22: staphylococci - jonathan Flashcards
What bacteria is the major cause of hospital bacteremias?
Staphylococcus aureus and Staph Epidermis
What are the major causes and concerns with hospital Staph infections?
IV catheters or other implanted devices
Resistance to Methicillin and even Vancomycin
High mortality and high costs
What are the lab Dx features that S. aureus, S. epidermis, and S. saprophyticus share?
All... G+ grape clusters Catalase Faculative anaerobes, although S. saprophyticus is slow anaerobic growth Teichoic acid
What color are the colonies for S. aureus, S. epidermis, and S. saprophyticus?
S. aureus is yellow
S. epidermis and S. saprophyticus is white
In terms of catalase, compare Staph from Strep.
Staph = catalase Strep = NO catalase
Which Staph is resistant to novobiocin?
S. saprophyticus
List the many positive tests for S. aureus that are not positive for S. epidermis and S. saprophyticus.
Coagulase Mannitol DNase hymolysis Protein A Phage receptor
Staph aureus epidemiology…
On what tissues is it normally found?
What patients are more susceptible?
Skin, mucous membranes, and nose
Diabetics, drug addicts, immunocompromised patients, and those with implanted devices.
How is S. aureus strains determined during outbreaks?
Doubtful we need to know the details
Serology Phage sensitivity/Phage typing DNA fingerprinting Ribotyping (rRNA) DNA of Protein A and Coagulase
T/F Staph aureus is pathogenic because it is an INVASIVE disease, rather than an exotoxin producing bacteria.
False.
S. aureus produces toxin-mediated diseases and invasive diseases.
What is the pathogenesis of S. aureus as a toxin-mediating bacteria.
bacterial colonization (food, tampons, vasculature, skin) and production of the toxin. Toxin can affect areas anywhere in the body, not just at the site of colonization
How does S. aureus contribute to colonization of vasculature and/or skin?
What is the tampon-related infection called?
Vasculature: S. aureus contains fibrinogen and fibrinogen receptors
Skin: S. aureus contains exfoliatins that bind to damaged skin (wound sites)
Tampon: Toxic Shock Syndrome toxin
As an invasive bacteria, what is the method of adhesion and invasion?
Lots of adhesive molecules that bind to host membranes (fibrinogen, fibronectin, collagen, platelets)
Bind to membranes, colonize, secrete toxins, and evade host defenses.
What are the notable toxins and enzymes through which S. aureus causes damage.
1) Alpha toxin: lyses host cell membrans
2) Coagulase: forms clot in human plasma
These were also mentioned…
Leukocidins: lyse leukocytes
Proteases
Staphylokinase: lysis of blood clot or fibrin
Hyaluronidase: disovles hyaluronic acid
Lipase: dissolves lipids and lipoproteins
What are the methods that S. aureus uses to evade host defenses?
1) Protein A: binds the “wrong end” of IgG
2) enterotoxins A-E, G, H, I
Protein A is a B-cell superantigen
The enterotoxins are T-cell superantigens
Also mentioned…
Capsule is antiphagocytic
Eap (Map) is a surface protein that impairs neutrophils
Note: S. aureus can be contained or become systemic. If it is systemic, it can affect any organ system.
Note: S. aureus can be contained or become systemic. If it is systemic, it can affect any organ system.
What are the three toxin-mediated diseases caused by S. aureus?
1) Food poisoning
2) Toxic Shock Syndrome (TSS)
3) Staphylococcal Scalded Skin Syndrome (SSSS)
What are the three toxin-mediated diseases caused by S. aureus?
What are the toxins in general?
For which is colonization necessary?
1) Food poisoning (by enterotoxin some are superantigens) colonization is NOT required. Toxin can cause illness.
2) Toxic Shock Syndrome (TSS) (TSST-1 supersuperantigen) Colonization REQUIRED
3) Staphylococcal Scalded Skin Syndrome (SSSS) by exfoliatins A and B. Infection site does not have to be the site of toxin action
Are food-poisoning enterotoxins secreted by S. aureus heat stable? To what temperature?
Heat stable.
Resists boiling.
What do the cytokines do the superantigens of the enterotoxin or TSST-1 elicit?
IL-1
IL-2
TNF
Yada Yada What are the clinical syndromes of food poisoning by S. aureus?
Nausea, vomiting, non-bloody diarrhea
Note: these are specifically caused by the T-cell superantigen.
What are the clincial syndromes associated with toxic shock syndrome TSS?
Fever, rash, desquamation of palms and soles.
Hypotension and shock.
What are the toxins that produce Staph Scalded Skin Syndrome?
Are they in the main genome or a plasmid?
Exfoliatins A and B
Plasmid
Detail: What strain of S. aureus contain exfoliatins A and B?
phage group I
What patient population does S. aureus SSSS usually affect?
What are the symptoms
infants.
Erythematous skin followed by exfoliation
Why are antibiotics not always helpful with S. aureus toxin-mediated diseases?
Immunological effects due to the superantigen are already in effect before symptoms develop.
What distinguishes S. aureus “invasive disease” from an toxin-mediated disease in terms of localization and presentation.
Suppuration and abscess formation according to anatomic locations
There is a huge list of invasive disease examples by S. aureus on page R-4 and R-5. There is only one example that is in bold. What is it?
Catheter site infections
What is the Tx for S. aureus abscesses…
Name 1 physical treatment
Name 3-4 antibiotics
Name antibiotic combo for tolerant S. aureus
Abscesses need to be drained
Semisynthetic penicillin: Dicloxacillin (oral) or Oxacillin (IV)
Vancomycin is a last resort (methicillin resistance)
Combo with Rifampin and/or Gentamicin
Prevention of S. aureus (Just general stuff. Nothing noteworthy)
handwashing
judicious use of antibiotics
intranasal mupirocin, when necessary
What do you need to know about the bacteriology of S. epidermidis?
Gram stain and other distinctive features…
Coagulase negative (S. epidermidis and S. saprophyticus only)
Gram +
Staphylococci with white colonies
Catalase + (distinguishes staph from strep)
Sensitive to NOVOBIOCIN
Detail: S. epidermidis and …
blood agar?
Mannitol?
Little hemolysis on blood agar
Does NOT ferment mannitol
Epidemiology of S. epidermidis... Colonizes on what tissue? How opportunistic? Adheres to what? Who is susceptible?
Normal skin flora
Very oppotunistic that adheres to medical implants very efficiently
Neonates, patients in renal failure, immunocompromised patients
Pathogenesis of Staphylococcus epidermidis…
Nothing exciting here. Just wing it.
colonizes prosthetics, produces biofilms, there is a carbohydrate that mediates biofilm
poorly misunderstood
What are the clinical syndromes of Staphylococcus…
How does it compare in intensity with S. aureus?
What should you suspect if the patient is symptom free but is blood positive for S. epidermidis?
Low grade fever, pain, and discomfort.
Less severe than S. aureus
If symptom negative, but blood positive, suspect skin flora contamination
What is Tx for Staphylococcus epidermidis?
1) remove implant
2) Vancomycin
3) possible combo with Rifampin and/or Gentamicin
Interesting. Infection seems more mild, but we whip out the big guns for antibiotics.
Bacteriology of Staphylococcus saprophyticus…
gram stain and distinctive features.
G +
Coagulase negative (S. epidermidis and saprophyticus are neg. S. aureus is positive)
Catalase + (distinguishes from Strep)
Resistant to novobiocin
Epidemiology of Staphylococcus saprophyticus
What is normal tissue?
What illness is it a common cause of?
skin commensal
2nd leading cause of UTI in women
What are symptoms of S. saprophyticus UTI?
UTI with poluria and dysuria
What is Tx for S. saprophyticus?
Why are these the drugs of choice?
Trimethoprim sulfamethoxazol (Bactrim) Norfloxacin (quinolone) excellent penetration into urinary bladder.
Why are the following used? On which staph? VANCOMYCIN RIFAMPIN GENTAMYCIN BACITRIM + Sulfonamide + Trimethoprim NORFLOXACIN (a Quinolone)
S. aureus and S. epidimidis use VANCO, RIFAMPIN, AND GENTAMYCIN
S. saprophyticus uses BACTRIM AND NORFLOXACIN
Vanco: Cidal, G+ multi resistannt enterococcus and MRSA, cell wall inhibitor
Rifampin: Cidal broad spectrum RNA synthesis inhibitor, often used in TB
Genta: Cidal, 30s aminoglycoside protein synth inhibitor
Bacitrim: static antimetabolite inhibits folic acid via DHF reductase and PABA
Quinolone: Cidal, G- and G+ DNA inhibitor (DNA gyrase). Note MRSA is resistant. Used for UTI and P. aeruginosa
