Abstracts of the Scientific Posters, 2013 AACC Annual Meeting ...

Infectious Disease
Wednesday, July 31, 9:30 am – 5:00 pm
B-123
First Report on identification of plasmid mediated quinolone resistance
genes in E. coli and K. pneumoniae strains from Pakistan
M. Faiz 1 , S. Rafique 2 , H. Batool 2 , A. Younis 2 , F. Anwar 3 , T. Bashir 1 , A.
Shahid 1 . 1 Institute of Nuclear Medicine and Oncology, Lahore, Pakistan,
2
Kinnaird college for Women, Lahore, Pakistan, 3 University of Lahore,
Lahore, Pakistan
Background: Multidrug resistance in Enterobacteriaceae including resistance
to quinolones is rising worldwide and complicating the treatment of serious
nosocomial infections. Resistance to quinolones in Enterobacteriaceae is classically
chromosomally mediated. However, most commonly it arises stepwise as a result
of mutation usually accumulating in the genes encoding primarily DNA gyrase or
changes in the expression of outer membrane and efflux pumps. Several recent studies
have indicated that plasmid-mediated resistance mechanisms also play a significant
role in fluoroquinolone resistance, and its prevalence is increasing worldwide . Now
quinolone resistance determinants (qnrA, qnrB, qnrC and qnrS) have been identified
in a series of enterobacterial species from the United States, Europe, Japan and
Near and Far East. In Pakistan, the presence of the qnr gene in the clinical isolates
of Enterobacteriaceae has not been reported. Objectives: This study, therefore aimed
to investigate the presence of the qnr gene in clinical isolates of E. coli and K.
pneumoniae from Pakistan.
Methods: A total of one hundred fifty, non-repetitive, ciprofloxacin resistant E. coli
(n=110) and K. pneumoniae strains (n=40) were isolated from urinary specimens
of patients from January 2010 to October 2010 using standard microbiological
techniques. Minimal inhibitory concentrations (MICs) of the antibiotics were
determined according to the Clinical and Laboratory Standards Institute (CLSI).
Screening of qnrA, qnrB, and qnrS by was performed by polymerase chain reaction
(PCR) amplification.
Results: PCR amplification of Qnr gene in 110 E. coli isolates and 40 K. pneumonia
isolates was performed. qnr gene was detected in 11% (17 out of 150) strains tested.
In E.coli, qnrB gene was detected in 6 out of 110 strains (6%). No qnrA, qnrS or
both were identified in any of the strains. Similarly 11 out of 40 (28%) Klebsiella
isolates had qnr genes where 7 (64%) samples showed qnrB, 3 (27%) qnrS and 1
(9%) showed both qnrS and qnrB while none showed qnrA (Figure). In both E.coli
and Klebsiella sp, none of the strains showed qnrA or qnrA and qnrB both. Plasmid
transfer was achieved in Klebsiella K-1 strain. MICs of ciprofloxacin for qnrB
positive transformants range from 8-16μg/ml than recipient strains.
Conclusion: In conclusion, this study constitutes the first report on the identification
of qnr-like determinants in Enterobacteriaceae from Pakistan. Further studies are
needed to document the prevalence of qnr in larger number of samples as well as role
of chromosomally-mediated or/ other mechanisms of resistance towards quinolone
resistance.
B-124
Molecular characterization of clinical isolates of Carbapenemase
producer Klebsiella pneumoniae (KPC) resistant to polimyxin in a
Hospital in São Paulo, Brazil
E. K. Gumpl 1 , R. C. M. Cabral 1 , J. Monteiro 2 , C. R. L. Fonsceca 3 , O. V. P.
Denardin 3 , A. C. C. Pignatari 3 . 1 UNIFESP, SÃO PAULO, Brazil, 2 Unifesp,
SÃO PAULO, Brazil, 3 DASA, SÃO PAULO, Brazil
Background: Polimyxin is one of the few remaining options for treatment of KPC,
a multiresistant opportunistic pathogen, responsible for nosocomial infections with
high morbidity and mortality. Recently, isolates of KPC resistant to polimyxin have
been described in the course of treatment with this antibiotic. The aim of the study
was to molecular characterize isolates resistant to polimyxin from patients admitted to
a hospital of São Paulo, Brazil.
Methods: From July 2011 to March 2012, 21 clinical isolates of Klebsiella
pneumoniae resistant to the carbapenem ertapenem , were identified by the automated
system Vitek2 (BioMerieux) in the clinical microbiology laboratory of a 300-beds
general private hospital. The isolates were tried for carbapenem resistance by the
Hodge modified test and for the presence of the blaKPC gene by polimerase chain
reaction (PCR). Resistance to polimixin was confirmed by broth microdilution.
The isolates were molecular typed by Pulsed Field Gel Electrophoresis (PFGE) and
Multilocus Sequence Typing (MLST).
Results: All 21 ertapenem resistant isolates were positive by the modified Hodge Test
and for blaKPC. Nine out of these 21 isolates were resistant to polimyxin (42%). The
PFGE analysis revealed 6 different clonal profiles. The clone “A” was observed in
76.2% (16) of the isolates, and the clones “B”, “C”, “D”, “E” e “F” were found in only
one isolate each. Eight of the 9 isolates resistant to polimixin were classified in the
clone “A”. The MLST was done only for clone “A” isolates showing sequence type
11 e 437 (only one allele difference).
Conclusion: The molecular techniques were useful to identify the persistence of the
same clonal profile of KPC in a period of 9 months in clinical isolates obtained from
patients admitted to the hospital, and also the emergence of polimixin resistant strains.
These data are important to better understand and to control the dissemination of these
multiresistant microorganism in hospitalized patients.
B-125
Metabolic Disorders Associated to HIV/AIDS Infection and Treatment
in Ceará, Brazil
C. M. M. PONTE 1 , M. G. CASTELO 1 , G. A. PONTE 2 , R. M.
MONTENEGRO JR 3 , P. M. PONTE 3 , M. O. GOMES 4 , T. J. P. G.
BANDEIRA 4 , I. V. ROCHA 4 , O. FERNANDES 5 . 1
UFC; DASA,
FORTALEZA, Brazil, 2
HSJ-SESA, FORTALEZA, Brazil, 3
UFC,
FORTALEZA, Brazil, 4 DASA, FORTALEZA, Brazil, 5 DASA, SÃO PAULO,
Brazil
Background: After the advent of antiretroviral therapy (ART), HIV/AIDS patients
have been observed to develop a chronic-degenerative profile characterized by the
presence of several endocrine and metabolic disorders such as metabolic syndrome,
type 2 diabetes mellitus (DM2), dyslipidemia and lipodystrophy, conditions known
to be associated with increased cardiovascular risk. Moreover, it is recognized that
HIV itself plays a significant role in the emergence of these changes. The aim of this
study was to determine the prevalence of metabolic disorders in patients with HIV /
AIDS followed at Hospital São José, considered a reference center for the treatment
of this condition.
Methods: We conducted a cross-sectional study which included 144 patients treated
in outpatient program for HIV / AIDS among the months from January to May 2010,
selected sequentially. For the control group were randomly selected 95 patients
without HIV infection. Patients underwent medical evaluation, physical examination,
meansurement of waist circumference (WC) and collection of blood samples fasting
in the morning, for determination of glucose, insulin, total cholesterol, high density
lipoprotein (HDL), triglycerides, lymphocyte count CD4 and viral load HIV. We
calculated the HOMA-IR to infer the insulin resistance and cardiovascular risk was
estimated by the Framingham Risk Score. Data were subjected to statistical analysis,
being used for this purpose, the program StataTM, version 9.1. In data analysis, we
used the Student t test, Mann-Whitney, Spearman’s linear correlation, chi-square test,
Fisher exact test and Mantel-Haenszel X2, with statistical significance level of 5%
(p