Bugs and Drugs Flashcards
Streptococcus pneumonia (pneumococcus) is the most common cause of what 4 diseases?
Pneumococcus MOPS pneumonic 1) Meningitis 2) Otitis Media (in children) 3) Pneumonia 4 Sinusitis
- “rusty sputum”
- sepsis in sickle cell anemia/asplenia
S. Pneumoniae Gram stain? capsule? Shape? Catalase +/- ? Hemolysis? Optochin/Bacitracin sensitive/resistant?
S. Pneumoniae Gram positive encapsulated cocci catalase negative alpha (partial/green) hemolytic optochin sensitive (differentiate from S. Viridans)
OVRPS pneumonic (Optochin-Viridans is Resistant; Pneumoniae is Sensitive)
Viridans streptococci Gram stain? capsule? shape? catalase +/- Hemolysis? Optochin/Bacitracin sensitive/resistant?
Viridans streptococci Gram positive nonencapsulated cocci catalase negative alpha hemolytic optochin resistant (differentiate from S. Pneumoniae)
OVRPS pneumonic (Optochin-Viridans is Resistant; Pneumoniae is Sensitive)
Also, bacitracin resistant (vs. S. Pyogenes which is succeptible to bacitracin.
S. Viridans
Colonization locations (normally and pathologically?)
Disease?
S. Viridans is part of the normal flora of the mouth. S. Mutans causes dental carries.
Also (S. Sanguis) causes subacute bacterial endocarditis of previously damaged valves. Classically after dental procedures.
S. Pyogenes (Group A Strep)
Causes what diseases?
Pyogenic- pharyngitis (strep throat), cellulitis, impetigo, endocarditis (uncommon)
Toxigenic- Scarlet fever, Toxic Shock-like syndrome, necrotizing fasciitis
Immunologic- Rheumatic fever, acute glomerulonephritis
Streptococcus Bovis (Nonenterococcus Gama hemolysis) If found in blood culture or as cause of subacute endocarditis, what do you need to check for?
S. Bovis bacteremia highly associated with GI malignancy (it is a normal comensal flora of gut)
Major virulance factor of Group A strep?
Group A strep = S. Pyogenes
M protein is the major virulance factor (prevents phagocytosis). Antibody to M protein causes resistance to organism. But antibodies to different M (3 and 18) proteins can lead to rheumatic fever (Always pharynx infection) or autoimmune complex deposition -> glomerulonephritis (PSGN, more commonly skin but can be pharynx)
N terminus is the variable region that Ab’s are created for.
Over 80 M protein serotypes
Streptolysin O?
Streptolysin O is virulence factor of S. Pyogenes. Binds to lipid/cholesterol -> polymerizes -> forms a pore -> hemolysis.
Antibody increases to Streptolysin O post infection (especially of pharynx)
ASO titer
Toxic Shock syndrome
A superantigen produced by Staph A. and Strep Pyogenes. The toxin binds MHC-II and TCR indiscriminately resulting in polyclonal T-cell activation -> cytokines/immune response. Fever, vomiting, rash, desquamation, shock, end organ failure.
Acute Rheumatic fever typically presents how long after S. Pyogenes infection?
PSGN?
ARF = 3-6 weeks (prevented by treatment)
PSGN = 2-4 wks (probably not prevented by treatment)
Group B Strep (S. Agalactiae)
Gram, catalase, hemolysis, differentiation
Colonize where?
Disease whom?
Gram + cocci, catalase -, Beta hemolysis, Bacitracin resistant (vs group A sensitive, B-BRAS)
Group B for Babies
Colonize 25% of women vagina
Causes pneumonia, meningitis, sepsis in babies
Tx; Prophylactic with PCN antibiotics prior to delivery.
Enterococci (Group D strep)
Gram stain, catalase, oxygen use?
Colonize where? Infections?
Hemolysis?
Normal colonic flora. Gram positive, Catalase negative, facultative anaerobe.
UTI, Biliary tract, subacute endocarditis, 4% meningitis
VRE (nosocomial)
Hemolysis (none/gamma)
Staph Aureus Gram Stain? Shape? chains/clusters? Catalase +/- Coagulase +/-
Gram Positive catalase positive Cocci in clusters
Coagulase positive
Differentiate S. epidermidis from S. saprophyticus
both these staphs are catalase +, coagulase negative
S. epidermidis is sensitive to novobiocin
S. Saprophyticus is Resistant
At staph retreat. NO StRESs
Novobiocin - saprophyticus is resistant, epidermitis is sensitive
Staphylococcus aureus
Virulence factors?
All in the Cell Wall
Protein A is the major virulence factor for S. aureus. Binds Fc-IgG, which inhibits complement fixation and phagocytosis.
clumping factor- (like coagulase) but binds fibrinogen to cell and clumps bacteria together
techoic acid- attach to human cells
Staphylococcus aureus
Colonization
Diseases?
Colonize anterior nares, some skin/nose/vagina
Inflammatory- skin infections, organ abscess, pneumonia, osteomyelitis, acute endocarditis
Toxin mediated-
1) Toxic Shock syndrome (TSST-1, superantigen, stimulates broad, nonspecific immune response)–> IL1,2,interferon, ect.
2) Scalded skin syndrome (exfoliative toxin A/B slough at desmosomes of granular skin layer),
3) rapid food poisoning (preformed enterotoxin ingestion)
-MRSA- resistant to B-lactams bc altered pcn binding protein
Staph epidermidis
Colonization?
Disease?
Normal skin flora. Often contaminates blood cultures. Can infect prosthetic devices and IV caths by making adherent biofilms
What does coagulase do?
It coagulates fibrinogen/fibrin. Can help microorginism form abscess
Macconkey agar
when negative?
Negative with catalase +
MacConkey is selective for gram negative organisms because GPs can’t grow in the presence of bile salts.
Gram negative organisms that ferment lactose will produce acid which lowers the pH and causes the medium to turn red.
GNRs that can’t ferment lactose, ferment peptone which creates ammonia –> raising pH. This produces clear colonies.
Staph Aureus resistance
Has plasmids, mostly transfers by transduction (bacteriophages)
PCN -> MRSA -> VISA/VRSA
Also 15% resistant clindamycin
Job’s Syndrome
Hyper IgE, poor neutrophil chemotaxis,
afflicted by boils (cold abscesses), like staph A.
FATED Mnemonic Facies (coarse) Abscesses (cold) Teeth (retain primary "baby" teeth) E -> Hyper IgE Dermatologic problems (eczema)
Catalase Positive Organisms
SLAP NECKS for catalase pos orgs.
S – S. aureus, L – Listeria, A – Aspergillus, P – Pseudomonas, N – Nocardia, E – E. coli, C – Candida, K – Klebsiella, S – Serratia
Encapsulated Bacteria
+
Vaccines for asplenic patients
SHiNE SKiS mnemonic for encapsulated bacteria – S. pneumonia, H. influenza type B, N. meningitides, E. coli, Salmonella, K. pneumonia, Group B Strep
+ vaccines
S. Pneumoniae, H. Flu, N. Meningitidis
Endocarditis
Acute organisms?
Subacute organisms?
S/S?
Acute Endocarditis usually: S. Aureus, B-hemolytic strep, pneumococcus
Subacute: Viridians strep > Enterococci > CoNS (coag negative staph, HACEK organisms
Community Prevalence: Nongroup A strep (40%) > Staph A. (28%) > Enterococci > others
Hospital Acquired: Staph A. (53%) > Enterococci (13%)
S/S Fever, chills, night sweats, myalgia, heart murmers, anemia, ESR, CRP, CHF (develops most often from valvular dysfunction), Osler’s Nodes (painful red immune complex depositions causing inflammation), splinter hemorrhage (vertical bleeding under nails), Roth’s spots (retinal hemorrhage)
FROM JANE Fever Roth's Spots (Retinal) Osler's Nodes (ouch) Murmur
Janeway Lesion (on palms and soles of feet)
Anemia
Night sweats
ESR increased/Emboli
Most common isolated nosocomial bacterial infection
2nd?
1) S. Aureus
2) Enterococcus (E. Faecalis and faecium predominantly)
Difficulty treating enterococci?
What two common Enterococci?
Resistances?
Prevalence Hosp. Aq. infections: E. Faecalis > E. faecium, but E. faecium is increasing
Both are resistant to PCN G
E. faecium is by far the most resistant and challenging enterococcal species to treat; indeed,
>80% of E. faecium resistant to vancomycin
>90% are resistant to ampicillin (historically the most effective β-lactam drug against enterococci)
Resistance to vancomycin and ampicillin in E. faecalis isolates is much less common (∼7% and ∼4%, respectively).
Factors increasing VRE colonization
The most important factors associated with VRE colonization and persistence in the gut include
prolonged hospitalization; long courses of antibiotic therapy; hospitalization in long-term-care facilities, surgical units, and/or intensive care units;
organ transplantation; renal failure (particularly in patients undergoing hemodialysis) and/or diabetes
VRE found on many inanimate objects in hospital. VRE can survive exposure to heat and certain disinfectants
Most common Bacterial causes of central line associated bacteremia
1st?
2nd?
1) S. Epidermidis (Coag neg. Staph)
2) Enterococci
Bacteria found in the intestine (7+4)
Gram Negative
Shigella
Salmonella
E. Coli
Yersinia
Campylobacter
Vibrio
Helicobacter
Gram positive
E. faecalis/faecium
Listeria
Clostridium
Enterobacteriaceae Gram stain? Morphology? oxidase +/-? ferment? Bugs with main causes of enteric infection?
Gram negative oxidase negative bacilli
All ferment glucose
Salmonella, Shigella, E. coli, Yersinia
“Shit Stink’s EspeCially Yours”
***campylobacter is distantly related and is top 3 cause of bacterial diarrhea
**others in enterbacteriaceae family include Klebsiella, Serratia, enterobacter, citrobacter, proteus….
Antigenic structures (3) of enteric bacteria (enterobacteriaceae)
All Gram negatives have LPS: consists of Lipid A, core polysaccharides, and O antigens (Lipid A portion is toxic). O for oligosacharide!!
H antigen (flagellar protein): Not all enterics have it
K antigen (polysaccharide capsule. Not all enterics have it, usually associated with increased virulence especially with bacteremias.
Vibrio Cholera S/S? mechanism of S/S? transmission/reservoir? Infectious dose? Treatment?
Abrupt onset diarrhea, abdominal cramps, some vomit. 15-20L/day diarrhea, High mortality if untreated.
Mechanism = Enterotoxin (A-B) B subunit binds cell surface receptor and injects subunit A. A ultimately constitutively activates Adenylyl cyclase which leads to cAMP concentrations and Cl- secretion and decreased Na+ absorption. Cytotonic.
Transmitted fecal/oral, reservoir aquatic environments
High infectious dose: 10/\8
Treatment:
1) Fluid replacement
2) Antibiotics (shorten course)
* *requires phage to transfer enterotoxin before virulent.
E. Coli Stain? shape? Oxygen? capsule? Colonize? Strains? Why? COMMON TO ALL Virulence factors?
Gram negative encapsulated bacilli, facultative anaerobe,
Colonize as normal small intestine flora: most abundant fac. anaerobe/GNBacilli in feces.
EIEC, ETEC, EPEC, EHEC (plasmid/phage differences)
general Virulence factors:
Fimbriae (adhesins): allow attachment to overcome peristalsis-> cystitis, pyelonephritis.
K capsule: virulence factor, antigenic -> pneumonia, neonatal meningitis
LPS - septic shock
ETEC (enterotoxigenic)
S/S
mechanism
Tx
S/S travelers diarrhea (70%), watery/secretory,
Toxin-noninvasive:
- Heat labile: similar to cholera (same mechanism cAMP by Ad. Cyclase)
- Heat stable: peptide toxin activates Guanylate cyclase -> cGMP -> fluid secretion
Tx; Fluid replacement. Bismuth. Generally don’t recommend antibiotics.
EPEC (enteropathogenic)
S/S
mechanism
Tx
common Pediatric and Persistent (can be weeks)
S/S watery diarrhea
Mechanism: Small intestine. noninvasive. no toxin. Adhere to enterocyte, TYPE III secretion, attach and efface/flatten villi -> poor absorption -> osmotic diarrhea
Tx; fluid replacement, rapid response to antibiotics
EHEC (O157:H7 most common) S/S mechanism Transmission Tx
Noninvasive but cytotoxic
Watery progress to Bloody diarrhea, hemorrhagic colitis, fever in severe cases, HUS (thrombocytopenia, hemolytic anemia, renal failure)
Mechanism: Shiga-like toxin. Stx-I and II. Encoded by phage. STx binds sphingolipid. Stx-I subunit A binds rRNA and cleaves (60s subunit) -> inhibit protein synthesis -> cell death. Stx-II subunit A inactivates Bcl-2 –> Apoptosis.
+ Otherwise also attach/efface enterocytes.
Transmission: Classically ground beef (cattle as reservoir), also fresh produce through manure runoff (spinach/lettuce/sprouts ect.)
Tx; Supportive. No proven benefit of antibiotics.
**Fecal leukocytes uncommon
LAB: does not ferment sorbitol, the rest of E. Coli do.
