HIV’s “Patient Zero” was exonerated long ago

The news over the past 24 hours has exclaimed over and over:

HIV’s Patient Zero Exonerated

How scientists proved the wrong man was blamed for bringing HIV to the U.S.

Researchers Clear “Patient Zero” from AIDS Origin Story

H.I.V. Arrived in the U.S. Long Before ‘Patient Zero’

Gaetan Dugas: “patient zero” not source of HIV/AIDS outbreak, study confirms

HIV’s supposed “Patient Zero” in the U.S., Gaetan Dugas, is off the hook! He wasn’t responsible for our outbreak!

This is presented as new information.

Gaetan Dugas, from Wikipedia.

It is not, and I think by focusing on the “exoneration” of Dugas, a young flight attendant and one of the earliest diagnosed cases of AIDS in the U.S., these articles (referencing a new Nature paper) are missing the true story in this publication–that Dugas was really a victim of Shilts and the media, and remains so, no matter how many times the science evidence has cleared his name.

First, the idea that Dugas served to 1) bring HIV to the U.S. and 2) spark the epidemic and infect enough people early on that most of the initial cases could be traced back to him is simply false. Yes, this was the hypothesis based on some of the very early cases of AIDS, and the narrative promoted in Randy Shilts’s best-selling 1987 book, “And the Band Played On.” But based on the epidemiology of first symptomatic AIDS cases, and later our understanding of the virus behind the syndrome, HIV, we quickly understood that one single person in the late 1970s could not have introduced the virus and spread it rapidly enough to lead to the level of infections we were seeing by the early 1980s. Later understanding of the virus’s African origin and its global spread made the idea of Dugas as the epidemic’s originator in America even more impossible.

When we think of Dugas’s role in the epidemiology of HIV, we could possibly classify him as, at worst, a “super-spreader“–and individual who is responsible for a disproportionate amount of disease transmission. Dugas acknowledged sexual contact with hundreds of individuals between 1979 and 1981–but his numbers were similar to other gay men interviewed, averaging 227 per year (range 10-1560). And while Shilts portrayed Dugas as a purposeful villain, actively and knowingly spreading HIV to his sexual partners, that does not jibe with both our scientific knowledge of HIV/AIDS or with the assistance Dugas provided to scientists studying the epidemic. Dugas worked with researchers to identify as many of his partners as he could (~10% of his estimated 750), as the scientific and medical community struggled to figure out whether AIDS stemmed from a sexually-transmitted infection, as several lines of evidence suggested. There’s no evidence Dugas was maliciously infecting others, though that was the reputation he received. Dugas passed away from complications of AIDS in March of 1984–weeks before the discovery of HIV was announced to the general public.

Furthermore, the information in the new publication is not entirely novel. Molecular analyses carried out in part by Michael Worobey, also an author on the new paper, showed almost a decade ago that Dugas could not have been the true “Patient Zero.” The 2007 paper, “The emergence of HIV/AIDS in the Americas and beyond,” had the same conclusions as the new paper: HIV entered the U.S. from the Caribbean, probably Haiti, and was circulating in the U.S. by the late 1960s–when Dugas was only about 16 years old, and long before his career as a flight attendant traveling internationally. So this 2007 molecular analysis should have been the nail in the coffin of the Dugas-as-Patient-Zero ideas.

But apparently we’ve forgotten that paper, or other work that has followed the evolution of HIV over the 20th century.

What is unique about the new publication is that it included a sample from Dugas himself, via a plasma contribution Dugas donated in 1983, and other samples banked since the late 1970s. The new paper demonstrated that Dugas’s sample is not in any way unique, nor is it a “basal” virus–one of the earliest in the country, from which others would diverge. Instead, it was representative of what was already circulating among others infected with HIV at that time. In supplemental information, the authors also demonstrated how notation for Dugas in scientific notes changed from Patient 057, then to Patient O (for “Outside California”) to Patient 0/”Zero” in the published manuscript–which Shilts then named as Dugas and ran with in his narrative.

Graphic of sexual network of early AIDS cases, from Auerbach et al., Am J Med 1984.


The media then extended Shilts’s ideas, further solidifying the assertion that Dugas was the origin of the U.S. epidemic, and in fact that he was outright evil. The supplemental material notes that Shilts didn’t want the focus of the media campaign initially to be about Dugas, but was convinced by his editor, who suggested the Dugas/Patient Zero narrative would result in more attention than the drier critiques of policy and inaction in response to the AIDS epidemic by the Reagan administration.

And the media certainly talked about it. A 1987 edition of U.S. News and World Report included a dubious quote attributed to Dugas: “‘I’ve got gay cancer,’ the man allegedly told bathhouse patrons after having sex with them. ‘I’m going to die, and so are you.’” NPR’s story adds “The New York Post ran a huge headline declaring “The Man Who Gave Us AIDS. Time magazine jumped in with a story called ‘The Appalling Saga Of Patient Zero.’ And 60 Minutes aired a feature on him. ‘Patient Zero. One of the first cases of AIDS. The first person identified as the major transmitter of the disease,’ host Harry Reasoner said.”

This is the real scandal and lingering tragedy of Dugas. His story was used to stoke fear of HIV-infected individuals, and especially gay men, as predators seeking to take others down with them. His story was used in part to justify criminalization of HIV transmission. So while science has exonerated him again and again, will the public–and the media–finally follow?





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.

MCR-1 has been identified in the United States–what is it, and what does it mean?

                      E. coli, from Wikipedia commons

We’ve been expecting it, and now it’s here.

Yesterday, two article were released showing that MCR-1, the plasmid-associated gene that provides resistance to the antibiotic colistin, has been found in the United States. And not just in one place, but in two distinct cases: a woman with a urinary tract infection (UTI) in Pennsylvania, reported in the journal Antimicrobial Agents and Chemotherapy, and a positive sample taken from a pig’s intestine as part of the National Antimicrobial Resistance Monitoring System (NARMS), which tracks resistant bacteria related to retail meat products. Not surprising, not unexpected, but still, not good.

Colistin is an old antibiotic. Dating back to the 1950s, it’s been used sparingly over the decades because it can cause serious damage to the kidneys and nervous system. It’s also typically administered intravenously in humans, so you can’t just pop a colistin pill and be sent home from the doctor. Newer preparations appear to be safer, and because of the problem with antibiotic resistance in general and limited treatment options for multidrug-resistant Gram-negative infections in particular, colistin has seen a new life in the last decade or so as a last line of defense against some of these almost-untreatable infections.

Because of its sparing use in humans, resistance has not been much of an issue until recently. And while human use is relatively rare compared to other types of antibiotics, in animals, the story is different. Because colistin is old and cheap, it’s used as an additive to feed in Chinese livestock, to make them grow faster and fatter. (We do this here in the U.S. too, but using different antibiotics than colistin). So as would be expected, use of this antibiotic led to the evolution and spread of a resistant strain, due to the presence of the MCR-1 gene. By the first time they saw this resistance, it was already present in 20% of the pigs they tested near Shanghai, and 15% of the raw meat samples they tested. In this case, the gene is on a plasmid, which makes it easier to spread to other types of bacteria. To date, most of the reports of MCR-1 have been in E. coli, but it’s also been found in Salmonella and Klebsiella pneunoniae–all gut bacteria that can be spread from animals via contaminated food products, or person-to-person when someone carrying the bacterium doesn’t wash their hands after using the bathroom.

So a question becomes, how exactly did it get here? And that’s very difficult to say right now. The hospital where the human case was reported notes that the patient reported no travel history in the past 5 months (so it’s unlikely that she traveled to China, for instance, and picked up the gene or bacterium carrying it there). The hospital says they’ve not found other MCR-1 positive isolates from other patients, but also that they’ve only been testing specimens for 3 weeks, so…yeah. Hard to say. People and animals (like the tested pig) can carry E. coli or other species that harbor MCR-1 in their gut without becoming ill, so it may have been in the population for awhile (as they’ve seen in Brazil) before it came to the attention of medical researchers. Perhaps it’s been circulating in some of our meat products, or spreading in a chain of miniscule transfers of shit from person to person to person to person, for longer than we realize. Or both.

I was asked on Twitter yesterday, “Should I panic today or put that off until next week?” I’m not an advocate of panic myself, but I do think this is yet another concern and another hit on our antibiotic arsenal. It’s not widespread in this country and as mentioned, colistin is luckily not a first-line drug, so it won’t affect all *that* many people–for now, at least.


There are already papers out there showing bacteria that have both NDM-1 (or related variants) and MCR-1 genes. NDM-1 is a gene that provides resistance to another class of last-resort antibiotics, the carbapenems. (Maryn McKenna has covered this extensively on her blog). When carbapenems fail, treatment with colistin sometimes works. But if the bacterium is resistant to both colistin and carbapenems, well…not good. That hasn’t been reported yet in the U.S., but it’s only a matter of time, as McKenna notes.

It doesn’t mean that we’re out of antibiotics (yet) or that everyone who has one of these resistant infections will be unable to find a treatment that works (yet). But we’re inching ever closer to those days, one resistant bacterium at a time.

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.

The microbiology of zombies, part IV: hidden infections

(As previously, spoilers abound)

So on this week’s Walking Dead soap opera, we find that Daryl/Michonne’s group is still out and about searching for medical supplies. Back at the prison, the food situation is dire (apparently all the food stores were in the cell block where the infection broke out), so Rick and Carol head out to look for both medicines and food from the local ‘burbs. During their outing, discussion ensues of Carol’s attempt to stop the prison’s apparent influenza outbreak by killing two people who, at that point, were the only ones showing symptoms of disease. Rick decides he can’t trust her, and ends up banishing her from the group.

Carol said multiple times that she was trying to do the right thing, to protect the rest of the group from those who were sick and was only trying to end the outbreak. However, here’s where some knowledge of infectious disease would have helped her. Every disease has an incubation period: the time when the microbe is multiplying in your body, but you’re not showing any physical disease symptoms yet. This can be short–as little as perhaps a few hours for something like Salmonella food poisoning. It can be extremely extended, as I mentioned with rabies virus in my previous post, where the incubation period can be months to years. With influenza, the typical incubation period is 2 days, but it can be as short as 1 or as long as 4-5. The kicker is that a person who’s incubating flu can still spread it even before they show symptoms of the illness. So just because Karen and David were the only ones actively coughing and looking miserable, Carol was mistaken in her assumption that they were the only ones infected, and that she could stop the outbreak by snuffing them.

This is the difference between two similar concepts, quarantine and isolation. People who have been *exposed* to an infectious agent, but are not yet showing any signs of illness, can be quarantined to keep them away from others due to their *potential* to spread a disease. Those who are already showing signs and symptoms are placed into *isolation* to keep them from spreading it–they’re a known quantity. The prison group has used primarily isolation to keep the infection from spreading: they’re putting the ill in the Death Row cell blocks as an isolation area, and those who are well can roam around as they choose. (Maggie, for instance, hasn’t been sent to quarantine even though she clearly was exposed to the illness by being in such close contact with Glenn).

However, one thing that the group hasn’t yet determined (probably because no one has recovered as of yet) is how long they’re going to keep anyone who gets better in the isolation area. Though adults usually stop releasing influenza virus even before their symptoms are completely gone, kids can shed the virus for a long time: up to two weeks after their symptoms started according to one study (and others have found similar results). So while right now they have the healthy young children segregated from everyone else for their own protection, in theory, if Lizzie (the flu-infected child currently in held in isolation) gets well and is released back to the healthy kid’s room, she could simply re-start the outbreak there, among the most susceptible. 

This is why disease eradication is so difficult, and why it’s been accomplished for so few pathogens to date: many pathogens can spread on the sly, even when people don’t know they’re sick. For influenza, even if it’s knocked down in this group (and of course, it soon will be one way or another–at some point, the susceptible hosts in the prison will be exhausted, either by infection & recovery or by death), there is always another reservoir of disease out there. It may be other humans. Darryl/Michonne’s group finally made it to the veterinary school mentioned two episodes ago, and the zombies they ended up fighting there had clinical signs that looked an awful lot like the survivors had seen at the prison: blood that had come from the eyes and nose. Had flu been circulating there as well? It’s a vet school, pigs could certainly be housed (there were a number of animal cages, and could easily be an outdoor space for livestock somewhere). So pigs could be serving as a reservoir. Flu can also come from a number of other animals–most notably, birds, who don’t even have to appear sick to transmit the infection to people.

Infections can be sneaky and unseen, as this group should well know.

See also:

Part I: the microbiology of zombies

Part II: ineffective treatments and how not to survive the apocalypse

Part III: “We’re all infected”

Did Yersinia pestis really cause Black Plague? Part 5: Nail in the coffin

Despite its reputation as a scourge of antiquity, Yersinia pestis–the bacterium that causes bubonic plague–still causes thousands of human illnesses every year. In modern times, most of these occur in Africa, and to a lesser extent in Asia, though we have a handful of cases each year in the U.S as well.

When Y. pestis was first confirmed as the cause of bubonic plague during an 1894 outbreak in Hong Kong, most people assumed that we also now knew the cause of the 14th-century Black Death, and the later plague outbreaks that resurfaced periodically. However, there has been lingering resistance to the idea that Y. pestis actually caused the Black Death. I covered the reasoning behind this resistance in a series of posts back in 2008, so I’ll just give the Cliff notes version here. Basically, many of those advocating “not Y. pestis” pointed to differences in the epidemiology of the Black Death compared to modern outbreaks of Y. pestis. Today, people are much less likely to die of plague; the outbreaks aren’t nearly as big; and the pneumonic form (which infects the lungs and is therefore able to spread directly person-to-person) seems too rare to account for the number of cases that occurred during the Black Death. Also, they argue that transmission across Europe was much too fast, given that rodents (typically rats) are the disease vector. Instead of Yersinia, some authors have suggested that the Black Death was instead caused by a hemorrhagic fever virus, or perhaps by an unknown microbe that went extinct sometime in the last 600 years.

More recently, we’ve been able to test these claims, using paleomicrobiology to look for molecular evidence of Y. pestis in skeletons that presumably died of plague. Many of these come from mass graves that have been dated to the time of the Black Death–some also have parish or other town records to attest to the timing of the grave. In most cases, investigators found Y. pestis DNA. In a few cases, they didn’t, which led to controversy and charges of contamination in the positive samples.

However, the tide has turned. In 2010 and 2011, three papers came out which, um, put the nail in the coffin for the Y. pestis naysayers. At the time, the papers got press not necessarily because of what they explained, but because the ancient Y. pestis strains looked fairly ordinary–there was nothing obvious to suggest why, from the bacterial point of view, the Black Death was so deadly. However, I hadn’t had a chance to read these closely until now, and one of the punches never made it into the mainstream media. From the discussion section of this paper, the authors note:

Two of the authors (SW and JM) have previously argued that the epidemiology, virulence, and population dynamics of the Black Death were too different from those factors of modern yersinial plague to have been caused by Y. pestis (13). Given the growing body of evidence implicating this bacterium as responsible for the pandemic, we believe scientific debates should now shift to addressing the genetic basis of the epidemic’s unique characteristics.

The reference cited within is this paper, where the authors cast doubt on another group’s finding of Y. pestis DNA in ancient corpses. So it took them 10 years and probably a dozen or more papers, but two “Black Death doubters” have now come around. Score one for the weight of scientific evidence changing minds.

Works cited

Schuenemann VJ, Bos K, DeWitte S, Schmedes S, Jamieson J, Mittnik A, Forrest S, Coombes BK, Wood JW, Earn DJ, White W, Krause J, & Poinar HN (2011). Targeted enrichment of ancient pathogens yielding the pPCP1 plasmid of Yersinia pestis from victims of the Black Death. Proceedings of the National Academy of Sciences of the United States of America, 108 (38) PMID: 21876176

Bos KI et al. A draft genome of Yersinia pestis from victims of the Black Death. Nature, 2011.

Haensch, S et al. Distinct Clones of Yersinia pestis Caused the Black Death. PLoS Pathogens, 2010.

Previous posts in the series

Part 1

Part 2

Part 3

Part 4

“Spillover” by David Quammen

Regular readers don’t need to be told that I’m a bit obsessed with zoonotic disease. It’s what I study, and it’s a big part of what I teach. I run a Center devoted to the investigation of emerging diseases, and the vast majority of all emerging diseases are zoonotic. I have an ongoing series of posts collecting my writings on emerging diseases, and far too many papers in electronic or paper format in my office to count. Why the fascination? Zoonotic diseases have been responsible for many of mankind’s great plagues–the Black Death, the 1918 “Spanish” flu pandemic, or more recently, HIV/AIDS. So you can imagine my delight when I read about Spillover, a new book by David Quammen on zoonotic diseases.

I’ve previously highlighted some of Quammen’s work on this site. That link goes to a 2007 story he wrote for National Geographic on “infectious animals,” which really serves as a preview to “Spillover,” introducing some of the concepts and stories that Quammen elaborates on in the book.

“Spillover” is wide-ranging, tackling a number of different infectious agents, including viruses like Nipah, Hendra, and Ebola; bacteria including Coxiella burnetii and Chlamydia psittaci; and parasites such as Plasmodium knowlesi, a zoonotic cause of malaria. HIV is a big part of the story; Quammen devotes the last quarter or so of the book to tracing the discovery and transmission of HIV from primates to humans, and from 1900 to present-day. He even takes the time to explain the basic reproductive number–something that’s not always a page-turner, but Quammen manages to do it well and without being too tangential to the rest of the story; much more of a Kate-Winslet-in-Contagion than Ben-Stein-in-Ferris Bueller delivery.

Indeed, “Spillover” is somewhat unique in that it doesn’t read quite like your typical pop science book. It’s really part basic infectious disease, part history, part travelogue. Quammen has spent a number of years as a correspondent for National Geographic, and it shows. The book is filled with not only well-documented research findings and interviews with scientists, but also with Quammen’s own experience in the field, which gives the book a bit of an Indiana Jones quality. In one chapter, he details his adventure tagging along with a research team to capture bats in China, entering a cave that “felt a little like being swallowed through the multiple stomachs of a cow.” This was after an earlier dinner in which he describes his encounters with the an appetizer of the “world’s stinkiest fruit” (I’ll keep the description of the smell to myself) with congealed pig’s blood for a main dish (bringing to mind the scooping out of monkey’s brains in “Temple of Doom”–and the various zoonotic diseases that could be associated with those, come to think of it).

Quammen’s book is an excellent, and entertaining, overview of the issues of zoonotic disease–why do they emerge? Where have they come from? How do they spread? The only thing that’s missing is more of a cohesive discussion about what to do about them. However, that’s rather understandable, as we certainly have less of a grasp of this question than we do about the others (and even with some of those, our knowledge is spotty at best). I hope “Spillover” will inspire another generation of future germ-chasers, as “The Coming Plague” did almost 20 years ago.

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.

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.



Concerned about Crypto?

This is the fourteenth of 16 student posts, guest-authored by Caroline Rauschendorfer. 

Cryptosporidiosis, known more commonly as crypto, is a gastrointestinal (GI) disease caused by parasites of the Cryptosporidium genus. If infected with crypto you may experience diarrhea, nausea, vomiting, fever, and abdominal cramps that can last up to two weeks. Definitely something you want to avoid, if possible, but at least it usually resolves on its own without medical intervention and is rarely fatal in otherwise healthy individuals. [3]

The most common disease causing organisms for crypto are C. hominis and C. parvum. C. hominis is a version of the parasite that sticks mainly to humans. Historically, large outbreaks of crypto tend to be caused by drinking water that has been contaminated with wastewater. In 1993 a large outbreak of crypto occurred in Milwalkee, Wisconsin, making 403,000 people ill. It was thought to be caused by a failure of drinking water purification. It is also possible to get crypto from a variety of other places as well: swimming in contaminated water, eating contaminated food, or from infected livestock. [3]

It is this last possibility for transmission that I am most concerned with. As I said earlier, C. hominis sticks primarily to people; but C. parvum, another type of Cryptosporidium, has the ability to infect most major domestic livestock. [2] As a second year veterinary student, this is a health concern for me. C. parvum is particularly common in cattle, and frequently causes infection in young calves. Crypto infected calves either come into a large animal clinic or are seen by a veterinarian on farm for being a “poor-doer” and having watery diarrhea. Veterinarians and veterinary students often come in close contact with these sick calves during treatment and can become infected themselves. As a matter of fact, contracting crypto as a veterinary student during your large animal rotation is practically a right of passage.

Many studies have been done looking at the prevalence of crypto in cattle, with a variety of results. One similarity between most studies, however, is that the prevalence of crypto is generally higher in calves than in adult cattle. Results from different studies ranged from 7.5 to 49% of U.S. dairy calves infected with crypto. [2] This means that working with calves puts you at an even greater risk of becoming infected with crypto.

No need to freak out yet, though. One thing that should be noted is: it is possible to come in contact with cryptosporidium and not become sick. Crypto is not difficult to kill, and will be removed from water by boiling it for at least 1 minute; however, routine chemical disinfection alone may not kill it. According to one study, crypto contaminates 65% to 95% of surface water and 45% to 65% of ground water in the U.S. This probably doesn’t sound like a good thing, but it actually might be.  According to another study, 35% of the U.S. population has antibodies to crypto. Repeated exposure to small doses of crypto may help build immunity against it. [4]

The body’s immune system fights disease in two ways: adaptive and innate immunity. Innate immunity is the part of your immune system that you are born with and involves the cells that patrol and recognize any type of foreign cell or molecule that might be inside your body, such as bacteria, viruses and parasites. Adaptive immunity is something that the immune system builds over time as your body is invaded by various infectious agents (viruses, bacteria, parasites, etc.). The cells that are part of the adaptive system produce a memory when they are exposed to these infectious agents so that if they encounter them again, they can mark them to be killed by other cells. In other words, innate immunity works very generally and very quickly, whereas adaptive immunity adapts to the specific infectious agent, but it takes longer to kick in. This works for crypto in that if your body is exposed to the parasite for the first time as a small amount in your drinking water, it may not be enough to make you sick, but if your adaptive immune system finds it and makes a memory it can fight off the parasite much better if you are ever exposed to it again. This would also be true if you were infected with crypto and had all the gross symptoms that go with it, it would just be more unfortunate. [5]

Immunity is also the reason why crypto, although not serious for health individuals, can be very harmful for the immunocompromised such as those on chemo drugs for cancer treatment, or people with HIV/AIDS. The number of immune cells in an immunocompromised person can be so low that they do not have enough to fight off an infection. If someone with HIV/AIDS becomes infected with crypto, it is much more likely to be lethal. [3]

Treatment of crypto for someone who is immunocompromised would be to administer blood serum, which contains immune cells, from a healthy person. This has been shown to help in some cases. Unfortunately there is no treatment for otherwise healthy individuals who become infected with crypto. Your only option is to wait out the two miserable weeks until your body fights off the parasite. In some cases, IV fluids may be helpful for people who become dehydrated from severe diarrhea. [3]

Thankfully, there are many ways to help protect yourself from crypto. The CDC recommends, as always, washing your hands, especially before eating or preparing food, after gardening, after using the bathroom, after changing children’s diapers, after tending to someone who is ill with diarrhea, or after handling animals and animal waste. The also recommend keeping your child out of daycare if they have diarrhea. At pools, lakes, and any other recreational water source, they recommend: not swimming if you have diarrhea, especially children with diapers; showering before entering the water; washing children thoroughly after changing their diaper or after they use the toilet before allowing them in the water; and not changing diapers at the poolside. The CDC recognizes livestock handling as a potential risk for crypto infection and have special recommendations for these people: minimize contact with animal feces, particularly young animals; always wear disposable gloves when cleaning up animal waste and wash hands when finished; and wash hands after contact with animals or their living areas. As a veterinary student these are all things I will have to keep in mind while treating animals to help prevent two weeks of misery for myself. [1]


1. Centers for Disease Control. Updated 2010.

2. Dixon B, Parrington L, Cook A, et al. The potential for zoonotic transmission of giardia duodenalis and cryptosporidium spp. from beef and dairy cattle in ontario, canada. Vet Parasitol. 2011;175(1-2):20-26.

3. Leitch GJ, He Q. Cryptosporidiosis-an overview. J Biomed Res. 2012;25(1):1-16.

4. Preiser G, Preiser L, Madeo L. An outbreak of cryptosporidiosis among veterinary science students who work with calves. J Am Coll Health. 2003;51(5):213-215.

5. Tizard IR. Veterinary immunology. 8th ed. Philadelphia, PA: Saunders; 2008.