bacteri infection

7/29/2019 bacteri infection

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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 erosionswith 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 nodesJaneway 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 ofthe 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 andpersistence.

Tinea is lower.

Herpes short lived

Pseudofolliculitis Barbea ingrown hair and papules.


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Sycosis Vulgaris
http://dermatology.cdlib.org/DOJvol5num2/media/duv-2.jpeg


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Sycosis Lupoides

Staph infection that through extension results incentral 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 resistantPCN.


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Furunculosis

Presentation: Perifollicular, round, tender abscessthat 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 withdefinite fluctuation.

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

Upper lip and nose ,danger triangle, requires prompttreatment 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 cleanserssoap, 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 500mg QID (or Clindamycin 150mg qd for 3 mo)


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Pyogenic Paronychia

Presentation: Tender painful swelling involving the skinsurrounding the fingernail.

Etiology: Moisture induced separation of eponychiumfrom nail plate by trauma or moisture leading to secondaryinfection. Often work related

Bacteria cause acute abscess formation, Candida causeschronic 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
http://www.aafp.org/afp/20010315/1113_f2.jpghttp://www.aafp.org/afp/20010315/1113_f2.jpghttp://www.aafp.org/afp/20010315/1113_f2.jpg


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Pyogenic Paronychia
http://www.aocd.org/skin/dermatologic_diseases/images/paronychia_nail_in_1.gif


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Other predominately Staph Infections.

Botrymycosis

Presentation: Chronic, indolent d/o characterized bynodular, 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 developsinto vesicles and bullae. Upon rupture a strawcolored seropurulent discharge dries to formyellow, friable crust.

Etiology: S. Aureus > S. Pyogenes. Lesions located on exposed parts of body.

Group A Strep can cause AGN

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 ofpemphigus. 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 generalizeddesquamation of the skin seen primarily in neonates andchildren. Begins with skin tenderness and erythema of neck groin, axillae

with sparing of palm and soles

Blistering occurs just beneath granular layer. Positive Nikolskys sign

Etiology: Exotoxin from S. Aureus infection located at amucosal surface..

Differentiate from TENS by location of blister plane highin epidermis.

Treatment as before. Prognosis is good.


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Syndrome


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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 1980s. Also:wounds, catheters, nasal packing. Mortality 12 %.

Group A Strep : necrotizing fasciitis. Mortality 30%.

Diagnosis: CDC

Temp >38.9C, erythematous eruption with desquamation of palmsand 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 bloodurine 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 overseveral days and becomes thickly crusted. Whencrust is removed a superficial saucer shaped ulcerremains 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: 2448 hrs after Strep. Pharyngitis onset. Cutaneous:

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

Pastias 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 iftesting 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 painfuland is warm to touch. Freq. associated with fever , HAand 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
http://umed.med.utah.edu/MS2/derm/lect6/slide5.jpg


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Erysipelas


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Cellulitis

Presentation: Local erythema and tendernesswhich 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: PCNaseresistant 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 progressto 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.

Erysipeloid of Rosenbach


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Erysipeloid of Rosenbach.

Presentation: Purple, often polygonal, sharply marginatedpatches occurring on the hands. The central portion of the

lesion may fade as the border advances. New purplishpatches appear at nearby sites ( or possibly distant sites).

Causative agent: Erysipelothrix Rhusopathiae. Rod shaped

grm (+) that forms long branching filaments. Culture onmedia fortified with serum at room temp.

Organism found on dead animal matter and the affliction isseen most commonly among fishermen, veterinarians, andin 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 whichspontaneously ruptures purulent or sanguineous contents.A dark brown eschar surrounded by vesicles then developswith induration. Regional lymph glands then enlarge andfrequently suppurate. The lesion is not tender or painful. Mild cases - gangrenous skin sloughs and eschar heals.

In severe cases erythema and extensive edema develops. Lesionsappear at other sites. Fever, prostration and death (20% ofuntreated 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 for4-6 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 andmalaise.

Risk to immunosuppressed

Neonates: Granulomatosis infanta peptica.

May be missed on bacteriologic exam. Serologic testuseful.

Treatment: sensitive to most ABX.


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Cutaneous Diphtheria

Corynebacterium Diphtheriae infection in unimmunizedindividual

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 fromunimmunized migrant workers.

Treatment: Diphtheria antitoxin, E-mycin is DOC. Also

rifampin and PCN.


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Desert Sore

Ulcerative disease endemic amongst bushmen andsoldiers 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 organismpresent 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 schoolchildren during the rainy season.

Usually occur at sites of cutaneous injury.


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Tropical Ulcer

Etiology: Many organisms found under description oftopical ulcer:

Bacteriodes Fusiformis, spirochetes, anaerobes.

Differential:

Vascular ulcers

Arteriosclerotic ulcerdeep to expose fascia and tendons.

HTN ischemic ulcershallow, painful mid to lower legs.

Venous ulcersshallow, varicosities. Above medial malleolus.

Other:

Desert ulcerC diptheriae

Gummatous ulcerpunched out, other syphilis signs. Tuberculous ulcernot usually on leg.

Mycotic ulcernodular with fungi on inspection.

Buruli ulcerMycobacterium ulcerans.

Leshmania ulcercontans 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, slightlyscaling patches located in intertrignous areas esp theaxillae, 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 lampcoral 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 dermatitiswhere 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

i


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Intertrigo

I i


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Intertrigo

Pi d K l i


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Pitted Keratolysis

Presentation: Thick weight bearing portions of thesoles 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.

Pi d K l i


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Pitted Keratolysis

Pi d K l i


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Pitted Keratolysis

G G


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Gas Gangrene

Presentation: Several hours after a patient receives a deeplaceration, 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.

G G


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Gas Gangrene

Chronic Undermining Burrowing


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g g

Ulcers ( Meleneys Gangrene)

Presentation: Pt who recently (1-2 wks) underwent surgicaldrainage of a peritoneal or lung abscess developscarbunculoid appearance at the sutures or wound site. Thelesion then differentiates into three zones: outer zone-bright red, middle zone-dusky purple, inner zone-

gangrenous with central areas of granulation tissue. Pain isexcruciating.

Etiology: Peptostreptococcus in periphery. S. Aureus orEnterobacteriaceae in zone of gangrene.

Bacterial synergetic gangrene

Differential: gangrenous ecthyma (pseudomonas), amebic(liver abscess associated), Pyoderma gangrenosa (nobacteria)

Treatment: Wide excision with ABX (PCN and

aminoglycoside).

Fourniers Gangrene of the Penis


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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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