Just how long does the Ebola virus linger in semen?

The 2013-2016 West African Ebola virus outbreak altered our perception of just what an Ebola outbreak could look like.

While none of the three primary affected countries–Liberia, Sierra Leone, and Guinea-have had a case since April 2016, the outbreak resulted in a total of over 28,000 cases of Ebola virus disease (EVD)–65 times higher than the previous largest EVD outbreak, and more than 15 times the total number of cases of all prior EVD outbreaks combined, from the virus’s discovery in 1976 to a concurrent (but unrelated) outbreak in the Democratic Republic of Congo in 2014.

In March 2016, cases were identified once again in both Liberia and Guinea, just after the outbreak had been declared over. Both countries were declared Ebola-free in June 2016; Guinea for the second time and Liberia for the fourth time. The last series of cases in these countries demonstrated just how different this epidemic was from prior ones, changing what we thought we knew about the virus:

Previous research suggested Ebola could persist in the semen for 40 to 90 days. But that window has been eclipsed in this epidemic by a considerable amount. A probable case of sexual transmission occurred approximately six months after the patient’s initial infection last year in Liberia. Another study found evidence of Ebola in the semen of 25% of surviving men tested seven to nine months after infection. And it takes only a single transmission to kick off a fresh recurrence of the disease.

A recent paper extended this window of virus persistence in the semen even longer–over 500 days. It also explains how the outbreaks began in both countries after being declared Ebola-free–so where did the virus come from?

In a convergence of old-fashioned, “shoe leather” epidemiology/tracing of cases and viral genomics, two converging lines of evidence led to the identification of the same individual: a man who had been confirmed as an EVD case in 2014, and had sexual contact with one of the new cases. Author Nick Loman discussed via email:

The epidemiologists told us independently that they had identified a survivor and we were amazed when we decoded the metadata to find that case was indeed the same person. The sequencing and epidemiology is tightly coordinated via Guinea’s Ministry of Health who ran National Coordination for the Ebola outbreak and the World Health Organisation.

It shows that the genomics and epidemiology works best when working hand-in-hand. If we’d just had the genomics or the epidemiology we’d still have an element of doubt.

The sequencing results also suggested that it was likely that the new viral outbreak was caused by this survivor, and unlikely that the outbreak was due to another “spillover” of the virus from the local animal population, according to author Andrew Rambaut:

If the virus was present in bats and jumped to humans again in 2016, it might be genetically similar to the viruses in the human outbreak but not have any of the mutations that uniquely arose in the human outbreak (it would have its own unique mutations that had arisen in the bat population since the virus that caused human epidemic).

It might be possible that the virus jumped from humans to some animal reservoir in the region and then back to humans in 2016 but because we have the virus sequence from the patients acute disease 15 months earlier we can see that it essentially exactly the same virus. So this makes it certain the virus was persisting in this individual for the period.

So the virus–persisting in the survivor’s semen for at least 531 days–sparked a new wave of cases. Ebola researcher Daniel Bausch noted elsewhere that “The virus does seem to persist longer than we’ve ever recognized before. Sexual transmission still seems to be rare, but the sample size of survivors now is so much larger than we’ve ever had before (maybe 3,000-5,000 sexually active males versus 50-100 for the largest previous outbreak) that we’re picking up rare events.”

And we’re now actively looking for those rare events, too. The Liberia Men’s Health Screening Program already reports detection of Ebola virus in the semen at 565 days following symptoms, suggesting we will need to remain vigilant about survivors in both this and any future EVD epidemics. The challenges are clear–we need to investigate EVD survivors as patients, research participants, and possible viral reservoirs–each of which comes with unique difficulties. By continuing to learn as much as we can from this outbreak, perhaps we can contain future outbreaks more quickly–and prevent others from igniting.

Zika: what we’re still missing

As you’ve probably seen, unless you’ve been living in a cave, Zika virus is the infectious disease topic du jour. From an obscure virus to the newest scare, interest in the virus has skyrocketed just in the past few weeks:

 
I have a few pieces already on Zika, so I won’t repeat myself here. The first is an introductory primer to the virus, answering the basic questions–what is it, where did it come from, what are its symptoms, why is it concerning? The second focuses on Zika’s potential risk to pregnant women, and what is currently being advised for them.

I want to be clear, though–currently, we aren’t 100% sure that Zika virus is causing microcephaly, the condition that is most concerning with this recent outbreak. The circumstantial evidence appears to be pretty strong, but we don’t have good data on 1) how common microcephaly really was in Brazil (or other affected countries) prior to the outbreak. Microcephaly seems to have increased dramatically, but some of those cases are not confirmed, and others don’t seem to be related to Zika; and if Zika really is causing microcephaly, 2) how Zika could be causing this, whether timing of the infection makes a difference, and whether women who are infected asymptomatically are at risk of medical problems in their developing fetuses.

The first question needs good epidemiological data for answers. This can be procured in a few ways. First, babies born with microcephaly, and their mothers, can be tested for Zika virus infection. This can be looked at a few ways: finding traces of the virus itself; finding antibodies to the virus (suggesting a past infection–but one can’t know the exact timing of this); and asking about known infections during pregnancy. Each approach has advantages and limitations. Tracking the virus or its genetic material is a gold standard, but the virus may only be present in body fluids for a short time. So if you miss that window, a false negative could result. This could be coupled with serology, to look at past infection–but you can’t be 100% certain in that case that the infection occurred during pregnancy–though with the apparently recent introduction of Zika into the Americas, it’s likely that infection would be fairly recent.

Serology coupled with an infection in pregnancy that has symptoms consistent with Zika (headache, muscle/joint pain, rash, fever) would be a step up from this, but has some additional problems. Other viral infections can be similar in symptoms to Zika (dengue, chikungunya, even influenza if the patient is lacking a rash), so tests to rule those out should also be done. On the flip side, about 80% of Zika infections show no symptoms at all–so a woman could still have come into contact with the virus and have positive serology, but she wouldn’t have any recollection of infection.

None of this is easy to carry out, but needs to be done in order to really establish with some level of certainty that Zika is the cause of microcephaly in this area. In the meantime, there are a few other possibilities to consider: that another virus (such as rubella) is circulating there. This is a known cause of multiple congenital issues, including microcephaly. This could explain why they’re seeing cases of microcephaly in Brazil, but none have been reported thus far in Colombia. Another is that there is no real increase in microcephaly at all–that, for some reason, people have just recently started paying more attention to it, and associated it with the Zika outbreak in the area–what we call a surveillance bias.

This is a fast-moving story, and we probably won’t have any solid answers to these questions for some time. In the interim, I think it’s prudent to take this as a possibility, and raise awareness of the potential this virus *may* have on the developing fetus, so that women can take precautions as they’re able. Public health is about prevention, and there have certainly been cases in the past of links between A and B that fell apart under further scrutiny. Zika/microcephaly may be one, but for now, it’s an unfortunate case where “more research is needed” is about the best answer one can currently give.

Can we “catch” breast cancer?

Third of five student guest posts by Dana Lowry

In 1911, Peyton Rous first discovered viruses can cause cancer.  A chicken with a lump in her breast had been brought to Rous by a farmer.  Rous prepared an extract that eliminated bacteria and tumor cells and injected this extract into other chickens—tumors grew.  Rous suggested “a minute parasitic organism” was causing the tumor growth, which is now known to be a virus.  However, Rous’ discovery remained very controversial, and it wasn’t until 1966 that he was awarded a Nobel Prize for his discovery.  Since Rous’s discovery, researchers have found an estimated 15 percent of all cancers worldwide are associated with viruses.  Some common virus and cancer associations are: human papilloma virus (HPV) and cervical cancer, hepatitis B and liver cancer and human T lymphotropic virus type 1 (HTLV-1) and T-cell leukemia.

Epstein-Barr virus (EBV), a member of the herpesvirus family, is one of the most common viruses worldwide.  Among 35 to 40 year olds in the U.S., up to 95% have been infected with EBV.  Oftentimes, children infected with EBV have no clinical signs or symptoms; however, 30% to 50% of adolescents and young adults exposed to EBV for the first time will develop infectious mononucleosis, commonly known as mono.  In the U.S., individuals are usually exposed to EBV in adolescence or young adulthood compared to developing countries, where oftentimes individuals are exposed as infants or young children.  EBV usually remains dormant in the body throughout an individual’s lifetime, similar to the varicella-zoster virus, the virus responsible for the chicken pox.  EBV is known to play a role in Burkitt ’s lymphoma (cancer of the immune cells), nasopharyngeal cancer (cancer of the upper throat) and Hodgkin’s lymphoma (cancer of the lymphatic system), but can EBV also play a role in breast cancer?

In 2010, James Lawson and Benjamin Heng reviewed 27 papers concerning EBV and breast cancer associations. EBV infections are universal in high and low risk breast cancer groups, making it unlikely that EBV is the sole contributor to forms of breast cancer [1].  However, the age at which EBV is contracted seems to play a role in the risk of developing breast cancer. Women in Western countries are at higher risk of developing breast cancer and tend to be infected with EBV during adolescence or young adulthood, whereas women from non-Western countries have a lower risk for developing breast cancer and tend be infected during infancy or early childhood.  Hodgkin’s lymphoma shares a similar correlation with higher rates in Western countries [2].  Although there seems to be a relationship between age of EBV infections and risk of breast cancer, potential confounders need to be considered.  Women in developing countries tend to have more children, have children at a younger age and breastfeed their children for longer periods of time.  Breastfeeding, having more children and having children earlier in life all seem to be protective factors against breast cancer.

Beyond epidemiological evidence, lies biological evidence.  Twenty two of the studies Lawson and Heng reviewed were based on polymerase chain reaction (PCR) techniques. Issues have been found with standard PCR procedures, but it is becoming widely accepted that EBV can be identified in breast cancer tissue through specific PCR techniques [1].  EBV genes have been found in breast cancers through polymerase chain reaction (PCR) analyses.  EBV has not only been shown to shed in human breast milk [3], but it has also been shown to stimulate growth of human breast-milk cells [4]. The mechanism by which EBV actually causes cell alterations is not known, but it is thought to be different from the mechanisms used in lymphomas and nasopharyngeal cancer [1].

It is unlikely that we can actually “catch” breast cancer, as EBV doesn’t seem to be the sole cause of breast cancer.  EBV may contribute to breast cancer by altering genes in the breast cells which eventually leads the uncontrolled cell division, known as cancer.  More importantly, it seems the age an individual is infected with EBV may play an even bigger role in the outcome of disease.  An EBV vaccination is in the works that will hopefully prevent infectious mononucleosis and EBV-associated cancers.  However, the vaccination may not prevent the EBV infection itself; it is targeted towards the most abundant protein on the virus and on virus-infected cells.  If the vaccination proves to be successful, it will be interesting to see if a reduction in breast cancer rates will follow, along with the known cancers associated with EBV. Only time will tell.

 

References:

  1. Lawson, J. and Heng, B. (2010). Viruses and Breast Cancer. Cancers 2010, 2(2), 752-772; doi: 10.3390/cancers2020752.

 

  1. Yasui et al. (2001). Breast cancer risk and “delayed” primary Epstein-Barr virus infection. Cancer Epidemiology, Biomarkers & Prevention, 10:9-16. http://cebp.aacrjournals.org/content/ 10/1/9.long.

 

  1. Junker et al. Epstein-Barr virus shedding in breast milk. (1991). The American Journal of the Medical Sciences, 302: 220–223. http://www.ncbi.nlm.nih.gov/pubmed/1656752.

 

  1. Xue et al. (2003). Epstein-Barr virus gene expression in human breast cancer: protagonist or passenger?. British Journal of Cancer, 89:113–119. http://www.nature.com/bjc/journal/ v89/n1/full/6601027a.html

 

 

Ebola resurfaces in Uganda–history and analyses of Ugandan Ebola

Uganda just can’t catch a break. They’ve recently been hit with nodding disease, a mysterious syndrome where children repeatedly nod their heads and undergo serious seizures, typically leading to death. Now they’re in the grips of another Ebola outbreak. This will be the fourth time the country has suffered through Ebola since 2000, when the virus was first found in the country:

The first occurred in August of 2000; the first case died in Gulu on the 17th of September. Despite an investigation, doctors were unable to determine where or how she had contracted the disease. Her death was followed by the deaths of her husband, two children, and several other family members. This was reported to the Ministry of Health in October of that year, near the peak of the epidemic. An investigation and intervention to control the disease followed, and the epidemic was declared to be over in January of 2001. A total of 425 patients from 3 villages (Gulu, Masindi, and Mbarara) across Uganda were identified based on symptoms and/or laboratory data. 224 of them died, with a resulting mortality rate of 53%; an eerie echo of the 1976 Ebola outbreak in Sudan. Indeed, sequence analysis showed the infecting strain to be the Sudan subtype of Ebola; the first time this type had surfaced since the 1979 outbreak in Sudan. It is hypothesized that Sudanese rebels, who carried out regular attacks around Gulu, may have accidentally introduced the virus in some manner, though this has not been confirmed.

Ebola returned to Uganda in August of 2007, causing 149 illnesses and 37 deaths until the outbreak was declared over in February of 2008. This mortality (36%) was significantly lower than most Ebola outbreaks. Interestingly, when scientists tested this virus, it also reacted strangely with their assays. Therefore, they determined the entire molecular sequence of the virus, and found that it was a whole new strain of Ebola, which they named Ebola Bundibugyo.

The third outbreak occurred just last year, as a single case in a 12-year-old girl, who died of the infection. I’ve not been able to find any follow-up identifying the 2011 strain, but Uganda has been hit previously by both the Sudan and the novel Bundibugyo strains of Ebola, and the current outbreak has been identified once again as Ebola Sudan.

In the current outbreak, which began in the Kibaale district in western-central Uganda, at least 20 have been affected and 14 have died. As of today, an additional six cases are suspected but not yet confirmed, and it appears to be affecting more than one village in the district. One death has also occurred at Mulago hospital in the capital of Kampala. The individual who died was reported to be:

… a health worker who “had attended to the dead at Kagadi hospital” in Kibale, Health Minister Christine Ondoa told reporters.

She is believed to have travelled independently to Kampala — possibly on public transport — after her three-month old baby died, Ondoa added.

Reports also note that other health care workers are in quarantine as a precaution. In Africa, Ebola has really been able to spread in previous outbreaks for two reasons: breakdowns in barrier nursing within hospitals (not wearing gloves/gowns; reusing needles; lack of handwashing/sanitation, etc.) and ritual funeral practices within villages, which put many family members in contact with the virus as they assist with cleansing the victim. Indeed, it appears that 9 of the deaths in this outbreak have come from a single family, so it’s quite possible many were sickened using this type of practice. However, now that Ebola has been confirmed and people are aware of this, stricter controls over these practices can be implemented, and health care workers are being urged to report any cases that may be Ebola to authorities.

Kampala is a city of a bit over a million people on Lake Victoria, southeast of the Kibaale district. The 2011 case originated from Luwero district, due east of the Kibaale district and north of Kampala. The 2000 outbreak occurred in the Gulu district in the north of the country, and the 2007 outbreak in the Bundibugyo district, in the west and neighboring Kibaale. It would seem that Ebola reservoirs (likely fruit bats) could very well be spread across Uganda’s central region, occasionally spilling over into the human populations and igniting these outbreaks. One story notes that “The site where most of the cases occurred are close to Kibale forest where there are a lot of monkeys and birdlife,” and while bats are not explicitly mentioned, they presumably would also be present. Non-human primates have also been implicated in previous outbreaks of Ebola as an amplifying species.

The reporting of the current outbreak was delayed, as patients didn’t have any noticeable bleeding–rather, diarrhea and vomiting were the main reported symptoms. However, while many reports I’ve seen are characterizing hemorrhagic symptoms as “typical,” these aren’t seen in all patients, and indeed the diarrhea, vomiting, and even hiccups are common symptoms of Ebola infection. As such, Uganda has been playing a bit of catch-up, but has certainly learned since the first (and worst) outbreak in 2000. Hopefully this one will end fairly quickly.

Using zombies to teach science

With my colleague Greg Tinkler, I spent an afternoon last week at a local public library talking to kids about zombies:

The Zombie Apocalypse is coming. Will you be ready? University of Iowa epidemiologist Dr. Tara Smith will talk about how a zombie virus might spread and how you can prepare. Get a list of emergency supplies to go home and build your own zombie kit, just in case. Find out what to do when the zombies come from neuroscientist Dr. Greg Tinkler. As a last resort, if you can’t beat them, join them. Disguise yourself as a zombie and chow down on brrraaaaiiins, then go home and freak out your parents.

Why zombies? Obviously they’re a hot topic right now, particularly with the ascendance of The Walking Dead. They’re all over ComicCon. There are many different versions so the “rules” regarding zombies are flexible, and they can be used to teach all different kinds of scientific concepts–and more importantly, to teach kids how to *think* about translating some of this knowledge into practice (avoiding a zombie pandemic, surviving one, etc.) We ended up with about 30 people there: about 25 kids (using the term loosely, they ranged in age from maybe age 10 to 18 or so) and a smattering of adults. I covered the basics of disease transmission, then discussed how it applied to a potential “zombie germ,” while Greg explained how understanding the neurobiology of zombies can aid in fleeing from or killing them. The kids were involved, asked great questions, and even taught both of us a thing or two (and gave us additional zombie book recommendations!)

For infectious diseases, there are all kinds of literature-backed scenarios that can get kids discussing germs and epidemiology. People can die and reanimate as zombies, or they can just turn into infected “rage monsters” who try to eat you without actually dying first. They can have an extensive incubation period, or they can zombify almost immediately. Each situation calls for different types of responses–while the “living” zombies may be able to be killed in a number of different ways, for example, reanimated zombies typically can only be stopped by destroying the brains. Discussing these situations allows the kids to use critical thinking skills, to plan attacks and think through choice of weapons, escape routes and vehicles, and consider what they might need in a survival kit.

Likewise, zombie microbes can be spread through biting, through blood, through the air, by fomites or water, even by mosquitoes in some books. Agents can be viral, bacterial, fungal, prions or parasitic insect larvae (or combinations of those). Mulling on these different types of transmission issues and asking simple questions:

“How would you protect yourself if infection was spread through the air versus only spread by biting?”

“How well would isolation of infected people work if the incubation period is very long versus very short?”

“Why might you want to thoroughly wash your zombie-killing arrows before using them to kill squirrels, which you will then eat?” (ahem, Daryl)

can open up avenues of discussion into scientific issues that the kids don’t even realize they’re talking about (pandemic preparedness, for one). And the great thing is that these kids are *already experts* on the subject matter. They don’t have to learn about the epidemiology of a particular microbe to understand disease transmission and prevention, because they already know more than most of the adults do on the epidemiology of zombie diseases–the key is to get them to use that knowledge and broaden their thinking into various “what if” situations that they’re able to talk out and put pieces together.

It can be scary going to talk to kids. Since this was a new program, we didn’t know if anyone would even show up, or how it would go over. Greg brought a watermelon for some weapons demonstrations (household tools only–a screwdriver, hammer and a crowbar, no guns or Samurai swords) which was a big hit. Still, I realize many scientists are more comfortable talking with their peers than with 13-year-olds. Talking about something a bit ridiculous, like an impending zombie apocalypse, can lessen anxiety because it takes quite a lot of effort to be boring with that type of subject matter; it’s entertaining; and kids will listen. And after all, what you don’t know, might eat you.

Is history repeating itself?

This is the fifteenth of 16 student posts, guest-authored by Cassie Klostermann. 

One of the major accomplishments that public health professionals pride themselves in is the reduction of people getting sick or dying from preventable infectious diseases. Unfortunately, these debilitating, historic diseases that health professionals had once thought they had under control are starting to rear their ugly heads once again in the United States (U.S.). One of these diseases that I am referring to is measles. Measles is a highly contagious virus (from the genus Morbillivirus) spread through the air when an infected person coughs or sneezes making measles extremely easy to get by being around someone who is sick with this disease. According to the Centers for Disease Control and Prevention (CDC), if someone has the measles virus they could potentially infect 9 out of 10 people they come in contact with who are not immune (i.e. not vaccinated) to the disease.

Some of the most common symptoms associated with measles are fever, runny nose, and cough which are also very similar to the symptoms of many other diseases. Measles also commonly causes a rash that can cover the entire body. Those who have measles can spread the virus to another person about 4 days before and after the rash shows up. There are also a few more rare but more serious complications that can develop from having the measles virus such as pneumonia and encephalitis and it can also lead to the death of those infected.

The word measles comes from the Middle Dutch word masel meaning “blemish.” The history of measles cases goes relatively far back into history with references of the virus appearing in records as early as 700 AD. In the U.S., before the vaccine was introduced in 1963, there were about 3-4 million cases (essentially every child had had the disease by the time they were 15 years old), about 1,000 people suffered deafness or permanent brain damage (from encephalitis, for example) and around 450 people died from measles each year. By 2000, naturally occurring cases of measles in the U.S. (meaning cases that originated in the U.S. rather than another country) had been eliminated, although there are normally about 50 measles cases per year in the U.S. that come from other countries where measles is endemic (or constantly present in their population) and with increased worldwide travel people need to be more aware of their risk for contracting measles. Throughout the world, there are an estimated 20 million cases leading to about 164,000 deaths from measles each year, which is a great improvement from the 2.6 million deaths that occurred before the measles vaccine was globally used. The number of measles cases, long-term diseases, and deaths caused by measles are going down year by year and much of this progress can be attributed to efforts that provide the measles vaccine worldwide.

While the overall number of measles cases throughout the world are decreasing (mostly from decreasing cases in developing countries) the U.S. and other developed countries are seeing the opposite trend. According to the Notifiable Diseases and Mortality Tables from the Morbidity and Mortality Weekly Report, there were 223 reported cases of measles for 2011 occurring over 17 outbreaks in the U.S. (the average number of outbreaks is 4). This is an increase from previous numbers (63 cases in 2010 and 71 cases in 2009, to name a couple) and the majority of people infected, about 65%, had not been vaccinated against measles even though most of them were eligible to get the vaccine. Out of the measles cases seen in 2011, 90% were traced back to measles viruses seen in endemic countries and brought back to the U.S. where it was spread person to person in the States. Even though historically measles cases have been high in developing countries (especially Africa and Asia) extensive immunization programs have greatly decreased the amount of cases per year. Now European countries are seeing a large increase in their numbers of measles cases since 2009 because the number of vaccinated people has decreased.

The only proven way to effectively protect someone against contracting measles is to get the MMR (measles, mumps, and rubella) vaccine. If you have not been vaccinated then you are leaving yourself vulnerable to getting the diseases included in the MMR vaccine. This issue doesn’t just stop with the individual person, it spreads to everyone that individual comes into contact with. As mentioned above, measles is highly contagious and is spread through the air when an infected person coughs or sneezes so it can easily infect anyone breathing the same air you breath that is also vulnerable to the disease. When people who are vulnerable to getting the disease breathe in the contaminated air, they have a fairly high chance of getting measles and it is important to keep in mind that there are people who cannot get the MMR vaccine because they are either too young (under 12 months old), too sick (i.e. cancer patients), or the elderly who may have lost some of their immunity. For these people, they do not have a choice as to whether or not they get the vaccine, but they still deserve to have some protection from diseases prevented by vaccines. This protection comes from a concept referred to as herd immunity where there are enough people in a community or country vaccinated against a disease so that is unable to be “kept alive” because there not enough vulnerable people for it to pass through. If we are able to keep herd immunity up high enough by having enough people vaccinated against the measles, then the number of measles cases per year could drop back down to the normal 50 per year instead of 220 per year.

Travelers especially need to keep in mind that although a disease, like measles, is usually a rare occurrence in the U.S., this is not the case in many other countries in Europe, Asia, and Africa as examples. People traveling to countries where measles is endemic really should consider being vaccinated because their risk of being infected is much greater due to the higher number of people in the country infected with the disease.

As with anything in medicine, vaccines can cause reactions in rare situations and I urge people to ask their healthcare provider any questions they have regarding the MMR vaccine. I also urge people to receive all of the recommended vaccines they can (unless they have had past allergic reactions to a specific vaccine) because the risk of contracting measles and dying from it is more common than having a more moderate reaction to the MMR vaccine. If you or your kids are eligible to receive the MMR vaccine, please, please get vaccinated and talk to your doctor if you have concerns about an allergic reaction. By getting vaccinated you are not only protecting yourself and your children but also those who are unable to get the vaccine to protect them from the measles. If vaccination rates do not improve, we may very well see case numbers approach historical highs present before the vaccine was used.

References

http://www.cdc.gov/measles/about/overview.html

http://www.cdc.gov/measles/about/transmission.html

http://wwwnc.cdc.gov/eid/article/12/4/et-1204_article.htm

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6104a3.htm?s_cid=mm6104a3_w

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6122md.htm?s_cid=mm6122md_w

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6115a1.htm?s_cid=mm6115a1_w

http://www.who.int/mediacentre/factsheets/fs286/en/

http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6047a1.htm

http://www.niaid.nih.gov/topics/pages/communityimmunity.aspx

http://www.cdc.gov/measles/travelers.html

http://www.cdc.gov/vaccinesafety/Vaccines/MMR/MMR.html

http://www.aap.org/en-us/about-the-aap/aap-press-room/Pages/Protect-Children-from-Vaccine-Preventable-Diseases-Including-Measles-.aspx

http://www.immunizationinfo.org/vaccines/measles

 

Great Plains Emerging Infectious Diseases Conference–Registration Open

I mentioned last month that we are planning an Emerging Diseases conference here in April. Things are moving quickly and registration is now open (here). Abstract submission is also up and running here.

The details:

Oral and poster presentation research abstracts are due by 5:00pm on March 23, 2012. Individuals may submit up to two research abstracts. Abstracts must not exceed 250 words in length. There are a limited number of spots available for those interested in providing a 15-minute oral presentation. Abstracts submitted for oral presentations that are not selected for a talk will automatically be considered for the poster session. Please do not submit an abstract if your attendance is questionable. Confirmation of participation must be received no later than April 1, 2012.

Monetary awards will be conferred upon the top three student presentations (oral or poster).

Authors will be notified of the review committee’s decision by April 2, 2012.

If you have any questions regarding the conference, registration, or abstract submission, drop me a line or visit the conference website. We’re also still accepting ideas for breakout sessions in an unconference format, so feel free to contact me about thoughts for those as well. Hope to see some of you there!

Holy influenza, batman!

Typically when we think of flying things and influenza viruses, the first images that come to mind are wild waterfowl. Waterbirds are reservoirs for an enormous diversity of influenza viruses, and are the ultimate origin of all known flu viruses. In birds, the virus replicates in the intestinal tract, and can be spread to other animals (including humans) via fecal material.

However, a new paper expands a chapter on another family of flying animals within the influenza story: bats.

I’ve written previously about the enormous diversity of microbes that bats possess. This shouldn’t be surprising–after all, bats are incredibly diverse themselves, encompassing about a fifth of all known mammalian species. Though rabies is probably the most famous bat-associated virus, other viruses that have been isolated from bats include Nipah and Hendra viruses, SARS coronavirus, Chikungunya virus, Japanese and St. Louis encephalitis viruses, Hantaan virus (a relative of the Sin Nombre hantavirus), and filoviruses, among many others. And of course, a bat->pig->human cross-species infection ended up being a plot line in the recent movie, Contagion (modeled after Nipah virus). However, bats still remain chronically under-studied, despite the fact that they can carry so many potential human pathogens.

This new research expands our knowledge of bat viruses a bit. The authors examined 316 bats from eight locations in Guatemala in 2009-10. Rectal swabs were obtained and screened for influenza virus using molecular methods (looking for influenza virus RNA). Three of the samples tested positive, and all were from little yellow-shouldered bats (Sturnira lilium). This could indicate some clustering and transmission of the virus within bat colonies–and indeed, two of the bats were from the same area in the same year (2009). However, the third bat was captured in 2010 at a location 50 km away from the other two, suggesting that the virus may be more widespread than in just one colony.

When we discuss the epidemiology of influenza viruses, we talk about two genes: the HA gene, which encodes the hemagglutinin protein and allows the virus to bind to host cells; and the NA gene, which encodes the neuraminidase protein and allows the virus to leave an infected cell and spread to others. This is where the “H1N1” or “H5N1” nomenclature come from. The novel bat virus was a completely new H type–type 17 (provisional, they note, pending further analyses). The NA gene was also highly divergent, but they are awaiting further analyses to more definitively classify this gene. (Currently there are 9 recognized types of NA genes).

Though they weren’t able to culture out the flu viruses, the authors did do some molecular work suggesting that these novel bat viruses could combine with human viruses and form a functional recombinant virus. What implications could this have for human health? Well, hard to say. We still know very little about all the implications of any distinct type of avian influenza virus, or swine influenza virus, much less something completely foreign like bat flu. It’s interesting that, like birds, influenza virus in bats was found in the intestine (though lung samples were also positive). Can it cause an intestinal infection as well as an upper respiratory infection (the latter being more common in other mammal species)? Does it cause any signs of disease in infected bats at all? If they can get this bat virus to grow, all sorts of interesting lines of research are just waiting.

The article also mentions that seroepidemiological studies are currently being carried out to better understand the epidemiology of bat flu. Looking at PubMed, there is one reference to some similar studies carried out in the early 1980s, but I can’t access anything beyond the title. There also is a report of H3N2 influenza in bats in Kazakhstan, but that article is in Russian and also not readily available. Either way, everything old is new again, and it looks like interest in bat influenza has resurfaced after a 30-year lull. Who knows what else we’ll find lurking out there as interest continues to increase in the wildlife microbiome.

Reference

Suxiang Tong, Yan Li, Pierre Rivailler, Christina Conrardy, Danilo A. Alvarez Castillo, Li-Mei Chen, Sergio Recuenco, James A. Ellison, Charles T. Davis, Ian A. York, Amy S. Turmelle, David Moran, Shannon Rogers, Mang Shi, Ying Tao, Michael R. Weil, Kevin Tang, Lori A. Rowe, Scott Sammons, Xiyan Xu, Michael Frace, Kim A. Lindblade, Nancy J. Cox, Larry J. Anderson, Charles E. Rupprecht, & Ruben O. Donis (2012). A distinct lineage of influenza A virus from bats PNAS Link.