This is a comprehensive and detailed summary on Antibiotics and Diabetic Agents from the book Pharmacology for Nursing Care by Richard A. Lehne.
*Essential Study Material!!
Basic Principles of Antimicrobial Therapy:
Antibiotic:
→ a chemical that is produced by one microbe and has the ability to harm
other microbes
→ drugs such as sulfonamides that are produced in the lab are not antibiotics by
“strict” definition
→ narrow spectrum antibiotics are preferred to broad spectrum antibiotics
→ broad spectrums can be used as initial treatment then switched to narrow when
identity of bacteria is known
→ samples of exudates and body fluids must be obtained before initiation of
antibiotic treatment
→ antibiotics should not be d/c prematurely; if they are→ recurrent infection
MULTIPLE ANTIBIOTIC THERAPY→ INFECTION HAS UNKNOWN ETIOLOGY AND PT IS
NEUTROPENIC
→ in some cases antibiotic combination can reduce toxicity to the host and in some cases it
can increase toxicity
Antimicrobial Drug:
→ any agent, natural or synthetic, that has the ability to kill or suppress
microorganisms
→ no benefit/ significant diff. in the terms antimicrobial drug and antibiotic so
they’re used interchangeably
→ Antimicrobial therapy: #1 rule catch the drug with the bug
⇒ objective not to kill infecting organism, it is to suppress microbial growth to
the point at which the balance is tipped in favor of the host
→additive response→ antimicrobial effect of the combination of two drugs is equal
to the sum of effects of the two drugs alone
→ potentiative/synergistic response→ the effect of the drug combination is greater
than the sum of the effects of the two drugs alone (ex penicillin combined w/
aminoglycoside to treat enterococcal endocarditis)
→ antagonistic response→ effect is less; not significant if host defense is intact
→ common when bactericidal agent (ex penicillin) is combined with
bacteriostatic agent (ex tetracycline)
Selective toxicity:
→ the ability of a drug to injure a target cell or target organism
without injuring other cells or organisms that are intimate contact with
the target
→ the ability of an antibiotic to kill or suppress microbial
pathogens without causing injury to the host
Bactericidal Drug:
,→ directly lethal to bacteria at clinical concentrations
Bacteriostatic Drug:
→ slow bacterial growth; does not cause cell death
Acquired resistance:
→ over time drug that is effective becomes useless
→ problems w c-diff, staph, enterococci, pseudomonas, acinetobacter, klebsiella
→ MICROBE becomes resistant not the patient
Superinfection:
→ a NEW secondary infection that appears during the course of a primary infection
→ develop when antibiotics eliminate the inhibitory influence of normal flora
→ example of emergence of drug resistance
DISINFECTANT→ KILL BACTERIA→ APPLY TO SURFACES AND INSTRUMENTS
ANTISEPTIC→ INHIBIT MICROORGANISMS→ APPLY TO SKIN
Bacterial Cell Wall:
-osmotic pressure w/in bacterium is high
-If not for the cell wall bacteria would absorb water and burst
-drugs that weaken cell wall (penicillin and cephalosporin) cause bacterial lysis
-mammals do not have cell walls
Sulfonamides:
-antimetabolite
-selectively toxic to specific microbes; deprives the bacteria of folic acid
-inhibit an ENZYME critical to BACTERIAL survival
→ para-aminobenzoic acid makes folic acid; humans can safely receive sulfonamides
as treatment because folic acid is received dietarily and is not produced w/in the
body→ toxicity only in microbes
→ sulfonamides block conversion of Para-Aminobenzoic Acid acid (PABA) into folic
acid
Bacterial Protein Synthesis:
-bacteria do not have identical ribosomes, unlike humans; antibiotics can impair
bacterial ribosomes leaving ribosomes of mammalian untouched
Mechanisms of Action: Drugs→
-inhibit cell wall synthesis (promote bacterial lysis and death)--> penicillin and
cephalosporin
-increase cell membrane permeability (causing leakage of intracellular material)-->
amphotericin B
-cause lethal inhibition of bacterial protein synthesis (kills bacteria)-->
aminoglycosides/gentamicin
-that cause non-lethal inhibition of bacterial protein synthesis(slow microbial growth
they do not kill them)--> tetracyclines
,-that inhibit bacterial synthesis of DNA and RNA or disrupt DNA function (bind
directly to nucleic acids or DNA/ interfere with nucleic acid synthesis)--> ciprofloxacin
-antimetabolites (disrupt biochemical reactions)--> sulfonamides
-drugs that suppress viral replication (inhibit protease, polymerase, transcriptase,
etc)
→
results from or from acquisition of DNA from an external
source ie -> these are independent of drug use
-Use of antibiotics promotes the emergence of drug resistant microbes
-If a drug resistant organism is present antibiotics will create selection pressure
favoring its growth by killing sensitive organisms that are not resistant to the drug
-All microbial drugs facilitate resistance, but broad spectrum facilitate the most
→ EXCEPTION=drugs to treat TB SUPPRESS RESISTANCE
-more antibiotics=faster drug resistance
-hospitals use large amount of antibiotics→ HAI’s; DIFFICULT TO TREAT
Microbial Mechanisms of Drug Resistance:
⇒ at site of action→ mostly intracellular→ microbes stop uptake of certain drugs
(gentamicin, tetracycline) or increase export of drug→ resistance
⇒ molecule structure is altered→ resistance
⇒ microbe synthesizes compound that antagonizes drug action→ resistance
Drug Inactivations
→ microbes can resist harm by producing drug metabolizing enzymes
→ penicillinase is produced to inactivate penicillin
→ New Delhi Metallo-Beta-Lactamase 1 or gene in bacteria that codes for
extreme resistance; Inactivates drugs with beta-lactam ring (penicillin, cephalosporin);
bacteria that have gene are resistant to ALL antibiotics except colistin and tigecycline
Spontaneous Mutation
-gradual→ low level resistance develops first, greater resistance with additional
mutations; confer resistance to only
Conjugation
-extrachromosomal DNA is transferred from one bacterium to another
-donor must possess 2 unique DNA segments
-takes place among gram negative bacteria
- resistance
→ 1 codes for the sexual apparatus required for DNA transfer
→ 1 codes for the mechanisms of drug resistance
→ the 2 combine= R Factor (resistance factor)
→ R factors are becoming common in NORMAL FLORA (resistance transfer from
normal flora to pathogen is a clinical concern)
, Selecting An Antibiotic→
1. Identity of infecting organism
a. Microscopic examination of gram stained preparation are quickest,
simplest, and most versatile
b. Samples for stain include blood, sputum, urine, and other body fluids
c. Most useful sample=direct aspirates from site of infection
d. Polymerase Chain Reaction test/ Nucleic Acid Amplification test can
detect low titers of bacteria and viruses
i. More specific and more sensitive than gram stain
2. Drug sensitivity of infecting organism
3. Host factors such as site of infection and status of host defenses
Determining Drug Susceptibility:
→ sensitivity testing is not always needed
→ indicated when resistance is common (ex staph and gram neg. bacilli)
Aka Kirby-Bauer test
Performed by seeding an agar plate with infected organism solution
and placing on plate with several paper disks that have been
impregnated with various antibiotics
The degree of drug sensitivity is proportional to the size of the bacteria
free zone
a. Bacteria are grown in a series of tubes containing direct concentrations
of an antibiotic
b. Provides more precise drug sensitivity
c. Good for est. therapy for infections very hard to treat
d. Establishes 2 clinical values
1. The lowest concentration of antibiotic that produces
complete inhibition of bacterial growth (does not kill)
2. Drug levels 4-8x the minimum inhibitory concentration is
desirable
1. The lowest concentration of drug that produces a 99.9%
decline (kills) in bacterial colonies
a. Similar to disk diffusion but finds more precise MIC
b. Uses narrow test strips instead of disk; and uses 15 concentrations of
same antibiotic instead of all different ones
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