Agents of Skin infections I and II Flashcards Preview

Microbio (12.5) > Agents of Skin infections I and II > Flashcards

Flashcards in Agents of Skin infections I and II Deck (39):
1

What strains cause Impetigo?

Group A streptococcus and Staphylococcus A

2

Erysipelas

Tender, superficial erythematous and edematous lesions mostly on the superficial lymphatics of the skin. Red and clearly demarcated, can be lethal

3

What is a furuncle? Carbuncle?

Boil and Group of Boils

4

What is folliculitis and how does it present/progress?

Inflammation in hair follicles. Starts typically as small red bumps or white-headed pimples around the follicles, turning into nonhealing crusty sores.

5

What is gas gangrene and what does it lead to?

Causes myonecrosis, brought on by Clostridium. Dangerous form of necrosis with necrotic bullae (large blisters)

6

What is Fasciitis and what does it lead to?

Caused by GAS, commonly known as flesh eating bacteria. Destruction of skin and subcutaneous tissue

7

What infections are brought on by Streptococci?

Impetigo
Erysipelas
Cellulitis
Synergistic Cellulitis
Necrotizing fasciitis

Think (NICE Strep)

8

What infections are brought on by Staphylococci?

Folliculitis
Carbuncles
Impetigo
Cellulitis

(staFilocoCCI)

9

What is the hemolytic test?

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

10

Out of staph and strep discuss the following:
- Catalase
- Hemolytics

Catalase
- Staph - +
- Strep - Negative

Hemolytics
- Both group A so they are B hemolytic

11

VRSA vs. VISA

VRSA - Complete Vancomycin resistance
VISA - Incomplete resistance

12

Lancefield Group A carbohydrate antigen?

Not a virulence factor, but is a marker on the cell wall on Group A Streptococci.

Don't always find this, but when you do, you know you have a GA Strep

13

Generalizations about Streptococci

They are gram positive and catalase negative. They can come in pairs or chains.
- Gram positive
- Catalase negative
- Beta hemolytic
- Bacitracin sensitive

14

M protein and who has it

M protein is a major virulence factor found in Strep pyogenes that binds to the epidermis and is antiphagocytic.

15

Hyaluronic acid and who has it

This capsule found in Strep pyogenes is identical to components of normal tissue, making it antiphagocytic. Antibodies do not work well on this guy as you might imagine.

16

Discuss pyrogenic exotoxins

These superantigens from Strep pyogenes stimulate production of cytokines, and are involved in the pathogenesis of scarlet fever and toxic shock syndrome

Normally, MHCII of an APC and the TCR of a T Cell bind fleetingly to activate

17

What is Streptolysin O?

An hemolytic toxin that hurts a variety of cells. We detect this in strep pyogenes with a anti-streptolysin test

18

Function of streptokinase

Released by Strep Pyogenes to lyse clots and help bacteria spread

19

Function of C5a peptidase

Degrades complement component C5a that attracts PMNs

20

Typical presentation of streptococcus

Petechiae on the soft palate with oropharyngeal inflammation

21

Three signs that we have Scarlet fever due to a strep infection that used the superantigen

- Strawberry tongue
- Circumoral pallor (white around the mouth)
- Rash with desquamation following

22

Discuss rheumatic fever and how it comes about

most often occurs in 6-15 year olds after throat infection with certain rheumatogenic M types of group A streptococci.

Autoimmune mechanisms likely -- cross-reaction between anti-M antibodies and heart tissue

23

PANDAs is a pediatric autoimmune neuropsychiatric disorder associated with Group A Strep and is characterized by 5 criteria. What are they?

- OCD
- Pediatric onset
- Abrupt onset and episodic course of symptoms
- Association with GAS infections
- Association with neurologic abnormalities, such as motoric hyperactivity, choreiform movements, or tics

24

How do we treat Group A Strep?

Penicillin G, drug of choice for GAS infections but oral cephalosporins also work. If co-infection with Staphylococcus aureus (as in impetigo or cellulitis), then use penicillinase-resistant antibiotic to treat both organisms.

25

How do we identify different strains of Staphy cocci on plates?

1. Yellow beta-hemolytic means we have a Staph Aureus while White non-hemolytic means we have a Staph epidermidis

2. Coagulase positive indicates staph aureus and coagulase negative indicates Staph epidermidis or saprophyticus

26

How does the catalase test work?

Positive means you broke down the hydrogen peroxide to oxygen and water, causing bubbling and foaming

27

How does the coagulase test work?

Add prothrombin in, and if fibrinogen turns to fibrin, you have a coagulase positive test

28

What three staph factors defend against phagocytes?

Protein A, Catalase and Leukocidin

29

Ribotechoic acid

Found in Staph aureus. This guy mimics the endotoxins seen in strep pyogenes.

Binds fibronectin and induces shock

30

Hyaluronidase

Virulence factor of staph aureus that acts on hyaluronic acid in connective tissue, facilitation dissemination through subcutaneous tissues

31

4 Toxin types found in Staph aureus

- Alpha hemolysis - opens pores
- Beta - AKA sphingomyelinase C, kills cells via hydrolysis of membrane phospholipids
- Delta - nonspecific detergent, cytolytic
- Gamma - pore forming and lysis of neutrophils and macrophages

32

If we see bullous impetigo, we should think

Staph Aureus

33

What causes scalded skin syndrome?

Exfoliatins (serine proteases) released by Staph Aureus cause splitting of desmosomes in the stratum granulosum

34

Vibrio Vulnificus

Salt water exposure, causes fluid filled blisters. Can cause sepsis and be lethal

35

What Staph do we suspect for dog bites?

Staphylococcus Intermedius since this is a normal flora on healthy dogs

36

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

37

What bacteria develops in biofilms?

Staph Epidermidis

38

Which bacteria do we mostly associate with UTI?

Staph. Saphrophyticus

39

How do Staph survive so well on the skin surface?

They make lipases and glycerol ester hydrolases that degrade the skin lipids to help them grow at high lipid and salt concentration environments.