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42 Cards in this Set
- Front
- Back
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Two main anaerobic families:
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1. Bacteriodaceae (most important): all gram-neg obligate anaerobes.
2. Bacillaceae are gram positive and spore forming. Anaerobic except for b. anthracis. |
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Bacteroides lack the _____ structure that other gram negatives possess.
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LPS
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Bacteroides are normal inhabitants of _____, _____, and _____.
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upper respiratory tract
intestine femal genital tract |
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Is b. anthracis spore-forming?
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Yes! Important, as they can survive in soil for many years.
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Bacillus anthracis
gram neg or gram pos? |
Gram positive
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B. anthracis is the only _____ disease causing microorganism from the family Bacillaceae.
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Aerobic
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Anthrax is a disease that mainly affects __(a)__, by entry through __(b)___. Humans are affected rarely by entering of spores through __(c)___.
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a. animals such as sheep, cattle, and horses
b. mouth to GI c. injured skin, mucous membranes, or inhalation |
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B. anthracis spores germinate in tissue, and cause _____.
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Gelatinous edema and congestion.
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Three types of anthrax can develop in humans:
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1. cutaneous
2. pulmonary 3. intestinal |
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Source of anthrax infection for humans?
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soil, infected animals, and contamination with their hair
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B. anthracis exotoxin is made up of three proteins that combine to form:
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protective antigen + edema factor = edema toxin
protective antigen + lethal factor = lethal toxin most lethal when we have all three; protective antigen is needed for damage, as it bores holes in membranes so as to share this lovely poison. |
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B. cereus can cause:
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Food poisoning from toxins leading to vomiting and diarrhea.
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_____ and _____ are the two main pathogenic species of bacillaceae.
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bacillus
clostridium |
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Is Clostridia anaerobic or aerobic?
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Anaerobic.
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Is Clostridia spore-forming?
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Yes
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Is Clostridia motile?
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Yes
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Three main strains of Clostridia.
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1. C. botulinum
2. C. perfringens 3. C. tetani |
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The alpha-toxin of C. perfringens causes:
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increases vascular permeability; hemolysin; produces necrotizing activity.
can ultimately cause gas gangrene if introduced into damaged tissue |
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Four toxins of C. perfringens (or welchii):
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1. alpha toxin: lecithinase
2. collagenase 3. hyaluronidase 4. deoxyribonuclease |
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Treatment for gas-gangrene:
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amputation
antibacterial drugs - penicillin hyperbaric oxygen polyvalent antitoxin |
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C. perfringens pathogenesis:
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spores enter tissue by contamination of traumatized tissue --> they then germinate in the tissue --> ferment carbohydrates --> and produce gas
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Is C. tetani spore-forming?
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yes!
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Is C. tetani gram-neg or gram-pos?
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Gram positive
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Main C. tetani reservoir?
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soil
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There are several different types of c. tetani, which all produce the same neurotoxin:
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tetanospasmin
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C. tetani pathogenesis:
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Not invasive. The infection remains localized in the wound, where the spore germinates. The toxin spreads via blood and nerves.
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Tetanus is characterized by:
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Convulsive tonic contraction of voluntary muscles. Death results because of interference with respiration (paralysis of diaphragm).
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How does tetanospasmin act in the central nervous system?
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1. Inhibits release of acetylcholine, which interferes with neuromuscular transmisssion.
2. Inhibits postsynaptic spinal neurons by blocking release of inhibitory mediator. |
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Tetanus prevention
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Active immunization with toxoid; proper care of wounds contaminated with soil; prophylactic use of antitoxin; administration of penicillin.
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What is a toxoid?
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The toxin detoxified.
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Clostridium Botulinium is found in:
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Soil and animal feces.
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How many antigenic varieties of the Cl. botulinium toxin are there? Which are the most common?
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There are eight antigenic varieties (A-H), with A, B, and E being the most common.
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Pathogenesis of Cl. botulinium:
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Intoxication results from ingestion of food containing the toxin or spores. This includes smoked, vacuum-packed, canned, etc.
Toxin acts by blocking release of acetylcholine at synapses and neuromuscular junctions. |
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Results of Cl. botulinium intoxication.
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Symptoms begin 18-96 hours after ingestion. There will be loss of coordination of eye muscle with double vision, inability to swallow, speech difficulty, and bulbar paralysis. Patient remains fully conscious with flaccid paralysis.
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Death from Cl botulinium is the result of:
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Respiratory paralysis and cardiac arrest.
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Treatment for botulism
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Antitoxins A, B, and E, which were prepared in animals.
Ventilation to the respiratory tract. |
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Exotoxins vs. endotoxins re: heat stability and general makeup.
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Exotoxins are proteins that are heat sensitive.
Endotoxins are lipopolysaccharide and proteins, and are heat stable |
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Exotoxins vs. endotoxins re: mode of action (specificity) and which bacteria contain them.
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Exotoxins have very exclusive modes of action and act at very low concentrations.
Endotoxins are not exclusive and need very high concentrations. Exotoxins are produced in any bacteria, while endotoxins are only in gram-negative. |
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Exotoxin vs. endotoxins re: excretion.
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Exotoxins are excreted during growth or after death.
Endotoxins are only liberated after death. |
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Cl. Botulinium
-toxin -disease -effect of toxin |
Toxin: botulinium toxin
Disease: botulism - food poisoning. Effect of toxin: flaccid paralysis, blocks release of ACh. |
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Cl. Tetani
-toxin -disease -effect of toxin |
Toxin: tetanospasmin
Disease: tetanus Effect of toxin: spastic paralysis of the skeletal muscle, blocks the transmitter release, so there is continuous stimulation |
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Cl. perfringens
-toxin -disease -effect of toxin |
Toxin: entero-toxin, among others
Disease: food poisoning, gas gangrene Effect of toxin: diarrhea and vomiting; gangrene of tissues - leading to toxemia and death :( |
