LEC.3 Flashcards by Cardenas Xaira Andrea

Gram-positive and spore-forming bacilli

Clostridium

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most are strictly anaerobes
widely distributed in soil and water
some are normal flora in the GI tract of man and other animals

Clostridium

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describe morphology of clostridium

Are endospore forming large Gram-positive bacilli

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How do we acquire diseases from this group of organisms?

Through the inoculation of the bacilli spores, ibig sabihin nagkakaroon tayo ng sakit kapag nagmultiply yung mga spores. Or pwede ring ingestion.

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C. perfringens aka

C. welchii
Bacillus aerogenes capsulatus
Gas gangrene bacillus

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Do not produce spores in ordinary media

C.perfringens

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has spores located at the terminal end of the cell

C.tetani

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C. tetani has spores located at the terminal end of the cell, giving it a characteristic

tack-head, drumstick, lollipop, and tennis racket appearance

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C.tetani aka

tack-head bacillus

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all clostridium are motile except

C.perfringens

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type of media used for isolation of clostridium spp.

nonselective,selective, and liquid media

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supplemented anaerobic Blood Agar

Nonselective

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C.perfringens hemolysis in nonselective media

double zone of hemolysis

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double zone of hemolysis

beta hemolysis surrounded by alpha hemolysis

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Egg yolk agar

nonselective,differential

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nonselective,differential media allows differentiation based on

Lecithinase(white precipitate)
Lipase(sheen around surface of colonies)
Protease production(clearing)

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C.botulinum aka

canned good bacillus

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agent of canned good-bacillus-botulism

C.botulinum

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example of antigenic toxin produce by botulinum

botulism toxin

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different type of toxins of C.botulinum

Type A
Type B
Type E
Type F
Type G

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most common and potent type of toxin in c. botulinum

Type A

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Toxins of botulinum block release of

acetylcholine

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C.botulinum causes

flaccid paralysis

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It works at the neuromuscular junction and in the
autonomic nervous system to prevent the release of
the neurotransmitter acetylcholine.

C.botulinum

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part of C.botulinum cleaves proteins that mediate the fusion of synaptic vesicles with the cell membrane and the subsequent release of acetylcholine.

toxic part

Symptoms appear [C.botulinum]

18-24 hours after toxin ingestion

[C.botulinum] visual disturbances

inability to swallow, speech difficulties, bulbar paralysis(ptosis

usually caused by respiratory paralysis(diaphragm), cardiac arrest

Death

In infants: poor feeding, weakness and the characteristic flaccid paralysis is found caused by [C.botulinum]

hypotonia

C.botulinum may also cause

Sudden Infant Death Syndrome

the organism germinates in the wound abscess

Wound botulism

TRIAD OF BOTULISM

Symmetric descending flaccid paralysis(with prominent bulbar involvement) Absence of fever Intact sensorium

[C.botulinum] Demonstration of toxin by

passive hemagglutination or radioimmunoassay

[C.botulinum] adults specimen of choice

Serum and left-over food

[C.botulinum] Infants specimen of choice

stool

Anaerobic, gram-positive, spore-forming rod

C.tetani C.perfringens C.difficile

Disease is tetanus with characteristic [C.tetani]

backward arching of the back muscles

C.tetani toxin is produced by

vegetative cells that reaches the CNS

C.tetani virulence factors

spores glycine gamma-aminobutyric acid

[C.tetani] terminally located, therefore germinate under anaerobic conditions

Spores

[C.tetani] inhibits muscle contraction

Glycine Gamma-aminobutyric acid

Lockjaw

trismus

Risus sardonicus

patient has a distorted grin

Opisthotonus

Arching of the back

two enterotoxins proiduced [C.tetani]

A hemolysin Tetanospasmin

can travel to the CNS humorally through blood and lymph, or neurally through tissue spaces of the peripheral nerves

Tetanospasmin

Accounts for the lockjaw and opisthotonus

Tetanospasmin

C. perfringens invasive infection

myonecrosis and gas gangrene

C.perfringens produces an enterotoxin which is a common cause of

food poisoning

C.perfringens appearance on BAP

double zone of hemolysis around colonies

Nonmotile but with rapidly spreading growth on culture media

C.perfringens

Produces milky or stormy fermentation due to the excessive gas production

Milk Media

C.perfringens Virulence Factors

Lecithinase Alpha Toxin Delta/Theta Toxin

When grown in EYA, there is a white precipitate

Lecithinase

Responsible for incomplete hemolysis in C.perfringens

Alpha toxin

Responsible for complete hemolysis in C.perfringens

Delta/Theta toxin

Localized edema and erythema with gas formation in soft tissue, and generally not painful

Cellulitis

Accumulation of pus in muscle planes without muscle necrosis or systemic symptoms

Suppurative Myositis

Infection spreads 1-3 days to produce crepitation (cracking or rattling sound) in the subcutaneous tissue and muscle

Myonecrosis

discharge rapidly progressing necrosis and fever

foul-smelling

Myonecrosis leads to

Toxemia,shock, and death

Acute necrotizing destruction of the jejunum with abdominal pain, vomiting, blood diarrhea and peritonitis

Necrotizing Enteritis

C.perfringens specimen

material from wounds, pus, and tissue

Special Stain C.perfringens

gram positive rod with sporeS

C.perfringens Reverse CAMP test

positive

final phase by which viral cells infect cells

cytopathic effect

potent enterotoxin, cytotoxic activity, binds to the brush borders of the GUT at the receptor site

Toxin A

potent cytotoxin

Toxin B

MOT C.difficile

fecal-oral route

Non-bloody diarrhea associated with pseudomembranes Yellow-White Plaques on the colonic mucosa.

PSEUDOMEMBRANOUS COLITIS