Scientists at the University of Washington and Kenya Medical Research Institute are working to discern whether antibiotics could help prevent thousands of child deaths from diarrheal disease.
A four-year, $2.5 million grant from the World Health Organization is supporting UW's role in the largest clinical trial to date examining diarrhea-management. It aims to determine potential benefits of antibiotics as well as potential harms, such as antibiotic resistance.
Diarrhea remains a leading cause of death in children, mostly affecting children under 2 years in sub-Saharan Africa and Asia. More than a half-million children under 5 died from diarrheal disease in 2013, according the UW Institute for Health Metrics and Evaluation.
“That children continue to die from diarrhea is unacceptable,” said Patty Pavlinac, UW acting assistant professor of global health and one of the lead researchers. Although interventions have greatly reduced diarrhea deaths attributed to dehydration, "young children with bacterial causes of diarrhea experience other severe consequences, including malnutrition, gastrointestinal dysfunction, and death, which are unaddressed with existing interventions," she said.
Showing posts with label antibiotics. Show all posts
Showing posts with label antibiotics. Show all posts
28 July, 2016
Pneumonia discovery may offer way to boost body's defenses
A molecule being targeted in cancer is also critical for the immune system’s ability to battle pneumonia, researchers at the School of Medicine have determined. The finding may offer a new way for doctors to boost patients’ ability to fight off the life-threatening infection as bacteria become more and more resistant to antibiotics.
“We’re interested in seeing if there are things we an do to strengthen the natural defenses of the host to help them fight the infection more effectively,” said Borna Mehrad, MBBS, of UVA’s Division of Pulmonary and Critical Care Medicine. “Potentially this would be the sort of thing you could do in addition to antibiotics to help patients with severe infections.”
Mysterious role
Mehrad and his team determined that the lack of the cytokine M-CSF (short for macrophage-colony stimulating factor) in infected mice worsened the outcome of bacterial pneumonia: Not having the protein resulted in 10 times more bacteria in the lungs, 1,000 times more bacteria in the blood and spread the infection to the liver, resulting in increased deaths.
Clearly M-CSF has an important role in battling pneumonia, but what exactly does it do? “M-CSF has previously been shown to help make a type of immune cell, called monocytes, so my idea was that if you take it away, infected hosts just stop making monocytes and that’s why they get sick,” Mehrad said, “and it turned out that was completely wrong.”
Instead, the researchers determined, M-CSF helped monocytes survive once they have arrived in the infected tissues. Mehrad credited a PhD student in his lab, Alexandra Bettina, with making key observations that completely changed the course of the research. “As I had expected, when we blocked the action of M-CSF … we saw fewer monocytes in the lung. And I thought, well, there you have it,” Mehrad said. “But what Alexandra did was look at the number of cells in the bone marrow, when they’re made, and the blood, which is how they get to the lung. And she found that, in the absence of M-CSF, the number of monocytes in the bone marrow and blood was completely unaffected … but was dramatically reduced in the lung.”
That meant the original hypothesis was wrong. The cells were being made despite the lack of the cytokine; they just weren’t surviving in the lungs to do their jobs. “To use an analogy, they are like soldiers mobilizing,” Mehrad said. “They’re being made in the right number, they’re arriving in the right number, but when they get there, they’re not very good soldiers.”
But by knowing more about M-CSF, doctors one day may be able to make them very good soldiers indeed. “If you take M-CSF away, the infections get worse, so that raises two important questions about therapy: Would more be better? It may be that during infection, the body is making the right amount of M-CSF and if we add extra, it won’t improve outcomes further,” he said. “The second possibility is that there is room for improvement: in the fight between monocytes and the bacteria, M-CSF may make monocytes live longer and give them an edge. In addition, some people with weakened immunity might not make enough of M-CSF. If that’s the case, you could augment that and improve their ability to fight the infection.”
“We’re interested in seeing if there are things we an do to strengthen the natural defenses of the host to help them fight the infection more effectively,” said Borna Mehrad, MBBS, of UVA’s Division of Pulmonary and Critical Care Medicine. “Potentially this would be the sort of thing you could do in addition to antibiotics to help patients with severe infections.”
Mysterious role
Mehrad and his team determined that the lack of the cytokine M-CSF (short for macrophage-colony stimulating factor) in infected mice worsened the outcome of bacterial pneumonia: Not having the protein resulted in 10 times more bacteria in the lungs, 1,000 times more bacteria in the blood and spread the infection to the liver, resulting in increased deaths.
Clearly M-CSF has an important role in battling pneumonia, but what exactly does it do? “M-CSF has previously been shown to help make a type of immune cell, called monocytes, so my idea was that if you take it away, infected hosts just stop making monocytes and that’s why they get sick,” Mehrad said, “and it turned out that was completely wrong.”
Instead, the researchers determined, M-CSF helped monocytes survive once they have arrived in the infected tissues. Mehrad credited a PhD student in his lab, Alexandra Bettina, with making key observations that completely changed the course of the research. “As I had expected, when we blocked the action of M-CSF … we saw fewer monocytes in the lung. And I thought, well, there you have it,” Mehrad said. “But what Alexandra did was look at the number of cells in the bone marrow, when they’re made, and the blood, which is how they get to the lung. And she found that, in the absence of M-CSF, the number of monocytes in the bone marrow and blood was completely unaffected … but was dramatically reduced in the lung.”
That meant the original hypothesis was wrong. The cells were being made despite the lack of the cytokine; they just weren’t surviving in the lungs to do their jobs. “To use an analogy, they are like soldiers mobilizing,” Mehrad said. “They’re being made in the right number, they’re arriving in the right number, but when they get there, they’re not very good soldiers.”
But by knowing more about M-CSF, doctors one day may be able to make them very good soldiers indeed. “If you take M-CSF away, the infections get worse, so that raises two important questions about therapy: Would more be better? It may be that during infection, the body is making the right amount of M-CSF and if we add extra, it won’t improve outcomes further,” he said. “The second possibility is that there is room for improvement: in the fight between monocytes and the bacteria, M-CSF may make monocytes live longer and give them an edge. In addition, some people with weakened immunity might not make enough of M-CSF. If that’s the case, you could augment that and improve their ability to fight the infection.”
More information can be found from University of Virginia website.
12 May, 2016
Early detection system for catheter infections
Urinary catheters are used in people who have difficulty passing urine naturally and are often used during or after surgery, for patients with enlarged prostates or in some cases to manage incontinence.
100 million urinary catheters are used annually across the globe, but associated infections can be experienced by up to half of patients using catheters long-term and can lead to kidney failure, septicaemia and death.
The research team led by the University of Bath and including scientists from the University of Brighton, has developed a chemical coating that can be applied to the catheter tip, which releases a coloured dye when the urine becomes alkaline due to a bacterial infection.
The prototype system gives a 12 hour warning of infections before they cause blockages, alerting healthcare professionals before an infection takes hold. This avoids the need for treating patients with antibiotics as a precaution, which can increase the worldwide problem of antibiotic resistance.
Dr Toby Jenkins, from the University of Bath’s Department of Chemistry, led the team. He explained: “Catheter infections are such a common problem that currently anyone using a catheter for more than seven days is given a course of antibiotics to prevent infection.
“The coating we’ve developed will give a 12 hour warning before an infection causes a blockage, meaning that only patients with an infection need to be treated with antibiotics.
“This system could therefore not only save lives but also reduce the threat of antibiotic resistance.”
Experiments by the researchers, using a glass bladder infection model, and published in the journal Biosensors and Bioelectronics, show that the dye is released around 12 hours before catheter blockage by the infective bacteria (Proteus mirablis). The system therefore gives an early warning to change the catheter and treat the infection before it causes serious damage.
Scarlet Milo, Annett Charitable Trust PhD scholar at Bath and first author of the paper, added: “When an infection develops, the bacteria converts a chemical called urea in the urine into ammonia, raising the pH of the urine.
“The coating we’ve developed consists of two layers which can be used with existing catheters: the top layer is a pH sensitive polymer which dissolves if the pH rises above 8, indicating infection.
“This exposes the bottom layer of the coating, which is a gel containing a non-toxic dye which is released into the urine drainage bag, turning it bright yellow.”
The researchers are now looking to work with an industry partner to develop the prototype further.
100 million urinary catheters are used annually across the globe, but associated infections can be experienced by up to half of patients using catheters long-term and can lead to kidney failure, septicaemia and death.
The research team led by the University of Bath and including scientists from the University of Brighton, has developed a chemical coating that can be applied to the catheter tip, which releases a coloured dye when the urine becomes alkaline due to a bacterial infection.
The prototype system gives a 12 hour warning of infections before they cause blockages, alerting healthcare professionals before an infection takes hold. This avoids the need for treating patients with antibiotics as a precaution, which can increase the worldwide problem of antibiotic resistance.
Dr Toby Jenkins, from the University of Bath’s Department of Chemistry, led the team. He explained: “Catheter infections are such a common problem that currently anyone using a catheter for more than seven days is given a course of antibiotics to prevent infection.
“The coating we’ve developed will give a 12 hour warning before an infection causes a blockage, meaning that only patients with an infection need to be treated with antibiotics.
“This system could therefore not only save lives but also reduce the threat of antibiotic resistance.”
Experiments by the researchers, using a glass bladder infection model, and published in the journal Biosensors and Bioelectronics, show that the dye is released around 12 hours before catheter blockage by the infective bacteria (Proteus mirablis). The system therefore gives an early warning to change the catheter and treat the infection before it causes serious damage.
Scarlet Milo, Annett Charitable Trust PhD scholar at Bath and first author of the paper, added: “When an infection develops, the bacteria converts a chemical called urea in the urine into ammonia, raising the pH of the urine.
“The coating we’ve developed consists of two layers which can be used with existing catheters: the top layer is a pH sensitive polymer which dissolves if the pH rises above 8, indicating infection.
“This exposes the bottom layer of the coating, which is a gel containing a non-toxic dye which is released into the urine drainage bag, turning it bright yellow.”
The researchers are now looking to work with an industry partner to develop the prototype further.
More information can be found from Bath University website by clicking this link.
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