The document discusses antibiotic resistance mechanisms in bacteria. It describes several key mechanisms:
1. Production of enzymes that inactivate antibiotics through destruction or modification. This includes beta-lactamases that break down beta-lactam antibiotics.
2. Decreased permeability of the cell membrane, preventing antibiotic penetration.
3. Active efflux of antibiotics from the bacterial cell via efflux pumps.
4. Modification of antibiotic target sites, such as altered penicillin-binding proteins or modifications to ribosomes.
Resistance can arise through mutation or acquisition of resistance genes via horizontal gene transfer. Multiple resistance mechanisms can provide high-level or multidrug resistance.
genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations, which may lead to cancer. While genotoxicity is often confused with mutagenicity, all mutagens are genotoxic, whereas not all genotoxic substances are mutagenic
genotoxicity describes the property of chemical agents that damages the genetic information within a cell causing mutations, which may lead to cancer. While genotoxicity is often confused with mutagenicity, all mutagens are genotoxic, whereas not all genotoxic substances are mutagenic
Introduction to chronology, chronotherapy, and chronopharmacology.
How chronopharmacology involved in asthma and helps to manage asthma?.
Biological rhythms in bronchial asthma.
Factors associated with nocturnal exacerbation of bronchial asthma.
Introduction to asthma and their symptoms.
Introduction to Antiasthmatic drugs like beta-blockers, leukotriene antagonists, steroids, etc.
Chronopharmacology division & their examples.
Advantages and disadvantages of chronopharmacology.
Marketed preparation and their images along with the price in India.
antiviral drugs medicinal chemistry by padala varaprasadVaraprasad Padala
medicinal chemistry of antiviral drugs by padala varaprasad
mainly includes structures, SAR , mechanism of action, uses and toxicity of antiviral drugs
Introduction to chronology, chronotherapy, and chronopharmacology.
How chronopharmacology involved in asthma and helps to manage asthma?.
Biological rhythms in bronchial asthma.
Factors associated with nocturnal exacerbation of bronchial asthma.
Introduction to asthma and their symptoms.
Introduction to Antiasthmatic drugs like beta-blockers, leukotriene antagonists, steroids, etc.
Chronopharmacology division & their examples.
Advantages and disadvantages of chronopharmacology.
Marketed preparation and their images along with the price in India.
antiviral drugs medicinal chemistry by padala varaprasadVaraprasad Padala
medicinal chemistry of antiviral drugs by padala varaprasad
mainly includes structures, SAR , mechanism of action, uses and toxicity of antiviral drugs
Antibiotics,antibiotics resistances,classification of antibiotics,misuse of antibiotics details discussed here. for more information visit my blog helpful for pharmacy and medical student.thanks.
http://mydreamlan.wordpress.com/category/education/
The most common mode of action for antibiotics is the inhibition of cell wall synthesis. Antibiotics that inhibit cell wall synthesis work because of the fact that most eubacteria have peptidoglycan-based cell walls but mammals do not. Growth is prevented by inhibiting peptidoglycan synthesis. Thus these antibiotics only work for actively growing bacteria. The cell wall of new bacteria that grew in the presence of cell-wall-synthesis inhibitors is deprived of peptidoglycan. These bacteria will be subjected to osmotic lysis.In addition, gram-negative bacteria generally are less susceptible to inhibitors of cell wall synthesis than are gram-positive bacteria. In the former cell wall synthesis inhibitors fail to reach the cell wall because they are blocked by the gram-negative outer membrane.Penicillin is the classic example of an inhibitor of cell wall synthesis. Other examples include: ampicillin, bacitracin, carbapenems, cephalosporin, methicillin, oxacillin and vancomycin
Mechanism Antibiotic Resistance
Intrinsic (Natural)
Acquired
Chromosomal
Extra chromosomal
Intrinsic Resistance
Lack target : No cell wall; innately resistant to penicillin
2. Drug inactivation: Cephalosporinase in Klebsiella
3. Innate efflux pumps:
It is an active transport mechanism. It requires ATP.
Eg. E. coli, P. aeruginosa
Altered target sites
PBP alteration
Ribosomal target alteration
Decreased affinity by target modification
Beta-lactamase
Beta-lactamases are enzymes produced by bacteria that provide resistance to β-lactam antibiotics such as penicillins, cephamycins, and carbapenems
Major resistant Pathogen
1. PRSP- Penicillin resistant Streptococcus pneumoniae2. MRSA/ORSA- Methicillin-resistant Staphylococcus Aureus (Super bug)3. VRE -Vancomycin-Resistant Enterococci4. Carbapenem resistant pseudomonas aeruginosa5. Carbapenem resistant Carbapenem resistant 6. Extended spectrum beta-lactamase (ESBL)-producing bacteria
mechanism of resistance of antibiotics, ESBL, b lactums, enterobactericae, metallobactums, carbapenemases, types of mechanism of resistance, history of antibiotics and resistance
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
5. • Enzymatic destruction of drug
• Prevention of penetration of drug
• Alteration of drug's target site
• Rapid ejection of the drug
6. Clinical resistance vs actual resistance
Resistance can arise by mutation or by gene transfer (e.g.
acquisition of a plasmid)
Resistance provides a selective advantage
Resistance can result from single or multiple steps
Cross resistance vs multiple resistance
› Cross resistance -- Single mechanism-- closely related
antibiotics
› Multiple resistance -- Multiple mechanisms -- unrelated
antibiotics
7.
8. Terminologies
Resistant organism
MICs of organism are higher than achieved drug
concentrations in tissues
Intermediately resistant
the antibiotic may still be effective but higher
doses should be used
Highly resistant
the antibiotic tissue concentrations are likely not
to exceed MICs of the microorganisms
9. Types of resistance
Intrinsic or natural resistance
G-neg bacteria are resistant to vancomycin (large
molecule)
Tetracyclines are hydrophobic, G-neg bacilli are
resistant
Acquired resistance
Mutations (PBP)
Disseminated by plasmids and transposons
Spontaneous mutations
10. Mechanisms of antibiotic resistance
1. Production of enzymes
destroying and modifying AB
ß-lactamases AG modifying
enzymes
2. Decrease of cell
membrane permeability
3. Active efflux of AB from
cell
4. Modification of AB target
sites
11. Genetics and spread of drug resistance
Viridans Streptococci
S.pneumoniae
S.Epidermidis
S.aureus
E.faecium
S.aureus
12. Transposon .
genes moving from one point to another (jumping genes)
Bacteriophage
virus, infecting bacteria (virus of bacteria)
Integron
slice(s) of DNA, cassette of gene that may be entered into
other cell
Plasmid
circular double stranded DNA molecule, located separately
of the chromosomal RNA
13. (1) Mechanisms of resistance
Production of enzymes inactivating (destroying)
antibiotics
ß-lactamases
Main mechanism of resistance in ß-lactam
antibiotics
Penicillin-resistant S.aureus
Ampicillin-resistant E.coli
Production of enzymes modifying antibiotics
Aminoglycosides, chloramphenicol
14. Resistance mechanisms: inactivating enzymes (2)
Degrading enzymes will bind to the Blocking enzymes attach side chains
antibiotic and essentially degrade it to the antibiotic that inhibit its function.
or make the antibiotic inactive E.g. ß-lactamases
15. PBP & ß-lactamase
Serine proteases (PBP) a metalloenzymes (Zn-binding thiole group as
coenzyme)
200 different enzymes e.g. penicillinases, cephalosporinases, ESBL,
AmpC
ESBL - extended spectrum ß-lactamases (broad spectrum of activity);
encoded in plasmids, can be transferred from organism to organism
16. Production of ß-lactamases: mechanism of
action
Examples
TEM-1 is a
widespread ß-
lactamase of
Enterobacteriaciae
that attacks
Penicillin G and
narrow spectrum
cephalosporins
>50% AmpR
E.coli isolates are
caused by TEM-1
26. Important terms among drug
resistant microorganisms
VRE . vancomycin-resistant enterococci
70% of E. faecium strains in USA
GISA . glycopeptide intermediately susceptible S.aureus
VISA . vancomycin intermediately susceptible S.aureus
VRSA & VRSE . vancomycin-resistant S.aureus and S.epidermidis
(MIC> 32 mcg/ml; 1st clinical case described in 2002 in USA)
ESBL producing K.pneumoniae . Extended spectrum ß-lactamase
producing K. pneumoniae
PRSP penicillin-resistant S. pneumoniae
35. Cephalosporins
Initially isolated form
the mould Cephalosporium
Compared with penicillins:
More resistant to ß-
lactamase hydrolysis
Wider antibacterial spectrum
Improved PK-properties
40. Vancomycin: mechanism of action
Mechanism - vancomycin inhibits cross linkage between
peptidoglycan layers
Vancomycin can bind only to D-Ala-D-Ala and not to D-Ala-D-lac
41. Originally obtained form
Streptomyces orientalis
Active only against G+
bacteria (large molecule
unable to penetrate outer
membrane of G+ bacteria)
Used for treatment of
oxacillin resistant G+
infections
42. Intrinsic resistance (pentapetide end with D-Ala-D-Lac)
Leuconostoc, Lactobacillus, Pediococcus
Or with D-Ala-D-Ser
Enetrococcus gallinarum, Enetercoccus caselliflavus
Acquired resistance
A thickening of the PG layer, and
Modification of the PG termini from D-Ala--D-Ala to D-Ala--D-lactate
Gene (vanA, B, C, D, G, E) is carried on plasmids & may be
transferred from organism to organism
Importance
VRE - vancomycin resistant E. faecium, E.faecalis
VISA - vancomycin intermediately resistant S.aureus
GISA - glycopeptide intermediately resistant S.aureus
VRSA - vancomycin resistant S.aureus (MIC> 32 µg/ml; 1st
clinical case reported 2002 in US)
44. Bacitracin (cyclic peptides) is isolated form Bacillus
licheniformis
Topically applied agent against G+ bacteria
Interferes with the dephoshorylation and recycling of the
lipid carrier responsible for moving peptidoglycan
precursors
Polymyxin (cyclic polypeptides) derived from Bacillus
polymyxa
Interact with the lipopolysaccharides and phospholipids in
the outer membrane and thus increase cell permeability
Mostly active against G- bacilli (G+ bacilli do not have
outer membrane)
45. Activity of antibiotics to bacterial
cell wall
polypeptides ß-lactams
glycopeptides
G-negative
G-positive
46. Inhibition of protein synthesis
Aminoglycosides
Tetracyclines
Oxazolidones
Chloramphenicol
Macrolides
Clindamycin
Streptogramins
51. Consists of aminosugars that are
linked through glycosidic rings
Origin
Streptomyces - streptomycin,
neomycin, kanamycin, tobramycin
Micromonospora - gentamicin,
Sisomicin
Synthetic derivates
Amikacin = kanamycin
Netilmycin = sisomycin
Mainly active against G-negative
bacteria
Gentamycin
52. Aminoglycoside: mode of action
AG pass through cell wall,
cytoplasmic membrane to
cytoplasma (mainly of Gbacteria,
no penetration through cytoplasmic
membrane of strepto- and
entrococci)
Bind irreversible to the 30S
subunit of bacterial ribosomes and
block the attachment of the 50S
subunit to the initiation complex
As a result production of
aberrant proteins and misreading
of RNA occurs
53. Aminoglycoside: mode of action
1. Passage through cytoplasmic membrane of G- bacteria (no penetration
through cytoplasmic membrane of strepto- and enterococci)
2. Binding to 30S subunit
3. Misreading the codon along mRNA
4. Inhibition of protein synthesis
54. Aminoglycoside resistance
Enzymatic modification (common) of the drug
High level resistance
>50 enzymes identified
Genes encoding resistance located in plasmids
Gene transfer occurs across species
Reduced uptake or decreased permeability of bacterial
cell wall
Resistance in anaerobes (transport through
cytoplasmic membrane depends on anaerobic respiration)
Altered ribosome binding sites (rare)
Microbes bind to multiple sites
Low level resistance
55. Tetracyclines
Origin
Tetracyclin, oxytetracyclin isolated from Streptomyces
Minocyclin, doxycyclin are synthetic
Broad spectrum bacteriostatic antibiotics
Antibacterial spectrum similar to macrolides (incl. Clamydia,
Mycoplasma, Rickettsia)
Resistance (widespread)
Energy dependent efflux pump (most common)
Alteration of ribosomal target (ribosome protection)
Enzymatic change
56. Tetracyclines
The tetracyclines block
bacterial translation by binding
reversibly to the 30S subunit and
distorting it in such a way that the
anticodons of the charged tRNAs
cannot align properly with the
codons of the mRNA
57. Oxazolidones: linezolid
Newest class of antibiotics; completely synthetic
Narrow spectrum of activity (G+ bacteria, includingVRE,
MRSA)
G-neg bacteria resistant due to efflux pump
Mode of action: unique mechanism among antibiotics;
interferes with the initiation complex at the 50S ribosome
subunit (V domain of 23S rRNA)
Resistance confers to mutation at 23S rRNA
Resistance is rare; cross-resistance unlikely because 23S
rRNA is encoded by several genes
58. Oxazolidones: mode of action
Inhibit the formation of an initiation complex by binding to the 50S
ribosomal subunit (domain V of the 23S rRNA), disrupting the preliminary
phases of protein synthesis
59. Chloramphenicol
Binds irreversible to peptidyl transferase component of 50S
ribosome and blocks peptide elongation, thus interferes with
protein synthesis
Bacteriostatic antibiotic with broad spectrum of antibacterial
activity
Interferes with the protein synthesis of bone marrow cells
causing aplastic anaemia
Limited clinical use in Western world due to side Effect
Resistance is associated with producing
acetyltransferase which catalyses acetylation of 3-hydroxy
group of chloramphenicol
60. Macrolides (1)
Erythromycin was derived from Streptomyces erythreus
The basic structure is a lactone ring
14-membered lactone ring . erthromycin, clarithromycin, roxithromycin,
telithromyin (ketolide)
15-membered lactone ring . Azithromycin
16-membered lactone ring . spiramycin, josamycin
Acitivity .
broad spectrum G+ bacteria and some G- bacteria including
Chlamydia, Mycoplasma, Legionella, Rickettsia, Neisseria
Azithromycin, Clarithromycin active against some mycobacteria
61. Macrolides: mode of action
Blocking Translation during Bacterial Protein
Synthesis erythromycin
The macrolides bind reversibly to the 50S subunit.
They can inhibit elongation of the protein by the peptidyltransferase, the
enzyme that forms peptide bonds between the amino acids.
62. Mode of Action of Macrolides in Blocking
Translation during Bacterial Protein
Synthesis
The macrolides bind reversibly to
the 50S subunit.
They can inhibit elongation of the
protein by blocking the translocation
of the ribosome to the next codon on
mRNA
64. Clindamycin, lincomycin
Family of lincosamide antibiotics originally isolated from
Streptomyces lincolnensis
Mode of action: bind 50S ribosome subunit and blocks
protein elongation
Resistance is related to 23S ribosomal RNA Methylation
Active against staphylococci and G-ve anaerobic bacilli.
No activity against aerobic
65. Replacement of a
sensitive pathway
› Acquisition of a
resistant enzyme
(sulfonamides,
trimethoprim)
66. Molecular Drug Susceptibility Testing
• Genotypic methods: the
drug target and nature of
the gene mutation are
known
• Usually molecular
amplification of target
DNA or RNA followed by
some means of detecting
mutation in the product.
67. Molecular methods of drug susceptibility testing
1. Sequencing
Universal and
reliable method
Expensive, time-
consuming and not
suitable for
everyday routine
testing
Applied as
reference method to
verify results of other
tests.
68.
69. 2. PCR-based methods
PCR-Single Strand
Conformation
Polymorphism (PCR-
SSCP)
Mutations cause
alterations in
conformation of single-
strand DNA fragments
and it is registered in
non-denaturizing PAGE
70. Other molecular methods of drug susceptibility
testing:
Real-Time fluorescent PCR
Molecular combines amplification and
beacons detection: minimises amplicon
contamination
71. PCR+hybridization
Based on amplification of fragments of genes
responsible for drug resistance development
follwed by hybridization with oligonucleotide
probes immobilized on membranes;
Both commercial kits and in-house macro-
arrays have been reported to demonstrate
high sensitivity and specificity
72. Molecular tests for the detection of resistance to RIF and INH
GenoType® MTBDRplus test procedure
74. Exposure to sub-optimal levels of
antimicrobial
Exposure to microbes carrying resistance
genes
75. Prescription not taken correctly
Antibiotics for viral infections
Antibiotics sold without medical supervision
Spread of resistant microbes in hospitals due
to lack of hygiene
76. Lack of quality control in manufacture or
outdated antimicrobial
Inadequate surveillance or defective
susceptibility assays
Poverty or war
Use of antibiotics in foods
77. Antibiotics are used in animal feeds and
sprayed on plants to prevent infection and
promote growth
Multi drug-resistant Salmonella typhi has
been found in 4 states in 18 people who ate
beef fed antibiotics
78. Infections resistant to
available antibiotics
Increased cost of
treatment
79.
80. Methicillin-Resistant Staphylococcus aureus
Most frequent nosocomial (hospital-acquired)
pathogen
Usually resistant to several other antibiotics
81. Speed development of new antibiotics
Track resistance data nationwide
Restrict antimicrobial use
Direct observed dosing (TB)
Use more narrow spectrum antibiotics
Use antimicrobial cocktails