Overview
Definition:
Methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-susceptible Staphylococcus aureus (MSSA) are both strains of the bacterium Staphylococcus aureus
The key difference lies in their susceptibility to beta-lactam antibiotics, including methicillin, oxacillin, and penicillin
MRSA strains possess a mecA gene that encodes for penicillin-binding protein 2a (PBP2a), which has a low affinity for these antibiotics, rendering them ineffective
MSSA strains lack this gene and remain susceptible
Skin and soft tissue infections (SSTIs) are the most common presentations of both, particularly in pediatric populations.
Epidemiology:
Staphylococcus aureus is a common colonizer of the skin and nasal passages, affecting approximately 30% of the healthy population
Community-acquired MRSA (CA-MRSA) infections have become increasingly prevalent in pediatric settings globally, often associated with close contact in schools, sports, and daycares
Pediatric MRSA SSTIs often present as purulent cellulitis, abscesses, or impetigo
MSSA infections remain more common overall but are seeing a resurgence of antibiotic resistance to other classes.
Clinical Significance:
Accurate differentiation between MRSA and MSSA is crucial for appropriate antibiotic selection
Misdiagnosis or delayed appropriate therapy for MRSA can lead to treatment failure, prolonged illness, increased morbidity, and spread of resistant strains
Understanding current local antibiograms and susceptibility patterns is paramount in pediatric infectious disease management, especially for DNB and NEET SS preparation.
Clinical Presentation
Symptoms:
Localized pain at the site of infection
Rapidly progressing swelling and erythema
Presence of a pustule, boil, or abscess with purulent drainage
Fever and chills may be present in more severe or invasive infections
Sometimes, a "spider bite" appearance or a small red bump that quickly enlarges and becomes painful.
Signs:
Erythematous, warm, and tender area of skin
Palpable fluctuant mass (abscess)
Purulent discharge
May have surrounding edema and satellite lesions
Regional lymphadenopathy can occur
Vital signs may be normal in uncomplicated cases, but fever and tachycardia may indicate systemic involvement.
Diagnostic Criteria:
Diagnosis is primarily clinical, supported by laboratory confirmation
Clinical suspicion for MRSA arises in the presence of characteristic lesions in an epidemiologically relevant context (e.g., recent hospitalization, contact with infected individual, participation in contact sports)
Definitive diagnosis requires isolation of S
aureus from a clinical specimen (wound culture, blood culture) with subsequent susceptibility testing
The presence of the mecA gene, detected by PCR, confirms MRSA.
Diagnostic Approach
History Taking:
Detailed history of lesion onset, progression, and associated symptoms
Recent contact with individuals with skin infections
History of antibiotic use
Presence of underlying medical conditions (e.g., eczema, diabetes, immunocompromise)
Recent hospitalizations or healthcare exposure
Participation in team sports or group activities
Travel history.
Physical Examination:
Thorough skin examination to assess the morphology, size, and location of the lesion
Palpation for fluctuance and tenderness
Examination for satellite lesions, purulent drainage, and surrounding erythema
Assessment for regional lymphadenopathy
Evaluation of vital signs for signs of systemic infection.
Investigations:
Gram stain and culture of purulent material from the lesion is essential for identifying S
aureus and determining antibiotic susceptibility
Blood cultures are indicated in patients with signs of systemic illness or invasive infection
Rapid diagnostic tests (e.g., PCR for mecA gene) can provide faster identification of MRSA
Complete blood count (CBC) with differential may show leukocytosis
Inflammatory markers like C-reactive protein (CRP) can be elevated.
Differential Diagnosis:
Bacterial abscesses caused by other organisms (e.g., Streptococcus pyogenes)
Folliculitis
Furuncle
Carbuncle
Ecthyma
Viral infections (e.g., herpes simplex virus)
Insect bites
Allergic reactions
Cellulitis of non-staphylococcal origin.
Management
Initial Management:
For localized, uncomplicated abscesses or purulent SSTIs: incision and drainage (I&D) is the cornerstone of therapy
Appropriate wound care, including dressing changes
Pain management with analgesics
Identification of the pathogen and its susceptibility profile is paramount.
Medical Management:
For MRSA SSTIs: Empirical antibiotic therapy should be guided by local antibiograms and risk factors for MRSA
Common choices include trimethoprim-sulfamethoxazole (TMP-SMX) (e.g., 8-10 mg/kg/day of TMP component divided q12h, max 320 mg TMP q12h) or clindamycin (e.g., 10-13 mg/kg/day divided q8h, max 1.8 g/day)
Doxycycline or linezolid may be options in specific situations
For MSSA SSTIs: Beta-lactam antibiotics like dicloxacillin or cephalexin are typically first-line (e.g., cephalexin 25-50 mg/kg/day divided q6-8h, max 4 g/day)
If penicillin allergy, alternatives like TMP-SMX or clindamycin can be used.
Surgical Management:
Incision and drainage (I&D) is indicated for all abscesses and fluctuant lesions
The goal is to remove purulent material and reduce bacterial burden
Necrotic tissue debridement may be necessary in severe cases
Surgical consultation may be required for complex or deep-seated infections.
Supportive Care:
Regular wound assessment and dressing changes
Elevating the affected limb to reduce edema
Monitoring for signs of worsening infection or systemic spread
Patient education on hygiene and wound care
Adequate hydration and nutrition
Fever control with antipyretics.
Complications
Early Complications:
Spread of infection to deeper tissues (e.g., fasciitis, osteomyelitis, septic arthritis)
Bacteremia and sepsis
Metastatic infections (e.g., endocarditis, pneumonia, abscesses in other organs)
Toxic shock syndrome.
Late Complications:
Chronic wound healing issues
Scarring
Recurrent infections
Development of antibiotic resistance.
Prevention Strategies:
Good hand hygiene practices among healthcare providers and caregivers
Prompt recognition and management of skin lesions
Education on wound care and infection prevention
Screening of high-risk individuals or populations
Judicious use of antibiotics to prevent resistance
Maintaining a clean environment, especially in childcare settings and sports facilities.
Prognosis
Factors Affecting Prognosis:
The presence of underlying comorbidities (e.g., immunocompromise, chronic skin conditions)
The extent and depth of the infection
Promptness of diagnosis and initiation of appropriate therapy
Development of systemic complications
Virulence factors of the specific bacterial strain.
Outcomes:
With appropriate management, including I&D and targeted antibiotic therapy, most pediatric MRSA and MSSA SSTIs have an excellent prognosis and resolve completely
However, invasive infections can lead to significant morbidity and mortality if not treated aggressively and promptly
Recurrence is possible if reservoirs for colonization are not addressed.
Follow Up:
Follow-up is usually required to ensure complete wound healing and resolution of infection
Close monitoring for signs of recurrence or development of complications
Patients with extensive infections or underlying risk factors may require more prolonged follow-up
Education on preventing future infections and recognizing early signs of recurrence is vital.
Key Points
Exam Focus:
Always consider MRSA in pediatric skin infections, especially purulent ones
Local antibiograms are critical for empirical therapy
Incision and drainage is the primary treatment for abscesses
Common MRSA outpatient choices: TMP-SMX, clindamycin
Common MSSA choices: dicloxacillin, cephalexin.
Clinical Pearls:
Even a small, red, tender bump can be a MRSA infection
Pus drainage is a classic sign of abscess
If in doubt, culture the wound before starting antibiotics
Consider decolonization strategies for recurrent MRSA carriers
Educate parents on recognizing and preventing skin infections.
Common Mistakes:
Treating all S
aureus skin infections with beta-lactams without susceptibility testing
Delaying incision and drainage of abscesses
Relying solely on antibiotics without addressing surgical drainage
Failing to consider MRSA in the differential diagnosis of purulent skin lesions
Not adhering to local resistance patterns.