Antibiotic alternatives: ‘We kind of pride ourselves in my research group of doing the crazy stuff’

As the world loses its upper hand in the antibiotic arms race, it raises the specter of un-treatable infections resulting from routine surgeries. But a Canadian scientist has discovered a surprising source of potential antibiotic options.

Over the past few months, there’s been grim evidence of the march to a post-antibiotic world. Last week, for instance, U.S. researchers said they’d identified what could be the first strain of E. coli resistant to antibiotics considered last-line defences.

Antibiotic resistance happens when bacteria change and become able to withstand the antibiotics used to treat the infections they cause. Overuse and misuse of antibiotics increase the development of resistant bacteria, the World Health Organization says.

Superbug headlines like the E. coli one reflect the need to develop new ways to kill bugs that develop resistance to antibiotics.

That’s where McMaster University scientist Eric Brown’s research comes in.

His team screens thousands of chemicals that are already used to treat other diseases to see if any will work against bacteria.

“We kind of pride ourselves in my research group of doing the crazy stuff. Screens that won’t be done say in a pharmaceutical setting.”

No new antibiotics in years

Since the early 1990s, there’s been little progress in the search for new antibiotics. A new one hasn’t been developed in years, partly because most obvious ones have already been found.

Another big reason is money, according to Dr. Anthony Fauci, head of the U.S. National Institute of Allergy and Infectious Diseases.

“Antibiotic development is not a big economic profit-making ticket item for pharmaceutical companies because antibiotics, unlike other drugs, are not used by everyone, every day,” Fauci said. “It is unusual for an antibiotic to be a blockbuster.”

Scientists at Brown’s lab take an alternative approach. The challenge is bacteria have multiple layers of defences that scientists need to dismantle.

“It’s sort of like you’re sitting on a four-legged stool, and if you remove one leg, the stool can still function as a stool with three legs,” Brown said. “But if you take away two, you’re going to land on your butt. That’s the sort of synergy we’re looking for in terms of looking for say two compounds that will act against a bacterial pathogen.”

He’s made some surprising discoveries: anti-diarrheal medication Imodium and anti-convulsant drug lamotrigine also seem to kill bacteria.

‘It’s getting worse’

Fortunately at this point, not every microbe can resist every drug. The concern is how many resistance genes float around for bacteria to swap, giving them the ability to disarm drugs. It means that if someone is infected with one, doctors are forced to try alternatives, no matter how toxic or expensive, to see if anything works.

Fauci says Canadians and Americans may not appreciate the seriousness of microbes with resistance to multiple antibiotics.

“It’s worse and it’s getting worse,” Fauci said. “That is one of the things we are concerned about.”

Former NFL star Daniel Fells is a case in point. Fells got a superbug infection in his foot after a simple injection of cortisone for an injured ankle. After almost a dozen surgeries to remove the infected tissue, the superbug ended his football career.

It’s a sign of how routine medical care is getting increasingly complicated as we try to stay a step ahead of the microbes.

Minor surgeries are already becoming more dangerous. Last year, researchers writing in The Lancet Infectious Diseases warned that between 39 and 50 per cent of bugs that cause infections in surgical sites are already resistant to standard antibiotics.

Chemotherapy will also be increasingly risky, the authors said. More than a quarter of pathogens that cause chemo-related infections are resistant.

Sense of urgency

The findings add a sense of urgency to Brown’s work in Hamilton, Ont.

“Think about just about any inpatient surgery that you can imagine. Something we take so for granted like a caesarean section. The risk of infection would suddenly go through the roof as a result of not having antibiotics to treat infection,” Brown said.

The advantage of repurposing old drugs to fight bacteria is they’ve already been tested and proven to be safe.

The pharmaceutical industry typically takes 15 years to develop a drug.

“I think though that we’ve got a chance to shorten the path to the clinic by starting with a lead that is already a drug,” Brown said.

They still need to be modified and tested as antibiotics, but in the face of growing resistance, repurposing could be part of the multifaceted solution, Fauci says, alongside more judicious use.

Source: CBC news

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Antibacterial Ingredients in Indoor Dust Could Contribute to Antibiotic Resistance

To better understand the problem of antibiotic-resistant bacteria, researchers have been piecing together its contributing factors. Now in the ACS journal Environmental Science & Technology, scientists report for the first time a link between antimicrobial substances such as triclosan in indoor dust and levels of antibiotic-resistance genes, which can transfer from one bacterial cell to another.

The overuse of antibiotics in both humans and livestock has largely been blamed for the rise in drug resistance. The ubiquity of antimicrobials in hand soaps, cosmetics and other personal care products that ultimately rinse down the drain and into wastewater has also contributed. Erica Hartmann and colleagues wanted to see whether their presence in indoor dust might play a role, too.

The researchers analyzed dust samples from an indoor athletic and educational facility and found six links between antimicrobial chemicals and antibiotic-resistance genes in microbes. For instance, dust samples with higher amounts of triclosan also had higher levels of a gene that’s been implicated in bacterial resistance to multiple drugs. Although the median concentration of triclosan in indoor dust was small — much lower than amounts used in toothpaste, for example — the researchers say their findings demonstrate the need to further investigate the role of antimicrobials in dust in the rise of antibiotic resistance.

The authors acknowledge funding from the Alfred P. Sloan Foundation, the National Science Foundation and the National Institutes of Environmental Health Sciences.

Source: American Chemical Society

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Pets and Children are a Potential Source of Clostridium difficile in the Community

Household transmission of Clostridium difficile to pets and children may be a source of community-associated C. difficile infections according to findings from a new study published today in Infection Control & Hospital Epidemiology. The study found that patients with this bacteria can colonize or infect household contacts following or during treatment for an infection.

“C. difficile is primarily a healthcare-associated infection, but we now know that it can spread beyond the hospital,” said Vivian Loo, MD, MSc, a lead author of the study and an infectious disease specialist and medical microbiologist at the McGill University Health Centre (MUHC), investigator at the Research Institute of the MUHC, and professor at McGill University. “These infections, causing diarrhea and inflammation of the colon, can be serious, so it is important that everyone follows simple hygienic practices, like hand-washing with soap and water, even in your own home.”

The prospective study included 51 patients treated for C. difficile infection in hospital or outpatient settings, along with members of their households, and pets. Researchers visited each household monthly, collecting stool samples or rectal swabs at each visit. The samples were tested for C. difficile, to determine whether those who tested negative for the bacterium initially eventually became infected or colonized. Colonized individuals with C. difficile have the bacteria present in their stool, but without diarrhea.

The results revealed 13.4 percent of the 67 human household contacts had C. difficile isolated from their stool or rectal samples. One adult household member had diarrhea and the remaining 8 were asymptomatically colonized. Sixty-six percent of those colonized were younger than five years old, including five in diapers.

More than a quarter (26.7 percent) of the 15 domestic pets were asymptomatic carriers of the bacterium, as well. When analyzing the bacteria strains from pets, researchers found that the strains carried by the pets and by their human contacts were indistinguishable or closely related, suggesting inter-species transmission. The study concluded that pets can be reservoirs for re-infection or transmission of C. difficile within the household.

“Our research suggests that household transmission from patients with C. difficile infection could be responsible for a bacterial reservoir for community-associated cases,” said Loo.

Reference: Loo V, Brassard P and Miller M. Household Transmission of Clostridium difficile to Family Members and Domestic Pets. Web (Aug. 8, 2016).

Source: Society for Healthcare Epidemiology of America

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New Zika Clone Could be New Model for Developing Vaccine

Stopping the explosive spread of Zika virus – which can lead to birth defects in babies born to infected mothers – depends on genetic insights gleaned through new tools and models. Researchers at the National Institutes of Health recently cloned an epidemic strain of the virus, creating a model that can help biologists develop and test strategies for stopping the pandemic.

In the latest issue of mBio, the researchers reported that the cloned virus replicated successfully in multiple cell lines, including placental and brain cells – tissue particularly vulnerable to damage from Zika. The clone will be used for the development of a live but attenuated vaccine.

“Our goal is to create long-term immunity after one short immunization,” says study leader and molecular biologist Alexander Pletnev, at the National Institute of Health’s National Institute of Allergy and Infectious Diseases in Bethesda, Md.

The goal of Pletnev’s group is to create a live, attenuated vaccine similar to the ones used in humans against other harmful viruses like polio, yellow fever, and Japanese encephalitis. Following up on their lab studies, Pletnev and his collaborators recently began mouse studies of the cloned virus. Pletnev says he invites other researchers to use his lab’s ZIKV clone to investigate and ultimately stop the harm caused by Zika.

The virus was first identified nearly 70 years ago in Uganda, but for decades it circulated only in a small geographic area in equatorial Africa and Asia, and mostly among primates. The current epidemic began in early 2015 in Brazil, and since then has spread throughout South and Central America. In February 2016, the World Health Organization declared the pandemic a public health emergency. Five months later, the US Centers for Disease Control and Prevention reported the first case of mosquito-borne infection in the US in residents of Florida, in a neighborhood near Miami. (The virus can also be transmitted through sex.)

The biological behavior of viruses is often unpredictable, which makes it difficult for scientists to figure out how to stop them, says Pletnev. Zika belongs to the Flavivirus group of viruses, which also includes West Nile, dengue, and yellow fever. Viruses in this family each have a single strand of RNA, but they’re notoriously difficult to manipulate and clone. With the tools of reverse genetics, biologists can study single-stranded RNA by using viral complementary DNA, or cDNA. Flaviviruses, however, are often toxic to their bacterial hosts, and biologists have pursued a variety of ways around the problem.

Pletnev and his group, including researchers from the University of Texas and the US Food and Drug Administration, began with a viral strain collected from an infected, febrile patient in Brazil in 2015. To reduce toxicity and increase the stability of the ZIKV cDNA clone during growth in Escherichia coli bacteria, they added introns – or specific nucleotide sequences – to the full viral cDNA genome. High-throughput sequencing revealed that the virus derived from the cDNA clone had less genetic diversity than its wild-type parent strain, and subsequent experiments showed that the clone was attenuated, compared to its parent.

The researchers made a few more genetic tweaks to customize their clone to grow in Vero cells – a line derived the kidneys of African green monkeys, commonly used in human vaccine manufacture.

In addition to their work on Zika, which began in early 2016, Pletnev’s group has worked extensively on other Flaviviruses. They produced a vaccine for West Nile virus, currently in clinical trials, and have worked on developing vaccines against St. Louis and Japanese encephalitis. Their current work on Zika was funded by the Division of Intramural Research Program of the National Institute of Allergy and Infectious Diseases, National Institutes of Health.

Source: American Society for Microbiology

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Time of Day Influences Our Susceptibility to Infection, Study Finds

We are more susceptible to infection at certain times of the day as our body clock affects the ability of viruses to replicate and spread between cells, suggests new research from the University of Cambridge. The findings, published today in the Proceedings of the National Academy of Sciences, may help explain why shift workers, whose body clocks are routinely disrupted, are more prone to health problems, including infections and chronic disease.

When a virus enters our body, it hijacks the machinery and resources in our cells to help it replicate and spread throughout the body. However, the resources on offer fluctuate throughout the day, partly in response to our circadian rhythms – in effect, our body clock. Circadian rhythms control many aspects of our physiology and bodily functions – from our sleep patterns to body temperature, and from our immune systems to the release of hormones. These cycles are controlled by a number of genes, including Bmal1 and Clock.

To test whether our circadian rhythms affect susceptibility to, or progression of, infection, researchers at the Wellcome Trust-Medical Research Council Institute of Metabolic Science, University of Cambridge, compared normal ‘wild type’ mice infected with herpes virus at different times of the day, measuring levels of virus infection and spread. The mice lived in a controlled environment where 12 hours were in daylight and 12 hours were dark.

The researchers found that virus replication in those mice infected at the very start of the day – equivalent to sunrise, when these nocturnal animals start their resting phase – was ten times greater than in mice infected 10 hours into the day, when they are transitioning to their active phase. When the researchers repeated the experiment in mice lacking Bmal1, they found high levels of virus replication regardless of the time of infection.

“The time of day of infection can have a major influence on how susceptible we are to the disease, or at least on the viral replication, meaning that infection at the wrong time of day could cause a much more severe acute infection,” explains professor Akhilesh Reddy, the study’s senior author. “This is consistent with recent studies which have shown that the time of day that the influenza vaccine is administered can influence how effectively it works.”

In addition, the researchers found similar time-of-day variation in virus replication in individual cell cultures, without influence from our immune system. Abolishing cellular circadian rhythms increased both herpes and influenza A virus infection, a dissimilar type of virus – known as an RNA virus – that infects and replicates in a very different way to herpes.

Dr. Rachel Edgar, the first author, adds: “Each cell in the body has a biological clock that allows them to keep track of time and anticipate daily changes in our environment. Our results suggest that the clock in every cell determines how successfully a virus replicates. When we disrupted the body clock in either cells or mice, we found that the timing of infection no longer mattered – viral replication was always high. This indicates that shift workers, who work some nights and rest some nights and so have a disrupted body clock, will be more susceptible to viral diseases. If so, then they could be prime candidates for receiving the annual flu vaccines.”

As well as its daily cycle of activity, Bmal1 also undergoes seasonal variation, being less active in the winter months and increasing in summer. The researchers speculate that this may help explain why diseases such as influenza are more likely to spread through populations during winter.

Using cell cultures, the researchers also found that herpes viruses manipulate the molecular ‘clockwork’ that controls our circadian rhythms, helping the viruses to progress. This is not the first time that pathogens have been seen to ‘game’ our body clocks: the malaria parasite, for example, is known to synchronise its replication cycle with the host’s circadian rhythm, producing a more successful infection.

“Given that our body clocks appear to play a role in defending us from invading pathogens, their molecular machinery may offer a new, universal drug target to help fight infection,” adds Reddy.

The research was mostly funded by the Wellcome Trust and the European Research Council.

Reference: Edgar, RS et al. Cell autonomous regulation of herpes and influenza virus infection by the circadian clock. PNAS; e-pub 15 Aug 2016; DOI: 10.1073/pnas.1601895113

Source: University of Cambridge

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Clinical Trial Will Examine Investigational Vaccine Against Mosquito-Borne Illness

As world leaders increasingly recognize the Zika virus as an international public health threat, the Center for Vaccine Development at the University of Maryland School of Medicine’s Institute for Global Health has been chosen as one of three study sites in a human safety trial of a new Zika vaccine. The early-stage study will evaluate the experimental vaccine’s safety and ability to generate an immune system response in participants.

The selection of the University of Maryland School of Medicine (UM SOM) marks the second time in two years that the School’s internationally-acclaimed Center for Vaccine Development (CVD) has been tapped to lead vaccine development efforts in the midst of a growing crisis. In 2014, the UM SOM was the only U.S. medical school asked to join an unprecedented international consortium formed by the World Health Organization. The Consortium resulted in the development of one of the first effective vaccines for Ebola. Recently, the CVD received FDA approval for the first vaccine approved in the U.S. for protection against Cholera. In July, the CVD began malaria vaccine trials in Burkina Faso.

The Zika vaccine trial, which will involve at least at least 80 volunteers at the sites in the United States, is being undertaken by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health (NIH). The early-stage study will evaluate the experimental vaccine’s safety and ability to generate an immune system response against Zika.

Scientists at NIAID’s Vaccine Research Center (VRC) developed the investigational vaccine—called the NIAID Zika virus investigational DNA vaccine—earlier this year.

Leading the effort at the UM SOM’s CVD is the Center’s director Kathleen Neuzil, MD, MPH, professor of medicine and deputy director of the UM SOM’s Institute for Global Health, who has extensive experience with vaccine research policy and introduction.

“As we learn more about the threat that Zika poses, and as it spreads further and further, the need for a vaccine becomes greater,” Neuzil said. “Our center is gratified that we have been chosen by NIH to be part of this extremely important collaborative effort.”

The study is part of the U.S. government response to the ongoing outbreak of Zika virus in the Americas. According to the Centers for Disease Control and Prevention (CDC), more than 50 countries and territories have active Zika virus transmission. In the United States and its territories, more than 6,400 Zika cases have been reported. Although Zika infections are usually asymptomatic, some people experience mild illness lasting about a week. However, Zika virus infection during pregnancy can cause a serious birth defect called microcephaly, as well as other severe fetal defects of the brain and other organs. There are no vaccines or specific therapeutics to prevent or treat Zika virus disease.

The NIAID Zika virus investigational DNA vaccine approach is similar to that used for another investigational vaccine developed by NIAID for West Nile virus. That vaccine candidate was found to be safe and induced an immune response when tested in a Phase 1 clinical trial.

The investigational Zika vaccine includes a small, circular piece of DNA—called a plasmid—that scientists engineered to contain genes that code for proteins of the Zika virus. When the vaccine is injected into the arm muscle, cells read the genes and make Zika virus proteins, which self-assemble into virus-like particles. The body mounts an immune response to these particles, including neutralizing antibodies and T cells. DNA vaccines do not contain infectious material—so they cannot cause a vaccinated individual to become infected with Zika—and have been shown to be safe in previous clinical trials for other diseases.

The Phase 1 clinical trial, called VRC 319, is led by Julie E. Ledgerwood, DO, chief of the VRC’s clinical trials program. Volunteers will be divided randomly into four study groups of 20 people each. After enrollment, all participants will receive a vaccination at their first visit via a needle-free injector that pushes the vaccine fluid into the arm muscle. Half of the participants will receive one additional vaccination eight weeks or 12 weeks later. The remaining participants will receive two additional vaccinations: one group of 20 participants will receive a second vaccine at week four and a third at week eight; the other group of 20 participants will receive a second vaccine at week four and a third at week 20. All participants will receive the same dose at each vaccination.

Following each vaccination, participants will remain at the study site for observation for a minimum of 30 minutes so clinicians can monitor for any adverse reactions. Participants will receive a diary card to use at home to record their temperature and any symptoms for seven days following each vaccination.

All participants will return for follow-up visits within a 44-week time period after the first vaccination so investigators can monitor their health to determine if the vaccine is safe. The study team will review patient data daily and weekly to monitor safety. A Protocol Safety Review Team will also conduct formal interim safety reviews.

At follow-up visits, investigators will also take blood samples for laboratory testing to measure the immune response to the vaccine. Participants will be asked to return for two follow-up visits at 18 months and two years following the initial vaccination so investigators can obtain additional blood samples to assess the durability of the immune response.

The other two study sites are Emory University in Atlanta and NIH in Bethesda, Md. Initial safety and immunogenicity data from the Phase 1 trial are expected by the end of 2016. If results show a favorable safety profile and immune response, NIAID plans to initiate a Phase 2 trial in Zika-endemic countries in early 2017.

“Zika is an urgent international public health threat, including, now, in parts of our own country,” said UM SOM Dean E. Albert Reece, MD, PhD, MBA, who is also vice president for medical affairs at the University of Maryland and the John Z. and the Akiko K. Bowers Distinguished Professor. “It is gratifying to see the University of Maryland’s Center for Vaccine Development continue to be involved on the front lines of addressing these global threats, as we have done with Ebola and other infectious diseases.”

Source: University of Maryland School of Medicine

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Glucose Transporters Blocked in Bacterial Meningitis

Escherichia coli K1 (E. coli K1) continues to be a major threat to the health of young infants. Affecting the central nervous system, it causes neonatal meningitis by multiplying in immune cells, such as macrophages, and then disseminating into the bloodstream

Meningitis can be caused by bacterial, fungal or viral pathogens. One hallmark of bacterial meningitis is reduced glucose levels in the cerebrospinal fluid (CSF) of patients, which allows a physician to quickly begin appropriate antibiotic treatment.

The reason for the reduced glucose levels associated with bacterial meningitis was believed to be the need for glucose as fuel by infiltrating immune cells in response to infection. However, the possibility that the bacteria itself could manipulate glucose concentrations in the brain had not been explored before now.

Scientists at the Saban Research Institute of Children’s Hospital Los Angeles (CHLA) report that glucose transporters, which transfer glucose from the blood to the brain, are inhibited by E. coli K1 during meningitis.

“We found that expression of glucose transporters is completely shut down by bacteria, leaving insufficient fuel for the immune cells to fight off the infection,” said the study’s first author, Subramanian Krishnan, PhD, of the Division of Infectious Diseases at CHLA.

Specifically, the study – reported online in The Journal of Infectious Diseases – shows that E. coli K1 modulates the protein peroxisome proliferator-activated receptor-gamma (PPAR-γ) and glucose transporter-1 (GLUT-1) levels at the blood-brain barrier in human brain microvascular endothelial cells. This causes inhibition of glucose uptake and the disruption of the blood-brain barrier integrity.

The suppression of PPAR-γ and GLUT-1 levels in mouse models of bacterial meningitis caused extensive neurological effects. The researchers showed that a two-day treatment regimen with partial or selective PPAR-γ agonists (Telmisartan and Rosiglitazone – both FDA-approved drugs) ameliorated the pathological outcomes of infection in mice by inducing expression of glucose transporters.

“Modulation of PPAR-γ and GLUT-1 levels may boost the immune system to fight infection,” said principal investigator Prasadarao V. Nemani, PhD of CHLA and the Keck School of Medicine of the University of Southern California. “Our findings could lead to a novel way of treating children with meningitis and reducing long-term neurological problems.”

Additional contributors to the study include Alexander C. Chang, PhD of CHLA and professor Brian M. Stoltz of the California Institute of Technology. This work was supported by funds from NIAID (AI40567) and NICHD (NS73115).

Source: Childrens Hospital Los Angeles


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Could Yellow Fever Virus Cause a Zika-like Epidemic in the Americas

Yellow fever virus (YFV), a close relative of Zika virus and transmitted by the same type of mosquito, is the cause of an often-fatal viral hemorrhagic fever and could spread via air travel from endemic areas in Africa to cause international epidemics. The recent reemergence and spread of YFV in Africa and Asia and the dire shortage of YFV vaccine have called attention to the potential public health threat of yellow fever and the need for specific measures to prevent infection and control spread of the virus and its mosquito carrier. These measures are clearly presented in a short communication and accompanying editorial published in Vector-Borne and Zoonotic Diseases, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers, and are available free on the Journal website until Aug. 26, 2016.

In the article “Yellow Fever Remains a Potential Threat to Public Health,” Pedro Vasconcelos, Ministry of Health, Ananindeua, Brazil, and Thomas Monath, NewLink Genetics Corp., state that urban epidemics caused by the spread of Aedes aegypti mosquitoes are currently of great concern due mainly to increasing urbanization, climate change, and air travel, which has put more than 130 countries infested with the mosquito and more than 4 billion people at risk of yellow fever. The authors describe the most recent YFV epidemic in Angola and the reasons for the lack of sufficient vaccine stockpiles. They propose actions to increase vaccine availability and the need for new approaches to combat Aedes aegypti mosquitoes, especially in urban environments.

“As we have recently seen with West Nile, chikungunya, and Zika viruses, vector-borne and zoonotic diseases continue to be a significant and unpredictable threat to mankind,” says Stephen Higgs, PhD, editor-in-chief of Vector-Borne and Zoonotic Diseases, and director of the Biosecurity Research Institute at Kansas State University. “Despite studies of yellow fever that span over more than 100 years, we still lack critical understanding and resources to combat these diseases. The number of cases of yellow fever in several African countries continues to increase despite a major vaccination campaign. We are also seeing travel-related cases in the People’s Republic of China. Elsewhere, yellow fever cases have been reported in Brazil, Chad, Colombia, Ghana, Guinea and Peru.”

Source: Mary Ann Liebert, Inc./Genetic Engineering News

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Public Health Officials Investigating Unique Case of Zika in Utah

Utah health officials confirmed today a new case of Zika in Utah and have launched an investigation to determine how the person became infected. The new case is a family contact who helped care for the individual who died from unknown causes and who had been infected with Zika after traveling to an area with Zika.

Laboratories at the Centers for Disease Control and Prevention and in Utah confirmed Zika infection in both Utah residents. A CDC team is in Utah to help with the investigation.

The new case is the eighth Utah resident to be diagnosed with Zika. Based on what is known now, the person has not recently traveled to an area with Zika and has not had sex with someone who is infected with Zika or who has traveled to an area with Zika. In addition, there is no evidence at this time that mosquitoes that commonly spread Zika (aedes species) virus are in Utah.

The investigation is focused on determining how the eighth case became infected after having contact with the deceased patient who had a uniquely high amount of virus in the blood.

“Our knowledge of this virus continues to evolve and our investigation is expected to help us better understand how this individual became infected,” said Dr. Angela Dunn, deputy state epidemiologist at the Utah Department of Health (UDOH). “Based on what we know so far about this case, there is no evidence that there is any risk of Zika virus transmission among the general public in Utah.”

Public health investigators are interviewing the person and family contacts to learn more about the types of contact they had with deceased patient. They are also collecting samples for testing from family members and others who had contact with the deceased patient while they were ill and are working in the communities where the two cases lived to trap and test mosquitoes.

“We’re doing our part as public health officials to learn more about the virus and about this specific case,” said Gary Edwards, executive director of the SLCOHD. “In the meantime, the public, and especially pregnant women, should continue to take recommended steps to protect themselves from Zika virus.”

Source: Utah Department of Health

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Discovery of a New Defense System Against Microbial Pathogens

Antibodies play an important role in host defense against microbial pathogens. However, microbial pathogens seem to have acquired a protease that destroys antibodies in order to evade host immune system. On the other hand, the host immune system appears to have acquired an immune activating receptor, LILRA2, that specifically recognizes microbially cleaved antibodies. Courtesy of Osaka University

For the first time in the world, a group of researchers discovered a human immune receptor, which detects the invasion of pathogenic microorganisms. They thereby succeeded in identifying a so far unknown host defense mechanism. These results will contribute to future developments in the treatment and prevention of infectious diseases.

Infectious diseases are a serious concern for societies around the world and continue to be a major cause of death. They are caused by pathogenic microorganisms that fight back against the host’s biological defense system by producing a variety of proteins. However, the various mechanisms of this biological defense system are yet to be fully understood. Assistant professor Kouyuki Hirayasu and professor Hisashi Arase as well as their research group at the Immunology Frontier Research Center/Research Institute for Microbial Diseases of Osaka University, Japan now made the discovery that certain types of microorganisms evade the immune system by producing protein-splitting enzymes (protease), which cleave and thereby disable the antibodies that trigger immune responses in the host. They further found a so far unknown receptor within the host that recognizes the cleaved antibodies and fight the immune evasion mechanisms of pathogenic microorganisms.

The research team came upon these receptors (LILRA2) when they analyzed human cell strains infected with Mycoplasma, which are extremely small bacteria possessing no cell walls. As with Mycoplasma, other pathogenic microorganisms such as Legionella (parasitic bacteria within cells causing pneumonia), pneumococcus and Haemophilus influenzae (both bacteria causing pneumonia and middle ear infection) as well as Candida (a type of fungus normally resident in areas such as the mouth or vagina; may cause infections when the body’s immune function drops) also produce protease that cleaves antibodies. In the case of Legionella, which infect and multiply within immune cells, findings show that their growth is inhibited when LILRA2 recognize the cleaved antibodies. Similarly, LILRA2-expressing cells were activated in other places infected with bacteria as well, such as tympanitis (middle ear infection), inflammatory atheroma (type of skin boil), and cellulitis (bacterial skin infection).

The discovery that LILRA2 immune receptors work as a biological defense system against pathogenic microorganisms is expected to contribute to the development of new treatments and prevention of infectious diseases via the development of drugs that control LILRA2 functions and vaccines.

This research is a joint research project by Osaka University, Chiba University, Kyoto University, Hokkaido University and Washington University School of Medicine.

Source: Osaka University

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