Cutaneous Bacterial Infections Flashcards Preview

Infection & Immunity Block > Cutaneous Bacterial Infections > Flashcards

Flashcards in Cutaneous Bacterial Infections Deck (26):
1

Mechanisms of Cutaneous Infections

Mechanisms of cutaneous infections
Break in skin
Toxin mediated skin damage (rashes)
Skin manifestation of systemic infections

2

Classifications of Cutaneous Infections

Classifications of cutaneous infections
Abscess formation
Spreading Infection
Necrotizing Infection

3

Host Defenses

Host defenses against growth on skin
Limited moisture (with exceptions), acidic pH and salt
Normal flora

4

Clostridium species

Anaerobic
Gram-positive
Spore forming rods

5

Spore Formation

Spore forming bacteria grow as vegetative cells and divide by binary fission during optimal conditions
When suboptimal conditions, DNA condenses and becomes a spore vegetative cell, which invaginates once DNA copied to form the forespore. The original (mother) cell engulfs the developing spore and is surrounded by two membranes with outside peptidoglycan. Dipicolinic acid is formed inside the developing spore and Ca2+ enters the cortex to remove the water in the spore. Protein coat forms exterior to become mature and resistant to outside conditions. Lastly, lytic enzymes degrade the mother cell and the mature spore is released.

6

Clostridium perfringens

Background:
Gram-positive, anaerobic rod [“rectangular”]
Rarely spore forming

Encounter:
GI tract of humans and other vertebrates
Ubiquitous in nature (soil)
Classic example: stepping on a nail

Cutaneous infections: cellulitis, suppurative myositis, clostridial myonecrosis (gas gangrene)
Food poisoning
Necrotizing Enteritis (rare)

7

Clostridium perfringens: Virulence Determinants

A: alpha
B: alpha, beta, and epsilon
C: alpha and beta
D: alpha and epsilon
E: alpha and iota

Alpha: cytotoxic, mediates tissue destruction
Beta: necrotizing enteritis (rare)
Epsilon: increases vascular permeability
Iota: necrotic activity and increases vascular permeability

8

Clostridium perfringens: Dx, Tx, Prevention

Diagnosis:
Confirmatory
Gram-staining and antigen detection

Treatment:
Surgical debridement
Penicillin
Hyperbaric oxygen

Prevention:
Proper wound care
Proper heating of food (heat labile enterotoxin)

9

Clostridium tetani

Background:
Gram-positive rod (bacilli)
Strict anaerobe
Spore-forming

Encounter:
GI tracts of humans
Many animal reservoirs
Often present in soil (metabolically inactive spores)

Disease:
Tetanus, usually associated with a traumatic wound where temp is high enough and O2 is low enough to facilitate growth

10

Clostridium tetani: Clinical Presentation

Muscles in the face contract and look like the person is smiling or snarling
In some cultures, the umbilical cords are packed with soil or manure and this can introduce this disease
Then all the muscles in the body contract and the patient will eventually die of respiratory failure because diaphragm cannot work

11

Clostridium tetani: Virulence Factors

Tetanolysin

Tetanospasmin:
Encoded on a non-mobilizable plasmid
AB toxin
Released by cell lysis
Prevents the release of inhibitory neurotransmitters

AB toxin (binding and active domains) and encoded on non-mobilizable plasmid (not all plasmids can be shared by conjugation); do not know of any specific secretion of toxin, just think it undergoes lysis (the cell) to release them; muscles are always getting inhibitory signals, but with the toxin only get activating signals and continue to contract

12

Clostridium tetani: Dx, Tx, and Preventation

Diagnosis:
Clinical Presentation
Culture is unreliable

Treatment:
Debridement of the wound
Antibiotic (Metronidazole)
Passive immunization with tetanus immunoglobulin

Prevention:
Vaccination with Tetanus toxoid
Series of 3 with booster every 10 years.

13

Pasteurella species

Gram-negative coccobacilli
Catalase positive
Non-spore forming
Anaerobic or facultative anaerobic

14

3 Types of Pasteurella species

P. multocida: bite wound infection, bacteremia, and meningitis; common

P. canis: bite wound infection; less common

P. bettyae, dagematic, and stomatis: opportunistic infections; rare

15

Pasteurella species: Encounter, Disease, and Virulence

Encounter
Commensal in oropharynx of animals
Animal bite or scratch

Disease
Localized cellulitis and lymphadenitis
Systemic infection in immuno-compromised hosts

Virulence factors: capsule

16

Pasteurella species: Dx, Tx, Prevention

Diagnosis: culture and staining of pus

Treatment:
Penicillin
Alternatives = macrolides, tetracyclines or fluoroquinolones

Prevention: avoid exposure and wound care

17

Propionibacterium acnes

Background:
Gram-positive rods
Arranged in short chains or clumps
Anaerobic (aerotolerant)
Non-spore forming

Exposure: normal flora of the skin, the oropharynx and the female genital tract

Disease: acne and opportunistic infections on implanted devices

18

P. acnes Virulence

Inflammatory Mediators: P. acnes is present as normal flora, but when there is hyper-secretion of sebum it causes breakdown of sebum to fatty acids thus causing an inflamed lesion

19

P. acnes: Dx, Tx, and Prevention

Diagnosis: clinical Presentation

Treatment: antibiotics, tetracylines or erythromycin

Prevention: antibiotics
Unrelated to the effectiveness of skin cleaning

20

Staphylococci species

Gram-positive cocci
Facultative anaerobe
Catalase positive

21

Staph aureus: Exposure

Exposure:
Ubiquitous in nature
Normal carriage in ~15% of people
Cutaneous infections require breach in immunity such as a break in skin or insertion of foreign object

22

Staph aureus Diseases

Cutaneous infections:
Impetigo
Folliculitis
Cellulitis
Furuncles (boils) and Carbuncles
Wound infection

Septic arthritis
Endocarditis
Pneumonia
Toxic Shock Syndrome - infection and toxin
Scalded Skin Syndrome- infection and toxin
Food poisoning - toxin alone

*the rest are frank suppurative infections with bacteria present

23

Staph aureus Virulence Factors

Capsule: anti-phagocytic and adhesion

Protein A: specific to staph genus; on surface of bacteria and binds all circulating Ab (upside down on Fc portion); it coats bacteria in human protein to hide itself, and blocks the binding of specific Ab to prevent opsonization/Ab mediated clearing

Coagulase: is positive for staph aureus ONLY; fibrinogen to fibrin (to dissolve clots)

Hyaluronidase: degrades hyaluronic acid

Lipase: hydrolyzes DNA

Penicillinases (plasmid): degrades penicillin; CANNOT use penicillin, unless some later generations

24

Staph aureus Toxins

Cytotoxins (a, b, d, gamma, leucocidin): toxic to macrophages, leukocytes, and other cells

Exfoliative toxins (ETA, ETB): proteases

Enterotoxins (A-E, G-I): superantigens

Toxic Shock Syndrome Toxin 1: superantigen

25

Staph aureus: Dx, Tx, and Prevention

Diagnosis:
Culture and Gram-stain
Antigen detection

Treatment: antibiotics **; there are so many resistance patterns, so important to know which area you are working in to know the resistance pattern there

Prevention:
No available vaccine
Frequent hand washing

26

Methicillin Resistant S. aureus (MRSA)

~30% of S. aureus strains are resistant to semisynthetic penicillins: methicillin, nafcillin, oxacillin, diclozocillin
Hospital and community acquired
Resistance due to acquisition of a single gene (mecA)

Molecular level: bacteria have a gene called mecA that is a penicillin binding protein (PBP) and functions to cross link NAM units in peptidoglycan; the drugs target PBPs, but the mecA is an extra PBP produces a second gene that encodes resistance to this