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R Gomez-Lus

Publications and source records attributed to R Gomez-Lus.

18 recordsLinked to original sources
PubMed2000

Emerging and reemerging pathogens.

From 1973 to 1995, 29 new and reemerging pathogenic microbes were recognized. However, in discussions about emerging infectious diseases, the focus is often on the clinical effects of the host-parasite relationship, rather than the examination of the biology of the pathogen. Many of what we refer to as emerging diseases are characterized better as 'diseases of human progress'. Thus, the aerosolization of water has played an important role in the emergence of Legionella pneumophila infections. New diseases are superimposed on endemic diseases such as diarrhoeal diseases, malaria and tuberculosis. In addition, many pathogens are becoming increasingly resistant to standard antimicrobial drugs, making treatment difficult and in some cases impossible. We summarize our experience on emerging parasitic diseases (primary amoebic meningoencephalitis, respiratory cryptosporidiosis, and diplogonoporiasis), and selected problems of bacterial resistance (MDR tuberculosis caused by Mycobacterium bovis and macrolide-resistance mechanisms of Streptococcus pneumoniae and S. pyogenes).

AIDS-Related Opportunistic Infections↗
PubMed2000

In vitro activity of cefepime and cefotaxime compared to six other agents against 350 penicillin-susceptible and penicillin-resistant Streptococcus pneumoniae.

From January 1996 to December 1997, we evaluated the in vitro activity of 8 antimicrobials (penicillin, amoxycillin, amoxycillin/clavulanate, cefuroxime, ceftazidime, cefepime, cefotaxime, and imipenem) against 350 Streptococcus pneumoniae clinical isolates collected from two hospitals. Imipenem, cefepime and cefotaxime were the most active antibiotics against penicillin-intermediate (PI) and highly penicillin-resistant (PR) S. pneumoniae with MICs 2- to 8-fold lower than penicillin. Against PI and PR pneumococci amoxycillin and amoxycillin/clavulanate were 2-times less active than cefepime and cefotaxime, while cefuroxime was 4-8-times less active. The majority of strains of serotypes 6B, 23F, 14, 9 and 19 were penicillin-resistant, both intermediate (68%) and highly resistant (32%).

Anti-Bacterial Agents↗
PubMed1996

Characterization of the chromosomal aminoglycoside 2'-N-acetyltransferase gene from Mycobacterium fortuitum.

A novel gene encoding an aminoglycoside 2'-N-acetyltransferase (AAC) was cloned from Mycobacterium fortuitum. DNA sequencing results identified an open reading frame that we have called aac(2')-Ib encoding a putative protein with a predicted molecular mass of 24,800 Da. The deduced AAC(2')-Ib protein showed homology to the AAC(2')-Ia from Providencia stuartii. This is the second member of a subfamily of AAC(2')-I enzymes to be identified. No homology was found with other acetyltransferases, including all of the AAC(3) and AAC(6') proteins. The aac(2')-Ib gene cloned in a mycobacterial plasmid and introduced in Mycobacterium smegmatis conferred resistance to gentamicin, tobramycin, dibekacin, netilmicin, and 6'-N-ethylnetilmicin. DNA hybridization with an intragenic probe of aac(2')-Ib showed that this gene was present in all 34 strains of M. fortuitum tested. The universal presence of the aac(2')-Ib gene in M. fortuitum was not correlated with any aminoglycoside resistance phenotype, suggesting that this gene may play a role in the secondary metabolism of the bacterium.

Acetyltransferases↗
PubMed1995

Aminoglycoside resistance in Haemophilus influenzae.

From September 1, 1990 to December 31, 1993 a total of 425 Haemophilus influenzae strains from clinical specimens were isolated in the Microbiology Laboratory of the Zaragoza University Hospital. Of these strains, 16 (33.33%) were resistant to kanamycin, neomycin, paromomycin, lividomycin and streptomycin. Demonstration of APH (3')-I activity by the phosphocellulose paper binding assay, based on the incorporation of radiolabel into lividomycin was sixfold greater than into butirosin. Two DNA probes were prepared to screen for the genes encoding APH(3') activity in kanamycin-resistant H. influenzae. Homology was observed between the aphA1 DNA probe and total cellular DNA from all 16 APH(3')-I producers. On the other hand, streptomycin-resistance was not through metabolic modification of the antibiotic.

Anti-Bacterial Agents↗
PubMed1994

Epidemiological markers of Acinetobacter baumannii clinical isolates from a spinal cord injury unit.

During a period of 28 months, 114 isolates of Acinetobacter baumannii obtained from urine samples of 57 patients, were recovered in a Spinal Cord Unit; an unusual increase in the number of A. baumannii isolates was observed between February 1991 and January 1992. Six different typing methods [biotyping, antimicrobial susceptibility, whole cell and cell-envelope protein analysis, plasmid analysis and chromosomal DNA analysis by pulsed-field gel electrophoresis (PFGE)] were used to study the isolates to establish any potential relationships among them. Chromosomal DNA analysis by digestion with ApaI and separation of the fragments by PFGE was the most powerful tool to determine the relatedness of isolates. The results suggest that the isolates from 1991 and 1992 may have originated from strains present in 1990 that subsequently acquired resistance to amikacin and tobramycin during the epidemic.

Acinetobacter↗
PubMed1993

In vitro antimicrobial production of beta-lactamases, aminoglycoside-modifying enzymes, and chloramphenicol acetyltransferase by and susceptibility of clinical isolates of Acinetobacter baumannii.

Antimicrobial susceptibility testing was performed on 54 epidemiologically unrelated clinical isolates of Acinetobacter baumannii by using a standard agar dilution technique. On the basis of the in vitro activities, imipenem and doxycycline were the most active agents, whereas amikacin, isepamicin, and the new fluorquinolones ciprofloxacin and ofloxacin presented moderate activity. Cephalosporinase activity was found in 98% of the strains, whereas lactamases of TEM type 1 and one with a pI of 7 to 7.5 were present in 16 and 11% of the strains, respectively. Resistance to aminoglycosides was explained by the production of the three classes of aminoglycoside-modifying enzymes, with predominance of aminoglycoside-3'-phosphotransferase VI in 28% of the strains.

Acinetobacter↗
PubMed1990

Transposition of an antibiotic resistance element in mycobacteria.

Bacterial resistance to antibiotics is often plasmid-mediated and the associated resistance genes encoded by transposable elements. Mycobacteria, including the human pathogens Mycobacterium tuberculosis and M. leprae, are resistant to many antibiotics, and their cell-surface structure is believed to be largely responsible for the wide range of resistance phenotypes. Antibiotic-resistance plasmids have so far not been implicated in resistance of mycobacteria to antibiotics. Nevertheless, antibiotic-modifying activities such as aminoglycoside acetyltransferases and phosphotransferases have been detected in fast-growing species. beta-lactamases have also been found in most fast- and slow-growing mycobacteria. To date no mycobacterial antibiotic-resistance genes have been isolated and characterized. We now report the isolation, cloning and sequencing of a genetic region responsible for resistance to sulphonamides in M. fortuitum. This region also contains an open reading frame homologous to one present in Tn1696 (member of the Tn21 family) which encodes a site-specific integrase. The mycobacterial resistance element is flanked by repeated sequences of 880 base pairs similar to the insertion elements of the IS6 family found in Gram+ and Gram- bacteria. The insertion element is shown to transpose to different sites in the chromosome of a related fast-growing species, M. smegmatis. The characterization of this element should permit transposon mutagenesis in the analysis of mycobacterial virulence and related problems.

Amino Acid Sequence↗
PubMed1990

Aminoglycoside acetyltransferase 3-IV (aacC4) and hygromycin B 4-I phosphotransferase (hphB) in bacteria isolated from human and animal sources.

Members of the family Enterobacteriaceae harboring an enzyme of the aminoglycoside acetyltransferase 3 class (AAC-3-IV) (apramycin and gentamicin resistance) and hygromycin B phosphotransferase 4 (HPH-4-I) (hygromycin B resistance) have been isolated from human clinical sources in Europe. A cluster of genes containing IS140, aacC4, and hphB was found in these strains. We demonstrate by Southern hybridization that this cluster is identical to the operon found in animals that also contains insertion sequences belonging to the ISO family. This provides another example of presumptive transfer of antibiotic resistance genes between bacteria of animal and human origin.

Acetylation↗
PubMed1988

Comparative activity of cefotetan against plasmid-encoded aminoglycoside-resistant enterobacteria strains.

304 strains of R-plasmid harbouring enterobacteria resistant to aminoglycosides were studied for their susceptibilities to a range of antibiotics, including cefotetan. Cefotetan and latamoxef were the most active of the four cephamycins tested and all were stable to the beta-lactamases produced by these strains. No new beta-lactamases (SHV-2, CTX-1, TEM-4, CAZ-1) were found in these strains capable of hydrolysing third generation cephalosporins. The activity of cefotetan against these multi-resistant, beta-lactamase producing strains may be of clinical value.

Aminoglycosides↗
PubMed1987

Structure and mobilization of an ampicillin and gentamicin resistance determinant.

A DNA segment originally found in an epidemic plasmid of Escherichia coli encoding an aminoglycoside-(3)-N-acetyltransferase gene (aacC5) and a TEM-type beta-lactamase gene was characterized. The two genes were adjacent and constituted a single transcriptional unit. In addition, these genes were simultaneously mobilized through the action of an insertion sequence related to IS26, IS140, and IS15-delta. This DNA segment is a composite transposon which has been called Tn2922.

Ampicillin↗
PubMed1987

Stability of dactimicin to aminoglycoside-modifying enzymes.

Dactimicin was active against strains expressing the activities of aminoglycoside acetylating enzymes [AAC(3)-II, III, IV and V, AAC(2'), AAC(6')-I and II], aminoglycoside-nucleotidylating enzymes [ANT(2"), AAD(3")] and aminoglycoside-phosphorylating enzymes [APH(3')-I-II and III], with the exception of AAC(3)-I and one staphylococcal AAC(6')-IV. Apparently this is the first report of one 6'-N-acetylating enzyme which modifies and inactivates dactimicin. The authors' data suggest that the differences in the behaviour of dactimicin, gentamicin and amikacin against the aminoglycoside-resistant strains tested were mainly due to the production of aminoglycoside-modifying enzymes. If the results are summarized, it may be concluded that dactamicin is the most stable to the majority of aminoglycoside-modifying enzymes demonstrated [APH(3'), APH(2"), APH(3"), ANT(2"), AAD(3"), AAC(2') and AAC(6')], with the exception of AAC(3)-I and staphylococcal AAC(6')-IV.

Acetylation↗
PubMed1986

Aminoglycoside-phosphotransferases APH(3')-IV and APH(3") synthesized by a strain of Campylobacter coli.

Campylobacter coli strain 981 of animal origin was resistant to erythromycin, tetracycline, streptomycin, kanamycin, ribostamycin, neomycin, paromomycin, lividomycin, and butirosin. Resistance to aminoglycosides of strain 981 was mediated by phosphotransferases APH (3') type-IV and APH (3"). C. coli 981 harboured three plasmids of 24, 34, and 40 Megadaltons respectively. None of these plasmids were transferable to Escherichia coli K-12 by conjugation.

Aminoglycosides↗
PubMed1977

Serological typing of Pseudomonas aeruginosa: use of commercial antisera and live antigens.

A practical slide agglutination test, with commercial antisera (Difco) and live antigens (antigens of live bacteria) taken directly from 24-h antimicrobial susceptibility plates, has been established for serotyping Pseudomonas aeruginosa. Until recently, the lack of both a standard antigenic scheme and a source of commercial antisera has made serological typing of this organism impractical. A simplified procedure with 17 unabsorbed antisera and live antigens prepared from materials readily available in most clinical microbiology laboratories makes epidemiological typing of this organism possible in hospital laboratories. The distribution of each serotype examined in this study was determined by using 425 consecutive patient isolates from six different hospitals. The distribution of O antigen groups (live antigen) was as follows: O1, 11.5%; O2, 1.6%; O3, 3.8%; O4, 7.8%; O5, 4.2% O6, 27.1%; O7,8, 5.9%; O9, 6.8%; O10, 2.4%; O11, 8.2%; O12 through O17, each less than 1%. Ten and six-tenths percent of the above agglutinated in two antisera, 3.3% agglutinated in more than two antisera, and 5.2% did not agglutinate in any antisera. A comparison of live and heated antigens shows that 93.2% were typable with the live antigen, and 94.5% were typable with the heated antigen. When both antigens were used, we typed 96.3% of 725 isolates. The reproductibility and specificity of the serological procedure were examined. We recommend using the live antigen for routine serological typing in clinical microbiology laboratories for "in house" epidemiology and reserving the heated antigen for reference and research typing (and for those few cases where results cannot be obtained using the live antigen). The application of serotyping in the study of outbreaks of P. aeruginosa is also presented.

Agglutination Tests↗