Transcript Bacterial Infections Chapter 14

Bacterial Infections
Chapter 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
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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
• 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
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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:
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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
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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
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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.
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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 Emycin.
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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:
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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 zonebright red, middle zone-dusky purple, inner zonegangrenous 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
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aminoglycoside).
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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