Cutaneous Bacterial Infections

Question 1

Mechanisms of Cutaneous Infections

Answer 1

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

Question 2

Classifications of Cutaneous Infections

Answer 2

Classifications of cutaneous infections
Abscess formation
Spreading Infection
Necrotizing Infection

Question 3

Host Defenses

Answer 3

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

Question 4

Clostridium species

Answer 4

Anaerobic
Gram-positive
Spore forming rods

Question 5

Spore Formation

Answer 5

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.

Question 6

Clostridium perfringens

Answer 6

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)

Question 7

Clostridium perfringens: Virulence Determinants

Answer 7

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

Question 8

Clostridium perfringens: Dx, Tx, Prevention

Answer 8

Diagnosis:
Confirmatory
Gram-staining and antigen detection

Treatment:
Surgical debridement
Penicillin
Hyperbaric oxygen

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

Question 9

Clostridium tetani

Answer 9

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

Question 10

Clostridium tetani: Clinical Presentation

Answer 10

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

Question 11

Clostridium tetani: Virulence Factors

Answer 11

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

Question 12

Clostridium tetani: Dx, Tx, and Preventation

Answer 12

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.

Question 13

Pasteurella species

Answer 13

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

Question 14

3 Types of Pasteurella species

Answer 14

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

P. canis: bite wound infection; less common

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

Question 15

Pasteurella species: Encounter, Disease, and Virulence

Answer 15

Encounter
Commensal in oropharynx of animals
Animal bite or scratch

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

Virulence factors: capsule

Question 16

Pasteurella species: Dx, Tx, Prevention

Answer 16

Diagnosis: culture and staining of pus

Treatment:
Penicillin
Alternatives = macrolides, tetracyclines or fluoroquinolones

Prevention: avoid exposure and wound care

Question 17

Propionibacterium acnes

Answer 17

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

Question 18

P. acnes Virulence

Answer 18

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

Question 19

P. acnes: Dx, Tx, and Prevention

Answer 19

Diagnosis: clinical Presentation

Treatment: antibiotics, tetracylines or erythromycin

Prevention: antibiotics
Unrelated to the effectiveness of skin cleaning

Question 20

Staphylococci species

Answer 20

Gram-positive cocci
Facultative anaerobe
Catalase positive

Question 21

Staph aureus: Exposure

Answer 21

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

Question 22

Staph aureus Diseases

Answer 22

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

Question 23

Staph aureus Virulence Factors

Answer 23

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

Question 24

Staph aureus Toxins

Answer 24

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

Question 25

Staph aureus: Dx, Tx, and Prevention

Answer 25

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

Question 26

Methicillin Resistant S. aureus (MRSA)

Answer 26

~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