INDIA ANNOUNCES TOUGHER RULES FOR OTC ANTIBIOTIC SALES
27 September 2013
The Indian government has tightened regulation of sales of over the
counter (OTC) antibiotics following widespread domestic and global
concern over growing antibiotic resistance in the country.
In late August this year the Indian Ministry of Health and Family
Welfare, through an official notification, brought 24 antibiotics under a
new ‘Schedule H1’ category of drugs, whose sale without a doctor’s
prescription could attract significant penalties. Pharmacists now have
to document details of the patient, the actual drug and the prescriber
in a separate register, subject to regular inspections by drug control
officials.
The drugs specified in Schedule H1, will be labelled with symbol ‘Rx’
and prominently displayed on the packaging in bold red colour with
following warning: “Schedule H1 Drug-Warning -It is dangerous to take
this preparation except in accordance with the medical advice. Not to be
sold by retail without the prescription of a Registered Medical
Practitioner”. The new rules will come in force in early March 2014.
In India, the issue of infections caused by multi-drug resistant
bacteria came to the spotlight with the discovery of the highly
resistant New Delhi Metallo beta lactamase-1 or NDM-1, which was found
on European patient who had been to India in 2009. While the Indian
government initially objected to the resistant bacteria being named
after ‘New Delhi’ the controversy also spurred the government to frame a
new antibiotic policy.
One of the recommendations of the committee set up to frame this
poicy was to regulate the sale of antibiotics by introducing “Schedule
H1” under the Drugs and Cosmetics rules, to regulate sale of
antibiotics.
The official notification of the list of drugs in Schedule H1 was
however held up over the last couple of years due to protests by the All
India Organization of Chemists and Druggists (AIOCD), which has pointed
out that in many rural areas, licenced doctors are scarce or
unavailable, making many drugs inaccessible to rural populations. Others
fear that new regulations will make life-saving drugs scarce, and lead
to increased costs as they will be routed through the gray market.
Another problem with regulation of antibiotics sales is that of poor
implementation. Antibiotics are already listed under Schedule H of the
Indian Drug Control Act, which includes over 536 drugs that cannot be
sold without prescription, but this has had little regulatory effect so
far.
According to the Chennai Declaration, a significant policy statement
made in 2012 by prominent medical professionals and their associations
in India, the problems that India faces in tackling anti-microbial
resistance are multi-factorial. The health infrastructure is very
diverse with uneven standards of hospital infection control or
antibiotic use and across such a diverse country uniform implementation
of restriction of antibiotic sales is a difficult task. In many rural
and remote areas with inaccessible medical facilities, there is hardly
any qualified doctor available to make "prescription only" policy for
sale of antibiotics. Due to the lack of laboratory infrastructure,
collecting and monitoring national data on antimicrobial resistance is a
challenging task.
Keeping these issues in mind the Chennai Declaration had suggested a
practical approach to regulating antibiotic sales that would be
implementable and not just remain on paper. According to it one of the
strategies that the government should consider is to formulate a list of
key antibiotics with strict monitoring on the dispensing of these
drugs. Once the success of the first stage is ensured step- by- step
introduction of other drugs to the restricted list could be tried.
The lastest government notification putting a list of selected
antibiotics for greater regulation seems to have taken up this
recommendation of the Declaration and the next move in this context will
be determined by how well this new approach works in practice.
Reff:http://www.reactgroup.org/news/332/18.html
Biocon launches drug for treating psoriasis
The drug will be about half the price of similar drugs offered by multinationals in the country, according to Biocon Chairman and Managing director Kiran Mazumdar-Shaw.
Indian biotech major Biocon announced on Saturday that it had launched
its first biologic drug for psoriasis, which affects about 10-20 million
Indians. The drug against the disease, which attacks the immune system,
will be about half the price of similar drugs offered by
multi-nationals in the country, said Chairman and Managing Director
Kiran Mazumdar-Shaw.
ALZUMAb, which took the company 10 years to develop, is available in
India at Rs.7,950 a vial. She claimed the drug was the world’s first
“novel” anti-CD6 antibody to treat psoriasis. Ms. Shaw said the cheaper
biologic would enable poorer patients to access a cure for psoriasis.
“Currently, the Indian market for biologics is very small, but the
availability of a cheaper option would expand the size of the market,”
she said.
The company was in talks with foreign companies for “partnerships” to
reach out to global markets. “The value of the global market for
biologics to address psoriasis is valued at more than $30 billion,” she
said. “We will start trials in these markets soon,” she said.
Ms. Shaw said the success of the company, which she attributed to a
large R&D budget, encouraged it to seek remedies for other
autoimmune diseases such as lupus, rheumatoid arthritis and Sjogren’s
disease. Biocon earned revenues of over Rs.2,500 crore in 2012-13. It
spent 10 per cent of overall revenues on R&D, Ms. Shaw said.
Reff:http://www.thehindu.com/business/Industry/biocon-launches-drug-for-treating-psoriasis/article5010115.ece
LeptoScan2 Developed by Dr. Arivudainambi Seenichamy with Proff. Dato Abdul Rani Bhaman,Post Doctoral Researcher, University of Putra Malaysia for leptospirosis it is a disease usually spread by rat urine. Salute for Tamilan Development. Malaysia Press meet was held on 01/0812013.
VIT moves up to 8th position in India Today 2013 ranking
VIT University will reach the top-1.
Silver makes antibiotics thousands of times more effective
Ancient antimicrobial treatment could help to solve modern bacterial resistance.
Silver may help in the fight against drug-resistant bacteria such as Stenotrophomonas maltophiliaby easing large antibiotic molecules through the microbes' outer coating.
COLOURED TRANSMISSION ELECTRON MICROGRAPH BY CFI/PHE/SCIENCE PHOTO LIBRARY
Like werewolves and vampires, bacteria have a weakness: silver. The precious metal has been used to fight infection for thousands of years — Hippocrates first described its antimicrobial properties in 400 bc — but how it works has been a mystery. Now, a team led by James Collins, a biomedical engineer at Boston University in Massachusetts, has described how silver can disrupt bacteria, and shown that the ancient treatment could help to deal with the thoroughly modern scourge of antibiotic resistance. The work is published today in Science Translational Medicine1.
“Resistance is growing, while the number of new antibiotics in development is dropping,” says Collins. “We wanted to find a way to make what we have work better.”
Collins and his team found that silver — in the form of dissolved ions — attacks bacterial cells in two main ways: it makes the cell membrane more permeable, and it interferes with the cell’s metabolism, leading to the overproduction of reactive, and often toxic, oxygen compounds. Both mechanisms could potentially be harnessed to make today’s antibiotics more effective against resistant bacteria, Collins says.
Resistance is futil
Many antibiotics are thought to kill their targets by producing reactive oxygen compounds, and Collins and his team showed that when boosted with a small amount of silver these drugs could kill between 10 and 1,000 times as many bacteria. The increased membrane permeability also allows more antibiotics to enter the bacterial cells, which may overwhelm the resistance mechanisms that rely on shuttling the drug back out.
That disruption to the cell membrane also increased the effectiveness of vancomycin, a large-molecule antibiotic, on Gram-negative bacteria — which have a protective outer coating. Gram-negative bacterial cells can often be impenetrable to antibiotics made of larger molecules.
“It’s not so much a silver bullet; more a silver spoon to help the Gram-negative bacteria take their medicine,” says Collins.
Toxic assets
Vance Fowler, an infectious-disease physician at Duke University in Durham, North Carolina, says the work is “really cool” but sounds a note of caution about the potential toxicity of silver. “It has had a chequered past,” he says.
In the 1990s, for example, a heart valve made by St. Jude Medical, based in St. Paul, Minnesota, included parts covered with a silver coating called Silzone to fight infection. “It did a fine job of preventing infection,” says Fowler. “The problem was that the silver was also toxic to heart tissue.” As a result the valves often leaked2.
Before adding silver to antibiotics, “we’ll have to address the toxicity very carefully”, says Fowler. Ingesting too much silver can also cause argyria, a condition in which the skin turns a blue-grey colour — and the effect is permanent.
Collins says that he and his colleagues saw good results in mice using non-toxic amounts of silver. But, he adds, there are ways to reduce the risk even further. “We’re also encouraging people to look at what features of silver caused the helpful effects, so they can look for non-toxic versions,” he says.
Source: doi:10.1038/nature.2013.13232 http://www.nature.com/news/silver-makes-antibiotics-thousands-of-times-more-effective-1.13232
TITUSVILLE, N.J., Dec. 31, 2012 -- Janssen Therapeutics, Division of Janssen Products, LP, today announced the U.S. Food and Drug Administration (FDA) has granted accelerated approval to SIRTURO™ (bedaquiline) Tablets for the treatment of pulmonary multi-drug resistant tuberculosis (MDR-TB) as part of combination therapy in adults. The accelerated approval is based on the surrogate endpoint of time to sputum culture conversion.
"SIRTURO™ was first discovered in our laboratories more than a decade ago and it is gratifying to see our discovery and development lead to the accelerated approval of the first TB therapy in 40 years with a new mechanism of action. This underscores our commitment as a company to discover, develop and responsibly deliver innovative medicines that address serious unmet medical needs," said Paul Stoffels, M.D., Chief Scientific Officer and Worldwide Chairman, Pharmaceuticals, Johnson & Johnson.
SIRTURO™ inhibits mycobacterial ATP (adenosine 5'‑triphosphate) synthase, an enzyme that is essential for the generation of energy in Mycobacterium tuberculosis.
Image source from-www.healthcarenets.com
SIRTURO™ is a diarylquinoline antimycobacterial drug indicated as part of combination therapy in adults (greater than or equal to 18 years) with pulmonary MDR-TB. Reserve SIRTURO™ for use when an effective treatment regimen cannot otherwise be provided. SIRTURO™ should be administered by directly observed therapy (DOT). This indication is based on analysis of time to sputum culture conversion from two controlled Phase 2 trials in patients with pulmonary MDR-TB. The safety and efficacy of SIRTURO™ for the treatment of latent infection due to Mycobacterium tuberculosis has not been established. The safety and efficacy of SIRTURO™ for the treatment of drug-sensitive TB has not been established. In addition, there are no data on the treatment with SIRTURO™ of extra-pulmonary TB (e.g., central nervous system). Therefore, use of SIRTURO™ in these settings is not recommended.
Read more: FDA Grants Accelerated Approval for SIRTURO™ (bedaquiline) as Part of Combination Therapy to Treat Adults with Pulmonary Multi-Drug Resistant Tuberculosis - FierceBiotech http://www.fiercebiotech.com/press-releases/fda-grants-accelerated-approval-sirturo-bedaquiline-part-combination-therap#ixzz2UBPSzRDT
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Beating Drug-Resistant TB
Reinvestigating a natural antibiotic compound reveals its potential as a tuberculosis drug.
By Ruth Williams | September 19, 2012
An antibiotic produced naturally by common soil bacteria kills Mycobacterium species that cause various human diseases, including tuberculosis (TB), according to a report published Monday (September 17) in EMBO Molecular Medicine. The antibiotic even kills drug-resistant strains that escape current TB treatments.
“I seldom get so tickled when I read a paper,” said William Jacobs, a microbiologist and immunologist at the Albert Einstein College of Medicine in New York, who did not participate in the research. The emergence of multidrug resistant strains of Mycobacterium tuberculosis “is a big problem,” he said. “This could be a godsend.”
Tuberculosis infections are commonly treated with a mixture of antibiotics, including one called isoniazid, which Jacobs described as “the cornerstone of TB therapy.” Unfortunately, the most common drug-resistant strains of M. tuberculosis are isoniazid-resistant, he said.
Many researchers, including Stewart Cole, chair of the microbial pathogenesis department at the École Polytechnique Fédérale de Lausanne in Switzerland, have thus been searching for new M. tuberculosis-killing drugs. “In the past we’ve been working a lot on TB drug discovery using target-based approaches… [but] this has been spectacularly unsuccessful,” said Cole. So instead, he and his colleagues looked back over decades of academic literature searching for reports of natural compounds with M. tuberculosis-killing activity.
They found pyridomycin. First described in the 1950s, the drug was reportedly produced by the bacteria Streptomyces pyridomyceticus and Dactylosporangium fulvum. Surprisingly, little was known about pyridomycin—perhaps, Cole suggested, because isoniazid was discovered around the same time and simply stole the limelight.
Cole’s team grew cultures of D. fulvum bacteria, figured out how to isolate and purify pyridomycin, and then showed that the drug was indeed capable of killing M. tuberculosis, as well as many otherMycobacterium species, in culture.
This indiscriminate Mycobacterium-killing ability is a bonus, said Cole. “One of the problems with isoniazid is that it only works against TB,” he said. “If pyridomycin makes it into the clinic, it could have applications in leprosy or Buruli ulcer or atypical mycobacterial infections that can occur in cystic fibrosis patients.”
The team went on to identify the bactericidal target of pyridomycin—a protein called inhA, which is involved in synthesis of bacterial cell wall components. As it happens, inhA is the same protein targeted by isoniazid, but there is a difference in the two drugs’ mechanisms. While isoniazid is a pro-drug that requires activation by an intracellular enzyme called KatG before it can bind to inhA, pyridomycin binds inhA directly.
This is an important distinction, explained Valerie Mizrahi, director of the Institute of Infectious Disease and Molecular Medicine at Cape Town University, South Africa, who was not involved in the study. The overwhelming majority of drug resistance mutations in M. tuberculosis occur in the KatGgene, she explained, and such mutant strains should not be resistant to pyridomycin. Indeed, the team showed that clinical isolates of isoniazid-resistant M. tuberculosis carrying KatG mutations were killed effectively by pyridomycin. “The efficacy against drug resistant forms of M. tuberculosis is particularly encouraging,” Mizrahi said.
There is, however, much to be done before pyridomycin can be used in the clinic. “We would [need to] test that it works in animal models and that it is safe and doesn’t have any side effects,” said Cole. “That will take a couple of years.”
“It’s a long journey,” agreed Mizrahi, “but the big plus is that they don’t really need to validate inhA as a drug target because inhA is already the most well validated drug target out there… [so] it has got a good head start.”
R. C. Hartkoorn et al., “Towards a new tuberculosis drug: pyridomycin – nature’s isoniazid,”EMBO Molecular Medicine, doi:10.1002/emmm.201201689, 2012
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What is NDM-1
NDM-1, which stands for New Delhi metallo-beta-lactamase-1 is a gene (DNA code) carried by
some bacteria. If a bacteria strain carries the NDM-1 gene it is resistant to nearly all antibiotics, including carbapenem antibiotics - also known as antibiotics of last resort.Carbepenems are the most powerful antibiotics, used as a last resort for many bacterial infections, such as E. coli andKlebsiella. The NDM-1 gene makes the bacterium produce an enzyme which neutralizes the activity of carbepenem antibiotics.
A bacterium carrying the NDM-1 gene is the most powerful superbug around.
Put simply:
- NDM-1(New Delhi metallo-ß-lactamase-1) is the gene (the DNA code) found in some types of bacteria
- This gene makes the bacteria produce an enzyme called a carbapenemase - making carbepenem antibiotics ineffective (as well as virtually all other antibiotics).
- Carbepenem antibiotics are extremely powerful and used to fight highly resistant bacteria (when other antibiotics have not worked).
- There are no current antibiotics to combat NDM-1
- There is no research in the pipeline on drugs to combat NDM-1
- A bacterium with the NDM-1 DNA code has the potential to be resistant to all our current antibiotics, as well as new antibiotics which may come into the market in the near future.
UK doctors say they had only ever seen a few cases which are resistant to carbapenems - and these had not been able to transfer resistance to other bacteria. The fact that NDM-1 can easily transfer to different bacteria strains is very worrying, they say.
Currently (12 August 2010) we know that some strains of bacteria, such as E. coli andKlebsiella pneumoniae carry the NDM-1 gene.
The origin of NDM-1
The gene was discovered by Young and team and was named after New Delhi, the Indian capital. The gene is widespread in India and Pakistan, especially in hospitals.Europeans who have undergone hospitalization in the Indian subcontinent have brought NDM-1 back to Europe. A significant number of Europeans who brought the gene back to Europe had undergone cosmetic surgery in India/Pakistan because it is cheaper there.
How untreatable is this superbug?
So far, doctors in the UK have managed to fight these infections with a combination of several different medications. However, scientists have detected some bacterial strains that are resistant to ALL antibiotics.The only way to currently combat the spread of NDM-1 is through surveillance, prompt identification and isolation of infected patients, disinfecting hospital equipment, and thorough hand-hygiene procedures in hospitals. This is going to be a challenge and will require international cooperation.
NDM-1 is widespread in India and Pakistan, and it has reached Europe, the USA, Canada and Australia.
Alerts in the UK
The Health Protection Agency (HPA), UK has issued an alert to medical professionals. Below is part of the alert:Allowing patterns of human travel and migration, and the many UK residents who receive medical treatment in India, we believe that UK healthcare will be repeatedly challenged by imported producers. These organisms mostly are resistant to ALL antibiotics except polymyxins and, less consistently, tigecycline. The activity of obscure agents (fosfomycin, arbekacin and isepamicin) and novel compounds is under investigation, but none is readily available for therapy. In these circumstances it is vital to detect producers and to prevent their onward transmission.
Actions advised
- Be alert to the increase in carbapenemase-producing Enterobacteriaceae, and the growing importance of NDM -1 enzyme.
- Recognise exposure to healthcare systems in India and Pakistan as additional major risk factors for infection or colonization with multiresistant, carbapenemase-producing Enterobacteriaceae
- Refer ALL carbapenem-resistant Enterobacteriaceae to ARMRL, except (i) Proteus spp. and Morganella spp. With borderline resistance only to imipenem (common in these genera) and (ii)
E. cloacae with intermediate resistance to ertapenem only, as these are generally just derepressed for AmpC. NDM production will be investigated promptly. - Patients infected with producers should be isolated to prevent onward transmission in hospitals; carriage in the patient's faecal flora should be examined for producers of the same or different species; similar screening of close unit contacts should be strongly considered.
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