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Volume 4, Issue 8 (Suppl) J Infect Dis Ther 2016
ISSN: 2332-0877, JIDT an open access journal Infection Control 2016
November 28-29, 2016
Page 44
Notes:
conferenceseries.com
November 28-29, 2016 Valencia, Spain
4th World Congress on
Infection Prevention and Control
Ampicillin resistance mechanisms in clinical Haemophilus influenzae
Haemophilus influenzae remains a key etiological agent of upper and lower respiratory tract infections. Two major
mechanisms are involved in ampicillin (AMP) resistance: β-lactam hydrolysis due to β-lactamase production (TEM-1 or
ROB-1) and decreased affinity of penicillin-binding protein 3 (PBP3) for β-lactam antibiotics as a result of ftsI gene mutations
encoding PBP3. Isolates exhibiting this latter resistant mechanism are termed β-lactamase-non-producing ampicillin-
resistant (BLNAR), while isolates with both resistant mechanisms are defined as β-lactamase-positive amoxicillin-clavulanic
acid-resistant (BLPACR). A variety of amino acid (AA) substitutions within the transpeptidase domain of PBP3 are mainly
responsible for resistance. According to specific substitutions, these isolates have been classified in one of three mutational
groups: I-III. Group II was further divided into subgroups IIa-IId. More recently, a new group was described, “III-like” with
additionally AA substitutions to the ones described in group III. Decreased ampicillin susceptibility have been associated to
group I and II, while group III is normally associated with high resistance levels to ampicillin. Isolates with the non-enzymatic
resistance mechanisms have been described and emerging worldwide. In this context, we aimed to characterize ampicillin
resistance mechanisms in clinical H. influenza e strains isolated in Portugal. Amplification and sequencing of ftsI gene was
performed in 568 clinical H. influenza isolates. Analysis of mutations characterized 61% of isolates as gBLNAR or gBLPACR.
Most of the strains were included in group II (85%) with predominance of IIb (61%). Rare isolates were of group I and no
isolate was classified in group III, although few strains were of group III-like. Our results are indicative of wide dissemination
of a non-enzymatic resistance mechanism to β-lactams among H. influenzae isolates circulating in our country, probably due
to inappropriate use of oral antibiotics, which is a matter of concern. A better understanding of this issue may help to establish
adequate therapeutic and preventive measures to avoid selection or dissemination of such strains.
Biography
Maria Paula Ramalho Bajanca-Lavado has completed her PhD in Biomedical Science, specialty Microbiology and is responsible for the Haemophilus influenzae
Reference Laboratory, Department of Infectious Diseases, National Institute of Health in Lisbon, Portugal. She has published several scientific publications in peer-
review journals, along with other scientific productions, including invited lectures, oral communications and posters presented in international conferences. Her
research is focused at H. influenzae infections, in different clinical and epidemiological aspects.
Maria Paula Ramalho Bajanca-Lavado
National Institute of Health, Portugal
Maria Paula Ramalho Bajanca-Lavado, J Infect Dis Ther 2016, 4:8 (Suppl)