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Normal Skin Flora & Bacterial Infections of the Integumentary System

STUDY
PLAY
Diversity of the skin @ different body sites
• Face
High density of sebaceous glands
Hair & eccrine glands
Environmentally exposed

• Palm (dry)
Thick stratum corneum
Hairless
High density of eccrine glands

• Axilla (moist)
Apocrine glands
High density of hair
Oclluded, humid environment
Functional associations w/ communities on the skin
• AMP = anti-microbial peptides
Models of dysbiosis
a) Driven by Microbial Communities
b) driven by host biology/pathology
Important colonizers*
•#1 Coagulase negative staphylococci, e.g.,
→→ Staphylococcus epidermidis: no associated skin disease despite large numbers on skin but involved in IV catheter infections & prosthetic device infections.

•Propionibacterium sp.: produce fatty acids which inhibit most bacteria including most Gram-negatives (except Acinetobacter)* Propionibacterium acnes associated with acnes & opportunistic infections.

•Staphylococcus aureus - small #s in moist areas; larger #s on cutaneous surfaces of diabetics, injection drug users, & some health care workers.
Less impt colonizers
• Viridans streptococci & peptostreptococci (anaerobic cousins)

• Corynebacterium spp.

• Brevibacterium spp. (cheesy foot odor)

• Propionibacterium spp. (but important for fatty acid production).

• Acinetobacter spp. (Gram negative) (no associated skin disease)

• Clostridium perfringens found in about 20% of healthy adults
Pathogens of the Dermatomuscular System
...
S. aureus*
• Gram (+) cocci, arranged in grape-like clusters
→→ From Greek staphyle - "bunch of grapes"

• Initially white colonies turn buff-golden (aureus)
• Most colonies β-hemolytic, facultative***
• Ability to grow in 7.5% NaCl, mannitol salt agar (selective/indicator medium)
S. aureus I.D. & Subtyping
• Coagulase distinguishes S. aureus from other staphylococci
• Most strains produce clumping factor
∆∆ "bound coagulase"
∆∆ Binds fibrinogen
S. aureus Epidemiology
Normal flora of skin and mucosa

• Can survive on dry surfaces for long periods
• Spread by person-to-person or by fomites (bed linens, clothing, etc.)

• Risk factors include:
→→ Foreign body (splinter, suture, etc.)
→→ Previous surgical procedure
→→ Antibiotic use suppressing normal flora

•Methicillin Resistant S. aureus (MRSA) most common cause community acquired skin & soft-tissue infections
S aureus Virulence Factors***
• Coagulase: fibrinogen->fibrin: coats cells with fibrin making them resistant to phagocytosis; also localizes infection; slows down WBC.

• Cytotoxin Alpha: inserts self to form pores in human membrane->cell leakage: RBC, WBC, platelets, other tissue

• Exfoliatins-split intracellular bridges in the stratum granulosum in Scalded Skin Syndrome

• Panton-Valentine Leukocidin (associated with community acquired methicillin resistant Staph aureus (CA-MRSA))*****

• ±TSST-1 (toxic shock syndrome toxin) - decreases LPS clearance, pyrogenic, capillary damage, hypotension, and shock; superantigen. Toxin is absorbed & disseminated*******
Community-Acquired MRSA
•812 army soldiers followed during basic training (8-10 weeks)
→→ 3% colonized with CA-MRSA, 38% developed infection (9/24) - 5/9 hospitalized
→→ 28% colonized with MSSA, 3% developed infection (8/229) - 1/8 hospitalized
→→ 5/5 CA-MRSA infections requiring hospitalization were associated with Panton-Valentine leukocidin (PVL, pore forming cytotoxin)

• Spider bites*** presenting with MRSA soft tissue infection require early aggressive treatment.
• 38 patients presented with infected "spider bites"
• 87% grew MRSA
Staphylococcal Skin Diseases*
• Bullous impetigo (bullae are fairly short lived.)
• Often secondary invader of GAS pustular impetigo

(impetigo probably mixed)
Clinical Manifestions: S. aureus/MRSA
• Furuncle & Carbuncle***
-Superficial infection of follicle
-Infection resolves upon spontaneous drainage

→→ Multiple boils yield a carbuncle
Clinical Manifestations 2: S. aureus
• S. aureus can cause a wide variety of infections of deep tissues
• 90% of acute osteomyelitis in children
• Pneumonia and deep tissue lesions highly destructive
• Initial infection may be skin related & travel to deeper tissues
Clinical Manifestations 3: Toxins*
• Scalded Skin syndrome
• Exfoliative toxins destroy the intracellular -connections separating the upper layers of the epidermis.
Clinical Manifestations 3b: Toxins
• Patient "toxic" 104 F
• Nasal surgery two days ago
→ ER

• 104F, hypotensive, in shock
• Kidneys beginning to fail → multi-organ
• Desquamation of skin on palms & soles.
Streptococcus pyogenes (pyogenic)*
• Group A Streptococcus
-Rebecca Lancefield - group A carbohydrate, Lancefield cell wall antigen A

• Gram (+) spherical or ovoid cells in short to medium chains (4 - 10 cells)
→→ β-hemolytic, facultative, hyaluronic capsule* catalase negative*
→→ Generally bacitracin suscetible*
S. pyogenes Morphology*
S. pyogenes Epidemiology***
• Pharyngitis
-Human reservoir
-Carriage rate ~5%

•Pharyngeal, nasal, anal
-Spread - contact with mucosa, secretions, or large droplet transmission

• Impetgio - preceded by skin colonization
-Poor hygiene
-Minor trauma
-Spread - direct contact or shared fomites

• Nosocomial wound & Puerperal infections
-Once a leading cause
-Transmission by hands & poor hygiene
-Now derived from patients/staff ill with pharyngitis

•Obstetrician anal carrier
•9 post-partum infections
S. pyogenes Virulence Factors*
•Antiphagocytic factors (C5a peptidase, M protein, Streptococcal inhibitor of complement, capsule)
•Streptolysins O & S - hemolysins
•Streptokinase - fibrinolytic
•Dnases - degrade free DNA in pus
•Streptococcal pyrogenic exotoxins - super antigens, toxic shock (SpeA, B, C, F)
S. pyogenes Clinical Manifestations
S. pyogenes Clinical Manifestations 2
• Necrotizing fasciitis
S. pyogenes Diagnosis
• Anaerobic blood agar plates: β-hemolysis
• Direct detection of group A antigen***
-Rapid strep test, sensitivity issues (75-80%)
-Negatives must be confirmed to protect against Acute Rheumatic Fever (ARF)

•PYR test positive: (FYI: hydrolyze L-pyrrolidonyl-β-naphthylamide)
Clostridium perfringens
• Gram-positive, sporeformer
• Non-motile, found in soil & human colon; 20% folks have on skin.
• Anaerobe (→→ gas in tissues cellulitis, suppurative myositis, & gas gangrene)
• Grows rapidly in damaged tissue!!
• Once started, nasty: produces at least 12 tissue destroying toxins***
Clostridial Soft Tissue Infections
•Cellulitis & supprative myositis

•Myonecrosis (gas gangrene)
-Painful, rapid destruction of muscle tissue, systemic spread with high mortality; trapped gas; shock, renal failure, death within 2 days

-Clinical & microscopic diagnosis; center of lesions have C. perfringens but no WBCs. (LACK OF WBCs)
Clostridium perfringens Toxins*
•α toxin
-a lecithinase (a.k.a. Phospholipase C)
-hemolyzes RBC, platelets, WBC, endothelial cells → massive hemolysis, tissue destruction, hepatic toxicity

•At least a dozen other destructive toxins & enzymes
•Hallmark of myonecrosis: pain, fever, rapid spread; white cells not seen in infected tissue & cannot control infection.
→→ Damage to platelets means clotting problems & hemorrhage. (Bullae reddish brown from heme.)
C. perfringens Naegler's Reaction
•Egg Yolk (lecithin) Agar Plate with antitoxin; anaerobic incubation

•Detects C. perfringens α toxin = lecithinase

•Naegler test has antitoxin to α toxin on one half of plate

→→ Breakdown of lecithin changes pH causing precipitate; antitoxin stops activity so none on side with the antitoxin.
(+Antitoxin (left): No antitoxin (right))
C. perfringens infected tissue w/ visible gas pockets
1. Accumulation of air in skeletal tissue
2. Stained bacteria
Clostridial Gas Gangrene*
•Tense tissue from hydrogen gas trapped in tissues; x-ray may show gas bubbles in tissue
•Crepitus - the cracking and popping sounds heard/experienced under the skin
•Marked swelling; yellow-bronze skin discoloration, brown bullae, green black patches of necrosis, serosanguinous discharge, myonecrosis (destruction of muscle tissue)
•Pain prominent, extremely rapid course, high fever; renal failure; shock; death with in 2 days.
Gas Gangrene Treatment
•First: general concept: anaerobes require débridement or amputation, delayed closure AND antibiotics
•Antibiotic: penicillin
•Second: general concept: Clindamycin* decreases protein synthesis & is often used here in conjunction with another drug because it reduces toxin production.

•Third: hyperbaric may increase oxygenation of tissues although animal studies suggest the addition of clindamycin is more important as is débridement.
Clostridium tetani*
• Gram +, anaerobic rod
• Spore former
• Soil/dust organism widely distributed in the world.
• Terminal spores (tetanus looks like a "tennis racket)
• Problem in unvaccinated people & babies of unvaccinated women. (Umbilical cord tetanus is a high risk in these babies in developing countries.)
C. tetani pathogenesis
•Spores traumatically implanted; if tissue has low oxygen level, spores will germinate & grow
•Vegetative cells elaborate neurotoxin tetanospasmin, which produces spastic paralysis.
•Toxin binds to & is taken up by endosomes in motor neurons, travels in axons to neuronal junctions where the endopeptidase activity cleaves core proteins involved in neurotransmission.
•Blocks the release of GABA & glycine resulting in a rigid spasm.
•A disease of unvaccinated. Often associated with fairly minor puncture wounds, umbilical cord at birth if Mom unvaccinated (neonatal tetanus.)

•Risus sardonicus or trismus ("lockjaw") first, then opisthotonus
Tetanus: Opisthotonus
Tetanus Treament
•Debridement of wound (may appear innocuous)

•Passive immunization with human tetanus immunoglobulin to neutralize toxin (Antitoxin TIG)

•Anti-spasmolytics

•Antibiotics (Metronidazole or Pen G)

•Does not produce immunity-vaccinate
Wound botulism*
•Clostridium botulinum in deep wounds with restricted oxygen (probably mixed infections.)

•Incubation period of 4 days or longer

•Symptoms are identical to foodborne botulism
Pseudomonas aeruginosa*
• Water organism & major hospital opportunist
• Gram- rod, motile • Oxidase (+)
• Aerobic, no special growth requirements
• VF: Exotoxin A (inhibits EF-2) & endotoxin
•Plants, cut flowers (water), raw veggies, standing water (incl. distilled), faucet aerators, drain U traps, not properly maintained: whirlpools, respiratory therapy equipment, blenders, etc.

• Fruity, grape-like odor
• Greenish-blue color due to pyocyanin & pyoverdin
• Some strains mucoid
Ecthyma gangrenosum
•Associated with Pseudomonas aeruginosa septicemias & pneumonias in severely neutropenic patients; less commonly infected burns***

•Looks like cutaneous anthrax but patient population differs and location on body generally differs.
* in zoonoses lecture
Other Pseudomonal Infections
• Pseudomonal folliculitis
-Generally all follicles neck down inflamed.
-Hot tubs
-If immunologically normal, generally no treatment needed.

• Malignant otitis externa in diabetics
-Bone invaded; diabetics; very serious infection

• Cellulitis from nail puncturing tennis shoe sole.
Vibrio vulnificus *
• Vibrio vulnificus
→→ Gram (-): curved rod
→→ oxidase positive (Not Entero-bacteriaceae)

• Infection
→→ Exposure to contaminated salt water
→→ Shucking oysters
Vibrio vulnificus cellulitis
• Commonly abrupt onset of malaise, fever, chills & headache.
• Rapidly advancing lesions.
• Hot, tender, red skin over involved area
• Fatalities
Bartonellas*
• Gram negative bacilli, pericellular
• Require special isolation - check with lab

• Bartonella henselae
→→ Bacillary angiomatosis****
→→ Subacute endocarditis
→→ Cat-scratch disease***

•Bartonella quintana
→→ Bacillary angiomatosis***
→→ Subacute endocarditis
→→ Trench fever
Bacillary angiomatosis*
• Vascular proliferative disease found in immunocompromised patients →→ Spread by exposure to feces of human body louse***

• B. quintana
→→ Disease involves skin, subcutaneous tissues, & bones
Bacillary angiomatosis 2*
• B. henselae
• Bacterium asymptomatically colonizes the oropharynx of cats & is carried by their fleas
→→ Bacillary angiomatosis in immunocompromised*

• Disease involves skin, lymph nodes, or liver and spleen
→→ Cat scratch disease in immunocompetent**

• Small initial papule followed by regional lymphadenopathy
•Self resolves in a few months w/o antibiotic
Bartonella Reservoir* (host-cell interactions & vascular tumor formation)
Erysipeloid (cellulitis): Erysipelothrix rhusiopathiae
• Gram +, non-sporulating rod; capsule
• facultative anaerobe
• Recover from tonsils or digestive tracts of mammals, birds, & fish
→→colonization is particularly high in turkeys & swine

• hazard of butchers, cooks, veterinarians***
• purplish red, indurated skin lesions on fingers or hands
→→ treated with penicillin
Skin & Soft Tissue Infections in IDU
• Common occurrence (most common reason for IDU admissions to hospital)

• Common organisms:
→→ Staph aureus most common with a high frequency of CA-MRSA
→→ Streptococci: Group A strep & other oral flora (from licking needles)

• From both iv injection & skin popping (drugs are injected into the fatty layer under the skin.)
• Commonly result in abscesses, cellulitis, or skin ulcers; but may cause necrotizing fasciitis & septic thrombophlebitis.

•But also wound botulism, tetanus, Candida, endocarditis, HIV & viral hepatitis.
Actinomyces spp.*
• Gram positive filamentous*
• Anaerobe (see thioglycollate; aerobic @ top, anaerobic @ bottom)
• Not acid fast
• Normal gingival flora (between teeth & gums)

•FYI:Other infections: CNS abscesses, endocarditis, pelvic
Cervicofacial actinomycosis/Lumpy jaw
• Recent tooth extraction
• Febrile
• More pain than yesterday.
• Drainage or surgical debridement followed by prolonged antibiotics
Mycobacterium marinum*
• Fish tank granuloma
• Swimming pool (non-chlorinated)
Osteomyelitis (HY)
•Bone pain (limping, etc.), fever, sometimes redness over area)
•S. aureus: if patient has not had trauma nor has hematological abnormalities*
•Salmonella: if patient has sickle cell disease*
•Pseudomonas if trauma*