Name: KIRAN BHATTI

University: Liaquat University of Medical and Health Sciences.

Pharm-D student.
Antibiotic resistance

• Antibiotics have always been considered one of the wonder

discoveries of the 20th century. This is true, but the real wonder
is the rise of antibiotic resistance in hospitals,
communities, and the environment concomitant with their use.
• The discovery of antibiotics more than 70 years ago initiated a period of
drug innovation and implementation in human and animal health and
agriculture. These discoveries were tempered in all cases by the
emergence of resistant microbes 1, 2. This history has been interpreted to
mean that antibiotic resistance in pathogenic bacteria is a modern
phenomenon; this view is reinforced by the fact that collections of
microbes that predate the antibiotic era are highly susceptible to antibiotics
3. Here we report targeted metagenomic analyses of rigorously
authenticated ancient DNA from 30,000-year-old Beringian permafrost
sediments and the identification of a highly diverse collection of genes
encoding resistance to β-lactam, tetracycline and glycopeptide antibiotics.
Structure and function studies on the complete vancomycin resistance
element VanA confirmed its similarity to modern variants. These results
show conclusively that antibiotic resistance is a natural phenomenon that
predates the modern selective pressure of clinical antibiotic use.
• Antibiotic-resistant bacteria that are difficult or impossible to
treat are becoming increasingly common and are causing a
global health crisis. Antibiotic resistance is encoded by several
genes, many of which can transfer between bacteria. New
resistance mechanisms are constantly being described, and
new genes and vectors of transmission are identified on a
regular basis.
• The synthesis of large numbers of antibiotics over the past three decades
has caused complacency about the threat of bacterial resistance. Bacteria
have become resistant to antimicrobial agents as a result of chromosomal
changes or the exchange of genetic material via plasmids and
transposons. Streptococcus pneumoniae, Streptococcus pyogenes, and
staphylococci, organisms that cause respiratory and cutaneous infections,
and members of the Enterobacteriaceae and Pseudomonas families,
organisms that cause diarrhea, urinary infection, and sepsis, are now
resistant to virtually all of the older antibiotics. The extensive use of
antibiotics in the community and hospitals has fueled this crisis.
Mechanisms such as antibiotic control programs, better hygiene, and
synthesis of agents with improved antimicrobial activity need to be
adopted in order to limit bacterial resistance.
•
Causes:
• The causes of antibiotic resistance are complex and include
human behaviour at many levels of society; the consequences
affect everybody in the world. Similarities with climate change
are evident. Many efforts have been made to describe the many
different facets of antibiotic resistance and the interventions
needed to meet the challenge.
Treatment:
• Antibiotic resistance is a problem of deep scientific concern both in hospital and
community settings. Rapid detection in clinical laboratories is essential for the
judicious recognition of antimicrobial resistant organisms. Production of
extended-spectrum β-lactamases (ESBLs) is a significant resistance-mechanism
that impedes the antimicrobial treatment of infections caused
by Enterobacteriaceae and is a serious threat to the currently available antibiotic
armory. ESBLs are classified into several groups according to their amino acid
sequence homology. Proper infection control practices and barriers are essential
to prevent spread and outbreaks of ESBL producing bacteria. As bacteria have
developed different strategies to counter the effects of antibiotics, the
identification of the resistance mechanism may help in the discovery and design
of new antimicrobial agents. The carbapenems are widely regarded as the drugs
of choice for the treatment of severe infections caused by ESBL-
producing Enterobacteriaceae, although comparative clinical trials are scarce.
Hence, more expeditious diagnostic testing of ESBL-producing bacteria and the
feasible modification of guidelines for community-onset bacteremia associated
with different infections are prescribed.
Reference:
• Authors
• Julian Davies, Dorothy Davies
• Microbiology and molecular biology reviews 74 (3), 417-433,
2010
• Philip S Stewart, J William Costerton
• The lancet 358 (9276), 135-138, 2001
• Jessica MA Blair, Mark A Webber, Alison J Baylay, David O
Ogbolu, Laura JV Piddock
• Nature reviews microbiology 13 (1), 42-51, 2015
• Ramanan Laxminarayan, Adriano Duse, Chand Wattal, Anita
KM Zaidi, Heiman FL Wertheim, Nithima Sumpradit, Erika
Vlieghe, Gabriel Levy Hara, Ian M Gould, Herman Goossens,
Christina Greko, Anthony D So, Maryam Bigdeli, Göran
Tomson, Will Woodhouse, Eva Ombaka, Arturo Quizhpe
Peralta, Farah Naz Qamar, Fatima Mir, Sam Kariuki, Zulfiqar A
Bhutta, Anthony Coates, Richard Bergstrom, Gerard D Wright,
Eric D Brown, Otto Cars
• The Lancet infectious diseases 13 (12), 1057-1098, 2013