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79 Cards in this Set
- Front
- Back
Name the 7 general of Gram-positive bacilli and categorize them: endospore forming, non-endospore forming, branching
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ENDOSPORE: 1 Bacillus, 2 Clostridium. NO ENDOSPORE: 3 Listeria, 4 Corynebacterium, 5 Gardnerella. BRANCHING: 6 Actinomyces, 7 Nocardia
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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)
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xxx
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2. Understand the process of sporulation, the structure and properties of endospores, and the organisms that form them.
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xxx
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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)
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xxx (take notes in class)
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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)
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xxx
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5. Know key culture media used to identify Gram-positive bacilli (p8)
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1 Loeffler coagulated serium medium for Corynebacteria diphtheria, 2 Potassium -tellurite medium that turns brown when C. diphtheria converts it to elemental tellurium
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Name the endospore forming bacilli (6)
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B. anthracis, B. cereus, C. tetani, C. perfringens, C. botulinum, C. difficile
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Name the non-endospore forming bacilli (3)
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L. monocytogenes, C. diphtheriae, G. vaginalis
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Name the branching bacilli (2)
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A. israelii, Nocardia
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B. anthracis: full name, the basics (1)
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Bacillus anthracis. Endospore-forming. Usually spores found in dry fields infect herbivores, which is why you can send it in the mail.
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B. anthracis: virulence factors (4)
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1 polyPEPTIDE capsule. ANTHRAX TOXINS: 1 PA, 2 LF, 3 EF.
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PA: acronym, mechanism of virulence
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protective antigen. Binds to cell and facilitates entry of LF and EF.
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LF: acronym, mechanism of virulence
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metalloprotease of MAP kinase; signals for cell death
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EF: acronym, mechanism of virulence
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Edema factor is a calmodulin-mediated adenylate cyclase. inc cAMP > membrane more permeable > cells lose water > pulmonary edema
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B. anthracis: infections (3) by body system
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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
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B. cereus: full name, source
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Bacillus cereus. Found in rice and vegetables. Endospore-forming.
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B. cereus: infections (2)
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1 emetic disease, 2 diarrheal disease
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emetic disease of B. cereus, pathogenesis
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From eating ENTEROTOXIN. Poorly refridgerated fried rice > bacteria eat protein in the rice > produce enterococcin > nausea, vomiting, diarrhea
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diarrheal disease of B. cereus, pathogenesis
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From eating BACTERIA. Contaminated meat > bacteria multiply in intestines > release enterotoxins > diarrhea (no vomiting).
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Clostridium: the basics
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anaerobic. Endospore-forming.
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C. tetani: full name, morphology, source, general preferred environment
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Clostridium tetani. Look like a tennis racket due to terminal endospores. From soil. Prefers low-oxygenated tissues.
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C. tetani: characteristic infection
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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
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Name the inhibitory nt's that are blocked by tetanus. (2)
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GABA, glycine
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C. perfringens: full name, source, typical infections
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Clostridium perfringens. From soil, feces. 1 wound infection, 2 gas gangrene
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wound infection by C. perfringens: pathogenesis and course of disease
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bacteria introduced into tissue by surgery or trauma > produce toxins, gas > gas gangrene > massive tissue destruction
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food poisoning by C. perfringens, pathogenesis
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eat contaminated meat > L secretory diarrhea > resolves within 24hr
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C. botulinum: full name, source, main virulence factor.
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Clostridium botulinum. Found in soil. Produces neurotoxin.
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C. botulinum: typical infections (3)
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1 food-born botulism, 2 infant botulism (most common form in USA), 3 wound botulism, (4) SoCal botulism aka Botox
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food-born botulism by C. botulinum: pathogenesis
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poorly canned green beans > incubates 1-2 days > bacteria produce botulism toxin which blocks ACh receptors > flaccid paralysis
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infant botulism by C. botulinum: pathogenesis
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eat honey > spores grow > floppy baby syndrome > respiratory arrest
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wound botulism by C. botulinum: pathogenesis
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bacteria infect wound > flaccid paralysis
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C. difficile: full name, source, main risk factor, types of strains, virulence factors.
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Clostridium difficile. Found in soil, feces. Overgrowth due to antibiotics. Can be toxigenic or non-toxigenic. Toxins A & B.
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C. difficile: typical infections (
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C. difficile associated disease (CDAD) 1 Environmental, or 2 endogenous
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environmental C. difficile associated disease: pathogenesis
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hospital worker touches a rectal thermometer > washes hands with alcohol that does not kill spores > transmits to next pt > mild diarrhea or pseudomembranous colitis
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pseudomembranous cholitis, ssx
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abd cramping, fever, diarrhea containing blood and pus
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endogenous C. difficile associated disease: pathogenesis
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oral antibiotics > changes enteric flora > overgrowth of bacteria
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L. monocytogenes: full name, morphology, metabolism, preferred growing conditions, source (3)
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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)
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gastroenteritis due to L. monocytogenes: pathogenesis
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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
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L. monocytogenes: typical infections (3)
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1 mild gastroenteritis in summertime, 2 septicemia of fetuses, 3 meningitis in immunocompromised renal transplant patients
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C. diphtheriae: full name, morphology, metabolism, source, mode of transmission
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Corynebacterium diphtheriae. Non-endospore forming. Club-shaped. Aerobes. Found in plants, animals, human skin & mucous membranes. Transmitted by droplets or skin contact.
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C. diphtheriae: virulence factors, typical infections (2)
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diptheria toxin, aka A-B toxin. Inhibits protein synthesis in the oropharyngeal mucosa, heart, nerve cells. Typical infections: 1 respiratory diphteria, 2 cutaneous diphtheria
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Respiratory infection by C. diphtheriae: pathogenesis, clinical outcomes leading to death (2)
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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
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Cutaneous infection by C. diphtheriae: pathogenesis
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skin contact with infected person > breaks through skin > papule > chronic nonhealing ulcer > toxins invade > myocarditis, cardiac dysfunction, laryngeal nerve palsy
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G. vaginalis: full name, metabolism, source, morphology
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Gardenerella vaginalis. Non-endospore forming. Facultative anaerobe. Gram-variable cells that form "clue cells"
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clue cell, def
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vaginal epithelial cell covered in bacteria
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Bacterial vaginosis due to G. vaginalis: pathogenesis
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Usually inhibited by acidic Lactobacillus > something kills it > fishy smelling vagina that gets worse with intercourse (semen is basic)
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A. israelii: full name, metabolism, source
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Actinomyces israelii. Branching bacillus. Anaerobic. Found in mucous membranes (gingiva, vagina).
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endogenous infection of A. israelii: pathogenesis
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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
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Nocardia: metabolism, morphology, source
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Branching bacilli. Aerobic. Filaments that break into rods. Found in soil.
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Nocardia: typical infections
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1 pulmonary nocardiosis, 2 cutaneous or subcutaneous infection, 3 brain abscess
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pulmonary nocardiosis or brain abscess due to Nocardia: pathogenesis
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inhalation of bacteria by immunocompromised individual > spreads to organs such as brain > can cause a brain abscess
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cutaneous infection due to Nocardia: pathogenesis
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traumatic implantation of bacteria > abscess
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calcium dipicolinate: fxn, producing cell genera
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calcium dipicolinatedehydrates nucleic acids. Produced by Bacillus, Clostridium.
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Name the stain used to detect endospores (and the counter-stain used).
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Schaefer-Fulton endospore stain w/ malachite green. Counter-stain: safranin.
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Name the layers of an endospore, innermost to outermost, starting with DNA. (5)
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1 core (DNA w/ calcium dipicolinate), 2 cytoplasmic membrane, 3 spore wall (peptidoglycan), 4 cortex (less cross-linked peptidoglycan), 5 keratin spore coat
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Name the organism with a polyPEPTIDE capsule. How do the effects of this differ from those of a normal capsule? (2)
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polypeptide capsule is 1 immunogenic, 2 antiphagocytic
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CLINICAL APPLICATION: A pt presents with a widened mediastinum on X-ray. Which organism?
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Indicative of hemorrhagic mediastinitis due to B. anthracis, a Gram-positive bacillus.
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toxins produced by C perfringens? (2)
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alpha toxins (aka phospholipase C, destroys membranes), theta toxins (destroys
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Name the Gram-positive bacilli that cause food poisoning and the type of food.
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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)
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Toxins produced by C. difficile, mechanisms (2)
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Toxin A: intestinal fluid secretion, mucosal injury. Toxin B: depolymerizes actin.
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Organisms covered by Tdap?
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Corynebacterium diphtheriae, Clostridium tetani
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CLINICAL APPLICATION: How can thrichomonas vaginalis and Gardnerella vaginalis be distinguished (ssx are similar)?
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wet mount - if clue cells are present, it's G. vaginalis
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From eating ENTEROTOXIN. Poorly refridgerated fried rice > bacteria eat protein in the rice > produce enterococcin > nausea, vomiting, diarrhea
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emetic disease of B. cereus, pathogenesis
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From eating BACTERIA. Contaminated meat > bacteria multiply in intestines > release enterotoxins > diarrhea (no vomiting).
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diarrheal disease of B. cereus, pathogenesis
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bacteria introduced into tissue by surgery or trauma > produce toxins, gas > gas gangrene > massive tissue destruction
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wound infection by C. perfringens: pathogenesis and course of disease
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eat contaminated meat > L secretory diarrhea > resolves within 24hr
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food poisoning by C. perfringens, pathogenesis
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poorly canned green beans > incubates 1-2 days > bacteria produce botulism toxin which blocks ACh receptors > flaccid paralysis
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food-born botulism by C. botulinum: pathogenesis
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eat honey > spores grow > floppy baby syndrome > respiratory arrest
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infant botulism by C. botulinum: pathogenesis
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bacteria infect wound > flaccid paralysis
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wound botulism by C. botulinum: pathogenesis
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hospital worker touches a rectal thermometer > washes hands with alcohol that does not kill spores > transmits to next pt > mild diarrhea or pseudomembranous colitis
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environmental C. difficile associated disease: pathogenesis
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|
abd cramping, fever, diarrhea containing blood and pus
|
pseudomembranous cholitis, ssx
|
|
oral antibiotics > changes enteric flora > overgrowth of bacteria
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endogenous C. difficile associated disease: pathogenesis
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|
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
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gastroenteritis due to L. monocytogenes: pathogenesis
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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
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Respiratory infection by C. diphtheriae: pathogenesis, clinical outcomes leading to death (2)
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skin contact with infected person > breaks through skin > papule > chronic nonhealing ulcer > toxins invade > myocarditis, cardiac dysfunction, laryngeal nerve palsy
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Cutaneous infection by C. diphtheriae: pathogenesis
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Usually inhibited by acidic Lactobacillus > something kills it > fishy smelling vagina that gets worse with intercourse (semen is basic)
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Bacterial vaginosis due to G. vaginalis: pathogenesis
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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
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endogenous infection of A. israelii: pathogenesis
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inhalation of bacteria by immunocompromised individual > spreads to organs such as brain > can cause a brain abscess
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pulmonary nocardiosis or brain abscess due to Nocardia: pathogenesis
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traumatic implantation of bacteria > abscess
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cutaneous infection due to Nocardia: pathogenesis
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