A baby who developed meticillin-resistant staphylococcus aureus (MRSA) infection without exposure to MRSA carriers suggests an alternative model for the acquisition of this virulent staphylococcal infection.
In a research letter in this week's issue of The Lancet, the authors conclude that a new MRSA genotype was formed in vivo by exchange of the meticillin-resistance gene between different staphylococcal species.
MRSA is responsible for many hospital-based infections worldwide. Its strong resistance is a result of its penicillin-binding protein 2a, which has a low affinity for all b-lactam antibiotics. Penicillin-binding protein 2a is encoded by the mecA gene, which is found on the chromosome of meticillin-resistant strains of many staphylococcal species.
Camiel Wielders and colleagues from University Hospital Utrecht, Netherlands, isolated a successive pair of mecA- and mecA+ S aureus strains from a baby whose initial meticillin-susceptible infection had just been treated with b-lactam antibiotics and who later unexpectedly developed an MRSA infection.
The investigators analyzed the molecular epidemiology of these isolates and found that, except for the mecA DNA, the two isolates were identical. The mecA DNA present in the MRSA strain was identical to that in a S epidermidis strain isolated from the baby, but different from other MRSA strains.
Camiel Wielders comments: "The new mecA+ MRSA genotype is difficult to explain since we isolated it from an infant younger than 2 months, who was neither transferred from a foreign hospital nor in contact with an MRSA carrier.
"We conclude that this MRSA isolate was formed in vivo, during treatment, by the horizontal transfer of mecA DNA from the S epidermidis strain. Many mecA+ MRSA might be formed by horizontal gene transfer, followed by the spread of multiresistant clones that are favoured most by antibiotic selection pressure".
(Reference: THE LANCET, 26th May 2001.)
[Contact: Dr. Camiel LC Wielders]