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Bacterial Infections Chapter 14 Infections Caused by Gram Positive Organisms. Michael Hohnadel, D.O. 10/7/03 Staphylococcal Infections General 20% of adults are nasal carriers. HIV infected are more frequent carriers.

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Bacterial Infections Chapter 14

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Bacterial infections chapter 14 l.jpg

Bacterial InfectionsChapter 14

Infections Caused by Gram Positive Organisms.

Michael Hohnadel, D.O.

10/7/03


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Staphylococcal Infections

  • General

    • 20% of adults are nasal carriers.

    • HIV infected are more frequent carriers.

  • Lesions are usually pustules, furuncles or erosions with honey colored crust.

    • Bullae, erythema, widespread desquamation possible.

    • Embolic phenomena with endocarditis:

      • Olser nodes

      • Janeway Lesions


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Embolic Phenomena With Endocarditis

Osler nodes

Janeway lesion


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Superficial Pustular Folliculitis

  • Also known as Impetigo of Bockhart

  • Presentation: Superficial folliculitis with thin wall, fragile pustules at follicular orifices.

    • Develops in crops and heal in a few days.

    • Favored locations:

      • Extremities and scalp

      • Face (esp periorally)

  • Etiology: S. Aureus.


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Sycosis Vulgaris(Sycosis Barbae)

  • Perifollicular, Chronic , pustular staph infection of the bearded region.

  • Presentation: Itch/burn followed by small, perifollicular pustules which rupture. New crops of pustules frequently appear esp after shaving.

  • Slow spread.

  • Distinguishing feature is upper lip location and persistence.

    • Tinea is lower.

    • Herpes short lived

    • Pseudofolliculitis Barbea ingrown hair and papules.


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Sycosis Vulgaris


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Sycosis Lupoides

  • Staph infection that through extension results in central hairless scar surrounded by pustules. Pyogenic folliculitis and perifolliculitis with deep extension into hair follicles often with edema.

  • Thought to resemble lupus vulgaris in appearance.

  • Etiology: S. Aureus


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Treatment of Folliculitis

  • Cleansing with soap and water.

  • Bactroban (Mupirocin)

  • Burrows solution for acute inflammation.

  • Antibiotics: cephalosporin, penicillinase resistant PCN.


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Furunculosis

  • Presentation: Perifollicular, round, tender abscess that ends in central suppuration.

  • Etiology: S. Aureus

  • Breaks in skin integrity is important.

    • Various systemic disorders may predispose.

  • Hospital epidemics of abx resistant staph may occur

    • Meticulous hand washing is essential.


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Furuncle


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Furuncle / Carbuncle


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Furunculosis

  • Treatment of acute lesions

    • ABX may arrest early furuncles.

    • Incision and drainage AFTER furuncle is localized with definite fluctuation.

      • No incision of EAC or nasal furuncles. TX with ABX.

    • Upper lip and nose ,‘danger triangle’, requires prompt treatment with ABX to avoid possible venous sinus thrombosis, septicemia, meningitis.


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Treatment of Chronic Furunculosis

Avoid auto-inoculation, Eliminate carrier state.

  • Nares, axilla, groin and perianal sites of colonization.

  • Use Anti-staph cleansers – soap, chlorhexidine.

  • Frequent laundering

  • Bactroban to nares of pt and family members

    • BID to nares for one week (q 4th week.).

  • Rifampin 600mg QD for 10 days with cloxacillin 500 mg QID (or Clindamycin 150mg qd for 3 mo)


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Pyogenic Paronychia

  • Presentation: Tender painful swelling involving the skin surrounding the fingernail.

  • Etiology: Moisture induced separation of eponychium from nail plate by trauma or moisture leading to secondary infection.

    • Often work related

  • Bacteria cause acute abscess formation, Candida causes chronic swelling.

  • Treatment:

    • Avoid maceration / trauma

    • I&D of abscess

    • PCN, 1st Gen Cephalosporin, augmentin.

    • Chronic infection requires fungicide and a bactericide.


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Pyogenic Paronychia


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Pyogenic Paronychia


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Other predominately Staph Infections.

  • Botrymycosis

    • Presentation: Chronic, indolent d/o characterized by nodular, crusted, purulent lesions.

      • Sinus tracts discharge sulfur granules. Scaring.

    • Uncommon disorder. Altered immune function.

    • S. Aureus most common. (Pseudo, E-coli, Proteus, Bacteroides, Strep.)

  • Pyomyositis

    • S. aureus abcess in deep, large striated muscle.

    • Most frequent location is thigh

    • Occurs in tropics and in children as well as AIDS pts.

    • Not associated with previous laceration.


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Pyomyositis


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Impetigo Contagiosa

  • Presentation: 2mm erythematous papule develops into vesicles and bullae. Upon rupture a straw colored seropurulent discharge dries to form yellow, friable crust.

  • Etiology: S. Aureus > S. Pyogenes.

  • Lesions located on exposed parts of body.

  • Group A Strep can cause AGN

    • Children <6 yrs old.

    • 2% to 5%

    • Serotytpes 49, 55, 57, 60 strain M2 most associated

    • Good prognosis in children.


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Impetigo Contagiosa

  • Treatment

    • PCN, 1st Gen. Cephalosporin.

    • Topical: bacitracin or mupirocin after soaking off crust.

  • Topical ABX prophylaxis of traumatic injury.

    • Reduced infection 47 %

  • Treatment of nares for carriers.


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Impetigo Contagiosa


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Impetigo Contagiosa


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Impetigo Contagiosa


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Bullous Impetigo

  • Presentation: Large, fragile bullae, suggestive of pemphigus. Rupture leaves a circinate, weepy crusted lesion (impetigo circinata). Collarette of scale present.

  • Affects newborns at the 4-10th days of life. Adults in warm climates


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Bullous Impetigo


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Bullous Impetigo


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Bullous Impetigo


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Staphylococcal Scalded Skin Syndrome.

  • Presentation: Febrile, rapidly evolving generalized desquamation of the skin seen primarily in neonates and children.

    • Begins with skin tenderness and erythema of neck groin, axillae with sparing of palm and soles

    • Blistering occurs just beneath granular layer.

    • Positive Nikolsky’s sign

  • Etiology: Exotoxin from S. Aureus infection located at a mucosal surface..

  • Differentiate from TENS by location of blister plane high in epidermis.

  • Treatment as before. Prognosis is good.


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Staphylococcal Scalded Skin Syndrome


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Staphylococcal Scalded Skin Syndrome


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Toxic Shock Syndrome

  • Acute, febrile, multisystem disease.

    • One diagnostic criteria is widespread maculopapular eruption.

  • Causes:

    • S. Aureus : cervical mucosa historically in early 1980’s. Also: wounds, catheters, nasal packing. Mortality 12 %.

    • Group A Strep : necrotizing fasciitis. Mortality 30%.

  • Diagnosis: CDC

    • Temp >38.9C, erythematous eruption with desquamation of palms and soles 1-2 wks after onset. Hypotension

    • AND involvement of three of more other systems

      • GI, muscular, renal, CNS.

    • AND Test for RMSF, Leptospirosis and rubeola as well as blood urine and CSF should be negative.


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Toxic Shock Syndrome

  • Treatment:

    • Systemic ABX,

    • Fluid therapy

    • Drainage of S. Aureus infected site.


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Streptococcal Skin Infections


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Ecthyma

  • Presentation: Vesicle/pustule which enlarges over several days and becomes thickly crusted. When crust is removed a superficial saucer shaped ulcer remains with elevated edges.

    • Nearly always on shins or dorsal feet.

    • Heals in a few weeks with scarring.

  • Agent: Staph or Strep.

  • Heal with scaring

  • Gangrene in predisposed individuals.

  • Treatment: Clean, topical and systemic ABX.


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Ecthyma


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Scarlet Fever

  • Presentation: 24 –48 hrs after Strep. Pharyngitis onset.

    • Cutaneous:

      • Widespread erythema with 1-2 mm papules. Begins on neck and spreads to trunk then extremities.

      • Pastia’s lines – accentuation over skin folds with petechia.

      • Circumoral pallor

      • Desquamation of palms and soles at appox two wks.

        • May be only evidence of disease.

    • Other: strawberry tongue

  • Causes: erythrogenic exotoxin of group A Strep.

  • Culture to recover organism or use streptolysin O titer if testing is late.

  • TX: PCN, E-mycin, Cloxacillin.


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Scarlet Fever


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Scarlet Fever


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Scarlet Fever


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Scarlet Fever


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Erysipelas

  • Presentation: erythematous patch with a distinctive raised, indurated advancing border. Affected skin is very painful and is warm to touch. Freq. associated with fever , HA and leukocytosis >20,000.

    • Face and Legs are most common sites.

    • Involves superficial dermal lymphatics

  • Cause: Group A strep., (Group B in newborns)

  • Differential:

    • Contact derm: more itching little pain.

    • Scarlet fever: widespread punctate erythema

    • Malar rash of Lupus and Acute tuberculoid Leprosy: Absence of fever pain and leukocytosis.

  • Treatment: Systemic PCN for 10 days.


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Erysipelas


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Erysipelas


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Erysipelas


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Cellulitis

  • Presentation: Local erythema and tenderness which intensifies and spreads. Often associated with a discernable wound. Lymphangitis, fever and streaking may accompany the infection.

  • Group A strep and S. Aureus are usually causative.

  • Gangrene and sepsis possible particularly in compromised pt.

  • Treatment: PCNase – resistant PCN, 1st Gen Ceph.


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Cellulitis


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Cellulitis


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Necrotizing Fasciitis

  • Presentation: Following surgery or trauma (24 to 48 hours) - erythema, pain and edema which quickly progress to central patches of dusky blue discoloration. Anesthesia of the involved skin is very characteristic. By day 4-5 the involved area becomes gangrenous.

  • Infection of the fascia.

  • Many causative agents. Aerobic and anaerobic cultures should be taken.

  • Treatment: Early debridement. ABX.

  • 20% mortality in best cases

  • Poor prognostic factors: Age >50, DM, Atherosclerosis, involvement of trunk, delay of surgery >7 days.


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More Staph and Strep Infections

  • Blistering Distal dactylitis

    • Superficial blisters on volar fat pads

    • Typical pt is 2-16 yrs old

  • Perianal Dermatitis

    • Superficial, perianal, well demarcated rim of erythema which is often confused with a dermatitis.

    • Typical pt is 1-8 yrs old.

  • Group B infection

    • Consider in any neonates. Also seen in adults with DM and peripheral vascular disease.

  • Staph Iniae

    • 1997 first reported

    • Cellulitis of hands assoc with preparation of tilapia fish.


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Perianal Dermatitis


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Other Gram Positive Infections.


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Erysipeloid of Rosenbach.

  • Presentation: Purple, often polygonal, sharply marginated patches occurring on the hands. The central portion of the lesion may fade as the border advances. New purplish patches appear at nearby sites ( or possibly distant sites).

  • Causative agent: Erysipelothrix Rhusopathiae. Rod shaped grm (+) that forms long branching filaments. Culture on media fortified with serum at room temp.

  • Organism found on dead animal matter and the affliction is seen most commonly among fishermen, veterinarians, and in the meat packing industry (esp pork)

  • Treatment: PCN 1.0 gm/day 5-10 days.


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Erysipeloid


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Anthrax

Three forms:

  • Cutaneous 95% of cases.

  • Inhalation

  • GI

  • Cutaneous presentation: Inflammatory papule rapidly becomes a bulla surrounded by intense erythema which spontaneously ruptures purulent or sanguineous contents. A dark brown eschar surrounded by vesicles then develops with induration. Regional lymph glands then enlarge and frequently suppurate. The lesion is not tender or painful.

    • Mild cases - gangrenous skin sloughs and eschar heals.

    • In severe cases erythema and extensive edema develops. Lesions appear at other sites. Fever, prostration and death (20% of untreated cases.)


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    Anthrax

    • Human infection generally from infected animals. Human to human transmission is possible.

    • Diagnosis: smear with gram stain and cultures of wound.

      • Gamma bacteriophage to identify

      • Mice serum titer.

      • Electrophoretic immunoblots.

    • Treatment: PCN G 2 million units IV q 6 hours for 4-6 days followed by oral PCN for 7-10 days.


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    Anthrax


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    Anthrax


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    Anthrax


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    Anthrax


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    Anthrax


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    Listeriosis

    • Listeria Monocytogenes

    • Ubiquitous organism which usually causes meningitis of encephalitis.

    • Rare cutaneous affliction causing erythematous, tender papules and pustules with lymphadenopathy, fever and malaise.

    • Risk to immunosuppressed

      • Neonates: Granulomatosis infanta peptica.

    • May be missed on bacteriologic exam. Serologic test useful.

    • Treatment: sensitive to most ABX.


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    Cutaneous Diphtheria

    • Corynebacterium Diphtheriae infection in unimmunized individual

    • Presentation:

      • Ulcer with a hard rolled border with a pale blue tinge. A leathery gray membrane often coves the lesion.

      • Eczematous, impetinginous, vesicular or pustular scratches.

    • Paralysis and cardiac complication from Diphtheria toxin are possible.

    • Common in tropical areas with most U.S. cases from unimmunized migrant workers.

    • Treatment: Diphtheria antitoxin, E-mycin is DOC. Also rifampin and PCN.


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    Desert Sore

    • Ulcerative disease endemic amongst bushmen and soldiers in Australia.

    • Presentaion: Grouped vesicles on extremities which rupture to form superficial, indolent ulcers that may be 2.0 cm in diameter.

    • Cause: Staph, Strep and Corynebacterium Diphtheria.

    • Treatment: Diphtheria antitoxin if organism present and topical ABX with oral PCN or E-mycin.


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    Tropical Ulcer

    • Presentation:

      • Inflammatory papule with vesiculation and ulcer formation frequently with undermined edges.

      • Pseudomembrane may be present or simply crusting.

      • Minimal distress other then mild itching.

      • Autoinnouculation

      • Usually single lesion on one extremity.

    • Most common in native laborers or school children during the ‘rainy season’.

    • Usually occur at sites of cutaneous injury.


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    Tropical Ulcer

    • Etiology: Many organisms found under description of ‘topical ulcer’:

      • Bacteriodes Fusiformis, spirochetes, anaerobes.

    • Differential:

      • Vascular ulcers

        • Arteriosclerotic ulcer – deep to expose fascia and tendons.

        • HTN ischemic ulcer – shallow, painful mid to lower legs.

        • Venous ulcers – shallow, varicosities. Above medial malleolus.

      • Other:

        • Desert ulcer – C diptheriae

        • Gummatous ulcer – punched out, other syphilis signs.

        • Tuberculous ulcer – not usually on leg.

        • Mycotic ulcer – nodular with fungi on inspection.

        • Buruli ulcer – Mycobacterium ulcerans.

        • Leshmania ulcer – contans Leishmania tropicans, not on leg.

        • Ulcer of blood abnormalities.


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    Tropical Ulcer


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    Tropical Ulcer


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    Erythrasma

    • Presentation: sharply delineated, dry, brown, slightly scaling patches located in intertrignous areas esp the axillae, genitocrural crease and webs of 4-5 toes. Rarely, widespread lesions will occur with lamellated plaques.

    • Lesion are generally asymtomatic except for the groin where minor itching may be reported.

    • Extensive involvement is associated with DM and other debilitating disease.

    • Etiology: Corynebacterium Minutissimum.

    • Diagnosis: Woods lamp – coral red.

    • Treatment: e-mycin 250 qid x 7 days. Tolnaftate, miconazole, e-mycin, clindamycin topicals also effective.


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    Erythrasma


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    Erythrasma


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    Intertrigo

    • Presentation: Superficial inflammatory dermatitis where two skin surfaces are in apposition.

    • Etiology: Friction and moisture allows infection by bacteria (Staph, Strep, Pseudo.) or fungi or both.


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    Intertrigo


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    Intertrigo


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    Intertrigo


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    Pitted Keratolysis

    • Presentation: Thick weight bearing portions of the soles gradually covered by asymtomatic round pits 1-3 mm in diameter. Pits may become confluent forming furrows. Rarely, palms may be affected.

    • Etiology: unknown. Micrococcus sedentarius in synergy with corynebacteria is suspected

    • Men with sweaty feet are most susceptible.

    • Treatment: Topical E-mycin, clindamycin. Miconazole, benzoyl perioxide gel, AlCl solution.


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    Pitted Keratolysis


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    Pitted Keratolysis


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    Gas Gangrene

    • Presentation: Several hours after a patient receives a deep laceration, severe pain and wound site crepitance develop as well as fever, chills and prostration. A mousy odor is characteristic.

    • Etiology: (2 types)

      • Clostridium types: perfringens, oedematiens, septicum and haemolyticum. Acute onset !

      • Peptostreptococcus. Delayed onset up to several days.

    • Treatment:

      • Clostridium: Wide debridement and PCN G, hyperbaric

      • Peptostreptococcus: Surgical debridement limited to glossy necrotic muscle.


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    Gas Gangrene


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    Chronic Undermining Burrowing Ulcers ( Meleney’s Gangrene)

    • Presentation: Pt who recently (1-2 wks) underwent surgical drainage of a peritoneal or lung abscess develops carbunculoid appearance at the sutures or wound site. The lesion then differentiates into three zones: outer zone- bright red, middle zone-dusky purple, inner zone-gangrenous with central areas of granulation tissue. Pain is excruciating.

    • Etiology: Peptostreptococcus in periphery. S. Aureus or Enterobacteriaceae in zone of gangrene.

      • Bacterial synergetic gangrene

    • Differential: gangrenous ecthyma (pseudomonas), amebic (liver abscess associated), Pyoderma gangrenosa (no bacteria)

    • Treatment: Wide excision with ABX (PCN and aminoglycoside).


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    Fournier’s Gangrene of the Penis and Scrotum

    • Presentation: Gangrenous infection of penis, scrotum or perineum which spreads along fascial planes.

    • Etiology: Group A Strep or mixed organism.

    • Ages 20-50

    • Culture for aerobic and anaerobic organisms.

    • Treatment: ABX as indicated.


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