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1 Bacterial Infections Chapter 14 Infections Caused by Gram Positive Organisms. Michael Hohnadel, D.O. 10/7/03.

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Presentation on theme: "1 Bacterial Infections Chapter 14 Infections Caused by Gram Positive Organisms. Michael Hohnadel, D.O. 10/7/03."— Presentation transcript:

1 1 Bacterial Infections Chapter 14 Infections Caused by Gram Positive Organisms. Michael Hohnadel, D.O. 10/7/03

2 2 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

3 3 Embolic Phenomena With Endocarditis Osler nodes Janeway lesion

4 4 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.

5 5 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.

6 6 Sycosis Vulgaris

7 7 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

8 8 Treatment of Folliculitis Cleansing with soap and water. Bactroban (Mupirocin) Burrows solution for acute inflammation. Antibiotics: cephalosporin, penicillinase resistant PCN.

9 9 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.

10 10 Furuncle

11 11 Furuncle / Carbuncle

12 12 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.

13 13 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 4 th week.). –Rifampin 600mg QD for 10 days with cloxacillin 500 mg QID (or Clindamycin 150mg qd for 3 mo)

14 14 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, 1 st Gen Cephalosporin, augmentin. Chronic infection requires fungicide and a bactericide.

15 15 Pyogenic Paronychia

16 16 Pyogenic Paronychia

17 17 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.

18 18 Pyomyositis

19 19 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.

20 20 Impetigo Contagiosa Treatment –PCN, 1 st Gen. Cephalosporin. –Topical: bacitracin or mupirocin after soaking off crust. Topical ABX prophylaxis of traumatic injury. –Reduced infection 47 % Treatment of nares for carriers.

21 21 Impetigo Contagiosa

22 22 Impetigo Contagiosa

23 23 Impetigo Contagiosa

24 24 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 4-10 th days of life. Adults in warm climates

25 25 Bullous Impetigo

26 26 Bullous Impetigo

27 27 Bullous Impetigo

28 28 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.

29 29 Staphylococcal Scalded Skin Syndrome

30 30 Staphylococcal Scalded Skin Syndrome

31 31 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.

32 32 Toxic Shock Syndrome Treatment: –Systemic ABX, –Fluid therapy –Drainage of S. Aureus infected site.

33 33 Streptococcal Skin Infections

34 34 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. Heal with scaring Gangrene in predisposed individuals. Treatment: Clean, topical and systemic ABX.

35 35 Ecthyma

36 36 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.

37 37 Scarlet Fever

38 38 Scarlet Fever

39 39 Scarlet Fever

40 40 Scarlet Fever

41 41 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.

42 42 Erysipelas

43 43 Erysipelas

44 44 Erysipelas

45 45 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, 1 st Gen Ceph.

46 46 Cellulitis

47 47 Cellulitis

48 48 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.

49 49 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.

50 50 Perianal Dermatitis

51 51 Other Gram Positive Infections.

52 52 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.

53 53 Erysipeloid

54 54 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.)

55 55 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.

56 56 Anthrax

57 57 Anthrax

58 58 Anthrax

59 59 Anthrax

60 60 Anthrax

61 61 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.

62 62 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.

63 63 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.

64 64 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.

65 65 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.

66 66 Tropical Ulcer

67 67 Tropical Ulcer

68 68 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.

69 69 Erythrasma

70 70 Erythrasma

71 71 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.

72 72 Intertrigo

73 73 Intertrigo

74 74 Intertrigo

75 75 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.

76 76 Pitted Keratolysis

77 77 Pitted Keratolysis

78 78 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.

79 79 Gas Gangrene

80 80 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).

81 81 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 Culture for aerobic and anaerobic organisms. Treatment: ABX as indicated.


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