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Bacterial InfectionsChapter 14

Infections Caused by Gram Positive Organisms.

Michael Hohnadel, D.O.

10/12/04

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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

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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

• Etiology: Staph. Aureus infection that, through extension, results in a central hairless scar surrounded by pustules.

• Histopathology: Pyogenic folliculitis and perifolliculitis with deep extension into hair follicles often with edema.

• Thought to resemble lupus vulgaris in appearance.

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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: A 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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Furunculosis Treatment of Chronic Furunculosis(Avoid auto-inoculation, Eliminate carrier state.)

– Sites of colonization: Nares, axilla, groin and perianal.

– 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 = acute abscess formation. Candida = 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. Assoc with 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. More frequent in children and AIDS

pts.– May not be associated with previous laceration.

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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% of infections– 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.

• Organism present in the lesions.

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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. – Primarily affects 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 (not in lesions).

• Differentiate from TENS • Treatment as before. Prognosis is good.

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Staphylococcal Scalded Skin Syndrome

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Blister plane in grannular layer

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Staphylococcal Scalded Skin Syndrome

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Toxic Shock Syndrome• Presentation:

– Acute, febrile, multi-system disease.– One diagnostic criteria is widespread

maculopapular eruption.

• Causes:– S. Aureus :

• Cervical mucosa historically in early 1980’s. • Also seen with: wounds, catheters, nasal packing.

Mortality 12 %.

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

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Toxic Shock Syndrome• 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.

• 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.• Heals with scaring• Gangrene in predisposed individuals.• Treatment: Clean, topical and systemic ABX.

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Ecthyma

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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

Rash with circumoral pallor

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Scarlet Fever

‘Sandpaper Rash’

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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

Sharp, raised border.

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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.– Less defined border than erythrasma

• 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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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.

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Necrotizing Fasciitis

• 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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Necrotizing Fasciitis

Necrosis of the subcutaneous fat and fascia of the inner aspect of the upper arm in an elderly patient with diabetes mellitus.

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More Staph and Strep InfectionsBlistering 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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AnthraxThree forms:

1. Cutaneous 95% of cases.2. Inhalation3. 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 complications from diphtheria toxin are possible.

• Common in tropical areas with most U.S. cases from non-immunized 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.

– Auto inoculation

– 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.

• Etiology: Many organisms found under description of ‘topical ulcer’:– Bacteriodes Fusiformis, spirochetes, anaerobes.

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Tropical UlcerDifferential:

– Vascular ulcers1. Arteriosclerotic ulcer – deep to expose fascia and tendons.

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

3. 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. (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 assoc. with DM

• 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 asymptomatic 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)1. Clostridium types: perfringens, oedematiens, septicum

and haemolyticum. Acute onset ! 2. 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. Pain is excruciating.

• The lesion then differentiates into three zones: 1.1. outer zone outer zone - bright red,

2.2. middle zone middle zone - dusky purple,

3.3. inner zone inner zone - gangrenous with central areas of granulation tissue.

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Chronic Undermining Burrowing Ulcers

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

• 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.