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bacteria that is spore-forming
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found in soil, water...
Clostridium ssp
Clostridium ssp
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non-spore forming
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found in mucosal tissues
Bacteroides, Actinomyces ssp
Bacteroides, Actinomyces ssp
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why is O2 toxic to bacteria?
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•bacteria lack catalase and/or superoxide dismutase which makes them susceptible to oxidative damage (NO WAY TO DETOXIFY!)
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metabolism of anaerobic bacteria
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- use other electron acceptors
•Less ATP is produced, so bacteria are typically slow-growers
•CO2 and H2 generated by these reactions, so bacteria often produce gas in tissues
Produce short chain fatty acids during metabolism → contributes to foul smell
•Less ATP is produced, so bacteria are typically slow-growers
•CO2 and H2 generated by these reactions, so bacteria often produce gas in tissues
Produce short chain fatty acids during metabolism → contributes to foul smell
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C. perfringens Virulence Factors
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- produce major lethal toxins
- produce enterotoxin (superantigen)
- produce enterotoxin (superantigen)
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major lethal toxins of C. perfringens
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- alpha (α)
- beta (β)
- epsilon (ε)
- Iota (I)
- theta (θ)
- beta (β)
- epsilon (ε)
- Iota (I)
- theta (θ)
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enterotoxin of C. perfringens
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•binds brush border cells of ileum and jejunum (not duodenum), altering membrane permeability and promoting fluid and electrolyte loss
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diseases of Clostridium perfringens
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- cellulitis
- fasculitis
- myonecrosis
- food poisoning (gastroenteritis)
- necrotizing enteritis
- fasculitis
- myonecrosis
- food poisoning (gastroenteritis)
- necrotizing enteritis
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C. tetani Virulence
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2 toxins
•Tetanolysin
•Tetanospasmin
•Tetanolysin
•Tetanospasmin
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tetanolysin
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hemolysin
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Tetanospasmin
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classic A/B toxin
•The A subunit is a Zn peptidase that cleaves SNARE proteins involved in trafficking and release of neurotransmitter-containing vesicles (see slide 38 for SNARE proteins)
•RESULT- inhibitory neurotransmitters glycine and GABA are not released, producing spastic paralysis
•Toxin binding is irreversible, so damage remains and recovery dependent on if/when new axonal termini are generated
•The A subunit is a Zn peptidase that cleaves SNARE proteins involved in trafficking and release of neurotransmitter-containing vesicles (see slide 38 for SNARE proteins)
•RESULT- inhibitory neurotransmitters glycine and GABA are not released, producing spastic paralysis
•Toxin binding is irreversible, so damage remains and recovery dependent on if/when new axonal termini are generated
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3 types of tetanus of C. tetani
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- localized
- cephalic
- neonatal
- cephalic
- neonatal
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localized tetanus
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•toxin does not disseminate to CNS, but stays localized to site of primary infection
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cephalic tetanus
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subset of localized tetanus when head is site of primary infection, very poor prognosis
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neonatal tetanus
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•infection at umbilical stump with disease progressing to generalized tetanus; high mortality rates with developmental defects in survivors
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C. botulinum Virulence
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- endospores found in soil
- Botulinum toxin
- Botulinum toxin
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Botulinum toxin
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heat-labile A/B neurotoxin - heavy (B) and light (A) chain
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mechanism of Botulinum toxin
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•Inhibits binding of vesicles with axon terminus thereby preventing release of acetylcholine at neuromuscular junction
•Muscle can't contract, so flaccid paralysis results (wrinkles gone)
•Muscle can't contract, so flaccid paralysis results (wrinkles gone)
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sources of infant botulism
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- honey and powdered formula
- spore-containing soil and dust (most common)
- spore-containing soil and dust (most common)
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susceptibility factor of infant botulism
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•Relative lack of intestinal microbiota (often a problem for babies!) allows adherence of spores and colonization of intestine upon germination of spore
•Adults routinely ingest spores which cannot colonize due to competition with normal GI flora
•Adults routinely ingest spores which cannot colonize due to competition with normal GI flora
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predisposing factors for Clostridioides difficile
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•Recent antibiotic therapy - reduces normal GI flora
•Recent contact with health care setting
•Reduced immune function (esp. elderly) - cannot control infection
•Recent contact with health care setting
•Reduced immune function (esp. elderly) - cannot control infection
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significance of C. difficile with healthcare setting
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•spores resistant to decontamination and persist in hospitals
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pathogenesis of C. difficile
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•Survival of spores in stomach (resistant to gastric acid) → germinate in small intestine
•polysaccharide capsule
•Adherence
•Produce Toxin A (enterotoxin) and Toxin B (cytotoxin)
•polysaccharide capsule
•Adherence
•Produce Toxin A (enterotoxin) and Toxin B (cytotoxin)
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Toxin A of C. difficile
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induces cytokine production
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Toxin B of C. difficile
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disrupts cytoskeleton by actin depolymerization causing tissue destruction
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current SHEA guidelines for C. difficile diagnosis
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1. screen stool sample for C. diff with EIA or NAAT assay
2. Toxin A/B EIA to identify toxin-producing infection
2. Toxin A/B EIA to identify toxin-producing infection
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actinomycosis
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•Characterized by chronic granulomatous lesions that form abscesses connected by sinus tracts, macroscopic colonies of the bacteria resemble yellow grains of sand "sulfur granules," lesions firm upon palpation
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appearance/structure of Actinomyces
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filamentous arrangement
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3 bacteria that are major components of natural flora in oropharynx, GI tract, and genital tract
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- Lactobacillus spp
- Bifidobacterium spp
- Eubacterium spp
- Bifidobacterium spp
- Eubacterium spp
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normal flora that are avirulent and NOT associated with disease
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- Bifidobacterium spp
- Eubacterium spp
- Eubacterium spp
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component of normal flora that is a key regulator in biome
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Lactobacillus
- used with probiotics
- used with probiotics
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major role of Lactobacillus
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•secretion of lactic acid, H2O2, and bacteriocins (antibacterial substances) which suppresses growth of pathogenic bacteria
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what happens with dysbosis occurs (lactobacilli are reduced)?
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•other organisms (Candida, anaerobes) overgrow and cause disease
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P. acne pathogenesis
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•Acne vulgaris (teenagers and young adults) - causes acne!
•Opportunistic infections (prosthetic devices or intravascular lines)
•Opportunistic infections (prosthetic devices or intravascular lines)
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P. propionicum Pathogenesis:
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•Associated with endodontic abscesses and infections of lacrimal apparatus (lacrimal canaliculitis)
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Prevotella: virulence factors
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polysaccharide capsule, degrade Ig; assoc. w/ upper respiratory tract infections & gynecological infections
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Porphyromonas gingivalis virulence
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pili for attachment, associated with periodontal disease
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Fusobacterium: associated with _____ infections
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upper respiratory tract
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Bacteroides fragilis characteristics
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•Gram negative bacilli
•Modified LPS (low endotoxin activity)
•capsule
•fimbriae
•Products of anaerobic metabolism inhibit phagocytosis and intracellular killing
•Modified LPS (low endotoxin activity)
•capsule
•fimbriae
•Products of anaerobic metabolism inhibit phagocytosis and intracellular killing
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reservoir of Bacteroides fragilis
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human large intestine
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pathogenesis of Bacteroides fragilis
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•Trauma lead spread to sterile sites in the body and cause infection
•Causes septicemia, abscess, peritonitis, pleuropneumonia, and genital infections
•In general: abdominal infections and abscesses
•Causes septicemia, abscess, peritonitis, pleuropneumonia, and genital infections
•In general: abdominal infections and abscesses
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major virulence factor of Porphyromonas
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adhesion
‒fimbriae of P. gingivalis can adhere to epithelium and extracelluar molecules (e.g. fibronectin, fibrinogen) that promotes binding
‒fimbriae of P. gingivalis can adhere to epithelium and extracelluar molecules (e.g. fibronectin, fibrinogen) that promotes binding
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major virulence factor of Pasturella multocida
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capsule containing hyaluronic acid
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HACEK organisms
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•a group of fastidious, slow-growing, gram-negative bacteria whose growth requires an atmosphere of carbon dioxide. (fastidious means hard to grow!)
normally reside in the oral cavity and have been associated with local infections in the mouth. They are also known to cause severe systemic infections—most often bacterial endocarditis, which can develop on either native or prosthetic valves
normally reside in the oral cavity and have been associated with local infections in the mouth. They are also known to cause severe systemic infections—most often bacterial endocarditis, which can develop on either native or prosthetic valves