • Toxin is produced during sporulation and released by lysis of vegetative cells
  • Role of this toxinin animals is not known
40
Q

What is the pathogenesis of Foodborne Enteritis?

A
  1. C. perfringens grows in the food
  2. Sporulates in the stomach
  3. Produces enterotoxin in the SI
  4. Signs 8-12 h after ingestion of food
    • Diarrhea, abdominal cramps
    • self-limiting infection
41
Q

What are some Foodborne Pathogens?

A
  • Staphylococcus aureus
  • Escherichia coli O157:H7
  • Salmonella enteric
  • Chronobacter sakazaki
  • Yersinia enterocolitia
  • Clostridium botulinum
  • Clostridium perfringens
42
Q

What are Type G C. perfringens infections?

A
  • Chickens and turkeys
  • Most common clostridial disease in poultry
  • Major virulence factor:
    • Necrotic enteritis beta-like toxin (NetB)
  • About 38% amino acid identity with beta toxin
43
Q

What is Necrotic Enteritis?

A
  • Chickens and turkeys
  • 2 forms: Acute and subacute
    • Acute form: Death in a few hours
      • Depression, anorexia, ruffled feather, diarrhea
    • Subacute Form: Diarrhea and poor growth rate
44
Q

What lesions are seen with Nerotic Enteritis?

A
  • Confined to the jejunum and ileum
    • Coagulative necrosis. Yellow to green pseudomembrane
    • Contents are dark brown or yellow-green
    • In chronic form: thickened intestinal wall
45
Q

How is Necrotic Enteritis Diagnosed?

A
  • Clinical signs
  • Demonstration of toxin in the contents: toxin neutralizaiton in mice; ELISA
  • Isolation of C. perfringens and PCR confirmation of netB gene
46
Q

How is Necrotic Enteritis Treated?

A
  • Antibiotics in feed or water
    • Lincomycin, bacitracin, oxyttracycline
  • Treat the anorexia, ruffled feathers, diarrhea
  • No vaccine available
47
Q

What Vaccines are available for C. perfringens?

A
  • Bacterins and/or toxoids
  • Mostly Toxoids: Monovalent or multivalent vaccines
  • Sows are vaccinatd during mid-gestation with type C toxoid
  • Sheep in feedlos: Type D toxoid
48
Q

What is Quail Disease?

A
  • Ulcerative entritis of Wild and Domestic Birds
  • Caused by Clostridium colinum
  • Secondary to coccidiosis or infectious bursal disease
49
Q

What is the Mode of infection of Quail Disease?

A
  • Oral
  • Infection ofthe GI tract
  • Through the blood to the liver to cause diffuse necrosis
  • Virulence factor unknown
50
Q

How is Quail Disease treated?

A
  • Tetracyclines in water
51
Q

What is Clostridium piliforme?

A
  • Causes “Tyzzer’s disease” in rabbits, rodents and horses
  • Gram -
  • Long slender rods and heavily fimbriated
  • Not cultivable in culture media
  • Grows in tissue culture or chick embryos (obligate intracellular pathogen)
  • Habitat: intestinal tract of rodents
52
Q

What is the mode of infection of Tyzzer’s Disease?

A
  • Ingestion of spores
53
Q

What is the Pathogenesis of Tyzzer’s Disease?

A
  • Invades intestinal epithelial cells - Enteritis, colitis
  • Invades hepatic cells - hepatitis
54
Q

What lesions are present in Tyzzer’s Disease?

A
  • Necrosis
55
Q

How is Tyzzer’s Disease prevented?

A
  • Tetracycline
56
Q

What is Tyzzer’s Disease in Horses?

A
  • Mainly in foals between 1 - 4 weeks
  • Mode of infection: ingestion of spores
  • Disease is profressive hepatitis
  • Clinical signs: lethargy, fever, seizures, death
  • Lesions: Heptomagaly with 1 - 5 mm necrotic foci Tetracycline
  • Diagnosis: Demonstration of the bacteria in the parenchymatic cells. Also PCR
  • Treatment: Penicillin, erythromycin, tetracycline
57
Q

What is C. spiroforme?

A
  • Spiral shaped, Gram + and spore forming
  • Virulence factor: Iota toxin
  • Causes Entertoxemia in weanling rabbits and laboratoy rodents
  • Clinica Signs: spontaneous diarrhea and death
  • Lesions: Cecum is dilated with watery contents. Necrosis of the lining
58
Q

What is Clostridium difficile?

A
  • First recognized as a human pathogen in 1977
  • Causes Pseudomembranous colitis
  • Part of the normal flora
  • Disease results from overgrowth of the organism and production of toxins
  • Major nosocomial pathogen
59
Q

What Antibiotic treat C. difficile?

A
  • Clindamycin, erythromycin, Ampicillin, Amoxicillin, Cephalosporins, and Fluoroquinolones
  • 25% of all Antibiotic-associateed diarrhea
    • Can be induced in lab animals - feeding antibiotics to guinea pigs and hamsters
  • Hypervirulent strains: Rapid spread and higher mortality
60
Q

What is Community-Associated CDI?

A
  • No history of antibiotic use
  • Food born? Zoonotic?
  • Isolated from raw and ready-to-eat meat from grocery stores
  • Foodborne illness not documented yet.
61
Q

What are the Virulence Factors of C. difficile?

A
  • Toxin A (TcdA): Enterotoxin
    • Causes fluid accumulation
  • Toxin B (TcdB): Cytotoxin
    • Does not cause fluid accmulation
  • Both act synergistically
  • Not all strains produce toxins
62
Q

What is Pseudomembranous Colitis?

A
  • Severe hemorrhgic colitis or ileitis
  • Watery and bloody diarrhea
  • Ulceration of the colonic mucosa
  • Formation of pseudomembrane
  • Diagnosis: Demonstration of toxins in the feces
63
Q

How do C. difficile infections (CDI) affect animals?

A
  • Most common in horses and swine
  • Rarely in cattle, dogs, and cats
  • Healthy animals carry the organism (5 - 40% fecal prevalence)
  • Mode of infection: Endogenou or exogenous
  • Organism has been isolated from raw meat intended for pet consumption
64
Q

How does CDI affect horses?

A
  • Not age dependent. More common in foals than adults
  • Adults: Hospital associated; antibiotic associated
  • Foals: Hemorrhagic necrotizing entercolitis. 1st week of birth
  • Clinical signs: Profuse diarrhea, colic, weak, and dehydration
  • Death usually within 24h
  • Treatment: Metronidazole or vancomycin
65
Q

How does CDI affect pigs?

A
  • Age dependent. Seen in piglets of 1-7 days of age
  • Infection of colon (colitis) and cecum (Cecitis); Typhlocolitis
  • Profuce diarrhea. Some exhibit dyspnea, abdominal distension and scrotal edema
  • Lesion: Necrotic lesions in the lamina propria of the colon and edema ofthe colon
  • Diagnosis: TcdA and TcdB toxins in the blood
66
Q

How is C. difficile a zoonotic pathogen?

A
  • C. difficile spores are shed in the feces of healthy humansand animals
  • High rates of carriage in healthy swine farmers and handlres
  • Identical genetic types in swine and clinical human cases

Bacteriology and Mycology (35 decks)

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