Ceftazidime-Resistant Salmonella enterica, Morocco

To the Editor: Nontyphoidal salmonellosis (NTS) is a major food-borne illness worldwide. Extended-spectrum cephalosporins (ESCs) are currently preferred drugs for treatment of children with NTS. However, resistance to ESCs has emerged worldwide and has become a serious public health problem. This resistance is caused by production of various class A extended-spectrum β-lactamases (ESBLs) and class C cephalosporinases in Salmonella enterica (1).


Ceftazidime-Resistant Salmonella enterica, Morocco
To the Editor: Nontyphoidal salmonellosis (NTS) is a major foodborne illness worldwide. Extendedspectrum cephalosporins (ESCs) are currently preferred drugs for treatment of children with NTS. However, resistance to ESCs has emerged worldwide and has become a serious public health problem. This resistance is caused by production of various class A extended-spectrum β-lactamases (ESBLs) and class C cephalosporinases in Salmonella enterica (1).
National surveillance systems, ideally based on integration of data for animals, food, and humans, are needed to develop strategies for containing antimicrobial drug resistance. Such systems are primarily based on a network of public or private clinical laboratories that refer Salmonella isolates to public health laboratories for identification. However, this laboratory-based surveillance system in developing countries is hampered by cost constraints and poor access to quality health facilities, resulting in a low rate of isolation of bacterial pathogens from patients having mild infections. These constraints account for the lack of data and underestimation of the number of NTS cases in many countries, including Morocco.
According to the World Health Organization Global Salm Surv database (www.who.int/salmsurv/activities/ en), the Moroccan National Institute of Hygiene reported only 210 human non-Typhi isolates and 999 animal non-Gallinarum isolates during 1999-2003. Antimicrobial drug resistance data are extremely rare. We report the presence of nontyphoidal Salmonella isolates resistant to ESCs during an outbreak of food poisoning and in food products in Morocco.
In March 2008, an S. enterica serotype Typhimurium strain was isolated from stool samples of 45 persons who had attended a wedding ceremony in Errachidia. Clinical symptoms were diarrhea, vomiting, and stomach cramps, beginning 24-72 hours after these persons had eaten a tagine prepared with poorly cooked broiler chickens. Five patients were hospitalized for 3 days, but no deaths were recorded. S. enterica serotype Typhimurium was isolated from leftovers of a broiler carcass stored in a refrigerator.
PulseNet (http://pulsenetinter national.org/pulsenet/pulsenet.asp) LETTERS standard pulsed-field gel electrophoresis (PFGE) of XbaI-digested chromosomal DNA showed that human and poultry isolates had identical profiles. Antimicrobial drug susceptibility was determined by the disk diffusion method and E-tests, as described (2). Isolates were resistant to penicillins and ceftazidime but were susceptible to other antimicrobial drug classes tested. A positive double-disk synergy test result suggested that these strains produced an ESBL. Isolates showed higher levels of resistance to ceftazidime (MIC 128 mg/L) than to ceftriaxone (MIC 8 mg/L).
For identification of the ESBL gene, we conducted PCR amplifications of bla TEM , bla SHV , and bla CTX-M group genes, as described (3). Only the SHV amplicon was obtained, and DNA sequencing showed this amplicon to be 100% identical to bla SHV-12 . Resistance to ESCs and the bla SHV-12 gene were transferred into Escherichia coli by conjugation. An ≈60-kb plasmid was isolated from E. coli transconjugants and the parental strain. PCR-based replicon typing analysis identified replicon IncI1 (4). Although the broilers had been reared locally, no environmental investigation was conducted.
In November 2007, an S. enterica serotype Newport strain was isolated from a pastry made with locally produced eggs during a food survey conducted in southern Morocco. The isolate was resistant to penicillins, cefoxitin (MIC 128 mg/L), ceftriaxone (MIC 64 mg/L), ceftazidime (MIC 128 mg/L), streptomycin, sulfonamides, chloramphenicol, and tetracycline. We identified the bla CMY-2 gene carried by a 210-kb nonconjugative plasmid of replicon IncA/C. These CMY-2-producing isolates are also known as Salmonella Newport multidrug-resistant (MDR)-AmpC. XbaI-PFGE showed a profile similar to the New8a profile described in 2003 in France during a small outbreak linked to consumption of imported horse meat (2). (5). This report described a serotype Typhimurium clone that produced TEM-3 that was isolated from 10 children hospitalized in Casablanca in 1994. Few studies have been conducted on ESC-resistant S. enterica in northern Africa, and most have reported hospital-acquired infections (1). Our study identified ESC-resistant Salmonella strains in the human food chain and in poultry for human consumption in Morocco. Salmonella isolates resistant to ESCs were not identified in food during 2002-2005 at the Institut Pasteur de Casablanca (104 Salmonella isolates from 11,516 food samples) (6). Emergence in poultry and humans of an MDR serotype Keurmassar strain that produced SHV-12 was reported in Senegal in 2001 (7).

ESC-resistant Salmonella isolates have been reported in Morocco
Although CMY-2 was originally identified in a serotype Senftenberg isolate from a child in Algeria (8)

Group B Streptococcus Meningitis in Child with Cochlear Implant
To the Editor: Streptococcus agalactiae, designated group B streptococcus (GBS), is a major cause of infections in neonates and young infants (1). Invasive GBS disease in children beyond infancy is uncommon, occurring mainly as bacteremia without a focus; meningitis caused by GBS is rarely reported (2). Cochlear implant recipients have been documented as having a higher rate of postimplantation bacterial meningitis than a cohort of the same age in the general US population (3). However, no cochlear implant recipient described has been reported to be infected with GBS. We report a case of GBS meningitis in a 6-year-old boy with a cochlear implant.
The patient was hospitalized in 2007 with a 1-day history of fever, headache, and vomiting. His medi-cal history indicated congenital bilateral deafness diagnosed at 1 month of age and consistent with Patterson syndrome (i.e., unusual facies, deafness, bronzed hyperpigmentation of the skin, cutis laxa, mental retardation, and bony deformities) (4). At 4 years of age, he received a right-ear cochlear implant with good functional result. Preoperative high-resolution computed tomography of the temporal bones showed bilateral inner ear malformations of both the cochlear and vestibular labyrinth, conditions consistent with bilateral Mondini deformity (5). Mastoids and middle ears were well aerated. No evidence of cerebrospinal fluid leak appeared during physical examination or imaging. He received a dose of 23-valent pneumococcal polysaccharide vaccine.
At the time of hospital admission, he was somnolent but could be aroused and was cooperative. He had nuchal rigidity, dysmorphic facies, and oligodactyly. Fundi, skin, and ears were unremarkable on examination. Lumbar puncture showed a total protein level of 204 mg/dL, a glucose level of 1.6 mmol/L (blood glucose 3 mmol/L), and 4,800 leukocytes/mm 3 with 88% neutrophils; no bacteria were seen on the Gram stain. Blood count was remarkable for leukocytosis of 30,000/mm 3 and neutrophil predominance.
The patient received treatment with dexamethasone, vancomycin, and ceftriaxone; after treatment, his condition improved rapidly. Blood culture was sterile, but GBS grew in the cerebrospinal fluid culture (the isolate being resistant only to tetracycline). Therapy was continued with ampicillin for 3 weeks. Repeated testing of his hearing and speech perception with the cochlear implant showed no deterioration.
GBS plays a major role in earlyand late-onset infections in neonates and young infants (1). Infections in older children and adults have been described, especially in elderly patients or those suffering from chronic conditions such as diabetes mellitus, malignancy, or HIV infection (6). A review of medical records of patients with GBS infections over a 7-year period at a children's hospital in Memphis, Tennessee, USA, showed that, among 18 patients >3 months of age (13% of all GBS infections in the study), bacteremia was most commonly reported; 3 cases of ventriculo-peritoneal shunt infections were recorded, but no cases of meningitis without foreign devices were found (2). GBS meningitis in children beyond infancy is rare; only a few cases have been reported (7).
Cochlear implantation is the standard treatment for children and adults affected by severe and severeto-profound sensorineural hearing loss. The implant is a neural stimulator with an electrode array surgically placed near the auditory nerve fibers in the scala tympani of the cochlea. Pediatric cochlear implant recipients were found to be at higher risk for developing bacterial meningitis than children in the general US population (3). Increased risk was evident in the perioperative period but extended to >2 years postimplantation (8). Most meningitis cases were associated with an implant with a positioner, a silastic wedge inserted next to the implanted electrode in the cochlea to position the electrode closer to the cochlear nerve endings and thus facilitate electrical signal transmission. Most of those infections were caused by Streptococcus pneumoniae, and none by GBS (3,8). In our patient, the implant did not include a positioner. The timing of meningitis was consistent with the timing indicated in previous reports, but the infecting organism was unique.
Inner ear malformations themselves are associated with increased risk for meningitis (9). The patient reported here had bilateral inner ear malformations; therefore, estimating the relative role of the deformity compared with the cochlear implant's role in the pathogenesis of meningitis in