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Lynch and Martinez, 2000; File, 2000; Chambers and Sande, 1996; Craig, 1998. However, a few
microcins, such as McC and MccJ25, bring into play a second and independent mechanism that
intervenes at higher concentrations. Please note that many of the page functionalities won't work as
expected without javascript enabled. Mutations can also eliminate the target in the cell of the bacteria
that the antibiotic attacks. A normal cell can be transformed into a cancerous cell. Many have a high
stability in the gastrointestinal tract where they can target a single pathogen whilst only slightly
perturbing the gut microbiota. American Academy of Otolaryngology, 2000; Low et al, 1997.
Patients should stop taking antibiotics as soon as they feel better to avoid developing resistance.
CDC, 2000; Jacobs et al, 1999; Temple and Nahata, 2000. There are many ways through which
mutations help bacteria develop resistance. Abhinav S Seminario Biologia Molecular Manuela
Alvarez Ramirez Seminario Biologia Molecular Manuela Alvarez Ramirez manuelaalvarezr USG,CT
AND MR IMAGING OF HEPATIC MASS LESIONS. No use, distribution or reproduction is
permitted which does not comply with these terms. This has been poorly explored until now, but is
however illustrated by MccPDI for which mutations in dsbA, dsbB genes induce resistance to
MccPDI ( Zhao et al., 2015 ). Genes dsbA, dsbB encode DsbA and DsbB thiol-redox enzymes that
usually catalyze disulfide bond formation for proteins that are transported into the periplasm, and
which would be possibly involved in formation of the disulfide bond that stabilizes this microcin. It
is the main causative agent in community acquired bacterial pneumonia, and it can also cause otitis
media, conjunctivitis, sinusitis and more severe diseases like meningitis and bacteremia. However,
although the presence of the siderophore PTM enhances its efficiency, the non-modified form of
MccE492 (without the C-terminal siderophore) is also able to kill sensitive bacteria, but at a
significantly lower level. However, by the late 1980s vancomycin resistance first appeared in
enterococci (VRE) and in recent years in S. Among their antigenic structures are the protein A,
which binds to Fc region of immunoglobulin G (IgG) and prevents complement activation; the
teichoic acids, which modulate mucosal adhesion and induce toxic shock through release of
interleukin 1 (IL-1) and tumor necrosis factor (TNF); and polysaccharide capsule, with 11 different
serotypes. Vancomycin-resistance is mediated by several van gene clusters such as vanR, vanS,
vanH, vanX and vanZ that are responsible for the replacement of D-Ala-D-Ala with D-alanyl-D-
lactate termini. A Antimicrobial therapy for hemodialysis-associated infections increases antibiotic
resistance. If a 'parent' cell contains a gene for drug resistance, this gene will be passed vertically,
down the family tree, on to its 'daughter' cells. Many lasso peptides produced by proteobacteria do
not show antibacterial activity ( Hegemann et al., 2013 ). This questions their ecological role or can
be due to difficulty to decipher the reasons for their narrow activity spectrum. A normal cell can be
transformed into a cancerous cell. International Journal of Translational Medicine (IJTM). It uses
FepA-, Cir-, Fiu-TonB dependent receptors to reach its inner membrane target ( Patzer et al., 2003 ).
The mechanism of action of the class IIa MccPDI is poorly identified. Several antibacterial lasso
peptides, have been shown to also target RNAP through binding to the secondary channel, although
their different antibacterial activity spectrum. American Academy of Otolaryngology, 2000; Low et
al, 1997. These include mainly negative structures, with a few being neutral or positive. They are
specific to the different siderophore chemical types, such as FhuA for ferrichrome or Cir, Fiu, and
FepA for catechol siderophores in enterobacteria. Article types Author guidelines Editor guidelines
Publishing fees Submission checklist Contact editorial office Submit your research Search Download
article. Mutations in the murA gene confer resistance to fosfomycin due to the replacement of
cysteine with aspartate in the active site of MurA, which prevents fosfomycin binding ( Falagas et
al., 2019 ). Moreover, resistance to fosfomycin can occur from chromosomal mutations in the
structural genes that encode the GlpT and UhpT membrane transporters.
For more information on the journal statistics, click here. Carbon and Poole, 1999; File, 2000; Jacobs
et al, 1999. Journal of Experimental and Theoretical Analyses (JETA). Craig, 1998; File and Slama,
2000; File 2000; Carbon and Poole, 1999. Lastly, etK can additionally phosphorylate the pmrE gene.
Taking an incomplete dose of an antibiotic not only allows slightly resistant bacteria to persist in the
patient, it also increases the likelihood that a re-emerging infection will now be resistant to the
previously administered antibiotic. Cell cytoskeleton and molecular motors.pdf Cell cytoskeleton and
molecular motors.pdf Emerging Issues In Bacterial Resistance 2. The gene coding for RRE, which
ensures leader peptide recognition in MccJ25 and MccJ25-like peptides is shown as hatched motif.
Nosocomial (hospital-acquired) infections: Refers to any infection acquired in hospital (e.g., P.
aeruginosa infections of patients undergoing burn therapy; immunocompromised patients picking up
opportunistic pathogens). Furthermore, the iron-free molecule, Apolactoferrin (ApoLF), is able to
interact with microbial cellular membranes, undergoing subsequent proteolysis which results in
release of smaller and more potent cationic peptides, especially those found in the N-terminal lobe:
Lactoferricin (LFcin), Lactoferrampin (LFampin) and LF1-11 ( Sinha et al., 2013 ). GlpT and UhpT
transport glycerol-3-phosphate and glycerol-6-phosphate sugars in bacteria, respectively and are used
by fosfomycin to facilitate its entry in bacteria. Bacteria resistance to specific antibiotics are difficult
to treat, it requires alternative medications with higher dose. In the case of loss of function of the
TonB system, MccE492, MccH47, and MccM retain antimicrobial activity, suggesting the
involvement of another translocator, such as the TolA-TolQ-TolC system known to mediate the
import of certain colicins ( Lazdunski et al., 1998 ). Similar observations were made for MccL and
MccV ( Gerard et al., 2005; Morin et al., 2011 ), suggesting that the function of the ExbB protein
could be replaced by its homolog TolQ in TonB-dependent microcin activity. Through the two
actions—increasing share of resistant bacteria in the existing population and creating a new
generation that’s fully resistant—the bacteria spread resistance against antibiotics. Vancomycin-
resistance is mediated by several van gene clusters such as vanR, vanS, vanH, vanX and vanZ that
are responsible for the replacement of D-Ala-D-Ala with D-alanyl-D-lactate termini. Similar to
fluoroquinolones, MccB17 targets the cleavage of both DNA strands, which is a critical step in the
DNA gyrase supercoiling cycle, but the MccB17-induced cleavage pattern is different from that of
quinolones (for a review on MccB17 activity see Collin and Maxwell, 2019 ). The present review
summarizes the strategies adopted by Gram-positive pathogenic bacteria to resist AMP action. Zenni
et al, 1995; Bluestone and Klein, 1995, American Academy of Pediatrics, 1997. American Thoracic
Society, 1995; American Lung Association, 2000; Ball et al, 1994; FDA, 1997. Although these
bacteria are genetically different, the resistance strategies that underlie the emergence and persistence
of these pathogens are widely shared among them including decreased drug uptake, drug target
alteration, drug inactivation and drug efflux pumps activation. Generally, resistant infections are
detected through trial and error; doctors will administer one antibiotic and then switch to another if
the bacteria do not respond. However, although most of produced McC is efficiently exported,
intracellular processing also occurs inside the producing cells that ineluctably leads to the
accumulation of the toxic entity that cannot be exported by the MccC pump and results in self-
poisoning. It is also exemplified by siderophore microcins (MccE492, MccM, MccH47) or the lasso
microcin MccJ25 that mimic the natural ligands of siderophore receptors to hijack them. Combination
therapy reduces the chance of single-mutation resistance. Bacteria achieve this type of resistance by
producing redundant proteins, or back-ups, that fulfill the same responsibilities of the inhibited
protein. Physicians should avoid antibiotics for possible UTIs and instead use oral hydration,
investigating other causes of pain and symptoms, and following results of urine culture for 48 hours.
GERIATRIC PHARMACOLOGY Geriatric pharmacology is a specialized field focusing. This
concentration is the MPC that can be defined as the MIC of the least-susceptible, single-step mutant.
Levinson and Jawetz, 1998; Chambers and Sande, 1996. Wadwa and Feigin, 1999; Klein, 1995;
Otitis Media Guideline Panel, 1994.
The gene is predicted to be an efflux pump against AMPs and a transposon-induced mutagenesis
caused a higher sensitivity against both AMPs in a plate-based minimum inhibitory concentration
(MIC) assay ( Boone and Tyrrell, 2012 ). Their analysis also correlates this resistance to an ecological
advantage over the less resistant strains, which reinforces the importance of AMPs in controlling S.
That means the germs are not killed and continue to grow. To further illustrate the role CAUTIs play
in the resistance epidemic, Woc-Colburn describes risk factors for uncomplicated versus complicated
UTIs. Presently, only two antimicrobial treatment options for MDR gram-negative are FDA-
approved: ceftazidime-avibactam and ceftolozane-tazobactam. Most GBS infections occur during
labor, but there is also a chance of infection after delivery. Arrows indicate individual microcin
genes; arrows are not drown to scale and their direction does not necessarily indicate the direction of
transcription that can change between homologous specific gene clusters. Antibiotic resistance can
sometimes be shared among bacteria. One proposed mechanism is that exposure to antimicrobial
peptides triggers CPS release, which trap the AMPs and shield the bacterium ( Llobet et al., 2008 ).
This capsule shedding has been demonstrated to occur in vivo, thus comprising a potential strategy to
prevent AMP-mediated killing. Typhimurium, both in static inhibition assays and in ecological
competition experiments. Therefore, other measures have been undertaken, including educating the
public about the proper use of antibiotics and the importance of completing a full regimen as
prescribed. The L-Ara4N modification is the most effective of the two modifications due to the
nature of the charge alteration. Check my posts here and give your valuable comments. Thus,
medical doctors and researchers are worried about the advancing number of cases involving multi
resistant bacteria as such infections are difficult or even impossible to treat. Otherwise, it is well
known that immunity genes are responsible for protecting the producing bacteria from their own
bacteriocin. In addition, a significant amount of phage-therapy research was conducted throughout
the 20th century in regions within the former Soviet Union. This effect highlights the importance of
proteinase SpeB in LL-37 degradation ( Schmidtchen et al., 2002 ). Consequently, in such strains,
the PagL-dependent deacylation of this lipid A increases polymyxin resistance ( Kawasaki et al.,
2007 ). This finding implies that the various forms of lipid A modifications, particularly L-Ara4N
and PEtN modifications and deacylation, may be compensatory to each other in certain bacteria,
such as Salmonella. Antibiotic resistance is spreading through a large population of bacteria due to
widespread antibiotic use. The released CPSs are able to trap or bind to polymyxins, thereby
reducing the quantity of drug that reaches the bacterial cell surface, leading to increased polymyxin
resistance ( Llobet et al., 2008 ). The underlying mechanism is attributed to electrostatic interactions
between the cationic polymyxins and anionic CPSs. The dawn of “SUPERBUGS”: Vancomycin-
resistant Enterococcus (VRE) Enterococcus is part of natural flora of human gut but is now a
concern now because of more invasive procedures, more immunocompromised people. We now know
that many transport protein complexes confer antibiotic resistance (and sometimes metalR) on the
bacterium by actively transporting toxic chemicals (i.e. antibiotics) OUT of the cell. In the following
decades, overuse and repeated exposure to antibiotic agents favoured the selection and replication of
numerous strains of antibiotic-resistant bacteria. However, by the late 1980s vancomycin resistance
first appeared in enterococci (VRE) and in recent years in S. Rajshri Namburi phased spot test -
NPST To identify bhasma and sindhura - A Qualitat. Seminario biologia molecular Kevin Duque
Seminario biologia molecular Kevin Duque SUNSCREEN, definition, classification, SPF value,
history, mechanism, develop. Which of the Following Statements About Antibiotic Resistance Is
False. Cole and Nadler, 1999; Pankuch et al, 1998; Davies et al, 1999. Zenni et al, 1995; Bluestone
and Klein, 1995, American Academy of Pediatrics, 1997. Bacteria resistance to specific antibiotics
are difficult to treat, it requires alternative medications with higher dose.
Mode of action and resistance mechanisms of antibiotics. Chromosomally mediated colistin
resistance occurs mainly via the addition of cationic moieties onto the negatively charged lipid A,
while the plasmid mediated colistin resistance (MCR) is acquired via a plasmid-borne copy of an
mcr gene. All articles published by MDPI are made immediately available worldwide under an open
access license. No special. According to the World Health Organization (WHO), the pathogenicity
and antibiotic resistance pattern of S. Antibiotics prevent infections from spreading and help the
immune system fight off invading pathogens like bacteria. Combating Drug Resistance.pptx 01.
Combating Drug Resistance.pptx PurushothamKN1 Similar to Emerging Issues In Bacterial
Resistance ( 20 ) Role of pharmacists in combating drug resistatnce Role of pharmacists in
combating drug resistatnce Role of pharmacists in combating drug resistatnce by neel ratnam. As a
result, today in Georgia, which was once under Soviet rule, bandages saturated with bacteriophages
against staphylococcus are commercially available as topical treatments for wounds and burns. It also
discusses the current state of AMR in the most critical resistant bacteria as determined by the
WHO’s global priority pathogens list. Felmingham et al, 1999; Geddes, 1997; Grossman, 1997;
Bartlett et al, 1998; Bartlett, 1997; Jacobs et al, 1999; Sethi, 1999; Thornsberry. For an overview on
siderophore microcins, see Massip and Oswald (2020). Which of the following statements about
bacterial antibiotic resistance genes is false. The second step implies either membrane perturbations or
inhibition of critical enzymes, and therefore vital functions in bacteria. These gene clusters are
generally plasmid-borne, except the chromosomally encoded class IIb microcins. Antibiotic resistance
cannot be conferred by conjugation as conjugation only affects the fertility of bacteria. However,
penicillin’s reign as a life-saving treatment was short lived; by 1947 scientists had already identified
bacteria that could resist the toxic effects of this molecule. Besides, a plasmid-mediated protection
of DNA gyrase and topoisomerase IV from the action of quinolones is ensured in a non-specific
manner by the gyrase interacting protein Qnr. Population of India and Family welfare
programme.pptx Population of India and Family welfare programme.pptx Artificial Radionuclide
Generators in Medicine Applications in Radiotherapy.pptx Artificial Radionuclide Generators in
Medicine Applications in Radiotherapy.pptx Analyzing Performance of the Twist Exome with CNV
Backbone at Various Probe D. Which of the following statements about antibiotic resistance in
bacteria is NOT true. It is responsible for the sturdiness of MccJ25 and is required for its
antibacterial activity ( Rebuffat et al., 2004; Wang and Zhang, 2018 ). Physicians should avoid
antibiotics for possible UTIs and instead use oral hydration, investigating other causes of pain and
symptoms, and following results of urine culture for 48 hours. Such as most bacteriocins, microcins
are active against phylogenetically related bacteria including enteropathogenic Klebsiella, Shigella,
Salmonella and E. Reviews Select overall rating (no rating) Your rating is required to reflect your
happiness. They also showed that this protection is type specific once M protein type 49 did not
protects the bacterium the same extension of M1, moreover, they found that strains isolated from
invasive diseases patients were more resistant to LL-37 action than the strains isolated from
asymptomatic patients ( Lauth et al., 2009 ). Moreover, various resistant isolates harbor double
mutations in pmrB, and these multimutant strains tend to display high levels of resistance to colistin (
Moskowitz et al., 2012 ). For P. aeruginosa, only one study has reported a mutation in pmrA that
may be responsible for resistance to date ( Lee and Ko, 2014 ), while the rest of the mutations have
been mainly localized to PmrB or generally distributed within the cognate regulators of TCSs (Figure
4B; Table 1 ). Infection by C. difficile (ICD) has been increasingly reported in the United States (
Lessa et al., 2015; Crobach et al., 2020 ). C. perfringens can also cause acute diarrhea, with an
estimated death toll of 200,000 each year in Nigeria according to The World Health Organization
(WHO) ( Fisher et al., 2005; Chukwu et al., 2016 ). Several microcins and antibiotics can bind to
similar bacterial receptors and use similar pathways to cross the double-membrane of Gram-negative
bacteria and reach their intracellular targets, which they also can share. Based on their high
immunogenicity and protective efficacy, capsular polysaccharides comprise the basis of the current
pneumococcal vaccines, alone or in fusion with carrier proteins ( Darrieux et al., 2015; Geno et al.,
2015; Converso et al., 2020 ). KavyasriPuttamreddy Population of India and Family welfare
programme.pptx Population of India and Family welfare programme.pptx Dr. Dheeraj Kumar
Artificial Radionuclide Generators in Medicine Applications in Radiotherapy.pptx Artificial
Radionuclide Generators in Medicine Applications in Radiotherapy.pptx Dr. Dheeraj Kumar
Analyzing Performance of the Twist Exome with CNV Backbone at Various Probe D. Such costs
have been observed in colistin-resistant isolates both in vitro and in vivo and include growth
retardation, impaired virulence, and substantially reduced clinical invasiveness ( Fernandez-Reyes et
al., 2009; Lopez-Rojas et al., 2011; Rolain et al., 2011; Pournaras et al., 2014 ). Furthermore, Hraiech
et al. For example, many patients will choose to cut their antibiotic regiment short after their
infection begins to subside.
Major seminar1 Major seminar1 Drug resistance Drug resistance Monoclonal antibodies drug
targeting particuler carrier system Monoclonal antibodies drug targeting particuler carrier system
Molecular mechanism of multi drug resistance Molecular mechanism of multi drug resistance
Mechanism Of Resistance Of Antibiotics Mechanism Of Resistance Of Antibiotics Chemotherapy
(2) Chemotherapy (2) S. Objective 1b. Microbial resistance and efflux pumps. Antibiotic resistance
can sometimes be shared among bacteria. Given the excellent pharmacokinetic properties (i.e.,
clearance, elimination half-life, large tissue penetration) of clindamycin, this lincosamide antibiotic is
the most favored agent for the treatment of serious infections, including those caused by macrolide
resistant S. Cole and Nadler, 1999; Pankuch et al, 1998; Davies et al, 1999. ISPRS International
Journal of Geo-Information (IJGI). Available online: (accessed on 18 December 2020). Cepas, V.;
Soto, S.M. Relationship between Virulence and Resistance among Gram-Negative Bacteria.
Namburi phased spot test - NPST To identify bhasma and sindhura - A Qualitat. GERIATRIC
PHARMACOLOGY Geriatric pharmacology is a specialized field focusing. The supplemented
strain showed a reduced susceptibility to the AMPs, which in this case was linked to a higher
rigidity in the cell membrane. Class II microcins result from a proteolytic processing of a precursor
with a leader peptide extension, which occurs at a conserved double-glycine (or Gly-Ala) cleavage
site, concomitantly with secretion. Bartlett, 1997; Felmingham et al, 1999, Grossman, 1997; Sethi,
1999; Niederman, 1996; Canadian Medical. Journal of Theoretical and Applied Electronic
Commerce Research (JTAER). Several mutations resulting in in-frame deletions, frameshifts or
truncations of the phoQ gene that consequently activate the arnBCADTEF operon have been
reported in resistant strains (Table 1 ) ( Miller et al., 2011; Lee and Ko, 2014 ). Learn about
techniques in RNA sequencing, western blotting, crystallography, and immunoassays that are helping
scientists explore proteins further. Moreover, it was proposed that the CD1d-dependent
immunomodulatory effect is limited by the size of the compounds, explaining the absence of effect
of native MccB17, although its content in oxazole rings. Physicians should avoid antibiotics for
possible UTIs and instead use oral hydration, investigating other causes of pain and symptoms, and
following results of urine culture for 48 hours. Those include Escherichia, Salmonella, Shigella,
Klebsiella, Enterobacter, and Citrobacter ( Gordon and O’Brien, 2006; Gordon et al., 2007; Budic et
al., 2011; Drissi et al., 2015; Wang et al., 2016; Cheung-Lee et al., 2019 ). The development of DNA
sequencing methods and the availability of an increasing number of genomes revealed that clusters of
genes orthologous to microcin biosynthesis and self-immunity genes are widespread in bacteria.
Combination therapy reduces the chance of single-mutation resistance. By the 1940s penicillin was
already widely used and previously fatal infections could be effectively cured by this miracle drug.
Seminario Biologia Molecular Manuela Alvarez Ramirez Seminario Biologia Molecular Manuela
Alvarez Ramirez USG,CT AND MR IMAGING OF HEPATIC MASS LESIONS. Author
Contributions Conceptualization, C.B. and G.M.; data curation, A.M. and E.G.; writing—original
draft preparation, G.M., A.M. and E.G.; writing—review and editing, C.B. All authors have read and
agreed to the published version of the manuscript. Until a few years ago, carbapenems like imipenem
and meropenem were the most effective agents to treat A. Several insertion sequences, such as those
of the IS5-like, IS903B, IS1F-like and ISKpn14 elements belonging to several IS families (especially
the IS5 family), have been observed to lead to the truncation of mgrB. In consequence, pneumococci
develop resistance to LL-37 and erythromycin in vitro ( Zahner et al., 2010 ). Efflux pumps eject
antibiotics from bacterial cells D. Such encodings are found on DNA molecules called plasmids and
a small part of the DNA called transposons. Seminario biologia molecular Kevin Duque Seminario
biologia molecular Kevin Duque SUNSCREEN, definition, classification, SPF value, history,
mechanism, develop. Antibiotic resistance is spreading through a large population of bacteria due to
widespread antibiotic use. Bacteria produce transport systems, called efflux pumps that actively
remove noxious substances from the cell.