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65 Cards in this Set
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Bacillus anthracis 1
General characteristics |
-gram +
-spore-forming -bacillus -aerobic! -the only aerobic microorganism causing disease from the Bacillus group |
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Bacillus anthracis 2
Epidemiology |
-disease of sheep, cattle, horses, & other animals.
-animals can be infected by soil or ingestion of contaminated vegetation. -humans' source of infection: soil, infected animals,inhalation of contaminatd dust, ingestion of contaminated food and contamination w/ infected animal hair, hides, wool -high percentage of death |
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Bacillus anthracis 3
Pathogenesis |
-disease that mainly affects animals, though rarely humans may be affected by entering of spores through injured skin, mucous membranes, or inhalation.
-in animals the entry is mouth to GI -spores germinate in tissue and cause gelatinous edema and congestion. |
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Bacillus anthracis 7
Treatment |
penicillin
tetracycline erythromycin quinolones |
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Bacillus anthracis 4
Effect in humans |
can develop:
-cutaneous anthrax - malignant pustule -pulmonary anthrax -intestinal anthrax |
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Bacillus anthracis 5
3 proteins that make up toxin (exotoxin) |
PA (proteolytic activation)
EF (edema factors) LF (lethal factors) PA binds to cell membrane, forms channel, EF and LF enter cell EF (adenlyly cycle) + PA --> Edema toxin LF + PA --> Lethal toxin (major virulence factor which causes death) *PA is necessary. w/out it LT nor ET form |
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Bacillus anthracis 6
virulence factors |
-spore-forming
-the only bacterium w/ capsule composed of protein (poly-D-glutamic acid) --> prevents phagocytosis -exotoxin |
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Bacillus cereus 1
General characteristics |
-anaerobic
-spore-forming -bacilli -motile |
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Bacillus cereus 2
causes 2 types of food intoxications (food poisoning) by secretion of 2 types of enterotoxins |
1. Emetic form: nausea, vomiting, abdominal cramps. incubation period 1-6 hrs. resembles staph. aureus in symptoms and incubation prd. (this is through heat stable enterotoxin)
2. abdominal cramps, diarrhea, incubation period 8-16 hrs. (occurs through heat labile enterotoxin) |
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Clostridia (Anaerobes) 1
General characteritics |
-gram +
-anaerobic -spore-forming -motile -bacilli |
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Clostridia (Anaerobes) 2
Growth conditions |
-unable to grow under oxygen conditions (anaerobic)
-unable to break H2O2 -ferment variety of sugars, proteins, produce gas -produce many enzymes like proteinases, collagenases, hyaluronidase, DNase which are potent exotoxins in vivo. |
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Clostridium perfringens 1
(gas gangrene) Epidemiology |
-produces clostridial myonecrosis when introduced into damaged tissue
-42-60% are caused by mixed infections -formerly known as Clostridium welchii -can also be a food-associated infection |
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Clostridium perfringens 2
(gas gangrene) Pathogenesis |
-spores enter traumatized tissue --> germinate --> ferment carbohydrates --> produce gas which pushes on nerve and causes pain
necrosis thus no blood, no oxygen, no materials to generate interference w/ blood supply + secretion of necrotizing toxin hyaluronidase favors spread of infection leading to severe toxemia & death |
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Clostridium perfringens 3
(gas gangrene) Clinical findings |
1-3 days incubation
-foul-smelling discharge -necrosis, fever, toxemia, shock, death -infections are invasive (due to the type of toxins) |
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Clostridium perfringens 5
(gas gangrene) Treatment |
(until specific therapy, early amputation was the only treatment)
current treatment involves: -surgical debridement -antibacterial drugs - penicillin -hyperbaric oxygen - "detoxification" -polyvalent antitoxin (antibody that neutralizes toxin) -don't do amputation b/c it can spread through body |
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Clostridium perfringens 4
(gas gangrene) Toxins |
-large variety of toxins
-most important are: *alpha toxin (Lecithinase) --> splits lecithin (in membranes) --> phosphorylcholine + diglyceride and *collagenase --> proteolytic --> collagen of muscles other toxins include: hyaluronidase and DNase |
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Clostridium perfringens 6
(gas gangrene) Diagnosis |
-smear from injury; gram stain
-culture on blood agar, anaerobic conditions, thioglycate -Lecithinase activity on Lecithin medium |
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Clostridium difficile 1
(Pseudomembranous Enterocolitis) Etiology |
-antibiotic-associated colitis after prolonged oral administration of Clindamycin and others.
-antibiotics kill normal flora and Clost. difficile can take over -Clost. diffiicile is drug resistant & proliferates in colon and produces necrotizing toxin |
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Clostridium difficile 2
(Pseudomembranous Enterocolitis) Treatment |
has high mortality rate unless the selecting drug is stopped and oral vancomycin is given
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Clostridium tetani
Epidemiology |
-worldwide in distribution in soil, feces of horse and other animals
-tetanus is not caused by rust. rusty objects simply have higher chances of being mixed w/ dirt and thus having spores. |
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Clostridium tetani
Basic characteristics |
gram +
spore forming bacilli look like tennis rackets |
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Clostridium tetani
Pathogenesis |
-not invasive (only toxin spreads, not the bacteria), the infection remains localized in the wound, burn, injury, surgical suture into which spore germinates.
-toxin can either travel through blood (toxemia) or nervous system. -need anaerobic conditions to germinate. |
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Clostridium tetani
Clinical findings |
-incubation 4-5 days till several weeks
-disease is characterized by convulsive tonic contraction of voluntary muscles -muscle spasms in injury area -any stimulus causes spasm -lockjaw (trismus) -spastic paralysis (opposing flexor and extensor muscles contract simulataneously) -the patient is conscious -death results from interference w/ respiration (contraction of diaphragm) -spinal cord can break -mortality w/out prevention --> 50% -few physicians have seen tetanus |
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Clostridium tetani
toxin |
-neurotoxin called tetanospasmin
-released only by lysis due to its large size (high MW) -VERY potent. 1 mg --> kills 2X10^7 mice (lethal dose = 2X10^7 mice) -acts on CNS by blocking release of inhibitory neurotransmitters GABA and glycine from presynaptic neuron. -thus postsynaptic neuron results in constant excitation -release of Ach is not inhibited from postsynaptic neuron --> results in generalized msucular spasm -toxin may reach the CNS via: retrograde axonal transport or via bloodstream -must neutralize toxin before it becomes fixed to gangliosides in spinal cord & brain stem *(there are several types (strains) which produce the same neurotoxin) |
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Clostridium tetani
Diagnosis |
-diagnosis is mostly clinical
-culture of tissues, Cl. tetani isolation, production of toxin and neutralization by specific antitoxin |
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Clostridium tetani
Prevention |
-active immunization w/ toxoid
-proper care of wounds contaminated w/ soil -prophylactic use of antitoxin (toxin which was injected to other animals (horse) and we took the antibodies) -administration of penicillin (prevent proliferation of toxin) |
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Clostridium tetani
Control |
toxoid - which is the toxin detoxified
-in 1st yr of life give 3 injections. -1x one yr later -1x booster upon entering school -boosters given every 7-10 yrs to maintain serum level (> 0.01 unti antitoxin/ml) -tetanus toxoid is given w/ pertussis & diptheria --> triple vaccine -if someone is injured, give shot every 2 yrs. |
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Clostridium tetani
the disease is toxemia and develops if: |
a. necrotic tissue
b. calcium salts c. secondary infection associated w/ pyogenic bacteria |
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Clostridium tetani
virulence factors |
-tetanospasmin - neurotoxin blocks release of neurotransmitters for inhibitory synapses
-tetanolysin - oxygen-labile hemolysin (unknown significance) -spore formation - allows organism to survive in unfavorable environments |
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Clostridium botulinum 2
Epidemiology |
-found in soil (thus can also contaminate fruit, vegetables, etc) and animal feces
-canned food prepared at home should be sufficiently heated -toxoids (active immunization, create memory cells) are used for cattle in south africa b/c they are herbivores and this food can have soil w/spores. -botulin bacteria produces little gas so cannot tell if a can is infected by seeing if it is swollen -spores cannot go into vegetative state in acidic food (ph<6) |
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Clostridium botulinum 4
Toxin |
-produced during growing & eliberated during growth & lysis
-8 antigenic varieties of toxin (A-H) currently known. A, B, & E are most common ones associated w/ human disease. -neurotoxin -MW 150,000 (large like tetanus) -most potent biological toxin known -used in biological warfare -Amount of toxin on a pin can cause a death to a person. -low lethal dose for humans (1-2 ug) -spores are very resistant -spores destroyed by autoclaving -neurotoxin destroyed by boiling (20 min at 100 deg. cel.) b/c it's a protein -toxin acts by blocking release of Ach at synapses & neuromuscular junctions (toxin prevents fusion of vesicle w/membrane) --> flaccid paralysis |
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Clostridium botulinum 3
Pathogenesis |
-the illness is intoxication, not infection
-results from ingestion of food containing toxin or Clost. botulinum or spores. -smoked, spiced, vacuum packed, canned alkaline foods eaten w/out cooking, fish, vegetables prepared in home conditions. |
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Clostridium botulinum 5
Clinical |
-symptoms begin 18-96 hrs after ingestion
-loss of coordination of eye muscle, double vision, inability to swallow, bulbar paralysis -death occurs from respiratory paralysis & cardiac arrest -patients remain fully conscious -high mortality rate 65% |
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Clostridium botulinum 6
Lab Diagnosis |
-has very little importance
-the food can be injected IV to mice or serum of patient |
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Clostridium botulinum 7
Treatment |
-antitoxins (passive immunization. used in emergencies when can't wait) of 3 types were prepared in animals
-toxoid is rarely used as treatment b/c can't wait that long. -ventilation to respiratory tract |
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Clostridium botulinum 1
General characteristics |
-gram +
-spore-forming -anaerobic -bacilli |
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Anaerobes (general)
Toxoid is... |
active immunization where we create memory cells
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Anaerobes (general)
Antitoxin is... |
-passive immunization
-used in emergency when don't have time to wait |
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Clostridium difficile 3
(Pseudomembranous Enterocolitis) virulence factors |
-Enterotoxin (toxin A) = produces chemotaxis, induces cytokine production w/ hypersecretion of fluid, produces hemorrhagic necrosis
-Cytotoxin (toxin B) = induces depolymerization of actin w/loss of cellular cytoskeleton. -Adhesin factor = mediates binding to human colonic cells -Hyaluronidase = produces hydrolytic activity -Spore formation = permits survival for months in hospital environment |
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Anaerobes (exotoxins)
exotoxin vs. endotoxin |
exotoxin - protein, sensitive to heat (heat labile b/c it's a protein), act in low conc., very specific mode of action, are named by their targets. exotoxin is produced by both gram + and -, can be secreted during growth and death.
endotoxin - LPS + proteins, heat resistant (heat stable), produced only by gram -, secreted only after death, mode of action is not exclusive, act at high conc. |
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Anaerobes (exotoxins)
some enzymes which are examples of exotoxins |
-coagulases
-phospholipases -DNAse -colagenases |
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Anaerobes (exotoxins)
some types of exotoxins name according to their target |
-neurotoxin
-enterotoxin -hemolysins -cytotoxins |
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Exotoxins
Toxin(s)of Clostridium botulinum & effect |
Botulinum toxin: flaccid paralysis (blocks release of Ach)
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Exotoxins
Toxin(s) of Clostridium tetani & effect |
Tetanospasmin = a. spastic paralysis of the skeletal muscle
b. blocks inhibitory neurotransmitter release --> continuous stimulation |
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Exotoxins
Toxin(s) of Clostridium perfringens (Clost. welchii)& effect |
1. entero-toxin = diarrhea & vomiting
2. other toxins = gangrene of tissues - toxemia --> death |
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Exotoxins
Toxin(s) of Clostridium difficile & effect |
Enterotoxin = after treatment w/antibiotics (clindamycin kills all flora, clost. difficile takes over). releases enterotoxin which is cytotoxic to GI cells
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Exotoxins
Toxin(s) of Corynebacterium diptheriae & effect |
Diptheria toxin = prevents protein synthesis by ribosomes - by inactivation of EF2. damage to internal organs (lung, heart, liver, kidneys, CNS)
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Exotoxins
Toxin(s) of Staphylococcus aureus & effect |
1. Entero-toxin = diarrhea, vomiting, nausea, cramps
2. Toxin-F1 = rash, diarrhea, shock, death |
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Exotoxins
Toxin(s) of Vibrio cholerae & effect |
cholerae enterotoxin = massive diarrhea, loss of water, cell nutrients, electrolytes, shock and death.
adenylyl cyclase increase --> cAMP increase --> GI electrolyte channels open |
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Exotoxins
Toxin(s) of E. coli & effect |
ST-enterotoxin
LT-enterotoxin diarrhea, loss of water and electrolytes. like cholera |
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Exotoxins
Toxin(s) of Pseudomonas aeruginosa & effect |
Exotoxin A = mode of action - like diptheria
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Exotoxins
Toxin(s) of Shigella dysenteriae & effect |
Neurotoxin = neurological syndrome
Enterotoxin = diarrhea, loss of water and electrolytes |
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Exotoxins
Toxin(s) of beta-hemolytic group A streptoccus (GAS) |
Erythrogenic toxin = rash on the body (by erythrogenic toxin)
Toxin(S)= gangrene to tissues, high temp, toxemia, destruction of fascia |
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Exotoxins
Disease caused by Clostridium botulinum |
botulism - food poisoning
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Exotoxins
Disease caused by Clostridium tetani |
tetanus
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Exotoxins
Disease caused by Clostridium perfringens (Clost. welchii) |
1. food poisoning
2. gas gangrene |
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Exotoxins
Disease caused by Clostridium difficile |
Antimicrobial enterocolitis
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Exotoxins
Disease caused by Cornyebacterium dyptheriae |
diptheria
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Exotoxins
Disease caused by Staphylococcus auerus |
1. food poisioning
2. TSS |
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Exotoxins
Disease caused by Vibrio cholerae |
cholera
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Exotoxins
Disease caused by E. coli |
acute gastroenteritis
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Exotoxins
Disease caused by Pseudomonas aeruginosa |
opportunistic infections
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Exotoxins
Disease caused by beta-hemolytic group A streptococcus (GAS) |
scarlet fever
necrotizing fasciitis |
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Bacteroidacae 1
General characteristics |
-grow on complex media
-anaerobic conditions -lack the LPS structure that other gram (-) possess (according to MRS only gram - bacteria that doesn't have lipid A) -normal inhabitant of upper respiratory, intestinal, & female genital tracts -normal stool contain 10^11/gr |
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Bacteroidacae 2
Infection |
-when Bacteroides cause infection (lung, brain, peritoneum, pelvis) associated w/ other anaerobic bacteria like peptostreptococcus and others.
-suppuration (pus) is followed by foul smell -Bacteroides fragilis = resisitant to penicillins; susceptible to clindamycin, metronidazole, chloramphenicol |
