Download SKIN AND SOFT TISSUE INFECTIONS

SKIN AND SOFT TISSUE INFECTIONS
1 : 11
Abdul Ghafur, PS Shareek, Chennai
INTRODUCTION
“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. This is
how we can define skin and soft tissue infections (SSTI) in the modern era. Added to this, the arsenal
of weapons carried by pathogens has changed dramatically over decades.”1
This quote depicts the importance of early diagnosis and correct management of the broad spectrum
of SSTI, ranging from simple boils to life threatening necrotising fasciitis. In this article we try to
provide a brief description of various SSTIs and their management.
SSTIs can be defined as an inflammatory microbial invasion of the epidermis, dermis and subcutaneous
tissues.2 the presence of bacteria over the skin surface or even on an ulcer doesn’t mean that this
microbe is responsible for the pathology. Unless there are signs of inflammation over the skin surface,
result of wound swab culture should be viewed with suspicion and all efforts should be undertaken
to differentiate pathogen from a colonizer before hunting for the sensitivity pattern and commencing
on a lengthy antibiotic regimen. Colonization doesn’t warrant antibiotics as a rule but infections may
need it. Over use of antibiotics is a global problem, even in countries with good antibiotic stewardship
policies. An excellent review article by Dryden on soft tissue infections, highlights the usage of
antibiotics to treat MRSA colonization rather than infection.3
Colonization of ulcers does not usually result in inflammation, but occasionally infection of the
surrounding tissues may result from lateral spread of the colonizing organisms. Direct infection of skin
occurs by invasion of epidermis usually by a breach in the skin. Hematogenous spread of microbes
also results in SSTI. Bacterial dissemination of Meningococcus and rickettsia can affect skin. Measles
and chicken pox are well known pathogens affecting skin. Staphylococcal scalded skin syndrome and
streptococcal scarlet fever are typical examples of toxin mediated skin damages.
CLASSIFICATION
There is no scarcity on the availability of various classifications of SSTI and despite all the advances in
modern medicine, managing severe types of these infections are still difficult. SSTI may be classified
according to the layer of infection, severity of infection and microbiologic etiology. Easiest of these
is the classification based on the layer of involvement (Table 1).
The practice guidelines of the Infectious Diseases Society of America (IDSA) for the diagnosis
and management of skin and soft tissue infections classifies SSTIs into five categories, comprising
superficial uncomplicated infection (includes impetigo, erysipelas and cellulitis), necrotizing
infection, infections associated with bites and animal contact, surgical site infections and infections in
the immunocompromised host.4 Eron classification, based on the severity of local and systemic signs is
also useful (Table 2). The advantage of this classification is that it guides the clinical management and
treatment decisions for patients with SSTIs more efficiently when compared with the previous ones.
WHAT IS COMPLICATED SSTI?
Complicated SSTI [cSSTI] represents more severe types of SSTI. Healthy people with unhealthy
wounds, immunocompromised patients with even healthy wounds, patients with extensive cellulitis
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Table 1: Types of infection affecting skin and soft tissue
structures
Anatomy
Infection
Table 2 : Eron classification.5
Category
Microbial cause
Epithelium
Varicella
Measles
Varicella virus
Measles virus
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
Muscle
Myositis
Toxic strains of Staph
Gangrene
Clostridium perfringens
Clinical features
Management
Class 1
SSTI but no signs or symp- Drainage (if required) and oral
toms of systemic toxicity or antibiotics as outpatient
co-morbidities
Class 2
Either systemically unwell or
systemically well but with comorbidity that may complicate
or delay resolution
Class 3
Toxic and unwell (fever, tach- Likely to require inpatient
ycardia, tachypnoea and/or hy- treatment with parenteral
potension)
antibiotics
Class 4
Sepsis syndrome and life- Likely to require admission to
threatening infection
ICU, urgent surgical
assessment and treatment with
parenteral antibiotics
Oral or outpatient intravenous
antibiotic therapy; may require
short period of observation in
hospital
response is weak in patients with streptococcal impetigo, as
skin lipids suppress Streptolysin O response, but anti–DNAase
B levels are consistently elevated.11-13
Matthew S. Dryden* Complicated skin and soft tissue infection. J Antimicrob Chemother 2010; 65(Suppl 3):iii35–44.
Treatment
Penicillin was the drug of choice for treating impetigo at
a time when Streptococci were the commonest cause of
impetigo. This antibiotic is no longer advisable now days, with
staphylococcus becoming the predominant cause. Penicillinase
resistant penicillin or a cephalosporin may be better treatment
choice currently to treat impetigo. Erythromycin or a newer
macrolide is used for penicillin allergic patients. Cotrimoxazole,
doxycycline and clindamycin has good activity against CA
MRSA.14 Topical antibiotic mupirocin may be used when
lesions are limited in number, but increasing mupirocin
resistance is a concern.15 Retapamulin is a recently approved
topical agent. Fusidic acid is another topical agent especially
in pediatric population.
and systemic symptoms, patients with necrotizing limbthreatening infection that requires life-saving surgery and
diabetic foot infections fall into this category. Infections
in areas where rate of complication is more as in perianal
region can also be classified as cSSTI. SSTIs accompanied
by signs and symptoms of systemic toxicity such as fever,
hypothermia, tachycardia (100 beats/min) and hypotension
(systolic blood pressure, 90 or 20 mmHg below baseline) can
be classified as complicated.6
IMPETIGO
Impetigo is an initially vesicular, later crusted, superficial
infection of the skin. Though previously it was most often
caused by Even though Group A streptococcus was the
commonest cause of this entity, now days Staphylococcus
has become the number one offender.7,8 Increasing prevalence
of MRSA as a cause of impetigo is indeed worrying.9 Nasal
colonization can act as a source of Staphylococcal impetigo.10
ERYSIPELAS
This is a superficial infection of skin, with prominent
lymphatic involvement. It is commonly caused by group A
streptococcus.
CLINICAL FINDINGS
Clinical findings
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. Pruritus is common and
scratching of lesions results in spreading of infection. Healing
generally occurs without scarring.
Erisipelas is more common in infants, young children and older
adults. Lower extremities are affected more, though rarely
face may also get involved in 5-20% of patients. Bacteria
enter through skin ulcers, local trauma, psoriasis or eczema or
fungal infections. Predisposing factors include lymphoedema,
venous stasis, obesity, paraparesis, diabetes mellitus, alcohol
abuse and nephrotic syndrome. Erysipelas is painful lesion
with a bright red, edematous, indurated appearance with an
advancing raising and sharply demarcated borders. Presence
of fever is a usual finding. Cellulitis, abscess and necrotizing
fasciitis are not uncommon complications.16
Laboratory findings
Gram stain may show gram positive cocci and culture of the
exudates may grow Staph aureus, streptococci or both. Assays
of streptococcal antibodies are not useful in the diagnosis
and treatment of impetigo, but positivity may indicate recent
streptococcal infection in patients suspected of having post
streptococcal glomerulonephritis. The antistreptolysin O
Laboratory findings
Leucocytosis is common. Cultures are usually sterile
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presentation. Fever and lymphadenopathy may be present.
The borders in cellulitis are not well demarcated. Bacteraemia,
thrombophlebitis, especially in older people, and local abscess
formation may develop. Though group A streptococci and
staphylococcus are the most common organisms rarely
organisms like H influenza, pneumococcus may also cause
cellulitis. . 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.
Laboratory findings
Neutrophil leucocytosis is a common finding. Cultures of
needle aspirates are routinely not recommended because
of low sensitivities. Aspiration is recommended only if we
suspect unusual pathogens, presence of abscess formation
or failed antimicrobial therapy. Blood cultures are usually
negative, even though Staph aureus or a Group A streptococcus
may be positive.
Treatment
Streptococcus cellulitis responds to β lactam. Penicillinase
resistant penicillin or a first or second generation cephalosporin
may be used if MRSA is less likely. Strong suspicion of MRSA
needs vancomycin (1gm twice daily) or linezolid 600 mg
twice daily.18 Daptomycin is another option and can be given
once a day. Step down to oral antibiotics is possible after
settling of fever and improvement in the skin lesions. Oral
agents can be tried in the outset in mild cases of cellulitis.
Immobilization and elevation of involved limbs will be useful.
Chronic suppressive usage of antibiotics may be necessary in
cases of recurrent cellulitis.
Fig. 1 : Necrotising fasciitis in a cancer chemotherapy patient,
treated with debridement and antibiotics and raw area covered
with skin graft.
especially from the surface of skin lesions.
Treatment
Mild cases can be treated with oral penicillin (500 mg every
6 hourly).Erythromycin (250 mg -500 mg orally every 6
hourly) can also be used, but resistant isolates are reported.
Severe cases need parenteral crystalline penicillin at a dose
of 2000000 units every 6 hrly. Presence of bullous erysipelas
or if associated cellulitis is cannot be ruled out penicillinase
resistant penicillin (cloxacillin) or a first generation
cephalosporin should be used. Recurrence of erysipelas may
be prevented by prolonged use of oral penicillin.17
GANGRENOUS CELLULITIS
CELLULITIS
Necrotizing fasciitis
Introduction
Introduction
Cellulitis is an acute spreading infection that involves
subcutaneous tissue, most commonly caused by group a
streptococcus and staph aureus. Trauma and underlying skin
lesion can lead to the development of cellulitis. Bacteraemia
can rarely be the cause of cellulitis. Cellulitis may also develop
due to the spread of adjacent infections like osteomyelitis.
Necrotizing fasciitis is a 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. Group A
beta-hemolytic streptococci (Streptococcus pyogenes) is the
number one culprit, but any other bacteria, either alone or
together (polymicrobial) can cause this disease. Occasionally,
even fungus can cause necrotizing fasciitis.
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
Clinical findings
Clinically rapidly intensifying pain and redness is a common
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Necrotising fasciitis can be divided into two forms. Type 1
necrotizing fasciitis is polymicrobial Type 2 is caused by
Group A streptococcus alone or in combination with other
organism especially staphylococcus.19 Necrotizing fasciitis
can affect any part of the body but is most common on the legs.
Abdominal wall, perianal and groin areas and postoperative
wounds are the other areas usually affected. 20 Organisms gain
entry through areas of trauma, surgery and ulcers. Diabetes
mellitus and alcoholism can increase the risk for necrotizing
fasciitis and parenteral drug abuse is other common risk
factors (Fig. 1).21,22
material containing spores of clostridium perfringens is the
key initiating factor of this condition. Non traumatic clostridial
myonecrosis is usually caused by Clostridium septicum
species can cause non traumatic clostridial myonecrosis.
Clinical findings
Lab findings
The affected area is erythematous, swollen, without sharp
margins, hot, very tender, and painful in the early stage. Within
3 to 5 days after onset, skin breakdown with bullae developing
to cutaneous gangrene. High grade fever is common. The
involved areas become non tender at this stage and this feature
helps in identifying necrotizing fasciitis. Subcutaneous gas is
often present in the polymicrobial form of necrotizing fasciitis
especially in diabetics.
Leucocytosis is a common feature, blood culture usually
negative. Gram stain usually shows gram positive bacilli
without spores. Presence of spore favours clostridium
septicum. Anaerobic culture turns positive in as early as 6
hours time, with the growth as fast as the clinical progress.
X ray of the area may show evidence of gas in muscles and
fascial planes.
Laboratory findings
Emergency surgical exploration is a must. Combination of
crystalline penicillin and clindamycin are the drugs of choice.
Hyperbaric oxygen has been tried with conflicting results.26
Clinical findings
Pain is the earliest symptom, with rapidly increasing severity
progressing to signs of toxicity and shock. Foul smelling
serosanguinous discharge from the wound is a feature.
Crepitus is usually present. The area later turns into greenish
black cutaneous necrosis.
Treatment
Leucocytosis is commonly seen. Gram-stain of the exudates
or the tissue can help in early identification of the possible
pathogen or pathogens. Blood cultures are frequently positive.
Progressive bacterial synergistic gangrene
Treatment
This develops as a complication of laparotomy wounds or
colostomy sites or as a chronic ulcer n the extremity, appearing
as a painful erythematous area, which later ulcerates,
progressing to gangrene. Staph aureus or streptococci are the
causative organisms.27
It is extremely important to diagnose this condition at a very
early stage to reduce the morbidity and mortality, as this
condition has a rapid clinical course. The overall mortality rate
for this condition varies from 24-34%.23 Immediate surgical
debridement is an essential part of the management. The
antibiotic choice depends on the local resistance pattern in the
community and health care settings. For group A streptococcal
necrotizing fasciitis, penicillin or plus clindamycin can be
used. Empirical broad spectrum antibiotics should be used
initially until cultures are back. Gram positives, gram negative
aerobes and anaerobes should be kept in mind.
Gangrenous cellulitis in immunocompromised patients
In an immunocompromised host, even unusual pathogens like
fungi can produce severe cellulitis progressing to gangrene.
Gram negative bacteria like pseudomonas and fungi like
mucormycosis can produce life threatening infections in these
patients. Cryptococcosis and histoplasmosis can also produce
skin lesions.
Fourniers gangrene
CA MRSA (Community-Acquired MRSA)
Fourniers gangrene is the necrotizing fasciitis of genitalia,
which usually affects scrotum but may spread to lower
abdominal wall and perianal area. Local trauma, diabetes and
perineal infections are predisposing factors.24
MRSA infections have already turned into a menace in
hospitals across the globe. In Indian hospitals the MDR
Gram negative saga has masked the importance of MRSA,
with multiple antibiotics available against MRSA, at a time
when the pipeline of Gram negative antibiotics is drying up.
Now there are increasing case reports of community acquired
MRSA infection even in India, while this problem has turned
to a routine problem in countries like USA.
Gas gangrene
Introduction
Gas gangrene is a rapidly progressive myonecrosis which can
be life threatening. It is usually caused by clostridia, especially
clostridium perfringens. This condition usually follows
muscle injury, but rarely can be seen in post operative patients
as well.25 Muscle injury and contamination with soil or foreign
What do we mean by community acquired MRSA (CAMRSA)?
CA-MRSA is entirely different from the MRSA circulating
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Skin and Soft Tissue Infections
daptomycin may be used in moderately severe infections
especially in the outpatient settings.Linezolid is another
alternative in this context.36
in hospitals (e MRSA/HA-MRSA). CA-MRSA is not due to
spread of hospital strains to community. They belong to a
different molecular class with different characteristics.CDC
Population-Based Surveillance Definition of cMRSA is;
MRSA culture positivity in outpatient setting or 1st 48 hours of
hospitalization AND Patient lacks risk factors for healthcareassociated MRSA, like Hospitalization, Surgery, Long-term
care Dialysis Indwelling devices,history of MRSA positivity.
Panton valentine toxin (PVL)
Panton valentine toxin (PVL) is a γ hemolysin toxin seen in
staph aureus which was first isolated in 1932 by Panton and
valentine. Prevalence of PVL gene varies among strains of
Staph aureus and MRSA. Presence of PVL in MSSA and HA
MRSA is less common, while majority of CAMRSA in USA
produce PVL. Other studies have reported a high incidence
of PVL production among strains of CA-MRSA.37 There have
been case reports of PVL producing strains from India also.
The first Indian case report of PVL producing CA MRSA was
in a pediatric patient from Chennai in 2009.38 In an excellent
study from Mumbai 64% of MRSA were PVL producers and
67% of the isolates from SSTIs were PVL producers.39
Salient differentiating features of CA MRSA are the acquisition
of infection in community setting, especially young otherwise
healthy individuals, while HA-MRSA is acquired in hospital
setting in patients with co-morbidities. CA-MRSA has SCC
mec IV-V cassette and in USA they belong to clone USA
300 and USA 400. CA-MRSA carry PVL (Pantone Valentine
Leucocidin) gene, producing PVL toxin, which is an important
virulent factor of CA-MRSA. PVL may be produced by some
strains of MSSA as well.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.
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. Flucloxacillin is bactericidal,
but the low sub inhibitory concentrations achievable in vivo
in necrotic tissue may further augment PVL toxin.40 Subinhibitory concentrations of clindamycin, linezolid and
fusidic acid induce a concentration dependent decrease in PVL
production, whereas low concentrations of oxacillin increase
the concentration of PVL up to threefold.41
Reports of community acquired MRSA cases started
appearing almost a decade ago in various countries28 in USA
the prevalence of CA-MRSA has increased rapidly over the
last 10 years. Incidence of CA MRSA rose to 76% of isolates in
Houston and 63%–72% of isolates in Atlanta.29 USA300 clone
of CA MRSA has become the most predominant one in USA,
accounting for 90%–99% of cases.30 CA-MRSA caused an
increasing percentage of hospital onset bacteraemias between
2000 and 2006 in Chicago (increasing from 24% to 49%).31
Mathematical models predict that within the next few years,
so-called community-associated strains will become the
predominant strains in hospitals throughout the USA.32 In a
2010 Indian study rate of CA MRSA was 9.6%.32 Another
big study from Mumbai revealed increasing prevalence of
CAMRSA in India. 54% of MRSA isolates were community
acquired.33 This interesting study by the Mumbai team should
be an eye opener on the possible extends of CA MRSA in
Indian set up. The CA MRSA rate is at its peak in USA and at
least in the race on the rate of CAMRSA, India is far behind
western countries in the resistance marathon.
Antibiotics used in SSTI
Introduction
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. The predominance of Gram positives over
the Gram negatives as the cause of cSSTI is in fact a solace
at a time when the Gram negative pipeline is getting drier
and the Gram positive one is still flowing at full velocity
and vigour. 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.
TREATMENT OF CA MRSA
Cotrimoxazole
Unlike HA MRSA, community acquired type is mostly not
multidrug resistant, being sensitive to many oral antibiotics
like cotrimoxazole, doxycycline and clindamycin. Can be used
in most outpatient setting.34 UK practice recommendations
gives emphasis to combination therapy in managing
CAMRSA. They include rifampicin and sodium fusidate,
doxycycline; rifampicin and trimethoprim or linezolid,
rifampicin+trimethoprim; or linezolid.35 Glycopeptides or
Cotrimoxazole has reemerged as a good antibiotic choice for
mild to moderate soft tissue infections due to CA MRSA.
Almost 90-100% of isolates are sensitive to cotrimoxazole in
western studies.42 History of sulpha allergy should carefully be
ruled out before starting this drug. Hyperkalaemia is another
side effect especially in elderly and patients already on ACE
inhibitors and ARB group of drugs.
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Medicine Update 2012  Vol. 22
Clindamycin
telavancin than among those treated with vancomycin. So
monitoring of renal functional tests is mandatory when using
this drug.50
Clindamycin has very good ant staphylococcal activity with
good soft tissue penetration and toxin suppressing activity,
making this drug a good choice for treating soft tissue
infections. Even though clindamycin resistance is common
in HAMRSA, it usually works well with CA MRSA, as
these isolates retain their sensitivity to 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.
Tetracyclines
Doxycycline is a good option for treating mild to moderate
MRSA soft tissue infection, even though increasing resistance
is concern. Tetracyclines are pregnancy category D and are
not recommended for children <8 years of age because of
the potential for tooth enamel discoloration and decreased
bone growth.
Daptomycin
Vancomycin
Daptomycin is a cyclic lipopeptide and is approved for
treatment of cSSTIs. Daptomycin is bactericidal drug acting
on the cell membrane of the bacteria. Daptomycin is active
against MRSA, glycopeptide- and linezolid-resistant S.
aureus and vancomycin-resistant enterococcal species. It has
good activity during the stationary phase growth of bacteria
as against the β lactams and has a good post antibiotic effect
against staph aureus.43 Daptomycin is highly protein bound
and renally excreted. Elevation in creatinine phosphokinase
(CPK) and associated myopathy is a well reported complication
of daptomycin, uncommon with the once a day dosing
pattern.CPK level should be monitored at least once a week
during daptomycin therapy. Development of eosinophilic
pneumonias is another but uncommon complication. This
drug is not licensed in children. It is pregnancy category B.
Daptomycin is non inferior to vancomycin for the treatment
of cSSTI.44
Vancomycin is probably the most commonly used drug used
for treating MRSA infections. Emergence of resistance and
“the MIC creep” is a serious issue to be kept in mind while
choosing this drug. Tissue penetration is highly variable and
depends upon the degree of inflammation. Vancomycin is
considered pregnancy category C.
Linezolid
Linezolid is a synthetic oxazolidinone and inhibits protein
synthesis at the 50S ribosome. Linezolid has 100% oral
bioavailability. Parenteral therapy is indicated only if
gastrointestinal absorption is compromised. Linezolid
resistance is rare, but has been reported.51 Long-term use can
produce hematologic toxicity, commonly thrombocytopenia
though anemia and neutropenia is also seen. Peripheral and
optic neuropathy and lactic acidosis are the other side effects
seen with use of linezolid. Although myelosuppression is
generally reversible, peripheral and optic neuropathy are
not reversible or are only partially reversible. Linezolid has
been associated with serotonin syndrome in patients taking
concurrent selective serotonin-receptor inhibitors. Linezolid
causes less bone marrow suppression in children than in
adults. It is considered pregnancy category C.52
TIGECYCLINE
Tigecycline belongs to the group glycylcycline. It inhibits
bacterial protein synthesis by binding to the 30S ribosomal
subunit but with a five times higher affinity than that for
the tetracyclines.45 It can overcome the normal tetracycline
resistance mechanisms and other bacterial resistance
mechanisms like ESBLs.46 Tigecycline was shown to be
noninferior to combination vancomycin-aztreonam regimens
and exhibited high clinical success rates for cSSTI.47Tigecycline
use has been associated with higher all cause mortality rates,
though it was not statistically significant, FDA has issued a
warning.48 No dosage adjustment of tigecycline is necessary in
patients with renal insufficiency or mild to moderate hepatic
impairment and the aged population, although in patients with
severe hepatic impairment, the initial dose should be 100 mg,
followed by a reduced maintenance dose of 25 mg every 12
hrs.49
SOLVE THE PROBLEMS!
1. A 22 year old man presents with multiple boils on thigh
with abscess, severe pneumonia and arthritis. Which
one of the following drugs should be avoided?
A.daptomycin
B.cephalexin
C.clindamycin
D.linezolid
2. 30 year old male patient admitted with severe sepsis and
cSSTI. Which of the following should be avoided in this
scenario?
Televancin
Telavancin is a novel parenteral lipoglycopeptide. It inhibits
cell wall synthesis. Televancin is used in settings of MRSA,
VISA, and VRSA. It is pregnancy category C. Nephrotoxicity
was more commonly reported among individuals treated with
A.linezolid
B.tigecycline
64
Skin and Soft Tissue Infections
C.daptomycin
2.
D.daptomycin+clindamycin
Dryden MS. Skin and soft tissue infection: microbiology and epidemiology. Int J Antimicrob Agents 2009;33Suppl3:2–7.
A. it has 100% oral bioavailability.
3. Dryden M, Andrasevic A, Bassetti M et al. A European survey
of antibiotic management of methicillin-resistant Staphylococcus
aureus infection: current clinical opinion and practice. Clin Microbiol Infect 2010;16Suppl1:3–30.
B. peripheral neuropathy is completely reversible.
4.
C. thrombocytopenia is the most common hematological abnormality.
Stevens DL, Bisno AL, Chambers H et al. Practice guidelines for
the diagnosis and management of skin and soft-tissue infections.
Clin Infect Dis 2005;41:1373–406.
D. hematological abnormalities are less common in
children
5.
Eron LJ, Lipsky BA, Low DE et al. Managing skin and soft tissue
infections: expert panel recommendations on key decision points.
J Antimicrob Chemother 2003;52Suppl1:i3–17.
6.
Matthew S. Dryden .Complicated skin and soft tissue infection. J
Antimicrob Chemother 2010;65Suppl3:iii35–44.
7.
Ferrieri et al. Natural history of impetigo, site sequence of acquisition and familial pattern of spread of cutaneous streptococci. J
Clin Insvet 1972;51:2851-2862.
8.
Bison AAL, Stevens DL. Streptococcal infections of skin and soft
tissues. New Engl J Med 1996;334:240-245.
9.
Forcade NA, Parchman ML, et al. Prevalence, Severity, and Treatment of Community-Acquired Methicillin-Resistant Staphylococcus Aureus (CA-MRSA) Skin and Soft Tissue Infections in 10
Medical Clinics in Texas: A South Texas Ambulatory Research
Network (STARNet) Study. J Am Board Fam Med 2011;24:54350.
3. One of the following is not true about linezolid.
4. The drug which is associated with eosinophilic pneumonia
A.linezolid
B.daptomycin
C.clindamycin
D. none of the above
5. D test is done on MRSA isolates to predict the resistance
of which antibiotic?
A.clindamycin
B.doxycycline
10. Durupt F et al. prevalence of staph aureus toxins and nasal carriage in furuncles and impetigo. Br J Dermatol 2007;157:1161-67.
C.linezolid
11. Kaplan EL, Anthony BF, Chapman SS, Ayoub EM, Wannamaker
LW. The influence of the site of infection on the immune response
to group A streptococci. J Clin Invest 1970;49:1405–14.
D.daptomycin
Answers
12. Bisno AL, Nelson KE, Waytz P, Brunt J. Factors influencing serum antibody response in streptococcal pyoderma. J Lab Clin Med
1973;81:410–20.
1. B: Cephalexin
This scenario is very suggestive of CAMRSA/CA
MSSA PVL toxin producing infection. Toxin suppressing antibiotics should be used and Beta lactam antibiotics should be avoided as these drugs can increase toxin
production.
13. Kaplan EL, Wannamaker LW. Suppression of the anti–streptolysin
O response by cholesterol and by lipid extracts of rabbit skin. J
Exp Med 1976;144:754–67.
14. Dellit TH, Duchin J. Guidelines for Evaluation & Management of
Community-Associated Methicillin-Resistant Staphylococcus aureus Skin and Soft Tissue Infections in Outpatient Settings. Olympia: Washington State Department of Health, Infectious Diseases
Society of Washington, December, 2007.
2. B: tigecycline. Tigecycline is not reliable for treatment
of bacteraemia due to inadequate concentration of this
drug in blood. In severe sepsis bacteraemia should be
anticipated.
15. Steven DL et al. IDSA practice guidelines for diagnosis and management of cSSTI. Clin Inf Diseases 2005:41;1373-1406.
3. B: linezolid induced thrombocytopenia is not always reversible.
16. Damstra RJ, van Steensel MA, Boomsma JH, et al. Erysipelas as
a sign of subclinical primary lymphoedema: A prospective quantitative scintigraphic study of 40 patients with unilateral erysipelas
of the leg.Br J Dermatol 2008;158:1210-1215.
4. B: Daptomycin
5. A: If D test is positive clindamycin therapy may fail.
This test should be performed if clindamycin is used in
MRSA infection.
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