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.

Are we *sure* Ebola isn’t airborne?

Since yesterday’s post, several people have asked me on various social media outlets about the airborne nature of Ebola. Didn’t I know about this paper (“Transmission of Ebola virus from pigs to non-human primates“), which clearly showed that Ebola could go airborne?

Indeed I do–I wrote about that paper two years ago, and it in no way changes my assertion that Ebola doesn’t spread between people in an airborne manner.

Let me back up. The paper in question was an experimental study done in the wake of the 2008 finding of the Reston Ebola virus in pigs and a previous study looking at the Zaire virus in pigs. In the air transmission study, they inoculated pigs with Ebola and examined transmission to macaques (who were not in direct contact with the infected pigs). They did find aerosolized Ebola in air samples, and some of the macaques did come down with symptoms of Ebola. So, it looked like pigs could spread Ebola through the air, which is something that had already been suggested by the epidemiology of the 2008 pig Ebola outbreak. It’s always nice when experimental data matches up with that observed during a real-life occurrence of the virus.

*However*, the kicker was not that Ebola is transmitted by air in human outbreaks, but rather that there may be something unique about pig physiology that allows them to generate more infectious aerosols as a general rule–so though aerosols aren’t a transmission route between primates (including humans, as well as non-human primates used experimentally), pigs may be a bigger threat as far as aerosols. Thus, this may be important for transmission of swine influenza and other viruses as well as Ebola.

So unless you’re sitting next to an Ebola-infected pig, seriously, airborne transmission of Ebola viruses isn’t a big concern. (Perhaps this corollary should be added to this handy diagram examining your risk of Ebola).


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Student guest post: Chirp, Chirp, Sneeze!

Student guest post by Julia Wiederholt

I don’t think there is a single person that can claim to have never had the joyous experience (sarcasm intended) of suffering from the influenza.  We all recognize the common symptoms that accompany this infectious little virus taking up residence in our bodies: the chills accompanying a fever, the total body ache, the nausea, and overall feeling of malaise.  Typically this virus comes and goes within a week without serious side effects.  When novel strains of the influenza pop up however, there can be more serious complications as your body lacks a sufficient immune recognition of the virus.  An example of a new strain of influenza that presents a great risk for the human population is the H7N9 influenza, also known as Avian Influenza A.

H7N9 was first recognized earlier this year in China and thankfully has yet to be reported in the US. The majority of the people infected have had direct contact with poultry or an environment that has contained infected poultry.  Some of the people diagnosed however, report having had no direct contact with poultry opening up the possibility of human to human transfer of the disease.  The infected poultry have shown no obvious symptoms of being infected, but when humans become infected it can cause severe respiratory problems and fever.  As of May this year, LiveScience reported that there have been a total of 131 reported human cases of H7N9 with 32 reported deaths.

While all of that may not sound too impressive, here’s what makes H7N9 such a concern as an emerging infectious disease.  The first major concern regarding this specific influenza is the fact that it is the first time the H7N9 virus has been reported in humans.  The H in the name H7N9 stands for hemaglutinin, which is the attachment protein found on influenza viruses.  This protein not only enables the virus to attach to the cells it is trying to infect, it also is provides the host’s immune system a way of recognizing the virus as a foreign threat.  The fact that this is the first time this specific virus has been found to infect humans means that we lack any prior immunity to it and are therefore, more susceptible.

Another factor that raises the alarm for this influenza is the fact that the infected poultry that have been found so far have shown no outward signs of being sick.  This is a huge concern because it makes controlling the spread of the disease much more difficult.  When poultry and livestock exhibit obvious signs of being infected, it allows the infected to be separated out from the healthy and either isolated or culled to prevent further spread of the disease.  In some cases, the disease may have already spread amongst all of the animals in the vicinity requiring the entire herd or flock to be culled.  When it is difficult to distinguish between healthy and infected animals however, any evidence that the disease has been found within the animals will more than likely lead to the entire herd or flock being culled.  This not only results in greater economic losses for the poultry farmers but also a higher number of people being exposed to infected animals before realizing the danger that is present.

Possibly the greatest concern with H7N9 is the fact that it could be jumping from person to person.  The original thought was that the only way it had been spreading was from direct contact with sick poultry, which would limit the at risk human population to people coming into contact with the infected birds.  Some of the people who have been diagnosed with H7N9 however, are claiming to have had no contact with poultry suggesting that the disease may be capable of human to human transmission.  This would greatly increase the reproductive rate of the disease because people would no longer need to come into contact with poultry to be exposed to it.  The reproductive rate, commonly referred to in scientific communities as the Ro, is a way of measuring the predicted number of new infections that one infectious case is likely to create.  Another factor that suggests the possibility of human to human transfer is the fact that there have been three reported family clusters of H7N9.  While this does not necessarily mean that the virus is capable of sustained human to human transfer, it is highly suggestive that human to human transmission has occurred in these particular instances and that with the right (or depending on how you look at it, wrong) mutation, it could transfer between humans with ease.

While all of these things explain why H7N9 is being watched so closely and why it is important to have a healthy respect for just how dangerous it could be, there’s no reason for people to start panicking quite yet.  As mentioned earlier, this strain of influenza has only been reported in people that either live in or have recently traveled to China.  Unless you are planning to travel out of the country in the near future, there is no reason to become overly concerned about H7N9 at the moment.  Also, the majority of the cases have either had direct contact with infected poultry or close contact with someone who has had contact with poultry.  This means that unless the virus becomes proficient at human to human transmission, the majority of the population is at a low risk.

For the germaphobes out there that are still freaking out over the possibility of catching H7N9, there are several ways to reduce the risk of catching it, or any other influenza for that matter.  Good hygiene practices such as frequently washing your hands and avoiding touching your face will help minimize the risk of introducing the influenza virus into your body.  Eating a well-balanced diet and getting plenty of rest will help keep your immune system in tip top shape in the event of a virus managing to get past your innate defense mechanisms.  In regards to reducing the risk of catching a zoonotic strain of influenza, practices such as thoroughly washing your hands after handling any animals and avoiding contact with sick poultry or livestock will reduce the risk of transmission.  So rest at ease, the world isn’t coming to an end due to H7N9…at least not yet.


Cong Dai, Min Jiang, “Understanding H7N9 Avian Flu,” BMJ, Available online 3 May 2013.  <http://www.bmj.com.proxy.lib.uiowa.edu/content/346/bmj.f2755?view=long&pmid=23645899>.

“Frequently Asked Questions on Human Infection Caused by the Avian Influenza A (H7N9) Virus.”

World Health Organization. WHO, 30 Apr. 2013. Web. 12 June 2013. <http://www.who.int/


Guang-Wu Chen, Michael M.C. Lai, Suh-Chin Wu, Shih-Cheng Chang, Li-Min Huang, Shin-Ru Shih, “Is avian influenza A (H7N9) virus staggering its way to humans?”, Journal of the Formosan Medical Association, Available online 3 June 2013, ISSN 0929-6646, 10.1016/j.jfma.2013.04.015. <http://www.sciencedirect.com/science/article/pii/S0929664613001654>.

“H7N9: Frequently Asked Questions.” Centers for Disease Control and Prevention. Centers for Disease

Control and Prevention, 22 Apr. 2013. Web. 12 June 2013. <http://www.cdc.gov/flu/avianflu/


Kannan Tharakaraman, Akila Jayaraman, Rahul Raman, Karthik Viswanathan, Nathan W. Stebbins, David Johnson, Zachary Shriver, V. Sasisekharan, Ram Sasisekharan, “Glycan Receptor Binding of the Influenza A Virus H7N9 Hemagglutinin,” Cell, Available online 6 June 2013, ISSN 0092-8674, 10.1016/j.cell.2013.05.034. <http://www.sciencedirect.com/science/article/pii/S0092867413006405>.

Rettner, Rachael. “H7N9 Bird Flu Cases Declining, Health Officials Say.” LiveScience. N.p., 10 May

2013. Web. 12 June 2013. <http://www.livescience.com/



Student guest post: Unintended Consequences

Student guest post by Naomi Kirschenbaum

Although we can never know, there are estimates in the range of 15,000 displaced pets in the wake of 2005 Hurricane Katrina.  Many of the dogs found their way to shelters and homes in our community around the Monterey Bay in California.  As a local veterinarian the most notable observation I saw was how it “seemed” that so many were heartworm positive.  Six years later we have a published study finding a 48.8% prevalence of heartworm in these dogs.

This story is an example of a few important lessons.  First, how things seemed to me, in my clinical practice turned out to be 48.8% of the dogs, not all.  (Of course in our area we may have had a different subset of positive dogs, but I thought, in general, they were nearly all heartworm positive). Secondly, how long it takes for a study to be done and published.  In this case the study I referenced has a six year interval between the event and publication of data examining an aspect of concern.

Now, let’s step into the present.  I’m currently taking courses for a Masters in Public Health at the University of Iowa to branch out from my basic training in veterinary medicine.

Yesterday, in a course I’m taking we had a lecture on a group of zoonotic diseases, Trypanosomes.  This group of little single celled organisms, protozoans, causes problems all over the world.   In Africa it causes, Sleeping Sickness, in Latin America, Chagas’ disease.  We don’t hear a lot about it here in North America.

What came to my attention was a disease described in dogs, here, in the U.S. caused by one in this group called Leishmania.  Dogs are a known reservoir in areas where these diseases are endemic but these U.S. reports starting in the late 1990’s were in two breeds with whopping over representation, specifically Foxhounds1 and Neapolitan Mastiffs.

That’s weird, I thought.  I’ve been a small animal veterinarian for a long time and those are not two very common breeds.  What’s up?

The first two things you need to know have to do with our basic understanding of where this parasite lives and how it infects mammals.  It has been traditionally thought a mammal becomes infected from the bite of an insect vector (tsetse fly in Africa or sand fly in South America), which is carrying the protozoa.  Also, although this occurs more rarely, you can become infected by direct contact with the blood of an infected animal into your tissue, read blood-to-blood transmission.  This second bit of information will be important later.

As well from studying these outbreaks in Foxhounds, one research group received a donated pregnant bitch they new was infected which allowed them to examine the puppies and look to see if they were also infected.  They found Leishmania in the puppies.  This lends evidence of transmission of the organism from mother to puppies in utero. Their thought is the Leishmania protozoan circulates in the mother’s blood and crosses over the placenta to infect the developing fetuses.

An important point here is the novel idea that transmission of the infection can be vertical and DOES NOT REQUIRE A VECTOR.  This would mean you could sustain the parasite in a mammal population where it has never lived before and would not normally be expected to be able to live.

This disease is endemic in parts of Europe and these two breeds, although fairly rare here in the U.S., often are imported from Leishmania endemic areas to be incorporated into U.S. breeding stock lines.   These imported dogs are very valuable and key to their breeding programs.

The work done showing vertical transmission from mother to pup suggests we can establish the infectious agent in a host indefinitely.  So far we are lucky and the areas where these dogs live don’t have vector insects readily available.  I wouldn’t count on that lasting too long.  Between global travel and climate change alone, and if historical record of disease spread with so many other zoonotic infectious agents is any guide, it’s really, likely, just a matter of time.

So a final concern, more immediate, goes back to that second route of traditional transmission I described above, the direct contact, blood-to-blood infection.   Here’s the thing.  These dogs, the Foxhounds and Neapolitan Mastiff’s that are infected are breeding dogs.  Breeding dogs, by definition, are sexually intact.  Dogs that have their “parts” can more often get into scrapes (read: fights).  When dogs fight they really can tear each other up.  The fighting often occurs around the head, neck and ears.  All fight wounds bleed, a lot.  Ears especially bleed like stuck pigs.

People try to break up the fighting dogs.  People get bitten all the time doing this.  (Read: Do not try to break up fighting dogs yourself, but that’s another essay of it’s own).  The dog blood that is all over the dogs is now all over you.  You have an open bite wound.  The dog’s blood now is mingling with your tissue and blood.  You now have Leishmania.  This is the problem.

The good news is if you are immune-competent you should mount a good response to this insult and have a very good likelihood of clearing the infection.  It will require a significant effort calling upon both arms of your immune systems, the cellular and the humoral.  Unfortunately you will not be immune to reinfection should another exposure event occur.  The bad news is if you are in anyway immune compromised, not so good.  You are likely to get clinical illness.

I guess our best hope at this point in time is to help breeders see the need and importance of choosing disease free dogs.  Encourage them to buy and bring only dogs that they have tested and know are free of Leishmania into the U.S.  I know breeding for phenotype and working characteristics and abilities is the holy grail of breeders, but can’t we do it looking at the bigger picture, the greater good?

1Monti, Dean (June 2000). “Hunters hounded as leishmaniasis is diagnosed in Foxhounds”. J Am Vet Med Assoc 216 (12): 1887, 1890.

Student guest post: Tuberculosis: A Real Problem With No Real Solution

Student guest post by Jack Hamersky

After successfully completing a job interview I had the opportunity to take the next step in my employment process: taking a Tuberculosis or TB test.  I have received the test before but never really understood the point of testing for a disease no one ever sees in my community. I always thought, “Why not focus all this effort and money on more prevalent infectious agents such as Ebola or HIV?” You know, focus on something important.  So, as the nurse called me in from the waiting room I began to curse that hard little bubble that would soon be forming under my skin, and the inconvenience it would be to have to come back to this same clinic to have it read.

This same type of experience is known throughout the United States and other developed countries.  However, many people like myself, do not know the importance of this test.  They might not know that this test is a crucial part of the much larger goal of eradicating a deadly and common worldwide disease.

What is tuberculosis and why is it even important?

Tuberculosis is a contagious disease that is found in both animals and humans. The human form of the disease is caused by a group of three bacteria: Mycobacterium bovis, Mycobacterium avium, and Mycobacterium tuberculosis.  This disease can come in two forms: latent and active.  The active form of tuberculosis causes pockets of pus called granulomatous lesions in lungs and has a death rate around 50%. It is estimated that TB infects around one third of the human population on earth and is the second leading cause of death by infectious disease, behind HIV, killing around million people annually, according to the Center for Disease Control and Prevention; CDC (4).  The greatest prevalence of TB occurs in developing countries and their low socioeconomic populations.  This is likely due to the limited availability of health care, poor nutrition, and overcrowding conditions these people face on a daily basis.  Immunosuppressed individuals, such as people infected with HIV, are also more likely to contract tuberculosis.  TB is also very hard to treat and many forms of the disease are resistant to antibiotics.

Another reason TB is so dangerous is the threat of Mycobacterium bovis. M. bovis is another strain of tuberculosis that mainly infects cattle, cervids (deer like animals), elephants, bison, etc (7,10). What makes this bacterium interesting is its been known to infect people through the consumption of raw (unpasteurized) milk or products that were made from that raw milk (1,5,7,10). This zoonotic microorganism is responsible for two percent of all new cases of TB in the US (7) with an even a greater percentage worldwide (6).  The zoonotic nature of M. Bovis allows for it to hide in wildlife populations which act as a reservoir for the disease (6,9). The good news is a campaign to eradicate M. Bovis from the US food supply began in 1993(5). The bad news is that TB remains endemic in wildlife and agricultural animal populations worldwide. The program in the United States has been a success and most of the United States is considered Bovine Tuberculosis free.  However some states, such as Michigan, still find M. bovis in their wild deer herds making the continual threat of reemergence a reality.

So what have we done about this problem?

The United States government has taken a leading role in the fight against TB. It formed the Advisory Council for the Elimination of Tuberculosis to address the growing resurgence of TB in the 1980’s (5). It also passed legislation like the Comprehensive Tuberculosis Elimination Act which called for the increase of federal funding, education, and international collaboration in the fight against TB.  Other non-governmental advancements have taken place over the years too.  A vaccine was created and is now available throughout the world.  Known as BCG, this vaccine is good at protecting children against the disease, however, it loses its effectiveness as children grow older and has not shown promising results in adults (8).  This, coupled with the increasing amount of antibiotic resistant cases (known as Multi Drug Resistant Tuberculosis or MDR TB) once again proves the fight to eradication or even control might be more of an uphill battle then we once thought.

So how is the fight to end TB going?

Over the past few decades we have made progress and in 2011, the World Health Organization reported “The absolute number to TB cases has been falling since 2006”. However, in that same report, the WHO also stated, even though TB cases had dropped, “In 2009 there were almost 10 million children who were orphans as a result of parental deaths caused by TB” (12,13).  As long as there TB is left to reside in our low income populations and in animal reservoirs it will continue to plague millions worldwide.

So where do we go from here?

The continuation and strengthening of surveillance and research projects worldwide is the key to combat tuberculosis.  The more we know about the disease and its ecology the better prepared we will be to face the challenges we may encounter during its eradication process.  Will we ever get to total world eradication of tuberculosis?  This writer thinks so but to quote the great Robert Frost it seems that “we have miles to go before we can sleep”.

1)      http://www.aphis.usda.gov/animal_health/animal_diseases/tuberculosis/

2)      http://www.cdc.gov/tb/publications/factsheets/general/mbovis.htm

3)      http://www.cdcnpin.org/scripts/tb/eliminate.asp

4)      http://www.cdc.gov/tb/statistics/default.htm

5)      http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5412a1.htm

6)      http://wwwnc.cdc.gov/eid/article/19/6/12-0543_article.htm

7)      http://www.cfsph.iastate.edu/Factsheets/pdfs/bovine_tuberculosis.pdf

8)      http://www.chop.edu/service/vaccine-education-center/a-look-at-each-vaccine/tuberculosis-vaccine.html

9)      http://www.mayoclinic.com/health/tuberculosis/DS00372/DSECTION=tests-and-diagnosis

10)  http://www.lung.org/lung-disease/tuberculosis/factsheets/multidrug-resistant.html

11)  http://www.ncbi.nlm.nih.gov/pubmed/20819249

12)  http://www.who.int/tb/publications/global_report/2011/gtbr11_full.pdf

13)  http://www.who.int/mediacentre/factsheets/fs104/en/index.html

14)  http://en.wikisource.org/wiki/Comprehensive_Tuberculosis_Elimination_Act_of_2008

15)  http://en.wikipedia.org/wiki/Mycobacterium_tuberculosis

16)  http://en.wikipedia.org/wiki/Mycobacterium_avium-intracellulare_infection

17)  http://en.wikipedia.org/wiki/Tuberculosis



E. coli update: sprouts as the culprit?

The E. coli story is moving quickly. A news report out today suggests that sprouts might be the culprit (though it should be emphasized that the outbreak strain hasn’t been isolated from these vegetables yet):

Mr Lindemann said epidemiological studies all seemed to point to the plant nursery in Uelzen in the state of Lower Saxony, about 100km (62m) south of Hamburg – though official tests had not yet shown the presence of the bacteria there.

“Further evidence has emerged which points to a plant nursery in Uelzen as the source of the EHEC cases, or at least one of the sources,” he said.

“The nursery grows a wide variety of beansprouts from seeds imported from different countries.”

As far as the molecular analyses, Kat Holt and David Holme have been doing some additional analyses of the released genome sequences, and it looks like this is an old strain of enteroaggregative E. coli (the type which usually cause more run-of-the-mill diarrhea; free review here, but it’s a bit dated) which has simply acquired the Shiga toxin. From Kat:

It will be interesting to see what more can be found as the assemblies of the strains are improved with additional data. While the analysis so far suggests that this is a classic case of E. coli sharing genes via various mechanisms of horizontal transfer (i.e. bacteria doing what bacteria do), it will be very interesting to tease out the subtleties of the virulence genes and how they interplay to result in this particularly virulent bug.

For me, another interesting unanswered question will be the origin–if it’s on the sprouts, how did it get there? Are animals in the area carrying this? Why so many antibiotic resistance genes? Still quite a bit to learn, even if the sprouts indeed turn out to be the vehicle.