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

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. Embolic Phenomena With Endocarditis
Osler nodes
Janeway lesion

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. 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. Sycosis Vulgaris

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

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. Furuncle

11. Furuncle / Carbuncle

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. 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)

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

15. Pyogenic Paronychia

16. Pyogenic Paronychia

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. Pyomyositis

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. 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.

21. Impetigo Contagiosa

22. Impetigo Contagiosa

23. Impetigo Contagiosa

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

25. Bullous Impetigo

26. Bullous Impetigo

27. Bullous Impetigo

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. Staphylococcal Scalded Skin Syndrome

30. Staphylococcal Scalded Skin Syndrome

31. Toxic Shock Syndrome Acute, febrile, multisystem disease. Causes:
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. Toxic Shock Syndrome Treatment: Systemic ABX, Fluid therapy
Drainage of S. Aureus infected site.

33. Streptococcal Skin Infections

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. Ecthyma

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. Scarlet Fever

38. Scarlet Fever

39. Scarlet Fever

40. Scarlet Fever

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. Erysipelas

43. Erysipelas

44. Erysipelas

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, 1st Gen Ceph.

46. Cellulitis

47. Cellulitis

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. 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. Perianal Dermatitis

51. Other Gram Positive Infections.

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. Erysipeloid

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. 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. Anthrax

57. Anthrax

58. Anthrax

59. Anthrax

60. Anthrax

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. 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. 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. 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. 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. Tropical Ulcer

67. Tropical Ulcer

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. Erythrasma

70. Erythrasma

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. Intertrigo

73. Intertrigo

74. Intertrigo

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. Pitted Keratolysis

77. Pitted Keratolysis

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. Gas Gangrene

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. 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.