Staphylococci & Streptococci Flashcards
Describe the virulence factors of staph
Produce toxins and induce pyogenic inflammation.
Virulence factors:
Staphyloxanthin- inactivates microbicidal effect of superoxidases and other ROS of neutrophils.
Coagulase- causes clotting (prothbn–>thrbn = fibrinogen–>fibrin); walling off infection from immune system
Hemolysins- lyse RBCs and use Fe
Protein A- binds IgG and prevents complement activation.
Teichoic acids- mediate adherence to mucosal cells.
Polysaccharide capsule- adherence and resist phagocytosis
Peptidoglycan- stimulates MP to produce cytokines, activates complement/coag. cascade.
Alpha toxin- pokes holes in host cells. Causes necrosis and hemolysis.
Panton Valentine Leukocidin (PVL)- membrane damaging hemolytic toxin & leukocyte destruction. (Found only in MRSA)
Gamma-toxin/leukotoxin- Lyses phagocytes/RBCs
Describe scalded skin syndrome
Toxin mediated. Looks like a full body sun burn.
Virulence factors: Exfoliatin/Exfoliative toxins A & B- cleave desmogleins in desmosomes.
Very common in newborns.
Febrile, irritable, diffuse blanching erythema, w/ blisters bullae
Exudate, dehydration, electrolyte imbalance.
Mucous membranes spared
No scarring bc only epidermal involvement.
Recovery 10 days
Describe the pathogenesis & clinical presentation of S. aureus food poisoning.
Toxin mediated.
Enterotoxin A: causes vomiting & non-bloody diarrhea.
Vomiting caused by cytokine storm that actives enteric nervous system that tells vomit center of brain to go to town.
Heat resistant, not inactivated by brief cooking.
Resistant to stomach acid/enzymes
Incubation: 1-8 hrs
Describe bullous impetigo of S. aureus.
Caused by exfoliative toxin.
Young children.
Flaccid bullae w/ clear, yellow fluid, later becoming dark, more turbid.
Trunk freq. affected.
Describe Toxic Shock Syndrome of Staph.
Toxin mediated/superantigen. Massive EPIdermal peeling.
Tampons, nasal packing (epistaxis), post-op infections, other infections.
TSST produced by S. aureus, then enters blood –> toxemia.
Blood cultures commonly negative.
Describe tx of S. aureus infection in MSSA & MRSA.
MSSA: Nafcillin/oxacillin
Cefazolin, ceftriaxone, cefepime, ceftaroline (advanced gen. cephalosporin)
Vanc
Augmentin (Amox/Clav acid) for mild infections
MRSA: Vanc Daptomycin Linezolid Ceftaroline Mild inf. - Bactrim, clinda, doxy
Vanc resistance: Dapto, linezolid, ceftaroline
How does Staph acquire resistance to penicillins/vanc?
Chances in PBP structure for pen
Unusually thick cell wall for vanc and subing D-lactate for D-alanine in peptidoglycan.
Describe Tx of TSS.
Supportive- get BP up (fluids, pressors)
Surgical- clean shit up.
Abx- Vanc/oxacillin + clindamycin (suppresses protein [toxin] synthesis)
Describe the lab tests to confirm S. aureus.
Gram stain: pos cocci in grape-like clusters Catalase: + Coagulase: + Beta hemolytic Ferments mannitol
Describe the lab tests to confirm S. epidermidis
Gram stain: pos cocci in clusters Catalase: + Coagulase: NEG Non-hemolytic Urease (pink tube): POS Does NOT ferment mannitol Novobiocin SENSITIVE * differentiates S. epi from S. sap
Describe how S. epi gets into you and hurts your feelings.
Biofilms on invasive instruments. Biofilms protect in once it is in your body from immune response. The biofilm is its most important virulence factor
Tx of S. epi
** Vanc ** assume S. epi is VRSE
Rifampin + Gentamycin for prosthetic valve endocarditis.
MRSE same mech of resistance as MRSA.
Describe the lab tests to confirm S. saprophyticus
Cat + Coag - Urease + No mannitol fermentation Novobiocin RESISTANT * differentiates S. epi from S. sap
Describe the pathogenesis and Tx of S. saprophyticus
2nd most common cause of UTIs in women. Most after sex.
Tx- Bactrim (trimethoprim/sulfamethoxazole) or Cipro
Describe the morphology and differential labs of the Strep genus in general
GPC in chains or pairs
Catalase neg
Hemolysis is important to distinguish
Tell me about the species of Strep that is the commonest cause of pharyngitis.
S. pyogenes (Group A Strep) is a GPC that forms chains Commonly causes pharyngitis and also skin infections Also causes: TTS Nec Fasc Scarlet Fever Puerperal sepsis Endometritis Rheumatic fever glomerulonephritis
Describe the virulence factors of Group A Strep (GAS- S. pyogenes)
M protein- Antiphagocytic
Polysaccharide capsule- antiphagocytic
Hyaluronidase - allows infection to spread thru tissue
Streptokinase- breaks down clots (science is not sure why this matters)
DNAse- for breaking out of NETs
C5a peptidase- prevents complement activation
Strep chemokine protease- Degrades IL-8 that attracts neutrophils to infection site.
Streptolysin O- hemolytic but O2 labile.
Streptolysin S- hemolytic in presence of O2.
Describe how to Dx and treat GAS.
Rapid Strep antigen (high spec. low sens)
If rapid neg but high suspicion, do culture.
Tx:
Oral penicillin V, amoxicillin, cephalexin (1st gen ceph)
Penicillin allergy? Hit them with macrolides. (azith, clarith, clinda [lincosamide])
Describe presenting features of Nec Fasc
Pain out of proportion to exam
Associated with M proteins type 1 & 3
Rapid progression over several days
Affected area erythematous, shiny, warm, exquisitely tender
Skin color change over several days
Crepitus felt sometimes
Advanced infection: fever tachycardia, systemic toxicity
IT IS A SURGICAL EMERGENCY
Discuss the toxins of GAS
Erythrogenic toxin- responsible for rash of Scarlett Fever.
Pyrogenic exotoxin A: Causes most cases of TSS.
Exotoxin B: protease that rapidly destroys tissue (nec fasc)
How do you Tx Strep TSS
Penicillin + clindamycin and surgical debridement for nec fasc
Discuss Scarlet fever.
Children ** Erythrogenic toxin ** Sore throat + later *erythema* (hint to toxin resp.) on head/neck Skin feels sand-papery Rash desquamates after several days STRAWBERRY TONGUE Usually associated w/ pharyngitis
Describe Post-Strep glomerulonephritis.
Caused by nephritogenic strains of GAS
Ag-Ab complexes on glomerular basement membrane
HTN, facial edema, dark urine due to presence of RBCs (nephritic)
Most pts recover completely
Describe Acute Rheumatic fever.
2 weeks after untreated GAS pharyngitis
Abs against GAS proteins cross-react with host proteins
Jones criteria:
Joint pain
Cardiac Probs
Nodules (subcutaneous)
Erythema
Sydenham chorea- abrupt, involuntary movements (neuropathy)
Tx- full course of Abx to eradicate remaining bacteria THEN intramuscular Abx monthly for years
Describe lab and clinical features of Group B strep.
Also describe tx.
In the Lab: Strep. agalactiae B hemolytic (narrowly) Hydrolyzes hippurate Bacitracin resistant (GAS is sensitive) CAMP + Polysaccharide capsule is antiphagocytic
Clinical:
Found in female genital tract & colon
Infection acquired in utero or during birth
Causes neonatal PNA, Sepsis, meningitis
Tx: Penicillin/ampicillin Vanc if allergic. Screen pregnant women
Talk about Group D Strep and its Tx
Group D Strep is the poop Strep. S. faecalis/faecium Grows in your butt. Treat with PCN/Vanc + aminoglycoside. Vanc resistant? Daptomycin or linezolid
Tell me about Viridans group Strep.
Grows in mouth/butt.
Sticks to heart valves.
Causes brain, heart, liver abscesses
Tx: PCN, ceftriaxone. Intermediate response w/ endocarditis? add Gentamycin
How do you distinguish between S. epi and S. saprophyticus in the lab?
Novobiocin sensitivity.
S. epi is novo sensitive. S. sap is not sensitive.
What is the main toxicity of Vanc?
Nephrotoxicity! Pts will go into renal failure from Vanc. Substitute Linezolid or daptomycin
Hemolysis by Strep occurs due to which toxins?
Streptolysin O and S
O- (O)xygen labile
S- Oxygen (S)table
What is special about Streptolysin S that makes it difficult to find in serology?
It is not immunogenic, so you would not see any Abs to Streptolysin S.
Name the 2 Strep VFs that help it to avoid phagocytosis.
M Protein
Polysaccharide capsule
A pt has a nasty ass mouth. They get some invasive dental work done. They present to the ED with a brain abscess. What organisms are likely responsible for the brain abscess?
Strep. viridans & Peptostreptococcus
“think mixed infection” - Sara Cross, M.D.
Your pt suffered from infection with S. bovis. Echo showed vegetation on his mitral valve. You treated him and he improved with time. What do you need to do when he gets better?
Colonoscopy.
S. bovis has a strong association w/ colon cancer.
What is a Janeway lesion?
Painless micro abscesses caused by septic emboli. Found on palms of hands and soles of feet.
What is an Osler’s node?
These are painful violaceous nodules found on pulp of fingers & toes. These are due to immune complex deposits
What are Roth Spots?
Exudative, edematous, hemorrhagic lesions of retina.
Describe the mechanism of resistance of Vanc Intermeidate Staph aureus (VISA).
Thickened cell wall to prevent abx penetration
Describe the mech of resistance of Vanc resistant endocarditis.
Substitution of D-Lactate for D-Ala in peptidoglycan
Which strep group is known to cause sepsis, meningitis, and PNA in neonates? How do you destinguish it from the other Streps?
GBS- Strep agalactiae
Hydrolyzes hippurate & is Bacitracin resistant
babies love stuffed hippos and bash’d racins
What is the most common cause of subacute bacterial endocarditis?
Viridans group strep
Subacute- sicker longer. Indolent illness. Fevers, night sweats, weight loss for weeks before presentation.
Acute endocarditis due to S. aureus. Present emergently, immediately.
Both S. viridans & S. pneumo are a-hemolytic. How do you distinguish the two in lab?
S. viridans is Optochin resistant, and displays resistance to lysis by bile.
