University:
West Coast University
Course:
PHAR 837 | IPC Infectious Diseases I
Academic year:

2024
Views:

53

Pages:

46
Author:

Asal A.

SKIN AND SOFT TISSUE INFECTIONS (SSTI) Su Lee, Pharm.D., M.S., BCPS-AQID Objectives • Epidemiology, risk factors, characteristics, pathophysiology, common organisms, appropriate antimicrobial therapy, monitoring strategies, and duration of therapy • -Impetigo • -Erysipelas • -Necrotizing Fasciitis • -Cellulitis • -CA-MRSA Skin infection • -Bite Wounds • -Diabetic foot infections 4 Introduction of Skin/Soft Tissue Infections (SSTI) • SSTIs are common and very widely in severity and classifications • Numerous factors influencing development of SSTIs • Important to understand potential infecting organism for specific classification Gorbach SL: Infectious diseases, ed 3. Philadelphia, 2003, Lippincott Williams & Wilkins 5 Pathophysiology Skin-Resistant to infection • Protective Host Factors -Dryness -Continuous epidermal renewal -Sebaceous secretion (sweat) • Predisposing Factors -Inoculum size ( high concentration of bacteria, more than 105 CFU) -Excessive moisture of the skin -Reduced vascular supply ( inadequate blood supply) -Bacterial nutrients -Damage/penetration of skin -Immunocompromised Classification of SSTIs • Simple uncomplicated (mostly G(+)) -Boils such as folliculitis, furuncles, carbuncles -Simple abscess -Erysipelas -Impetigo -Cellulitis • Complicated (G (+), G(-), anaerobes) -Diabetic foot infections -Decubitus ulcers (Pressure sores) -Necrotizing fasciitis -Cellulitis -Gangrene 7 Stevens DL, et al., CID 2014:59:1-43 8 Classification /Etiology • Non-purulent -Erysipelas -Cellulitis -Necrotizing Infection -Streptococci -S. aureus • Purulent -Folliculitis -Furuncles -Carbuncles -Abscess -S. aureus • MSSA • MRSA (CA-MRSA) • MRSA (empiric coverage if severe patients) • Empiric coverage 9 Severity of Purulent SSTI vs. Non-Purulent SSTI • Mild infections • Mild infections -local infection • Moderate infections -SSTI with systemic signs of infection • Severe infection -SSTI patient who have failed incision and drainage plus oral antibiotics -SSTI With SIRS (= Sepsis*) -Immunocompromised patients -typical cellulitis/erysipelas with no focus of purulence • Moderate infections -typical cellulitis/erysipelas with systemic signs of infection • Severe infection -patients who failed oral antibiotic treatment -SSTI With SIRS (= Sepsis*) -Immunocompromised patients -those with clinical signs of deeper infection such as bullae, skin sloughing, hypotension, or evidence of organ dysfunction Sepsis* = SIRS + Infection Definition : Dysregulated host response causing organ failure due to infections • Systemic Inflammatory Response Syndrome (SIRS) -Systemic response to a variety of insults • Infection • Trauma • Burns • Cirrhosis • Drugs • Pancreatitis • Cancer • SIRS Criteria -Must meet 2 or more • Temperature > 38 °C (100.4 °F) or < 36°C (96.8 °F) • Heart Rate > 90 beats/min • White Blood Cells > 12,000 cells/mm3 or < 4,000 cells/mm3 or >10% bands • Respiratory Rate > 20 breaths/min or PaCO2 < 32 mmHg 11 Purulent : Folliculitis, Furuncles, ad Carbuncles • Folliculitis • inflammation of the hair follicle • caused by physical injury, chemical irritation, or infection • Stye: Infection occurring at the base of the eyelid • superficial infection with pus present only in the epidermis • Furuncles and carbuncles : follicular infection extends from around the hair shaft to involve deeper areas (subcutaneous tissue) of the skin • Furuncles: commonly known as a boil, is a walled-off mass of purulent material arising from a hair follicle • Carbuncles: when adjacent furuncles coalesce to form a single inflamed area • S. aureus is the most common cause of folliculitis, furuncles, and carbuncles • Outbreaks of furunculosis caused by S. aureus and CA-MRSA have been reported in settings involving close contact (eg, families, prisons), especially when skin injury was common (such as with athletes) Figures from http://www.webmd.com/skin-problems-and-treatments/ss/slideshow-boils, accessed 9/9/17 Purulent : FolliculitisTC) > Macrolides (Erythromycin, Azithromycin) > TMP/SMX • Re-evaluation after 3-4 months • J Am Acad Dematol 2016;74:945-73 Treatment of CA-MRSA • Large abscess, cellulitis, or systemic symptoms -Incision and drainage -Empiric oral antimicrobial therapy • Trimethoprim-sulfamethoxazole (TMP-SMX) DS q12h (160 x 2 = 320 mg TMP/day) • Minocycline 100mg q 12 h • Doxycycline 100mg q 12 h • Clindamycin 300 – 450mg q 12 h (IF D-zone test is negative) • Linezolid PO • Newer agents -Severe, Conventional MRSA therapy • • • • • Vancomycin IV Linezolid IV Daptomycin IV Tigecycline IV Newer agents Impetigo • Superficial -Group A streptococci (GAS, S. pyogenes) -S. aureus • Small, fluid-filled vesicles, lesions dry to form golden-yellow crusts commonly on hands or face in children • Is transmittable • Treatment : for GAS and MSSA -Penicillinase-Resistant Penicillins (dicloxacillin) or 1st generation cephalosporins (cephalexin) for 7 days if MRSA is suspected or confirmed: Doxycycline, TMP/SMX, or clindamycin -Mupirocin (Bactroban®) or retapamulin x 5 days, but less effective than oral agents Erysipelas • Fiery red in color (no focus of purulence) -Painful lesion with defined demarcated edges -Superficial often with extensive lymphatic involvement -Common on lower extremities but can occur on face -Often in elderly or infant • S. pyogenes (Group A streptococci) -30% of pts. have had a streptococcal respiratory inf. • Treatment -Penicillin V PO or Penicillin G IV/IM , preferred (PO or IV depending on clinical severity) -If S. aureus suspected Nafcillin / Cefazolin IV or Dicloxacillin / Cephalexin PO 17 Lymphangitis • Inflammation involving the subcutaneous lymphatic channels • Secondary to puncture wounds, infected blisters, or other skin lesions • Most common pathogen is S. pyogenes • S/S • Systemic S/S( fever, chills, malaise, and headache) often develop rapidly before or after local sign of infection • Lymph nodes are enlarged and tender • Peripheral edema of the involved extremity • Leukocytosis • Treatment • Penicillin • Initial IV penicillin G 1-2 million units q 4-6 hours for 48-72 hours, followed by penicillin VK PO for 10 days (Clindamycin for Penicillin-allergic pts) • Immobilization and elevation of the affected extremity and warm water soak q 2-4 hours Cellulitis • Acute, spreading infectious process affecting • Majority of infections : • • -S. aureus -Streptococcus pyogenes (group A streptococcus) • Considerations : -MRSA -VRE -Gram negatives: Pseudomonas, E. coli -Anaerobes: Clostridium, Bacteroides, peptostreptococcus • • • • epidermis and dermis Inflammation with little or no necrosis, edema Lymphatic involvement; infection spread through lymphatic tissue and the bloodstream Number of ambulatory care clinics and ED = 9.6 million in 2005, 4 million pts hospitalized for cellulitis between 1998 and 2006, representing 10% of all infection related admission Fever, chills, leukocytosis Bacteremia up to 30% of cases Complications (1% of outpatients, 17% of hospitalized pts): -local Abscess, myositis, osteomyelitis, septic arthritis, bacteremia, endocarditis, and sepsis 19 Cellulitis (Dipiro 12 th ed) Signs • Characterized by erythema and edema of the skin. • Lesions are non-elevated and have poorly defined margins. • Affected areas generally are warm to touch. • Inflammation generally is present with little or no necrosis or suppuration of soft tissue. • Lesions may be associated with purulent drainage, exudates, and/or abscesses. • Tender lymphadenopathy associated with lymphatic involvement is common. Laboratory Tests • Cultures of fluid should be collected when purulent drainage, exudates, or abscesses are present. • Gram stain of fluid obtained by injection and aspiration of 0.5 mL of saline (using a small 22-gauge needle) into the advancing edge of the lesion may aid the microbiologic diagnosis but often yields negative results. • Diagnosis usually is made on clinical grounds rather than by culture. Other Diagnostic Tests • Complete blood cell count is often performed as leukocytosis is common. • Blood cultures often useful because bacteremia may be present in up to 30% of cases. Treatment of Cellulitis Duration : 5 - 7 days or until clinical improvement • Blood culture or cutaneous aspirate, biopsies, or swabs are not routinely recommended -Except Immunocompromised patients or animal bite • Non-purulent Mild : PO for Group A Streptococci -Penicillin VK, Cephalexin, Dicloxacillin, or Clindamycin • Non-purulent Moderate : IV for MSSA or Group A strep -Nafcillin, Ceftriaxone, Cefazolin, or Clindamycin • Non-purulent Severe : MRSA, strep, G(-), anaerobes -Vancomycin + (Pip/tazo, imi/cilastatin or meropenem) 21 Treatment of Cellulitis • Moderate or severe non-purulent cellulitis • Empiric treatment of MRSA Risk Factors • Penetrating trauma • Evidence of infection at nasal/other MRSA colonization • Injection drug use • In patients with two or more SSTI SIRS criteria = SEVERE • MRSA and Group A ẞ-hemolytic streptococci • Clindamycin alone or (amoxicillin + (TMP/SMX*, Doxycycline*, or Minocycline*)} *very poor Group A ẞ-hemolytic streptococci coverage • Severe purulent cellulitis (MRSA parenteral antibiotics) - Vancomycin, Daptomycin, linezolid or tedizolid, telavancin, and ceftaroline 22 Necrotizing Fasciitis Clostridial Myonecrosis (Gas gangrene) • Deep, devastating infection • Involves subcutaneous tissue -Along fascial planes to superficial fascia -May continue and involve muscle (myositis) • Necrosis of area -Gangrene (70%) • Causing Organisms -Monomicrobial or • S. pyogenes, S. aureus • Vibrio vulnificus, Aeromonas hydrophila • Clostridial spp. Including C. perfringens (Gas gangrene-often associated with trauma) -Polymicrobials 24 Treatment of Necrotizing Fasciitis Severe : emergent surgical inspection/debridement, IV • Empiric Tx : Broad : Vanco + Pip/Taz • (Vancomycin or Linezolid) + {(Pip/Taz or Cabapenem) or (Ceftriaxone + Metronidazole)} • Definitive : -Monomicrobial • S. pyogenes: Penicillin + Clindamycin (anti-toxin effect, as Linezolid with less evidence) • Clostridial sp. : Penicillin + Clindamycin • Vibrio vulnificus (G(-) rod) : Doxycycline + Ceftazidime • Aeromonas hydrophilia (G(-) rod) : Doxycycline + Ciprofloxacin -Polymicrobial : Vanco + Pip/Taz 25 New Agents for ABSSSI (Acute Bacterial Skin and Skin Structure Infections) • Ceftaroline (5th generation cephalosporin) : 600 mg IV q 12 hrs -MRSA, strep, Enterobacterales • Tedizolid (oxazolidinone) IV/PO : 200 mg q 24 hrs -Gram-positive including MRSA • Lipoglycopeptides IV -Telavancin 10 mg/kg Q 24 h : Renal adjustment -Dalbavancin T1/2 = 346 hrs; 1500 mg as a single dose or 2 doses (1000 mg day 1 & 500 mg day 8) -Oritavancin T1/2 = 245 hrs; 1200 mg single dose • Delafloxacin : 450 mg PO q 12 hrs or 300 mg IV q 12 hrs • Omadacycline : 300 mg PO qday or 100 mg IV qday Diabetic Foot Infections • • • • Most common and severe complications of DM lower extremity (LE) ulcer most frequent reason for hospitalization in DM DM is the leading cause of lower-extremity amputations in US Retrospective studies indicate a 2-year mortality rate of 35-50% and a cumulative amputation rate over 1-3 years of 40% • Almost all subsequent amputations precipitated by previous foot ulcer-stressing need for preventive foot care • At 2 years, relative risk of death 2.4 times in diabetic subjects with foot ulcers compared to those without Diabetic Foot Ulcer Etiology • Polymicrobial (multiple pathogens ) -3 to 9 organisms per infection in hospitalized patients -Aerobes • Gram (+)(80% of cases) -Staphylococci, Streptococci, or Enterococci • Gram (-)(50% of cases) -Enterobacter spp., or Pseudomonas -Anaerobes (50% of cases) • Gram (+) cocci or bacteroides Pathogenesis • Neuropathy • Sensory-NOT aware of mechanical/thermal injury • Motor-predisposition to gait disturbance/foot deformalities, leads to weight maldistribution, elevated focal pressure, and increase risk of ulceration • Vascular insufficiency-diminished arterial blood supply Factors Affecting Antimicrobial Selection • Vascular impairment – penetration of abx • Impaired renal function – caution Vanco/AGs • Autonomic neuropathy/gastroparesis • Decreased absorption of oral abx • Abx resistance patterns, previous abx exposure (Review Cultures at least for 1 year) • Drug allergies (PCN, Sulfa) • Linezolid : myelosuppression (up to 45% of pts) • Severe infections more likely polymicrobial Treatment : Wound Care • Apligraf ®: living/biological dressing made from neonatal foreskin • Approved for adjunct treatment of mild diabetic foot ulcers • Becaplermin (Regranex ® ) Gel 0.01% : topical recombinant human platelet-derived growth factor (rhPDGF) • Limited effects due to elevated proteases in ulcers • Promogran® : collagen & oxidized regenerated cellulose, sterile & freeze dried matrix sheet binds/inactivates proteases, protects growth factors • Indicated for use in exuding wounds • Vacuum Assisted Closure(VAC) ® : negative pressure wound therapy through sterile, latex-free foam dressing 31 Severity assessment using IDSA/IWGDF classification Lipsky BA at al, DMRR 2019;36(S1):e3280 IDSA Classification of Diabetic Foot Infections • Mild : Ulcer with < 2 cm of superficial inflammation -Gram (+) S. aureus (assume MRSA) S. agalactiae (Group B Strep) S. pyogenes • Moderate : Ulcer with ≥ 2cm of inflammation with extension of fascia -G(+) + GNB(Gram Negative Bacilli) • Severe : Extensive local inflammation + SIRS (≥2)= Sepsis -As above + anaerobic bacteria Diagnosis -Adjunctive measure for Dx: Inflammatory serum biomarkers- CRP, ESR, PCT -Osteomyelitis o Plain X-ray and clinical/laboratory finding o MRI, CT, leukocyte scintigraphy Lipsky BA et al., CID 2012; 54(12):132-173 Lipsky BA at al, DMRR 2019;36(S1):e3280 33 Treatment of Diabetic Foot Infections Severity of Infection Route of Administration Setting Duration of Therapy Mild Topical or PO Out patient 1-2 Wks, May extended up to 4 wks if slow to resolve Moderate PO (or initial IV) Outpatient (Inpatient) 1-3 Wks Severe Initial IV Switch to PO if clinically improved (OM after 5-7 days) Inpatient, then Outpatient 2-4 Wks (osteomyelitis up to 6 wks) Lipsky BA at al, DMRR 2019;36(S1):e3280 34 Empiric Abx for DFI Lipsky BA at al, DMRR 2019;36(S1):e3280 35 Lipsky BA at al, DMRR 2019;36(S1):e3280 36 37 38 Decubitus Ulcer (Pressure Sores) Stage 1 Intact skin with a localized area of nonblanchable erythema. Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration; these may indicate deep tissue pressure injury. Stage 2 Partial-thickness loss of skin with exposed dermis. Wound bed is viable, pink or red, moist, and may also present as an intact or ruptured serum-filled blister. Adipose tissue is not visible and deeper tissues are not visible. Granulation tissue, slough, and eschar are not present. a Stage 3 Full-thickness loss of skin, in which adipose tissue is visible in the ulcer and granulation tissue and epibole (rolled wound edges) are often present. Slough and/or eschar may be visible. Depth of tissue damage varies by anatomical location; areas of significant adiposity can develop deep wounds. Undermining and tunneling may occur. Fascia, muscle, tendon, ligament, cartilage and/or bone are not exposed. a Stage 4 Full-thickness skin and tissue loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer. Slough and/or eschar may be visible. Epibole (rolled edges), undermining and/or tunneling often occur. Depth varies by anatomical location. Unstageab Full-thickness skin and tissue loss in which the extent of tissue damage within a le the ulcer cannot be confirmed because it is obscured by slough or eschar. If slough or eschar is removed, a stage 3 or stage 4 pressure injury will be revealed. DeepIntact or nonintact skin with localized area of persistent nonblanchable tissue (discoloration of the skin that does not turn white when pressed) deep red, pressure maroon, purple discoloration or epidermal separation revealing a dark wound injury bed or blood filled blister. Pain and temperature change often precede skin color changes. This injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface. The wound may evolve rapidly to reveal the actual extent of tissue injury, or may resolve without tissue loss. 39 Supine view of areas where pressure sore formation tends to occur, Dipiro 12e 40 Management of Decubitus Ulcer • Prevention : Relief for a period of only 5 minutes once every 2 hours • > Stage 3 : Surgical intervention, debridement of necrotic tissue as needed • Wound cleansing, dressing, prevention, diagnosis and treatment of infection • Topical antibiotics (Silver sulfadiazine, triple antibiotics) up to 2 weeks • Systemic antibiotics on bacteremia, sepsis, cellulitis, fasciitis, or osteomyelitis • MRSA, anaerobes, enterococci, pseudomonas coverage based on cultures Bite Wounds (human, dog, or cat) • 4 million people bitten by dogs annually • 40% cat bites/scratches become infected • Etiology -Pasteurella multocida (most common, dogs and cats) -Streptococcus, S. aureus, Eikenella (human) -Anerobes : Bacteroides and Fusobacterium • Treatment (Tetanus-diphtheria toxoids vaccine , Rabies-observe the dog for 10 days) Antimicrobial prophylaxis for 3-5 days for minor wound: all human bite due to high infection risk or animal bite in immunocompromised pts or deeper wounds (asplenic; advanced liver disease; pre-existing or resultant edema of the affected area; moderate to severe bite related injuries to hands or face; deep puncture wounds that cannot be adequately irrigated; or penetrated to periosteum or joint capsule) -Amoxicillin-clavulanate -Doxycycline* or moxifloxacin (not in children or pregnant women) -Levofloxacin*, Ciprofloxacin*, TMP/SMX*, cefuroxime* *Add anaerobe coverage (metronidazole or clindamycin) • Cf. Severe wound: hospitalization with IV Abx (Unasyn, Zosyn, Cefoxitin, Ertapenem, {(Doxy or FQs) + (Metronidazole or Clindamycin)} 42 Rabies • Vaccine-preventable, zoonotic, viral disease affecting • • • • • • the CNS. Serious public health problem mainly in Asia and Africa, that causes tens of thousands of deaths annually with 40% being children under 15. In US, only 1 to 3 cases reported each year, but 60,000 Americans receive PEP following an exposure Dog bites are scratches cause 99% of the human rabies cases, and can be prevented through dog vaccination and bite prevention Once the virus infects the CNS and clinical symptoms appear, rabies is fatal in 100% of cases. Incubation period typically 2-3 months but may vary from one week to one year, depending on factors such as the location of virus entry and the viral load. Initial symptoms of rabies include generic signs like fever, pain and unusual or unexplained tingling, pricking, or burning sensations at the wound site. • Rabies deaths are preventable with prompt post exposure prophylaxis (PEP) by stopping the virus from reaching the CNS. • PEP include wound washing, administration of a course of human rabies vaccine and, when indicated, rabies immunoglobulin (RIG) WHO Rabies version 6/5/2024, https://www.who.int/news-room/factsheets/detail/rabies#:~:text=Rabies%20is%20a%20vaccine%2Dpreventable,%2C%20cats%2C%20livestock%20and%20wildlife, retrieved on 9/30/24. 43 Lyme Disease • Caused by Borrelia burgdorferi through bite of infected blacklegged ticks. • Typical symptoms • fever, headache, fatigue, and a characteristic skin rash called “erythema migrans” (Bull’s eye). • If left untreated, infection can spread to joints, the heart, and the nervous system • Diagnosis • based on symptoms, physical findings (e.g., rash), and the possibility of exposure to infected ticks • Laboratory test • helpful if used correctly and performed with validated methods • Treatment • Early Localized Ds: Doxycycline 100 mg PO BID x 10 days, Amoxicillin 500 mg PO TID x 14 days, or Cefuroxime 500 mg PO BID x 14 days • Early Disseminated Ds: Doxcycline 100 mg PO BID, Ceftriaxone 2 G IV qday, Cefotaxime 2 G IV q8h x 14-21 days • Late Disseminated Dx: Ceftriaxone 2 G IV 14-28 days https://www.cdc.gov/lyme/index.html, accessed on 8/14/21 44 Lyme Disease Sanchez E et al., JAMA 2016;315(16):1767-77 45 RxPrep ORAL Antibiotic Dosing Name Usual adult dose (skin infection) Dicloxacillin 250-500 mg po q6h Amoxicillin/clavulanate* 875/125 mg po q12h Cephalexin* 250 mg to 500mg po q6h Cefuroxime* 250 – 500 mg po q12h Doxycycline 100 mg po q12h, (NOT in age<8 y or pregnancy) Clindamycin 300-450 mg po TID Erythromycin 250 – 500 mg po q6h TMP/SMX DS* 8-12mg/kg/day (TMP), 1-2 tabs po q8-12h *Renal adjustment necessary PARENTERAL Antibiotic Dosing Name Usual adult dose Oxacillin 1-2 gm IV q6h Cefazolin* 1-2 gm IV q8h Vancomycin* 15 mg/kg IV q12h to achieve target AUC (400-600) Daptomycin* 4 -6 mg/kg IV q24h Linezolid 600 mg IV/po q12h Quinupristin/dalfopristin 7.5 mg /kg IV q8h Ampicillin-sulbactam* 1.5-3 gm IV q6h Piperacillin-tazobactam* 3.375 to 4.5 gm IV q6h Clindamycin 600mg IV q8h TMP/SMX 8-12mg/kg/day (TMP component) divided q6h Tigecycline 100 mg x1, then 50mg IV q12h Telavancin* 10 mg/kg IV q24h *Renal adjustment necessary Summary • Epidemiology, risk factors, characteristics, pathophysiology, common organisms, monitoring strategy, appropriate antimicrobial therapy, and duration of therapy • Impetigo • Erysipelas • Cellulitis • Necrotizing Fasciitis • Diabetic foot Infections • Bite Wounds

Skin and Soft Tissue Infections (SSTI)

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