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258 Cards in this Set
- Front
- Back
Fxn: Peptidoglycan
|
- gives rigid support
- protects against osmotic pressure |
|
CC: Peptidoglycan
|
Sugar backbone w/cross-linked peptide and chains
|
|
Fxn: Cell wall/cell membrane (G+)
|
Surface antigen
|
|
CC: Cell wall/cell membrane (G+)
|
- Peptidoglycan -> support
- Lipoteichoic acid -> induces TNF and IL-1 |
|
Fxn: Outer membrane (G-)
|
- Site of endotoxin (LPS)
- Major surface antigen |
|
CC: Outer membrane (G-)
|
- Lipid A -> induces TNF and IL-1
- Polysaccharide = antigen |
|
Fxn: Plasma membrane
|
Site of oxidative and transport enzymes
|
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CC: Plasma membrane
|
Lipoprotein bilayer
|
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Fxn: Ribosome
|
Protein synthesis
|
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CC: Ribosome
|
50S and 30S subunits
|
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Fxn: Periplasm
|
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
|
Protects against phagocytosis
|
|
CC: Capsule
|
Polysaccharide
(Bacillus anthracis is exception -> contains D-Glutamate) |
|
Fxn: Pilus/Fimbriae
|
Mediates adherence of bacteria to cell surface --> sex pilus attachment between two bacteria during conjugation
|
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CC: Pilus/fimbriae
|
Glycoprotein
|
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Fxn: Flagellum
|
Motility
|
|
CC: Flagellum
|
Protein
|
|
Fxn: Spore
|
Provides resistance to dehydration, heat and chemicals
|
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CC: Spore
|
- Keratin-like coat
- Dipicolinic acid |
|
Fxn: Plasmid
|
Contains genes for antibody resistance, enzymes, toxins
|
|
CC: Plasmid
|
DNA
|
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Fxn: Glycocalyx
|
Mediates adherence to surfaces, especially foreign surfaces (e.g., indwelling catheters)
|
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CC: Glycocalyx
|
Polysaccharide
|
|
Cell wall components common to both G+ and G- bacteria
|
- Flagellum
- Pilus - Capsule - Peptidoglycan - Cytoplasmic membrane |
|
Cell wall component unique to G+ organisms
|
Lipoteichoic acid
|
|
Components of lipoteichoic acid
|
- lipid
- teichoic acid |
|
Cell wall component unique to G- organisms
|
Endotoxin/LPS (outer membrane)
|
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Circular (coccus): G+
|
- Staphylococcus
- Streptococcus |
|
Circular (coccus): G-
|
Neisseria
|
|
Rod (bacillus): G+
|
- Clostridium
- Cornyebacterium - Bacillus - Listeria - Mycobacterium |
|
G+ rod stained using acid-fast stains
|
Mycobacterium
|
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Rod (bacillus): G- enterics
|
- E. coli
- Shigella - Salmonella - Yersinia - Klebsiella - Proteus - Enterobacter - Serratia - Vibrio - Campylobacter - Heliobacter - Pseudomonas - Bacteroides |
|
Rod (bacillus): G-, not enteric
|
- Haemophilus
- Legionella - Bordetella - Francisella - Brucella - Pasteurella - Bartonella - Gardnerella |
|
G- rod using silver stain
|
Legionella
|
|
G- rod that's actually gram-variable
|
Gardnerella
|
|
Branching filamentous
|
- Actinomyces (G+)
- Nocardia (G+) |
|
Gram + branching filamentous that weakly stains acid fast
|
Nocardia
|
|
Pleomorphic organisms
|
- Rickettsiae (G-)
- Chlamydiae (G-) |
|
Spiral (Spirochetes) organisms
|
- Leptospira
- Borrelia - Treponema |
|
Organisms stain with Giemsa
|
- Chlamydiae
- Borrelia |
|
Organisms with cell wall
|
Mycoplasma
|
|
Mycoplasma: composition of CW/CM
|
Sterols, no cell wall
|
|
Mycobacteria: composition of CW/CM
|
Mycolic acid, high lipid content
|
|
Which bugs don't gram stain well (and why?)
|
- Treponema
- Rickettsia - Mycobacteria - Mycoplasma - Legionella pneumoniae - Chlamydia (These Rascals May Microscopically Lack Colour) |
|
Why can't Treponema gram stain well?
|
too thin to be visualised
|
|
Why can't Rickettsia gram stain well?
|
intracellular parasite
|
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Why can't Mycobacteria gram stain well?
|
high-lipid-content CW requires acid-fast stain
|
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Why can't Mycoplasma gram stain well?
|
no CW
|
|
Why can't Legionella pneumoniae gram stain well?
|
primarily intracellular
|
|
Why can't Chlamydia gram stain well?
|
intracellular; lacks muramic acid in its CW
|
|
What does Giemsa stain?
|
- Borrelia
- Plasmodium - Trypanosomes - Chlamydia |
|
What does PAS (periodic-acid-Schiff) stain?
|
- Glycogen
- Mucopolysaccharides |
|
What can you use PAS to diagnose (and what organism)?
|
Whipple's disease (Tropheryma whippelii)
|
|
What does Ziehl-Neelsen (carbol fuschin) stain?
|
Acid-fast organisms
|
|
What does India Ink stain?
|
Cryptococcus neoformans
|
|
What can also be used to stain cryptococcus neoformans (besides India Ink)?
|
Mucicarmine (stains thick polysaccharide capsule red)
|
|
What does silver stain stain?
|
- Fungi (e.g., Pneumocystis)
- Legionella |
|
What are the culture requirements for H. influenzae?
|
Chocolate agar with Factor V (NAD+) and Factor X (hematin)
|
|
What are the culture requirements for N. gonorrhoeae?
|
Thayer-Martin media
|
|
What are the components of Thayer-Martin media (and what do they select for?)
|
- Vancomycin (inhibits G+)
- Polymyxin (inhibits G-) - Nystatin (inhibits fungi) |
|
"to connect to Neiserria, please use your VPN client"
|
Vancomycin, Polymixin, Nystatin
|
|
What are the culture requirements for B. pertussis?
|
Bordet-Gengou (potato) agar
(Bordet for Bordetella) |
|
What are the culture requirements for C. diptheriae?
|
- Tellurite plate
- Loffler's media |
|
What are the culture requirements for M. tuberculosis?
|
Lowenstein-Jensen agar
|
|
What are the culture requirements for M. pneumoniae?
|
Eaton's agar
|
|
What are the culture requirements for Lactose-fermenting enterics?
|
- 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 |
|
What are the culture requirements for Legionella?
|
Charcoal yeast agar buffered with cysteine and iron
|
|
What are the culture requirements for fungi?
|
Sabouraud's agar
|
|
Obligate anaerobes: how they generate energy?
|
Use 02-dependent system to generate ATP
|
|
Obligate anaerobes: examples
|
- Nocardia
- Pseudomonas aeruginosa - Mycobacterium tuberculosis - Bacillus (Nagging Pests Must Breathe) |
|
Where would one typically encounter P. Aeruginosa?
|
(P. AERuginosa is an AERobe seen in:)
- burn wounds - nosocomial pneumonia - pneumonia in cystic fibrosis pts. |
|
Why does M. tuberculosis prefer the apices of the lung upon reactivation (e.g., after immune compromise or TNF-a inhibitor use)?
|
Has the highest PO2 levels in lung
|
|
Obligate anaerobes: examples
|
- Clostridium
- Bacteroides - Actinomyces (Anaerobes Can't Breathe Air) |
|
Where are obligate anaerobes found? Are they pathogenic anywhere?
|
Normal in GI tract, pathogenic everywhere else
|
|
Can you use aminoglycosides with anaerobes? Why or why not?
|
No. Aminoglycosides require oxygen to enter the bacterial cell
|
|
Obligate anaerobes: important things to remember
|
- 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) |
|
Which antioxidative enzymes do obligate anaerobes lack?
|
- Catalase
- Superoxide dismutase |
|
Why do obligate anaerobes smell?
|
Short chain fatty-acids
|
|
Which gases does obligate anaerobes produce?
|
CO2 and H2
|
|
Are obligate anaerobes easy to culture?
|
Nope
|
|
Name the obligate intracellular bugs. Why are they obligate?
|
- Rickettsia
- Chlamydia (Stay inside cells when it's Really Cold) They don't make their own ATP. |
|
Name the facultative intracellular bugs.
|
- Salmonella
- Neisseria - Brucella - Mycobacterium - Listeria - Francisella - Legionella - Yersinia pestis (Some Nasty Bugs May Life FacultativeLY) |
|
What happens in a positive Quelling reaction? What is this indicative of?
|
Bugs with capsules --> capsule swells when specific anti-sera are added
|
|
Which bugs can be detected via the Quellung reaction?
|
- Streptococcus pneumoniae
- Haemophilus influenzae B - Neisseria meningitidis - Salmonella - Klebsiella pneumoniae - Group B strep (SHiN SKiS) (Group B) |
|
What do capsules serve to do? What use are they clinically?
|
- Anti-phagocytic virulence factor
- If conjugated with a protein --> vaccine |
|
What problems do asplenic individuals face with encapsulated pathogens?
|
- Decreased ability to opsonize encapsulated pathogens --> risk for severe infections
|
|
Which vaccines should you give to an asplenic individual?
|
- S. pneumonia
- H. influenzae - N. meningiditis |
|
Fxn: Catalase
|
Degrades H2O2 before it can be converted to microbicidal products by myeloperoxidase
|
|
What problems do people with chronic granulomatous disease face with catalase-positive organisms?
|
Have NADPH oxidase deficiency --> recurrent infections with Cat+ organisms b/c remaining H2O2 is degraded
|
|
Catalase+ organisms
|
- S. aureus
- Serratia - Pseudomonas - Actinomyces - Candida - E. coli (You need SSPACE for your CATs) |
|
How do vaccines with polysaccharide capsule antigens work?
|
Protein is conjugated to polysaccharide antigen to promote T-cell activation and subsequent class switching.
|
|
Why can't a polysaccharide antigen alone work as a vaccine?
|
It would not be recognized and presented by T-cells --> only IgM antibodies would be produced
|
|
What are the urease-positive bugs?
|
- Proteus
- Ureaplasma - Nocardia - Cryptococus - H. pylori - Klebsiella (PUNCH-K) |
|
What pigment does Actinomyces israelii produce?
|
Yellow "sulfur" granules (mass of filaments, formed in pus)
(ISRAEL has YELLOW SAND) |
|
What pigment does S. aureus produce?
|
Yellow pigment (aureus = gold)
|
|
What pigment does Pseudomonas aeruginosa produce?
|
blue-green pigment
(AERUGula is GREEN) |
|
What pigment does Serratia marcescens produce?
|
Red pigment
(RED MARASCHINO cherries) |
|
What is the purpose of virulence factors?
|
To promote evasion of host immune response
|
|
Protein A: primary organism, action, effect
|
- PO: S. aureus
- Action: Binds Fc portion of Ig - Effect: Prevents opsonization and phagocytosis |
|
IgA Protease: primary organisms, action, effect
|
- PO: S. pnuemoniae, H. influenzae type B, Neisseria (SHiN)
- Action: Cleaves IgA - Effect: Secreted to colonize respiratory mucosa |
|
M Protein: primary organism, action
|
- PO: Group A Streptococcus
- Action: Helps prevent phagocytosis |
|
Source: exo- vs. endotoxin
|
Exo: certain species of G+ and G-
Endo: Outer CM of G- |
|
Secretion from cell: exo- vs. endotoxin
|
Exo: Yes
Endo: No |
|
Chemistry: exo- vs. endotoxin
|
Exo: Polypeptide
Endo: LPS (structural part of bacteria; released when lysed) |
|
Location of genes: exo- vs. endotoxin
|
Exo: Plasmid or bacteriophage
Endo: Bacterial chromosome |
|
Toxicity: exo- vs. endotoxin
|
Exo: High (fatal dose = 1 ug)
Endo: Low (fatal dose = 100 ug) |
|
Clinical effects: exo- vs. endotoxin
|
Exo: Various
Endo: Fever, shock |
|
Mode of action: exo- vs. endotoxin
|
Exo: Various
Endo: Induces TNF and IL-1 |
|
Antigenicity: exo- vs. endotoxin
|
Exo: Induces high-titer antibodies (antitoxins)
Endo: Poorly antigenic |
|
Vaccines: exo- vs. endotoxin
|
Exo: Toxoids used as vaccines
Endo: No toxoids formed, no vaccine available |
|
Heat stability: exo- vs. endotoxin
|
Exo: Destroyed rapidly at 60C (NOT staphylococcal enterotoxin)
Endo: Stable at 100C for 1h |
|
Which bug's exotoxin is not destroyed rapidly at 60C?
|
Staphylococcus
|
|
Typical diseases: exo- vs. endotoxin
|
Exo: tetanus, botulism, diptheria
Endo: meningococcemia, sepsis by G- rods |
|
Bacteria that inhibit protein synthesis
|
- Cornybacterium diptheriae
- Pseudomonas aeruginosa - Shigella spp. - Enterohemorrhagic E. coli (EHEC), including O157:H7 |
|
Mechanism of action: C. diptheriae and P. aeruginosa
|
Inactivate elongation factor (EF-2)
|
|
Toxin: C. diptheriae
|
Diptheria toxin
|
|
Manifestation C. diptheriae
|
- Pharyngitis
- Pseudomembrane in throat |
|
Toxin: P. aeruginosa
|
Exotoxin A
|
|
Manifestation: P. aeruginosa
|
Host cell death
|
|
Mechanism of action: Shigella and EHEC
|
Inactivate 60S ribosome by cleaving rRNA
|
|
Toxin: Shigella
|
Shiga Toxin (ST)
|
|
Manifestation: Shigella
|
GI mucosal damage --> dysentery
ST enhances cytokine release --> HUS |
|
Toxin: EHEC
|
Shiga-like toxin (SLT)
|
|
Manifestation: EHEC
|
SLT enhances cytokine release --> HUS (but does not invade host cells)
|
|
Bacteria that increase fluid secretion
|
- Enterotoxigenic E.coli (ETEC)
- Yersinia enterocolitica - Bacillus anthracis - Vibrio cholerae |
|
What are the two types of toxins ETEC produce?
|
- Heat-LABILE toxin (LT)
- Heat-STABLE toxin (ST) |
|
Mech. of action: Heat-labile ETEC
|
Overactivates cAMP --> increased Cl- secretion in gut and H2O efflux
(LABILE in the AIR, stable on the ground) |
|
Manifestation: Heat-labile AND heat-stable ETEC
|
Watery diarrhea
|
|
Mech. of action: Heat-stable ETEC and Yersinia Enterocolitica
|
Overactivate cGMP --> decreased reabsorpbtion of NaCl and H2O in gut
(Labile in the air, STABLE on the GROUND) |
|
Manifestation: Yersinia enterocolitica
|
BLOODY diarrhea (Y. enterocolitica invades/destroys cells --> dysentery)
|
|
MoA: Bacillus anthracis
|
Mimics adenylate cyclase (increases cAMP)
|
|
Toxin: B. anthracis
|
Edema factor
|
|
Manifestation: B. anthracis
|
Likely responsible for characteristic edematous borders of black eschar in cutaneous anthrax
|
|
MoA: Vibrio cholerae
|
Permanently activating Gs --> overactivates adenylate cyclase (increases cAMP) --> increased Cl- secretion in gut, H2O efflux
|
|
Toxin: V. cholerae
|
Cholera toxin
|
|
Manifestation: V. cholerae
|
Volumnious rice-water diarrhea
|
|
Bacteria that inhibit phagocytic ability
|
Bordetella pertussis
|
|
MoA: Bordetella pertussis
|
Disables Gi -> impairs phagocytosis to permit survival of microbe, overactivates adenylate cyclase (inc. cAMP)
|
|
Toxin: B. pertussis
|
Pertussis toxin
|
|
Manifestation: B. pertussis
|
WHOPPING COUGH
- Child coughs and "whoops" on inspiration - Toxin may not actually be cause of cough |
|
Bacteria that inhibit release of neurotransmitter
|
- Clostridium tetani
- Clostridium botulinum |
|
MoA: C. tetani and C. botulinum
|
Cleave SNARE protein required for NT release
|
|
Toxin: C. tetani
|
Tetanospasmin
|
|
Toxin: C. botulinum
|
Botulinum toxin
|
|
Manifestation: C. tetani
|
- Muscle rigidity, lockjaw
- Toxin prevents release of INHIBITORY NT's (GABA and Glycine) in spinal cord |
|
Manifestation: C. botulinum
|
- Flaccid paralysis, floppy baby
- Toxin prevents release of STIMULATORY signals (ACh) at musculoskeletal junction |
|
Bacteria that lyse cell membranes
|
- Clostridium perfringens
- Streptococcus pyogenes |
|
MoA: C. perfringens
|
Phospholipase --> degrades tissues, cell membranes
|
|
MoA: S. pyogenes
|
Protein that degrades cell membrane
|
|
Toxin: C. perfringens
|
Alpha toxin
|
|
Toxin: S. pyogenes
|
- Streptolysin O (SLO)
- Exotoxin A (superantigen) |
|
Manifestation: C. perfringens
|
Degradation of phospholipids:
- myonecrosis (gas gangrene) - hemolysis ('double zone' of hemolysis on blood agar) |
|
Manifestation: S. pyogenes (SLO)
|
- 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) |
|
Bacteria with Superantigens that cause shock
|
- Streptococcus pyogenes (Exotoxin A)
- Staphylococcus aureus (Toxic shock syndrome toxin, TSST-1) |
|
Manifestation: toxic-shock syndrome
|
- Fever
- Rash - Shock |
|
Manifestation: S. pyogenes (ExoA)
|
Toxic-shock syndrome
|
|
Manifestation: S. aureus
|
- Toxic-shock syndrome
- Other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin) |
|
MoA: ADP-ribosylating toxins
|
- B-component binds to host cell receptor --> endocytosis
- A-component attaches ADP-ribosyl --> disrupts host cell proteins (active) |
|
Examples: ADP-ribosylating toxins
|
- Diptheria toxin (C. diptheriae)
- Exotoxin A (P. aeruginosa) - Heat-labile toxin (EHEC) - Cholera toxin (V. cholerae) - Pertussis toxin (B. pertussis) |
|
What is an endotoxin?
|
LPS found in OM of G- bacteria
(N-dotoxin is an intergral part of gram-Negative OM. heat STABLE.) |
|
Three effects of endotoxin
|
1) Activates macrophages
2) Activates complement (alternate pathway) 3) Activates hageman factor |
|
What do activated macrophages produce in response to endotoxin? What is the effect?
|
- IL-1 --> fever
- TNF --> fever, hemorrhagic tissue necrosis - Nitric Oxide --> hypotension (shock) |
|
What complement components are activated in the alternate pathway in response to endotoxin? Effect?
|
- C3a --> hypotension, edema
- C5a --> Neutrophil chemotaxis |
|
What happens when Hageman factor is activated in response to endoxtoxin? Effect?
|
Coagulation cascade --> DIC
|
|
Bacterial Growth Curve:
1) X-axis 2) Y-axis |
X) time
Y) Number of viable bacteria |
|
Bacterial Growth Curve: Phases
|
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 |
|
At what phase on the BGC do penicillins and cephalosporins act?
|
Exponential/log phase. P/C act here as peptidoglycan is being made.
|
|
At what phase are spores formed in some bacteria?
|
Stationary phase
|
|
Transformation (definition, bugs that do it)
|
- Ability to take up DNA from environment (competence). Any DNA can be used.
- S. pneumoniae, H. influenzae type B, Neisseria (SHiN) |
|
Conjugation (F+ x F-)
|
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. |
|
Conjugation (Hfr x F-)
|
Hfr cell: F+ plasmid incorporated into bac chromosomal DNA
Transfer of plasmid and chromosomal genes |
|
Transposition
|
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 |
|
Generalized transduction
|
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 |
|
Specialized transduction
|
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 |
|
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) |
|
G+ --> Branching filaments --> Anaerobe, not acid fast
|
Actinomyces
|
|
G+ --> Branching filaments --> Aerobe, acid fast
|
Nocardia
|
|
G+ --> Cocci --> Catalase + --> Coagulase +
|
S. aureus
|
|
G+ --> Cocci --> Catalase (+) --> Coagulase (-) --> Novobiocin sensitive
|
S. epidermidis
|
|
G+ --> Cocci --> Catalase (+) --> Coagulase (-) --> Novobiocin resistant
|
S. saphrophyticus
|
|
G+ --> Cocci --> Catalase (-) --> Partial hemolysis (green, alpha):
- Quellung(+) - Bile soluble (does not grow in bile) - Optochin SENSITIVE |
S. pneumoniae
|
|
G+ --> Cocci --> Catalase (-) --> Partial hemolysis (green, alpha):
- Quellung(-) - Bile insoluble - Optochin INSENSITIVE |
S. viridans
|
|
G+ --> Cocci --> Catalase (-) --> Complete hemolysis (clear, beta): Bacitracin SENSITIVE
|
S. pyogenes (Group A)
|
|
G+ --> Cocci --> Catalase (-) --> Complete hemolysis (clear, beta): Bacitracin INSENSITIVE
|
S. agalacticae (Group B)
|
|
G+ --> Cocci --> Catalase (-) --> No hemolysis (gamma): enterococcus
|
E. faecalis
|
|
G+ --> Cocci --> Catalase (-) --> No hemolysis (gamma): Non-enterococcus, growth in bile, NOT 6.5% NaCl
|
S. bovis
|
|
Novobiocin susceptibility
|
Staphylococci
Resistant: Saphrophyticus Sensitive: Epidermidis (On the office's STAPH retreat, there was NO StRES) |
|
Optochin susceptibility
|
Streptococci
Resistant: Viridans Sensitive: Pneumoniae (OVRPS) |
|
Bacitracin susceptibility
|
Streptococci
Resistant: group B strep Sensitive: group A strep (B-BRAS) |
|
alpha-hemolytic bacteria
|
Form GREEN RING around colonies on blood agar
- S. pneumoniae (cat-, op-sens) - S. viridans (cat-, op-res) |
|
beta-hemolytic bacteria
|
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) |
|
S. aureus: action of Protein A
|
Binds Fc-IgG --> inhibits complement fixation and phagocytosis
|
|
S. aureus: how to ID microscopically
|
Gram-positive cocci in clusters
|
|
S. aureus: effects
|
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 |
|
Action of TSST
|
Superantigen that binds to MHC-II and T-cell receptor --> polyclonal T-cell activation
|
|
Cause of S. aureus induced food poisoning
|
Ingestion of preformed toxin (enterotoxins)
|
|
Staphylococcus epidermidis: action, effects
|
Produces adherent biofilms --> infects prosthetic devices and IV catheters
- Component of normal skin flora - Contaminates blood cultures |
|
S. pneumoniae: effects
|
MOPS (Most OPtochin Sensitive)
- Meningitis - Otitis media - Pneumonia - Sinusitis |
|
S. pneumoniae: common facts (microscopic ID, toxin) and associations
|
- Lancet-shaped, G+ diplococci
- Encapsulated - IgA Protease - Associated with: rusty sputum, sepsis (sickle cell anemia), splenectomy |
|
S. viridans: effects
|
- Dental carries (S. mutans)
- Subacute bacterial endocarditis at damaged valves (S. sanguis) (Sanguis = blood...lots of blood in the heart) |
|
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 |