Sudden-onset bilateral deafness revealing early neurosyphilis.

INTRODUCTION: Rapid-onset of sensorineural hearing loss in a patient at risk of genital or oral exposure to treponema can be secondary to early neurosyphilis, for which delayed treatment may result in irreversible sequelae. SUMMARY OF THE CASE REPORT: A 40-year-old, HIV seropositive man with a CD4 lymphocyte count greater than 500/mm(3) presented with rapid-onset of bilateral sensorineural hearing loss over a period of one week. Otorhinolaryngological examination was normal. The audiogram showed bilateral hearing loss of 25 and 30 decibels, respectively. He subsequently developed loss of visual acuity, leading to the diagnosis of syphilitic meningitis affecting the optic and auditory nerves. DISCUSSION: In about one half of cases, neurosyphilis is an early manifestation of the disease occurring several weeks or months after contamination. Rapid- or even sudden-onset of hearing loss may be due to auditory neuritis. Clinical interview and syphilis serology in a patient at risk of exposure can allow rapid diagnosis and treatment, consisting of two weeks parenteral penicillin. Recovery of hearing loss is inconstant but can be complete.

[Using a 48-hour delay from admission to the first positive culture without any other consideration: an accurate method to differentiate acquired and imported methicillin-resistant Staphylococcus aureus?]. / Retenir un délai de 48 heures entre l'admission des patients et le premier prélèvement positif est-il suffisant pour différencier les souches acquises à l'hôpital et importées de Staphylococcus aureus résistant à la méticilline?

To differentiate imported and acquired strains of methicillin-resistant Staphylococcus aureus (MRSA), a 48-hour delay from hospital admission to the first MRSA-positive culture is usually considered. To assess if taking into account this delay without any other consideration is an accurate method, we defined 3 situations for whom we considered the MRSA acquisition status as questionable. The other situations were defined as either acquired MRSA or imported MRSA. We determined the acquisition status of MRSA (acquired, imported, or questionable) isolated during a 20-month period by considering or not considering screening samples performed on admission. The ratio "imported MRSA/acquired MRSA" (I/A) was calculated according to (1) the consideration of MRSA with questionable status as imported or acquired, and (2) the consideration of screening samples or not in the calculation of the ratio. The acquisition status in our hospital was questionable in 3.6% of patients when all samples were considered and in 12,0% when only clinical samples were taken into account (p = 0,01). The ratio I/A was 4-fold higher by considering both clinical and screening cultures and questionable status as imported than by considering only clinical samples and questionable status as acquired. Using a 48-hour delay without any other consideration is probably an accurate method to differentiate acquired and imported MRSA when a selective screening programme at admission in operational. Conversely, this definition seems to be more hazardous in the absence of screening.

Brain abscess caused by Nocardia cyriacigeorgica in a patient with human immunodeficiency virus infection.

Nocardia cyriacigeorgica is a recently characterized species within the genus of Nocardia. We report a brain abscess, following a primary pulmonary colonization, due to this species in a human immunodeficiency virus-infected patient. This case confirms that isolation of Nocardia in sputum is associated with a high risk of disseminated infection in immunocompromised patients.

Estimation of methicillin-resistant Staphylococcus aureus transmission by considering colonization pressure at the time of hospital admission.

Our objective was to evaluate the accuracy of a methicillin-resistant Staphylococcus aureus (MRSA) rate using the imported MRSA reservoir identified at the time of hospital admission. Two indicators were used: the number of imported MRSA patient-days/total number of patient-days [representing colonization pressure (CP) at the time of admission] and the incidence of hospital-acquired MRSA isolated from clinical samples expressed as density/100 patient-days for carriers identified at the time of admission [representing the incidence taking CP into account (ICP)]. The variations of these indicators were analysed and compared with two more common indicators: percentage of MRSA acquired in our hospital and the incidence of hospital-acquired MRSA isolated from clinical samples expressed as density/1000 patient-days within three four-month periods during 2002. Common indicators varied similarly, with marked decline during the third period; first-period CP was twice that of other periods (P<10(-6)) and the highest (>two-fold) ICP was seen in the summer (second) period (P<0.001) when the personnel/patient ratio was the lowest. Thus, comparison of different indicators within four-month periods underlines important differences between common and novel indicators. Despite several limitations, ICP should be helpful in the interpretation of MRSA surveillance data, particularly for estimating the extent of MRSA transmission.

Impact of screening for MRSA carriers at hospital admission on risk-adjusted indicators according to the imported MRSA colonization pressure.

We evaluated the impact of the different components of a screening programme of methicillin-resistant Staphylococcus aureus (MRSA) carriers at hospital admission on the value of two risk-adjusted rates: the proportion of imported MRSA and an indicator of the MRSA colonization pressure (ICP), and the incidence of MRSA acquired and detected in our hospital. Indicators were calculated: (1) with no screening programme; (2) with a programme limited to the intensive care unit (ICU); (3) with a programme extended to patients with risk factors for MRSA carriage hospitalized in non-ICU wards. The programme included an automatic alert. Systematic sampling of patients with risk factors hospitalized in non-ICU settings detected nearly 50% of carriers at admission. The proportion of MRSA imported into our hospital varied from 35.4% without any screening programme to 71.8% when all components of our screening programme were considered (P<10(-4)). The ICP varied from 3.1% (31/985) with the complete programme to 10.4% (31/297) without any screening programme (P<10(-6)). Screening patients with risk factors for MRSA carriage hospitalized in non-ICU wards resulted in a 51% increase of the calculated proportion of imported strains and a 58% decrease of the ICP. The two studied indicators were strongly dependent on the screening strategy for MRSA carriers implemented at admission. The screening strategy for patients admitted to non-ICU wards who have risk factors for MRSA carriage seems to be the determinant for the interpretation of certain risk-adjusted indicators of MRSA cross-transmission. Comparisons of these indicators must consider the setting in which the screening programmes are implemented.

Dissemination of CTX-M-type beta-lactamases among clinical isolates of Enterobacteriaceae in Paris, France.

We analyzed 19 clinical isolates of the family Enterobacteriaceae (16 Escherichia coli isolates and 3 Klebsiella pneumoniae isolates) collected from four different hospitals in Paris, France, from 2000 to 2002. These strains had a particular extended-spectrum cephalosporin resistance profile characterized by a higher level of resistance to cefotaxime and aztreonam than to ceftazidime. The bla(CTX-M) genes encoding these beta-lactamases were involved in this resistance, with a predominance of bla(CTX-M-15). Ten of the 19 isolates produced both TEM-1- and CTX-M-type enzymes. One strain (E. coli TN13) expressed CMY-2, TEM-1, and CTX-M-14. bla(CTX-M) genes were found on large plasmids. In 15 cases the same insertion sequence, ISEcp1, was located upstream of the 5' end of the bla(CTX-M) gene. In one case we identified an insertion sequence designated IS26. Examination of the other three bla(CTX-M) genes by cloning, sequencing, and PCR analysis revealed the presence of a complex sul1-type integron that includes open reading frame ORF513, which carries the bla gene and the surrounding DNA. Five isolates had the same plasmid DNA fingerprint, suggesting clonal dissemination of CTX-M-15-producing strains in the Paris area.

Selection during cefepime treatment of a new cephalosporinase variant with extended-spectrum resistance to cefepime in an Enterobacter aerogenes clinical isolate.

Enterobacter aerogenes resistant to cefepime (MIC, 32 microg/ml) was isolated from a patient treated with cefepime for an infection caused by a strain of E. aerogenes overproducing its AmpC beta-lactamase (MIC of cefepime, 0.5 microg/ml). The AmpC beta-lactamase of the resistant strain had an L-293-P amino acid substitution and a high k(cat)/K(m) ratio for cefepime. Both of these modifications were necessary for resistance to cefepime.

Clostridium difficile brain empyema after prolonged intestinal carriage.

Clostridium difficile, the most common cause of antibiotic-associated diarrhea, is occasionally isolated from extraintestinal sites and is usually found as part of a polymicrobial flora. We report a case of brain empyema that occurred after the recurrent intestinal carriage of a nontoxigenic strain of C. difficile. Brain abscess cultures contained both toxigenic and nontoxigenic isolates. Pulsed-field gel electrophoresis showed that nontoxigenic isolates from the intestine and from the brain were identical.

Extension of resistance to cefepime and cefpirome associated to a six amino acid deletion in the H-10 helix of the cephalosporinase of an Enterobacter cloacae clinical isolate.

Enterobacter cloacae CHE, a clinical strain with overproduced cephalosporinase was found to be highly resistant to the new cephalosporins, cefepime and cefpirome (MICs> or =128 microg ml(-1)). The strain was isolated from a child previously treated with cefepime. The catalytic efficiency of the purified enzyme with the third-generation cephalosporins, cefepime and cefpirome, was 10 times higher than that with the E. cloacae P99 enzyme. This was mostly due to a decrease in K(m) for these beta-lactams. The clinical isolate produced large amounts of the cephalosporinase because introduction of the ampD gene decreased ampC expression and partially restored the wild-type phenotype. Indeed, MICs of cefepime and cefpirome remained 10 times higher than those for a stable derepressed clinical isolate (OUDhyp) transformed with an ampD gene. Sequencing of the ampC gene showed that 18 nucleotides had been deleted, corresponding to the six amino acids SKVALA (residues 289--294). According to the crystal structure of P99 beta-lactamase, this deletion was located in the H-10 helix. The ampR-ampC genes from the clinical isolates CHE and OUDhyp were cloned and expressed in Escherichia coli JM101. The MICs of cefpirome and cefepime of E. coli harboring ampC and ampR genes from CHE were 100--200 times higher than those of E. coli harboring ampC and ampR genes from OUDhyp. This suggests that the deletion, confirmed by sequencing of the ampC gene, is involved in resistance to cefepime and cefpirome. However, the high level of resistance to cefepime and cefpirome observed in the E. cloacae clinical isolate was due to a combination of hyperproduction of the AmpC beta-lactamase and structural modification of the enzyme. This is the first example of an AmpC variant conferring resistance to cefepime and cefpirome, isolated as a clinical strain.

Genotypic characterisation of endemic VanA Enterococcus faecium strains isolated in a paediatric hospital.

A total of 36 vancomycin-resistant Enterococcus faecium isolates obtained from 30 patients during a 28-month period in a paediatric university hospital was analysed by pulsed-field gel electrophoresis (PFGE) combined with Southern hybridisation of a vanA-specific DNA probe. All the isolates hybridised with the vanA probe. Seventeen different PFGE patterns and 11 PFGE subtypes were identified among the 36 clinical isolates, and the size of probe-positive bands ranged from c. 30 to 300 kb. These data are consistent with an increase in the overall genomic diversity of vancomycin-resistant E. faecium isolates during the study period. Two periods were distinguished. The prevalence of a single clone in the initial period suggested transmission between patients in three wards. During the following period, multiple genotypes of vancomycin-resistant E. faecium were identified, indicative of multiple introductions or the dissemination of resistance genes by recombinant transposition.

A novel integron in Salmonella enterica serovar Enteritidis, carrying the bla(DHA-1) gene and its regulator gene ampR, originated from Morganella morganii.

The genetic organization of the gene coding for DHA-1 and the corresponding ampR gene was determined by PCR mapping. These genes have been mobilized from the Morganella morganii chromosome and inserted into a complex sulI-type integron, similar to In6 and In7. However, they are not themselves mobile cassettes. This integron probably includes a specific site for recombination allowing the mobilization of diverse resistance genes, as observed for bla(CMY-1) and bla(MOX-1).

Salmonella enteritidis: AmpC plasmid-mediated inducible beta-lactamase (DHA-1) with an ampR gene from Morganella morganii.

DHA-1, a plasmid-mediated cephalosporinase from a single clinical Salmonella enteritidis isolate, conferred resistance to oxyimino-cephalosporins (cefotaxime and ceftazidime) and cephamycins (cefoxitin and moxalactam), and this resistance was transferable to Escherichia coli HB101. An antagonism was observed between cefoxitin and aztreonam by the diffusion method. Transformation of the transconjugant E. coli strain with plasmid pNH5 carrying the ampD gene (whose product decreases the level of expression of ampC) resulted in an eightfold decrease in the MIC of cefoxitin. A clone with the same AmpC susceptibility pattern with antagonism was obtained, clone E. coli JM101(pSAL2-ind), and its nucleotide sequence was determined. It contained an open reading frame with 98. 7% DNA sequence identity with the ampC gene of Morganella morganii. DNA sequence analysis also identified a gene upstream of ampC whose sequence was 97% identical to the partial sequence of the ampR gene (435 bp) from M. morganii. The gene encoded a protein with an amino-terminal DNA-binding domain typical of transcriptional activators of the LysR family. Moreover, the intercistronic region between the ampC and ampR genes was 98% identical to the corresponding region from M. morganii DNA. AmpR was shown to be functional by enzyme induction and a gel mobility-shift assay. An ampG gene was also detected in a Southern blot of DNA from the S. enteritidis isolate. These findings suggest that this inducible plasmid-mediated AmpC type beta-lactamase, DHA-1, probably originated from M. morganii.

Cloning and sequencing of the gene encoding the AmpC beta-lactamase of Morganella morganii.

The chromosomal beta-lactamase gene of a clinical isolate of Morganella morganii was cloned in Escherichia coli and sequenced. The beta-lactamase had a pI of 7.4 and conferred a typical AmpC susceptibility pattern. The insert obtained was found to encode a protein of 379 amino acids. Its deduced amino acid sequence revealed it to be a class C beta-lactamase: 39-56% identity with chromosomal AmpC beta-lactamases of Serratia marcescens, Yersinia enterocolitica, Citrobacter freundii, Enterobacter cloacae and Escherichia coli; and 37-56% identity with plasmid-mediated beta-lactamases (MOX-1, CMY-1, FOX-1, ACT-1, LAT-1, BIL-1 and CMY-2). The ampC gene was linked to a gene only part of which (450 bp) was cloned homologous to the regulatory ampR genes of chromosomal class C beta-lactamases.