Extensively Drug-Resistant Tuberculosis
In vitro microbiological characterization of novel cyclic homopentapeptides, CP-101,680 and CP-163,234, for animal health use. (1/49)Two cyclic homopentapeptides, CP-101,680 and CP-163,234 [6a-(3',4'-dichlorophenylamino) analogs of viomycin and capreomycin, respectively], were identified as novel antibacterial agents for the treatment of animal disease, especially for livestock respiratory disease. The in vitro microbiological characterization of both CP-101,680 and CP-163,234 was carried out using their parent compounds, viomycin and capreomycin, as controls. This characterization included antibacterial spectrum, influence of media, inoculum size, pH, EDTA, polymixin B nonapeptide (PMBN), serum, cell-free protein synthesis inhibition, and time-kill kinetics. Our results indicated that the capreomycin analog, CP-163,234, showed slightly improved in vitro potency over the viomycin analog, CP-101,680. Both analogs showed very potent cell-free protein synthesis inhibition activity and were bactericidal against Pasteurella haemolytica, P. multocida and Actinobacillus pleuropneumoniae at the level of 4 times and 8 times MICs. CP-163,234 was bactericidal at the level of 4x and 8x MIC against E. coli, but re-growth was observed after 24 hours incubation at both concentrations of CP-101,680. (+info)
In vitro activity of C-8-methoxy fluoroquinolones against mycobacteria when combined with anti-tuberculosis agents. (2/49)OBJECTIVES: To examine the effect of first-line and second-line anti-tuberculosis agents on the ability of fluoroquinolones to kill mycobacteria. METHODS: A clinical isolate of Mycobacterium tuberculosis and a laboratory strain of Mycobacterium smegmatis were grown in liquid medium and treated with a fluoroquinolone in the presence or absence of anti-tuberculosis agents. Bacterial survival was determined by viable colony counts on agar medium. RESULTS: When moxifloxacin activity was examined in two-drug combinations containing traditional anti-tuberculosis agents, activity was greater than either compound alone with isoniazid, capreomycin and low, but not high, concentrations of rifampicin. Cycloserine contributed no additional activity, and ethambutol interfered with the lethal action of moxifloxacin and gatifloxacin. Experiments with M. smegmatis confirmed that both rifampicin and ethambutol reduce fluoroquinolone lethality. Moreover, ethambutol increased the recovery of fluoroquinolone-resistant mutants newly created by ethyl methanesulphonate treatment. CONCLUSIONS: The intrinsic bactericidal activity of C-8-methoxy fluoroquinolones can be adversely affected by some agents currently used for treatment of tuberculosis. (+info)
Unilamellar vesicles as potential capreomycin sulfate carriers: preparation and physicochemical characterization. (3/49)The aim of this work was to evaluate unilamellar liposomes as new potential capreomycin sulfate (CS) delivery systems for future pulmonary targeting by aerosol administration. Dipalmitoylphosphatidylcholine, hydrogenated phosphatidylcholine, and distearoylphosphatidylcholine were used for liposome preparation. Peptide-membrane interaction was investigated by differential scanning calorimetry (DSC) and attenuated total internal reflection Fourier-transform infrared spectroscopy (ATIR-FTIR). Peptide entrapment, size, and morphology were evaluated by UV spectrophotometry, photocorrelation spectroscopy, and transmission electron microscopy, respectively. Interaction between CS and the outer region of the bilayer was revealed by DSC and ATIR-FTIR. DSPC liposomes showed enhanced interdigitation when the CS molar fraction was increased. Formation of a second phase on the bilayer surface was observed. From kinetic and permeability studies, CS loaded DSPC liposomes resulted more stable if compared to DPPC and HPC over the period of time investigated. The amount of entrapped peptide oscillated between 10% and 13%. Vesicles showed a narrow size distribution, from 138 to 166 nm, and a good morphology. These systems, in particular DSPC liposomes, could represent promising carriers for this peptide. (+info)
Mutation of tlyA confers capreomycin resistance in Mycobacterium tuberculosis. (4/49)Capreomycin, an important drug for the treatment of multidrug-resistant tuberculosis, is a macrocyclic peptide antibiotic produced by Saccharothrix mutabolis subspecies capreolus. The basis of resistance to this drug was investigated by isolating and characterizing capreomycin-resistant strains of Mycobacterium smegmatis and Mycobacterium tuberculosis. Colonies resistant to capreomycin were recovered from a library of transposon-mutagenized M. smegmatis. The transposon insertion site of one mutant was mapped to an open reading frame in the unfinished M. smegmatis genome corresponding to the tlyA gene (Rv1694) in the M. tuberculosis H37Rv genome. In M. smegmatis spontaneous capreomycin-resistant mutants, the tlyA gene was disrupted by one of three different naturally occurring insertion elements. Genomic DNAs from pools of transposon mutants of M. tuberculosis H37Rv were screened by PCR by using primers to the tlyA gene and the transposon to detect mutants with an insertion in the tlyA gene. One capreomycin-resistant mutant was recovered that contained the transposon inserted at base 644 of the tlyA gene. Complementation with the wild-type tlyA gene restored susceptibility to capreomycin in the M. smegmatis and M. tuberculosis tlyA transposon mutants. Mutations were found in the tlyA genes of 28 spontaneous capreomycin-resistant mutants generated from three different M. tuberculosis strains and in the tlyA genes of capreomycin-resistant clinical isolates. In in vitro transcription-translation assays, ribosomes from tlyA mutant but not tlyA(+) strains resist capreomycin inhibition of transcription-translation. Therefore, TlyA appears to affect the ribosome, and mutation of tlyA confers capreomycin resistance. (+info)
Capreomycin is active against non-replicating M. tuberculosis. (5/49)BACKGROUND: Latent tuberculosis infection (LTBI) is affecting one-third of the world population, and activation of LTBI is a substantial source of new cases of tuberculosis. LTBI is caused by tubercle bacilli in a state of non-replicating persistence (NRP), and the goal of this study was to evaluate the activity in vitro of various antimicrobial agents against non-replicating M. tuberculosis. METHODS: To achieve a state of NRP we placed broth cultures of M. tuberculosis (three strains) in anaerobic conditions, and in this model tested all known anti-TB drugs and some other antimicrobial agents (a total of 32 drugs). The potential effect was evaluated by plating samples from broth cultures for determining the number of viable bacteria (CFU/ml) during a prolonged period of cultivation. Besides drug-free controls we used metronidazole for positive controls, the only drug known so far to be effective against tubercle bacilli in anaerobic setting. RESULTS: On a background of non-replicating conditions in drug-free cultures and clear bactericidal effect of metronidazole none of the antimicrobial agents tested produced effect similar to that of metronidazole except capreomycin, which was as bactericidal at the same level as metronidazole. CONCLUSION: The unique ability of capreomycin to be bactericidal in vitro among the anti-TB drugs against non-replicating tubercle bacilli may justify the search for other drugs among peptide antibiotics with similar activity. This phenomenon requires further studies on the mechanism of action of capreomycin, and evaluation of its activity in appropriate animal models. (+info)
Molecular analysis of cross-resistance to capreomycin, kanamycin, amikacin, and viomycin in Mycobacterium tuberculosis. (6/49)Capreomycin, kanamycin, amikacin, and viomycin are drugs that are used to treat multidrug-resistant tuberculosis. Each inhibits translation, and cross-resistance to them is a concern during therapy. A recent study revealed that mutation of the tlyA gene, encoding a putative rRNA methyltransferase, confers capreomycin and viomycin resistance in Mycobacterium tuberculosis bacteria. Mutations in the 16S rRNA gene (rrs) have been associated with resistance to each of the drugs; however, reports of cross-resistance to the drugs have been variable. We investigated the role of rrs mutations in capreomycin resistance and examined the molecular basis of cross-resistance to the four drugs in M. tuberculosis laboratory-generated mutants and clinical isolates. Spontaneous mutants were generated to the drugs singularly and in combination by plating on medium containing one or two drugs. The frequencies of recovery of the mutants on single- and dual-drug plates were consistent with single-step mutations. The rrs genes of all mutants were sequenced, and the tlyA genes were sequenced for mutants selected on capreomycin, viomycin, or both; MICs of all four drugs were determined. Three rrs mutations (A1401G, C1402T, and G1484T) were found, and each was associated with a particular cross-resistance pattern. Similar mutations and cross-resistance patterns were found in drug-resistant clinical isolates. Overall, the data implicate rrs mutations as a molecular basis for resistance to each of the four drugs. Furthermore, the genotypic and phenotypic differences seen in the development of cross-resistance when M. tuberculosis bacteria were exposed to one or two drugs have implications for selection of treatment regimens. (+info)
Capreomycin binds across the ribosomal subunit interface using tlyA-encoded 2'-O-methylations in 16S and 23S rRNAs. (7/49)The cyclic peptide antibiotics capreomycin and viomycin are generally effective against the bacterial pathogen Mycobacterium tuberculosis. However, recent virulent isolates have become resistant by inactivation of their tlyA gene. We show here that tlyA encodes a 2'-O-methyltransferase that modifies nucleotide C1409 in helix 44 of 16S rRNA and nucleotide C1920 in helix 69 of 23S rRNA. Loss of these previously unidentified rRNA methylations confers resistance to capreomycin and viomycin. Many bacterial genera including enterobacteria lack a tlyA gene and the ensuing methylations and are less susceptible than mycobacteria to capreomycin and viomycin. We show that expression of recombinant tlyA in Escherichia coli markedly increases susceptibility to these drugs. When the ribosomal subunits associate during translation, the two tlyA-encoded methylations are brought into close proximity at interbridge B2a. The location of these methylations indicates the binding site and inhibitory mechanism of capreomycin and viomycin at the ribosome subunit interface. (+info)
In Vitro activities of isepamicin, other aminoglycosides, and capreomycin against clinical isolates of rapidly growing mycobacteria in Taiwan. (8/49)The in vitro activities of isepamicin against 117 Mycobacteria abscessus, 48 Mycobacterium fortuitum, and 20 Mycobacterium chelonae isolates were evaluated by a microdilution test. Isepamicin MIC(90)s were < or =16 microg/ml for the three species. Isepamicin was as active as amikacin and kanamycin and more active than tobramycin, capreomycin, gentamicin, and streptomycin. (+info)
Capreomycin is an antibiotic drug that is primarily used to treat tuberculosis (TB) that is resistant to other first-line medications. It belongs to a class of drugs called cyclic polypeptides, which work by inhibiting bacterial protein synthesis. Capreomycin is administered via intramuscular injection and is typically used in combination with other anti-TB drugs as part of a multidrug regimen.
The medical definition of 'Capreomycin' is:
A cyclic polypeptide antibiotic derived from Streptomyces capreolus, used in the treatment of tuberculosis, particularly drug-resistant strains. It inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit and is administered intramuscularly.
Viomycin is an antibiotic that belongs to the class of drugs known as aminoglycosides. It works by binding to bacterial ribosomes and interfering with protein synthesis, leading to bacterial cell death. Viomycin is primarily used to treat tuberculosis and other mycobacterial infections that are resistant to other antibiotics. However, its use is limited due to its potential toxicity to the kidneys and hearing.
Here's a medical definition of Viomycin from Stedman's Medical Dictionary:
"A crystalline, basic polypeptide antibiotic produced by certain strains of Streptomyces floridae var. violaceusniger; used in the treatment of tuberculosis and other mycobacterial infections."
I'm sorry for any confusion, but "enviomycin" doesn't appear to be a recognized term in medical or scientific literature. It's possible that there may be a spelling error or it could be a term specific to a certain context. If you have more information or if there's a different term you meant to ask about, I'd be happy to help further!
Kanamycin is an aminoglycoside antibiotic that is derived from the bacterium Streptomyces kanamyceticus. It works by binding to the 30S subunit of the bacterial ribosome, thereby inhibiting protein synthesis and leading to bacterial cell death. Kanamycin is primarily used to treat serious infections caused by Gram-negative bacteria, such as Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae. It is also used in veterinary medicine to prevent bacterial infections in animals.
Like other aminoglycosides, kanamycin can cause ototoxicity (hearing loss) and nephrotoxicity (kidney damage) with prolonged use or high doses. Therefore, it is important to monitor patients closely for signs of toxicity and adjust the dose accordingly. Kanamycin is not commonly used as a first-line antibiotic due to its potential side effects and the availability of safer alternatives. However, it remains an important option for treating multidrug-resistant bacterial infections.
Antitubercular agents, also known as anti-tuberculosis drugs or simply TB drugs, are a category of medications specifically used for the treatment and prevention of tuberculosis (TB), a bacterial infection caused by Mycobacterium tuberculosis. These drugs target various stages of the bacteria's growth and replication process to eradicate it from the body or prevent its spread.
There are several first-line antitubercular agents, including:
1. Isoniazid (INH): This is a bactericidal drug that inhibits the synthesis of mycolic acids, essential components of the mycobacterial cell wall. It is primarily active against actively growing bacilli.
2. Rifampin (RIF) or Rifampicin: A bactericidal drug that inhibits DNA-dependent RNA polymerase, preventing the transcription of genetic information into mRNA. This results in the interruption of protein synthesis and ultimately leads to the death of the bacteria.
3. Ethambutol (EMB): A bacteriostatic drug that inhibits the arabinosyl transferase enzyme, which is responsible for the synthesis of arabinan, a crucial component of the mycobacterial cell wall. It is primarily active against actively growing bacilli.
4. Pyrazinamide (PZA): A bactericidal drug that inhibits the synthesis of fatty acids and mycolic acids in the mycobacterial cell wall, particularly under acidic conditions. PZA is most effective during the initial phase of treatment when the bacteria are in a dormant or slow-growing state.
These first-line antitubercular agents are often used together in a combination therapy to ensure complete eradication of the bacteria and prevent the development of drug-resistant strains. Treatment duration typically lasts for at least six months, with the initial phase consisting of daily doses of INH, RIF, EMB, and PZA for two months, followed by a continuation phase of INH and RIF for four months.
Second-line antitubercular agents are used when patients have drug-resistant TB or cannot tolerate first-line drugs. These include drugs like aminoglycosides (e.g., streptomycin, amikacin), fluoroquinolones (e.g., ofloxacin, moxifloxacin), and injectable bacteriostatic agents (e.g., capreomycin, ethionamide).
It is essential to closely monitor patients undergoing antitubercular therapy for potential side effects and ensure adherence to the treatment regimen to achieve optimal outcomes and prevent the development of drug-resistant strains.
Amikacin is a type of antibiotic known as an aminoglycoside, which is used to treat various bacterial infections. It works by binding to the 30S subunit of the bacterial ribosome, inhibiting protein synthesis and ultimately leading to bacterial cell death. Amikacin is often used to treat serious infections caused by Gram-negative bacteria, including Pseudomonas aeruginosa, Escherichia coli, and Klebsiella pneumoniae. It may be given intravenously or intramuscularly, depending on the severity and location of the infection. As with all antibiotics, amikacin should be used judiciously to prevent the development of antibiotic resistance.
Antitubercular antibiotics are a class of medications specifically used to treat tuberculosis (TB) and other mycobacterial infections. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis, which can affect various organs, primarily the lungs.
There are several antitubercular antibiotics available, with different mechanisms of action that target the unique cell wall structure and metabolism of mycobacteria. Some commonly prescribed antitubercular antibiotics include:
1. Isoniazid (INH): This is a first-line medication for treating TB. It inhibits the synthesis of mycolic acids, a crucial component of the mycobacterial cell wall. Isoniazid can be bactericidal or bacteriostatic depending on the concentration and duration of treatment.
2. Rifampin (RIF): Also known as rifampicin, this antibiotic inhibits bacterial DNA-dependent RNA polymerase, preventing the transcription of genetic information into mRNA. It is a potent bactericidal agent against mycobacteria and is often used in combination with other antitubercular drugs.
3. Ethambutol (EMB): This antibiotic inhibits the synthesis of arabinogalactan and mycolic acids, both essential components of the mycobacterial cell wall. Ethambutol is primarily bacteriostatic but can be bactericidal at higher concentrations.
4. Pyrazinamide (PZA): This medication is active against dormant or slow-growing mycobacteria, making it an essential component of TB treatment regimens. Its mechanism of action involves the inhibition of fatty acid synthesis and the disruption of bacterial membrane potential.
5. Streptomycin: An aminoglycoside antibiotic that binds to the 30S ribosomal subunit, inhibiting protein synthesis in mycobacteria. It is primarily used as a second-line treatment for drug-resistant TB.
6. Fluoroquinolones: These are a class of antibiotics that inhibit DNA gyrase and topoisomerase IV, essential enzymes involved in bacterial DNA replication. Examples include ciprofloxacin, moxifloxacin, and levofloxacin, which can be used as second-line treatments for drug-resistant TB.
These antitubercular drugs are often used in combination to prevent the development of drug resistance and improve treatment outcomes. The World Health Organization (WHO) recommends a standardized regimen consisting of isoniazid, rifampicin, ethambutol, and pyrazinamide for the initial two months, followed by isoniazid and rifampicin for an additional four to seven months. However, treatment regimens may vary depending on the patient's clinical presentation, drug susceptibility patterns, and local guidelines.
Mycobacteriaceae is a family of gram-positive, aerobic bacteria that are characterized by their high content of mycolic acids in the cell wall. This family includes several medically important genera, most notably Mycobacterium and Mycobacteroides. Many species within this family are environmental organisms, found in soil and water, but some are significant human pathogens. They are known for their ability to resist decolorization by acid after being stained with a basic fuchsin stain, known as acid-fast bacilli (AFB). This property is due to the unique structure of their cell walls, which contain mycolic acids and other lipids that make them resistant to many chemical and physical agents.
Mycobacterium tuberculosis, the causative agent of tuberculosis (TB), is the most well-known pathogen within this family. Other important human pathogens include Mycobacterium leprae (leprosy), Mycobacterium avium complex (MAC) species that can cause pulmonary and disseminated infections, and Mycobacterium abscessus, which can cause various types of skin and soft tissue infections.
Mycobacteriaceae are typically slow-growing organisms, with some species taking weeks to grow in culture. Diagnosis of mycobacterial infections often involves microbiological culture, histopathology, and sometimes molecular techniques such as PCR and gene sequencing. Treatment usually requires a combination of antibiotics that target different components of the bacterial cell wall due to their inherent resistance to many conventional antibiotics.
Extensively Drug-Resistant Tuberculosis (XDR-TB) is a term used to describe a rare, severe form of tuberculosis (TB) that is resistant to the majority of available drugs used to treat TB. This means that the bacteria that cause TB have developed resistance to at least four of the core anti-TB drugs, including isoniazid and rifampin, as well as any fluoroquinolone and at least one of the three injectable second-line drugs (amikacin, capreomycin, or kanamycin).
XDR-TB can be challenging to diagnose and treat due to its resistance to multiple drugs. It is also more likely to cause severe illness, spread from person to person, and result in poor treatment outcomes compared to drug-susceptible TB. XDR-TB is a public health concern, particularly in areas with high rates of TB and limited access to effective treatments.
It's important to note that XDR-TB should not be confused with Multi-Drug Resistant Tuberculosis (MDR-TB), which refers to TB that is resistant to at least isoniazid and rifampin, but not necessarily to the other second-line drugs.
'Mycobacterium tuberculosis' is a species of slow-growing, aerobic, gram-positive bacteria that demonstrates acid-fastness. It is the primary causative agent of tuberculosis (TB) in humans. This bacterium has a complex cell wall rich in lipids, including mycolic acids, which provides a hydrophobic barrier and makes it resistant to many conventional antibiotics. The ability of M. tuberculosis to survive within host macrophages and resist the immune response contributes to its pathogenicity and the difficulty in treating TB infections.
M. tuberculosis is typically transmitted through inhalation of infectious droplets containing the bacteria, which primarily targets the lungs but can spread to other parts of the body (extrapulmonary TB). The infection may result in a spectrum of clinical manifestations, ranging from latent TB infection (LTBI) to active disease. LTBI represents a dormant state where individuals are infected with M. tuberculosis but do not show symptoms and cannot transmit the bacteria. However, they remain at risk of developing active TB throughout their lifetime, especially if their immune system becomes compromised.
Effective prevention and control strategies for TB rely on early detection, treatment, and public health interventions to limit transmission. The current first-line treatments for drug-susceptible TB include a combination of isoniazid, rifampin, ethambutol, and pyrazinamide for at least six months. Multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains of M. tuberculosis present significant challenges in TB control and require more complex treatment regimens.
Multidrug-resistant tuberculosis (MDR-TB) is a form of tuberculosis (TB) infection caused by bacteria that are resistant to at least two of the first-line anti-TB drugs, isoniazid and rifampin. This makes MDR-TB more difficult and expensive to treat, requiring longer treatment durations and the use of second-line medications, which can have more severe side effects.
MDR-TB can occur when there are errors in prescribing or taking anti-TB drugs, or when people with TB do not complete their full course of treatment. It is a significant global health concern, particularly in low- and middle-income countries where TB is more prevalent and resources for diagnosis and treatment may be limited.
MDR-TB can spread from person to person through the air when someone with the infection coughs, speaks, or sneezes. People at higher risk of contracting MDR-TB include those who have been in close contact with someone with MDR-TB, people with weakened immune systems, and healthcare workers who treat TB patients.
Preventing the spread of MDR-TB involves early detection and prompt treatment, as well as infection control measures such as wearing masks, improving ventilation, and separating infected individuals from others. It is also important to ensure that anti-TB drugs are used correctly and that patients complete their full course of treatment to prevent the development of drug-resistant strains.
A ribosome is a complex molecular machine found in all living cells, responsible for protein synthesis. It consists of two subunits: the smaller **ribosomal subunit** and the larger **ribosomal subunit**. These subunits are composed of ribosomal RNA (rRNA) and ribosomal proteins.
The small ribosomal subunit is responsible for decoding messenger RNA (mRNA) during protein synthesis, while the large ribosomal subunit facilitates peptide bond formation between amino acids. In eukaryotic cells, the small ribosomal subunit is composed of one 18S rRNA and approximately 30 ribosomal proteins, whereas the large ribosomal subunit contains three larger rRNAs (5S, 5.8S, and 28S or 25S) and around 45-50 ribosomal proteins.
In prokaryotic cells like bacteria, the small ribosomal subunit consists of a single 16S rRNA and approximately 21 ribosomal proteins, while the large ribosomal subunit contains three rRNAs (5S, 5.8S, and 23S) and around 30-33 ribosomal proteins.
These ribosome subunits come together during protein synthesis to form a functional ribosome, which translates the genetic code present in mRNA into a polypeptide chain (protein).
In the context of medical terminology, "powders" do not have a specific technical definition. However, in a general sense, powders refer to dry, finely ground or pulverized solid substances that can be dispersed in air or liquid mediums. In medicine, powders may include various forms of medications, such as crushed tablets or capsules, which are intended to be taken orally, mixed with liquids, or applied topically. Additionally, certain medical treatments and therapies may involve the use of medicated powders for various purposes, such as drying agents, abrasives, or delivery systems for active ingredients.
Dry powder inhalers (DPIs) are medical devices used to administer medication in the form of a dry powder to the lungs. They are commonly used for treating respiratory conditions such as asthma and chronic obstructive pulmonary disease (COPD).
To use a DPI, the patient places a pre-measured dose of medication into the device and then inhales deeply through the mouthpiece. The force of the inhalation causes the powder to become airborne and disperse into small particles that can be easily inhaled into the lungs.
DPIs offer several advantages over other types of inhalers, such as metered-dose inhalers (MDIs). For example, DPIs do not require the use of a propellant to deliver the medication, which can make them more environmentally friendly and cost-effective. Additionally, because the medication is in powder form, it is less likely to deposit in the mouth and throat, reducing the risk of oral thrush and other side effects.
However, DPIs can be more difficult to use than MDIs, as they require a strong and sustained inhalation to properly disperse the medication. Patients may need to practice using their DPI regularly to ensure that they are able to use it effectively.
Microbial sensitivity tests, also known as antibiotic susceptibility tests (ASTs) or bacterial susceptibility tests, are laboratory procedures used to determine the effectiveness of various antimicrobial agents against specific microorganisms isolated from a patient's infection. These tests help healthcare providers identify which antibiotics will be most effective in treating an infection and which ones should be avoided due to resistance. The results of these tests can guide appropriate antibiotic therapy, minimize the potential for antibiotic resistance, improve clinical outcomes, and reduce unnecessary side effects or toxicity from ineffective antimicrobials.
There are several methods for performing microbial sensitivity tests, including:
1. Disk diffusion method (Kirby-Bauer test): A standardized paper disk containing a predetermined amount of an antibiotic is placed on an agar plate that has been inoculated with the isolated microorganism. After incubation, the zone of inhibition around the disk is measured to determine the susceptibility or resistance of the organism to that particular antibiotic.
2. Broth dilution method: A series of tubes or wells containing decreasing concentrations of an antimicrobial agent are inoculated with a standardized microbial suspension. After incubation, the minimum inhibitory concentration (MIC) is determined by observing the lowest concentration of the antibiotic that prevents visible growth of the organism.
3. Automated systems: These use sophisticated technology to perform both disk diffusion and broth dilution methods automatically, providing rapid and accurate results for a wide range of microorganisms and antimicrobial agents.
The interpretation of microbial sensitivity test results should be done cautiously, considering factors such as the site of infection, pharmacokinetics and pharmacodynamics of the antibiotic, potential toxicity, and local resistance patterns. Regular monitoring of susceptibility patterns and ongoing antimicrobial stewardship programs are essential to ensure optimal use of these tests and to minimize the development of antibiotic resistance.
23S rRNA (cytidine1920-2'-O)-methyltransferase
16S rRNA (cytidine1409-2'-O)-methyltransferase
Extensively drug-resistant tuberculosis
Totally drug-resistant tuberculosis
Health in Bangladesh
North West England
ATC code J04
List of drugs: C-Ca
List of MeSH codes (D04)
List of MeSH codes (D12.644)
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- capreomycin, or kanamycin. (cdc.gov)
- The second-line injectable drugs are amikacin, kanamycin, and capreomycin. (cdc.gov)
- However, the following antituberculosis drugs are contraindicated in pregnant women - Streptomycin, Kanamycin, Amikacin, Capreomycin and Fluoroquinolones (Ciprofloxacin / Ofloxacin). (ndtv.com)
- Extensively drug resistant-tuberculosis is defined as multidrug-resistant tuberculosis that is also resistant to any one of the fluoroquinolones and to at least one of three injectable second-line antibiotics (amikacin, capreomycin or kanamycin). (who.int)
- Extensively drug-resistant (XDR) tuberculosis is defined as disease caused by Mycobacterium tuberculosis with resistance to at least isoniazid and rifampicin, any fluoroquinolone, and at least one of three injectable second-line drugs (amikacin, capreomycin, or kanamycin). (nih.gov)
- MDR-TB that is also resistant to any one of the fluoroquinolones and to at least one of three injectable second-line medicines (amikacin, capreomycin or kanamycin).6 MDR-TB and XDR-TB are principally a result of inadequate or poorly administered treatment regimens. (who.int)
- The latest evidence from individual patient data meta-analyses of 50 observational studies published since 2009 indicates that kanamycin and capreomycin are inferior and should be replaced by amikacin (or streptomycin, if susceptible) or, even better, by oral agents such as bedaquiline [ 13 , 14 ]. (ersjournals.com)
- In this type the bacteria causing tuberculosis is resistant to isoniazid, rifampin, any fluoroquinolone and at least one of three injectable second-line drugs (i.e., amikacin, kanamycin, capreomycin). (centerhears.com)
- It was observed that 2% of rifampin, 6% of isoniazid, 24% of fluoroquinolone and 32% of aminoglycoside/capreomycin resistance in XDR M. tuberculosis strains would be undetected if only these common hot-spot regions were tested. (who.int)
- Capreomycin was discovered from Streptomyces capreolus in 1960. (wikipedia.org)
- Capreomycin is an antibiotic which is given in combination with other antibiotics for the treatment of tuberculosis. (wikipedia.org)
- Capreomycin, an antiphlogistic antibiotic which was produced in the United States in 1960, and be applied in clinic in 1968. (wikipedia.org)
- Capreomycin is an old antibiotic for treatment of pulmonary tuberculosis [ 7 ] with recently increasing interest. (hindawi.com)
- Additional genetic loci need to be tested for detection of mutations conferring fluoroquinolone, aminoglycoside and capreomycin resistance in order to improve molecular diagnosis of regional XDR M. tuberculosis strains. (who.int)
- Yet, the knowledge in this area is fundamentally limited and only a few drugs, notably capreomycin and PA-824, have been shown to be active against non-replicating persistent TB bacilli. (hindawi.com)
- In this study, we performed a new bioinformatics analysis on microarray-based gene expression data obtained from the public domain to explore genes that were differentially induced by drugs between the group of capreomycin and PA-824 and the group of mainly the first-line TB drugs. (hindawi.com)
- Recently, much research effort has been focused on testing capreomycin and PA-824 for TB treatment with emphasis on their unique bactericidal effect on persistent tubercle bacilli. (hindawi.com)
- amphotericin B deoxycholate and capreomycin both increase nephrotoxicity and/or ototoxicity. (medscape.com)
- capreomycin and gentamicin both increase nephrotoxicity and/or ototoxicity. (medscape.com)
- Capreomycin is an injectable broad spectrum antibiotic used in the therapy of drug resistant tuberculosis as a second line agent, always in combination with other antituberculosis drugs. (nih.gov)
- however, their mothers were also exposed to several drugs during pregnancy and during breastfeeding, so the problems cannot necessarily be attributed to capreomycin. (nih.gov)
- 2010) The structures of the anti-tuberculosis antibiotics viomycin and capreomycin bound to the 70S ribosome. (nih.gov)
- capreomycin and neomycin PO both increase nephrotoxicity and/or ototoxicity. (medscape.com)
- capreomycin and carboplatin both increase nephrotoxicity and/or ototoxicity. (medscape.com)
- capreomycin and elvitegravir/cobicistat/emtricitabine/tenofovir DF both increase nephrotoxicity and/or ototoxicity. (medscape.com)
- In 1979, capreomycin was used in the area of antituberculosis by inhibiting the growth of mycobacterium tuberculosis. (wikipedia.org)
- Capreomycin is an antibiotic which is given in combination with other antibiotics for the treatment of tuberculosis. (wikipedia.org)
- Phase I, single-dose, dose-escalating study of inhaled dry powder capreomycin: a new approach to therapy of drug-resistant tuberculosis. (nih.gov)
- Capreomycin is commonly grouped with the aminoglycoside family of medications. (wikipedia.org)
- Some specialists monitor capreomycin concentrations routinely, regardless of renal function. (ladiligenciarural.es)