Community-Acquired MRSA Bacteraemia in a Healthy 6-Year-Old Female

Methicillin-resistant Staphylococcus aureus (MRSA) is a worldwide problem with high rates of prevalence in the United States. The epidemiology of MRSA has shifted since the late 1990s and is affecting more healthy individuals without healthcare-associated MRSA risk factors. Ninety-five percent of community-acquired MRSA (CA-MRSA) is isolated from skin and soft-tissue infections, however, in rare circumstances it may result in severe infection and even death. CA-MRSA is easily transmitted between close contacts in households, day-care centres, competitive sports teams, and military installations. We present the case of CA-MRSA bacteraemia in a 6-year-old female without MRSA risk factors who received treatment at Children’s Hospital of Nevada at UMC.

The traditional teaching that MRSA is a hospital pathogen has changed due to the increasing number of reports of community-acquired MRSA infections in healthy individuals. CA-MRSA is a pressing public health issue due to high rates of transmission by asymptomatic MRSA carriers and the introduction of the pathogen into hospitals. Clinicians must be aware of the threat posed by CA-MRSA infections in paediatric populations and judiciously select antibiotic coverage based on local resistance rates for MRSA isolates [1,2].

A 6-year-old female without established MRSA risk factors presented to the emergency department at Children’s Hospital of Nevada at UMC with a 6-day history of limping and a dull, aching pain overlying the left medial malleolus. Low-grade fever was also reported prior to admission. The left leg pain was described as sudden in onset, non-radiating and 4/10 in intensity. Ambulation and palpation of the affected area exacerbated the pain, while rest and Motrin were remitting factors. One day prior to admission, the patient’s pain intensified, and she was unable to bear weight on her left leg [3-5]. There was no history suggestive of trauma, and there was no history of redness, swelling, or warmth overlying the left leg. On physical examination, the patient was an ill-appearing female. Vital signs were as follows: temperature of 39 degrees Celsius, pulse of 146, respiratory rate of 28, and oxygen saturation of 97% on room air. There was an area of tenderness, erythema, and swelling overlying the left distal tibia, approximately 21.5 cm in diameter. The patient was unable to bear weight on her left leg and range of motion was difficult to assess due to pain. The rest of the physical examination on presentation was unremarkable. Of note, on day 3 of hospitalization, the leg swelling progressed to involve both the distal and proximal tibia and red streaking developed. Subsequently, the patient clinically worsened and became toxic-appearing with high fevers and tachypnea. A radiograph and ultrasound of the left ankle demonstrated mild soft tissue swelling. An MRI of the left lower leg showed marrow edema and enhancement in the distal tibial metaphysis and epiphysis compatible with osteomyelitis. Repeat MRI on day 3 of hospitalization showed progression of osteomyelitis to the mid and proximal tibia along with progressive cellulitis and myositis in the anterior and medial subcutaneous tissues [6-10] (Figures 1 and 2).

Figure 1: 6-year-old female diagnosed with CA-MRSA osteomyelitis and bacteremia: Radiograph of left lower extremity

Figure 2: 6-year-old female diagnosed with CA-MRSA osteomyelitis and bacteremia: Physical examination finding of LLES.

Laboratory results include a CBC which showed a WBC count of 12,400 wbc/mcL with 78% neutrophils; Hgb of 13.7 g/dL, haematocrit of 38.3%, and platelets of 299 platelets/mcL. CRP was initially elevated at 93 mg/L and peaked at 184 on day 3 of hospitalization. ESR was elevated at 70 mm/hr. On day 2 of hospitalization, gram stain demonstrated gram-positive cocci in clusters, and blood culture resulted positive for methicillin-resistant Staphylococcus aureus on day 4 of hospitalization. The patient was initially treated with IV Clindamycin without clinical improvement. The treatment was transitioned on day 3 of hospitalization to Vancomycin to treat the MRSA bacteraemia and osteomyelitis. The patient was also given fluid resuscitation for early compensated shock and features of systemic inflammatory response syndrome (SIRS). The repeat blood culture drawn on day 4 of hospitalization demonstrated no growth. On day 5 of hospitalization, the patient demonstrated clinical improvement with stabilization of vital signs and improvement of her pain. The patient was ultimately discharged in stable condition on a course of oral Linezolid [11-15].

There is a significant degree of alarm regarding CA-MRSA and its predilection for targeting healthy hosts, namely children. Prior to the mid-1990s, it was rare for MRSA strains to cause disease in otherwise healthy people. Now, outbreaks of CA-MRSA infections affect healthy hosts and hit hardest in ‘closed populations’ such as children who attend daycare, competitive athletes, inmates, and personnel in military installations [16-25]. Evidence also suggests that children from socially disadvantaged minority groups are at greater risk of acquiring CA-MRSA infections. Approximately thirty percent of the general population and up to fifty percent of people with chronic medical conditions may be colonized with S. aureus [26]. The bacteria colonize the nares, axillae, groin, perineum, and gastrointestinal tract of carriers. Many patients are colonized without demonstrating signs of disease and may later suffer an infection from the strain. The clinical presentation, severity of disease, and outcome vary significantly. Skin and soft-tissue infections account for the majority of CA-MRSA infections in young patients, however, five percent of all infections cause invasive diseases such as pneumonia, osteomyelitis, bacteraemia, endocarditis, and necrotizing fasciitis. MRSA strains express a penicillin-binding protein (PBP2a) that creates high-level resistance to beta-lactam antibiotics. Furthermore, the epidemiology of MRSA has shifted, and community-acquired infections are increasingly common in the general population. The virulence of CA-MRSA infections is attributed to the presence of Panton-Valentine leucocidin genes which code for cytotoxins that lead to tissue necrosis and leukocyte destruction [27]. These factors contribute to the versatility of CA-MRSA and make it a challenging pathogen to treat.

According to the CDC, incision and drainage is the recommended primary treatment for patients who present with a cutaneous abscess, or other skin and soft-tissue infections [28]. For smaller lesions not amenable to incision and drainage, hot compress may be applied to promote drainage. For patients with purulent skin lesions, empiric antibiotic treatment may be administered in combination with incision and drainage. Factors that support supplementation with antimicrobial therapy include the presence of cellulitis, severe and spreading SSTI, signs and symptoms of systemic illness, lack of response to incision and drainage alone, associated co-morbidities, or immune suppression. The choice of empiric antibiotic therapy for CA-MRSA skin and soft-tissue infection requires that clinicians differentiate between uncomplicated versus complicated SSTI’s. For empiric coverage of CA-MRSA in paediatric outpatients with uncomplicated skin and soft-tissue infections, oral antimicrobial options include the following: clindamycin, trimethoprim-sulfamethoxazole, and linezolid. Tetracyclines are not a viable option in children less than 8 years of age. In hospitalized children with complicated SSTI’s, vancomycin is the treatment of choice. However, if the paediatric patient is stable and has no signs or symptoms of bacteraemia, clinicians may use empiric clindamycin therapy if the local resistance rate is less than ten percent [29,30].

1. Know the clinical presentation and antibiotic susceptibility of CA-MRSA.
2. Have a high suspicion for CA-MRSA in a patient with a syndrome compatible with S. aureus infection, including bacteraemia, pneumonia, osteomyelitis, and septic arthritis.
3. Tailor therapy based on local anti-bio grams, local prevalence, and resistance data regarding S. aureus species.
4. Determine when a patient requires incision and drainage, or when antimicrobial therapy should be administered.
5. Promote the role of hygiene and contact precautions in the prevention of CA-MRSA.
6. Know the CA-MRSA risk factors characterized by the CDC as the “5 C’s”: crowding, close contact, compromised skin, contaminated surfaces, and lack of cleanliness.

No conflict of interest to declare.

1. Crawford SE, Vavra BS, Daum RS. Community-associated methicillin-resistant Staphylococcus aureus. Emerging infections. Washington DC. ASM Press. 2007; 7: 153-179.
2. Herold BC, Immergluck LC, Maranan MC, Diane SL, Gaskin RE, Vavra S, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no predisposing risk. JAMA. 1998; 279: 593-598.
3. Naimi TS, LeDell KH, Sabetti CK, Boxrud DJ. Comparison of community and health care-associated methicillin-resistant Staphylococcus aureus infection. JAMA. 2003; 290: 2976-2984.
4. Vandenesch F, Naimi T, Enright MC. Community-acquired methicillin-resistant staphylococcus aureus carrying panton-valentine leukocidin genes: worldwide emergence. Emerg Infect Dis. 2003; 9: 978-984.
5. Maree CL, Daum RS, Vavra BS, Matayoshi K, Miller LG. Community-associated methicillin-resistant Staphylococcus aureus isolates causing healthcare-associated infections. Emerg Infect Dis. 2007; 13: 236-242.
6. Dietrich DW, Auld DB, Mermel LA. Community-acquired methicillin-resistant staphylococcus aureus in southern New England children. Pediatrics. 2004; 113: 347-352.
7. Gorwitz RJ, Jernigan DB, Powers JH, Jernigan JA. Strategies for clinical management of MRSA in the community: summary of an experts meeting convened by the Centers for Disease Control and Prevention. 2006.
8. Moore MR, Remington F, Chambers HF. Vancomycin treatment failure associated with heterogeneous vancomycin-intermediate Staphylococcus aureus in a patient with endocarditis and in the rabbit model of endocarditis. Antimicrob Agents Chemother. 2003; 47: 1262-1266.
9. Markowitz N, Quinn EL, Saravolatz LD. Trimethoprim-sulfamethoxazole compared with vancomycin for the treatment of Staphylococcus aureus infection. Ann Intern Med. 1992; 117: 390-398.
10. Thompson RL, Cabezudo I, Wenzel RP. Epidemiology of nosocomial infections caused by methicillin-resistant Staphylococcus aureus. Ann Intern Med. 1982; 97: 309-317.
11. Jorgensen JH. Laboratory and epidemiologic experience with methicillin-resistant Staphylococcus aureus in the USA. Eur J Clin Microbiol. 1986; 5: 693-696.
12. Brumfitt W, Miller HJ. Methicillin-resistant Staphylococcus aureus. N Eng J Med. 1989; 320: 1188-1196.
13. Fowler VG Jr, Boucher HW, Corey GR, Abrutyn E, Karchmer AW, Levine DP, et al. Daptomycin versus standard therapy for bacteremia and endocarditis caused by Staphylococcus aureus. N Engl J Med. 2006; 355: 653-665.
14. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus. Minnesota and North Dakota. JAMA. Centers Disease Control Prevention. 1999; 282: 1123-1125.
15. Suggs AH, Maranan MC, Vavra S, Daum RS. Methicillin-resistant and borderline methicillin-resistant asymptomatic Staphylococcus aureus colonization in children without identifiable risk factors. Pediatr Infect Dis J. 1999; 18: 410-414.
16. Adcock PM, Pastor P, Medley F, Patterson JE, Murphy TV. Methicillin-resistant Staphylococcus aureus in two child care centers. J Infect Dis. 1998; 178: 577-580.
17. Outbreaks of community-associated methicillin-resistant Staphylococcus aureus skin infections. California. Centers Dis Control Preven. 2003; 52: 88.
18. Methicillin-resistant Staphylococcus aureus infections among competitive sports participants. Centers Disease Control Prevention. 2003; 52: 793-795.
19. Fridkin SK, Hageman JC, Morrison M. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med. 2005; 352: 1436-1444.
20. Fraser C, Riley S, Anderson RM, Ferguson NM. Factors that make an infectious disease outbreak controllable. Proc Natl Acad Sci. USA. 2004; 101: 6146-6151.
21. Colley EW, McNicol MW, Bracken PM. Methicillin resistant staphylococci in a general hospital. Lancet. 1965; 191: 595-597.
22. Barrett FF, McGehee RF, Finland M. Methicillin-resistant Staphylococcus aureus at Boston City Hospital. Bacteriologic epidemiologic observations. N Engl J Med. 1968; 279: 441-448.
23. Saravolatz LD, Markowitz N, Arking L, Fisher E . Methicillin-resistant Staphylococcus aureus. Epidemiologic observations during a community-acquired outbreak. Ann Intern Med. 1982; 96: 11-16.
24. Saravolatz LD, Pohlod DJ, Arking LM. Community acquired methicillin-resistant Staphylococcus aureus infections: a new source for nosocomial outbreaks. Ann Intern Med. 1982; 97: 325-329.
25. Johnson LB, Bhan A, Pawlak J. Changing epidemiology of community-onset methicillin-resistant Staphylococcus aureus bacteremia. Infect Control Hosp Epidemiol. 2003; 24: 431-435.
26. Tong SY, Davis JS, Eichenberger E, Holland TL, Fowler VG. Staphylococcus aureus infections: epidemiology, pathophysiology, clinical manifestations, and management. Clin Microbiol Rev. 2015; 28: 603-661.
27. Katayama Y, Ito T, Hiramatsu K. A new class of genetic element, staphylococcus cassette chromosome mec, encodes methicillin resistance in Staphylococcus aureus. Antimicrob Agents Chemother. 2000; 44: 1549-1555.
28. Stevens DL, Bisno AL, Chambers HF, Dellinger P, Kaplan SL, Montoya JG, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005; 41: 1373-1406.
29. Catherine L, Bayer A, Sara E, Michael JR, David A, Henry F, et al. Chambers, clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant staphylococcus aureus infections in adults and children. Clinical Inf Dis. 2011; 52: 18-55.
30. Zinderman CE, Conner B, Malakooti MA, LaMar JE, Armstrong A, Bohnker BK, et al. Community-acquired methicillin-resistant Staphylococcus aureus among military recruits. Emerg Infect Dis. 2004; 10: 941-944.