“Organizational silos,” and how they prevent effective zoonotic disease tracking

It appears that the agencies that we rely on to track disease outbreaks need to start tracking disease, not just their own jurisdiction.

An article in Sociology of Health and Illness piqued my interest this last week that reveals the amount of segregation different government agencies have when dealing with zoonotic disease. The understanding of the goals and connections between livestock, wildlife, and human health among these agencies are often apathetic at best, and antagonistic at worst.

The author of the article took it upon himself to interview several government agencies with different species and regional jurisdictions, and was able to reveal what he calls “organizational silos” that develop when the values and cultures of these different agencies prevent them from working with outside groups. When attempting to monitor emerging infectious disease (EID), identification of cross-species movement is critical to predicting and preventing pandemics. Unfortunately, while they may be able to acknowledge the geographical movement of EID’s, many organizations are blinded by their specific oversight of humans or animals.

Copied from the article: Diagram showing the crossover between domestic animals, wildlife, and human EID. Important emergence factors for each circle are listed on the outside.

There are many telling comments contained in his interviews, and I encourage you to read the article to get the whole scope of the problem, but I’ve chosen to list a few of my favorites here:

From the Director of Animal Health Division at a state Department of Agriculture:

“‘We got a positive [flu result] on one of our routine surveillance tests’ of a poultry farm, Spencer complained, and ‘we were required to contact the USDA right away because of the pandemic Asian strain’. Spencer added, ‘It seems a little silly because there was no clinical illness on the property, and the strain came back something pretty common…’ In Spencer’s eyes, it was ‘hard to justify’ reporting the flu strain to the USDA… These days, Spencer said he passes on information about disease events to the state DOH and leaves it to them to tell local health boards. ‘If somebody screws up’, he shrugged, ‘at least we can blame the [Department of Health]’.”

Not an uncommon perspective for many organizations, or even coworkers! Let’s hear from another director at the USDA Animal and Plant Health Inspection Service (APHIS):

 “Clinton argued that the ‘single biggest threat for disease’ comes from ‘wildlife intermingling with domestic livestock’. He told me, ‘You can’t control the birds’ and he rightly pointed out that ducks are flu incubators. If the bird flu – which Clinton called the top priority of his agency – becomes pandemic in humans, he told me, it will come from waterfowl.”

Interesting, I might argue that we have much more interaction with domestic fowl (can’t remember the last time I handled a wild duck), but let’s see what others had to say about this viewpoint.

“Nina Marano, a zoonotic disease expert at the CDC, told me that ‘most of the outbreaks have occurred through interaction with domestic poultry’. Another example: though poultry farmers singled out wild birds called cattle egrets as the source of a 2004 flu outbreak in California, the egrets tested negative – it turned out that contaminated egg containers circulating between farms were the culprit (McNeil 2004).”

Finally, one last example of how a zoonotic disease often isn’t treated as such by human health agencies. From a Director of the Infectious Disease Bureau of a city Public Health Commission:

“When I asked Sanders to describe a zoonose that she responded to, she mentioned a recent outbreak of salmonella…and she believed that the pathogen came from two live poultry markets in Chinatown. What I found telling was that, in Sanders’ lengthy discussion of this outbreak, she did not mention any communication with veterinary medicine agencies.While the Disease Bureau’s response to salmonella followed protocol, it did not turn to the Department of Agriculture, the USDA, or any other agencies involved in animal health for help or information. Nor did it share information with them.”

Clearly here the city health board considered this a food safety issue, but payed no attention to the implications of getting meat from an approved source (a domain which definitely belongs to the USDA), or the fact that other agriculture agencies may be interested in a salmonella outbreak. There are many other telling quotes within these interviews, and I again encourage you to check out the article.

The author of the study concludes that the only examples we get of harmonious collaboration are for those diseases which are in the public eye such as rabies and influenza (H5N1 and H1N1), though we still have lines drawn even when the public is asking for action (“‘we have enough H1N1 to worry about without worrying about turkeys’. He
concluded that turkey infection is ‘a Department of Agriculture issue’”). The most shining example of the failure to communicate by these institutions in the article is the discovery of Bird Flu in the US.

The first human cases of H5N1 in the US were wrongly diagnosed with St. Louis encephalitis, resulting in the deaths of 3 patients. A veterinary pathologist at the Bronx zoo observed neurological symptoms in some of the zoo’s birds and suspected a link, however encephalitis would not have killed her birds. Both the CDC and local DOH would not accept new information from her, instead keeping the encephalitis diagnosis. She then sent specimens to a friend at an Army Medical Research Institute of Infectious Diseases, who revealed the etiology of the disease and I’m sure had a hilarious conversation with the CDC and DOH (could you please explain to us why this veterinarian is doing your job casually on the side, and doing it better?). By the time the CDC received/accepted this information, H5N1 was endemic in the area.

Nothing against the CDC, it’s a fantastic organization, but this highlights the closed lines of communication that exist between human and animal agencies the author discusses. In order to prevent the next EID crisis, rigorous epidemiology is critical. Refusing to acknowledge the importance of cross-species movement to the virulence and emergence of a disease that falls under your agency does not only prevent you from identifying the next source of infection, but leaves you with nothing but reactive measures catered to a epidemic that you refuse to fully appreciate.


Jerolmack, C. (2012). Who’s worried about turkeys? How ‘organisational silos’ impede zoonotic disease surveillance Sociology of Health & Illness DOI: 10.1111/j.1467-9566.2012.01501.x

Staphylococcus aureus diversity and subclinical mastitis

This is the first study I’ve found that was interested in cataloging bacterial diversity among subclinical (or asymptomatic) infections. While they may be less threatening to the animal’s overall health, these infections have great significance in the world of animal agriculture, where they restrict growth (or in this case, milk production), and encourage the use of medicated feeds which in turn motivate people to purchase organic products. Identifying the risk factors and causes of these infections could therefore impact both the management of food animals, and any legislation defining how and when medications can be used. With that in mind, let’s jump back into mastitis, and everyone’s favorite gram-positive, S. aureus.

It’s because of my plasmids, people can’t help but stare.
Image from http://cellimagelibrary.org/

S. aureus is one of many bacteria that cause mastitis, however it is of additional importance as it often causes chronic or recurring cases of mastitis that result in unusable milk and discomfort of the animal. In this study, the authors investigated 11 dairy farms where they expected to find S. aureus, based on previous culture findings at each farm. They defined cows that they took milk samples from as having new or chronic infections based on somatic cell counts (SCC) in the milk. If values were >200,000 cells/mL for the month of collection the infections were considered new, whereas if cell counts were  >200,000 cells/mL for more than 2 months, those infections were considered chronic. They took a single milk sample from each teat of the infected cows, for a total of 1,354 mammary glands from 350 cows.

Pulse field electrophoresis was used to identify the different subspecies/serotypes/pulsotypes (pick your word), and to identify the genes coding for enterotoxin production that had been amplified by PCR. An ELISA test was used last to detect the presence of several enterotoxins.

As the majority of exposure to enterotoxins produced my S. aureus is through milk and dairy products, subclinical infections of S. aureus are very important as a food safety control point. Unlike cows with clinical cases that are removed from production, cows with subclinical infections continue to contribute milk that makes it to the consumer, provided that the SSC is <750,000 cells/mL. The authors were unable to detect a large amount of enterotoxin in their samples, but many of the pulsotypes contained the genes coding for their production. Other studies cited by the author report the common presence of these genes in S. aureus  samples, but expression rates are inconclusive or unexplored. This means that theoretically, subclinical cows could be introducing these bacterial toxins into consumer milk in small amounts.

It’s difficult to tell how significant these amounts might be. Toxic doses of one of the enterotoxins, “Toxic Shock Syndrome Toxin 1”, has been found to be as low as 100 micrograms/Kg in miniature pigs. The concentrations that may be introduced through contaminated milk, and the bioavailability when ingested, should be explored. Takeuchi et al. (1998) were able to detect the presence of TSST- 1 in bulk milk tanks, but no one has yet to quantify the amounts of TSST- 1 potentially present in pasteurized milk.

All that being said, what good is this new information? It can be argued that because these infections are chronic and/or subclinical that these strains of S. aureus aren’t very pathogenic, but they’re still causing inflammation. By identifying common serotypes and factors leading to the subclinical infection of a herd, perhaps there are simple management changes that can prevent infection. Milking is an almost sterile procedure, with sanitation of the teats both prior and following milking, wearing gloves, and forestripping; but there could be other tricks that would target risk factors related to the spread of subclinical pathogens, especially those that are specific to a location.



Bulanda M, Zaleska M, Mandel L, Talafantova M, Travnicek J, Kunstmann G, Mauff G, Pulverer G, & Heczko PB (1989). Toxicity of staphylococcal toxic shock syndrome toxin 1 for germ-free and conventional piglets. Reviews of infectious diseases, 11 Suppl 1 PMID: 2928643

Oliveira L, Rodrigues AC, Hulland C, & Ruegg PL (2011). Enterotoxin production, enterotoxin gene distribution, and genetic diversity of Staphylococcus aureus recovered from milk of cows with subclinical mastitis. American journal of veterinary research, 72 (10), 1361-8 PMID: 21962279

Takeuchi, S., Ishiguro, K., Ikegami, M., Kaidoh, T., & Hayakawa, Y. (1998). Production of toxic shock syndrome toxin by Staphylococcus aureus isolated from mastitic cow’s milk and farm bulk milk Veterinary Microbiology, 59 (4), 251-258 DOI: 10.1016/S0378-1135(96)01253-9

Do organic animal operations encourage management decisions that negatively impact animal welfare? Part 3

Here’s the final portion of my paper: Do organic animal operations encourage management decisions that negatively impact animal welfare?

If you’ve missed the other posts, you can check out part 1, part 2,  or read the entire paper here.



Conflict Between the Organic Approach and Welfare Ideals
Despite measures taken to promote prevention, a certain amount of disease is permissible in a healthy ecosystem and the restrictions placed on organic producers by both their certification requirements and ethos can create dilemma’s that could potentially harm animals. Several classic examples of species specific situations have been examined where the animal welfare approach taken by organic producers can be considered detrimental to the animal.

It should be noted that while there is evidence that there is a reluctance to use prohibited medications and chemicals to treat disease on organic farms (Vaarst and Bennedsgaard, 2001), both the Code of Federal Regulations (CFR) and IFOAM standards explicitly state that organic livestock producers must not withhold medical treatment from a sick animal in an effort to preserve that animals organic status (IFOAM, 2005; National Archives and Records Administration, 2012a; Riddle, 2008, 2012).
Management of mastitis in organic dairies is a commonly discussed example of when health of the individual and a reluctance to accept the financial loss associated with antibiotic use can potentially harm the animal. Herd health, in general, has not been shown to be significantly different between organic and conventional dairy herds, and some data suggests that the incidence of disease may actually be lower in organic herds, though the reasons for this are unknown (Lund and Algers, 2003; Lund, 2006). Interestingly, the ban on antibiotics for clinical use is more of a concern within U.S. boarders, as the majority of certification standards in the European Union allow antibiotic use to treat clinical disease without jeopardizing the organic status of the animal (Ruegg, 2009). However, the strict FDA guidelines for organic milk production not only prohibit the use of antibiotics in organic livestock, but do not allow the use of any compounds with an antimicrobial effect that are not approved by the FDA for organic production (National Archives and Records Administration, 2012a). Currently, there are zero antimicrobials approved for use in organic animals (Ruegg, 2009). This leaves organic dairy producers extremely limited in their options for treatment when faced with a cow that has mastitis. With few options available, Zwald et al. (2004) were able to find that farmers who switched to organic production began to seek information on treatments from other organic farmers as opposed to veterinarians. This trend is not seen in countries where antibiotic options are available to organic dairy farmers (Hamilton et al., 2006).

So what options are available to organic dairy producers in the U.S.? Once again, prevention is key, but research has shown that rates of mastitis are similar between organic and conventional dairy operations (Lund and Algers, 2003; Lund, 2006). This indicates that treatment must be part of a management plan, even if the organic ethos prevents any attempts to interfere with natural processes through antimicrobial intervention. Certain drugs are available for use on the CFR’s approved substances list with increased withdrawal times to maintain the high standards expected in organic milk production (Riddle, 2008; National Archives and Records Administration, 2012a). These drugs include certain anti-inflammatory drugs that would be useful in treating fever and inflammation associated with mastitis. Beyond pharmaceuticals, therapeutic care including frequent milking is a recognized way to discourage bacterial growth within the affected quarters. Combined with approved anti-inflammatory drugs, frequent milking and supportive care constitutes a common mastitis treatment on organic dairies in the United States (Ruegg, 2009).

Many organic farmers will also attempt to utilize complementary and alternative medicines; however, almost all of the products available have not been evaluated in peer reviewed studies for efficacy. Immunoboost, a USDA licensed immune stimulant sold in the U.S., has been evaluated but has not shown to have any significant effect on the treatment of mastitis (Ruegg, 2009). Other various remedies including peppermint, aloe, and garlic have been utilized by organic farmers as intramammary treatments, however the efficacy of these options is doubted, and their use is prohibited by the FDA (National Archives and Records Administration, 2012a). It appears that without recovery using simple supportive care, any medical intervention necessary to prevent unnecessary pain or distress for non-responsive mastitis cases will result in the loss of a producing animal for that organic operation. This creates a potential welfare risk, as the USDA organic requirements do not specify a point when prohibited treatments must be used, and the decision to discontinue organic treatment resides solely with the farmer.
Poultry producers face a distinctive management change when converting to organic as free choice medicated feeds containing antibiotics are commonly used to manage disease and promote growth (Love et al., 2010). Organic poultry is also currently under increased pressure from consumers (Love et al., 2012) to provide a safe and antibiotic free product, which could indicate an increased reluctance to treat conditions using pharmaceuticals. Following the prevention management strategy, organic poultry producers may use a variety of feed supplements including probiotics, prebiotics, organic acids, and plant extracts that have had minimal and sometimes contradictory efficacy reviews (Griggs and Jacob, 2005). Once again, treatment needs to be a key part of the management strategy of the organic producer, and the increased public scrutiny over medication use in poultry has the potential to encourage famers to withhold medication as has been shown in other species (Lund, 2006).

One of the most contested animal welfare debates surrounding organic poultry is regarding the space required by the USDA regulations to remain organic (Kijlstra and Eijck, 2006). While the law only requires year-round access to the outdoors, shade, shelter, exercise areas, fresh air, clean water for drinking, and direct sunlight (appropriate for the species, age, and climate) (National Archives and Records Administration, 2012a); organic farmers have adopted the term “free-range”, which unfortunately like the word “natural,” has no legal meaning. Nonetheless, open access to runs follows the third of Frasier et al.’s welfare ideals in allowing chickens to exhibit natural behaviors and thus have better welfare. The trade-off, however, is that while we have defined the major focus of disease management in organic operations as prevention based, free ranging chickens are more susceptible to predation, outbreaks of cannibalism, parasite exposure, coccidiosis and ascarid infections, and interactions with wild fowl that transmit dangerous diseases such as avian influenza (Verhoog et al., 2004; Kijlstra and Eijck, 2006; Lund, 2006). In order to keep with organic standards, all of these animals must continue to have access to the outdoors, and prohibited pharmaceuticals cannot be fed to treat outbreaks of disease or treat the higher rate of parasites that are found on organic operations (Lund, 2003). Clearly, should there be an outbreak of disease or cannibalism, an ethical dilemma is created between the first two ideals concerning the physical and mental needs of the animal, and the third to maintain natural conditions.

The various dilemmas discussed indicate that organic producers face additional pressure, both financially and in public relations, to avoid the use of treatments that would compromise the organic status of that animal. However, prioritizing animal welfare to include aspects beyond the scope of the clinical health of individual animals can potentially change the way welfare is perceived by conventional farmers and the general public. If an ecocentric rather than an individualistic perspective is considered, and positive experiences can be provided for the animal by indulging its natural behaviors and ecological niche, perhaps some stress events like occasional infections are an acceptable trade-off. Given that a higher incidence of disease has not been found, and that organic producers are required by law not to restrict care to maintain an organic status, it can be determined that organic livestock production does not encourage decisions that negatively impact animal welfare. However, it is recommended U.S. should adopt the EU policy of allowing antibiotics to be used in clinical cases without removing the organic status of that animal. With adequately increased withdrawal times in place to reflect the strict requirements that define organic products and enough consumer education, the organic market should recognize and accept the benefits of this policy change. Livestock would benefit by receiving more aggressive medical intervention as financial pressure not to treat animals could be alleviated as it has been in the EU (Ruegg, 2009), and having prescription antibiotics available as a treatment option could encourage more contact with veterinarians instead of neighbors to discuss animal health. Additional research is needed to support this position that could come from data determining if financial and public pressure are enough to encourage farmers to withhold treatments. In that case, additional actions such as stricter enforcement of the law may be necessary to promote a higher standard of care for organic animals.

Banned antibiotics in feather meal – A discussion with an author of the study

Following my recent post where I examined an article from Johns Hopkins that found multiple contaminants in commercial feather meal (including fluoroquinolones, a class of antibiotics that have been banned from use in poultry since 2005), I was honored to be contacted by one of the Authors, Dr. David Love. Dr. Love offered to continue the discussion with me, and was happy to answer my questions regarding the study, the media frenzy it has inspired, and some of the goals of the research conducted at the Center for a Livable Future. I immediately jumped at the chance, and was able to speak with him on the phone earlier this week.

As those who read the post last week have seen, my primary concern with the study was not to do with it’s results or conclusion, but in how the press release was worded. He didn’t feel that it was as misrepresentative as I initially interpreted it, and we quickly moved on discussing just why this article was picked up so quickly.

“I’m not sure how much more clear it could be, we specifically said feather meal, and the title of the study says ‘feather meal, a previously unrecognized route for reentry into the food supply’…I think on the whole we were careful, I don’t think we can come out of this paper with twelve samples and make sweeping generalizations, it’s important to point out that our big recommendation of the study in the last line was that more research should be done…It’s really at the intersection of the media and what they’re interested in, the consumer and what their interests are, and then our story as the authors. Consumers are so interested in what’s going on with their food. We say we did a study on chicken, there’s energy there, and if that’s what they want to talk about, it tells me that we need more transparency in packaging, labeling, and more consumer education. “

I agree, everyone is interested in what they eat, and he makes a great point that we shouldn’t ignore that interest as scientists or producers as it reflects consumer demand. Another point I wanted clarification on was the statement that self-regulation and our current FDA guidelines aren’t sufficient to keep contaminants out of food.

“From the looks of the latest FDA Guidance there’s a lot of strong language, but no teeth in the language. I think for the draft guidance for 213 we’re hopeful, as there will be a larger role for veterinarians in prescribing antibiotics. As for self regulation, I would be more willing to support it if there was more transparency. Many other countries go out of their way to report use, and we in the U.S. have trouble dividing up which antibiotics are used for growth promotion, prophylaxis, and therapy. It would be hard to go about but if we could get that, and reduce or cut growth promotion uses, we would be able to actually measure progress on how we’re reducing antibiotic use in animals.”

He made a very strong point, and following publishing my post last week I came upon  a commentary published by the authors discussing the issue created by unintentional overuse of antibiotics in feed. The article actually provided many of the citations supporting their arguments that I mockingly asked for last week, and I encourage anyone interested to check out the data behind the conclusions. In wrapping up our discussion, I asked where the authors planned to go next with follow-up research.

“A lot of people want to know. Well we found this stuff in feathers, now lets look at meat, at the consumer level with what you buy at the grocery store.”

A logical next step, and one that I’m sure will have even more interest than the findings from feather meal.

Out of our discussion, I discovered a different perspective of the research that I believe was reflected in the discussion, but was completely missed by the media and myself. While the source of the contaminants is obviously a big question, that wasn’t the purpose of the study. The authors were examining feather meal as a route to antibiotic introduction that could have implications in terms of creation of AB-resistant bacteria. Regardless of how it got there (like through contaminated groundwater, as I suggested), a small percentage of chicken producers use it as a feed supplement, thus introducing fluoroquinolones into our food supply through a previously unknown method, and thus not subject to withdrawal times that prevent meat contamination. Further exploration of this research goal will probably concern testing the meat of chickens being fed feather meal for the presence of fluoroquinolones, and seeing if they do allow a sufficient amount to reenter the food supply that may warrant a withdrawal period.

In reflecting on my first post on the subject, I believe that my own response to the press release provided an excellent example of the point I was making. As this case and my interpretation of it reveal, it’s extremely easy to think that your statements were clear and representative of the science at the time, but under outside scrutiny can still be misinterpreted whether in a press release or a blog post. I’m sure I’ll remember this article when I get to publish my first paper, and take a good, hard look at the press release before approving it.



I want to sincerely thank Dr. David Love for taking the time to speak with me about his research, food safety, and agriculture research in general. I greatly enjoyed our discussion and hope that I get to work with him again. Quotes used in this post are transcribed from my notes I took during our discussion, and are used with his prior review and permission.

If you are still interested in this topic I encourage you to read all you can about it, there’s no end to the depth of the science and social issues involved. I’ve linked to the original article several times, but you can also read the supplementary material here that includes some of the anecdotal evidence in support of the presence of some of the contaminants. You can also read the National Chicken Council’s response to the NY times opinion piece that first made this research so popular. Finally, here’s some research from Chile correlating concentrations of enrofloxacin (a fluoroquinolone)  in feathers with withdrawal times in chickens treated with the drug.

Additional government resources on AB-resistant bacteria statistics and USDA residue testing: FDA NARMS report and USDA Redbook.

Please feel free to leave comments on how you feel about the research, the media presentation, and my own interpretation! I know for a fact all you people from ResearchBlogging.org have opinions, I read them all the time!

Love, D., Davis, M., Bassett, A., Gunther, A., & Nachman, K. (2010). Dose Imprecision and Resistance: Free-Choice Medicated Feeds in Industrial Food Animal Production in the United States Environmental Health Perspectives, 119 (3), 279-283 DOI: 10.1289/ehp.1002625

Love, D., Halden, R., Davis, M., & Nachman, K. (2012). Feather Meal: A Previously Unrecognized Route for Reentry into the Food Supply of Multiple Pharmaceuticals and Personal Care Products (PPCPs) Environmental Science & Technology, 46 (7), 3795-3802 DOI: 10.1021/es203970e

San Martín B, Cornejo J, Iragüen D, Hidalgo H, & Anadón A (2007). Depletion study of enrofloxacin and its metabolite ciprofloxacin in edible tissues and feathers of white leghorn hens by liquid chromatography coupled with tandem mass spectrometry. Journal of food protection, 70 (8), 1952-7 PMID: 17803156

What your intoor/outdoor cat could be sharing with the local pumas

Image from Pet-peeves.org

Generally not small talk, though I imagine they might be interested in the projections for this year’s salmon run (pause for polite awkward laughter). A new article from PLoS ONE has been discussed, implying that, while direct contact may not be routine, exchange of disease between domesticated and wild cats may be fairly common.

The group of scientists involved were examining the occurrence of Toxoplasmosis, Bartonellosis, and FIV. They went out to rural Colorado and California and trapped 260 bobcats and 200 pumas to take blood samples. They also collected blood from 275 domestic cats that lived in the areas investigated, most of whom were feral and free ranging. They tested the serum of these animals for antigens that indicated infection, and ran a statistical analysis that looked at the prevalence of each disease compared to factors such as age, location, sex, and species. The data was collected over a ten year period.

I’m not going to discuss much of the wild species data, but there are some important trends for those interested in pet health, though it’s not very surprising. The researchers revealed that the prevalence of disease was much higher in domestic animals near urban areas than in those rural. This indicates that even though there is a larger number of hosts and vectors (fleas and ticks primarily) in rural areas, clearly the higher concentration of animals in urban areas and increased interactions between domestic cats and wild species (created by human expansion into undeveloped areas) plays a much larger role in the transmission of infectious diseases.

There are also some cool snippets about FIV here as well. The discussion mentions that male cats were slightly more likely to be carrying FIV, which is to be expected due to the higher rate of sex hormone driven behaviors such as roaming and fighting. The FIV strains found in the wild felids also had greater genetic diversity, suggesting that the FIV we know and vaccinate for may be a relatively new disease (at least in comparison to wild FIV serovars). The data shows that the highest combination of pathogens that the domestic cats tested positive for were FIV and Bartonellosis, and the authors mention that because Bartonellosis and FeLV infection have also been correlated in other studies, this data implies that there may be a relationship between the three. However, that relationship may be as simple as having similar risk factors.

The take home message of the study is that wild populations can serve as an important reservoir for multiple zoonotic diseases, and that exposure to this reservoir is mediated by the domestic cats we frequently come into contact with. Just one more reason to think about convincing your kitten that the outside world is scary, and that they don’t necessarily have to go check out what the big cats are doing. Feel free to check out the paper yourself, its light on jargon and easy to read. I’m actually a little disappointed to see that they collected this data over a ten year span, but chose not to do any comparison of the rates of disease from year to year. It would have been interesting to see how climate differences and population growth may have affected the number of vectors and associated risk. Additionally, because all of the samples were collected opportunistically when wild animals were trapped for other non-related studies, there was no way to ensure sampling without replacement, which may have skewed the data.

Sarah N. Bevins1*, Scott Carver2, Erin E. Boydston, Lisa M. Lyren, Mat Alldredge, Kenneth A. Logan, Seth P. D. Riley, Robert N. Fisher, T. Winston Vickers, Walter Boyce, Mo Salman, Michael R. Lappin, Kevin R. Crooks, & Sue VandeWoude (2012). Three Pathogens in Sympatric Populations of Pumas, Bobcats, and Domestic Cats: Implications for Infectious Disease Transmission PLoS ONE

Article review: Mechanisms of Viral Emergence

It’s funny how reading these articles is incredibly relieving for me. They confirm that I actually did learn and do remember principals and details from my classes. Today’s article comes from Veterinary Research, and discusses the mechanisms and variables involved in the emergence of a virus.

A viral emergence is generally defined as the appearance of a new pathogen for a host, such as human immunodeficiency virus (HIV)-1 for humans in the twentieth century. Viral re-emergence often refers to the reappearance of a viral pathogen after a period of absence, such as the periodic human influenza epidemics or pandemics.” (Domingo, 2010)

There’s a huge amount of information on viral evolution and mutation, a concept that (like everything else you haven’t specifically studied) I had greatly oversimplified. It was incredibly fascinating to read how viruses can recombine and splice gene segments from other unrelated infections, and the various pathways new genes can be created or introduced that allow viruses to jump host species. I’m not going to try to summarize all of those, the article explains them much better than I could, but there’s still a few broad topics in the paper worth discussing.

The concept of viral quasispecies is something I’ve never heard about. I’ve discussed viral serovars on here before, but I believe that term specifically refers to antigen variation. Quasispecies refers to groups of virus that are labeled and operate as one species (for example, Influenza H1N1) but contain different genomes. For example, if I get the flu this winter, the virus I am exposed to may contain several quasispecies, that are the same virus, but contain different genes. Now any deleterious mutations or reassortments will probably be wiped out by my immune system, but the ones with a fitness advantage will reproduce and take over. Here’s the extra interesting part, even if I had been infected with just one quasispecies, I could still shed several while I’m infected. There is so much mutation and variation in viral reproduction that I would be generating new ones as a single host.

Quasispecies are important in emergence because they are a major source of viral evolution. We identify the “wild type” gene amongst quasispecies as a distribution of genes that characterize that viral species (consensus gene); even though amongst different quasispecies they may be found in different places in the genome. This is where the existence of quasispecies propels viral evolution forward. When you mix up the genome so much, you can create mutations that change nothing in the functional portions of the genome, but create subpopulations that are fine tuned to conditions that may not yet be occurring. As an example, it’s been assumed that SARS was introduced to humans through Civet cats, when it was originally a virus transmitted by bats. Contact with civets is common in areas surrounding SARS outbreaks (where they are raised for food), where contact with bats is much less common. It is possible that there was a quasispecies subpopulation of SARS carrying a mutation allowing it to jump species to humans long before it was even introduced to civets. When the disease was contained to bats, this mutation has no fitness advantage, but it can sit idle until a change in the environment (higher infection rates in civets, civets brought from more rural areas, there are unlimited possibilities) gives it an advantage. This essentially allows virus to be proactive in its evolution. Instead of waiting for selective pressure, new genes are created spontaneously in the event that they may become useful.

Civet, image from healthjockey.com

The article continued to discuss different factors in emergence, primarily focusing on new host emergence, and brought it all together as an example of biological complexity. My personal favorite example for biological complexity is the realization that we’ll probably never fully understand the complete pharmacology associated with feelings of hunger and satiety. Alternatively you can illustrate this principal by asking someone to model the weather. The idea is that there are so many variables, all interdependent on each other, that it is pretty much impossible to trace all of the factors that led to an event such as the host change SARS made from civets to humans. They illustrate this by showing that even if viral variation is sufficient to promote a host change, there are numerous other roadblocks that have to be surmounted to allow it to take place (interaction with the new host, sufficient amounts of virus introduced to the system of the new host, fitness of the mutated virus, exposure to multiple quasispecies or serovars, future shedding of virus adapted to that host species, etc.). It’s a paradoxal idea, because we have been able to successfully model systems like these through the CDC and WHO, and we have been able to successfully model complex systems like the weather, even when there are countless interactions that we can’t even begin to measure.

Read this article if you have any interest in virology at all. I learned a lot, and it’s interesting and fluid reading if you have a basic understanding of cell biology.

ResearchBlogging.orgDomingo, E. (2010). Mechanisms of viral emergence Veterinary Research, 41 (6) DOI: 10.1051/vetres/2010010

Article Review: Leptospira and Leptospirosis

In my latest ScienceDirect purge, I came across this article covering Leptospirosis. I had no idea it would be such a dense read, figuring it would be a simple review of the disease with emphasis on new discoveries. I ended up using a lot of immunology references and Google searches. This article isn’t just an entry from the Merck manual.

The article does a very good job of covering Lepto microbiology, but I was especially impressed with the point they made to identify everything we don’t know. Indeed that was the emphasis of the article, that lepto contains so many pathways unique to it as a bacterium that we don’t know nearly as much about it as we do something like E. Coli. Additionally, Lepto is extremely hard to culture, as you end up with non-virulent colonies. They identify and isolate the virulent daughters by inoculating lab animals.

You might assume that immunity to Lepto is a simple thing, given how prevalent Lepto vaccination is due to the zoonotic risk. However the article makes the point multiple times that immunity to one Lepto serovar does not grant immunity to others, though occasionally it can help grant passive immunity or resistance across different species. While the exchange of genetic material between parent and daughter lepto colonies is not well understood, it appears to be slow mutating, which is interesting given how unique the antigens between serovars seem to be.

There’s a lot of complicated immunology discussed in the article that I don’t feel qualified to comment on, but it’s very interesting, and I recommend glancing through. The more microbiology I learn the more I understand that 99% of the workings of the cell happen on membranes (a statement that probably produces a loud “duh” from any student, biologist, or doctor). For a more clinical discussion of Lepto, a simpler reference like Merck or Blackwells will help, as well as several peer-reviewed sources that the article itself recommends for information on clinical presentations.

Adler, B., & de la Peña Moctezuma, A. (2010). Leptospira and leptospirosis Veterinary Microbiology, 140 (3-4), 287-296 DOI: 10.1016/j.vetmic.2009.03.012