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258 Cards in this Set
- Front
- Back
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Fxn: Peptidoglycan
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- gives rigid support
- protects against osmotic pressure |
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CC: Peptidoglycan
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Sugar backbone w/cross-linked peptide and chains
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Fxn: Cell wall/cell membrane (G+)
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Surface antigen
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CC: Cell wall/cell membrane (G+)
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- Peptidoglycan -> support
- Lipoteichoic acid -> induces TNF and IL-1 |
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Fxn: Outer membrane (G-)
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- Site of endotoxin (LPS)
- Major surface antigen |
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CC: Outer membrane (G-)
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- Lipid A -> induces TNF and IL-1
- Polysaccharide = antigen |
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Fxn: Plasma membrane
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Site of oxidative and transport enzymes
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CC: Plasma membrane
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Lipoprotein bilayer
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Fxn: Ribosome
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Protein synthesis
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CC: Ribosome
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50S and 30S subunits
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Fxn: Periplasm
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Space between cytoplasmic membrane and peptidoglycan wall in G- bacteria
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CC: Periplasm
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Contains hydrolytic enzymes (e.g., beta-lactamases)
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Fxn: Capsule
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Protects against phagocytosis
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CC: Capsule
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Polysaccharide
(Bacillus anthracis is exception -> contains D-Glutamate) |
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Fxn: Pilus/Fimbriae
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Mediates adherence of bacteria to cell surface --> sex pilus attachment between two bacteria during conjugation
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CC: Pilus/fimbriae
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Glycoprotein
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Fxn: Flagellum
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Motility
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CC: Flagellum
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Protein
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Fxn: Spore
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Provides resistance to dehydration, heat and chemicals
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CC: Spore
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- Keratin-like coat
- Dipicolinic acid |
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Fxn: Plasmid
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Contains genes for antibody resistance, enzymes, toxins
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CC: Plasmid
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DNA
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Fxn: Glycocalyx
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Mediates adherence to surfaces, especially foreign surfaces (e.g., indwelling catheters)
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CC: Glycocalyx
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Polysaccharide
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Cell wall components common to both G+ and G- bacteria
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- Flagellum
- Pilus - Capsule - Peptidoglycan - Cytoplasmic membrane |
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Cell wall component unique to G+ organisms
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Lipoteichoic acid
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Components of lipoteichoic acid
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- lipid
- teichoic acid |
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Cell wall component unique to G- organisms
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Endotoxin/LPS (outer membrane)
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Circular (coccus): G+
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- Staphylococcus
- Streptococcus |
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Circular (coccus): G-
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Neisseria
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Rod (bacillus): G+
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- Clostridium
- Cornyebacterium - Bacillus - Listeria - Mycobacterium |
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G+ rod stained using acid-fast stains
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Mycobacterium
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Rod (bacillus): G- enterics
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- E. coli
- Shigella - Salmonella - Yersinia - Klebsiella - Proteus - Enterobacter - Serratia - Vibrio - Campylobacter - Heliobacter - Pseudomonas - Bacteroides |
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Rod (bacillus): G-, not enteric
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- Haemophilus
- Legionella - Bordetella - Francisella - Brucella - Pasteurella - Bartonella - Gardnerella |
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G- rod using silver stain
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Legionella
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G- rod that's actually gram-variable
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Gardnerella
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Branching filamentous
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- Actinomyces (G+)
- Nocardia (G+) |
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Gram + branching filamentous that weakly stains acid fast
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Nocardia
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Pleomorphic organisms
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- Rickettsiae (G-)
- Chlamydiae (G-) |
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Spiral (Spirochetes) organisms
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- Leptospira
- Borrelia - Treponema |
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Organisms stain with Giemsa
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- Chlamydiae
- Borrelia |
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Organisms with cell wall
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Mycoplasma
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Mycoplasma: composition of CW/CM
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Sterols, no cell wall
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Mycobacteria: composition of CW/CM
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Mycolic acid, high lipid content
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Which bugs don't gram stain well (and why?)
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- Treponema
- Rickettsia - Mycobacteria - Mycoplasma - Legionella pneumoniae - Chlamydia (These Rascals May Microscopically Lack Colour) |
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Why can't Treponema gram stain well?
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too thin to be visualised
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Why can't Rickettsia gram stain well?
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intracellular parasite
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Why can't Mycobacteria gram stain well?
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high-lipid-content CW requires acid-fast stain
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Why can't Mycoplasma gram stain well?
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no CW
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Why can't Legionella pneumoniae gram stain well?
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primarily intracellular
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Why can't Chlamydia gram stain well?
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intracellular; lacks muramic acid in its CW
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What does Giemsa stain?
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- Borrelia
- Plasmodium - Trypanosomes - Chlamydia |
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What does PAS (periodic-acid-Schiff) stain?
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- Glycogen
- Mucopolysaccharides |
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What can you use PAS to diagnose (and what organism)?
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Whipple's disease (Tropheryma whippelii)
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What does Ziehl-Neelsen (carbol fuschin) stain?
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Acid-fast organisms
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What does India Ink stain?
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Cryptococcus neoformans
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What can also be used to stain cryptococcus neoformans (besides India Ink)?
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Mucicarmine (stains thick polysaccharide capsule red)
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What does silver stain stain?
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- Fungi (e.g., Pneumocystis)
- Legionella |
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What are the culture requirements for H. influenzae?
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Chocolate agar with Factor V (NAD+) and Factor X (hematin)
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What are the culture requirements for N. gonorrhoeae?
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Thayer-Martin media
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What are the components of Thayer-Martin media (and what do they select for?)
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- Vancomycin (inhibits G+)
- Polymyxin (inhibits G-) - Nystatin (inhibits fungi) |
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"to connect to Neiserria, please use your VPN client"
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Vancomycin, Polymixin, Nystatin
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What are the culture requirements for B. pertussis?
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Bordet-Gengou (potato) agar
(Bordet for Bordetella) |
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What are the culture requirements for C. diptheriae?
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- Tellurite plate
- Loffler's media |
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What are the culture requirements for M. tuberculosis?
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Lowenstein-Jensen agar
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What are the culture requirements for M. pneumoniae?
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Eaton's agar
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What are the culture requirements for Lactose-fermenting enterics?
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- Pink colonies on MacConkey's agar (fermentation produces acid --> turns plate pink)
- E. coli also grown on eosin-methylene blue (EMB) agar as black-blue colonies with metallic sheen |
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What are the culture requirements for Legionella?
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Charcoal yeast agar buffered with cysteine and iron
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What are the culture requirements for fungi?
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Sabouraud's agar
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Obligate anaerobes: how they generate energy?
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Use 02-dependent system to generate ATP
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Obligate anaerobes: examples
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- Nocardia
- Pseudomonas aeruginosa - Mycobacterium tuberculosis - Bacillus (Nagging Pests Must Breathe) |
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Where would one typically encounter P. Aeruginosa?
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(P. AERuginosa is an AERobe seen in:)
- burn wounds - nosocomial pneumonia - pneumonia in cystic fibrosis pts. |
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Why does M. tuberculosis prefer the apices of the lung upon reactivation (e.g., after immune compromise or TNF-a inhibitor use)?
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Has the highest PO2 levels in lung
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Obligate anaerobes: examples
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- Clostridium
- Bacteroides - Actinomyces (Anaerobes Can't Breathe Air) |
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Where are obligate anaerobes found? Are they pathogenic anywhere?
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Normal in GI tract, pathogenic everywhere else
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Can you use aminoglycosides with anaerobes? Why or why not?
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No. Aminoglycosides require oxygen to enter the bacterial cell
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Obligate anaerobes: important things to remember
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- Lack catalase and/or superoxide dismutase --> susceptible to oxidative damage
- Foul-smelling (short-chain fatty acids) - Difficult to culture - Produce gas in tissue (CO2 and H2) |
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Which antioxidative enzymes do obligate anaerobes lack?
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- Catalase
- Superoxide dismutase |
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Why do obligate anaerobes smell?
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Short chain fatty-acids
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Which gases does obligate anaerobes produce?
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CO2 and H2
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Are obligate anaerobes easy to culture?
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Nope
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Name the obligate intracellular bugs. Why are they obligate?
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- Rickettsia
- Chlamydia (Stay inside cells when it's Really Cold) They don't make their own ATP. |
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Name the facultative intracellular bugs.
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- Salmonella
- Neisseria - Brucella - Mycobacterium - Listeria - Francisella - Legionella - Yersinia pestis (Some Nasty Bugs May Life FacultativeLY) |
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What happens in a positive Quelling reaction? What is this indicative of?
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Bugs with capsules --> capsule swells when specific anti-sera are added
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Which bugs can be detected via the Quellung reaction?
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- Streptococcus pneumoniae
- Haemophilus influenzae B - Neisseria meningitidis - Salmonella - Klebsiella pneumoniae - Group B strep (SHiN SKiS) (Group B) |
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What do capsules serve to do? What use are they clinically?
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- Anti-phagocytic virulence factor
- If conjugated with a protein --> vaccine |
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What problems do asplenic individuals face with encapsulated pathogens?
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- Decreased ability to opsonize encapsulated pathogens --> risk for severe infections
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Which vaccines should you give to an asplenic individual?
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- S. pneumonia
- H. influenzae - N. meningiditis |
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Fxn: Catalase
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Degrades H2O2 before it can be converted to microbicidal products by myeloperoxidase
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What problems do people with chronic granulomatous disease face with catalase-positive organisms?
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Have NADPH oxidase deficiency --> recurrent infections with Cat+ organisms b/c remaining H2O2 is degraded
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Catalase+ organisms
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- S. aureus
- Serratia - Pseudomonas - Actinomyces - Candida - E. coli (You need SSPACE for your CATs) |
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How do vaccines with polysaccharide capsule antigens work?
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Protein is conjugated to polysaccharide antigen to promote T-cell activation and subsequent class switching.
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Why can't a polysaccharide antigen alone work as a vaccine?
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It would not be recognized and presented by T-cells --> only IgM antibodies would be produced
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What are the urease-positive bugs?
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- Proteus
- Ureaplasma - Nocardia - Cryptococus - H. pylori - Klebsiella (PUNCH-K) |
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What pigment does Actinomyces israelii produce?
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Yellow "sulfur" granules (mass of filaments, formed in pus)
(ISRAEL has YELLOW SAND) |
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What pigment does S. aureus produce?
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Yellow pigment (aureus = gold)
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What pigment does Pseudomonas aeruginosa produce?
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blue-green pigment
(AERUGula is GREEN) |
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What pigment does Serratia marcescens produce?
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Red pigment
(RED MARASCHINO cherries) |
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What is the purpose of virulence factors?
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To promote evasion of host immune response
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Protein A: primary organism, action, effect
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- PO: S. aureus
- Action: Binds Fc portion of Ig - Effect: Prevents opsonization and phagocytosis |
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IgA Protease: primary organisms, action, effect
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- PO: S. pnuemoniae, H. influenzae type B, Neisseria (SHiN)
- Action: Cleaves IgA - Effect: Secreted to colonize respiratory mucosa |
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M Protein: primary organism, action
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- PO: Group A Streptococcus
- Action: Helps prevent phagocytosis |
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Source: exo- vs. endotoxin
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Exo: certain species of G+ and G-
Endo: Outer CM of G- |
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Secretion from cell: exo- vs. endotoxin
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Exo: Yes
Endo: No |
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Chemistry: exo- vs. endotoxin
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Exo: Polypeptide
Endo: LPS (structural part of bacteria; released when lysed) |
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Location of genes: exo- vs. endotoxin
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Exo: Plasmid or bacteriophage
Endo: Bacterial chromosome |
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Toxicity: exo- vs. endotoxin
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Exo: High (fatal dose = 1 ug)
Endo: Low (fatal dose = 100 ug) |
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Clinical effects: exo- vs. endotoxin
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Exo: Various
Endo: Fever, shock |
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Mode of action: exo- vs. endotoxin
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Exo: Various
Endo: Induces TNF and IL-1 |
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Antigenicity: exo- vs. endotoxin
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Exo: Induces high-titer antibodies (antitoxins)
Endo: Poorly antigenic |
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Vaccines: exo- vs. endotoxin
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Exo: Toxoids used as vaccines
Endo: No toxoids formed, no vaccine available |
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Heat stability: exo- vs. endotoxin
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Exo: Destroyed rapidly at 60C (NOT staphylococcal enterotoxin)
Endo: Stable at 100C for 1h |
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Which bug's exotoxin is not destroyed rapidly at 60C?
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Staphylococcus
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Typical diseases: exo- vs. endotoxin
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Exo: tetanus, botulism, diptheria
Endo: meningococcemia, sepsis by G- rods |
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Bacteria that inhibit protein synthesis
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- Cornybacterium diptheriae
- Pseudomonas aeruginosa - Shigella spp. - Enterohemorrhagic E. coli (EHEC), including O157:H7 |
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Mechanism of action: C. diptheriae and P. aeruginosa
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Inactivate elongation factor (EF-2)
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Toxin: C. diptheriae
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Diptheria toxin
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Manifestation C. diptheriae
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- Pharyngitis
- Pseudomembrane in throat |
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Toxin: P. aeruginosa
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Exotoxin A
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Manifestation: P. aeruginosa
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Host cell death
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Mechanism of action: Shigella and EHEC
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Inactivate 60S ribosome by cleaving rRNA
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Toxin: Shigella
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Shiga Toxin (ST)
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Manifestation: Shigella
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GI mucosal damage --> dysentery
ST enhances cytokine release --> HUS |
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Toxin: EHEC
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Shiga-like toxin (SLT)
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Manifestation: EHEC
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SLT enhances cytokine release --> HUS (but does not invade host cells)
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Bacteria that increase fluid secretion
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- Enterotoxigenic E.coli (ETEC)
- Yersinia enterocolitica - Bacillus anthracis - Vibrio cholerae |
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What are the two types of toxins ETEC produce?
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- Heat-LABILE toxin (LT)
- Heat-STABLE toxin (ST) |
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Mech. of action: Heat-labile ETEC
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Overactivates cAMP --> increased Cl- secretion in gut and H2O efflux
(LABILE in the AIR, stable on the ground) |
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Manifestation: Heat-labile AND heat-stable ETEC
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Watery diarrhea
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Mech. of action: Heat-stable ETEC and Yersinia Enterocolitica
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Overactivate cGMP --> decreased reabsorpbtion of NaCl and H2O in gut
(Labile in the air, STABLE on the GROUND) |
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Manifestation: Yersinia enterocolitica
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BLOODY diarrhea (Y. enterocolitica invades/destroys cells --> dysentery)
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MoA: Bacillus anthracis
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Mimics adenylate cyclase (increases cAMP)
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Toxin: B. anthracis
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Edema factor
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Manifestation: B. anthracis
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Likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax
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MoA: Vibrio cholerae
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Permanently activating Gs --> overactivates adenylate cyclase (increases cAMP) --> increased Cl- secretion in gut, H2O efflux
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Toxin: V. cholerae
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Cholera toxin
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Manifestation: V. cholerae
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Volumnious rice-water diarrhea
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Bacteria that inhibit phagocytic ability
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Bordetella pertussis
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MoA: Bordetella pertussis
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Disables Gi -> impairs phagocytosis to permit survival of microbe, overactivates adenylate cyclase (inc. cAMP)
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Toxin: B. pertussis
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Pertussis toxin
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Manifestation: B. pertussis
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WHOPPING COUGH
- Child coughs and "whoops" on inspiration - Toxin may not actually be cause of cough |
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Bacteria that inhibit release of neurotransmitter
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- Clostridium tetani
- Clostridium botulinum |
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MoA: C. tetani and C. botulinum
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Cleave SNARE protein required for NT release
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Toxin: C. tetani
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Tetanospasmin
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Toxin: C. botulinum
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Botulinum toxin
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Manifestation: C. tetani
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- Muscle rigidity, lockjaw
- Toxin prevents release of INHIBITORY NT's (GABA and Glycine) in spinal cord |
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Manifestation: C. botulinum
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- Flaccid paralysis, floppy baby
- Toxin prevents release of STIMULATORY signals (ACh) at musculoskeletal junction |
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Bacteria that lyse cell membranes
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- Clostridium perfringens
- Streptococcus pyogenes |
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MoA: C. perfringens
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Phospholipase --> degrades tissues, cell membranes
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MoA: S. pyogenes
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Protein that degrades cell membrane
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Toxin: C. perfringens
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Alpha toxin
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Toxin: S. pyogenes
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- Streptolysin O (SLO)
- Exotoxin A (superantigen) |
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Manifestation: C. perfringens
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Degradation of phospholipids:
- myonecrosis (gas gangrene) - hemolysis ('double zone' of hemolysis on blood agar) |
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Manifestation: S. pyogenes (SLO)
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- Lyses RBC's
- Contributes to b-hemolysis - Host ab's against toxin (ASO) used to dx rheumatic fever (DO NOT CONFUSE with immune complexes of post-strep glomerulonephritis) |
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Bacteria with Superantigens that cause shock
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- Streptococcus pyogenes (Exotoxin A)
- Staphylococcus aureus (Toxic shock syndrome toxin, TSST-1) |
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Manifestation: toxic-shock syndrome
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- Fever
- Rash - Shock |
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Manifestation: S. pyogenes (ExoA)
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Toxic-shock syndrome
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Manifestation: S. aureus
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- Toxic-shock syndrome
- Other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin) |
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MoA: ADP-ribosylating toxins
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- B-component binds to host cell receptor --> endocytosis
- A-component attaches ADP-ribosyl --> disrupts host cell proteins (active) |
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Examples: ADP-ribosylating toxins
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- Diptheria toxin (C. diptheriae)
- Exotoxin A (P. aeruginosa) - Heat-labile toxin (EHEC) - Cholera toxin (V. cholerae) - Pertussis toxin (B. pertussis) |
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What is an endotoxin?
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LPS found in OM of G- bacteria
(N-dotoxin is an intergral part of gram-Negative OM. heat STABLE.) |
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Three effects of endotoxin
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1) Activates macrophages
2) Activates complement (alternate pathway) 3) Activates hageman factor |
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What do activated macrophages produce in response to endotoxin? What is the effect?
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- IL-1 --> fever
- TNF --> fever, hemorrhagic tissue necrosis - Nitric Oxide --> hypotension (shock) |
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What complement components are activated in the alternate pathway in response to endotoxin? Effect?
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- C3a --> hypotension, edema
- C5a --> Neutrophil chemotaxis |
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What happens when Hageman factor is activated in response to endoxtoxin? Effect?
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Coagulation cascade --> DIC
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Bacterial Growth Curve:
1) X-axis 2) Y-axis |
X) time
Y) Number of viable bacteria |
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Bacterial Growth Curve: Phases
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1) Lag --> metabolic activity w/o division
2) Exponential/log --> rapid cell division 3) Stationary --> nutrient depletion slows growth 4) Death --> prolonged nutrient depletion and buildup of wast products lead to death |
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At what phase on the BGC do penicillins and cephalosporins act?
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Exponential/log phase. P/C act here as peptidoglycan is being made.
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At what phase are spores formed in some bacteria?
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Stationary phase
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Transformation (definition, bugs that do it)
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- Ability to take up DNA from environment (competence). Any DNA can be used.
- S. pneumoniae, H. influenzae type B, Neisseria (SHiN) |
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Conjugation (F+ x F-)
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F+ plasmid --> genes for conjugation
F- bacteria --> bacteria without F+ plasmid Plasmid replicated and transferred through pilus from F+ cell. Plasmid DNA ONLY, NO CHROMOSOMAL TRANSFER. |
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Conjugation (Hfr x F-)
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Hfr cell: F+ plasmid incorporated into bac chromosomal DNA
Transfer of plasmid and chromosomal genes |
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Transposition
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Segment of DNA that "jumps" between locations and can transfer genes from plasmid to chromosome and vice versa.
Excision --> can include chromosomal DNA --> incorporated into plasmid --> transferred into another bac |
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Generalized transduction
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Packaging event.
LYTIC phage infects bac --> cleavage of bac DNA, synthesis of viral proteins --> Parts of bac chromosomal DNA packaged into viral capsid --> Phage infects another bac --> transfer of genes |
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Specialized transduction
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Excision event.
LYSOGENIC phage infects bac --> viral DNA incorporated into bac chromosome --> DNA excised: flanking bac genes excised also --> packaged into viral capsid --> infects another bacterium |
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Bacterial toxins whose genes are encoded in a lysogenic phage
|
ShigA-like toxin
Botulinum toxin Cholera toxin Diptheria toxin Erythrogenic toxin of S. pyogenes (ABCDE) |
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G+ --> Branching filaments --> Anaerobe, not acid fast
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Actinomyces
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G+ --> Branching filaments --> Aerobe, acid fast
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Nocardia
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G+ --> Cocci --> Catalase + --> Coagulase +
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S. aureus
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G+ --> Cocci --> Catalase (+) --> Coagulase (-) --> Novobiocin sensitive
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S. epidermidis
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G+ --> Cocci --> Catalase (+) --> Coagulase (-) --> Novobiocin resistant
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S. saphrophyticus
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G+ --> Cocci --> Catalase (-) --> Partial hemolysis (green, alpha):
- Quellung(+) - Bile soluble (does not grow in bile) - Optochin SENSITIVE |
S. pneumoniae
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G+ --> Cocci --> Catalase (-) --> Partial hemolysis (green, alpha):
- Quellung(-) - Bile insoluble - Optochin INSENSITIVE |
S. viridans
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G+ --> Cocci --> Catalase (-) --> Complete hemolysis (clear, beta): Bacitracin SENSITIVE
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S. pyogenes (Group A)
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G+ --> Cocci --> Catalase (-) --> Complete hemolysis (clear, beta): Bacitracin INSENSITIVE
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S. agalacticae (Group B)
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G+ --> Cocci --> Catalase (-) --> No hemolysis (gamma): enterococcus
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E. faecalis
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G+ --> Cocci --> Catalase (-) --> No hemolysis (gamma): Non-enterococcus, growth in bile, NOT 6.5% NaCl
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S. bovis
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Novobiocin susceptibility
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Staphylococci
Resistant: Saphrophyticus Sensitive: Epidermidis (On the office's STAPH retreat, there was NO StRES) |
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Optochin susceptibility
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Streptococci
Resistant: Viridans Sensitive: Pneumoniae (OVRPS) |
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Bacitracin susceptibility
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Streptococci
Resistant: group B strep Sensitive: group A strep (B-BRAS) |
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alpha-hemolytic bacteria
|
Form GREEN RING around colonies on blood agar
- S. pneumoniae (cat-, op-sens) - S. viridans (cat-, op-res) |
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beta-hemolytic bacteria
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Form CLEAR AREA of hemolysis on blood agar
- S. aureus (cat+, coag+) - S. pyogenes: group A strep (cat-, bacitracin-sens) - S. agalactiae: group B strep (cat-, bacitracin-res) - Listeria monocytogenes (tumbling motility, meningitis in newborns, unpasterurized milk) |
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S. aureus: action of Protein A
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Binds Fc-IgG --> inhibits complement fixation and phagocytosis
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S. aureus: how to ID microscopically
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Gram-positive cocci in clusters
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S. aureus: effects
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1) Inflammatory disease --> skin infections, organ abcesses, pneumonia
2) Toxin mediated diseases: - Toxic-shock syndrome (TSST-1) - Scalded skin syndrome (exfoliative toxin) - Rapid-onset food poisoning (enterotoxins) 3) MRSA infection: serious nosocomial and community-acquired infections - Altered penicillin-binding protein --> resistance to beta-lactams 4) Acute bacterial endocarditis 5) Osteomyelitis |
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Action of TSST
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Superantigen that binds to MHC-II and T-cell receptor --> polyclonal T-cell activation
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Cause of S. aureus induced food poisoning
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Ingestion of preformed toxin (enterotoxins)
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Staphylococcus epidermidis: action, effects
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Produces adherent biofilms --> infects prosthetic devices and IV catheters
- Component of normal skin flora - Contaminates blood cultures |
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S. pneumoniae: effects
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MOPS (Most OPtochin Sensitive)
- Meningitis - Otitis media - Pneumonia - Sinusitis |
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S. pneumoniae: common facts (microscopic ID, toxin) and associations
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- Lancet-shaped, G+ diplococci
- Encapsulated - IgA Protease - Associated with: rusty sputum, sepsis (sickle cell anemia), splenectomy |
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S. viridans: effects
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- Dental carries (S. mutans)
- Subacute bacterial endocarditis at damaged valves (S. sanguis) (Sanguis = blood...lots of blood in the heart) |
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S. viridans: how to differentiate from S. pneumoniae
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Optochin-SENSITIVE (both are alpha-hemolytic)
(Viridans group live in the mouth because they are NOT AFRAID OF-THE-CHIN.) |
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S. pyogenes: pyogenic effects
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- Pharyngitis
- Cellulitis - Impetigo |
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S. pyogenes: toxigenic effects
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- Scarlet fever
- Toxic shock-like syndrome |
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S. pyogenes: immune effects
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- Rheumatic fever
- Acute glomerulonephritis |
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Rheumatic fever: signs/symptoms
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- Subcutaneous plaques
- Polyarthritis - Erythema marginatum - Chorea - Carditis (No "rheum" for SPECCulation) |
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S. pyogenes: how to detect (antibiotic and titers)
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- Bacitracin SENSITIVE
- ASO titer detects RECENT infection |
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S. pyogenes: effect of M-protein antibodies
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- Enhances host defenses against S. pyogenes
- Can give rise to rheumatic fever |
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S. agalacticae: where to find, effects
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Colonises vagina
Mainly in babies (Group B for Babies!) - Pneumonia - Meningitis - Sepsis |
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S. agalacticae: products and their effects
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CAMP factor (NOT cAMP) --> enlarges area of hemolysis formed by S. aureus
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S. agalacticae: screening and prophylaxis
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Screen: pregnant women at 35-37 weeks --> if (+): receive intrapartum penicillin prophylaxis
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Enterococci (Group D): where they colonise, effects
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- Colonic flora
- Penicillin-resistant - UTI - Subacute endocarditis |
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On what does the Lancefield grouping base its categories?
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Based on the C carbohydrate on the bacterial CW.
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Enterococci (Group D): growth medium
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6.5% NaCl and bile
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S. bovis (Group D): where they colonize, effects
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- Colonises gut
- Causes bacteremia and subacute endocarditis in colon CA pts. |
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C. diptheriae: toxin+effects, symptoms
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Diptheria via exotoxin encoded by beta-prophage --> inhibits protein synthesis via ADP ribosylation of EF-2
Sx: pseudomembranous pharyngitis (gray-white membrane) w/lymphadenopathy |
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C. diptheria: lab stuff
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- Grows on tellurite agar
- Lab Dx: G+ rods with metachromatic (red and blue) granules |
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C. diptheria: test for toxin
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Elek test
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C. diptheria: vaccine
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Toxoid vaccine --> prevents diptheria
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ABCDEFG's of C. diptheria
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ADP Ribosylation
Beta-prophage Corynebacterium Diptheria Elongation Factor 2 Granules |
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Spores: who produces them, when during BCG?
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G+ rods, when resources are limited (end of STATIONARY phase)
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Organisms that produce spores in soil
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- Bacillus anthracis
- Clostridium perfringens - Clostridium tetani |
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Organisms that produce spore (not in the soil)
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- Bacillus cereus
- Clostridium botulinum - Coxiella burnetii |
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Spores: durability/resistance, and how to kill
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- Highly resistant to heat and chemicals --> have dipicolinic acid in core, no metabolic activity
- To kill: autoclave by steaming at 121C for 15m |
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Clostridia: how to ID
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G+, spore-forming, obligate anaerobic bacilli
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C. tetani: toxin+effect
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Tetanospasmin: exotoxin causing tetanus
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Tetanus: what it is, action, effects
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- Tetanic paralysis
- GABA and glycine release inhibited from Renshaw cells in spinal cord --> inhibited inihibition - Spastic paralysis, trismus (lockjaw), risus sardonicus |
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C. botulinum: toxin+effect
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Preformed/heat-labile toxin --> inhibits ACh release at NMJ --> causes botulism
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C. botulinum: cause of disease in adults and babies
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Adults: ingestion of preformed toxin
Babies: ingestion of bacterial spores --> floppy baby syndrome (BOTulinum is from bad BOTtles of food and honey --> flaccid paralysis) |
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C. perfringens: toxin+effect
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- alpha-toxin: "lecithinase", a phosopholipase
- Myonecrosis (gas gangrene), hemolysis (PERFringens PERForates a gangrenous leg.) |
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C. dificile: toxins+effects
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- Toxin A (enterotoxin): binds to brush border of gut
- Toxin (cytotoxin): destroys cytoskeletal structure of enterocytes --> causes pseudomembranous colitis |
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C. dificile: treatment
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Metronidazole or oral vancomycin
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C. dificile: causes, Dx
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- Cause: secondary to antibiotic abuse (clindamycin, ampicillin)
- Diagnosis: detection of one or both toxins in the stool |
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What two antibiotics can cause an exacerbation of C. dificile related problems?
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- Clindamycin
- Ampicillin |
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What bacterium is the only one with a polypeptide capsule?
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Bacillus anthracis (contains D-glutamate)
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Anthrax: skin lesion appearance and cause
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Black eschar (necrosis) surrounded by edematous ring. Caused by lethal factor and edema factor.
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Cutaneous anthrax
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Contact --> black eschar (painless ulcer) --> progresses to bacteremia and death
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Pulmonary anthrax
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Inhalation of spores --> flulike symptoms --> rapid progression to fever, pulmonary hemorrhage, mediastinitis, shock
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Woolsorter's disease
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Inhalation of spores from contaminated wool
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Listeria monocytogenes: ID, acquisition
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ID: facultative intracellular microbe
Acquisition: - Ingest unpasteurized milk/cheese, deli meats - Vaginal transmission during birth |
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Listeria monocytogenes: motility/movement
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- Forms "actin rockets" --> how it moves from cell to cell
- Tumbling motility = characteristic |
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L. monocytogenes: effects
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- Pregnant women: amnionitis, septicemia, spontaneous abortion
- Granulomatosis infatiseptica - Neonatal meningitis - Meningitis in immunocompromised pts. - Mild gastroenteritis (healthy people) |
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L. monocytogenes: treatment
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- Self-limited
- Ampicillin: infants, immunocompromised, elderly --> use in empirical treatment of meningitis |
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Appearance: actinomyces and nocardia
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G+ rods, form long branching filaments resembling fungi
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Actinomyces israelii: ID, where it colonises, effects
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- G+ anaerobe
- Normal oral flora - Oral/facial abcesses --> drain through sinus tracts in skin (Forms yellow "sulfur granules" in sinus tracts) |
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Nocardia asteroides: ID, effects
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- G+, weakly acid-fast aerobe in soil
- Pulmonary infection in immunocompromised pts. |
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Tx: actinomyces and nocardia
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- Nocardia: Sulfas
- Actinomyces: Penicillin (SNAP) |
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1* vs 2* TB: who gets it/what circumstances?
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1* TB: nonimmune host (child)
2* TB: partially immune hypersensitised host (usually host) - Reactivation TB of the lungs |
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1* vs 2* TB: points of localization of lesions
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1* TB: hilar nodes, lower lobes (Ghon focus)
2* TB: upper lobes (fibrocaseous cavitary lesion) |
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What makes up the Ghon complex?
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TB granulomas:
- Lobar/perihilar lymph nodes - Ghon focus (lower lobes) Reflects 1* infection of exposure |
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Four effects of 1* TB and their consequences
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1) Heals by fibrosis --> immunity/hypersensitivity --> tuberculin positive
2) Progressive lung disease (HIV/malnutrition) --> (rarely) death 3) Severe bacteremia --> miliary tuberculosis --> death 4) Preallergic lymphatic or hematogenous dissemination --> dormant tubercle bacilli in several organs --> reactivation in adult life |
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Two consequences of reactivation TB in the lungs
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1) 2* tuberculosis
2) Extrapulmonary tuberculosis |
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Extrapulmonary TB: affected areas (and assn. diseases)
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- CNS (parenchymal tuberculoma, meningitis
- Vertebral body (Pott's disease) - Lymphadenitis - Renal - GI |
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Mycobacteria: important types+effects
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- M. tuberculosis (TB, resistant to multiple Rx)
- M. kansaii (pulmonary TB-like symptoms) - M. avium-intracellulare (many Rx-resistant, causes disseminated disease in AIDS; Tx: prophylaxis with azithromycin) - M. leprae (leprosy) All are acid-fast organisms |
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Symptoms of TB
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- Fever
- Night sweats - Weight loss - Hemoptysis |
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Leprosy (Hansen's disease): causes
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- M. leprae: acid-fast bacillus, likes cool temps (infects skin, superficial nerves), cannot be grown in vitro
- Reservoir: armadillos (US) |
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Leprosy (Hansen's disease): two forms
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1) Lepromatous:
- spread diffusely over skin, communicable - low cell-mediated immunity --> humoral Th2 response (LEpromatous can be LEthal) 2) Tuberculoid: - few hypoesthetic skin plaques - high cell-mediated immunity --> Th1-type immune response |
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Leprosy (Hansen's disease): Tx
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Long-term: oral dapsone
- Toxicity: hemoptysis, methemglobinemia Alternate tx: - Rifampin - Clofazimine/dapsone |
