SSTIs. Dr Carlos Dobles R. San José, 29 de abril de 2017

Transcription

1 SSTIs Dr Carlos Dobles R. San José, 29 de abril de 2017

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3 NORMAL SKIN FLORA Propionibacterium acnes Corynebacterium sp. Staphylococci Staphylococcus epidermidis Staphylococcus aureus Streptococci sp. Candida albicans (yeast) Many others

4 TYPES The various types of SSTIs, listed according to clinical presentation and anatomic location, include the following: Impetigo Folliculitis Furuncles Carbuncles Erysipelas Cellulitis Necrotizing fasciitis Pyomyositis

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6 Erysipela Is an acute infection of the upper dermis and superficial lymphatics, usually caused by streptococcus bacteria. Erysipelas is more superficial than cellulitis, and is typically more raised and demarcated.

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8 Impetigo-Presentation Impetigo is characterised by blisters that rupture and coalesce to become covered with a honey-coloured crust.

9 Tinea cruris

10 Furuncles and carbuncles

11 Cellulitis Is an inflammation of the dermal and subcutaneous tissues due to non suppurative bacterial invasion. Misnomer as lesion is one of the connective tissues and interstitial tissue and not of the cells. The common causative organisms are GAS and staphylococcus.

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13 Folliculitis

14 Impetigo

15 Herpes Zoster

16 Paronychia

17 What is Localized skin infection? Localized SSSIs include lesions such as furuncles, carbuncles, and abscesses, which would generally be treated by incision and debridement with drainage.

18 Clinical presentations of SSTIs Necrotising SSTI Surgical site infection Cellulitis Skin and soft tissue infections Diabetic foot infection Abscess Infected ulcer Infected wound ~0.1% of adult population requires hospital treatment for SSTIs each year 1 SSTIs may become complicated if require hospitalisation, surgery, involve deeper tissues, co-morbidities or systemic symptoms 1. Eron LJ, et al. J Antimicrob Chemother 2003; 52 Suppl1:i3 17.

19 When to consider it complicated? Surrounding cellulitis, immunocompromised, or the presence of potentially infectable prostheses, such as cardiac valves, orthopedic devises or vascular grafts, mandates antibiotic use and might well mean that the infection would be classed as complicated

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22 Comorbidities In particular, there are a number of underlying comorbidities that should be sought and excluded as being particularly relevant to the patient with an SSSI. Diabetes Vascular insufficiency in the area of the infection Chronic renal or hepatic disease Potentially infectable prostheses Immunosuppression Debilitation or advanced age Recent antimicrobial therapy Recent surgery; and Recent hospitalization

23 Skin Abscess

24 Animal Bites

25 Animal Bites

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27 What can you expect? superficial Gram Positives Anaerobes GN Deep

28 What are the three main organisms? FIRST :S. aureus Is the commonest Two potent and clinically relevant exotoxins from S. aureus are the enterotoxins (responsible for food poisoning) and toxic shock syndrome toxin (TSST-1) SECOND : Group A streptococci ( GAS) (S. pyogenes), much like S. aureus can produce a variety of virulence factors. Group A streptococci secrete an array of soluble exotoxins some of which are extremely potent causing systemic toxicity known as streptococcal toxic shock syndrome 9STSS) and necrotizing fascitis. THIRD : Clostridium perfringens is the most frequently isolated, although isolates of C. septicum, C. histolyticum, C. bifermentans, and C. novyii can be equally pathogenics.

29 Physiology and Resistance Mechanisms of S aureus S aureus is a virulent human pathogen with the ability to elaborate a range of virulence factors and toxins; gram positive cocci in clusters Resistance to methicillin first appeared in 1961, attributed to inheritance of a meca gene found on the mobile staphylococcal cassette chromosome mec (SCCmec) Genetic analysis suggests that meca has been transferred to S aureus over 20 times, resulting in 5 major lineages MecA gene cassette leads to genetic alteration of penicillin binding protein, conferring resistance to all penicillin and cephalosporin family of antibiotics WTA=wall teichoic acid; PVL=Panton-Valentine leukocidin; CHIP=chemotaxis inhibitory protein. Zetola N et al. Lancet Infect Dis. 2005;5: Deresinski S. Clin Infect Dis. 2005;40: Foster TJ. J Clin Invest. 2004;114:

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31 Why increasing?? Initially we thought it is pure Ping Pong effects, i e, the same hospital acquired MRSA is now living in the community. But it is clear now that this is not the complete story There is emergence of new CA-MRSA

32 Risk Factors for Community-Associated (CA) MRSA Athletes (close physical contact) Military personnel Children Native Americans HIV MSM Prisoners Young sexually active Family members (don t forget to ask!) Majority of patients have no identifiable risk factors

33 Community-Associated (CA) MRSA Increasing cause of community skin infections Genotypically and phenotypically unique from nosocomial MRSA Less resistant to non-beta-lactam agents Often susceptible to TMP-SMX, clinda, tetracyclines, +/- fluoroquinolones Panton-Valentine leukocidin (PVL) virulence factor Risk Factors Athletes, inmates, military recruits, men who have sex with men, injection drug user, prior antibiotic use Increases need to culture.

34 The emergence of VRE, VRSA and VISA 1997: VISA first reported, in United States 1 and Japan. 2 Developed spontaneously, without genetic exchange 1958: Vancomycin first licensed Mid-1980s: Use of vancomycin increases in response to surge in MRSA 2006: Nine confirmed isolates of VISA and one of VRSA in Europe 3 TODAY: VRE encountered in hospitals in most countries Reports of VISA increasing; VRSA still rare : VRE first reported, in Europe : VRSA first reported, in United States. 5 Result of transfer of VanA gene from VRE to MRSA 6 Increasing reports of S. aureus with heterointermediate resistance to vancomycin (hvisa) 1. CDC. MMWR 1997; 46: Hiramatsu K, et al. J Antimicrob Chemother 1997; 40: EARSS. EARSS annual report, Uttley AH, et al. Lancet 1988; 1: CDC. MMWR 2002; 51: CDC.

35 Percentage of isolates (van MIC = 1 µg/ml) Number of isolates MIC shift: S. aureus susceptibility to vancomycin is decreasing MRSA MSSA Year MRSA MSSA Year S. aureus isolates submitted to UCLA Clinical Microbiology Laboratory (n = 6,003) Wang G, et al. J Clin Microbiol 2006; 44:

36 What the history says? Boucher & SAkoulas CID 2007

37 IDSA GUIDELINE 2005 CID,2005, 41:

38 CLSI vancomycin breakpoints against S. aureus were lowered in 2006 to take account of MIC shift Old breakpoint (µg/ml) New breakpoint (µg/ml) VSSA 4 2 VISA VRSA Tenover FC & Moellering RC Jr. CID 2007; 44:

39 Linezolid first Oxazolidinon O Linezolid N F N O O N H O C CH 3 337,35 Dalton 1449,27 Dalton H 3 C HO + H 3 N CH 3 O HO O O HO O CH 2OH O O Cl Vancomycin Size relationship 1 : 4 O HO O NH N H O Cl H N O O N H O H N O OH O N H CH 3 NH 2 + CH 3 O HO OH OH NH 2 CH 3

40 Emergence of a New Kind of MRSA The majority of CA-MRSA infections are SSSI and adequate drainage/debridement and/or antibiotics is sufficient therapy for cure these infections. Other reports of invasive CA-MRSA infections include necrotizing pneumonia and necrotizing fascitis CA-MRSA prevalence rate was 30.2% (range %), whereas for the prospective studies 636 patients) the prevalence rate was 37.3% (range %).

41 PVL toxin: a toxin produced by MRSA The Panton-Valentine leukocidin (PVL) toxin,a potent dermatoxin, act synergistically to form pores in the cell membrane of mononuclear and polynmorphonuclear (PMN) cells. of the PVL toxin is predominately found in SCCmecA IV types, in particular the USA300 pulse field pattern.

42 Skin and soft tissue infections (SSTIs) Include infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis. Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection.

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45 Necrotizing Fasciitis Flesh Eating Strep Streptococcus pyogenes (Group A Strep) Tissue digesting enzymes Hyaluronidase Streptokinase Streptolysins Rapidly spreading cellulitis may lead to loss of limb

46 Skin and Soft Tissue Infections Moreover, these infections are commonly associated with the early onset of shock and organ failure. Predisposing factors include varicella, penetrating injuries, minor cuts, burns, splinters, surgical procedures, childbirth, blunt trauma, and muscle strain.

47 Complicated skin and soft tissue infection

48 Diagnosis-LRINEC The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score. It uses six serologic measures: C-reactive protein, total white blood cell count, hemoglobin, sodium, creatinine and glucose. A score greater than or eqaul to 6 indicates that necrotizing fasciitis should be seriously considered.

49 LRINEC-Criteria The scoring criteria are as follows: CRP (mg/l) 150: 4 points WBC count ( 103/mm3) <15: 0 points 15 25: 1 point >25: 2 points

50 LRINEC-Criteria cont. Hemoglobin (g/dl) >13.5: 0 points : 1 point <11: 2 points Sodium (mmol/l) <135: 2 points Creatinine (umol/l) >141: 2 points Glucose (mmol/l) >10: 1 poin

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53 Infections in, Skin Subcutaneous tissue Fasciae Muscles

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55 Staphylococcal Scalded Skin Syndrome Pathogen and virulence factors Some Staphylococcus aureus strains One or two different exfoliative toxins cause SSSS Pathogenesis No scarring because dermis is unaffected Death is rare but may be due to secondary infections Epidemiology Disease occurs primarily in infants Transmitted by person-to-person spread of bacteria

56 Desquamation

57 Toxic Shock Syndrome Group A Strep: Any invasive GAS infection (bacteremia, nec fasc, gangrenous myositis flesh eating ) complicated by case definition of TSS Exotoxin superantigens (complicated about 1/3 of invasive GAS infections) Associated bacteremia common Staph aureus toxins: Food poisoning staph enterotoxin Staph Scalded Skin exfoliative toxin CA-MRSA Panton-valentine leukocidin toxin TSS TSST-1 superantigen (interact directly with invariant region of MHC II molecule with activation of up to 20% of all T cells with massive cytokine storm) Previous association with tampons Usually MSSA but MRSA has been reported

58 Necrotizing fascitis A severe and extensive necrosis of the superficial fascia and subcutaneous fat with destruction of those tissues. Gram + and bacteria involved

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63 Diagnosis of Nec. Fas. History and Physical examination of the patient!!!!! This is a simple diagnostic test that works every time. Microbiology: group A Streptococcus pyogenes, Coliforms, Staphylococcus Aureus, Bacteroides species, and rarely Clostridium septicum

64 Nec.Fasc. Leg shows extensive redness and necrosis.

65 Imaging of Nec. Fas. Radiology Plain x-ray shows gas in tissues only 30% of cases Ultrasound: not useful

66 Radiology Standard x-rays of little use. CT more sensitive. MRI and CT can delineate and determine extent of surgical resection.

67 Nec.Fasc-Symptoms pain or soreness of a muscle. The skin may be warm with red or purplish areas of swelling that spread rapidly. There may be ulcers, blisters or black spots on the skin. Fever, chills, fatigue (tiredness) or vomiting may follow the initial wound or soreness

68 NECROTIZING INFECTIONS Necrotizing fasciitis, type 1 Mixed infection; anaerobes plus strep or GNR Incubation = h; progression = hrs days Marked pain, tenderness, swelling, crepitus, foul-smelling Necrotizing fasciitis, type 2 Grp A strep ( flesh-eating bacteria) Incubation = 6-48 h; progression = a few days Often with toxic shock, bullae, no crepitus Pain out of proportion to exam

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74 Six Clinical Criteria of Nec. Fas. 1) Necrosis of the superficial fascia with undermining of the surrounding tissues 2) Systemic toxic reaction with altered mental status 3) Absence of muscle involvement 4) No Clostridia species isolated 5) No arterial inflow occlusion 6) Pathological exam of debrided tissue shows intense leukocytic infiltration, focal fascial and surrounding tissue necrosis and thrombosis of microvasculature ref: Fisher s criteria

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76 Necrotizing Fasciitis Disease starts as localized infection Pain in area, flu-like symptoms Invasive and spreading May lead to toxic shock (drop in blood pressure) Incidence 1-20/100, % mortality Surgical removal, antibiotics

77 Necrotizing Fasciitis

78 Fasciitis

79 What are the Clinical Features of Necrotizing Fasciitis? The most common site of infection is the distal lower limb, although fascial extension up the leg is common. The progression is often alarmingly rapid from a silent or apparently minor process to a fulminant condition with clinical features of systemic toxicity, extensive destruction with threat to the affected limb, and even imminent death. The first clue may be unexplained and rapidly worsening pain By the time the bullae have appeared, there is usually already extensive necrosis.

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81 Clinical findings in necrotising fasciitis Early findings 1. Pain 2. Cellulitis 3. Pyrexia 4. Tachycardia 5. Swelling 6. Skin anesthesia Late findings 1. Severe pain 2. Skin discoloration (purple or black) 3. Blistering 4. Hemorrhagic bullae 5. Crepitus 6. Discharge of dishwater fluid 7. Severe sepsis or systemic inflammatory response syndrome 8. Multi-organ failure

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83 Pyomyositis Pyomyositis, also known as tropical pyomyositis or myositis tropicans, is a bacterial infection of the skeletal muscles which results in a pus-filled abscess Deep infection of muscle usually caused by S. aureus and occasionally by group A streptococci or enteric bacilli. Patients present with fever and tender swelling of the muscle;following exercise or muscle injury, the skin is usually minimally involved.

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85 Pyomyositis S. aureus & Streptococcus infection of the skeletal muscles pus-filled abscess most common in tropical areas- myositis tropicans can affect any skeletal muscle most often infects the large muscle groups e.g.-quadriceps or gluteal muscles

86 Pyomyostis-Diagnosis Most often infects the large muscle groups. The diagnosis can be readily made, if suspected, by needle aspiration and x-rays. Within 1-2 days of injury, the involved extremity becomes painful and swollen. Gas present in tissue may be obvious by physical exam, x-ray or CT.

87 Fever, Sepsis, Localized inflammation Muscle pain Predisposing factors- Immunodeficiency, IVDAs, Trauma and malnutrition Complications- Abscess, sepsis Rx- Drain surgically and antibiotics

88 Clostridial Myonecrosis Principally C. perfringens but C. novyi and C. septicum also seen. Predisposing event Deep trauma with gross contamination Surgical wound Hematogenous spread from colonic lesion Incubation Period 2-3 days; then explosive spread.

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90 Gas Gangrene Pathogenesis and epidemiology Traumatic event must introduce endospores into dead tissue Mortality rate exceeds 40% Diagnosis, treatment, and prevention Appearance is usually diagnostic Rapid treatment is crucial Surgical removal of dead tissue Administration of antitoxin and penicillin Prevent with proper cleaning of wounds

91 Gas Gangrene (Clostridial myonecrosis) Clostridium perfringens Extensive tissue destruction gas production by fermentative action of bacteria. Swollen reddish-black foul smelling tissue with crepitus.

92 Clinical Features Severe pain at the site of initial infection Tissue necrosis. spreading erythema pain soft tissue crepitus (infection tracks rapidly along the tissue planes) Fever,Tachycardia

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94 Gas Gangrene Signs and symptoms Blackening of infected muscle and skin Presence of gas bubbles Pathogens and virulence factors Caused by several Clostridium species Bacterial endospores survive harsh conditions Vegetative cells secrete 11 toxins

95 Gas Gangrene Diagnose on signs and symptoms. Imaging- air in the tissues.

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97 What can you expect? superficial Gram Positives Anaerobes GN Deep

98 Infectious Gangren and gangrenous cellulitis

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100 SSTIs.. COMPLICADA LOCALIZACION De riesgo NO NO CMPLICADA SINDROME COMPARTIMENTAL presente ausente INMUNOSUPRESION presente ausente HALLAZGOS DE IMAGENES Gas y/o colecciones NO SINDROME DE SHOCK TOXICO presente ausente PROGRESION FULMINANTE SI NO SIGNOS LOCALES clásicos (tardíos) ausentes INTENSIDAD DEL DOLOR ++++/4 + o ++/4 COMPROMISO HEMODINAMICO y/o ORGANICO By Dr Dobles R-UCI HCG presente ausente

101 TREATMENT Supportive, often hemodialysis, pressors, ICU care (intractable hypotension/capillary leak) Strep: Emergent surgical debridement if soft tissue primary source ( pain out of proportion to exam ) Empiric: Clinda (900 iv q8) + imi/dori/meropenem or pip/tazo Taylored: PCN G + Clinda IVIG?immunomodulators ex TNFa inhibitors? MSSA: clinda + oxacillin/naf/cefazolin, IVIG MRSA: clinda + vancomycin, IVIG

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103 Treatment usually surgical debridement amputation (if necessary) Antibiotics alone are not effective

104 urgent surgical exploration Extensive debridement or amputation (if necessary) Necrotizing fasciitis after debridement

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111 Predisposing factors Diabetes Alcoholism Malignancy Drug abuse venous stasis lymphoedema

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116 Pyomyositis-Treatment Surgical debridement and appropriate antibiotics are curative (nafcillin-oxacillin or vanco 1 gm q12h IV)

117 Treatment Debridement and excision, with amputation necessary in many cases. Antibiotics alone are not effective because they do not penetrate ischaemic muscles sufficiently to be effective.

118 Staphylococcal Scalded Skin Syndrome Diagnosis, treatment, and prevention Diagnosed by characteristic sloughing of skin Treated by administration of antimicrobial drugs Widespread presence of S. aureus makes prevention difficult 2012 Pearson Education Inc.

119 Necrotizing Skin Infections Characteristics Often perineal or lower extremity (especially for mixed infections) Abnormal inflammatory response (less purulent ) Often rapidly spreading Putrid discharge (what organisms?)/crepitance often present Associated with DM Vascular disease Trauma (bites included) Surgery

120 Skin and Soft Tissue Infections The diagnosis of necrotizing fasciitis should be suspected in a patient with a toxic appearance, bullae, crepitus or anaesthesia of the involved skin, overlying skin necrosis, and laboratory evidence of rhabdomyolysis or DIC. While these findings may be present with severe cellulitis and bacteremia, it is essential to rule out necrotizing fasciitis because rapid surgical debridement is essential.

121 INFECTIONS ASSOCIATED WITH UNDERLYING CONDTIONS Infections Post Op wound infections Lower extremity cellulitis Diabetic foot ulcers Decubitus ulcers Bite wound infections Post Trauma infections Perforated bowel Photo courtesy of T. File MD

122 Skin and Soft Tissue Infections Pyomyositis is a deep infection of muscle usually caused by S. aureus and occasionally by group A streptococci or enteric bacilli. Most cases occur in warm or tropical regions, and most among children. Patients present with fever and tender swelling of the muscle;following exercise or muscle injury, the skin is usually minimally involved.

123 Skin and Soft Tissue Infections The diagnosis of necrotizing fasciitis should be suspected in a patient with a toxic appearance, bullae, crepitus or anaesthesia of the involved skin, overlying skin necrosis, and laboratory evidence of rhabdomyolysis or DIC. While these findings may be present with severe cellulitis and bacteremia, it is essential to rule out necrotizing fasciitis because rapid surgical debridement is essential.

124 Ncrotizing Facitis is LIMB + LIFE threatening Immediate extensive surgical debridement must be done ASAP CLINDAMYCIN must be give, it also has antitoxin action

125 Who gets CA-MRSA?

126 Necrotizing Fascitis Necrotizing fascitis is a fulminating inflammation of the fascia that results in thrombosis of the subcutaneous blood vessels and necrosis of the underlying tissue Necrotizing fascitis itself is generally divided into two broad Type I, caused by mixed aerobic/anaerobic bacteria, including enterococci and non-group A streptococci (usually C or G); and Type 2, caused by group A streptococci, either alone or in combination with other organisms

127 When to consider it complicated? Surrounding cellulitis, immunocompromised, or the presence of potentially infectable prostheses, such as cardiac valves, orthopedic devises or vascular grafts, mandates antibiotic use and might well mean that the infection would be classed as complicated

128 Anatomy of the skin

129 csssi Definition Abscess Cellulitis Ulcer Skin/skin structure infections that: Involve deep, soft tissue Require surgical intervention Are associated with significant underlying disease that complicate the response to treatment 36

130 In particular, there are a number of underlying comorbidities that should be sought and excluded as being particularly relevant to the patient with an SSSI. Diabetes Vascular insufficiency in the area of the infection Chronic renal or hepatic disease Potentially infectable prostheses Immunosuppression Debilitation or advanced age Recent antimicrobial therapy Recent surgery; and Recent hospitalization

131 Clostridial Myonecrosis Presentation Severe pain out of proportion to clinical findings Erythema and cutaneous blisters Gangrene Crepitus Brown foul smelling discharge Loss of motor function

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