Clinical and Health Affairs
Community-Acquired Methicillin-Resistant Staphylococcus aureus Necrotizing Fasciitis in a Healthy Adolescent Male
By Ian J. Lalich, M.D., and Nadia A. Sam-Agudu, M.D., DTM&H
Abstract
Recently, the rate of severe, invasive community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) infection has been increasing in healthy children. The single most common cause of necrotizing fasciitis in children is group A Streptococcus. Empiric therapy is usually targeted at this organism, which is uniformly sensitive to penicillin. Necrotizing fasciitis caused by CA-MRSA is a potentially life-threatening infection that has not been extensively reported in the U.S. pediatric population. The limited literature includes reports of neonatal cases and reports of pediatric cases embedded in articles about adults with underlying risk factors. We present a case of CA-MRSA necrotizing fasciitis in a previously healthy 11-year-old male with no risk factors.
The rate of methicillin-resistant Staphylococcus aureus (MRSA) infections in healthy individuals in the community setting is increasing.1-4 In addition, community acquired-MRSA (CA-MRSA) strains are increasingly responsible for manifestations of severe S. aureus disease. Skin and soft-tissue infections are the predominant manifestations of CA-MRSA, accounting for 77% to 96% of CA-MRSA infections.1
Necrotizing fasciitis caused by CA-MRSA is an uncommon, life-threatening disease that requires prompt recognition and surgical debridement because of its rapid progression.5 Typical risk factors include IV drug use, diabetes, and chronic hepatitis C.6 The presentation and disease course for CA-MRSA necrotizing fasciitis has been said to differ from typical necrotizing fasciitis in that it may assume a more indolent nature.6 We present a case of rapidly developing MRSA necrotizing fasciitis in a previously healthy adolescent with no underlying risk factors.
Case Presentation
Three days prior to admission, our patient, an 11-year-old Caucasian male, noticed a papular lesion that was approximately 0.5 cm in diameter on his right elbow. There was no associated pain or pruritus, and he did not recall being bitten by insects. He denied having such lesions in the past; however, his siblings had developed similar lesions that had spontaneously resolved. During the next two days, the lesion increased in size to approximately 1 cm, and the patient noticed increased tenderness with induration of skin surrounding the lesion.
One day prior to admission, the patient sustained an injury to the lesion after a fall, causing it to rupture. By the next morning, the lesion had increased to approximately 1.5 cm in size and was draining thick, purulent fluid. He was seen in an outpatient clinic and subsequently admitted to our facility for evaluation later that day.
On admission, the patient reported experiencing fever, chills, headache, diaphoresis, poor appetite, and myalgias since that morning. On physical exam, height, weight, and BMI were in the 75th percentile. His pulse was 122 bpm, respirations 24 breaths/min, temperature 39.1 degrees C, blood pressure 118/72 mmHg in his left arm, and oxygen saturation 97% on room air. He was alert and oriented to person, place, and time.
Skin exam showed a circular 2-cm draining abscess overlying the extensor surface of the elbow on the ulnar side of the right upper extremity. The ruptured lesion continued to drain purulent greenish-yellow material. The surrounding redness and induration had progressed to involve the right elbow, forearm, and the lower half of the upper arm. Movement of the extremity was limited by significant pain and swelling. The patient denied any numbness, tingling, or loss of motor function in his right arm. No crepitus was noted in the involved skin; however, there was significant tenderness even to light palpation. No other abnormal skin lesions were noted. The right extremity was without cyanosis; right brachial and radial pulses were palpated and strong.
The patient exhibited significant limitation in active flexion and extension of the right arm at the elbow. Passive movement was limited secondary to severe pain. Movement of the right wrist and hand was intact; strength was 4/5. Deep-tendon reflexes were normal and symmetric. Sensation in the right upper extremity remained intact throughout. The remainder of the physical exam was unremarkable.
The patient lived in western Minnesota. He had dogs, cats, and cockatoos in his home but had no recent history of scratches or wounds inflicted by these pets. He denied recent travel or exposure to toxins or other chemicals. The patient was not taking any medications other than ibuprofen. He did not report any allergies, and he was up-to-date on his immunizations. The patient’s mother works in patient transport at the local hospital. No other family members worked in a health care setting, and there was no known history of MRSA in the family. With the mother’s limited patient contact, we presumed that this was a case of community-acquired MRSA without any specific personal risk factor.
Complete blood count showed leukocytosis (white blood cell count: 23,200/mm3) with left shift (Bands: 17%). Basic metabolic panel was unremarkable. Antistreptolysin O (ASO) titer was moderately elevated at 515 IU/mL. Blood cultures were not obtained. MRI of the right elbow (Figure) showed no evidence of abnormal enhancement of marrow or cartilage to suggest osteomyelitis. There was diffuse subcutaneous edema extending to the myofascial margins consistent with significant cellulitis; myositis could not be excluded.
Outcome
The patient was promptly started on IV clindamycin and vancomycin to provide broad-spectrum coverage. Within an hour, incision and drainage with debridement was completed. Sections of abnormal-appearing fascia were surgically removed and sent for pathologic examination. The wound was thoroughly irrigated and closed.
Pathologic examination of tissue specimens showed marked acute necrotizing inflammation. Wound culture was positive for MRSA sensitive to trimethoprim/sulfamethoxazole, clindamycin, gentamicin, levofloxacin, rifampin, and vancomycin. The patient was treated with two days of IV clindamycin and vancomycin followed by 10 days of oral trimethoprim/sulfamethoxazole. He did well and completely healed without complications.
Discussion
Rates of MRSA in previously healthy individuals with no underlying risk factors have been rising.1 Most of the MRSA infections in this group of patients are skin and soft-tissue infections. Necrotizing fasciitis, especially in a healthy child with no risk factors (very young age, IV drug use, diabetes, chronic hepatitis) is rare. Thus, this case illustrates an uncommon presentation of an increasingly common infection in a pediatric patient with no risk factors. Important clinical decisions were made regarding the choice of empiric therapy and the need for surgical intervention. The initial antibiotic selections (clindamycin and vancomycin), which are generally effective against MRSA, and the prompt surgical management may have saved this patient from loss of a significant amount of tissue or his limb, or other complications. Necrotizing fasciitis is typically caused by group A Streptococcus, a mixture of aerobic and anaerobic organisms, or organisms of the Clostridia species.4 Group A Streptococcus is responsible for most cases of single-organism necrotizing fasciitis infections.7,8 However, reports of MRSA necrotizing fasciitis have increased significantly in the last several years, with most of those being reported in adults.2-4, 6,9,10 Although the ASO titer was moderately elevated in this patient, it only indicated that he had had prior exposure to group A Streptococcus; ASO can be elevated for weeks to months after exposure. Culture of the wound and tissue is important for definitive diagnosis.
Conclusion
This is one of a few non-neonatal pediatric cases of CA-MRSA necrotizing fasciitis reported in the literature. Providers should realize that CA-MRSA can cause necrotizing fasciitis in the healthy pediatric population and should, therefore, consider MRSA as a possible etiologic agent in virtually every presentation of acute skin and soft-tissue infection, unless there is strong evidence to the contrary. For pediatric providers who routinely empirically prescribe antibiotics for MRSA in patients presenting with necrotizing fasciitis, this case illustrates that it actually does occur and may do so in a patient who has no risk factors whatsoever. Therefore, this case supports this practice.
We acknowledge that a single case is not representative of the entire pediatric population, however. More studies of pediatric MRSA necrotizing fasciitis are needed for us to know about special risk factors that may ultimately change our approach to prevention and management. MM
At the time of manuscript preparation, Ian Lalich was a fourth-year medical student at the University of North Dakota School of Medicine and Health Sciences in Grand Forks. He is currently completing a residency in otorhinolaryngology/head and neck surgery at Mayo Clinic in Rochester. Nadia Sam-Agudu is a consultant in pediatric infectious diseases at Sanford Children’s Hospital and Clinic in Fargo, North Dakota, and is an adjunct assistant professor in the department of pediatrics at the University of Minnesota Medical School.
We thank the patient, his family, and the medical staff involved with this case at the MeritCare Children’s Hospital for their assistance and support. No financial support was received for this report.
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