INTRODUCTION:
Different
antibiotics kill bacteria in a variety of different ways. The billions of
bacteria that normally live in our body always include a few mutants that by
chance have become antibiotic-resistant. If they are exposed to antibiotics,
the mutants that are resistant survive while the others are killed off. In
essence, repeated exposure to antibiotics over time can make these resistant
mutant bugs predominant. According to new research, it is found that new
biosensors have the potential to detect antiobiotic resistance in bacteria,
which is viewed optimistically for the near future. This review article
explores the various forms of superbugs and the harmful role played by them.
WHAT ARE SUPERBUGS...??
SUPER
BUGS are not space aliens, they are not insectoid monsters roaming the streets
and they are definitely not super heroes. Superbugs are drug-resistant, human
killing microbes that modern medicine struggle to combat. The term has morphed
over time, however.
EVOLUTION OF SUPERBUGS:
The
increasing frequency with which antimicrobial-resistant microorganisms have
emergad in hospitals and communities has alarmed public health officials
worldwide. The emergence of resistance results from the evolution of the
elegant resistance mechanisms that create so-called superbugs, which
disseminate by clonal spread or exchange resistance traits with other
microorganisms. Their genetic organisation includes structures that probably
evolved in order to resist naturally occuring chemicals contained rival living
things, just as plants, insects, birds, animals and indeed, we humans have
evolved means to resist predators
According
to microbiologists actually antibiotics, creates or excerts "selective pressure"
on bacteria. This pressure distorts and accelerates their evolution and so
previously vulnerable species become drug resistant.
When
an antibiotics attach any bacterial species, only the fittest survive where as
among the millions of bacteria only one kills the other species which is
invulnerable to drugs due to mutants. This bacteria grows and multiplies,
colonise the space left by the destruction of other bacteria. so, in future
drug does not work.
There
are many varieties of bacteria in this world where they have the capability of
spreading or causing serious and sometimes deadly infections. We have only
relied on the antibiotics to treat them. Incritably, these bacteria have
learned to resist each new drugs, making these infections more costly to
treat-and increasing deadly.
But
however at the same time the pipe line of new antibiotics to treat these
infections have slowed to a trickle. "WE NEED NEW AND BETTER DRUGS.....
"The range of new antibiotics is disturbingly limited [1].
STRAINS OF SUPERBUGS:
The
bacteria which are resistant to most of the antibiotics are generally referred
as superbugs. The most common types of superbugs.
<
VRSA (staphylococcus aureus)
<
VRE (Vancomycin-resistant enterococcus)
<
MRSA (Methillin-resistant staphylococcus aureus)
The
antibiotics vancomycin, may be effective for some MRSA [2]. The individual who
have break in the skin will become infected and illness due to these bacterias.
The patient on intrvenous, catheters or dialysis and surgical patient are
particularly vulnerable [3]. Superbugs are also potentially like threatening to
patients already by ailments [4] and to the elderly and very young [5].
VRSA (Staphylococcus aureus):
Staphylococcus aereus (colloquially known as "Staph
infection" or a "Staph aureus")
is one of the major resistant pathogens. Found on the mucous membranes and the
human skin of around a third of the population. The first documented strain
with complete resistance to VANCOMYCIN, termed vancomycin-resistant Staphylococcus
aureus (VRSA) appeared in the UNITED STATES in 2002 [6].
S. aureus is a catalase-positive (meaning it can produce the enzyme
catalase). Catalase converts hydrogen peroxide to water and oxygen.
Catalase-activity tests are sometimes used to distinguish staphylococci from
enterococci and streptococci. Previously, S. aureus was differentiated
from other staphylococci by the coagulase test. However it is now known that
not all S. aureus are coagulse
positive [7][8] and that incorrect species identification can impact effective
treatment and control measures [9].
ROLE IN DISEASE:
< S.aureus is responsible for many infections but it may also occur as a
commensal.The presence of S. aureus does not always indicate infections.
S. aureus can survive from hours to weeks, or even months, on dry
environment surfaces, depending on strain [10].
<
It can infect tissues when the skin or mucosal barrier have been breached. This
can lead to many different types of infections including furuncles and
carbuncles (which is collection of furuncles).
<
Strains of S. aureus can host phages, that produces Panton-valentine
leukocidin which increases virulence.
<
S. aureus is extremly prevalent in atopic dermititis patients. It is
most commonly found in fertile, active places, including armpits, hair and
scalp. Large pimples that appear in those areas may exacerbate if lacerated.
This can lead to staphylococcal scaled syndrome(SSSS). A severe form of this,
Ritter's disease can be observed in neonates [11].
<
S. aureus can survive on dogs [12], cats [13] and horses [14] and can
cause bumblefoot in chickens [15].
VRE (Vancomycin-resistance enterococcus):
Multidrug-resistance
Enterococcus faecalis and Enterococcus faecium are associated
with nosocomial infections. Among these strains, penicillin-resistant
Enterococcus was seen in 1983' vancomycin resistant Enterococcus in
1987, and linezolid-resistant Entrococcus in late 1990s [16].
High
level vancomycin-resistant E. faecalis and E. faaecium clinically
isolates were first documented in Europe in late 1980s [17][18]. since then, VRS
have been associated with outbreaks of hospital-acquired (nosocomial)
infections around the world. In the United States, vancomycin-resistant E.
faecium was associated with 4% of healthcare-associated infections reported
to the Centers for Disease Control and Prevention National Healthcare Safety
Network from January 2006 to October 2007 [19].
ROLE IN DISEASE:
<
VRE can be carried by healthy people who have come into contact with bacteria.
<
The most likely place where such contact can occur is in hospital (nosocomial
infection), although it is a thought that significant percentage of intensively
farmed chicken also carry VRE [20][21].
PREVENTION AND TREATMENT OF VRE INFECTION:
Cephalosporin
use is a risk factor for colonization by VRE, and restriction of cephalosporin
usage has been associated with decreased VRE infection and transmission in
hospitals [22]. In 2005, Lactobacillus rhamnosus GG (LGG), a strain of L.
rhamnousus, was uesd successfully for the first time to treat
gastrointestinal carriage of VRE in renal patients [23].
Resistance in Pseudomonas aeruginosa:
P.aeruginosa can cause disease at multiple sites in the body. It is a common
cause of blood infections, pneumonia, and also cause intra-abdominal infections
[24]. Multiple resistance mechanisms within one bacterium are also common and
combinations of antibiotics are typically used as first-line therapy to
circumvent potential resistance [25].
It
is a common bacterium that can cause disease in animals, including human
beings. It is found in soil, water, skin flora, and most man-made environments
throughout the world. It thrives not only in normal atmosphers, but also in
hypoxic atmospheres, and has thus, colonized many natural and artificial
environments.
Risk factors for a resistant Pseudomonas aeruginosa infection
include:
<
Pattients in hospital setting, including intensive care units and burns
victims.
<
Patients with previous broad spectrum to antibiotics.
<
Patients with cystic fibrosis are very susceptible because they are prone to
lungs infections and are aggressively
treated with variety of antibiotics.
This
bacterium uses a wide range of organic materials for food. In animals, the
versatility enables the organism to infect damaged tissues or those with
reduced immunity. The symptoms of such infections are generalized inflammation
and sepsis. If such colonizations occurs in critical body organs, such as
lungs, the urinary tract and kidneys, the results can be fatal [26]. because it
strives on the moist surface, this bacterium is also found on and in medical
equipment, including catheters, causing cross-infections in hospitals and
clinics. It is implicated in hot-tub rash.
Resistance in Clostridium difficilis:
Clostridium difficilis is a species of Gram-positive spore forming
bacteria that is best known for causing antibiotic-associated diarrhea(AAD).
Initially named Bacillus difficilis by Hall and O'Toole in 1935
becauseit was resistant to early attempts at isolation and grew very slowly in
culture, it was renamed in 1970 [27][28].
With
the introduction of Broad-spectrum antibiotics and chemotherapeutic
antineoplastic drugs in the second half of the 20th century, antibiotic and
chemotheraphy-associated diarrhea became more common. pseudomembranous colitis
was first described as a complication of C. diffile infections in 1978s,
when a toxin was isolated from patients suffering from pseudomembranous colitis
and koch's postulates were met [29].
SIGNS AND SYMPTOMS:
Symptoms
range from mild diarrhea to severe life-threatrning colitis [30]. In adults, a
clinical predictions rule found the best signs to be significant diarrhea,
recent antibiotic exposure, abdominal pain, fever and a distinctive pain had a
sensitivity of 86% and a specificity of 45% [31].
Resistance in Mycobacterium tuberculosis:
Mycobacterium tuberculosis (MTB) is a pathogenic bacterial species in
the family Mycobacteriaceae and the causative agent of most cases of
tuberculosis. First discovered in 1882 by Robert Koch, M. tuberculosis has an unusual,
waxy coating on it's cell surface, which makes the cells impervious to Gram
staining. Acid-fast detection techniques are used instead. The physiology of M.
tuberculosis is highly aerobic and requires high level of oxygen. primarily
a pathogen of the mammalian respiratory system, MTB infects the lungs. The most
frequently used diagnostic methods for TB are tuberculin skin test, acid-fast
stain, and chest radiographs [32].
In
1720, though, the history of tuberculosis started to take shape into what is
known of it today; as the physician Benjamin Marten described in his Theory of
Consumption, tuberculosis may be caused by small living creatures that are
transmitted through the air to other patients.
SUPERBUG NDM-1:
Generally
a type of carbepenem resistance gene, designated as NDM-1 gene. It is coded
with ND Mettalo-beta-lactamase enzyme (ND-New Delhi).
New
Delhi Metallo Beta Lactamase-1(NDM-1) is an enzyme of beta lactamase family and
recently has been in news after 'The Lancet Infectious Disease' reported the
world wide pressure of NDM-1 among severaal bacterial species viz K. pneumonia, E. coli, E. cloacae, specially in the Indian subcontinent region,
where abuse of antibiotics is more common [33].
To
date the presence of NDM-1 have been reported in many countries including
Sweden, United Kingdom, India, Pakistan, Bangladesh, Australia, USA, Canada,
China [34].
NDM-1 SYMPTOMS:
<
NDM-1 symptoms are reported to be associated with the bacteria it attaches to.
<
The currently known bacteria's hosting this gene are E. coli and Klebsiella
pneumonia.
<
The majority of the patients treated to date who are positive for NDM-1 were
those with G.I. tract infections, bacteraemia, or pneumonia.
<
May cause multi-organ failure leading to death.
CONCLUSION:
Bacteria
that have a high Minimum Inhibitory Concentration (MIC) and require doses of
antibiotics that have not been demonstrated to be safer or tolerable for
patients; these bacteria are resistant to multiple antibiotics and may no longer
treatable with available medicine. Bacteria that have high MIC and require
doses of antibiotic that have not been demonstrated to be safe or tolerable for
patients. Healthy adults are vulnerable to antibiotic-resistant infections, but
children, seniors, the chronically ill, and military personnel often are particularly
susceptible.
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