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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

Bacterial InfectionsChapter 14

Infections Caused by Gram Positive Organisms.

Michael Hohnadel, D.O.


staphylococcal infections
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
embolic phenomena with endocarditis
Embolic Phenomena With Endocarditis

Osler nodes

Janeway lesion

superficial pustular folliculitis
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.
sycosis vulgaris sycosis barbae
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.
sycosis lupoides
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
treatment of folliculitis
Treatment of Folliculitis
  • Cleansing with soap and water.
  • Bactroban (Mupirocin)
  • Burrows solution for acute inflammation.
  • Antibiotics: cephalosporin, penicillinase resistant PCN.
  • 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.
  • 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.
treatment of chronic furunculosis
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)
pyogenic paronychia
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.
other predominately staph infections
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.
impetigo contagiosa
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.
impetigo contagiosa20
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.
bullous impetigo
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
staphylococcal scalded skin syndrome
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.
toxic shock syndrome
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.
toxic shock syndrome32
Toxic Shock Syndrome
  • Treatment:
    • Systemic ABX,
    • Fluid therapy
    • Drainage of S. Aureus infected site.
  • 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.
scarlet fever
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.
  • 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.
  • 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.
necrotizing fasciitis
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.
more staph and strep infections
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.
erysipeloid of rosenbach
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.

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.)
  • 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.
  • 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.
cutaneous diphtheria
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.
desert sore
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.
tropical ulcer
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.
tropical ulcer65
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.
  • 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.
  • 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.
pitted keratolysis
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.
gas gangrene
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.
chronic undermining burrowing ulcers meleney s gangrene
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).
fournier s gangrene of the penis and scrotum
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.