September 01, 2011
4 min read

What to tell parents about CA-MRSA

A Q & A session with an expert to help inform parents on how to prevent MRSA infection and how to recognize when to seek medical care.

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In recent years, the tremendous increase in the frequency of community-associated methicillin-resistant Staphylococcus aureus has led to significant fears and concerns in many of our patients’ families.

Because it is difficult for families to ascertain the often-subtle differences between the various presentations of CA-MRSA (eg, symptomatic colonization, uncomplicated skin and soft tissue infections, deep abscesses), it is imperative that, as health care providers, we offer clear advice on the prevention and management of pediatric staphylococcal disease.

C. Buddy Creech, MD, MPH
C. Buddy Creech, MD, MPH

Where did my child’s CA-MRSA come from?

This is one of the most common questions we hear as infectious diseases consultants, and it is often the most difficult. Approximately one in every three adults harbors S. aureus in their anterior nares. Risk factors for carriage include race/ethnicity, exposure to staphylococci (whether in the community or health care setting), smoking, and undoubtedly host factors that have yet to be elucidated. MRSA carriage has also increased in recent years, with as many as 10% of healthy children in the Nashville, Tenn., area colonized in the nares. In addition, extranasal sites of colonization, particularly with USA300 S. aureus, seem to be important reservoirs for carriage, particularly oropharyngeal, perirectal and inguinal colonization. Regardless of the site of colonization, it appears that S. aureus, playing a mere commensal role initially, seizes an advantage afforded it by an antecedent respiratory infection or skin breakdown, resulting in clinically apparent disease.

What makes CA-MRSA so virulent?

This question takes many different forms from families. Why did my child get so sick? Why did it happen so fast? Why did his sister only get a skin abscess and he has a bone infection? These are critical questions to the field and, as yet, remain unsolved. What we know is that the spectrum of disease produced by CA-MRSA is entirely consistent with that of other strains of staphylococci, although there are differences regarding severity and resultant complications. For example, S. aureus is classically the most common cause of acute hematogenous osteomyelitis in children. Now, in many areas in the US, CA-MRSA represents most staphylococcal strains recovered from these patients. Data from Texas Children’s Hospital demonstrate that children with CA-MRSA isolates that produce Panton-Valentine leukocidin (PVL) have more extensive disease, higher inflammatory markers (erythrocyte sedimentation rate and C-reactive protein), higher likelihood of deep venous thrombosis and greater need for ICU care. Thus, although the spectrum of disease is similar, the severity of many of these infections is quite different.

What governs this difference is the topic of much research in the US and abroad. Three converging theories of virulence predominant: 1) the presence of novel virulence determinants (such as PVL or other cytolytic toxins); 2) the overexpression of common staphylococcal virulence factors (such as alpha-toxin); or 3) exposure of novel strains of S. aureus to a population without substantial pre-existing immunity to one or more novel antigens.

How contagious is CA-MRSA?

We often do not think of CA-MRSA as a communicable disease in the same way as we do tuberculosis, measles or varicella, but CA-MRSA is transmitted from person-to-person, both in the community and the health care system. Parents typically are attuned to this communicability when health care providers, adhering to standard infection control policies, don gowns and gloves before entering the room. This simple maneuver establishes that the organism is capable of spread and that protection is indicated.

I recommend two ways to communicate this to families. The first is to reinforce the idea of asymptomatic colonization and staphylococci’s prominent role as normal (and likely healthy) flora in most patients. Second, we should highlight our infectious diseases version of the “two-hit hypothesis,” that it is not merely exposure to CA-MRSA, but antecedent respiratory disease, trauma or surgery that places patients at risk. Beyond this, however, we should take time to investigate whether other close family members are at high risk for staphylococcal disease. Those with chronic pulmonary diseases, chronic skin breakdown or those undergoing surgery may be at higher risk for disease after exposure to virulent strains of S. aureus. Therefore, although many conversations should focus on reducing anxiety regarding communicability, there remains an opportunity to control subsequent infections in close contacts.

What do I do if the boils continue?

If a child continues to have boils from CA-MRSA, there are three steps to approach this with patients and their families. The first is to ensure that the patient is normal immunologically. In these days of CA-MRSA, this is often done by ensuring a normal growth curve; obtaining a history that specifically focuses on the presence of recurrent infections, adenopathy and unusual organisms (eg, Serratia); and documenting a normal number of circulating neutrophils. For some patients, enough concern for chronic granulomatous will exist that formal evaluation will be required; however, for most, eradication of CA-MRSA from the environment, skin and mucosal membranes may interrupt the cycle of recurrent furunculosis.

The second step is to help families recognize that as many as 15% to 20% of children, after a skin and soft tissue infection caused by CA-MRSA, will experience a recurrence within 1 year. The last step remains the most difficult to standardize because only preliminary data exist to guide our interventions. Many providers, seeking to eradicate CA-MRSA from the nose, skin and environment of patients, will prescribe nasal mupirocin (twice daily for 5-7 days), topical disinfection (via either chlorhexidine showers or dilute bleach baths) and environmental disinfection (through careful laundering of bedding, clothes, towels, etc.). In many situations, these maneuvers are associated with interruption of recurrent furunculosis, although their causal effect remains debated. Ongoing clinical trials will help define this strategy, including whether index patient alone vs. household decolonization should be attempted, and whether extranasal sites of carriage should be addressed as well (eg, oropharynx, gastrointestinal tract).


The problem of staphylococcal disease in pediatrics is not new, although the scope and severity have increased with the advent of CA-MRSA. Unfortunately, this moving target has become the most common invasive bacterial pathogen in the United States, replacing Haemophilus influenzae and Streptococcus pneumoniae. As a result, considerable efforts are under way to develop new therapeutics and primary preventions through vaccinations. As we counsel parents about staphylococcal disease, reminding them of how S. aureus fits into the pantheon of pediatric pathogens, the successes we currently enjoy through vaccination may provide a sense of comfort moving forward.

C. Buddy Creech, MD, MPH, is an Assistant Professor, Pediatric Infectious Diseases, Associate Director, Vanderbilt Vaccine Research Program and is Co-Director, Pediatric Infectious Diseases Fellowship Program, Vanderbilt University School of Medicine and Monroe Carell Jr. Children’s Hospital. Dr. Creech is also a member of the Infectious Diseases in Children Editorial board. Disclosure: Dr. Creech reports no relevant financial disclosures.

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