Cutaneous Bacterial Infections Flashcards
Mechanisms of Cutaneous Infections
Mechanisms of cutaneous infections
Break in skin
Toxin mediated skin damage (rashes)
Skin manifestation of systemic infections
Classifications of Cutaneous Infections
Classifications of cutaneous infections
Abscess formation
Spreading Infection
Necrotizing Infection
Host Defenses
Host defenses against growth on skin Limited moisture (with exceptions), acidic pH and salt Normal flora
Clostridium species
Anaerobic
Gram-positive
Spore forming rods
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.
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)
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
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)
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
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
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
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.
Pasteurella species
Gram-negative coccobacilli
Catalase positive
Non-spore forming
Anaerobic or facultative anaerobic
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
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
Pasteurella species: Dx, Tx, Prevention
Diagnosis: culture and staining of pus
Treatment:
Penicillin
Alternatives = macrolides, tetracyclines or fluoroquinolones
Prevention: avoid exposure and wound care
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
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
P. acnes: Dx, Tx, and Prevention
Diagnosis: clinical Presentation
Treatment: antibiotics, tetracylines or erythromycin
Prevention: antibiotics
Unrelated to the effectiveness of skin cleaning
Staphylococci species
Gram-positive cocci
Facultative anaerobe
Catalase positive
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
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
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
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
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
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
