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Revista argentina de microbiología

versión impresa ISSN 0325-7541

Rev. argent. microbiol. vol.44 no.4 Ciudad Autónoma de Buenos Aires dic. 2012



A case of familial transmission of community-acquired methicillin-resistant Staphylococcus aureus carrying the lnu(A) gene in Santa Fe city, Argentina


Emilce de los A. Méndez1*, María L. Roldán1, María R. Baroni1,2, María A. Mendosa1, Sabrina A. Cristóbal1, Stella M. Virgolini2, Diego Faccone3

1Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, Ciudad Universitaria, Paraje "El Pozo" (3000), Santa Fe;
2Hospital de Ninos "Dr O. Alassia", Mendoza 4115 (3000), Santa Fe;
3 Servicio Antimicrobianos, INEI - ANLIS "Dr. Carlos G. Malbrán", Av. Vélez Sársfeld 563 (1282) Ciudad Autónoma de Buenos Aires, Argentina.

*Correspondence. E-mail:



Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is increasingly recognized as an important pathogen causing skin and soft tissue infections as well as necrotizing pneumonia. We describe a case of familial transmission of CA-MRSA between a 6-month-old boy and his mother in Santa Fe City, Argentina. Both isolates showed an identical antimicrobial susceptibility profile, carried type IV SCCmec and harboured the pvl and the lnu(A) genes. Isolates showed indistinguishable SmaI-PFGE patterns confirming their genetic relationship. These results corroborate the intrafamilial transmission of CA-MRSA and might associate this strain with the repetitive events of furunculosis within the family.

Key words: CA-MRSA; Familial transmission; PVL; SCCmec IV.


Caso de transmisión familiar de Staphylococcus aureus resistente a la meticilina adquirido en la comunidad portador del gen lnu(A) en la ciudad de Santa Fe, Argentina. Staphylococcus aureus resistente a la meticilina adquirido en la comunidad (SARM-AC) es reconocido como un patógeno importante que causa infecciones de piel y partes blandas y neumonía necrotizante. Describimos un caso de transmisión familiar de SARM-AC entre un nino de 6 meses de edad y su madre en la ciudad de Santa Fe, Argentina. Ambos aislamientos mostraron idéntico perfil de sensibilidad a los antimicrobianos, tenían el SCCmec tipo IV, y contenían los genes pvl y lnu(A). Los aislamientos presentaron patrones de SmaI-PFGE indistinguibles entre sí, lo cual confirmó su relación genética. Estos resultados corroboran la transmisión intrafamiliar de SARM-AC; asimismo, este aislamiento podría asociarse con los eventos repetitivos de furunculosis en la familia.

Palabras clave: SARM-AC; Transmisión familiar; LPV; SCCmec IV.


Community-acquired methicillin-resistant Sta-phylococcus aureus (CA-MRSA) is a common cause of primary skin infections, mainly furunculosis and abscesses, but can also cause necrotizing tissue in-fections and fulminant pneumonia in young and pre-viously healthy people (5, 6). Several cases of intrafa-milial CA-MRSA transmission have been described in the last decades, especially in families with young children (1, 8, 9, 10). Most CA-MRSA isolates har-bour the virulence factor Panton-Valentine leukoci-din (PVL) and the mecA gene which is carried in the staphylococcal cassette chromosome mec (SCC-mec) type IV or V (5). Resistance to macrolides, lincosamides and streptogramins in S. aureus is mainly mediated by erm (MLS phenotype) and msrA (MSB phenotype) genes. However, an unusual mechanism of lincosamide resistance mediated by lnu(A) gene (L phenotype) has been occasionally described in clini-cal isolates (7, 11). In this report we describe a case of familial transmission of PVL producing CA-MRSA carrying SCCmec IV and the unusual lnu(A) gene.

Case report. In October 2010, a previously healthy 6-month-old boy was admitted to a private hospital in Santa Fe City, presenting with fever, shortness of breath, dysphagia and productive cough that had started 6 days earlier. The patient had no risk factors associated to hospital infection, such as immunosuppression, corticoid treatment, diabetes, recent infuenza, presence of any permanent indwelling catheter or percutaneous device, residence in a long-term care facility or others (e.g., daycare center) or previous S. aureus colonization/ infection.

Laboratory data showed hemoglobin levels of 8.2 g/dl and a white blood cells count of 36,000/µl (86 % neutrophils, 2 % eosinophils, 10 % lymphocytes, 2 % monocytes). Arterial blood gas was: pH = 7.4, Pa CO2 32.9 mmHg. Erythrocyte sedimentation rate was 30 mm/h and was positive for C-reactive protein. Chest X-ray and lung ecography showed a 10 mm pleural displacement and a pleural drainage tube insertion was required.

Despite empirical treatment with ceftriaxone 100 mg/kg for 4 days and since the patient's condition continued to worsen, he was transferred to a high-complexity public hospital for further treatment.

At the hospital, he was diagnosed with severe community-acquired pneumonia presenting with septic shock and he was transferred to the Intensive Care Unit (ICU) where he was intubated and ventilated.

Staphylococcus aureus (MRSA-1) was recovered from pleural fluid culture but not from blood cultures. The isolate was identifed by the Vitek System (bioMerieux, Marcy l'Etoile, France) and the coagulase test. Susceptibility testing was performed by the disk diffusion method according to CLSI standards (3). MRSA-1 isolate was categorized as susceptible to erythromycin, ciprofoxacin, cotrimoxazole, rifampin, and linezolid, but resistant to ß-lactam antibiotics and gentamicin. Although a susceptible inhibition zone was observed around the clindamycin disk, the lincomycin inhibition zone was of 9 mm, suggesting the presence of a mechanism of resistance to lincosamides. The minimal inhibitory concentration (MIC) of vancomycin was 0.75 μg/ml by Etest (bioMerieux). Considering these results, the antibiotic therapy was switched to intravenous vancomycin (40 mg/kg bid) plus rifampin (10mg/kg bid).

The patient remained ventilator-dependent for 4 days. He showed clinical improvement and intravenous antibiotic therapy was continued for 20 days. On day 24th of hospitalization he was discharged on oral cotrimoxazole treatment (10 mg/ kg/day for 15 days).

In an attempt to detect the infection source, household contact information was evaluated, revealing a history of repetitive furunculosis affecting the mother and all siblings. The mother was screened by taking a sample from an abdominal furuncle, obtaining a methicillin-resistant S. aureus (MRSA-2). MRSA-2 showed identical antibiotic susceptibility profile than MRSA-1, and the same MIC value to vancomycin. Detection of mecA and pvl genes was positive in both MRSA-1 and MRSA-2 isolates by polymerase chain reaction (PCR) as previously described (6, 13). Both isolates, MRSA-1 and MRSA-2, harbored the SCCmec type IV characterized by the multiplex PCR assay described by Oliveira (12). Interestingly, the lnu(A) gene was also detected in both isolates using lnuA-F: 5´- GGC GTA GAT GTA TTA ACT GG-3´, and lnuA-R2: 5´-GAA AAA GAA GTT GAG CTT C-3´, specific primers and confirmed by DNA sequencing. The presence of the unusual lnu(A) gene has been sporadically described in others countries, while only an MRSA-outbreak in a neonatal ward has been reported in Argentina (4, 7, 11) .

The clonal relationship determined by pulsed feld gel electrophoresis (PFGE) using SmaI enzyme for genomic DNA digestion showed that both isolates displayed indistinguishable electrophoretic patterns (2). These results confirm the genetic relationship between both isolates and the familial transmission of CA-MRSA harbouring SCCmec type IV and positive pvl gene.

The patient and household contact had no history of surgical procedures or of antimicrobial therapies. A repetitive history of furunculosis affecting the mother and all the siblings was registered; however no additional MRSA-positive samples were recovered.

The fact that both CA-MRSA isolates harbored the lnu(A) gene, limits the use of clindamycin as an option for the treatment of primary skin infections. However, it is important to note that none of the family had previously received clindamycin treatment.

In the present work, we confirm the familial transmission of CA-MRSA between a child and his mother, highlighting the importance of the search of contact carriage in community-onset MRSA infections.

Acknowledgment: this work was partly supported by research grants from the Universidad Nacional del Litoral, Santa Fe, Argentina (CAI+D 2009).


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Recibido: 29/5/2012
Aceptado: 8/11/2012

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