Human tuberculosis (TB), a devastating disease caused by the gram-positive, acid-fast eubacterium Mycobacterium tuberculosis, was classified as a global health emergency by the World Health Organization in 1993. TB remains one of the deadliest infectious diseases with an estimated 1.8 million deaths occurring per year, mainly in the developing world (World Health
Hi dear Dr . Yazi
Due to newly acquired mutations that confer further resistance.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988520/
Good morning Dr.Taif Majid Abdulhussein.
Thanks for your answer
Article Antibiotic resistance mechanisms in M. tuberculosis: an update
Dear dr
The Prolonged regimens using the same few drugs have resulted in poor patient compliance and, as a result, the emergence of strains that are increasingly resistant to the available anti-TB drugs. The careless use of antibiotics has created a selective pressure pushing a rapid evolution of M. tuberculosis, marching from mono-drug resistant to multidrug resistant (MDR), extensively drug resistant (XDR), and eventually totally drug resistant (TDR), through sequential accumulation of resistance mutations.
Hi Dr.
can see this link
https://www.google.com/url?sa=t&source=web&cd=&ved=2ahUKEwikj8T8g7PpAhVInaQKHdTJA8AQFnoECAgQAA&url=https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC1831743%2F&usg=AOvVaw1ihLV3ikURQGlQHmBfOM6b
https://www.google.com/url?sa=t&source=web&rct=j&url=https://academic.oup.com/femsre/article/41/3/354/3089982&ved=2ahUKEwin2s7UnrPpAhUDNOwKHTUxCIEQFjALegQIBRAB&usg=AOvVaw2w3GZGLUTztNnh8KyxV2m0
Dear Dr.
Treatment of tuberculosis (TB) has been a therapeutic challenge because of not only the naturally high resistance level of Mycobacterium tuberculosis to antibiotics but also the newly acquired mutations that confer further resistance. Currently standardized regimens require patients to daily ingest up to four drugs under direct observation of a healthcare worker for a period of 6–9 months. Although they are quite effective in treating drug susceptible TB, these lengthy treatments often lead to patient non-adherence, which catalyzes for the emergence of M. tuberculosisstrains that are increasingly resistant to the few available anti-TB drugs. The rapid evolution of M. tuberculosis, from mono-drug-resistant to multiple drug-resistant, extensively drug-resistant and most recently totally drug-resistant strains, is threatening to make TB once again an untreatable disease if new therapeutic options do not soon become available. Here, I discuss the molecular mechanisms by which M. tuberculosis confers its profound resistance to antibiotics. This knowledge may help in developing novel strategies for weakening drug resistance, thus enhancing the potency of available antibiotics against both drug susceptible and resistant M. tuberculosis strains.
A fundamental problem in the treatment of tuberculosis (TB) is the long duration of therapy required for cure. The recalcitrance of Mycobacterium tuberculosis (MTB) to eradication is thought to result from its achieving a nonreplicating (dormant) state in the host. Because virtually all classes of antibiotics require bacterial replication for their action, the nonreplicating state is thought to render MTB phenotypically resistant to otherwise bactericidal antibiotics.
Tuberculosis drug discovery efforts have been guided by the belief that MTB achieves this nonreplicating state as the result of specific interactions with the host, particularly residence in certain types of tuberculous granulomas. This belief has placed the imperative on understanding and overcoming TB-specific mechanisms by which the nonreplicating state is achieved. Yet, it is also known that many other pathogenic bacteria display phenotypic drug resistance in vivo, accounting for the need for longer durations of antibiotic therapy than would be predicted from the time required for in vitro bacterial killing. Only recently has attention been given to these general mechanisms to explain the need for prolonged TB therapy.
In this article, we consider general versus MTB-specific models of phenotypic antibiotic resistance (see Glossary) in light of our review of human TB treatment data. These data suggest that the duration of therapy required for cure correlates with overall bacterial burden. This correlation between bacterial burden and time to cure is not unique to TB, as it has been found in other bacterial infections, both acute and chronic. High bacterial burden infections, in turn, are associated with an increased frequency of phenotypically drug-resistant bacteria. We argue that understanding and countering general bacterial mechanisms of phenotypic antibiotic resistance may hold the key to reducing the duration of treatment of all recalcitrant bacterial infections, including TB
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988520/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1831743/
BR
Hello dear dr. Yazi .. see attached link please Article Why Is Long-Term Therapy Required to Cure Tuberculosis?
Hi Dr.
https://www.researchgate.net/deref/https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4988520%2F
https://www.researchgate.net/deref/https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4988520%2F
https://www.researchgate.net/deref/https%3A%2F%2Fwww.google.com%2Furl%3Fsa%3Dt%26source%3Dweb%26rct%3Dj%26url%3Dhttps%3A%2F%2Facademic.oup.com%2Ffemsre%2Farticle%2F41%2F3%2F354%2F3089982%26ved%3D2ahUKEwin2s7UnrPpAhUDNOwKHTUxCIEQFjALegQIBRAB%26usg%3DAOvVaw2w3GZGLUTztNnh8KyxV2m0
https://www.researchgate.net/deref/https%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fpmc%2Farticles%2FPMC4988520%2F
Treating drug susceptible TB, these lengthy treatments often lead to patient non-adherence, which catalyzes for the emergence of M. tuberculosis strains that are increasingly resistant to the few available anti-TB drug
Hi Dr.
Antibiotic resistance mechanisms in M. tuberculosis: an update.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988520/
Good morning Dr. Thualfakar Hayder Hasan Abusaiba
Thank you for your answer
Treating drug susceptible TB, these lengthy treatments often lead to patient non-adherence, which catalyzes for the emergence of M. tuberculosis strains that are increasingly resistant to the few available anti-TB drug
… Read more
The length treatments often lead to patient non-adherence, which catalyzes for the emergence of M. tuberculosis strains that are increasingly resistant to the few available anti-TB drugs.
hi dr.
The rapid evolution of M. tuberculosis, from mono-drug-resistant to multiple drug-resistant, extensively drug-resistant and most recently totally drug-resistant strains, is threatening to make TB once again an untreatable disease if new therapeutic options do not soon become available.
Article Antibiotic resistance mechanisms in M. tuberculosis: an update
@Yazi Abdullah Jassim
The fast expansion of M. Tuberculosis, running the gamut from mono-drug-resistant to larger drug-resistant, exhaustively drug-resistant and therefore most briefly absolutely drug-resistant strains, risks making TB an untreatable disease once again if no therapeutic strategies options exist soon.
Dear Dr.
Treatment of tuberculosis (TB) has been a therapeutic challenge because of not only the naturally high resistance level of Mycobacterium tuberculosis to antibiotics but also the newly acquired mutations that confer further resistance. Currently standardized regimens require patients to daily ingest up to four drugs under direct observation of a healthcare worker for a period of 6–9 months. Although they are quite effective in treating drug susceptible TB, these lengthy treatments often lead to patient non-adherence, which catalyzes for the emergence of M. tuberculosisstrains that are increasingly resistant to the few available anti-TB drugs. The rapid evolution of M. tuberculosis, from mono-drug-resistant to multiple drug-resistant, extensively drug-resistant and most recently totally drug-resistant strains, is threatening to make TB once again an untreatable disease if new therapeutic options do not soon become available. Here, I discuss the molecular mechanisms by which M. tuberculosis confers its profound resistance to antibiotics. This knowledge may help in developing novel strategies for weakening drug resistance, thus enhancing the potency of available antibiotics against both drug susceptible and resistant M. tuberculosis strains.
A fundamental problem in the treatment of tuberculosis (TB) is the long duration of therapy required for cure. The recalcitrance of Mycobacterium tuberculosis (MTB) to eradication is thought to result from its achieving a nonreplicating (dormant) state in the host. Because virtually all classes of antibiotics require bacterial replication for their action, the nonreplicating state is thought to render MTB phenotypically resistant to otherwise bactericidal antibiotics.
Tuberculosis drug discovery efforts have been guided by the belief that MTB achieves this nonreplicating state as the result of specific interactions with the host, particularly residence in certain types of tuberculous granulomas. This belief has placed the imperative on understanding and overcoming TB-specific mechanisms by which the nonreplicating state is achieved. Yet, it is also known that many other pathogenic bacteria display phenotypic drug resistance in vivo, accounting for the need for longer durations of antibiotic therapy than would be predicted from the time required for in vitro bacterial killing. Only recently has attention been given to these general mechanisms to explain the need for prolonged TB therapy.
In this article, we consider general versus MTB-specific models of phenotypic antibiotic resistance (see Glossary) in light of our review of human TB treatment data. These data suggest that the duration of therapy required for cure correlates with overall bacterial burden. This correlation between bacterial burden and time to cure is not unique to TB, as it has been found in other bacterial infections, both acute and chronic. High bacterial burden infections, in turn, are associated with an increased frequency of phenotypically drug-resistant bacteria. We argue that understanding and countering general bacterial mechanisms of phenotypic antibiotic resistance may hold the key to reducing the duration of treatment of all recalcitrant bacterial infections, including TB
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988520/
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