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Seminar on
Topic :-Literature Survey Antibiotic Resistance
Presented by:-
TUHIN SAMANTA
INTRODUCTION
• Antibiotic: A drug used to treat bacterial infections. Antibiotics
have no effect on viral infections. Originally, an antibiotic was a
substance produced by one microorganism that selectively inhibits the
growth of another. Synthetic antibiotics, usually chemically related to
natural antibiotics, have since been produced that accomplish
comparable tasks.
 In 1926, Alexander Fleming discovered penicillin, a substance
produced by fungi that appeared able to inhibit bacterial growth.
 In 1939, Edward Chain and Howard Florey further studied penicillin
and later carried out trials of penicillin on humans (with what were
deemed fatal bacterial infections).
It is a specific type of drug
resistance.
The most important problem
associated with infectious disease
today is the rapid development of
resistance to antibiotics.
There are more large cities in the
world today.
Large numbers of people in
relatively small areas
Passing antibiotic-resistant
pathogens is easier.
Many large urban populations have
poor sanitation.
Antibiotic Resistance:-
IT MAINLY TWO TYPES:-
• Intrinsic resistance
Occurs naturally in all or most strains of that species
Chromosomally encoded
Grams negative are resistance to Vancomycin
• Acquired resistance
Results from a mutation in the existing DNA often organism
of new DNA
OBJECTIVES
• Antimicrobial resistance is a global problem now a day. Many of the
bacteria grow resistance against a number of antibiotics. Many
developing and developed countries are greatly concerned with the
problem of resistance of microorganism against a good number of
antibiotics.
So, this topic is selected in order to give and overall idea about
antimicrobial resistance and its remedy.
LITERATURE SURVEY
J Davies, Science 15 Apr 1994, the emergence of multidrug resistant
bacteria is a phenomenon of concern to the clinician and the
pharmaceutical industry, as it is the major cause of failure in the
treatment of infectious diseases. The most common mechanism of
resistance in pathogenic bacteria to antibiotics of the amino glycoside,
beta-lactam (penicillin’s and cephalosporin’s), and chloramphenicol
types involves the enzyme inactivation of the antibiotic by hydrolysis or
by formation of inactive derivatives. Such resistance determinants most
probably were acquired by pathogenic bacteria from a pool of
resistance genes in other microbial genera, including antibiotic
producing organisms. The resistance gene sequences were subsequently
integrated by site-specific recombination into several classes of
naturally occurring gene expression cassettes (typically "integrons")
and disseminated within the microbial population by a variety of gene
transfer mechanisms1
J. M. Goodson, † S. Offenbacher, D. H. Farr, † and P.E. Hogan†, the sub
gingival microbiologic composition of diseasedperiodontal sites was
evaluated by dark field microscopy before and after scaling of
tetracycline. A standardized sampling and counting method using a
reticular washing technique was developed to determine both numbers
and proportions of morph types using dark field microscopy.
Tetracycline loaded hollow fibers established an initial intramuscular
concentration of 200,000 μg/ml, which decreased exponentially to15
μg/ml in 24 hours. Repetitive intramuscular placement of these fibers at
periodontitis sites produced an incremental reduction in bacterial counts
over a 10day period. Monolithic fibers made of ethylene vinyl acetate
loaded with 25% tetracycline hydrochloride provided sustained release
for 10 days under in vitro test conditions. Ten patients were treated in a
study comparing the effects of these fibers with scaling2
Clay B. Walker,† Janet D. Pappas,† Kathy Z. Tyler,† Samuel Cohen,†
and Jeffrey M. Gordon‡, In VITRO SUSCEPTIBILITIES OF 369 TO 966
BACTERIAL isolates from periodontal lesions to eight antibiotics were
determined by agar dilution technique as a means of determining which
antimicrobial agents were inhibitory for bacteria frequently associated
with destructive periodontal diseases. Although most bacteria were
relatively susceptible to the penicillin’s, greater activity was generally
noted with amoxicillin than with either penicillin or ampicillin with the
exception of Selenomonas sputigena and Peptostreptococcus.
Antibacterial activities obtained with minocycline were significantly
higher than with tetracycline for Actinobacillus actinomycetemcomitans
and Streptococcus but comparable for most other taxa. Clindamycin and
metronidazole both demonstrated excellent activity against the
anaerobic Gram-negative rods but were less effective against some of
the capnophilic and facultative organisms3 .
Max A. Listgarten, ChernHsiung Lai, and Virginia Young, a series of 993
microbial samples sent to a diagnostic microbiology laboratory included
196 samples that could be identified as compatible with a clinical
diagnosis of refractory or recurrent periodontitis. In descending order
of prevalence the associated micro biota included Bactericides forsythias
(84%), spirochetes (83%), motile rods (76%), Fusobacterium species
(68%), Porphyromonas gingival is (63%), Campylobacter rectus (47%),
Capnocytophaga species (38%), Prevotella intermediary (23%),
Peptostreptococcus micros (18%), Actinobacillus
actinomycetemcomitans (16%), Candida (14%), enteric rods (9%),
Staphylococcus species, not including aureus (5.6%). Eikenella
corrodens (3%), Staphylococcus aureus (1.5%), and Enterococcus
species (<1%). Antibiotic resistance to tetracycline, penicillin G, or
metronidazole was particularly noticeable for enteric rods,
Fusobacterium species, Capnocytophaga species, Staphylococcus, and
Actinobacillus actinomycetemcomitans4 .
J. Bacteriol, certain erythromycin-resistant strains of Staphylococcus
aureus remain sensitive to other macrolide antibiotics. If these strains are
exposed to low levels of erythromycin, resistance to other antibiotics is
induced. The antibiotics to which resistance is induced by erythromycin
include: other macrolides as well as lincosaminide, streptogramin (group
B) antibiotics but not chloramphenicol, amice tin, streptogramin (group
A) antibiotics, tetracyclines, and amino glycosides. Hence erythromycin
induces resistance exclusively towards inhibitors of 50S ribosomal
subunit function and, thus far, only with respect to three of six known
classes of inhibitors which act on this subunit. In the four strains tested,
erythromycin did not induce resistance to pactamycin or bottromycin, to
fusidic acid (which inhibits a function involving both subunits), or to
other antibiotics which do not inhibit ribosomal function5.
CONCLUSION
Based on the above literature review, it may be concluded that
Antibiotic resistance can be minimized by awareness of people using
proper dose of antibiotic at proper time interval with view
prescription.
With the rising of awareness of common people this major
global problem can be removed from the developing and developed
countries in the days to come.
REFERANCES
• 1. Davies J
Topic- Inactivation of antibiotics and the dissemination of resistance
genes 264, 1994, 375-382
• 2. Goodson J.M, Offenbacher.S, Farr D.H, Hogan P.E
Topic- Journal of Periodontology 56(5)1985, 155-161
• 3. Walker clay B, Pappas Janet D, Tyler Kathy Z, Cohen Samuel,
Gordon Jeffrev M
Topic- Journal of Periodontology 56(11s) 1985, 67-74
• 4. Listgarten Max A, Lai Chern Hsiung, Young Virginia
Topic- Journal of Periodontology 64(3)1993, 155-161
• 5. Bacteriol J
Topic- Journal of Bacteriology 98(2) 1969 447-452
Literature Survey Antibiotic Resistance

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Literature Survey Antibiotic Resistance

  • 1. Seminar on Topic :-Literature Survey Antibiotic Resistance Presented by:- TUHIN SAMANTA
  • 2. INTRODUCTION • Antibiotic: A drug used to treat bacterial infections. Antibiotics have no effect on viral infections. Originally, an antibiotic was a substance produced by one microorganism that selectively inhibits the growth of another. Synthetic antibiotics, usually chemically related to natural antibiotics, have since been produced that accomplish comparable tasks.  In 1926, Alexander Fleming discovered penicillin, a substance produced by fungi that appeared able to inhibit bacterial growth.  In 1939, Edward Chain and Howard Florey further studied penicillin and later carried out trials of penicillin on humans (with what were deemed fatal bacterial infections).
  • 3. It is a specific type of drug resistance. The most important problem associated with infectious disease today is the rapid development of resistance to antibiotics. There are more large cities in the world today. Large numbers of people in relatively small areas Passing antibiotic-resistant pathogens is easier. Many large urban populations have poor sanitation. Antibiotic Resistance:-
  • 4. IT MAINLY TWO TYPES:- • Intrinsic resistance Occurs naturally in all or most strains of that species Chromosomally encoded Grams negative are resistance to Vancomycin • Acquired resistance Results from a mutation in the existing DNA often organism of new DNA
  • 5. OBJECTIVES • Antimicrobial resistance is a global problem now a day. Many of the bacteria grow resistance against a number of antibiotics. Many developing and developed countries are greatly concerned with the problem of resistance of microorganism against a good number of antibiotics. So, this topic is selected in order to give and overall idea about antimicrobial resistance and its remedy.
  • 6. LITERATURE SURVEY J Davies, Science 15 Apr 1994, the emergence of multidrug resistant bacteria is a phenomenon of concern to the clinician and the pharmaceutical industry, as it is the major cause of failure in the treatment of infectious diseases. The most common mechanism of resistance in pathogenic bacteria to antibiotics of the amino glycoside, beta-lactam (penicillin’s and cephalosporin’s), and chloramphenicol types involves the enzyme inactivation of the antibiotic by hydrolysis or by formation of inactive derivatives. Such resistance determinants most probably were acquired by pathogenic bacteria from a pool of resistance genes in other microbial genera, including antibiotic producing organisms. The resistance gene sequences were subsequently integrated by site-specific recombination into several classes of naturally occurring gene expression cassettes (typically "integrons") and disseminated within the microbial population by a variety of gene transfer mechanisms1
  • 7. J. M. Goodson, † S. Offenbacher, D. H. Farr, † and P.E. Hogan†, the sub gingival microbiologic composition of diseasedperiodontal sites was evaluated by dark field microscopy before and after scaling of tetracycline. A standardized sampling and counting method using a reticular washing technique was developed to determine both numbers and proportions of morph types using dark field microscopy. Tetracycline loaded hollow fibers established an initial intramuscular concentration of 200,000 μg/ml, which decreased exponentially to15 μg/ml in 24 hours. Repetitive intramuscular placement of these fibers at periodontitis sites produced an incremental reduction in bacterial counts over a 10day period. Monolithic fibers made of ethylene vinyl acetate loaded with 25% tetracycline hydrochloride provided sustained release for 10 days under in vitro test conditions. Ten patients were treated in a study comparing the effects of these fibers with scaling2
  • 8. Clay B. Walker,† Janet D. Pappas,† Kathy Z. Tyler,† Samuel Cohen,† and Jeffrey M. Gordon‡, In VITRO SUSCEPTIBILITIES OF 369 TO 966 BACTERIAL isolates from periodontal lesions to eight antibiotics were determined by agar dilution technique as a means of determining which antimicrobial agents were inhibitory for bacteria frequently associated with destructive periodontal diseases. Although most bacteria were relatively susceptible to the penicillin’s, greater activity was generally noted with amoxicillin than with either penicillin or ampicillin with the exception of Selenomonas sputigena and Peptostreptococcus. Antibacterial activities obtained with minocycline were significantly higher than with tetracycline for Actinobacillus actinomycetemcomitans and Streptococcus but comparable for most other taxa. Clindamycin and metronidazole both demonstrated excellent activity against the anaerobic Gram-negative rods but were less effective against some of the capnophilic and facultative organisms3 .
  • 9. Max A. Listgarten, ChernHsiung Lai, and Virginia Young, a series of 993 microbial samples sent to a diagnostic microbiology laboratory included 196 samples that could be identified as compatible with a clinical diagnosis of refractory or recurrent periodontitis. In descending order of prevalence the associated micro biota included Bactericides forsythias (84%), spirochetes (83%), motile rods (76%), Fusobacterium species (68%), Porphyromonas gingival is (63%), Campylobacter rectus (47%), Capnocytophaga species (38%), Prevotella intermediary (23%), Peptostreptococcus micros (18%), Actinobacillus actinomycetemcomitans (16%), Candida (14%), enteric rods (9%), Staphylococcus species, not including aureus (5.6%). Eikenella corrodens (3%), Staphylococcus aureus (1.5%), and Enterococcus species (<1%). Antibiotic resistance to tetracycline, penicillin G, or metronidazole was particularly noticeable for enteric rods, Fusobacterium species, Capnocytophaga species, Staphylococcus, and Actinobacillus actinomycetemcomitans4 .
  • 10. J. Bacteriol, certain erythromycin-resistant strains of Staphylococcus aureus remain sensitive to other macrolide antibiotics. If these strains are exposed to low levels of erythromycin, resistance to other antibiotics is induced. The antibiotics to which resistance is induced by erythromycin include: other macrolides as well as lincosaminide, streptogramin (group B) antibiotics but not chloramphenicol, amice tin, streptogramin (group A) antibiotics, tetracyclines, and amino glycosides. Hence erythromycin induces resistance exclusively towards inhibitors of 50S ribosomal subunit function and, thus far, only with respect to three of six known classes of inhibitors which act on this subunit. In the four strains tested, erythromycin did not induce resistance to pactamycin or bottromycin, to fusidic acid (which inhibits a function involving both subunits), or to other antibiotics which do not inhibit ribosomal function5.
  • 11. CONCLUSION Based on the above literature review, it may be concluded that Antibiotic resistance can be minimized by awareness of people using proper dose of antibiotic at proper time interval with view prescription. With the rising of awareness of common people this major global problem can be removed from the developing and developed countries in the days to come.
  • 12. REFERANCES • 1. Davies J Topic- Inactivation of antibiotics and the dissemination of resistance genes 264, 1994, 375-382 • 2. Goodson J.M, Offenbacher.S, Farr D.H, Hogan P.E Topic- Journal of Periodontology 56(5)1985, 155-161 • 3. Walker clay B, Pappas Janet D, Tyler Kathy Z, Cohen Samuel, Gordon Jeffrev M Topic- Journal of Periodontology 56(11s) 1985, 67-74 • 4. Listgarten Max A, Lai Chern Hsiung, Young Virginia Topic- Journal of Periodontology 64(3)1993, 155-161 • 5. Bacteriol J Topic- Journal of Bacteriology 98(2) 1969 447-452