920 likes | 1.97k Views
Bacterial Infections Chapter 14. Infections Caused by Gram Positive Organisms. Michael Hohnadel, D.O. 10/12/04. Staphylococcal Infections. General 20% of adults are nasal carriers. HIV infected are more frequent carriers.
E N D
Bacterial InfectionsChapter 14 Infections Caused by Gram Positive Organisms. Michael Hohnadel, D.O. 10/12/04
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 Osler nodes Janeway lesion
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) • 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 • 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.
Treatment of Folliculitis • Cleansing with soap and water. • Bactroban (Mupirocin) • Burrows solution for acute inflammation. • Antibiotics: cephalosporin, penicillinase resistant PCN.
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.
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.
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)
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.
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.
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.
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 • 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.
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.
Staphylococcal Scalded Skin Syndrome Blister plane in grannular layer
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%.
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.
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.
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.
Scarlet Fever Rash with circumoral pallor
Scarlet Fever ‘Sandpaper Rash’
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.
Erysipelas Sharp, raised border.
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.
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.
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.
Necrotizing Fasciitis Necrosis of the subcutaneous fat and fascia of the inner aspect of the upper arm in an elderly patient with diabetes mellitus.