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34 Cards in this Set

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  • Back
What is carbuncle and pathogenesis?
a
infection that drains to adjacent tissue rather than to surface. Abscess must drain prior to resolution of the wound.

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What is the coagulase test? What is the signifigance in seperation of the staph species?
a
The coagulase test is a bch to test if it causes the plasma to coagulate.

Coagulase + is staph aureus
Coagulase - is staph epidermis or staph saprophytico (both are less virulent)
What is the MOA of Alpha Toxin? Where does it act?
a
Alpha toxin is a pore forming complex. It acts locally. It is found in virtually all strains of Staph Aureus.
What is the MOA of StaphSAgs? How frequently is it found? What disease does it cause?
StaphSAg causes massive cytokine release by non-specifically activating APC and T cells.

StaphSAg is found in 5-10% of strains

It causes Toxic shock syndrome iin the blood. It causes food poisoning if it is ingested.
How is Staph spread? What is the source?
Transmission - airborne or direct contact

Autoinfection - Nasal shedding from ant. nares

Person2person - via carrier, lesion, and poor handwashing
What is the local disease caused by staphylcoccus?
Local lesion called: Furuncle or boil. This infection results from minor trauma or hair follicles. The infection causes tissue destruction through alpha toxin. The infection drains to surface

Carbuncle is same but drains to adjacent tissues rather than surface.

.
Describe Impetigo etiology in Staph Aureas? What is generally the major cause of impetigo?
Staph Aureas - occasionally causes bullous intraepidermal splitting when local exfoliatin local toxin is released.

Impetigo is more commonly a GAS etiology
What are the local acting toxins in Staph Aureas and the MOA for them to cause disease?
Staph binds to Fibronectin on cell surface. Secretes alpha toxin and Exfoliatin local toxins. Abcess forms from PMNs forming fibrosis in response.

Bacteremia may lead to spread to bone.
What is a rare finding found in neonates? What is the outcome?
SSSS (Staphylcoccal Scalded Skin Syndrome) is found in neonates when Exfoliatin is absorbed into the systemic circulation.

Despite grave appearance. Has good outcomes.
Describe who gets Toxic Shock Syndrome? What is the minority group?
The majority of pts w/ TSST get it in association w/ high absorbance tampons, during menses. Staph aureus grows and releases TSST-1.

The minority group of pts get a similar syndrome from skin infections from strains that produce TSST as well.
What are the pathogenesic steps leading to menstral TSST? What are the probability to develop the disease?
Tampons promote Staph Aureus growth and secretion of TSST-1. TSST-1 superantigen circulates (not the microbe) causing toxic shock syndrome.

5% of vaginas are colonized w/ S. Aureas. 5-10% of strains secrete TSST-1. This is a perfect storm.
What type of staph has glycocalyx and what are their virulence?
Coagulase negative staph (epidermis & saprophyticus) have glycocalyxs. Infections with these microbes are associated w/ foreign bodies.

The glycocalyx binds plastic in IV catheters & Prosthetic valves or joints.
Staphylcoccus Aureas bacteriology
Gram +, cocci , Acinar arrangement
Catalase + (differentiates from streptococci)
Coagulase + (coagulate plasma NOT serum)
Exfoliatin toxin
This is only produced by a minority of strains.
Causes intraepidermal splitting resulting in impetigo

In neonate may result in SSSS
What is the systemic exotoxin disease?
Refers to StaphSAg which facilitates the non specific activation and release of cytokines between APC & T cells. This causes TSS.
Where is Staph found?
Picking zone of nose, skin. Infections are often from self.
Contrast strep and Staph skin lesions.
Staph produces more focal lesion where strep produces more diffuse cellulitis
How does staph cause food poisoning? Describe the food poisoning disease
Staph Aureas replicates in food & forms StaphSAg toxin. The result of preformed ingested toxin is a VERY short incubation period. (think airplane sickness mid-flight & need to emergency land). The toxin activates GI receptors resulting in CNS stimulation of the vomiting center.

Symptoms are - vomiting, diarrhea only a few hours after ingestion
How do you diagnose Staph
culture site sample on routine blood agar
Also, culture blood (bacteremia?)
How do you prevent staph?
For pts with multiple recurrences of staph - special soap
Proper tampon use to decrease TSS
What are the methods of resistance seen in Staph? and the percentages of Staph infections that have them?
Penicillinase (beta-lactamase) found in 80-90% of strains

Altered peptidoglycan transpeptidase target is MRSA and occurs in 10-50% of infections
What is the association of coag neg staph?
catheters, foreign bodies (prosthetics)
Who has biofilms?
Staph coag neg & p. aureginosa (CF pts)
What factors are generally required for S. Aureas to initiate disease?
Generally requires a break in barrier such as in trauma or surgery. A skin wound or lesion on the umbilicus can also promote epidermal infection.
What are the minimum requirements for development of Staph Toxic Shock Syndrome? What actions can the community & individual take to decrease the incidence of the disease?
TSS requires some type of infection w/ Staph aureas strain that produces TSST.

Proper tampon use is the best prophylaxis. Would be hard to decrease the skin infections.
What is the typical setting for Staph food poisoning?
Food is contaminated by a carrier of strain that produces enterrotoxins. Time is needed to produce StaphSAg. The SAg toxin is heat and acid stable to get past the stomach.
How can we distinguish Staph Aureas from other staph species?
Staph aureus is the only coagulase positive staphylcoccus.
How can we distinguish Staph aureas from other streptococci species?
Staphylcoccal species are all catalse positive. Streptoccoci are catalase negative.
What are the systemic toxins and their MOA of causing disease?
The only staph systemic exotoxin is StaphSAg. Their is TSST-1 (also a 2) and enterotoxins (A,B,C).

Enterotoxins - bind receptor that activates the vomiting center in CNS
StaphSAg - binds non-specifically to APC/T cell to cause release of cytokines
What evidence is required to diagnose S. Aureas local infection and Toxic shock syndrome?
Positive cultures & catalase +, coagulase + BCH tests

Detection of StaphSAg
What is the mechanism for Staph Aureas resistance to beta-lactam antibiotics? What other resistance can they sometimes have?
Beta-lactamases are found in the majority of Staph aureas strains. The other resistance mechanism is a change in target. The peptidoglycan transpeptidase no longer binds Methicillin (MRSA) making it inactive Antibioitc.
What kind of disease do low virulent species of Staphylcocci cause?
Staph Saprophyticus - UTI
Staph Epidermidis - Polysaccharide binds to prosthetic & inoculates internal site
What is the MOA of Exfoliatin? Where does it act? How often is it found?
Exfoliatin acts locally to split intraepidermal. It is found in a minority of strains.
What are the symptoms of Staph Toxic Shock Syndrome?
Fever, diarrhea, shock, and renal failure.