Tag Archives: Infectious Disease

New Grant, Post-Doc Opportunity

Biological and Human Dimensions of Primate Retroviral Transmission
One of the great enduring mysteries in disease ecology is the timing of the AIDS pandemic. AIDS emerged as a clinical entity in the late 1970s, but HIV-1, the retrovirus that causes pandemic AIDS, entered the human population from wild primates many decades earlier, probably near the turn of the 20th century. Where was HIV during this long interval? We propose a novel ecological model for the delayed emergence of AIDS. Conceptually, in a metapopulation consisting of multiple, loosely interconnected sub-populations, a pathogen could persist at low levels indefinitely through a dynamic balance between localized transmission, localized extinction, and long-distance migration between sub-populations. This situation might accurately describe a network of villages in which population sizes are small and rates of migration are low, as would have been the case in Sub-Saharan Africa over a century ago.
We will test our model in a highly relevant non-human primate system. In 2009, we documented three simian retroviruses co-circulating in a metapopulation of wild red colobus monkeys (Procolobus rufomitratus) in Kibale National Park, Uganda, where we have conducted research for over two decades. We will collect detailed data on social interactions, demography, health, and infection from animals in a core social group.
We will also study a series of 20 red colobus sub-populations, each inhabiting a separate, isolated forest fragment. We will determine the historical connectivity of these sub-populations using a time series of remotely sensed images of forest cover going back to 1955, as well as using population genetic analyses of hypervariable nuclear DNA markers. We will assess the infection status of each animal over time and use viral molecular data to reconstruct transmission pathways.
Our transmission models will define the necessary conditions for a retrovirus to persist, but they will not be sufficient to explain why a retrovirus might emerge. This is because human social factors ultimately create the conditions that allow zoonotic diseases to be transmitted from animal reservoirs and to spread. We will therefore conduct an integrated analysis of the root eco-social drivers of human-primate contact and zoonotic transmission in this system. We will study social networks to understand how social resources structure key activities relevant to human-primate contact and zoonotic transmission risk, and we will explore knowledge, beliefs, and perceptions of human-primate contact and disease transmission for a broad sample of the population. We will reconcile perceived risk with actual risk through a linked human health survey and diagnostic testing for zoonotic primate retroviruses.
The ultimate product of our research will a data-driven set of transmission models to explain the long-term persistence of retroviruses within a metapopulation of hosts, as well as a linked analysis of how human social factors contribute to zoonotic infection risk in a relevant Sub-Saharan African population. Our study will elucidate not only the origins of HIV/AIDS, but also how early-stage zoonoses in general progress from “smoldering” subclinical infections to full-fledged pandemics.

I am thrilled to report that our latest EID project proposal, Biological and Human Dimensions of Primate Retroviral Transmission, has now been funded (by NIAID nonetheless!).  I will briefly describe the project here and then shamelessly tack on the full text of our advertisement for a post-doc to work as the project manager with Tony Goldberg, PI for this grant, in the College of Veterinary Medicine, University of Wisconsin, Madison.  This project will complement the ongoing work of the Kibale EcoHealth Project. The research team includes: Tony, Colin Chapman (McGill), Bill Switzer (CDC), Nelson Ting (Iowa), Mhairi Gibson (Bristol), Simon Frost (Cambridge), Jennifer Mason (Manchester), and me. This is a pretty great line-up of interdisciplinary scholars and I am honored to be included in the list.

Biological and Human Dimensions of Primate Retroviral Transmission

One of the great enduring mysteries in disease ecology is the timing of the AIDS pandemic. AIDS emerged as a clinical entity in the late 1970s, but HIV-1, the retrovirus that causes pandemic AIDS, entered the human population from wild primates many decades earlier, probably near the turn of the 20th century. Where was HIV during this long interval? We propose a novel ecological model for the delayed emergence of AIDS. Conceptually, in a metapopulation consisting of multiple, loosely interconnected sub-populations, a pathogen could persist at low levels indefinitely through a dynamic balance between localized transmission, localized extinction, and long-distance migration between sub-populations. This situation might accurately describe a network of villages in which population sizes are small and rates of migration are low, as would have been the case in Sub-Saharan Africa over a century ago.

We will test our model in a highly relevant non-human primate system. In 2009, we documented three simian retroviruses co-circulating in a metapopulation of wild red colobus monkeys (Procolobus rufomitratus) in Kibale National Park, Uganda, where we have conducted research for over two decades. We will collect detailed data on social interactions, demography, health, and infection from animals in a core social group.

We will also study a series of 20 red colobus sub-populations, each inhabiting a separate, isolated forest fragment. We will determine the historical connectivity of these sub-populations using a time series of remotely sensed images of forest cover going back to 1955, as well as using population genetic analyses of hypervariable nuclear DNA markers. We will assess the infection status of each animal over time and use viral molecular data to reconstruct transmission pathways.

Our transmission models will define the necessary conditions for a retrovirus to persist, but they will not be sufficient to explain why a retrovirus might emerge. This is because human social factors ultimately create the conditions that allow zoonotic diseases to be transmitted from animal reservoirs and to spread. We will therefore conduct an integrated analysis of the root eco-social drivers of human-primate contact and zoonotic transmission in this system. We will study social networks to understand how social resources structure key activities relevant to human-primate contact and zoonotic transmission risk, and we will explore knowledge, beliefs, and perceptions of human-primate contact and disease transmission for a broad sample of the population. We will reconcile perceived risk with actual risk through a linked human health survey and diagnostic testing for zoonotic primate retroviruses.

The ultimate product of our research will a data-driven set of transmission models to explain the long-term persistence of retroviruses within a metapopulation of hosts, as well as a linked analysis of how human social factors contribute to zoonotic infection risk in a relevant Sub-Saharan African population. Our study will elucidate not only the origins of HIV/AIDS, but also how early-stage zoonoses in general progress from “smoldering” subclinical infections to full-fledged pandemics.

Post Doctoral Opportunity

The Goldberg Lab at the University of Wisconsin-Madison invites applications for a post-doctoral researcher to study human social drivers of zoonotic disease in Sub-Saharan Africa.   The post-doc will be an integral member of a new, international, NIH-funded project focused on the biological and human dimensions of primate infectious disease transmission in Uganda, including social drivers of human-primate contact and zoonotic transmission.  This is a unique opportunity for a post-doctoral scholar with training in the social sciences to study human-wildlife conflict/contact and health and disease in a highly relevant ecological setting.  The following criteria apply.

  1. Candidates must have completed or be near to completing a PhD in the social sciences, in a discipline such as anthropology, geography, sociology, behavioral epidemiology, or a relevant discipline within the public health fields.
  2. Candidates must have a demonstrated interest in health and infectious disease.
  3. Candidates must have prior field experience in Sub-Saharan Africa.
  4. Candidates must be willing to relocate to Madison, Wisconsin for three years.
  5. Candidates must be willing to spend substantial time abroad, including in Sub-Saharan Africa and at partner institutions in the United Kingdom.
  6. Candidates must have experience with collection and analysis of both quantitative and qualitative data.  Familiarity with methods such as social network analysis, GIS, participatory methods, and survey design would be advantageous.

The successful candidate will help lead a dynamic international team of students and other post-docs in a multi-institutional, multidisciplinary project.  Duties involve a flexible combination of fieldwork, analyses, and project coordination, in addition to helping to mentor students from North America, Europe, and Africa.  The successful applicant will be expected to explore new research directions of her/his choosing, assisted by a strong team of collaborators.

University of Wisconsin-Madison is a top-notch institution for research and training in the social and health sciences.  Madison, WI, is a vibrant city with outstanding culture and exceptional opportunities for outdoor recreation.

Applicants should send a current CV, a statement of research interests and qualifications (be sure to address the six criteria above), and a list of three people (names, addresses, e-mails) who can serve as references.

Materials and inquiries should be sent to Dr. Tony L. Goldberg (tgoldberg@vetmed.wisc.edu).  Application materials must be received by September 12, 2011 for full consideration; the position is available starting immediately and requires a three-year commitment.

A New Vector for Leishmania

It isn’t every day that we learn about the discovery of an entirely new vector for an important vector-borne disease. A new report by the Australian Department of Agriculture and Fisheries has identified a new species of Leishmania that is transmitted by midges, not the usual vector, sandflies. Leishmania is a vector-borne protozoan parasite that causes an ulcerative disease known as Leishmaniasis or Kala-azar. Leishmaniasis is a disease primarily of the tropics and subtropics and is considered one of the most neglected infectious diseases in the world. The usual vectors are phlebotomine sandflies.

Australia (along with Antarctica) was thought to be the only continent free of Leishmania when locally-acquired infection was detected in kangaroos in Northern Territory in 2003.  Researchers investigating this infection thought that the local sandflies (Sergentomyia spp.) seemed highly unlikely vectors because they show a strong preference for feeding on reptiles. Indeed, screening for Leishmania in 3046 Sergentomyia sandflies yielded none infected with Leishmania. This led the researchers to expand the vectors tested. What they found was an unnamed species of day-feeding midge (Lasiohelea sp.) that was infected with a prevalence of up to 15 percent. This is the first identified vector for Leishmania that is not a phlebotomine sandfly. Not much is known about this midge.  The researchers were unable to find breeding sites, for example. The presence of prolegs on the midge larvae suggest that it is not aquatic but is terrestrial or semi-acquatic.  The authors suggest looking for midge breeding sites in the moist soil near water troughs where kangaroos drink.

Finding a totally new vector for a disease carries with it implications for eradication and control. One possibility raised by this work is that the difficulty some control programs have experienced may reflect the fact that Leishmania is being transmitted by multiple vectors. This is an hypothesis well worth investigating in areas other than Australia.

This work formed the basis of the Ph.D. dissertation for Annette Dougall at Charles Darwin University, Menzies School of Health Research.  Nice work, Annette!

Measuring Epidemiological Contacts in Schools

I am happy to report that our paper describing the measurement of casual contacts within an American high school is finally out in the early edition of PNAS. Stanford’s great social science reporter, Adam Gorlick, has written a very nice overview of our paper for the Stanford Report (also here in the LA Times and here on Medical News Today). The lead author, and general force of nature behind this paper, is Marcel Salathé, who until recently was a post-doc here at Stanford in Marc Feldman‘s lab.  This summer, Marcel moved to the Center for Infectious Disease Dynamics at Penn State, a truly remarkable place and now all the better for having Marcel.  From the Penn State end, there is a nice video describing our results as well as well as a brief note on Marcel’s blog.  This paper has not been picked up quite like our paper on plague dynamics this summer, probably because measuring casual contacts in an American high school generally does not involve carnivorous mice.

With generous NSF funding, we were able to buy a lot of wireless sensor motes — enough to outfit every student, teacher, and staff member at a largish American high school so that we could record all of their close contacts in a single, typical day. By “close contact,” we mean any more-or-less face-to-face interaction within a radius of three meters.  As Marcel was putting together this project, we were (once again) exceptionally lucky to find ourselves at Stanford along with one of the world authorities on wireless sensor technology, Phil Levis, of Stanford’s Computer Science department.  Phil and his students, Maria and Jung Woo Lee, made this work come together in ways that I can’t even begin to fathom.  This actually leads me to a brief diversion to reflect on the nature of collaboration.  As with our plague paper or SIV mortality paper, this paper is one where collaboration between very different types of researchers (viz., Biologists, Computer Scientists, Anthropologists) is absolutely fundamental to the success of the work.  In coming up for tenure — and generally living in an anthropology department — the question of what I might call the partible paternity of papers (PPP) comes up fairly regularly. “I see you have a paper with five co-authors; I guess that means you contributed 17% to this paper, no?”  Well, no, actually.  I call this the “additive fallacy of collaboration.” When a paper is truly collaborative, then the contributions of the paper are not mutually exclusive from each other and so do not simply sum.  To use a familiar phrase, the whole is greater than the sum of the parts.  Our current paper is an example of such a truly collaborative project.  Without the contributions of all the collaborators, it’s not that the paper would be 17% less complete; it probably wouldn’t exist. I can’t speak particularly fluently to what Phil, Maria, and Jung Woo did other than by saying, “wow” (thus our collaboration), but I can say that we couldn’t have done it without them.

I’ll talk more about our actual results later.  For now, you’ll either have to read the paper (which is open access), watch the video, or read the overview in the Stanford Report.

Ah, Ape-Scat, Pleasing is the Fragrance of Your Perfumes

One of the fundamental ontological questions of our day is surely, “is there anything you can’t do with ape scat?” Well, OK, this might be pushing it a bit far, but a recent article in the New York Times makes a pretty strong case for the blessings of this pungent goo.  My collaborator Beatrice Hahn, quoted in this article as saying that ape scat is “worth its weight in gold,” has been collecting fecal samples gathered by far-flung ape researchers throughout Africa. In addition to providing fundamental data on the landscape-level distribution of SIV (the work on which I have collaborated with her), Beatrice’s ape scat collection has now yielded the secret of the origin of Plasmodium falciparum, the most deadly of the five species that cause human malaria infection. The paper by Liu and colleagues appeared in the 23 September issue of Nature.  There is a nice accompanying piece by Eddie Holmes as well. It turns out that P. falciparum malaria spilled over into human populations from western gorillas, rather than from chimpanzees as had long been thought. Makes all that smelly collecting actually seem worthwhile…

The Little Mouse on the Prairie

We have a new paper in the Early Edition of PNAS on the ecology of plague in prairie dogs. The Stanford News Service did a nice little write-up of the paper (and Mark Shwartz’s full version is available on the Woods Institute site) and it has now been picked up by a number of media outlets including USA Today, ScienceDaily, The Register (UK), as well as a couple of radio news shows. This paper has been a real pleasure for me because of my incredible collaborators.  Dan Salkeld, who has been a post-doctoral fellow with me and now splits his time between teaching in Human Biology at Stanford and working as an epidemiologist for the California Department of Health, is the lead author.  Dan is clearly one of the leading young disease ecologists working today and his understanding of the field and willingness to do the sometimes unglamorous grunt work of ecology in pursuit of important research questions continually impresses me. The paper uses data that he collected while he worked for co-author Paul Stapp on Paul and collaborators’ plague project in the Pawnee National Grasslands in Colorado. Dan and Paul had the idea that grasshopper mice (see below) might have something to do with the episodic plague outbreaks in prairie dog towns.  Apparently, this idea was met with skepticism by their colleagues. When Dan came to Stanford, I suggested that we could probably put together a model to test the hypothesis. While we were waiting for our research permits to come through for a project in Indonesia (also dealing with plague; another long story), we decided to take up the challenge. What really made the whole project come together was the fortuitous office-pairing of Dan with Marcel Salathé, another post-doc with whom I have collaborated extensively on questions of social networks and infectious disease.  In addition to being a brilliant theoretical biologist, Marcel is an ace Java programmer.  Following a few white-board sessions in the studio near our offices, Dan and Marcel put together an amazing computer simulation that achieves that perfect balance between simplicity and realism that allows for scientific insight.

I don’t think anyone would have predicted this particular collaboration and this particular outcome.  The results described in this paper come from an incredibly interdisciplinary collaboration. I am really struck at how great science can come from a few simple ingredients: (1) long-term ecological data collection facilitated by a visionary program at the National Science Foundation, (2) a space where people from quite different disciplines and with different scientific sensibilities can get together and brain-storm, (3) flexible funding that permits researchers to explore the interesting – if offbeat – scientific questions that arise from such interactions.  So, I have many debts to acknowledge for this one.  The field data come from the project for which Mike Antolin at Colorado State is the PI (out co-author Paul Stapp is a Co-PI for that as well).  The funding source for this project was the joint NSF/NIH Ecology of Infectious Disease program. This is a cross-cutting program that “supports the development of predictive models and the discovery of principles governing the transmission dynamics of infectious disease agents” (from the EID home page).  The space – both physical and intellectual – that permitted this work to happen was provided by the Woods Institute for the Environment.  This paper literally came into being in the project studio on the third floor of Y2E2 in the Land Use and Conservation area.  Amazingly, this is exactly what these studios were designed to do.  My office in Y2E2 has adjoining office space for grad-students and post-docs and this is where Marcel and Dan did most of their hashing. It was always amusing to pop my head in and see them both huddled around a computer, having animated discussions about how best to represent the complex ecology in a computational model that is simple enough to understand and flexible enough to allow us to test hypotheses.  Finally, funding. Dan was funded by a Woods Environmental Ventures Project grant for which I am the PI.  Marcel was funded by the Branco Weiss Science in Society Fellowship.  My own flexibility was assured by a career grant form the National Institutes of Health. Research funding is almost always important, but the requirements of research funding can sometimes be too constraining to permit exploration of really new ideas.  All three of these mechanisms (Woods EVP, Branco Weiss, NIH K01) provide exactly the type of flexibility that fosters creativity. I wish there were more programs like these.

One of the fundamental questions in disease ecology is how extremely pathogenic infectious agents persist both through time and across landscapes.  Plague is a bacterial disease that affects a wide range of rodents throughout the world and, in North America, particularly afflicts prairie dogs (Cynomys ludovicianus).  Plague epizootics (the animal equivalent of epidemics in humans) are dramatic affairs with almost complete mortality of massive prairie dog ‘towns’ of thousands of animals. If plague is so deadly to prairie dogs, how does it persist?  Is there another reservoir (i.e., an other host species that can maintain an infection in the absence of prairie dogs)?  Does plague get into the soil and persist in some sort of suspended state (the way that some Mycobacteria do, for example) waiting to reinfect a re-colonized prairie dog town? Or is plague really enzootic (i.e., when an infection persists at low levels in an animal population) and we just haven’t detected it? This question has wide applicability. Consider diseases of people such as Ebola Hemorrhagic Fever or SARS, or, going back a few hundred years in human history, that nastiest of bacterial diseases, bubonic plague. Yes, the same beastie.  A disease that killed a third of the population of Europe in the fourteenth century exists in prairie dogs in North America today (and sometimes spills over to produce human infections).

Prairie dogs are a keystone species of the grasslands of the American West. They are  threatened by various anthropogenic forces, including habitat destruction and human persecution.  But most importantly, prairie dog viability is threatened by plague.

Plague, a disease caused by the bacterium (Yersinia pestis) and the causative agent of Black Death, arrived in USA via San Francisco ca. 1900, and still infects (or threatens to infect) people each year, including in California. Plague killed as many as 200 million people in Medieval Europe. It is still important in Africa and Asia.  There have been sizable epidemics as recently as the middle twentieth century in India and China and a substantial outbreak in Surat, India in 1994 that, in addition to death, caused widespread panic and social disruption.

Previous modeling and ecological work tended to assume that die-outs occur very rapidly.  But questions dogged this work (as it were): were the apparently rapid die-offs simply an artifact of finally seeing dead dogs dropping all over the place? Prairie dogs do live underground, after all, and they live in enormous towns.  Who would miss a few dead dogs underground in a town of thousands?  Our paper suggests that previous modeling efforts get the story wrong. They fail to account for observed patterns because they missed key elements of the picture.  Previous models that could describe the phenomena lacked an actual explanation – it’s a magical reservoir? It’s a carnivore? Certainly it’s something somewhere?

While prairie dogs live in enormous towns, they are highly territorial within the towns.  Towns form because of the benefits of predator defense. They live in small family groups known as coteries, and these coteries form a more-or-less regular grid of small defended territories within the towns. Because of this regular structure induced by their territoriality, a directly-transmitted infectious disease can only move so quickly through a town since it could only be transmitted to immediate neighbors and each coterie only has a couple of these.  Plague is not directly transmitted though.  It is carried by flea vectors, but if the dispersal distance of a flea is less than the diameter of a coterie’s territory, then the transmissibility of this vector-borne disease is similar to something that is directly transmitted.  Prairie dogs are territorial and this territoriality limits the rate of disease propagation through prairie dog towns. However, prairie dogs are not alone on their eponymous prairies.

Grasshopper mice – smelly, carnivorous mice, happy to eat through prairie dog carcasses – get swamped by fleas that normally live on prairie dogs. And grasshopper mice have no respect for prairie dog territories. They spread fleas across prairie dog coteries. This is the critical piece of the puzzle provided by our analysis.  Grasshopper mice are the key amplifying hosts for plague in prairie dogs.  Grasshopper mice increase the spread of disease by moving fleas across the landscape, similar to the way that highly promiscuous people may spread HIV or so-called ‘super-spreders‘ transmitted SARS in the global outbreak of 2003.  Of course, there are interesting differences between the plague model and these other diseases. Grasshopper mice are like super-spreaders in that they push the system over the percolation threshold.  They are unlike super-spreaders in that they don’t have that many more contacts than the average – they just connect otherwise unconnected segments of a population already near the threshold of an epidemic.

Without grasshopper mice, plague still kills prairie dog families, one at a time, but it moves very slowly, and it is extremely hard to detect (who misses 5 dead prairie dogs in a colony that stretches for 200 hectares and has upwards of 5000 animals?).  The grasshopper mice take a spatially-organized system that is on the verge of an epizootic and push it over the threshold.  The term ‘percolation threshold’ in the title of our paper relates to a branch of theory from geophysics that explains how and when a fluid can pass through a porous random medium.  This theory uses random graphs, which are the same mathematical structure that we use to model social networks, to understand when, for example, a medium will let water pass through it – i.e., to percolate. When the density of pores in, say, a layer of sandstone passes a critical density, water can pass from the surface through to recharge the aquifer. Similarly, when the density of susceptible prairie dog families crosses a critical threshold, plague can sweep through and wipe out a town of thousands of individuals.  The spatial structure induced by prairie dog territoriality turns out, on average, to be not quite at the percolation threshold (though it’s close).  What the grasshopper mice do is provide the critical connectivity that puts the system over the threshold and allows a slowly simmering enzootic infection turn into a full-blown epizootic.

It is in thinking about percolation thresholds that we see how important the behavior of affected species is for understanding disease dynamics.  Plague in Asian great gerbils, while effectively modeled using the same mathematical formalism, only requires one species in order to achieve the percolation threshold. Because great gerbils roam more widely and mix more, what matters for plague epizootics in this species is simply overall gerbil density.

It seems quite likely that this pattern of diseases smoldering at low-level below the detection threshold before some dramatic occurrence brings them to general attention is common, particularly with emerging infections. For example, there is evidence for extensive transmission of H1N1 ‘swine flu’ in Mexico before a large number of deaths appeared seemingly quite suddenly in April of 2009.  A number of other diseases – both of people and wildlife – show this pattern of being seemingly completely lethal, burning through host communities, and disappearing only to reappear some years later.  Important examples include Ebola in both humans and gorillas, hantavirus in people, anthrax in zebra, or chytrid fungi and frogs.

What are the key take-home messages of this paper? There are five, as far as I see it: (1) plague is enzootic in prairie dogs and there is no need to posit an alternate reservoir, (2) this said, the transition from enzootic to epizootic infection in prairie dogs is mediated by grasshopper mice, (3) understanding disease ecology – including species interactions – is a key to understanding (and predicting) dynamics, (4) behavior matters for disease dynamics, and (5) epidemiological surveillance is essential for controlling infectious disease – just because you don’t see a disease, doesn’t mean it’s not there!

I’m sure I’ll have more to say about this.  I did want to note that the publication of this paper coincides with a personnel transition here in our group at Stanford. Marcel has moved on to a faculty position, joining the spectacular Center for Infectious Disease Dynamics at Penn State.  Peter Hudson and his crew have assembled an amazing and eclectic group of scientists in Happy Valley and kudos to them for landing Marcel.  I frequently think that only a total fool would pass up an offer to join this exciting and productive group, but that’s another story. I expect Marcel to do great things there and look forward to continued collaborations.

Mutant Fungus Threatening World Wheat Supplies

A mutant strain of the wheat stem rust fungus, Puccinia graminis f. sp. tritici, has emerged that threatens as much as 60 million tons of world wheat production.  The story of this emergence can be found here.  There is a clearinghouse of information on the Borlaug Global Rust Initiative website. The emergence of such a potentially devastating crop pathogen highlights once again the practical importance of evolutionary biology for understanding major world problems.

Update on Salmonellosis Saintpaul

The Centers for Disease Control and Prevention have just issued a new report on the ongoing outbreak of Salmonella serotype Saintpaul infection. Since April, 1237 people have been infected.  The investigation has continued to focus on raw tomatoes but also jalepeño (and serrano) chiles and cilantro.  This further supports my previous speculation, based on the age profile of the cases, that salsa consumed while drinking alcoholic beverages might be implicated in this outbreak.  Epidemiological investigations are greatly complicated when multiple vehicles that are typically consumed together are implicated.

There is an interesting caution that accompanies the epidemic curve:

Salmonellosis Saintpaul Epidemic Curve

This has to do with the fact that it can be very misleading to read too much into an epidemic curve for an ongoing outbreak. Consider the epidemic curve for the 2003 SARS outbreak in Singapore:

Singapore 2003 SARS Epidemic Curve

Now imagine we were looking at the curve as it evolved on 12 March.  We might have be tempted to say that the epidemic was coming to an end and, man, would we ever have been wrong! There are a couple of things at work here.  First, epidemics often have multiple introductions and while theory tells us that an epidemic curve will be more or less bell shaped, this is based on the assumption of a single introduction.  If you look at the SARS epidemic curve hard enough, you can see several more-or-less bell-shaped components added together.  The second issue with SARS is that there is extreme heterogeneity in transmission.  Patient #1 probably infected 21 other cases, patient #4 probably infected 62.  The great majority of others infected none.  Individuals who infect more than 10 others are what is known as “superspreaders.”  There were five in the Singapore outbreak out of a total of 201 probable cases of SARS and 722 suspect cases.  Finally, there is often a delay between when people get sick and when their cases are reported.  This means that the trailing edge of the epidemic curve always looks like it’s closing off its bell shape. The full case report for the Singapore outbreak can be found here

So, is the current Salmonellosis outbreak on the wane?  Let’s hope so, but as CDC warns:

It can be difficult to say when the outbreak is over, because of the reporting delay.   The delay means that the curve for the most recent three weeks always looks like the outbreak could be ending even during an active outbreak. The full shape of the curve is only clear after the outbreak is over.

With a vehicle-borne disease, we don’t have to worry about superspreaders, but the fact that we still don’t know the source of the infection or the ultimate cause of the contamination is troubling.  Who knows how much contaminated (presumably) produce is lurking out there?  I, for one, will make sure to wash my produce well!