Skin and Soft Tissue
Infections (SSTIs)
by MOHAMED FATHY ZAIDAN (M.D)
Lecturer of general surgery
Definitions and introduction of SSTIs
 Suffered by everyone at least once in life time, most common
infection, and challenge to a physician in his day to day practice but
unfortunately the most misdiagnosed and mismanaged these
days..
 SSTIs can be defined as an inflammatory microbial invasion of the
epidermis, dermis and subcutaneous tissues.
 Over use of antibiotics is a global problem.
 occurs by invasion of epidermis usually by a breach in the
skin. Hematogenous spread of microbes also results in SSTI.
Classifications
SSTI may be classified according to the layer of infection, severity of
infection and microbiologic etiology.
A-The practice guidelines of the Infectious Diseases Society of
America (IDSA) for the diagnosis and management of SSTIs
classifies into five categories, comprising
1-superficial uncomplicated infection (includes impetigo, erysipelas
and cellulitis)
2- necrotizing infection
3-infections associated with bites and animal contact
4-surgical site infections
5- infections in the immunocompromised host.
Classifications (continued)
B- Eron classification, based on the severity of local and systemic
signs is also useful
1-Class 1 : SSTI but NO signs or symptoms of systemic toxicity or
co-morbidities.
2-Class 2 : Either systemically unwell or systemically well but with
COMORBIDITY that may complicate or delay resolution.
3-Class 3: TOXIC & UNWILL (fever, tachycardia, tachypnoea
and/or hypotension).
4-Class 4 SEPSIS SYNDROME and life-threatening infection
Classifications (continued)
C-Classification according to the layer affected
Epithelium Varicella &Measles
Keratin layer Ring worm (Dermatophyte fungi)
Epidermis Impetigo (Streptococcus pyogenes Staph aureus)
Dermis Erisepelas (Streptococcus pyogenes)
Hair follicles Folliculitis, boils,carbuncles (S. aureus)
Sebum glands Acne (Propionobacterium acnes)
Subcutaneous fat Cellulitis (Beta hemolytic Strepto)
Fascia Necrotizing fasciitis (Strept. pyogenes and mixed anaerobic infection)
D-Purulent OR non-purulent
1-purulent: e.g. Furuncle-abscess, carbuncles
2-Non-purulent :Cellulitis-erysipelas,, necrotizing fasciitis
IMPETIGO
 Def. Initially vesicular, later crusted, superficial infection of the skin.
 Etiology: Group A streptococcus was the commonest cause of this entity, now
days Staphylococcus has become the number one offender. Increasing prevalence
of MRSA as a cause of impetigo is indeed worrying.
 C/P: Streptococcal impetigo starts on exposed surfaces appearing as small vesicles
that pustulate rapidly and ruptures readily. This purulent discharge dries and forms
the characteristic golden yellow, stuck on, crusts. Healing generally occurs without
scarring.
 TTT: Penicillin (drug of choice)
  Benzathine penicillin
  Penicillin v
  PCN-allergic: erythromycin
  Cotrimoxazole, doxycycline and Clindamycin has good activity against CA
MRSA.
IMPETIGO
ERYSIPELAS
 Def. Superficial infection of skin, with prominent
lymphatic involvement.(streptococcal infection)
 C/P painful lesion with a bright red, edematous, indurated
appearance with an advancing raising and sharply
demarcated borders.
 TTT:Mild cases can be treated with oral penicillin, Severe
cases need parenteral crystalline penicillin or if associated
cellulitis is cannot be ruled out penicillinase resistant
penicillin (cloxacillin) or a first generation cephalosporin
should be used.
ERYSIPELAS
CELLULITIS
 Def.: acute spreading infection that involves
subcutaneous tissue (strept. and staph.)
 C/P: rapidly intensifying pain and redness .Fever and
lymphadenopathy may be present.The borders in
cellulitis are not well demarcated.
Acutely presenting and rapidly progressing lesions are
due to most commonly with streptococcus and vice
versa is true for staph aureus. This is a useful clue for the
physician when selecting the antimicrobial.
CELLULITIS vs ERYSIPELAS
GANGRENOUS CELLULITIS
This is a rapidly progressive cellulitis with extensive necrosis
of skin and subcutaneous tissues. They can be divided into
A. Necrotizing fasciitis
B. Gas gangrene
C. Progressive bacterial synergistic gangrene
D. Gangrenous cellulitis in immunocompromised host
Necrotizing fasciitis
 Def.:
 Term that describes a disease condition of rapidly
spreading infection, usually located in fascial planes of
connective tissue that results in tissue necrosis. Any part
of the body may be affected.
 Types:
 a- polymicrobial,,
 b- Monomicrobial (Group A beta-hemolytic streptococci)
Necrotizing fasciitis (continued)
C/P:
Tissue necrosis, spreading, bullae, severe pain, pain out
of proportion, pain then no pain. (this is a clue for
diagnosis)
Often severe intensity of illness
DD:
Necrotizing fasciitis; gas gangrene others Cannot easily
differentiate syndromes on basis of initial clinical
presentation
Initial approach is similar: Early surgery and
antibiotics
TREATMENT of Necrotizing fasciitis
 It is extremely important to diagnose this condition at a
very early stage to reduce the morbidity and mortality,
overall mortality rate for this condition varies from 24-
34%.
 Immediate surgical debridement
 Directed initially against mixed aerobic/anaerobic flora
 Ampicillin/sulbactam or Piperacillin/tazobactam PLUS
clindamycin (theoretically to inhibit protein synthesis and
supress bacterial toxin) PLUS ciprofloxacin;
 Other regimens: imipenem, meropenem, ertapenem,
clindamycin PLUS aminoglycoside or fluoroquinolone
Necrotizing fasciitis
Clues Suggesting NF vs. Cellulitis
 Pain more severe than expected (followed by anesthesia)
 Rapidly spreading swelling and inflammation
 Bullae (but can be seen with cellulitis as well)
 Necrosis
 Toxic shock syndrome
 Elevated CK
Fourniers gangrene
 Necrotizing fasciitis of genitalia,which usually affects
scrotum but may spread to lower abdominal wall and
perianal area. Emergency surgical exploration is a must.
Combination of crystalline penicillin and clindamycin are
the drugs of choice.
Progressive bacterial synergistic
gangrene Meleney gangrne
 This develops as a complication of laparotomy wounds or
colostomy sites.
Clostridial skin infections
 Clostridial cellulitis
 Infection limited to the dermis and epidermis
 Abundance of gas, usually not systemically ill
 Clostridial myonecrosis (classic gas gangrene)
 Rapid onset of necrosis, pain, and toxic state
 Usually associated with devitalized tissue (trauma, surgery,
peripheral vascular disease)
 Clostridial toxins (alpha toxin)
 Lyses blood cells and causes tissue destruction
 Therapy – Immediate surgery, antibiotics +/- hyperbaric O2?
 Clostridium septicum
 Consider adenoCA of Colon, leukemia.
Community-Associated (CA) MRSA
 Patient has no medical history in the past year of:
 Hospitalization
 Admission to a nursing home, skilled nursing facility or hospice
 Dialysis
 Surgery
 The patient has no indwelling catheters or medical
devices that pass through the skin
Community-Associated (CA) MRSA
 Increasing cause of community skin infections.
 in USA the prevalence of CA-MRSA has increased rapidly
over the last 10 years. Incidence of CA MRSA rose to
76% of isolates.
 CA MRSA has become the most predominant one in
USA, accounting for 90%–99% of cases.
 Genotypically and phenotypically unique from nosocomial
MRSA
 Less resistant to non-beta-lactam agents
 Often susceptible to Clindamycin , Tetracyclines, +/-
Fluoroquinolones
 Panton-Valentine leukocidin (PVL) – virulence factor
Diabetic Foot Infections
 Predisposing Factors
 Peripheral Neuropathy
 Maldistribution of weight (trophic ulcers)
 Failure to sense problems (corns, calluses)
 Vascular insufficiency
 Bacterial etiology
 Early, superficial – Strep, Staph
 Late, deep – Mixed
 Therapy – Surgery and antimicrobial agents
 Multi-disciplinary approach
TREATMENT of diabetic foot
infection
 MILD INFECTIONS
 Oral Regimens :
1. Cephalexin 500 mg PO QID OR Clindamycin 300 mg PO TID (covers MRSA)
2. OR Amoxicillin/clavulanate 875 mg PO BID
 Parenteral Regimens :
1. Clindamycin 600 mg IV q8h (covers CA-MRSA if no inducible Clindamycin
resistance)
2. OR :Cefazolin 1 g IV q8h
 MODERATE INFECTIONS
 Ertapenem 1g IV q24h OR Ciprofloxacin 500 mg PO BID / 400 mg IV q12h PLUS
EITHER Clindamycin 600 mg IV q8h/300 mg PO TID OR Metronidazole 500 mg
IV/PO TID
TREATMENT of diabetic foot
infection(continued)
 If patient at risk for MRSA, add Vancomycin to
regimens that do not include Clindamycin (see
dosing section)
 Risk factors for MRSA
1. History of colonization or infection with MRSA
2. Recent (within 3 months) or current prolonged
hospitalization > 2 weeks
3. Transfer from a nursing home or subacute facility
4. Injection drug use
Surgical Site Infections
 Suture removal plus incision and drainage
 If associated with a significant systemic response , such as
erythema and induration extending >5 cm from the
wound edge, temperature >38.5°C, heart rate >110
beats/minute, or white blood cell (WBC) count >12
000/μL Adjunctive systemic antimicrobial therapy
 When risk factors for MRSA are high (nasal colonization,
prior MRSA infection, recent hospitalization, recent
antibiotics) Vancomycin or clindamycin is recommended.
Antibiotics used in SSTI
 Introduction:
1. Complicated skin and soft tissue infections caused by
wide spectrum of bacteria, especially at an era of
increasing resistance and new virulence factors makes
empirical antibiotic section a real challenge.
2. The appearance of CA MRSA has changed the scenario of
antibiotic management of CSSTI, forcing us to choose
antibiotics which can suppress toxins, even for MSSA; rather
than blindly choosing beta lactam agents.
Panton valentine toxin (PVL)
 Is a γ hemolysin toxin seen in staph aureus which was
first isolated in 1932 by Panton and valentine.
 Presence of PVL in MSSA and HA MRSA is less common,
while majority of CAMRSA in USA produce PVL.
 PVL producing MSSA and MRSA infections usually
present as recurrent boils, especially in close groups like
family members, contact sports team members.
 Severe soft tissue infections, rapidly progressive
necrotizing pneumonia and severe arthritis are well
known manifestations of these bacteria.
Panton valentine toxin (contiued)
 The choice of antibiotic selection is extremely important
while treating PVL producing MSSA or MRSA.
 Betalactam antibiotics even though active against MSSA
will trigger release of toxins further contribute to the
pathogenesis.
 Clindamycin and linezolid are active against MRSA and
also suppress toxin production.
Clindamycin
 FDA-approved to treat serious infections due to
S. aureus with Clindamycin
 Good soft tissue penetration
 Toxin suppressing activity
 Even though clindamycin resistance is common in
HAMRSA, it usually works well with CA MRSA, as
these isolates retain their sensitivity to clindamycin.
D-Test FOR CLINDAMYCIN
MRSA isolates resistant to erythromycin must have a D
test done in the laboratory and if positive, clindamycin
should be avoided, as therapeutic failure can occur.
Clindamycin and pseudomembranous
colitis
 A retrospective survey of 15 019 patients treated with
clindamycin for a soft tissue infection was carried out to
determine whether the incidence of serious side effects was
sufficient to preclude the continuing use of this antibiotic.
 13 patients were found to have had severe diarrhea and 2
of these required inpatient treatment for
pseudomembranous colitis. Certain limitations of the use
of clindamycin are suggested but, in view of the recently
improved understanding of the nature of
pseudomembranous colitis and more effective methods of
treatment of this complication,
 It is concluded that this antibiotic still has a useful role to
play in the treatment of acute soft tissue infection.
Practice Guidelines for the Diagnosis and Management of
Skin and Soft Tissue Infections: 2014 Update by the
Infectious Diseases Society of America (recommendation
regarding DALACIN)
1-Impetigo:
When MRSA is suspected or confirmed, clindamycin,
sulfamethoxazole-trimethoprim,or doxycycline,in a 7 days
regamin.
2-Purulent SSTIs (I&D)
antibiotic active against MRSA (Clindamycin) is
recommended for patients with carbuncles or abscesses
who have 1-failed initial antibiotic treatment or 2-have
markedly impaired host defenses or in patients with 3-
SIRS and hypotension
Practice Guidelines for the Diagnosis and Management of
Skin and Soft Tissue Infections: 2014 Update by the
Infectious Diseases Society of America (recommendation
regarding DALACIN) coninued..
3-Necrotizing Fasciitis, Including Fournier Gangrene
 Penicillin plus clindamycin is recommended for
treatment of documented group A streptococcal
necrotizing fasciitis
4-Clostridial Gas Gangrene or Myonecrosis (surgery)
Definitive antimicrobial therapy with penicillin and
clindamycin is recommended for treatment of clostridial
myonecrosis
Recommended empiric antibiotics in
NSTI
Ampicillin/sulbactam 3 gm IV Q6hr +/- vancomycin
+/- clindamycin 900 mg IV Q8hr
Penicillin allergy: Ertapenem IV 1 gm Q24hr +/-
vancomycin +/- clindamycin 900 mg IV Q8hr
Thank you

SSTI's moh zidan

  • 1.
    Skin and SoftTissue Infections (SSTIs) by MOHAMED FATHY ZAIDAN (M.D) Lecturer of general surgery
  • 2.
    Definitions and introductionof SSTIs  Suffered by everyone at least once in life time, most common infection, and challenge to a physician in his day to day practice but unfortunately the most misdiagnosed and mismanaged these days..  SSTIs can be defined as an inflammatory microbial invasion of the epidermis, dermis and subcutaneous tissues.  Over use of antibiotics is a global problem.  occurs by invasion of epidermis usually by a breach in the skin. Hematogenous spread of microbes also results in SSTI.
  • 3.
    Classifications SSTI may beclassified according to the layer of infection, severity of infection and microbiologic etiology. A-The practice guidelines of the Infectious Diseases Society of America (IDSA) for the diagnosis and management of SSTIs classifies into five categories, comprising 1-superficial uncomplicated infection (includes impetigo, erysipelas and cellulitis) 2- necrotizing infection 3-infections associated with bites and animal contact 4-surgical site infections 5- infections in the immunocompromised host.
  • 4.
    Classifications (continued) B- Eronclassification, based on the severity of local and systemic signs is also useful 1-Class 1 : SSTI but NO signs or symptoms of systemic toxicity or co-morbidities. 2-Class 2 : Either systemically unwell or systemically well but with COMORBIDITY that may complicate or delay resolution. 3-Class 3: TOXIC & UNWILL (fever, tachycardia, tachypnoea and/or hypotension). 4-Class 4 SEPSIS SYNDROME and life-threatening infection
  • 5.
    Classifications (continued) C-Classification accordingto the layer affected Epithelium Varicella &Measles Keratin layer Ring worm (Dermatophyte fungi) Epidermis Impetigo (Streptococcus pyogenes Staph aureus) Dermis Erisepelas (Streptococcus pyogenes) Hair follicles Folliculitis, boils,carbuncles (S. aureus) Sebum glands Acne (Propionobacterium acnes) Subcutaneous fat Cellulitis (Beta hemolytic Strepto) Fascia Necrotizing fasciitis (Strept. pyogenes and mixed anaerobic infection) D-Purulent OR non-purulent 1-purulent: e.g. Furuncle-abscess, carbuncles 2-Non-purulent :Cellulitis-erysipelas,, necrotizing fasciitis
  • 6.
    IMPETIGO  Def. Initiallyvesicular, later crusted, superficial infection of the skin.  Etiology: Group A streptococcus was the commonest cause of this entity, now days Staphylococcus has become the number one offender. Increasing prevalence of MRSA as a cause of impetigo is indeed worrying.  C/P: Streptococcal impetigo starts on exposed surfaces appearing as small vesicles that pustulate rapidly and ruptures readily. This purulent discharge dries and forms the characteristic golden yellow, stuck on, crusts. Healing generally occurs without scarring.  TTT: Penicillin (drug of choice)   Benzathine penicillin   Penicillin v   PCN-allergic: erythromycin   Cotrimoxazole, doxycycline and Clindamycin has good activity against CA MRSA.
  • 7.
  • 8.
    ERYSIPELAS  Def. Superficialinfection of skin, with prominent lymphatic involvement.(streptococcal infection)  C/P painful lesion with a bright red, edematous, indurated appearance with an advancing raising and sharply demarcated borders.  TTT:Mild cases can be treated with oral penicillin, Severe cases need parenteral crystalline penicillin or if associated cellulitis is cannot be ruled out penicillinase resistant penicillin (cloxacillin) or a first generation cephalosporin should be used.
  • 9.
  • 10.
    CELLULITIS  Def.: acutespreading infection that involves subcutaneous tissue (strept. and staph.)  C/P: rapidly intensifying pain and redness .Fever and lymphadenopathy may be present.The borders in cellulitis are not well demarcated. Acutely presenting and rapidly progressing lesions are due to most commonly with streptococcus and vice versa is true for staph aureus. This is a useful clue for the physician when selecting the antimicrobial.
  • 11.
  • 12.
    GANGRENOUS CELLULITIS This isa rapidly progressive cellulitis with extensive necrosis of skin and subcutaneous tissues. They can be divided into A. Necrotizing fasciitis B. Gas gangrene C. Progressive bacterial synergistic gangrene D. Gangrenous cellulitis in immunocompromised host
  • 13.
    Necrotizing fasciitis  Def.: Term that describes a disease condition of rapidly spreading infection, usually located in fascial planes of connective tissue that results in tissue necrosis. Any part of the body may be affected.  Types:  a- polymicrobial,,  b- Monomicrobial (Group A beta-hemolytic streptococci)
  • 14.
    Necrotizing fasciitis (continued) C/P: Tissuenecrosis, spreading, bullae, severe pain, pain out of proportion, pain then no pain. (this is a clue for diagnosis) Often severe intensity of illness DD: Necrotizing fasciitis; gas gangrene others Cannot easily differentiate syndromes on basis of initial clinical presentation Initial approach is similar: Early surgery and antibiotics
  • 15.
    TREATMENT of Necrotizingfasciitis  It is extremely important to diagnose this condition at a very early stage to reduce the morbidity and mortality, overall mortality rate for this condition varies from 24- 34%.  Immediate surgical debridement  Directed initially against mixed aerobic/anaerobic flora  Ampicillin/sulbactam or Piperacillin/tazobactam PLUS clindamycin (theoretically to inhibit protein synthesis and supress bacterial toxin) PLUS ciprofloxacin;  Other regimens: imipenem, meropenem, ertapenem, clindamycin PLUS aminoglycoside or fluoroquinolone
  • 16.
  • 17.
    Clues Suggesting NFvs. Cellulitis  Pain more severe than expected (followed by anesthesia)  Rapidly spreading swelling and inflammation  Bullae (but can be seen with cellulitis as well)  Necrosis  Toxic shock syndrome  Elevated CK
  • 18.
    Fourniers gangrene  Necrotizingfasciitis of genitalia,which usually affects scrotum but may spread to lower abdominal wall and perianal area. Emergency surgical exploration is a must. Combination of crystalline penicillin and clindamycin are the drugs of choice.
  • 19.
    Progressive bacterial synergistic gangreneMeleney gangrne  This develops as a complication of laparotomy wounds or colostomy sites.
  • 20.
    Clostridial skin infections Clostridial cellulitis  Infection limited to the dermis and epidermis  Abundance of gas, usually not systemically ill  Clostridial myonecrosis (classic gas gangrene)  Rapid onset of necrosis, pain, and toxic state  Usually associated with devitalized tissue (trauma, surgery, peripheral vascular disease)  Clostridial toxins (alpha toxin)  Lyses blood cells and causes tissue destruction  Therapy – Immediate surgery, antibiotics +/- hyperbaric O2?  Clostridium septicum  Consider adenoCA of Colon, leukemia.
  • 21.
    Community-Associated (CA) MRSA Patient has no medical history in the past year of:  Hospitalization  Admission to a nursing home, skilled nursing facility or hospice  Dialysis  Surgery  The patient has no indwelling catheters or medical devices that pass through the skin
  • 22.
    Community-Associated (CA) MRSA Increasing cause of community skin infections.  in USA the prevalence of CA-MRSA has increased rapidly over the last 10 years. Incidence of CA MRSA rose to 76% of isolates.  CA MRSA has become the most predominant one in USA, accounting for 90%–99% of cases.  Genotypically and phenotypically unique from nosocomial MRSA  Less resistant to non-beta-lactam agents  Often susceptible to Clindamycin , Tetracyclines, +/- Fluoroquinolones  Panton-Valentine leukocidin (PVL) – virulence factor
  • 23.
    Diabetic Foot Infections Predisposing Factors  Peripheral Neuropathy  Maldistribution of weight (trophic ulcers)  Failure to sense problems (corns, calluses)  Vascular insufficiency  Bacterial etiology  Early, superficial – Strep, Staph  Late, deep – Mixed  Therapy – Surgery and antimicrobial agents  Multi-disciplinary approach
  • 24.
    TREATMENT of diabeticfoot infection  MILD INFECTIONS  Oral Regimens : 1. Cephalexin 500 mg PO QID OR Clindamycin 300 mg PO TID (covers MRSA) 2. OR Amoxicillin/clavulanate 875 mg PO BID  Parenteral Regimens : 1. Clindamycin 600 mg IV q8h (covers CA-MRSA if no inducible Clindamycin resistance) 2. OR :Cefazolin 1 g IV q8h  MODERATE INFECTIONS  Ertapenem 1g IV q24h OR Ciprofloxacin 500 mg PO BID / 400 mg IV q12h PLUS EITHER Clindamycin 600 mg IV q8h/300 mg PO TID OR Metronidazole 500 mg IV/PO TID
  • 25.
    TREATMENT of diabeticfoot infection(continued)  If patient at risk for MRSA, add Vancomycin to regimens that do not include Clindamycin (see dosing section)  Risk factors for MRSA 1. History of colonization or infection with MRSA 2. Recent (within 3 months) or current prolonged hospitalization > 2 weeks 3. Transfer from a nursing home or subacute facility 4. Injection drug use
  • 26.
    Surgical Site Infections Suture removal plus incision and drainage  If associated with a significant systemic response , such as erythema and induration extending >5 cm from the wound edge, temperature >38.5°C, heart rate >110 beats/minute, or white blood cell (WBC) count >12 000/μL Adjunctive systemic antimicrobial therapy  When risk factors for MRSA are high (nasal colonization, prior MRSA infection, recent hospitalization, recent antibiotics) Vancomycin or clindamycin is recommended.
  • 27.
    Antibiotics used inSSTI  Introduction: 1. Complicated skin and soft tissue infections caused by wide spectrum of bacteria, especially at an era of increasing resistance and new virulence factors makes empirical antibiotic section a real challenge. 2. The appearance of CA MRSA has changed the scenario of antibiotic management of CSSTI, forcing us to choose antibiotics which can suppress toxins, even for MSSA; rather than blindly choosing beta lactam agents.
  • 28.
    Panton valentine toxin(PVL)  Is a γ hemolysin toxin seen in staph aureus which was first isolated in 1932 by Panton and valentine.  Presence of PVL in MSSA and HA MRSA is less common, while majority of CAMRSA in USA produce PVL.  PVL producing MSSA and MRSA infections usually present as recurrent boils, especially in close groups like family members, contact sports team members.  Severe soft tissue infections, rapidly progressive necrotizing pneumonia and severe arthritis are well known manifestations of these bacteria.
  • 29.
    Panton valentine toxin(contiued)  The choice of antibiotic selection is extremely important while treating PVL producing MSSA or MRSA.  Betalactam antibiotics even though active against MSSA will trigger release of toxins further contribute to the pathogenesis.  Clindamycin and linezolid are active against MRSA and also suppress toxin production.
  • 30.
    Clindamycin  FDA-approved totreat serious infections due to S. aureus with Clindamycin  Good soft tissue penetration  Toxin suppressing activity  Even though clindamycin resistance is common in HAMRSA, it usually works well with CA MRSA, as these isolates retain their sensitivity to clindamycin.
  • 31.
    D-Test FOR CLINDAMYCIN MRSAisolates resistant to erythromycin must have a D test done in the laboratory and if positive, clindamycin should be avoided, as therapeutic failure can occur.
  • 32.
    Clindamycin and pseudomembranous colitis A retrospective survey of 15 019 patients treated with clindamycin for a soft tissue infection was carried out to determine whether the incidence of serious side effects was sufficient to preclude the continuing use of this antibiotic.  13 patients were found to have had severe diarrhea and 2 of these required inpatient treatment for pseudomembranous colitis. Certain limitations of the use of clindamycin are suggested but, in view of the recently improved understanding of the nature of pseudomembranous colitis and more effective methods of treatment of this complication,  It is concluded that this antibiotic still has a useful role to play in the treatment of acute soft tissue infection.
  • 33.
    Practice Guidelines forthe Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America (recommendation regarding DALACIN) 1-Impetigo: When MRSA is suspected or confirmed, clindamycin, sulfamethoxazole-trimethoprim,or doxycycline,in a 7 days regamin. 2-Purulent SSTIs (I&D) antibiotic active against MRSA (Clindamycin) is recommended for patients with carbuncles or abscesses who have 1-failed initial antibiotic treatment or 2-have markedly impaired host defenses or in patients with 3- SIRS and hypotension
  • 34.
    Practice Guidelines forthe Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America (recommendation regarding DALACIN) coninued.. 3-Necrotizing Fasciitis, Including Fournier Gangrene  Penicillin plus clindamycin is recommended for treatment of documented group A streptococcal necrotizing fasciitis 4-Clostridial Gas Gangrene or Myonecrosis (surgery) Definitive antimicrobial therapy with penicillin and clindamycin is recommended for treatment of clostridial myonecrosis
  • 35.
    Recommended empiric antibioticsin NSTI Ampicillin/sulbactam 3 gm IV Q6hr +/- vancomycin +/- clindamycin 900 mg IV Q8hr Penicillin allergy: Ertapenem IV 1 gm Q24hr +/- vancomycin +/- clindamycin 900 mg IV Q8hr
  • 36.