Flashcards in Agents of Skin Infections I and II Deck (89):
What strains cause Impetigo?
Group A streptococcus and Staphylococcus A
Exogenous vs. endogenous skin infections
Exogenous is direct invasion of microbe from external environment and endogenous is invasion of a microbe from an internal source such as the blood or an infected organ.
Tender, superficial erythematous and edematous lesions mostly on the superficial lymphatics of the skin. Red and clearly demarcated, can be lethal.
What layer of the skin is cellulitis predominantly affective in?
Subcutaneous fat layer
What is a furuncle?
Group of Boils
Inflammation in hair follicles. Starts typically as small red bumps or white-headed pimples around the follicles, turning into nonhealing crusty sores.
Causes myonecrosis, brought on by Clostridium. Dangerous form of necrosis with necrotic bullae (large blisters)
Caused by GAS, commonly known as flesh eating bacteria. Destruction of skin and subcutaneous tissue
What infections are brought on by Streptococci?
Think (NICE Strep)
What infections are brought on by Staphylococci?
What infections are brought on by Clostridium?
What gram stain is streptococci?
What bacteria are catalase positive? Negative?
Negative - Streptococci
Positive - Staphylococci
Alpha - You can lyse cells but can't break down hemoglobin (looks green)
Beta - Complete hemolysis including hemoglobulin
Gamma - Can't break down blood cells at all
Hemolytic results for bacteria
Streptococcus Group A - B hemolytic
Staph A - B hemolytic
Staph - Epidermidis - Gamma
VRSA vs. VISA
VRSA - Complete Vancomycin resistance
VISA - Incomplete resistance
Strep vs. Staph catalase tests
Strep - Negative
Staph - Positive
Lancefield Group A carbohydrate antigen
Not a virulence factor, but is a marker on the cell wall on Group A Streptococci
Specificity of test is great, but sensitivity is poor
Describe a GAS culture
- Glistening due to capsules
- Form clear zones (we can see through them with light)
- Sensitive to Basitracen
Antimicrobial that acts against the cell wall. We can use this to distinguish GAS on an agar plate
Make sure that you have streptococcus. If positive, you have Group A
2. Important for binding to epidermis
3. Homologous to many self proteins making it tricky to target (molecular mimicry)
Hyaluronic Acid capsule
Antiphagocytic, disguises bacteria due to similarity to our own proteins
Describe Super Antigens
Bind MHCII and TCR together nonspecifically. Causes 20% of our T cells to activate instead of the normal 0.01%. Leads to a shit storms of cytokines
Nosocomial transmissions of bacteria
P Aeruginosa - On biofilms on medical equipment
S Epidermidis- UTIs and other infections caused by surgeries and implanted medical equipment like catheters
S Aureus - EVERYWHERE
How do bacteria get these resistances?
DNA gets inserted into the bacterial DNA by bacterial phages giving them the ability to make toxins
Horizontal gene transfer OR spontaneous mutations
What is the lysonogenic phase
Phase when the virus that infected the bacteria (phage) is not doing anything. Advantages are that the bacteria can not be infected by other viruses and can gain virulence factors
When the virus inside of the bacteria is replicating like crazy
Virulence factor that is toxic to a wide variety of cells. Lyses cells around a colony
Neutrophils have a second attack method, NET (neutrophil extracellular trap) made up of toxic compounds and DNA fragments that trap and kill pathogens. DNAases released by the bacteria can break these NETs
Lyses blood clots to help bacteria spread
Virulence factor - Degrades complement protein C5a which is what attracts PMNs
What causes Rheumatic fever?
Caused usually after a sore throat from GAS. It causes a cross reaction between antiM antibodies and the heart = autoimmune
Renal injury due to deposition of antigen-antibody complexes on glomeruli
Streptococci Group A
5 PANDAS criteria
2. Pediatric Onset
3. Abrupt onset with episodic course
4. Association with Group A Strep infections
5. Neurological abnormalities like motoric hyperactivity, tics, etc.
Treatment for GAS
PCN-G and/or oral cephalosporins
What is the treatment if GAS is mixed with Staph Aureus?
PCN-ase resistant antibiotic to treat both
Are staphylococci gram positive or negative?
Blood agar result for S. Aureus
Yellow beta hemolytic
Blood agar result for S. Epidermidis
White non hemolytic (gamma)
Coagulase test results
Positive = Staph Aureus
Negative - Staph epidermidis and S Saprophyticus
Bubbling is positive. Take the colony put in H2O2. If it bubbles then you have staphylococci, if there is no bubbling then it is streptococci
Aureus makes protein coagulase that turns fibrinogen to fibrin causing a clot around the bacteria to mask it and grow in size
Infection of the epidermis manifested by intraepidermal vesicles that are filled with exudate and eventually become weeping and crusted lesions
Treatment for Furuncle
Heat and drain it
Muciprocin antibiotic treatment to eliminate nasal carriages
Salt water exposure, causes fluid filled blisters. Can cause sepsis and be lethal
Can cause Ecthyma gangrenosum, a necrotic reaction
Lesions caused by Staph A
Remember Staph (janitors) MOPS
Bacteremia caused by Staph A
Risk factors for boils from Staph A
Wet working conditions
Risk factors for wound infections being caused by Staph Aureus
Number one host defense against Staph Aureus?
What complement subunit deficiency puts you at high risk for Staph A?
What virulence factors help Staph A defend directly against phagocytosis?
Binds Fc Receptor
Breaks down H2O2 and makes leukocidin
Pokes holes in neutrophil membranes
Binds fibronectin in our ECM proteins which help it break into the cell
Acts on hyaluronic acids in connective tissue which facilitates dissemination through subcutaneous tissues
Cytotoxins of Staph Aureus
Gamma Toxins and PVLs
potent pore-former that is toxic to many types of cells
Also called Sphingomyelinase C, kills cells via hydrolysis of membrane phospholipids
Cytolytic for many cells, nonspecific detergent-like action
Gamma Toxins and PVLs
Panton-Valentine Leukocidin - pore forming toxins that lyse neutrophils and macrophages
What Staph do we suspect for dog bites?
Staphylococcus Intermedius since this is a normal flora on healthy dogs
Caused by Staph A, gets into the skin and causes abscesses. Usually localized. Big fluid filled sacs everywhere
Scalded Skin Syndrome
Staph A toxin that creates exfoliatin which gets into the bloodstream and causes shedding of the outermost layer of the skin. Looks like a dark red peeling sunburn all over
Treatment for Scalded Skin Syndrome
Antibiotics and hydration
How does Exfoliatin work?
Serine protease that causes splitting of desmosomes in the stratum granulosum. We develop antibodies to this toxin later in life
Super antigen involved with Toxic Shock Syndrome
Immediate symptoms of TSS
Fever, chills, vomiting, diarrhea, muscle pains, rash
Delayed symptoms of TSS
Hypotension, involvement of mucous memranes and multiple systems with desquamation (skin peeling)
Risk groups for TSS
1. Menstruating women
2. Women with contraceptive devices
3. People with nasal surgery
What condition do we see strawberry tongue with?
Scarlet Fever (sometimes brought on by TSS)
Most common cause of pyoderma
Alcohol soaps in hospitals help with what?
Staph Aureus spread
Pulse-field gel electrophoresis
Isolates related clones by cutting chromosomes up into large fragments and seeing if there are mutations, which will change gel migration of the fragments
When you use phages on different staph colonies to see which ones die. The ones that live already have that phage in them
Story of PCN, MRSA and VRSA
Started with PCN, but the bacteria developed PCNase, we fought back with methicillin, but then MRSA came about when the bacteria developed mec A gene which altered PCN binding protein.
Now we use Vancomycin, a glycopeptide that inhibits further production of peptidoglycans (PG) by binding to the PG precursors. This is the current treatment for MRSA, although, continuing the trend, VRSA has developed which is full resistance and VISA which is partial resistance. Acquisition of vanA gene which changed the terminus of the PG chain to stop Vancomycin binding
What bacteria develops in biofilms?
Which bacteria do we mostly associate with UTI?
Types of Spread of bacteria and examples that do this
Commensual Staph - Colonizers of normal skin and rarely causes deeper infection unless physically introduced there via a catheter or something. S. epidermidis follows this.
Virulent Staph may cause skin infections from which organisms disseminate to almost any organ or tissue. Staph. Aureus is a good example of this.