Month: March 2018

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Vaccines don’t overload babies’ immune systems, study finds

Kids who get more vaccines don’t get sick more often than kids who get fewer.

by Maggie Fox / 

 

Some parents may be afraid that babies and toddlers get too many vaccines all at once, but a new study can help put such worries to rest.

It found that kids who got more vaccines were not any more likely to get unrelated infections than kids who got fewer vaccines, or who had them spaced out more than recommended.

There was not much reason to think that vaccinating children might make them somehow more susceptible to diseases in general, but the researchers said it is important to keep testing, to reassure parents.

The new study, published Tuesday in the Journal of the American Medical Association, looks carefully not just at the number of vaccines, but at the number of antigens — the molecules that actually stimulate immune response.

“Some parents are concerned that multiple vaccines in early childhood could weaken their child’s immune system,” Jason Glanz of the Institute for Health Research at Kaiser Permanente Colorado and colleagues wrote.

It’s true that kids are vaccinated against more diseases than in the past.

 “In the past three decades, the routine childhood immunization schedule in the first two years of life expanded from three vaccines against seven diseases to 10 vaccines against 14 diseases,” the team wrote.

Babies are vaccinated against diphtheria and tetanus, whooping cough, measles, mumps and rubella, chickenpox, polio, hepatitis and bugs that cause meningitis, pneumonia and diarrhea.

“Some parents believe this increase in vaccine exposure is harmful to children, with specific concerns that early childhood immunization ‘overloads’ the immune system and increases the risk for future infection,” Glanz and colleagues added.

“Based in part on this concern, an estimated 10 percent to 15 percent of parents are choosing delayed or alternative immunization schedules for their children.”

Several studies have shown this is not the case, and a 2013 report by the Institute of Medicine, now the National Academy of Medicine, found no evidence that the childhood immunization schedule is not safe.

Furthermore, vaccines have been fine-tuned. “Although the number of vaccinations recommended is greater than ever before, the vaccines used in the current immunization schedule actually have fewer antigens (inactivated or dead viruses and bacteria, altered bacterial toxins, or altered bacterial toxins that cause disease and infection) because of developments in vaccine technology. From 1980 to 2000, the immunization schedule’s total number of antigens decreased by approximately 96 percent,” that 2013 report reads.

A 2005 Danish study found no evidence of vaccine overload, but the hypothesis had not been tested in U.S. kids given the current U.S. vaccine schedule.

Glanz’s team did that, studying 944 kids aged 2 to 4 who caught infections covered by vaccines as well as those not targeted by vaccines, including respiratory and gastrointestinal infections. For instance, many causes of colds and flu-like symptoms are not covered by vaccines, nor is norovirus, the most common cause of “stomach flu”.

Glanz’s team did not simply measure the number of vaccines the children got, but the total number of antigens in those vaccines.

Kids brought to the doctor for a variety of infections were compared to similar healthy children.

The children who got sick got almost precisely the same number of vaccine antigens as those who did not get sick, the study found.

The study proves “robust and reassuring results”, Dr. Sean O’Leary of the University of Colorado and Dr. Yvonne Maldonado of the Stanford University School of Medicine wrote in an editorial.

But it may not stop the vaccine deniers who have become much more active as social media gives them an easy way to voice their opinions without contradiction from experts.

“For example, insistence by such groups that vaccines cause autismpersists, despite overwhelming science to the contrary.”

But they agreed that such studies are useful.

“Simply providing scientific information and assuming parents will make the decision to vaccinate is not enough. Delivering evidence-based information to parents and clinicians in ways that inspire confidence in the robust and safe childhood immunization schedule is critical for maintaining the health of children,” they wrote.

Some parents argue that it is harmless to space out vaccines, but pediatricians say that it can in fact be dangerous or at least troublingto do so.

For instance, older kids are more likely to get fevers after receiving the measles, mumps and rubella (MMR) vaccine. And people who catch measles naturally suffer from suppressed immune systemsafterwards.

In addition, the immune systems of teenagers often respond less effectively to vaccines.

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In multiple myeloma, high levels of enzyme ADAR1 are associated with reduced survival

Date:December 5, 2017Source:University of California – San DiegoSummary:Using a database of multiple myeloma patient samples and information, researchers found that high ADAR1 levels correlate with reduced survival rates. They also determined that blocking the enzyme reduces multiple myeloma regeneration in experimental models derived from patient cancer cells.

 

 

Multiple myeloma is the second most common blood cancer in the United States. Thirty to 50 percent of multiple myeloma patients have extra copies of the gene that encodes the enzyme ADAR1. Using a database of multiple myeloma patient samples and information, researchers at University of California San Diego School of Medicine found that high ADAR1 levels correlate with reduced survival rates. They also determined that blocking the enzyme reduces multiple myeloma regeneration in experimental models derived from patient cancer cells.

The study, published December 4 in Nature Communications, also suggests that a class of commercially available drugs could be used to dampen ADAR1 activity, and ultimately prevent progression or relapse in multiple myeloma.

“Despite new therapies, it’s virtually inevitable that a patient with multiple myeloma will experience relapse of the disease at some point,” said senior author Catriona Jamieson, MD, PhD, professor of medicine, Koman Family Presidential Endowed Chair in Cancer Research and chief of the Division of Regenerative Medicine at UC San Diego School of Medicine. “That’s why it’s exciting that this discovery may allow us to detect the disease earlier, and address the root cause.”

The enzyme at the center of this study, ADAR1, is normally expressed during fetal development to help blood cells form. ADAR1 edits the sequence of RNA, a type of genetic material related to DNA. By swapping out just one RNA building block for another, ADAR1 alters the carefully orchestrated system cells use to control which genes are turned on or off at which times.

ADAR1 is known to promote cancer progression and resistance to therapy. In previous studies, Jamieson’s team described ADAR1’s contributions to leukemia. The enzyme’s RNA-editing activity boosts cancer stem cells — a special population of cells that can self-renew, giving rise to cancer, increasing recurrence and allowing some cancers to resist treatment.

In their current study, the team investigated ADAR1’s role in multiple myeloma. Analyzing a database of nearly 800 multiple myeloma patient samples, they discovered that 162 patients with low ADAR1 levels in their tumor cells survived significantly longer over a three-year period compared to 159 patients with high ADAR1 levels. While more than 90 percent of patients with low ADAR1 levels survived longer than two years after their initial diagnosis, fewer than 70 percent of patients with high ADAR1 levels were alive after the same period of time.

To unravel exactly how ADAR1 is connected to disease severity at a molecular level, the researchers transferred multiple myeloma patient tissue to mice, creating what’s known as a xenograft or “humanized” model.

“This is a difficult disease to model in animals — there isn’t a single gene we can manipulate to mimic multiple myeloma,” said co-senior author Leslie A. Crews, PhD, assistant professor at UC San Diego School of Medicine. “This study is important, in part because we now have a new xenograft model that will for the first time allow us to apply new biomarkers to better predict disease progression and test new therapeutics.”

Using their new model, Jamieson, Crews and team found that two events converge to activate ADAR1 in multiple myeloma — a genetic abnormality and inflammatory cues from the surrounding bone marrow tissue. Together, these signals activate ADAR1, which edits specific RNA in a way that stabilizes a gene that can make cancer stem cells more aggressive.

They also found that silencing the ADAR1 gene in the xenograft model reduced multiple myeloma regeneration. Five to 10-fold fewer tumor cells were able to self-renew in mice lacking ADAR1, suggesting a new therapeutic target.

Clinical trials that specifically test ADAR1-targeted therapeutics for their safety and efficacy against multiple myeloma are still necessary before this approach could become available to patients. To advance their initial findings, Jamieson and Crews are exploring ways to leverage ADAR1 to detect multiple myeloma progression as early as possible. They are also testing inhibitors of JAK2, a molecule that influences ADAR1 activity, for their ability to eliminate cancer stem cells in multiple myeloma models. Several JAK2 inhibitors have already been approved by the FDA or are currently in clinical trials for the treatment of other cancers.

“Several major advances in recent years have been good news for multiple myeloma patients, but those new drugs only target terminally differentiated cancer cells and thus can only reduce the bulk of the tumor,” said Jamieson, who is also deputy director of the Sanford Stem Cell Clinical Center, director of the CIRM Alpha Stem Cell Clinic at UC San Diego and director of stem cell research at Moores Cancer Center at UC San Diego Health. “They don’t get to the root cause of disease development, progression and relapse — cancer stem cells — the way inhibiting ADAR1 does. I like to call our approach ‘precision regenerative medicine.'”

 

Story Source:

Materials provided by University of California – San Diego. Original written by Heather Buschman, PhD.

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Determining the cause of difficult-to-control mitochondrial diseases (AMA)

Date:March 7, 2018Source:Kumamoto UniversitySummary:A research group has discovered that the ‘non-essential’ amino acid taurine is important for protein translation in mitochondria and is involved in mitochondrial disease development. The group also discovered that a taurine-conjugated compound was able to ameliorate the symptoms of mitochondrial dysfunction through taurine-deficiency.

 

A Japanese research group has discovered that taurine is conjugated with mitochondrial transfer RNAs (tRNAs), small RNAs that decode genetic information, and that taurine deficiency in tRNA dramatically reduces both mitochondrial protein translation and impairs mitochondrial membrane integrity. Subsequently, many mitochondrial proteins are unable to localize on mitochondria and end up forming toxic aggregates inside the cell. Furthermore, researchers also found that some symptoms of mitochondrial dysfunction can be improved by maintaining protein quality.

Mitochondria are intracellular organelles that function as the power plants of eukaryotic cells. Proteins gathered in mitochondria work on maintaining various functions. Thirteen species of mitochondrial proteins are encoded by mitochondrial DNA and produced in the mitochondria itself, while thousands of other mitochondrial proteins are produced in the cytosol and transported into the mitochondria.

When mutations occur in genes that design mitochondrial proteins, severe neurological disorders in the form of mitochondrial diseases can develop. Mitochondrial myopathy, encephalomyopathy, lactic acidosis, stroke-like symptoms (MELAS) or Myoclonic Epilepsy with Ragged Red Fibers (MERRF) are major mitochondrial diseases that are characterized by whole body muscle weakness and declining cardiac function. To date, there are no effective treatments and many patients die a few years after onset.

The molecular mechanism underlying the pathogenesis of MELAS and MERRF is not yet fully understood, but it has been reported that taurine, one of the functional amino acids, is involved. In mitochondria, it is known that taurine binds to tRNA, which is also known to be related to protein synthesis, and that this binding is reduced in patients with MELAS and MERFF. However, the detailed molecular mechanisms by which the decrease of taurine binding to tRNA induces these serious symptoms was unknown.

To elucidate this mystery, the research group first identified the enzyme that conjugates taurine to the tRNA molecule. They then deleted the enzyme in a mouse model and found that protein translation in the mitochondria was greatly reduced. This result demonstrated that taurine is essential for protein synthesis in mitochondria.

Proteins produced in the mitochondria also serve to maintain mitochondrial structure. When examining mitochondria that had decreased taurine function, the researchers discovered that the inner mitochondria membrane had collapsed. Consequently, the various proteins produced outside the mitochondria, which are usually transported inside, could not enter the mitochondria. With nowhere to go, these protein structures eventually broke down, accumulated in the cytoplasm, and became highly toxic aggregates. The researchers believe this to be one of the causes of cytotoxicity that occurs in patients with MELAS and MERRF.

In recent years, compounds that inhibit abnormal protein aggregation have been developed. One of these compounds, TUDCA (ursodeoxycholic acid), is a substance originally present as a secondary bile acid in the body. Administering TUDCA to cells without taurine-tRNA binding resulted in the near complete disappearance of aggregates and the reduction of cellular stress. Moreover, when TUDCA was administered to mitochondrial disease model mice with reduced taurine-tRNA binding, cell damage was also improved.

“We believe that this research will lead to the development of therapeutic drugs for mitochondrial diseases in which taurine’s activity declines, such as MELAS and MERRF,” said Associate Professor Wei Fan-Yan of Kumamoto University, leader of the research project. “TUDCA, which has been shown to be effective in cell and model animals, is used as a remedy for liver diseases in Italy and other European countries, so its pharmaceutical safety has already been confirmed. We are planning to conduct clinical trials in the near future to determine whether TUDCA is an effective remedy for mitochondrial diseases in humans.”

This research result was posted online in the journal Cell Reportson 9 January 2018.

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Ticks Creep Into Canada, Bringing Lyme Disease (and Confusion) With Them

Joanne Seiff, a resident of Manitoba, contracted Lyme disease a couple of years ago but didn’t remember pulling off the tick that bit her; nor did she have the telltale bullseye rash of a tick bite. Her husband Jeff Marcus, who grew up in New York’s Hudson Valley, about an hour and a half from the eponymous town of Lyme, Connecticut, recognized her symptoms immediately because Lyme disease was common there.

Canadian doctors, however, were not convinced.

“Even though we had been telling people for months that she had Lyme disease and that all she needed was about four weeks of antibiotics, we were seeing specialist after specialist, and getting the same run-around,” Marcus says. “She was getting sicker and sicker.” At their wits’ end, they paid thousands of dollars for testing at a certified lab in the United States, which finally convinced a Canadian doctor to treat her.

Ticks carried by migratory birds have been raining down on Canada for years. But it’s only in the last 10 to 15 years, amid a changing climate and the creation of new habitats in the north, that populations of deer ticks (Ixodes scapularis) have been able to establish a permanent beachhead in Canada. They have brought with them a variety of tick-borne diseases, the most common of which is Lyme.

According to Canada’s Lyme surveillance efforts, the number of reported Lyme cases increased more than six-fold from 2009 (144 reported cases) to 2016 (987 reported cases). And while public awareness of the disease is increasing in Canada as caseloads surge, many patients still struggle to get diagnosed and treated — enough so that many of them have been driven to seek help beyond the country’s borders, or even from alternative medicine practitioners with questionable expertise but in some cases, a more sympathetic ear.

“There are people who are really suffering,” says Tara Moriarty, an associate professor in the Faculty of Dentistry at the University of Toronto who studies the dissemination of blood-borne pathogens. That suffering, she says, “has made a lot of people feel very marginalized.”

Of course, diagnosing Lyme is far from foolproof, no matter where the bacterium that causes it, Borrelia burgdorferi, has surfaced. As many Americans already know — particularly those in the tick-infested Northeast — diagnosis of Lyme disease is most straightforward when patients present with a signature bullseye rash at the site of the bite. If the tick and/or rash are missing, which can happen in as many as half of all cases, diagnostic testing for Lyme disease in Canadian government labs follows the guidelines from the Infectious Diseases Society of America, which recommends a two-tiered test developed by the U.S. Centers for Disease Control and Prevention. This involves an initial test to determine if the body has mounted an immune response and is producing antibodies to Borrelia burgdorferi. If the test is positive, the second test seeks to confirm the infection by identifying proteins specific to Borrelia burgdorferi.

The tests, however, are imperfect. It can take several weeks for the body to produce antibodies to Lyme, for example, and if the test is administered too early, it will produce a false negative. Similarly, there are a variety of geographically distinct strains of Borrelia, which can sometimes produce equivocal western blot results.

Complicating matters further, ticks often carry more than one pathogen, such as the bacterium anaplasma or the malaria-like parasite babesia, which are not detected with the standard tests for Lyme. These pathogens can produce co-infections with Lyme. Kateryn Rochon, an assistant professor at the University of Manitoba who has been sampling the expanding range of ticks throughout the province for the last three years, and her collaborator, Jeff Marcus, husband of Joanne Seiff and an associate professor of biology at the university, estimate that 65 percent of the deer ticks in Manitoba are carrying either Lyme disease and/or one of the other two commensal human pathogens.

 

This all makes for a muddy diagnostic regimen even in regions with a long history of Lyme, but with Canada’s exposure still comparatively new, many doctors may not even suspect Lyme in an ailing patient. And even when they do, there are often systemic and cultural barriers to testing, according to Jim Wilson, the founder of the Canadian Lyme Disease Foundation, who contracted Lyme disease many years ago and was very sick for several years before he found effective treatment. After his daughter contracted Lyme in 2001, he decided to found the organization to raise awareness of the issue.

Many medical doctors feel caught in a Catch-22, Wilson suggested — simultaneously discouraged from making a diagnosis on clinical symptoms alone, and limited to laboratory tests that are often inconclusive. Doctors that diagnose and treat Lyme disease effectively — through a mixture of educated clinical diagnosis and testing — “have been policed out of business,” Wilson says, leaving them hesitant to diagnose and treat the disease at all. This leaves many patients with little recourse but to turn elsewhere — including seeking diagnosis via for-profit labs the U.S.

Moriarty at the University of Toronto thinks that’s a mistake, arguing that the lack of regulation at such labs leaves the door open for errors and even exploitation. The commercial labs in the U.S. aren’t as tightly regulated as the government labs in Canada, she argues, and many for-profit labs “diagnose Lyme disease in people who are not infected as often as they diagnose it in people who are.” A review of studies published in the Canadian Medical Association Journal in 2015 supported this assertion, showing that some analyses of U.S. specialty labs had false-positive rates ranging from 2.5 percent to as high as 25 percent. One lab showed false-positives in 57 percent of samples taken from a control group known to be Lyme-free.

Many Canadian patients are also turning to naturopathic physicians for help. Such practitioners are not restricted to government-approved laboratory tests, and they have more freedom to clinically diagnose and treat Lyme. The problem is — with the exception of British Columbia, naturopathic physicians are not able to prescribe the only scientifically proven treatment for addressing Lyme: a long course of antibiotics.

Not surprisingly, given his prescription-writing ability, naturopathic physician Eric Chan at the Pangaea Clinic of Naturopathic Medicine in British Columbia sees patients from all over Canada, and he has developed a practice focus in treating patients with chronic Lyme. “Not all infections are really simple,” Chan says, adding that patients with chronic Lyme may need antibiotic treatment to get rid of the infection, as well as treatment for the physiological symptoms of chronic stress, poor sleep, and pain. “When we take this multi-faceted approach, then patients start to feel better,” he says.

In conjunction with — or sometimes in lieu of — antibiotics, Chan uses a variety of approaches to treat Lyme, including ozone therapy by “major autohemotherapy”, that is, by withdrawing the patient’s blood, adding ozone to it, and then reinjecting it into the patient. According to Chan’s website, ozone therapy stimulates the immune system to clear the infection. Other naturopathic treatments offered for Lyme “involve sauna therapy with oxygen, IV vitamin C, IV glutathione for flares, DMSA and EDTA chelation, and oral chlorella, cilantro, garlic,” according to the site.

But Moriarty and other experts are quick to note that, aside from treatments with antibiotics, much of this is bunkum. “There is absolutely no evidence that any naturopathic treatment does anything to help Lyme disease. It is absolutely costly. There is zero evidence,” Moriarty says. “And anyone who promises or markets a treatment that is naturopathic for this disease is in my belief acting unethically.

“There are people that are very sick,” she adds, “and there are people that are exploiting them.”

All of this leaves many Canadian patients and their doctors on uncertain footing when it comes to diagnosing and treating a growing problem. Last year, the Canadian government pledged an additional $3 million ($4 million Canadian) to fund more Lyme research, and in response to that, Moriarty is co-leading a grant proposal application for a network of approximately 50 scientists and physicians across Canada to be submitted to the Canadian Institutes of Health Research and the Public Health Agency of Canada in March 2018. The multi-pronged proposal includes work to improve diagnostics, to conduct surveillance, to educate general practitioners about Lyme, and to build a biobank of patient samples.

Until we can actually test different ideas and figure out if they are right or wrong, all guidelines have to be based on evidence and what we know because otherwise they wouldn’t be guidelines,” Moriarty says.

“It’s our job to be professionally skeptical,” she adds.

Of course, some patients and advocates argue that the current guidelines are not based on the best evidence and that they are beholden to powerful interests. Disability insurance companies in Canada often claim that chronic Lyme disease does not exist, for example, so that they don’t have to pay disability claims. Such companies sometimes hire infectious disease doctors as experts to testify in court to deny claims, Wilson explains.

At the same time, many insurance companies deny life insurance to potential clients who have had a Lyme disease diagnosis, says Janet Sperling, a Lyme disease researcher at University of Alberta. Sperling — who was a stay-at-home mother when her son contracted Lyme disease and doctors couldn’t diagnose or treat him — suggests that such inconsistencies show that Lyme disease is “becoming politicized.” The experience with her son prompted her to pursue a Ph.D. at the University of Alberta so she could help start untangling Canada’s growing Lyme challenge. She’s currently investigating tick-borne pathogens that often co-occur with Lyme. “If it’s not Lyme disease, then what is it?” she asks.

Although the pace of progress has been glacial in the face of this rapidly spreading infectious disease, there is potential hope on the not-too-distant horizon: The French pharmaceutical company Valneva is currently working to develop a Lyme vaccine. Such a vaccine previously existed in the U.S., where it became FDA approved in 1998. But after complaints about side effects that led to lawsuits and falling vaccine sales, it was withdrawn in 2002. But a new and better vaccine could play a major role in controlling Lyme.

“If it works and it is safe, the Canadian government should be putting a lot of money into getting this out there,” Moriarty says, “because I think that’s going to be single-handedly more effective than anything else.”

In the meantime, there are no immediate solutions. But Marcus, witnessing the Canadian medical and public health system struggling to keep up with this emerging infectious disease, feels a sense of déjà vu.

“I grew up about an hour and a half from Lyme, Connecticut, in the 1980s when the Lyme epidemic was being recognized, and I remember the people who were sick for years and years without treatment because they weren’t showing symptoms that people first recognized as being associated with Lyme,” he says. “And it’s happening again in Canada, as the bacteria and the ticks are establishing themselves here.”

Viviane Callier is a San Antonio-based science writer covering biology, medicine, and STEM workforce and training issues. Her work has appeared in Science, Nature, Scientific American, Quanta, Wired.com, Smithsonian.com, The Atlantic.com, and National Geographic News, among other publications.

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Health Department: Food Service Employee Worked While Having Hepatitis A

BOYD COUNTY, KY (WOWK) – The Ashland-Boyd County Health Department is investigating one case involving the diagnosis of Hepatitis A in a food service worker at both Waffle House locations in Boyd County, Kentucky.

According to a release from the Ashland-Boyd County Health Department, the single employee worked at each location during the infectious period.

The window of possible exposure was February 12 – 28, 2018.

The Centers for Disease Control and Prevention (CDC) states it can take up to 50 days from exposure to hepatitis A for symptoms to develop.

Waffle House restaurant owner and employees have cooperated fully with the local and state health officials to identify all employee contacts. In addition, Waffle House seeks to notify patrons of the potential exposure that occurred to Hepatitis A.

Waffle House employees are receiving post-exposure Hepatitis A injections.

“Hepatitis A is a vaccine-preventable, communicable disease of the liver caused by the hepatitis A virus (HAV). It is usually transmitted person-to-person through the fecal-oral route or consumption of contaminated food or water. Hepatitis A is a self-limited disease that does not result in chronic infection. Most adults with hepatitis A have symptoms, including fatigue, low appetite, stomach pain, nausea, and jaundice, that usually resolve within 2 months of infection; most children less than 6 years of age do not have symptoms or have an unrecognized infection. Antibodies produced in response to hepatitis A infection last for life and protect against reinfection. The best way to prevent hepatitis A infection is to get vaccinated”, says the CDC.

There is a two-week window for an exposed individual to receive the Hepatitis A vaccine.

After the two week period the post-exposure vaccine is not effective. The last date for the post-exposure vaccine is March 13, 2018.

Anyone who is experiencing symptoms should immediately contact their physician or seek other medical attention.

Anyone with a possible exposure and not experiencing symptoms is encouraged to receive a Hepatitis A post-exposure vaccine from their healthcare provider. Most insurance plans will pay for the Hepatitis A vaccine.

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Restaurant worker in Boyd County, Ky. diagnosed with Hepatitis A

BOYD COUNTY, Ky. (WSAZ) — A food service worker employed at both Waffle House locations in Boyd County was diagnosed with Hepatitis A, and the Ashland-Boyd County Health Department is warning the public about possible exposure.

The agency says the window of exposure was from Feb. 12 to 28. According to the Centers for Disease Control and Prevention (CDC), it can take up to 50 days from exposure to Hepatitis A for symptoms to develop.

All employees at the affected Waffle Houses have since received post-exposure Hepatitis A injections, the Ashland-Boyd County Health Department said Wednesday.

The CDC reports that Hepatitis A is a virus transmitted from person-to-person in different ways, including consumption of contaminated food or water.

Hepatitis A does not result in chronic infection. Symptoms may include fatigue, poor appetite, stomach pain, nausea and jaundice.

The Ashland-Boyd County Health Department reports that a post-exposure vaccine must be given within two weeks of exposure. The last date for the post-exposure vaccine in this case is March 13.

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Louisville records first hepatitis A death as state continues battling outbreak

LOUISVILLE, Ky. (WDRB) – A Jefferson County resident has died after contracting hepatitis A.

The announcement came from Louisville Metro Department of Public Health and Wellness Tuesday afternoon as the state continues to battle an outbreak of acute hepatitis A among the the city’s homeless and drug users.

The person who died has not been identified, but officials say the victim had other health issues whose symptoms and lab results met the case definition of acute hepatitis A infection.

Kentucky declared an outbreak of acute hepatitis A in several counties on Nov. 21. So far, there have have been 150 cases in Kentucky — and 124 of those cases were in Louisville.

Officials with Louisville Metro Department of Public Health and Wellness said they started noticing a few cases last August. By November, the county documented at least 30 cases.

Director Lori Caloia said the state of Kentucky usually only see 20 cases each year.

“For the outbreak itself, the at-risk populations are a little bit different than what the CDC’s website would say,” Caloia said.

The department is focused on vaccinating as many people in the high-risk categories, including the homeless and drug users, as possible. Caloia said it’s a misconception that drug users will avoid getting Hepatitis A if they avoid using needles.

“It’s not just IV drug use,” she said. “Hepatitis B and C are spread through IV use, but Hepatitis A is spread more through contact with contaminated surfaces.”

Hepatitis A is a disease that affects the liver. It is preventable with a vaccine, and is usually transmitted person-to-person through contaminated surfaces.

Caloia said the spread of the virus could start once someone with Hepatitis A does not properly wash his or her hands and then touches any surface, object, food or liquid.

“It’s the fecal-oral route,” Caloia said. “So someone has perhaps used the bathroom and has hepatitis A, they may wash their hands but may have contaminated a surface. Someone else touches that same surface, and they can contract the virus.”

She says common symptoms include nausea, vomiting, abdominal or stomach pain, jaundice or yellowing of the skin or eyes, light-colored stool, dark-colored urine, fever, chills and body aches.

“Hepatitis A is more of an acute illness, typically,” Caloia said. “So you get sick, you get pretty sick all at once. And then you tend to recover and get better pretty rapidly.”

Caloia warned that hepatitis A can be deadly for those with liver conditions.

The best way to prevent hepatitis A infection is to get vaccinated.

The department is offering free hepatitis A vaccines to at-risk groups, including the homeless and drug users.

Since November, the department has given nearly 6,000 hepatitis A immunizations at homeless shelters, homeless camps, recovery houses and at agencies such as Family Health Centers’ Phoenix Health Center. It has also provided immunizations at Metro Corrections, both at intake and in the general population.

Plus immunizations are being provided at the health department’s syringe exchange sites, its Specialty Clinic and at the MORE Center.

In addition, the University of Louisville pharmacy has been providing immunizations for first responders at agencies such as EMS, Public Works and Louisville Fire, and the health department is also working with Kroger Little Clinics and Walgreen’s to immunize other first responders.

The department is encouraging other Kentucky residents to contact their doctors or pharmacists for the vaccine.