EMERGING THREAT OF ANTIBIOTIC RESISTANCE
By SOWNDHARYA. S
WHY ANTIBIOTICS?
Antibiotics are medicines that fight infections caused
by bacteria in humans and animals by either killing the bacteria or making it
difficult for the bacteria to grow and multiply. Antibiotics ONLY
treat certain infections caused by bacteria
THE RISE OF ANTIBIOTIC RESISTANCE:
Since
antibiotic regimens are often only used temporarily, they are much less
lucrative than medications used to treat long-term illnesses. Furthermore,
newly approved medications for the majority of other illnesses are quickly
provided, while new antibiotics are often kept on hand and only used to treat
infections that are resistant to more established medicines.
The
spread of resistance genes among bacterial populations is the other component
promoting antibiotic resistance. There are numerous ways in which people have
unintentionally sped up the evolution of bacterial resistance. One such
unfavorable policy has historically been the over-prescription of antibiotics
by physicians for symptoms that, in many circumstances, may not be brought on
by bacteria. However, measures have been taken recently to reduce the use of
antibiotics without a prescription. In surveys of medical visits from 1995 to
2005, the proportion of visits that ended in antibiotic prescriptions fell for
all symptoms, including sinusitis, ear infections, colds, bronchitis, and sore
throats. The use of combination medicines, switching between different classes
of antibiotics often and avoiding the use of broad-spectrum and last-resort
antibiotics whenever possible have also been used as measures to counteract the
evolutionary pressure that hastens resistance. Antimicrobial stewardship
programs are becoming more commonplace in hospital settings and have been
correlated in many cases to significant reductions in some strains of resistant
bacteria.
In some
circumstances, excessively protracted or ineffective treatment regimens may
place needless evolutionary pressure on bacteria. When a phenotypically
sensitive majority of bacteria is eliminated, a minority resistant bacterial
phenotype may find itself in a less competitive and hence more beneficial
environment. This might result in acquired drug resistance. A lack of knowledge
about antibiotics has also led to their overuse, which in turn resulted in
antimicrobial resistance.
In a
2009 survey conducted in Europe, 20% of people who had taken antibiotics within
the previous year claimed to have done so for influenza, a viral illness. Only
36% of those polled correctly identified the fact that medicines do not kill
viruses. This specific type of abuse is particularly prevalent in nations where
antibiotics are available without a prescription.
The use
of antibiotics in animal feedstocks has also exacerbated the spread of
antibiotic resistance. Their usage for prophylaxis, metaphylaxis, and growth
promotion, which according to one estimate amounted to 25–50% of all antibiotic
intake in the early 2000s, is particularly egregious. There is strong evidence
that the use of fluoroquinolones in food animals has led to the emergence of
fluoroquinolone-resistant Escherichia coli, salmonella, and Campylobacter.
HUMAN INDEPENDENT RESISTANCE:
Although
there is no doubt that humans have made a significant contribution to the
evolution of bacterial resistance, resistance has also arisen in nature without
human influence. Even bacteria whose DNA was kept isolated in permafrost for
30,000 years contained resistance components. According to calculations based
on the genetic divergence of genes involved in the biosynthesis of antibiotics,
some antibiotics may have originated hundreds of millions of years ago.
Antibiotic
use (and misuse) by humans has undoubtedly subjected bacteria to abnormal
selective pressure, speeding up their evolutionary process to the disadvantage
of all living things. Faster development of novel medicines and more judicious
usage of antibiotics currently on the market are unquestionably required to
solve this issue.
EMERGENT BACTERIAL THREATS :
|
BACTERIUM |
GRAM STAIN |
RESPIRATION |
PROBLEMATIC RESISTANCE |
|
Staphylococcus aureus |
+ |
Facultative anaerobe |
β-lactams,
glycopeptides |
|
Clostridium difficile |
+ |
Obligate anaerobe |
β-lactams,
quinolones |
|
Klebsiella pneumoniae |
- |
Facultative anaerobe |
β-lactams,
quinolones, aminoglycosides |
|
Enterobacter |
- |
Facultative anaerobe |
β-lactams,
quinolones |
ANTIBIOTICS OF 21st CENTURY:
|
CLASS |
CLINICALLY INTRODUCED SINCE 2000 |
IN PAHSE II OR III TRIALS |
|
Beta lactams |
Biapenem,
ceftaroline , doripenem, ertapenem |
Ceftobiprole,
ceftolozane, razupenem |
|
Aminoglycosides |
None |
Plazomicin |
|
Macrolides |
Telithromycin |
Cethromycin, Solithromycin |
|
Tetracyclines |
Tigecycline |
Eravacycline, Omadacycline |
|
Rifamycin |
Rifaximin |
None |
|
Glycopeptides |
Telavancin |
Dalbavancin, Oritavancin |
|
Quinolones |
Balafoxacin,
gemifloxacin, pazufloxacin, prulifloxacin |
Avarofloxacin,
delafloxacin finafoxacin, |
|
Oxazolidinones |
Linezolid |
AZD5847,
radezolid, sutezolid, tedizolid. |

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