Portal field news

Portal field news

in ,

🛋 | Check before cleaning the humidifier!What is the different care method for each type?


写真 

Check before cleaning the humidifier!What is the different care method for each type?

 
If you write the contents roughly
In addition, there are many types that use antibacterial filters.
 

Humidifiers play an active role when the humidity starts to drop with the temperature.However, the humidifier is suitable because it tends to collect dirt. → Continue reading

 ARUHI Magazine

Everyday events begin one day. Various articles useful for "living life" such as interview articles that are useful for finding a home, mortgage columns by FP, news about housing and news that can be used for living are being delivered every day!


Wikipedia related words

If there is no explanation, there is no corresponding item on Wikipedia.

Antibacterial drug

Antibacterial drug(Koukinyaku,English: Antibacterial drugs) IsBacteriaHas the function of suppressing or killing the growth ofchemical treatmentThe agent.FungusIf you do not haveAntibacterial drugTomo.

BacteriabyInfectionUsed to treatMedicineIs. Also,Antibacterial soapContained in household items such asTriclosanThe same applies to synthetic antibacterial agents such as and.

Sort

Effect classification

Bactericidal antibacterial agent
An antibacterial drug that kills bacteria.
Bacteriostatic antibacterial drug
An antibacterial drug that suppresses the growth of bacteria.

Structural classification

It is classified as follows.

 Antibacterial agents ┣ Natural antibacterial agents (antibiotics) ┃ ┣ β-lactam system ┃ ┣ Aminoglycoside system ┃ ┣ Lincomycin system ┃ ┣ Chloramphenicol system ┃ ┣ Macrolide system ┃ ┣ Ketride system ┃ ┣ ┃ ┗ Tetracycline ┃ ┗ Semi-synthetic antibacterial ┃ ┗ Doxycycline / minocycline ┗ Synthetic antibacterial ┣ Pyridone carboxylic acid (quinolone) ┣ New quinolone ┣ Oxazolidinone ┗

Mechanism of action of antibacterial drugs

Cell wall synthesis inhibitor

Antibacterial agents classified as cell wall synthesis inhibitors include β-lactams, fosfomycin, and vancomycin.

Cell wall synthetic pathway

Most bacteriaCell membraneOutside ofCell wallAnimal cells do not have this, whereas they have a structure called.Bacteria are generallyGram stainIt is classified into Gram-positive bacteria and Gram-negative bacteria according to the stained image of, and both are distinguished by the difference in cell wall structure, but both cell walls are common.PeptidoglycanAs a constituent component.In particular, cells of Gram-positive bacteria have a high internal pressure, and the peptidoglycan-based structure present on the cell wall prevents rupture due to this pressure.Therefore, bacteria lacking peptidoglycan die because their cell membranes rupture.[1].

Bacterial cell walls, also called peptidoglycan, are twoAmino sugarAnd 10amino acidThe cell wall is constructed by assembling the Murrain monomer composed of the above like a wall made of brick.The Murrain monomer is synthesized intracellularly and then transported extracellularly.Glycosyltransferase With an enzyme called (GT)Penicillin binding protein By the action of both enzymes called (PBP), the cells are cross-linked to the existing cell wall, and the synthesis of the cell wall is promoted.Note that these two enzymes are not necessarily different proteins,E. coliIn the case of, PBP doubles as two enzymes.Among cell wall synthesis inhibitors, β-lactams and vancomycin inhibit the action of PBP, while fosfomycin inhibits the synthesis of murain monomers in cells.[1].

β-lactam

Beta-lactam antibiotics are the most popular antibiotics, and 65% of the antibiotics prescribed in the United States belong to this family. Among β-lactamsCephem systemIs often prescribed in particular, and about half of β-lactam prescriptions are cephem antibiotics.[2].

The β-lactam system exerts its pharmacological effect by inhibiting the action of penicillin-binding protein (PBP). D-alanine-D-alanine plays an important role in cell wall synthesis because PBP recognizes D-alanine-D-alanine present in the molecule of the murain monomer and forms crosslinks to promote cell wall synthesis. ..penicillinSince β-lactam antibiotics represented by the above have a structure similar to this D-alanine-D-alanine, they bind to PBP, and PBP cannot bind to the murein monomer.As a result, the cross-linking of the cell wall becomes insufficient, and the bacteria rupture to death.This is the mechanism of action of β-lactams[1][3].

As the name implies, the β-lactam system has a structure called a β-lactam ring. Accompanying this in β-lactamsSide chainVarious antibacterial agents with different antibacterial spectra have been derived and developed by changing the structure of[1]..Side effects are mainly allergic reactions, especiallyAmpicillinCephalexinCross-allergic reactions are likely to occur between penicillins and cephems with similar side chains, such as the combination of.On the other hand, unlike the penicillin system and the cephem system, it does not have a 5-membered ring or a 6-membered ring associated with the β-lactam ring.MonobactamIs also used by patients who have less allergic reactions and are allergic to penicillin[2][4][5][6].

Vancomycin

The β-lactams bind to PBP and inhibit cell wall synthesis, whereasVancomycinIs said to act by binding to D-alanine-D-alanine, which is a part of the murain monomer, and inhibiting the polymerization of the murain monomer by GT.It is sometimes called a "last resort" because of its large size, which makes it difficult to pass through the outer membrane of the cell, and its high toxicity when administered to humans, but its mechanism of action is different from that of β-lactams. For,Methicillin-resistant Staphylococcus aureusUsed as a therapeutic agent against bacterial infections that are resistant to β-lactam antibiotics, such as[1][7]..However, vancomycin-resistant enterococci (VRE) also appeared.

Fosfomycin

Unlike the above two cell wall synthesis inhibitors,FosfomycinIs a part of Murrain MonomerN-Acetylmuramic acidInhibits the production of.Therefore, when used in combination with β-lactams, it shows a synergistic effect.[1][8].

Protein synthesis inhibitor

The information stored in the DNA of an organismTranscriptionBymConverted to mRNA翻 訳BeenproteinUsed for the synthesis of.RibosomeIs a place for protein synthesis, and in the case of bacteria, the 70S ribosome is composed of a combination of 30S and 50S subunits.[3]..Bacterial ribosomes have a partially different structure from human ribosomes, which allows protein synthesis inhibitors to act with high affinity for bacterial ribosomes.The selectivity of protein synthesis inhibitors is simply affinity dependent and exhibits quantitative selective toxicity.[1]..Protein synthesis inhibitors can be broadly classified into two types, one that targets the 30S subunit and the other that targets the 50S subunit, depending on the target of inhibition.The former includes aminoglycosides and tetracyclines, and the latter includes chloramphenicol and macrolides.[3][Annotation 1].

Amino glycoside(Aminoglycoside) in 1943Streptomyces griseusSeparated fromstreptomycinIt is an antibiotic represented by, and has a wide antibacterial spectrum against both Gram-positive and Gram-negative bacteria.[9]..On the other hand, the uptake of amino glycosides into cells requires aerobic respiration and is not effective against anaerobic bacteria.[10][11].

Macrolide systemIs a large molecule with a structure called a macrocyclic lactone composed of 12-16 atoms.[12]Low toxicity[13]Shows excellent antibacterial activity against gram-positive bacteria such as staphylococci[14]..Discovered in 1952 as a representative exampleerythromycinEtc. are known[12].

tetracyclineThe system is also an antibiotic with an extremely wide antibacterial spectrum, and has four continuous cyclic structures as nuclei.In addition to tetracycline, the side chain of tetracycline was changed to improve lipophilicity.Doxycycline,MinocyclineIs known.Tetracycline antibiotics bind to ribosomes and inhibit protein synthesis by inhibiting the binding of aminoacyl-tRNA to ribosomes.[15].

ChloramphenicolIs an antibiotic with an extremely broad antibacterial spectrum.However, it is highly toxic, such as showing bone marrow toxicity, and is not often used for therapeutic purposes.[1][16].

Nucleic acid synthesis inhibitor

Nucleic acid synthesis inhibitors are classified into RNA synthesis inhibitors and DNA synthesis inhibitors, both of which exhibit quantitative selective toxicity.The former isRNA polymeraseInhibitmSuppresses the synthesis of.RifampicinIs a representative example of this and is important as an anti-tuberculosis drug.[1].

Other antibacterial agents

QuinolonesSulfa drugWas mechanismd by inhibition of nucleic acid synthesisSynthetic antibacterial drugIt is different from antibiotics in a narrow sense.

Quinolones are also DNA synthesis inhibitors,DNA gyraseTopoisomerase IVInhibits DNA replication by inhibiting DNA replication.Humans do not have folic acid metabolism inhibitorsFolic acidIt has high selective toxicity because it inhibits the metabolic system.Sulfa drugs are folic acid metabolism inhibitors that block other pathways in the same folic acid metabolism system.TrimethoprimWithST mixtureUsed as. ST mixture includes Gram-positive and Gram-negative bacteria, as well asProtozoa,FungusAlso shows the effect[1].

Pharmacology of antibacterial drugs

Among antibiotics, drugs used as antibacterial agents act on some metabolic pathways necessary for bacteria to grow, resulting in selective toxicity, that is, less harmful to the organism to which they are administered, and are selected against bacteria. It is a compound that is highly toxic.For example, β-lactam antibiotics have an affinity for penicillin-binding protein (PBP) and inhibit cell wall synthesis, but all of them are peculiar to prokaryotic organisms and are therefore almost toxic to human cells. Does not show[17].

However, some antibiotics show not only antibacterial activity but also antiviral, antifungal, antiparasitic, and antitumor activity.[17]..There are also antibiotics that are toxic to all organisms without showing selective toxicity.for examplePuromycin ThetRNAHas a structure similar to aminoacyl-tRNA with amino acids added toActinomyceteAlthough it is an antibiotic derived from, it has a function of inhibiting protein synthesis in all organisms including producing bacteria.Antibiotics that do not have such selective toxicity are not used for the treatment of infectious diseases, but are widely used for research purposes such as research on protein synthesis systems.[18].

In addition, the action of antibacterial agents is generally classified into bactericidal and bacteriostatic.Bactericidal antibacterial drugs, as the name implies, kill bacteria.On the other hand, the bacteriostatic antibacterial agent only suppresses the growth of the bacterium, and if the concentration of the bacteriostatic antibacterial agent decreases, the bacterium can grow again.In addition, "antibacterial spectrum" is used as a term indicating the range of bacteria for which antibacterial agents are effective.The antibacterial spectrum is described according to the bacterial classification system[19].

Antibacterial drugs also act on non-pathogenic bacteria, so when used in large amounts, they can be used in the body.Often presentMay lose the balance.As a result, when the number of indigenous bacteria is extremely reduced, other bacteria and fungi (molds) may explode and become pathogenic.In addition, the surviving bacteria become resistantResistant bacteriaThe appearance of is also a problem.

Antimicrobial susceptibility

When an antibacterial drug is used for chemotherapy for a bacterial infectious disease, it is ideal to select the antibacterial drug to be administered after examining the susceptibility of the infection-causing bacteria to the antibacterial drug.To hit quickly,Gram stainStain the sample with.To accurately determine the susceptibility of antibacterial drugs,Minimum inhibitory concentration Measure (Minimum Inhibitory Concentration; MIC).

This can be carried out not only with antibiotics used as antibacterial agents but also with all antibiotics.In other words, it is a method to determine the minimum concentration of antibiotics that can suppress the growth of bacteria. There are two known methods, the liquid dilution method and the agar plate dilution method, and the simple sensitive disk method is widely used in medical practice. Have been[1].

Other indicators to evaluate antibacterial propertiesMinimum bactericidal concentration There is also (Minimum Bacteicidal Concentration; MBC), which means the minimum concentration of antibiotics needed to kill as well as suppress the growth of bacteria.In general, MBC has a higher value than MIC, and when the difference is small, it means that the antibacterial agent is bactericidal, and when the difference is large, it means that it is bacteriostatic.[19]..These indicators are used not only for the purpose of examining antibiotic resistance in clinical practice, but also for determining the activity of newly developed antibiotics.[20].

Treatment with antibacterial drugs

Antibiotics are used to treat or prevent bacterial infections[21],MetronidazolelikeProtozoan infectionThere are also things that show an effect on.

When an antibacterial drug is used for chemotherapy for a bacterial infectious disease, it is ideal to select the antibacterial drug to be administered after examining the susceptibility of the infection-causing bacteria to the antibacterial drug.However, if a symptom is suspected to be due to an infection and the pathogen that causes it is unclear.Empiric treatmentMay be done[22]..This is because it is necessary to administer antibacterial drugs as soon as possible, especially when a serious infection has occurred.This is the case, for example, when a patient may die from an infectious disease while waiting for a pathogen investigation.As a result, many emergency departments that may carry patients with serious infections are equipped with antibiotics.[23]..Empiric therapy involves the administration of broad-spectrum antibiotics based on symptoms without waiting for the results of culture tests, which can take several days to produce results.[21][22]..However, in order to strictly identify the infection-causing bacteria, it is necessary to carry out tests such as culture, but it may be possible to estimate the pathogen from the symptoms.for example,CellulitisSince streptococci and staphylococci can be presumed to be the most likely pathogens, treatment with antibacterial agents can be started even if the culture does not give a positive result.[22]..In this way, it may be possible to narrow down effective antibacterial agents to some extent.[22]..Also to avoid surgeryAcute appendicitisAntibacterial drugs may be prescribed for[24].

On the other hand, if the pathogenic microorganism is known in advance or identified by inspection, an antibacterial agent having a narrow antibacterial spectrum is administered.Identification of pathogens is important to reduce the cost of administering antibacterial agents, prevent the occurrence of adverse effects due to the administration of ineffective antibacterial agents, and suppress the emergence of resistant bacteria.[22]..If the culture identifies the pathogen, thenDrug susceptibility testAnd test whether the pathogen can grow in the presence of certain antibacterial agents.Based on the MIC value obtained in the drug susceptibility test, it is determined whether the pathogen is sensitive, resistant, or intermediate to each drug.In the case of susceptibility, it means that the usual dose of the antibiotic can treat the infection.

Antibiotics may be used prophylactically, but prophylactic administrationImmunosuppressive drugThose who are taking medication, those who have a weakened immune system such as cancer patients, those who are going to undergo surgery, such as those who are supposed to be sterile, invasion of bacteria into the body by surgical operation Limited to administration to, especiallyHuman immunodeficiency virusAdministered to prevent pneumonia in infected individuals[21]..Administration of antibacterial agents in surgery prevents infection at the incision site.Prophylactic antibiotic administration plays an important role in oral surgery, followed by bloodstream infectionsInfective endocarditisTo prevent.again,NeutropeniaIt is also used to prevent infections inchemical treatmentFor those who receive cancer treatment[25][26][27].

However, it is possible that the effectiveness of prophylactic administration has decreased since the frequent detection of antibiotic-resistant bacteria.[28].

In the case of antibacterial drugs, even if the prescription is appropriate, the patient'sMedication complianceIf it is bad, this is also regarded as a problem as it increases the risk of emergence of resistant bacteria.

Combination therapy with antibacterial drugs

There are several types of infectious diseases caused by microorganisms that easily develop resistance, such as tubercle bacilli.Anti-tuberculosis drugTo use at the same time,Combination therapyIs done[29].

Combination therapy is performed for the purpose of expanding the antibacterial spectrum in empirical treatment, increasing the therapeutic effect by synergistic effect, and suppressing the emergence of resistant bacteria.[30]..In acute bacterial infections, in order to improve the therapeutic effect, multiple antibacterial agents combined so as to have a stronger antibacterial effect than a single agent may be administered aiming at a synergistic effect.[31][32].

For example,Methicillin-resistant Staphylococcus aureusIn the infection ofFusidic acidRifampicinTreatment is performed in combination with[31]..For example, when treating Gram-negative bacterial infection with combination therapy, β-lactam antibiotics are combined with aminoglycoside antibiotics or new quinolone antibiotics.[30].

However, depending on the combination of antibacterial agents, the antibacterial activity may be lower than that of single agent administration, which is called an antagonistic effect.[31]..In general, the combination of bacteriostatic and bactericidal antibiotics is antagonistic.[31][32].

In addition, the effectiveness of combination therapy may only be demonstrated under experimental conditions, and some have questioned the clinical efficacy of combination therapy against Gram-negative bacteria, for example.[30].

Relationship between side effects of antibiotics and illness

In the treatment of bacterial infections, antibiotics are used with the expectation that they will kill or suppress the growth of pathogenic bacteria, but they can sometimes be harmful to those who receive them.Universal so that most antibiotics can cause diarrhea by oral administrationSide effectsHowever, some antibiotics may cause inherent side effects.[33]..Often the side effects of using antibioticsAllergiesHowever, allergic reactions are only part of the side effects of antibacterial drugs.Side effects of antibiotics can be divided into direct and indirect[22].

Allergic reactions represent the direct side effects of the use of antibacterial agents.IgEDependentImmediate allergic reactionWhen,Cellular immunitybyDelayed allergic reactionBoth can occur, but the most serious is anaphylactic shock due to an immediate allergic reaction. According to a survey conducted in the United States in 2008[34], 19% of emergency outpatient visits due to drug adverse events are related to antibiotics, 79% of which are classified as allergic reactions[22].

Side effects due to the toxicity of antibacterial agents are also direct and occur when the amount of antibacterial agent administered is large or the administration period is long.especiallykidney,liverAs a result of the functional deterioration of antibacterial drugsclearanceCare should be taken when using it in the treatment of patients with disabilities[22]..Mild side effects include yellowing of teeth with tetracyclines and gastrointestinal tract with erythromycin.PeristalsisIt is known to be enriched and pigmented by rifampicin.More serious side effects include irreversible hearing loss due to aminoglycosides, joint toxicity and retinopathy due to fluoroquinolone, methrinidazole andLinezolidPeripheral neuropathy due to linezolidLactic acidosis,Serotonin syndromeand so on[33].

Indirect side effectsBacterial floraIt is caused by bacterial change caused by the effect on Clostridium difficile, and is represented by enteritis caused by Clostridium difficile.[22],OtherVaginal candidiasisKnown to be related to[35].

Clostridium difficile enteritis due to antibacterial agents

ThisClostridium difficile enteritisIs normal due to the administration of antibacterial drugs, etc.Intestinal floraIs thought to occur when the bacteria are disturbed and bacterial alternation occurs.[36].. Disturbing the normal intestinal flora isClostridium difficile Gives the opportunity to grow[37].. So this disease(English editionIs one of[38].Clostridium difficile The outbreak of enteritis is an antibacterial drugNew quinolone,Cephalosporins,ClindamycinStrongly correlated with the use of[39].

Some researchers are routine(English edition Clostridium difficile Pointed out that there is a risk of leading to trends such as[40].

Vitamin deficiency due to antibacterial drugs

As a result of antibacterial agents affecting the intestinal flora, the vitamins that were biosynthesized by the intestinal flora are not fully biosynthesized by the intestinal flora, which can lead to vitamin deficiency. be.

Administration of antibacterial drugs to livestock

The most controversial is to promote growthEconomic animalLong-term use of low-dose antibiotics against.This is not an administration aimed at treating animals, but an antibacterial drug is administered because of its economic advantages in the livestock industry.However, when a low-dose antibacterial drug is used for a long period of time, resistant bacteria are likely to appear because many bacteria survive even if the antibacterial drug acts.And resistant strains can be transmitted not only between livestock animals but also to humans through diet and environment.[41]..In addition, there is no or, if any, economic benefit from the use of antimicrobials in the livestock industry, which is a small amount compared to the damage caused by the emergence of resistant strains.[41].

Since the 1950s, livestock administration of low-dose antibiotics to livestock has been used by farmers in the United States to significantly accelerate livestock weight gain.Antibacterial agents classified as antibiotics used for fattening purposes include, for example, penicillin, oxytetracycline, erythromycin, etc.Spiramycin,Tylosin,(English edition,(English editionAnd so on[42]..Weight gain was also shown by low dose administration of antibacterial agents to mice of experimental animals.Antibiotics and weight gain were also associated with 6-month-old human infants[43].

However, such use of antibacterial agents increases the risk of developing resistant bacteria to antibacterial agents.For example, an antibacterial drug similar to vancomycin.AvoparcinIs used for fattening poultry and pigs as an antibacterial agent that is effective against Gram-positive bacteria, but on farms that use avoparcin.Vancomycin resistant enterococciIs more likely to be detected.Vancomycin-resistant enterococci have been detected in livestock in the United Kingdom, Germany, and Denmark, and it is believed that these resistant bacteria spread rapidly in Western medical facilities.[44].

The EU banned the use of antibacterial drugs to fatten livestock in 2006[43]..In a study in Denmark, the ban on the use of avoparcin for the purpose of fattening livestock alone did not reduce the detection rate of vancomycin-resistant enterococci, whereas the ban on the use of macrolide antibiotics also banned vancomycin-resistant enterococci. The detection rate of cocci decreased.This is a vancomycin resistance genevanAAnd macrolide resistance genesermB chainIt is explained that it is to propagate[44].

The Ministry of Agriculture, Forestry and Fisheries of Japan is demanding "responsible and careful use" to reduce the risk of developing antibacterial drug-resistant bacteria in livestock.[45].

In addition,US Food and Drug Administrationによると、2019年の1年間でアメリカ合衆国内において動物用に販売された、医療用にも使用される抗菌薬の量は6,189,260 kgに上り、その内67%をテトラサイクリン系抗生物質が占めていた。なお、動物に対する抗菌薬の使用量は2015年の9,702,943 kgが最大であり、それと比べると36%減少した。また、動物の種別では牛と豚に対する抗菌薬の使用がそれぞれ2,529,281 kgと2,582,399 kgに及び、これは動物に対する抗菌薬の使用量のそれぞれ41%と42%を占めていた[46].

Tolerance and abuse

Antimicrobial resistance mechanism

The mechanism of resistance of antibacterial drugs is large

(1) Prevention of accumulation of antibacterial agents by reducing uptake and promoting excretion of antibacterial agents[47][3].
(2) Inactivation by decomposition or modification of antibacterial agents[47][3].
(3) It is classified as a decrease in affinity due to mutation or modification of the target molecule of the antibacterial drug or quantitative ineffectiveness of the antibacterial drug due to overproduction.[47][3].

As an example of the resistance mechanism by preventing the accumulation of antibacterial agents by reducing the uptake and excretion of antibacterial agentsPseudomonas aeruginosaNatural resistance of.All antibacterial agents exert their functions by passing through the outer membrane of bacteria and accumulating in the cells, but the outer membrane of Pseudomonas aeruginosa has low permeability of antibacterial agents, and antibacterial agents are generally difficult to work.It is also resistant to excretion of β-lactam antibiotics and quinolone antibiotics that have permeated into cells.[47][48].

Inactivation by degradation or modification of antimicrobial agents is the main mechanism of resistance to β-lactam antibiotics.As a typical exampleβ-lactamaseThe mechanism of resistance to β-lactam antibiotics is known, and β-lactamase inhibits the binding of PBP to β-lactam antibiotics such as penicillin by hydrolyzing the beta-lactam ring structure, and is resistant to bacteria. Bring[47]..Hundreds of lactamase have been discovered so far, and are generally classified into four classes, A, B, C, and D.[1][3][49].. EspeciallyNew Delhi Metallo β-lactamase-1 Unlike other lactamases, β-lactamase called (NDM-1) is shared not only by a specific bacterial species but also by a large number of bacterial species, because the plasmid having the NDM-1 gene also has resistance genes of other strains. Bacteria that carry plasmids acquire multidrug resistance and can be transmitted to Escherichia coli, which causes diarrhea in children, so they are easily spread in the environment and are recognized as a global health threat. ing[50][51].

Unlike antibiotics and semi-synthetic antibacterial agents derived from natural products, no enzyme has been found that decomposes or modifies synthetic antibacterial agents such as sulfa drugs and quinolones.Resistance to such antibacterial agents is acquired by reducing affinity due to mutation or modification of the target molecule of the antibacterial agent or quantitatively nullifying the antibacterial agent due to overproduction.[47]..For example, resistance to quinolone antibioticsDNA gyrase,DNA topoisomeraseOccurs as a result of mutations in genes encoding enzymes such as[3]..Resistance to not only synthetic antibacterial agents but also natural product-derived antibiotics and semi-synthetic antibacterial agents may be acquired by the same mechanism.for exampletetracycline The16S ribosomal RNAIt is an antibiotic that inhibits protein synthesis by binding toHelicobacter pyloriReported resistance acquisition by mutation of 16S ribosomal RNA gene[49].

Multidrug resistant bacteria

In recent yearsMethicillin-resistant Staphylococcus aureus,Multidrug-resistant tuberculosisBacteria that are resistant to multiple antibacterial agents have emerged.Resistance to multiple antibacterial drugs is called multidrug-resistant (MDR), and bacteria with multidrug resistance are called multidrug-resistant (MDR).Multidrug resistant bacteriaCalled.In addition, bacteria that are more resistant than multidrug-resistant bacteria are called extremely drug-resistant (XDR) bacteria, and bacteria that are resistant to all antibiotics are called pandrug-resistant (PDR) bacteria. Called a threat to public health[52][53]. For example,Center for Disease Control and PreventionEstimates that more than 23,000 people die annually in the United States from infections with multidrug-resistant bacteria[54].Mycobacterium tuberculosisMultidrug-resistant strains have emerged in a large number of bacteria, including those with increased morbidity and mortality due to resistance to therapeutic antibiotics, sometimes referred to as superbug.[55]..Methicillin-resistant Staphylococcus aureus or a group of bacterial species called ESKAPE for the acronym (,Staphylococcus aureus,Klebsiella pneumoniae,,Pseudomonas aeruginosa,andEnterobacter) Is included in this, and it is regarded as a problem as a nosocomial infection-causing bacterium showing multidrug resistance.[51][56].

Abuse prevention campaign

Organizations trying to solve the problem of resistant bacteria are campaigning to reduce the use of unnecessary antibiotics[57]..A cross-ministerial task force on resistant strains has been created in the United States to address the issue of resistant strains.For the task forceCenter for Disease Control and Prevention (CDC),US Food and Drug Administration (FDA),National Institutes of Health (NIH), etc. are participating[58].

Percentage of inappropriate antibiotic prescriptions[59]
Dialysis facility12 - 37%
Pediatrics4.0 - 46.7%
Critical care14 - 60%
Outpatient10.5 - 69.0%
Hospital / tertiary medical institution21 - 73%
Long-term care facility21 - 73%
General medical care (GP)45 - 90%

OECD says more than 5% of antimicrobial prescriptions are inappropriate[59]..The most inappropriate prescription isGeneral medical careWas (GP)[59].

There is also a campaign for the general public in the United StatesChoosing Wisely,FranceThe government launched an “Antibiotics are not automatic” campaign (2002), aiming to reduce unnecessary antimicrobial prescriptions.[59][60].

Clinical guidelines

The first rule of antibiotics is try not to use them, and the second rule is try not to use too many of them.[61]
(The first rule of antibacterial drugs is not to use, and the second rule is not to use too many types.)

Paul L. Marino, ICU Book 3rd Edition[62]

Choosing WiselyRecommendations do not prescribe antibiotics for respiratory viral infections[59].. The (AAFP) guidelines recommend that "antibacterial drugs should not be used for colds in children and adults (level of evidence A).[63].(English editionIn HEDIS by (NCQA), "acute bronchitisAntimicrobial prescriptions should be zero. "[64].

UK National Institute of Medical Technology(NICE) guidelines indicate that patients should refrain from or delay the prescription of antibiotics.Acute otitis media, / Acute pharyngitis / Acute tonsillitis, Cold ,, Acute cough /acute bronchitisAre listed[65].Japanese Society of Infectious DiseasesIn principle, antibiotics are not recommended for viral acute bronchitis unless you have chronic respiratory illness (recommended level A, level of evidence I).[66].

Drug resistant bacteriaProper use of antibacterial drugs is called for even infectious diseases, and improper use of antibacterial drugs in non-infectious diseases is warned.[67].

Types

β-lactam

Penicillin

Cephem system

  • First generation
  • Second generation
  • Third generation
  • Fourth generation
    • (CPR Broact Keiten)
    • (CZOP First Shin)
    • Cefepime(CFPM Maxi Pime)
  • Cephem system containing β-lactamase inhibitor

Carbapenem system

Monobactam system

Penem system

Aminoglycoside

Lincomycin system

Fosfomycin system

Tetracycline

Chloramphenicol system

Macrolide system

Ketolide system

  • (TEL Ketec)

Polypeptide system

Glycopeptide system

Streptogramin system

Quinolone

Pyridone carboxylic acid type or old quinolone type

New quinolone system

Sulfa drug

Folic acid metabolism inhibitor

Oxazolidinone system

Related item

footnote

[How to use footnotes]

注 釈

  1. ^ However,Kanamycin,GentamicinAlthough it is an aminoglycoside system, there are exceptions such as binding to both the 30S subunit and the 50S subunit.

Source

  1. ^ a b c d e f g h i j k l Edited by Keiichi Hiramatsu and Osamu Nakagome, "Chapter III General Bacteriology", "Standard Microbiology", 2009, 10.ISBN 978-4-260-00638-5.
  2. ^ a b Bush, Karen; Bradford, Patricia A. (2016-08). “Β-Lactams and β-Lactamase Inhibitors: An Overview” (English). Cold Spring Harbor Perspectives in Medicine 6 (8): a025247. two:10.1101 / cshperspect.a025247. ISSN 2157-1422 . PMC PMC4968164. PMID 27329032. http://perspectivesinmedicine.cshlp.org/lookup/doi/10.1101/cshperspect.a025247. 
  3. ^ a b c d e f g h Kapoor, Garima; Saigal, Saurabh; Elongavan, Ashok (2017). “Action and resistance mechanisms of antibiotics: A guide for clinicians” (English). Journal of Anaesthesiology Clinical Pharmacology 33 (3): 300. two:10.4103 / joacp.JOACP_349_15. ISSN 0970-9185 . PMC PMC5672523. PMID 29109626. http://www.joacp.org/text.asp?2017/33/3/300/214313. 
  4. ^ Mirakian, R .; Leech, SC; Krishna, MT; Richter, AG; Huber, PAJ; Farooque, S .; Khan, N .; Pirmohamed, M. et al. (2015-02). “Management of allergy to penicillins and other beta-lactams” (English). Clinical & Experimental Allergy 45 (2): 300–327. two:10.1111 / cea.12468. https://onlinelibrary.wiley.com/doi/10.1111/cea.12468. 
  5. ^ Trubiano, Jason A .; Stone, Cosby A .; Grayson, M. Lindsay; Urbancic, Karen; Slavin, Monica A .; Thursky, Karin A .; Phillips, Elizabeth J. (2017-11). “The 3 Cs of Antibiotic Allergy—Classification, Cross-Reactivity, and Collaboration” (English). The Journal of Allergy and Clinical Immunology: In Practice 5 (6): 1532–1542. two:10.1016 / j.jaip.2017.06.017. PMC PMC5681410. PMID 28843343. https://linkinghub.elsevier.com/retrieve/pii/S2213219817305019. 
  6. ^ Jeimy, Samira; Ben-Shoshan, Moshe; Abrams, Elissa M .; Ellis, Anne K .; Connors, Lori; Wong, Tiffany (2020-12). “Practical guide for evaluation and management of beta-lactam allergy: position statement from the Canadian Society of Allergy and Clinical Immunology” (English). Allergy, Asthma & Clinical Immunology 16 (1): 95. two:10.1186 / s13223-020-00494-2. ISSN 1710-1492 . PMC PMC7653726. PMID 33292466. https://aacijournal.biomedcentral.com/articles/10.1186/s13223-020-00494-2. 
  7. ^ Butler, Mark S; Hansford, Karl A; Blaskovich, Mark AT; Halai, Reena; Cooper, Matthew A (2014-09). “Glycopeptide antibiotics: Back to the future” (English). The Journal of Antibiotics 67 (9): 631–644. two:10.1038 / ja.2014.111. ISSN 0021-8820 . http://www.nature.com/articles/ja2014111. 
  8. ^ Falagas, Matthew E .; Vouloumanou, Evridiki K .; Samonis, George; Vardakas, Konstantinos Z. (2016-04). “Fosfomycin” (English). Clinical Microbiology Reviews 29 (2): 321–347. two:10.1128 / CMR.00068-15. ISSN 0893-8512 . PMC PMC4786888. PMID 26960938. https://journals.asm.org/doi/10.1128/CMR.00068-15. 
  9. ^ Jospe-Kaufman, Moriah; Siomin, Liza; Fridman, Micha (2020-07-01). “The relationship between the structure and toxicity of aminoglycoside antibiotics”. Bioorganic & Medicinal Chemistry Letters 30 (13): 127218. two:10.1016 / j.bmcl.2020.127218. ISSN 1464-3405 . PMC 7194799. PMID 32360102. https://pubmed.ncbi.nlm.nih.gov/32360102. 
  10. ^ Ramirez, Maria S .; Tolmasky, Marcelo E. (2010-12). “Aminoglycoside modifying enzymes”. Drug Resistance Updates: Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy 13 (6): 151–171. two:10.1016 / j.drup.2010.08.003. ISSN 1532-2084 . PMC 2992599. PMID 20833577. https://pubmed.ncbi.nlm.nih.gov/20833577. 
  11. ^ Krause, Kevin M .; Serio, Alisa W .; Kane, Timothy R .; Connolly, Lynn E. (2016-06). “Aminoglycosides: An Overview” (English). Cold Spring Harbor Perspectives in Medicine 6 (6): a027029. two:10.1101 / cshperspect.a027029. ISSN 2157-1422 . PMC PMC4888811. PMID 27252397. http://perspectivesinmedicine.cshlp.org/lookup/doi/10.1101/cshperspect.a027029. 
  12. ^ a b Vázquez-Laslop, Nora; Mankin, Alexander S. (2018-09). “How Macrolide Antibiotics Work”. Trends in Biochemical Sciences 43 (9): 668–684. two:10.1016 / j.tibs.2018.06.011. ISSN 0968-0004 . PMC 6108949. PMID 30054232. https://pubmed.ncbi.nlm.nih.gov/30054232. 
  13. ^ Brook, Itzhak; Wexler, Hannah M .; Goldstein, Ellie JC (2013-07). “Antianaerobic antimicrobials: spectrum and susceptibility testing”. Clinical Microbiology Reviews 26 (3): 526–546. two:10.1128 / CMR.00086-12. ISSN 1098-6618 . PMC 3719496. PMID 23824372. https://pubmed.ncbi.nlm.nih.gov/23824372. 
  14. ^ Takeshi Nishino "Research on the resistance mechanism of drug-resistant bacteria-especially elucidation of the natural resistance mechanism-"Journal of the Japan Society of Chemotherapy," Vol. 62, No. 2, 2014, pp. 177-191.
  15. ^ Griffin, Michael O .; Fricovsky, Eduardo; Ceballos, Guillermo; Villarreal, Francisco (2010-09). “Tetracyclines: a pleitropic family of compounds with promising therapeutic properties. Review of the literature” (English). American Journal of Physiology-Cell Physiology 299 (3): C539–C548. two:10.1152 / ajpcell.00047.2010. ISSN 0363-6143 . PMC PMC2944325. PMID 20592239. https://www.physiology.org/doi/10.1152/ajpcell.00047.2010. 
  16. ^ Oong, Ginny C .; Tadi, Prasanna (2021). Chloramphenicol. Treasure Island (FL): StatPearls Publishing. PMID 32310426. http://www.ncbi.nlm.nih.gov/books/NBK555966/ 
  17. ^ a b Dalhoff, Axel (2021-02). “Selective toxicity of antibacterial agents-still a valid concept or do we miss chances and ignore risks?”. Infection 49 (1): 29–56. two:10.1007 / s15010-020-01536-y. ISSN 1439-0973 . PMC 7851017. PMID 33367978. https://pubmed.ncbi.nlm.nih.gov/33367978. 
  18. ^ Aviner, Ranen (2020). “The science of puromycin: From studies of ribosome function to applications in biotechnology” (English). Computational and Structural Biotechnology Journal 18: 1074–1083. two:10.1016 / j.csbj.2020.04.014. PMC PMC7229235. PMID 32435426. https://linkinghub.elsevier.com/retrieve/pii/S2001037020300921. 
  19. ^ a b Ishida, Tsuneo (2011-02-28) (Japanese), Antibacterial properties and antibacterial mechanism, Material Life Society, two:10.11338 / mls.23.21, https://doi.org/10.11338/mls.23.21 2021/8/24Browse. 
  20. ^ Andrews, Jennifer M. (2001-07-01). “Determination of minimum inhibitory concentrations” (English). Journal of Antimicrobial Chemotherapy 48 (suppl_1): 5–16. two:10.1093 / jac / 48.suppl_1.5. ISSN 1460-2091 . https://academic.oup.com/jac/article/48/suppl_1/5/2473513. 
  21. ^ a b c Antibiotics Simplified.. Jones & Bartlett Publishers. (2011). Pp. 15–17. ISBN 978-1-4496-1459-1. https://books.google.com/books?id=vIRgA57q414C&q=Antibiotics 
  22. ^ a b c d e f g h i “General principles of antimicrobial therapy”. Mayo Clinic Proceedings 86 (2): 156–167. (February 2011). two:10.4065 / mcp.2010.0639. PMC 3031442. PMID 21282489. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031442/. 
  23. ^ “Cross-sectional study on emergency department management of sepsis”. Hong Kong Medical Journal = Xianggang Yi Xue Za Zhi 24 (6): 571–578. (December 2018). two:10.12809 / hkmj177149. PMID 30429360. 
  24. ^ Rollins KE, Varadhan KK, Neal KR, Lobo DN (October 2016). “An Updated Meta-Analysis of Randomised Controlled Trials”. World Journal of Surgery 40 (10): 2305–2318. two:10.1007 / s00268-016-3561-7. PMID 27199000. 
  25. ^ “Antimicrobial prophylaxis and outpatient management of fever and neutropenia in adults treated for malignancy: American Society of Clinical Oncology clinical practice guideline”. Journal of Clinical Oncology 31 (6): 794–810. (February 2013). two:10.1200 / JCO.2012.45.8661. PMID 23319691. 
  26. ^ “Infection in neutropenic patients with cancer”. Critical Care Clinics 29 (3): 411–441. (July 2013). two:10.1016 / j.ccc.2013.03.002. PMID 23830647. 
  27. ^ Freifeld, Alison G .; Bow, Eric J .; Sepkowitz, Kent A .; Boeckh, Michael J .; Ito, James I .; Mullen, Craig A .; Raad, Issam I .; Rolston, Kenneth V. et al. (2011-02-15). “Clinical Practice Guideline for the Use of Antimicrobial Agents in Neutropenic Patients with Cancer: 2010 Update by the Infectious Diseases Society of America” (English). Clinical Infectious Diseases 52 (4): e56–e93. two:10.1093 / cid / cir073. ISSN 1058-4838 . https://academic.oup.com/cid/article/52/4/e56/382256. 
  28. ^ Keiji Okinaka "About infectious disease measures in patients treated with anticancer drugs"Journal of the Japan Society of Chemotherapy," Vol. 68, No. 1, 2020, pp. 132-142.
  29. ^ Kerantzas, Christopher A .; Jacobs, William R. (2017-05-03). Rubin, Eric J .; Collier, R. John. Eds. “Origins of Combination Therapy for Tuberculosis: Lessons for Future Antimicrobial Development and Application” (English). mBio 8 (2). two:10.1128 / mBio.01586-16. ISSN 2161-2129 . PMC PMC5350467. PMID 28292983. https://journals.asm.org/doi/10.1128/mBio.01586-16. 
  30. ^ a b c Tamma, Pranita D .; Cosgrove, Sara E .; Maragakis, Lisa L. (2012-07). “Combination Therapy for Treatment of Infections with Gram-Negative Bacteria” (English). Clinical Microbiology Reviews 25 (3): 450–470. two:10.1128 / CMR.05041-11. ISSN 0893-8512 . PMC PMC3416487. PMID 22763634. https://journals.asm.org/doi/10.1128/CMR.05041-11. 
  31. ^ a b c d “Antagonism between bacteriostatic and bactericidal antibiotics is prevalent”. Antimicrobial Agents and Chemotherapy 58 (8): 4573–4582. (August 2014). two:10.1128 / AAC.02463-14. PMC 4135978. PMID 24867991. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135978/. 
  32. ^ a b Bollenbach T. (October 2015). “Antimicrobial interactions: mechanisms and implications for drug discovery and resistance evolution”. Current Opinion in Microbiology 27: 1–9. two:10.1016 / j.mib.2015.05.008. PMID 26042389. 
  33. ^ a b Barnhill, Alison E .; Brewer, Matt T .; Carlson, Steve A. (2012-08). “Adverse Effects of Antimicrobials via Predictable or Idiosyncratic Inhibition of Host Mitochondrial Components” (English). Antimicrobial Agents and Chemotherapy 56 (8): 4046–4051. two:10.1128 / AAC.00678-12. ISSN 0066-4804 . PMC PMC3421593. PMID 22615289. https://journals.asm.org/doi/10.1128/AAC.00678-12. 
  34. ^ Shehab, Nadine; Patel, Priti R .; Srinivasan, Arjun; Budnitz, Daniel S. (2008-09-15). “Emergency Department Visits for Antibiotic-Associated Adverse Events” (English). Clinical Infectious Diseases 47 (6): 735–743. two:10.1086/591126. ISSN 1058-4838 . https://academic.oup.com/cid/article-lookup/doi/10.1086/591126. 
  35. ^ Gonçalves, Bruna; Ferreira, Carina; Alves, Carlos Tiago; Henriques, Mariana; Azeredo, Joana; Silva, Sónia (2016-11). “Vulvovaginal candidiasis: Epidemiology, microbiology and risk factors” (English). Critical Reviews in Microbiology 42 (6): 905–927. two:10.3109 / 1040841X.2015.1091805. ISSN 1040-841X. https://www.tandfonline.com/doi/full/10.3109/1040841X.2015.1091805. 
  36. ^ Infectious disease of topic. Basic and clinical of infectious disease of Difficile bacterium. Modern Media October 2010 Issue (Volume 10 Issue 56) (PDF)
  37. ^ Curry J (July 2007, 7). “Pseudomembranous Colitis”. WebMD. 2008/11/17Browse.
  38. ^ Yasuo Suzuki,Medical treatment of antibiotic-induced enteritis Journal of the Japanese Society of Gastroenterology, Vol. 107 (2010) No. 12, p.1897-1904, two:10.11405 / nisshoshi.107.1897
  39. ^ Luciano, JA; Zuckerbraun, BS (December 2014). “Clostridium difficile infection: prevention, treatment, and surgical management ”. The Surgical clinics of North America 94 (6): 1335–1349. two:10.1016 / j.suc.2014.08.006. PMID 25440127. 
  40. ^ “Scientists probe whether It's hard is linked to eating meat ”. CBC News. (October 2006, 10). オ リ ジ ナ ルArchived as of October 2006, 10.. https://web.archive.org/web/20061024034645/http://www.cbc.ca:80/health/story/2006/10/04/cdifficile-meat.html 
  41. ^ a b McEwen, Scott A .; Collignon, Peter J. (2018-04-06). Aarestrup, Frank Møller; Schwarz, Stefan; Shen, Jianzhong et al .. eds. “Antimicrobial Resistance: a One Health Perspective” (English). Microbiology Spectrum 6 (2). two:10.1128 / microbiolspec.ARBA-0009-2017. ISSN 2165-0497 . https://journals.asm.org/doi/10.1128/microbiolspec.ARBA-0009-2017. 
  42. ^ Nobuo Tanaka and Shoshiro Nakamura "Overview of Antibiotics-Chemistry and Biological Activity (3rd Edition Supplement)" p.26 Published October 1984, 10, University of Tokyo Press ISBN-4 13-062020-7
  43. ^ a b Translated by Rob Knight, Takuji Yamada, etc., "Bacteria Make People" p139, TED Books, May 2018, 5,ISBN 978-4-255-01057-1
  44. ^ a b Wegener, Henrik C (2003-10). “Antibiotics in animal feed and their role in resistance development” (English). Current Opinion in Microbiology 6 (5): 439–445. two:10.1016 / j.mib.2003.09.009. https://linkinghub.elsevier.com/retrieve/pii/S1369527403001206. 
  45. ^ "About antibacterial substances used for livestock”. Ministry of Agriculture, Forestry and Fisheries (April 2016, 10). 2016/11/1Browse.
  46. ^ "2019 Summary Report on Antimicrobials Sold or Distributed for Use in Food-Producing Animals | FDA". www.fda.gov. 2021/9/29Browse.
  47. ^ a b c d e f Yoneyama, Hiroshi; Katsumata, Ryoichi (2006-05-23). “Antibiotic Resistance in Bacteria and Its Future for Novel Antibiotic Development” (English). Bioscience, Biotechnology, and Biochemistry 70 (5): 1060–1075. two:10.1271 / bbb.70.1060. ISSN 0916-8451 . https://academic.oup.com/bbb/article/70/5/1060-1075/5953912. 
  48. ^ Lambert, PA (2002). “Mechanisms of antibiotic resistance in Pseudomonas aeruginosa”. Journal of the Royal Society of Medicine 95 Suppl 41: 22–26. ISSN 0141-0768 . PMC 1308633. PMID 12216271. https://pubmed.ncbi.nlm.nih.gov/12216271. 
  49. ^ a b Alekshun, Michael N .; Levy, Stuart B. (2007-03). “Molecular Mechanisms of Antibacterial Multidrug Resistance” (English). Cell 128 (6): 1037–1050. two:10.1016 / j.cell.2007.03.004. https://linkinghub.elsevier.com/retrieve/pii/S009286740700311X. 
  50. ^ Nordmann, Patrice; Poirel, Laurent; Carrër, Amélie; Toleman, Mark A .; Walsh, Timothy R. (2011-02). “How To Detect NDM-1 Producers” (English). Journal of Clinical Microbiology 49 (2): 718–721. two:10.1128 / JCM.01773-10. ISSN 0095-1137 . PMC PMC3043507. PMID 21123531. https://journals.asm.org/doi/10.1128/JCM.01773-10. 
  51. ^ a b Moellering, Robert C. (2010-12-16). “NDM-1 — A Cause for Worldwide Concern”. New England Journal of Medicine 363 (25): 2377–2379. two:10.1056 / NEJMp1011715. ISSN 0028-4793 . PMID 21158655. https://doi.org/10.1056/NEJMp1011715. 
  52. ^ Magiorakos, A.-P .; Srinivasan, A .; Carey, RB; Carmeli, Y .; Falagas, ME; Giske, CG; Harbarth, S .; Hindler, JF et al. (2012-03). “Multidrug-resistant, extensively drug-resistant and pandrug-resistant bacteria: an international expert proposal for interim standard definitions for acquired resistance” (English). Clinical Microbiology and Infection 18 (3): 268–281. two:10.1111 / j.1469-0691.2011.03570.x. https://linkinghub.elsevier.com/retrieve/pii/S1198743X14616323. 
  53. ^ Toshihide, Okajima; Masayuki, Igarashi; Yoko, Eguchi; Ryutaro, Utsumi (2019). "Next-generation antibacterial drug effective against multidrug-resistant bacteria". Chemistry and biology 57 (7): 416–427. two:10.1271 / kagakutoseibutsu.57.416. https://www.jstage.jst.go.jp/article/kagakutoseibutsu/57/7/57_570706/_article/-char/ja/. 
  54. ^ Munita, Jose M .; Arias, Cesar A. (2016-03-25). Kudva, Indira T .; Zhang, Qijing. Eds. “Mechanisms of Antibiotic Resistance” (English). Microbiology Spectrum 4 (2). two:10.1128 / microbiolspec.VMBF-0016-2015. ISSN 2165-0497 . PMC PMC4888801. PMID 27227291. https://journals.asm.org/doi/10.1128/microbiolspec.VMBF-0016-2015. 
  55. ^ Davies, Julian; Davies, Dorothy (2010-09). “Origins and Evolution of Antibiotic Resistance” (English). Microbiology and Molecular Biology Reviews 74 (3): 417–433. two:10.1128 / MMBR.00016-10. ISSN 1092-2172 . PMC PMC2937522. PMID 20805405. https://journals.asm.org/doi/10.1128/MMBR.00016-10. 
  56. ^ Rice, Louis B. (2008-04-15). “Federal Funding for the Study of Antimicrobial Resistance in Nosocomial Pathogens: No ESKAPE” (English). The Journal of Infectious Diseases 197 (8): 1079–1081. two:10.1086/533452. ISSN 0022-1899 . https://academic.oup.com/jid/article-lookup/doi/10.1086/533452. 
  57. ^ Larson E (2007). “Community factors in the development of antibiotic resistance.”. Annu Rev Public Health 28: 435–447. two:10.1146 / annurev.publhealth.28.021406.144020. PMID 17094768. 
  58. ^ CDC --Antibiotic / Antimicrobial Resistance (Report). Center for Disease Control and Prevention. (2009-03-12). http://www.cdc.gov/drugresistance/index.html. 
  59. ^ a b c d e Tackling Wasteful Spending on Health, OECD, (2017-01), two:10.1787 / 9789264266414-en, ISBN 9789264266599 
  60. ^ Sabuncu E, David J, Bernède-Bauduin C et al. (2009). Klugman, Keith P .. ed. “Significant reduction of antibiotic use in the community after a nationwide campaign in France, 2002–2007”. PLoS Med 6 (6): e1000084. two:10.1371 / journal.pmed.1000084. PMC 2683932. PMID 19492093. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2683932/. 
  61. ^ Marino PL (2007). “Antimicrobial therapy”. The ICU book. Hagerstown, MD: Lippincott Williams & Wilkins. P. 817. ISBN 978-0-7817-4802-5 
  62. ^ Paul L. Marino, ICU Book 3rd Edition, Medical Science International, March 2008.ISBN 978-4-89592-500-6. 
  63. ^ Fashner J, Ericson K, Werner S (2012). “Treatment of the common cold in children and adults”. Am Fam Physician 86 (2): 153–159. PMID 22962927. http://www.aafp.org/afp/2012/0715/p153.html. 
  64. ^ Barnett, Michael L .; Linder, Jeffrey A. (2014). “Antibiotic Prescribing for Adults With Acute Bronchitis in the United States, 1996-2010”. JAMA 311 (19): 2020. two:10.1001 / jama.2013.286141. ISSN 0098-7484 . 
  65. ^ CG69: Respiratory tract infections (self-limiting): prescribing antibiotics (Report). National Institute for Health and Care Technology. (2008-07). https://www.nice.org.uk/guidance/cg69/. 
  66. ^ Japan Society of Chemotherapy JAID / JSC Infectious Disease Treatment Guide / Guideline Development CommitteeJAID / JSC Infectious Disease Treatment Guidelines-Respiratory Infections-"Journal of the Japan Society of Chemotherapy," Vol. 62, Japan Society of Chemotherapy, Japan Society of Chemotherapy, January 2014, p. 1.
  67. ^ Tuberculosis Infectious Diseases Division, Health Bureau, Ministry of Health, Labor and Welfare (2017-06) (pdf). Guidance on proper use of antimicrobial agents First edition (Report). Ministry of Health, Labor and Welfare. https://www.mhlw.go.jp/file/06-Seisakujouhou-10900000-Kenkoukyoku/0000166612.pdf 2017/12/10Browse.. 

 

Back to Top
Close