• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/79

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

79 Cards in this Set

  • Front
  • Back
Name the 7 general of Gram-positive bacilli and categorize them: endospore forming, non-endospore forming, branching
ENDOSPORE: 1 Bacillus, 2 Clostridium. NO ENDOSPORE: 3 Listeria, 4 Corynebacterium, 5 Gardnerella. BRANCHING: 6 Actinomyces, 7 Nocardia
1. Understand key details of the 7 different Gram-positive bacilli: basics, virulence mechanisms and infections (a summary appears at the end of these notes on pp. 11-12)
xxx
2. Understand the process of sporulation, the structure and properties of endospores, and the organisms that form them.
xxx
3. Be able to pick up on key “trigger words” for each organism (play my bacilli trigger word game after the G-ve bacilli lectures. Answers will be posted on Canvas)
xxx (take notes in class)
4. Learn the primary bacterial toxins used by Gram-positive bacilli and their mechanisms of action (summary of bacterial toxins is in red font on p10)
xxx
5. Know key culture media used to identify Gram-positive bacilli (p8)
1 Loeffler coagulated serium medium for Corynebacteria diphtheria, 2 Potassium -tellurite medium that turns brown when C. diphtheria converts it to elemental tellurium
Name the endospore forming bacilli (6)
B. anthracis, B. cereus, C. tetani, C. perfringens, C. botulinum, C. difficile
Name the non-endospore forming bacilli (3)
L. monocytogenes, C. diphtheriae, G. vaginalis
Name the branching bacilli (2)
A. israelii, Nocardia
B. anthracis: full name, the basics (1)
Bacillus anthracis. Endospore-forming. Usually spores found in dry fields infect herbivores, which is why you can send it in the mail.
B. anthracis: virulence factors (4)
1 polyPEPTIDE capsule. ANTHRAX TOXINS: 1 PA, 2 LF, 3 EF.
PA: acronym, mechanism of virulence
protective antigen. Binds to cell and facilitates entry of LF and EF.
LF: acronym, mechanism of virulence
metalloprotease of MAP kinase; signals for cell death
EF: acronym, mechanism of virulence
Edema factor is a calmodulin-mediated adenylate cyclase. inc cAMP > membrane more permeable > cells lose water > pulmonary edema
B. anthracis: infections (3) by body system
SKIN: cutaneous anthrax > eschar. GI (rare): GI inflammation. INHALATION: inhalation > eaten by macrophages > carried lymph node > start eating the macrophage and then the lymph node and then produce exotoxins > hemorrhagic mediastinitis, pulmonary edema > bacteria enter bloodstream through thoracic duct > septicemia > death
B. cereus: full name, source
Bacillus cereus. Found in rice and vegetables. Endospore-forming.
B. cereus: infections (2)
1 emetic disease, 2 diarrheal disease
emetic disease of B. cereus, pathogenesis
From eating ENTEROTOXIN. Poorly refridgerated fried rice > bacteria eat protein in the rice > produce enterococcin > nausea, vomiting, diarrhea
diarrheal disease of B. cereus, pathogenesis
From eating BACTERIA. Contaminated meat > bacteria multiply in intestines > release enterotoxins > diarrhea (no vomiting).
Clostridium: the basics
anaerobic. Endospore-forming.
C. tetani: full name, morphology, source, general preferred environment
Clostridium tetani. Look like a tennis racket due to terminal endospores. From soil. Prefers low-oxygenated tissues.
C. tetani: characteristic infection
Incubation of several weeks. Produce tetanus toxin > acts on anterior horn cells > retrograde transport (dynien) > destroys synaptobrevin II > prevents inhibitory nt release > uninhibited nerve impulses > death from paralysis of throat and respiratory muscles
Name the inhibitory nt's that are blocked by tetanus. (2)
GABA, glycine
C. perfringens: full name, source, typical infections
Clostridium perfringens. From soil, feces. 1 wound infection, 2 gas gangrene
wound infection by C. perfringens: pathogenesis and course of disease
bacteria introduced into tissue by surgery or trauma > produce toxins, gas > gas gangrene > massive tissue destruction
food poisoning by C. perfringens, pathogenesis
eat contaminated meat > L secretory diarrhea > resolves within 24hr
C. botulinum: full name, source, main virulence factor.
Clostridium botulinum. Found in soil. Produces neurotoxin.
C. botulinum: typical infections (3)
1 food-born botulism, 2 infant botulism (most common form in USA), 3 wound botulism, (4) SoCal botulism aka Botox
food-born botulism by C. botulinum: pathogenesis
poorly canned green beans > incubates 1-2 days > bacteria produce botulism toxin which blocks ACh receptors > flaccid paralysis
infant botulism by C. botulinum: pathogenesis
eat honey > spores grow > floppy baby syndrome > respiratory arrest
wound botulism by C. botulinum: pathogenesis
bacteria infect wound > flaccid paralysis
C. difficile: full name, source, main risk factor, types of strains, virulence factors.
Clostridium difficile. Found in soil, feces. Overgrowth due to antibiotics. Can be toxigenic or non-toxigenic. Toxins A & B.
C. difficile: typical infections (
C. difficile associated disease (CDAD) 1 Environmental, or 2 endogenous
environmental C. difficile associated disease: pathogenesis
hospital worker touches a rectal thermometer > washes hands with alcohol that does not kill spores > transmits to next pt > mild diarrhea or pseudomembranous colitis
pseudomembranous cholitis, ssx
abd cramping, fever, diarrhea containing blood and pus
endogenous C. difficile associated disease: pathogenesis
oral antibiotics > changes enteric flora > overgrowth of bacteria
L. monocytogenes: full name, morphology, metabolism, preferred growing conditions, source (3)
Listeria monocytogenes. Non-endospore forming. Coccobacilli. Facultative anaerobes. Can grow in wide pH, salt, and temp range, and can grow inside cells. Found in GI tracts of animals, soil, food (deli items like cheese and meats)
gastroenteritis due to L. monocytogenes: pathogenesis
enters intestines > adheres to epithelial cells via E-cadherin > taken up by intestinal cells > uses listeriolysin to poke holes in phagosomes > moves to adjacent cells > infection is usually asymptomatic
L. monocytogenes: typical infections (3)
1 mild gastroenteritis in summertime, 2 septicemia of fetuses, 3 meningitis in immunocompromised renal transplant patients
C. diphtheriae: full name, morphology, metabolism, source, mode of transmission
Corynebacterium diphtheriae. Non-endospore forming. Club-shaped. Aerobes. Found in plants, animals, human skin & mucous membranes. Transmitted by droplets or skin contact.
C. diphtheriae: virulence factors, typical infections (2)
diptheria toxin, aka A-B toxin. Inhibits protein synthesis in the oropharyngeal mucosa, heart, nerve cells. Typical infections: 1 respiratory diphteria, 2 cutaneous diphtheria
Respiratory infection by C. diphtheriae: pathogenesis, clinical outcomes leading to death (2)
incubate in oropharynx 2 days > exudative pharyngitis > dirty white pseudomembrane (can obstruct airway leading to suffocation) > toxins (not bacteria) invade into body > "bull necked" appearance, myocarditis, cardiac failure
Cutaneous infection by C. diphtheriae: pathogenesis
skin contact with infected person > breaks through skin > papule > chronic nonhealing ulcer > toxins invade > myocarditis, cardiac dysfunction, laryngeal nerve palsy
G. vaginalis: full name, metabolism, source, morphology
Gardenerella vaginalis. Non-endospore forming. Facultative anaerobe. Gram-variable cells that form "clue cells"
clue cell, def
vaginal epithelial cell covered in bacteria
Bacterial vaginosis due to G. vaginalis: pathogenesis
Usually inhibited by acidic Lactobacillus > something kills it > fishy smelling vagina that gets worse with intercourse (semen is basic)
A. israelii: full name, metabolism, source
Actinomyces israelii. Branching bacillus. Anaerobic. Found in mucous membranes (gingiva, vagina).
endogenous infection of A. israelii: pathogenesis
trauma (tooth extraction, IUD) compromises tissue blood flow > bacteria grow with no respect for anatomic boundaries > lump, abscess (possibly brain), sinus formation with hard yellowish microcolonies > may be misdiagnosed a sa neoplasm
Nocardia: metabolism, morphology, source
Branching bacilli. Aerobic. Filaments that break into rods. Found in soil.
Nocardia: typical infections
1 pulmonary nocardiosis, 2 cutaneous or subcutaneous infection, 3 brain abscess
pulmonary nocardiosis or brain abscess due to Nocardia: pathogenesis
inhalation of bacteria by immunocompromised individual > spreads to organs such as brain > can cause a brain abscess
cutaneous infection due to Nocardia: pathogenesis
traumatic implantation of bacteria > abscess
calcium dipicolinate: fxn, producing cell genera
calcium dipicolinatedehydrates nucleic acids. Produced by Bacillus, Clostridium.
Name the stain used to detect endospores (and the counter-stain used).
Schaefer-Fulton endospore stain w/ malachite green. Counter-stain: safranin.
Name the layers of an endospore, innermost to outermost, starting with DNA. (5)
1 core (DNA w/ calcium dipicolinate), 2 cytoplasmic membrane, 3 spore wall (peptidoglycan), 4 cortex (less cross-linked peptidoglycan), 5 keratin spore coat
Name the organism with a polyPEPTIDE capsule. How do the effects of this differ from those of a normal capsule? (2)
polypeptide capsule is 1 immunogenic, 2 antiphagocytic
CLINICAL APPLICATION: A pt presents with a widened mediastinum on X-ray. Which organism?
Indicative of hemorrhagic mediastinitis due to B. anthracis, a Gram-positive bacillus.
toxins produced by C perfringens? (2)
alpha toxins (aka phospholipase C, destroys membranes), theta toxins (destroys
Name the Gram-positive bacilli that cause food poisoning and the type of food.
B. cereus (fried rice if emetic, contaminated meat if diarrheal), C. perfringens (reheated meat dishes), C. botulinum (poorly canned beans, honey NOTE: only food poisoning that is neurotoxic)
Toxins produced by C. difficile, mechanisms (2)
Toxin A: intestinal fluid secretion, mucosal injury. Toxin B: depolymerizes actin.
Organisms covered by Tdap?
Corynebacterium diphtheriae, Clostridium tetani
CLINICAL APPLICATION: How can thrichomonas vaginalis and Gardnerella vaginalis be distinguished (ssx are similar)?
wet mount - if clue cells are present, it's G. vaginalis
From eating ENTEROTOXIN. Poorly refridgerated fried rice > bacteria eat protein in the rice > produce enterococcin > nausea, vomiting, diarrhea
emetic disease of B. cereus, pathogenesis
From eating BACTERIA. Contaminated meat > bacteria multiply in intestines > release enterotoxins > diarrhea (no vomiting).
diarrheal disease of B. cereus, pathogenesis
bacteria introduced into tissue by surgery or trauma > produce toxins, gas > gas gangrene > massive tissue destruction
wound infection by C. perfringens: pathogenesis and course of disease
eat contaminated meat > L secretory diarrhea > resolves within 24hr
food poisoning by C. perfringens, pathogenesis
poorly canned green beans > incubates 1-2 days > bacteria produce botulism toxin which blocks ACh receptors > flaccid paralysis
food-born botulism by C. botulinum: pathogenesis
eat honey > spores grow > floppy baby syndrome > respiratory arrest
infant botulism by C. botulinum: pathogenesis
bacteria infect wound > flaccid paralysis
wound botulism by C. botulinum: pathogenesis
hospital worker touches a rectal thermometer > washes hands with alcohol that does not kill spores > transmits to next pt > mild diarrhea or pseudomembranous colitis
environmental C. difficile associated disease: pathogenesis
abd cramping, fever, diarrhea containing blood and pus
pseudomembranous cholitis, ssx
oral antibiotics > changes enteric flora > overgrowth of bacteria
endogenous C. difficile associated disease: pathogenesis
enters intestines > adheres to epithelial cells via E-cadherin > taken up by intestinal cells > uses listeriolysin to poke holes in phagosomes > moves to adjacent cells > infection is usually asymptomatic
gastroenteritis due to L. monocytogenes: pathogenesis
incubate in oropharynx 2 days > exudative pharyngitis > dirty white pseudomembrane (can obstruct airway leading to suffocation) > toxins (not bacteria) invade into body > "bull necked" appearance, myocarditis, cardiac failure
Respiratory infection by C. diphtheriae: pathogenesis, clinical outcomes leading to death (2)
skin contact with infected person > breaks through skin > papule > chronic nonhealing ulcer > toxins invade > myocarditis, cardiac dysfunction, laryngeal nerve palsy
Cutaneous infection by C. diphtheriae: pathogenesis
Usually inhibited by acidic Lactobacillus > something kills it > fishy smelling vagina that gets worse with intercourse (semen is basic)
Bacterial vaginosis due to G. vaginalis: pathogenesis
trauma (tooth extraction, IUD) compromises tissue blood flow > bacteria grow with no respect for anatomic boundaries > lump, abscess (possibly brain), sinus formation with hard yellowish microcolonies > may be misdiagnosed a sa neoplasm
endogenous infection of A. israelii: pathogenesis
inhalation of bacteria by immunocompromised individual > spreads to organs such as brain > can cause a brain abscess
pulmonary nocardiosis or brain abscess due to Nocardia: pathogenesis
traumatic implantation of bacteria > abscess
cutaneous infection due to Nocardia: pathogenesis