SLA Biomedical & Life Sciences Division Blog

The Bedbugs Aren’t Coming, They’re Already Here

Bedbugs (primarily Cimex lectularius, but occasionally in warmer climes the tropical version Cimex hemipterus)  are tiny (about ¼ inch) blood-sucking human parasites. They are  typically found living  in bedding, but are also found hidden in closets, thin cracks in headboards, floorboards, baseboards and walls. In short they are found anywhere that brings them in close proximity to the humans on which they feast. They generally come out at twilight (Romero, Potter & Haynes 2010), wait for their victims to drift off to sleep, and then puncture the skin with their proboscis to suck up the blood, while coincidentally injecting  a local anesthetic which masks the intrusion.

Bedbugs  have been around for tens of thousands of years (they have been found in the wrappings of Egyptian mummies) but  were once thought to have been almost completely wiped out in the United States , Canada, and most of the major economically advanced countries in Europe and Asia.

But now they have resurged to the point that they are found in all 50 US states and the Provinces of Canada, and virtually the major business cities and political capitals around the world (Benac 2010, Burleigh 2010,How & Yee 2010a, 2010b, Manuel 2010.

Most major city exterminators report now having a thriving practice in attempts to eliminate or control bedbugs, whereas as recently as ten years ago, their presence was an exception (Motoki 2010, Radcliffe 2010).  

While private homes do report infestations, the majority of calls for assistance come from places where there are multiple and often continuingly changing occupants of rooms and their furniture. Breakouts are most common in hotels, motels and college dormitories, but in recent years many reports have come in from hospitals,  movie theaters, and passenger seats on planes and trains (Anders, Brocker & Hamm 2010, ED Management Editors 2010, Johns Hopkins Medical Letter for Health After 50 Editors 2010, Mayo Clinic  Womens Healthsource Editors 2010, Von Drehle 2010, Yaguchi & Kasai 2010).

How has this come to happen? Answer 1: Mobility of victims & vermin

It takes only one person with bedbugs in  his or her suitcase or clothing to infest an entire hotel, a college dorm, or even a bus, but people rarely examine their own clothing or luggage for possible bedbug infestation, must less exterminate the bedbugs that are coming along for the ride by steam blasting them, or putting possibly odorous pest strips inside. (Chalupka 2010). Today,  when sales personnel and tourists can  visit a different country every day and sleep in a different time zone every night, there is an unprecedented opportunity for them to be unwitting carriers of bedbugs (Potter, Rosenberg & Henriksen 2011) .  

In addition, bedbugs can temporarily feast on other animals between human feedings, with the most recent temporary vector for them  turning out to be New York City pigeons (Haag-Wackernagel & Bircher 2010).

How has this come to happen? Answer 2: In the  decaying public housing sector, cockroaches stole the limelight away from bedbugs long enough for bedbugs to recover

One of the most fascinating articles dealing with this question is by Biehler (2009). Bedbugs used to be the number one insect pest of the interiors of communal housing or sleeping quarters. They were aggressively attacked and treated in a cooperative  effort by building managers and vigilant cooperating residents, often involving  a vigorous campaign of joint inspection, cleaning, and fumigation.

However, after the 1950s in the US at least, housing for the middle class and returning WWII veterans shifted from sometimes subsidized apartments in the cities, to individual private homes in the suburbs.

The  population that remained behind in public housing were often the poor and elderly.   The demographics of the poor in public housing also became more black and Hispanic, while the ownership or management often remained white,  and was in any case, affluent by comparison, and distant from “the projects” in terms of their personal home locations. There was a substantial breakdown in the sense of shared social responsibility for  keeping up the property. Housing units fell into greater and greater disrepair. Services like regularly scheduled fumigations and cooperative inspections for bedbugs fell by the wayside.

This did not end the need for exterminators, and in cities, public housing  projects provided one  of their greatest sources of revenue. However, the target pest species changed. For most of the latter 20^th century, the cockroach took precedence as insect public enemy number one (Ebeling 1965.  Meanwhile the diminished population of bedbugs began to rebuild its numbers.

How has this come to happen? Answer 3:  Pesticide Resistance on the Part of Both the Bedbug and the Apartment Dweller

Initially bedbug infested apartment buildings were evacuated for the better part of a day to allow for highly toxic, but also highly effective, hydrocyanic gas fumigation of the whole complex.  But in the 1950s and 1960s, localized spraying of DDT, organophosphates and organochlorines  in individual apartments took over as the technology of choice for extermination. The advantages of these liquid spray spot treatments were that whole buildings did not need to shut down, and to some degree, neighboring units in apartment complexes did not need to know about infestations, perhaps preserving privacy but also diminishing communal buy-in.

Eventually, insects of all types developed increasing resistance to these more common pesticides (Romero et al 2007) and a search for alternative pesticides developed in earnest. Several were in fact found, but at about the same time, apartment dwellers and public health officials began to worry that the chemical killing of the bedbugs presented almost as much of a chemical danger to residents as it did to the insects (Berg 2010).

Fortunately, for about 20 years the pyrethins , natural neurotoxins derived from chrysanthemums, which naturally biodegraded and had seemingly negligible toxicity to humans , served to keep down both cockroaches and the rising tide of bedbugs.

No longer, alas (Hirao & Tomita 2010, Iwamoto 2010, Seong et al 2009, Zhu et al 2010) and combinations of these mild toxins now often need to be combined with additional activating chemicals  in order to remain effective (Romero, Haynes & Potter 2009).

Taking off the chemical gloves in the fight against bedbugs

But owing to an increased concern about bedbugs transmitting some fairly serious diseases (Delaunay et al 2010), it now seems as if some new generation chemical agents, or retired chemical agents, are likely to be approved for deployment or redeployment.  The most likely candidate in the US and Canada is propoxur, which had been pulled off the market in 2007(Benac 2009), although certain folk remedies are being reinvestigated in Europe (Soukand, Kalle & Svanberg 2010).   

Nonetheless, public health officials whose concerns have in more recent years focused on potential toxicity to humans, are still urging more environmentally friendly Integrated Pest Management approaches that will limit blunt force chemical applications (Rossi & Jennings 2010). Heat treatment with live steam, and even flash freezing are now being tried against bedbugs with varying degrees of effectiveness (Benoit et al 2009, Watanabe 2010), often in combination or in alteration with chemical sprays.

Will a better understanding of bedbug biology lead to more innovative approaches?

If bedbugs have a weakness in their life cycle, it is in their reproductive behavior. Adult male bedbugs practice what is referred to as traumatic insemination on females (Reinhardt & Siva-Jothy 2007, Siva Jothy 2006, Stutt & Siva Jothy 2001).

Imagine that in order to have sex, male humans would have to slash open female stomach at roughly their navels, and then stuff their penis in and deposit their sperm, and hope they find their way to the uterus and ovaries. Indeed, this is a highly inefficient approach because it is estimated that it takes as many as 20 rapes to produce a successful pregnancy.

This is a rather dangerous proposition for  bedbug females and even for immature bedbug males which  are often homosexually raped (Ryne 2009). Not surprisingly some female bedbugs have evolved a special entry port which makes penetration bt violent males easier (Reinhardt, Naylor & Siva-Jothy 2003).

But other females and nymphs have developed certain chemical countersignals that forestall these violent mating attacks by the males, largely by confusing, alarming or even positively repelling them (Haraca, Ryne & Ignell 2010, Levin, Levinson & Maschwitz 1974, Siljander et al 2008, Morrow & Arnqvist 2003).

It is through chemically duplicating the bedbug's own sexually defensive sprays that we may one day hold the key to interrupting the further spread of bedbugs, by keeping bedbugs  from reproducing, by using  a kind of nontoxic but effective pheromone fog (Haynes, Goodman & Potter 2010).

Tony Stankus, FSLA [email protected], Life Sciences Librarian, Science Coordinator & Professor

University of Arkansas Libraries MULN 233 E

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Voice: 479-409-0021

Fax: 479-575-4592

 

Anders, D., E. B. Brocker, and H. Hamm. 2010. Cimex lectularius - an unwelcome train attendant. European Journal of Dermatology 20 (2): 239-40.

Benac, Nancy. 2010. Bedbug bites becoming bigger battle. CMAJ 182 (15): 1606.

Benoit, J. B., G. Lopez-Martinez, N. M. Teets, S. A. Phillips, and D. L. Denlinger. 2009. Responses of the bed bug, Cimex lectularius, to temperature extremes and dehydration: Levels of tolerance, rapid cold hardening and expression of heat shock proteins. Medical and Veterinary Entomology 23 (4): 418-25.

Berg, R. 2010. Bed bugs: The pesticide dilemma. Journal of Environmental Health 72 (10): 32-5.

Biehler, D. D. 2009. Permeable homes: A historical political ecology of insects and pesticides in US public housing. Geoforum 40 (6): 1014-23.

Burleigh, Nina. 2010. Nightmare on bedbug street. Time 176 (9): 63-4.

Chalupka, S. 2010. Preventing bedbug infestation. AAOHN Journal 58 (11): 500-.

Cohen, P. R., J. A. Tschen, F. W. Robinson, and J. M. Gray. 2010. Recurrent episodes of painful and pruritic red skin lesions. American Journal of Clinical Dermatology 11 (1): 73-8.

Delaunay, P., V. Blanc, P. Del Giudice, A. Levy-Bencheton, O. Chosidow, P. Marty, and P. Brouqui. 2011. Bedbugs and infectious diseases. Clinical Infectious Diseases 52 (2): 200-10.

Ebeling, W. 1965. Cockroach control in public housing. Pest Control Operator News 25 (12): 21-24.

ED Management Editors 2010. EDs trying not to let the bed bugs bite. ED Manag 22 (9): 100-1.

Haag-Wackernagel, Daniel, and Andreas J. Bircher. 2010. Ectoparasites from feral pigeons affecting humans. Dermatology (Basel) 220 (1): 82-92.

Hawkins, C. N., and B. Barankin. 2010. Can you identify this condition? Canadian Family Physician 56 (6): 553,+.

Haynes, K. F., M. H. Goodman, and M. F. Potter. 2010. Bed bug deterrence. BMC Biology 8 .

Hirao, Motokazu, and Takashi Tomita. 2010. Insecticide resistance of bedbugs. Medical Entomology and Zoology 61 (3): 223-9.

How, Y. F., and C. Y. Lee. 2010a. Effects of life stages and feeding regimes on active movement behavior of the tropical bed bug, Cimex hemipterus (hemiptera: Cimicidae). Journal of Medical Entomology 47 (3): 305-12.

———. 2010b. Survey of bed bugs in infested premises in Malaysia and Singapore. Journal of Vector Ecology 35 (1): 89-94.

Iwamoto, Tatsuhiko. 2010. The present condition of bedbug management in the US: Some tips on promoting unification of laws regulating pesticides in Japan. Medical Entomology and Zoology 61 (3): 255-60.

Johns Hopkins Medical Letter for Health After 50 Editors. 2010. Don't let the bedbugs bite. Johns Hopkins Med Lett Health After 50 22 (2): 3.

Manuel, J. 2010. Invasion of the bedbugs. Environmental Health Perspectives 118 (10): A429-.

Mayo Clinic  Womens Healthsource Editors. 2010. I've heard that bedbugs have become a problem in hotels. How can I avoid them when I'm traveling? Mayo Clin Womens Healthsource 14 (8): 8.

Morrow, E.H., & G. Arnqvist. 2003. Proceedings of the Royal Society of London 270: 2377-2381.

Motoki, Mitsugu. 2010. Current status and problems of bedbug control in the pest-control industry. Medical Entomology and Zoology 61 (3): 251-3.

Pfeister, M. P.G. Koehler, & R.M. Pereira. 2009. Sexual conflict to the extreme: Traumatic insemination in bed bugs. American Entomologist 55: 244-249.

Radcliffe, Mark. 2010. Bedbugs and consultants are both bleeding us dry. Nurs Times 106 (34): 24.

Reinhardt, K., & M.T. Siva-Jothy.  2007. Biology of the bed bugs (Cimicidae). Annual Review of Entomology  52:351-374.

Reinhardt, K., R. Naylor, & R. Siva-Jothy. 2003. Reducing a cost of traumatic insemination: Female bedbugs evolve a unique organ. Proceedings of the Royal Society of London B Biological Sciences 270: 2371-2375.

Richard, S., P. Seng, P. Parola, D. Raoult, B. Davoust, and P. Brouqui. 2009. Detection of a new bacterium related to 'Candidatus midichloria mitochondrii' in bed bugs. Clinical Microbiology and Infection 15 : 84-5.

Romero, A., M. F. Potter, and K. F. Haynes. 2009. Evaluation of piperonyl butoxide as a deltamethrin synergist for pyrethroid-resistant bed bugs. Journal of Economic Entomology 102 (6): 2310-5.

Romero, Alvaro, Michael F. Potter, and Kenneth F. Haynes. 2010. Circadian rhythm of spontaneous locomotor activity in the bed bug, Cimex lectularius L. Journal of Insect Physiology 56 (11): 1516-22.

Rossi, L., and S. Jennings. 2010. Bed bugs: A public health problem in need of a collaborative solution. Journal of Environmental Health 72 (8): 34-5.

Ryne, C. 2009. Homosexual interactions in bed bugs: Alarm pheromones as male recognition signals. Animal Behaviour 78: 1471-1475.

Seong, K. M., D. Y. Lee, K. S. Yoon, D. H. Kwon, H. C. Kim, T. A. Klein, J. M. Clark, and S. H. Lee. 2010. Establishment of quantitative sequencing and filter contact vial bioassay for monitoring pyrethroid resistance in the common bed bug, Cimex lectularius. Journal of Medical Entomology 47 (4): 592-9.

Siljander, E., R. Gries, G. Khaskin & G. Gries. 2008. Identification of the airborne aggregation pheromone of the common bed bug, Cimex lectularius. Journal of Chemical Ecology 34: 708-718.

Siva-Jothy, M.T. 2001. Trauma, disease and collateral damage: Conflict in cimicids.  Philosophical Transactions of the Royal Society of London B Biological Sciences 361: 269-275.

Soukand, R., R. Kalle, and I. Svanberg. 2010. Uninvited guests: Traditional insect repellents in Estonia used against the clothes moth Tineola bisselliella, human flea Pulex irritans and bedbug Cimex lectularius. Journal of Insect Science 10 .

Straub, R. D., H. L. Salvaggio, D. R. Adams, and A. L. Zaenglein. 2009. Diffuse clusters of vesicles on the face and extremities of a 10-month-old girl. Pediatric Dermatology 26 (6): 747-8.

Tomita, Takashi. 2010. Insecticide resistance of bedbugs. Medical Entomology and Zoology 61 (3): 223-9.

Von Drehle, David. 2010. This really sucks. Time 176 (14): 36-8.

Watanabe, Mamoru. 2010. Insecticide susceptibility and effect of heat treatment on bedbug, Cimex lectularius. Medical Entomology and Zoology 61 (3): 239-44.

Yaguchi, Noboru, and Shinji Kasai. 2010. Current situation and problem of bedbug infestation in Tokyo, Japan: From public health officer's angle. Medical Entomology and Zoology 61 (3): 231-7.

Zhu, F., J. Wigginton, A. Romero, A. Moore, K. Ferguson, R. Palli, M. F. Potter, K. F. Haynes, and S. R. Palli. 2010. Widespread distribution of knockdown resistance mutations in the bed bug, Cimex lectularius (hemiptera: cimicidae), populations in the United States. Archives of Insect Biochemistry and Physiology 73 (4): 245-57.

Genetically Modified "GM" Salmon Raised In Self-Contained Systems: Much More Likely To Be Part of a Solution and Not a Problem

A New York Times article (Pollack 2010) appeared on Tuesday, September 21, 2010,   and discussed whether or not specially genetically engineered farmed salmon might be approved for sale in the US. There were representatives of the aquaculture industry and of the firm pushing the idea, AquaBounty  Technologies, speaking in support before an FDA panel, and a number of special environmentalist or consumer’s groups going on record as against the idea in general, or some particular aspect that they felt was underexplored or held potential danger. 

The critics brought up a number of issues that  were treated as being so important of themselves, that the approval process should be delayed or cancelled altogether. But such a single-issue-based disapproval  sometimes overlooked other factors and realities of  salmon ecology,  economics,  and even human medicine, when a more holistic and  interdisciplinary view of the risks and benefits of this AquAdvanatge™  salmon and its method of being aquacultured might be more revealing.

What’s the big deal with salmon?

Salmon now leads in US sales of all fresh, refrigerator case finfish in supermarkets and is the third most consumed seafood product just behind frozen shrimp and canned tuna (National Fisheries Institute 2009). It’s considered to be particularly good for you. It is nationally promoted, responsibly endorsed,  and widely perceived as having health benefits, especially its polyunsaturated fats and omega-3 fatty acid content (Harel et al 2001, Horrocks & Yeo 1999) that outweigh  its risks from mercury for most categories of consumers (Foran et al 2005, Smith & Guentzel 2010). Demand is expected to grow in the restaurant and institutional food service trade not the least because salmon is one of the most popular types of sushi and sashimi  among both high school (FoodServiceDirector 2010) and college age  consumers (Boss 2009).

Why do they farm salmon anyway? Can’t we just catch more wild salmon in the ocean?

Atlantic salmon are still caught in the wild, but their reproductive carrying capacity has long ago been reached, and Atlantic salmon fisheries have basically harvested (and often polluted) themselves out of business in many locales, including most of New England, formerly a rich salmon fishing area. Indeed most wild Atlantic salmon served in the US has been imported from Canada, the UK, or Scandinavian countries, but even so, catches have been declining: In 1996 we imported 566 tons of wild caught salmon, but by 2008 that amount was down to 58 tons.

It should be noted that while the Alaskan wild salmon fishery ----involving a number of different salmon species but not the Atlantic salmon----remains reasonably healthy, the other West coast native salmon fisheries running from Northern California through to British Columbia, have been in severe decline owing to overfishing and environmental calamities, and thus will not provide a ready, sustainable alternative in the future (US Fish & Wildlife Service 2010). The only realistic  alternative source for a growing demand for salmon is to use aquacultured salmon.

Can’t we just stock the rivers with more salmon from salmon hatcheries, and let them grow up in the wild in the ocean and have them return to the rivers where we stocked them, just like wild salmon do?

This is being done in Alaska and Northern Europe with some success (and in the Great Lakes although the population cannot reproduce there)  but there are still problems: The stocked fish generally behave like escaped farmed fish and sometimes out-compete the wild fish, and it is not always clear that wild and stocked fish interbreed  successfully, even though they are of the same species. This means that it is sometimes possible to end up, not with an overall increase in the total number of available salmon, but rather the displacement of one type of salmon by another without any net gain in salmon supply.  (Crozier 1993, Erkinaro et al 2010, Skaala,  Glover &  V. Wennevik  2006, Soto, Jara & Moreno 2006,  Uusitalo, Kuikka & Romakkaniemi 2005).

 

 Why do they want to genetically engineer a naturally perfectly good fish in the first place?

The principal reason is that these fish, when farmed, grow to harvest size in about half the time as non-genetically-engineered farm-raised salmon, and that this quick turnaround time means that they can be economically grown in closed aquatic systems, meaning not in pens in the open ocean or nearby brackish waters, but rather in clean artificial ponds  much like modern American catfish farming, ponds or tanks which do not connect to rivers or the ocean. As seen in the catfish farming industry (Stankus 2010), many more variables regarding fish wholesomeness and taste,  water quality, the presence of parasites and diseases, the management of waste products, are much more controllable, although realistically never perfectly controllable, in such closed systems. Salmon farming in a closed system represents a serious incremental improvement in the food safety, economics and as we will see shortly, in the environmental impact of salmon aquaculture.  Genetically modified salmon raised in closed systems will go a long way to exploding the simplistic folkloric natural foods ideology  that Norwegian fisheries researcher  Oivind Bergh (2007) calls the dual myth: That wild fish are always healthier (and therefore always better for you) and that farmed fish are always unhealthy (and therefore always worse for you).  

How do these genetically modified salmon grow so fast?

Basically, two genes have been inserted into their genomes. One gene simply enables internal growth hormone production year round despite the cold (salmon ordinarily stop making growth hormone in cold weather and therefore stop growing during winter months). The second gene basically enables the first gene to activate and do its work.

Most importantly, no hormones that are not native to fish are introduced to this  fish, nor are they fed hormones in their rations. There is no reasonable scientific basis for suggesting that these fish are somehow hormonally disruptive of humans or other animals that might eat them, or even that the enhanced growth hormone production, is damaging to the fish themselves, the arguments used against hormones given to livestock and dairy cows through feed or direct injection.

Why can’t we just wait for the traditional growing out period of non-genetically engineered salmon farmed in bays and estuaries?

There are at least three reasons that make quicker growing farmed salmon, grown in closed systems, a better idea than farmed non-genetically modified  salmon raised in sea pens.

The first is ironically ecological or environmental: Salmon farmed in the traditional manner in pens in bays and estuaries tend to become infested with sea lice, which, while not known to be harmful to humans, stunt the growth and well-being of the salmon being farmed. Unfortunately, once the sea lice find themselves a fertile home base, such as the trapped farmed salmon, they spread, not only to nearby wild salmon, but to other fish species as well, sometimes decimating their number(Costello 2009, Frazer 2009).

The second is also ecological and environmental: The sea floor beneath and areas surrounding sea pens are typically fouled with fecal products, uneaten food, and trace chemicals used to keep the cages from becoming coated with barnacles,  weeds, and the like. Perversely, the increased organic matter in the waters near the cages actually decreases the oxygen levels in the water as well as  the number of toxic compounds in the immediate area by binding with agents that would otherwise remain in solution and generally in a diluted state (Musclow 2005, Mayor et al 2010). See the following for more details.

The third reason is also environmental but includes some clinical implications as well: Quicker growing fish raised in closed aquatic systems with closely monitored water quality show demonstrably lower rates of bioaccumulation of environmental toxins including heavy metals, runoff fertilizer compounds, and especially trace pharmaceuticals like antibiotics used to suppress assorted bacterial and fungal infections in salmon penned up in bays and estuaries (Burridge 2010, Cabello 2006, Fortt, Cabello & Buschman  2007). These materials are not only generally bad for the sea life around them, but, should they accumulate within human consumers, poisonous and potential enablers of diminished antibiotic effectiveness, as they encourage the proliferation of drug resistant bacteria in the environment (Herwig, Gray & Weston 1997).  

What will happen to wild salmon if these genetically engineered fish somehow escape their closed systems and mate with natural salmon populations?

First, at least as currently planned in terms of their major sites of production, the salmon will be raised in places where even the nearest sea and river waterways are seriously unfavorable to them, so it is likely that they would die out because they were in such unsupportable circumstances.

Second, all of these fish are females,  and by design, about  five out of every six are demonstrably sterile. Such a sex ratio and high rate of infertility does not bode well for them to be able to establish a viable invasive population which can compete with local, native fish. (Which generally do not include members of the salmonid family with which they could conceivably try to mate.)

What about possible allergic reactions?

It is unfortunately true that there are a great many people allergic, and sometimes severely so, to proteins in seafood, including proteins in Atlantic salmon (Pitsios et al 2010). However, there is as yet no evidence that the two genes that have been inserted into these AquaAdvantage Atlantic salmon will cause the production of any proteins that are not already likely to be in any other type of Atlantic salmon. A safe and sensible recommendation  would be for people who are known to be allergic to Atlantic salmon not to eat any Atlantic salmon, AquAdvantage type or not, and for the rest of us to eat available Atlantic salmon including AquAdvantage salmon when we want to, because we like it and it is a generally healthy food.

Shouldn’t there be warning labels on such salmon?

Given that there are no known differences in the food safety or nutritional value of these salmon, there is no scientific justification for putting any kind of warning label on them. It might be fair to consumers who, for whatever reason, prefer wild-caught salmon or farmed salmon, to have the salmon labeled simply as wild-caught or farm raised salmon, and mention the country of origin.  This is pretty much the standard procedure in most supermarkets anyway, and as noted below, seems to have little effect on sales. People buy what looks good to them at the lowest price they can get.

Are there any foreseeable disadvantages to genetically modified salmon of this type raised by this method?

Overexpectation, too much “hype” in terms of  certain ecological and economic impacts  is about the only forseeable problem.

At least three pre-existing dilemmas will likely persist despite the adoption of this genetically modified salmon and its method of being raised, but these dilemmas  would also continue without them.

1. Detrimental impact on the global population of small fish and supply of fish byproducts. While all the science thus far suggests that with proper care, these fish can be raised safely within closed systems with virtually no risk to the local fish population by direct invasion of their waterways  and competition for food within them, problems remain with the need of all carnivorous fish (and this includes salmon, farmed or wild) for smaller forage fish, usually caught in the wild to be turned into fish meal for the pellets fed to the salmon, and this can cause population declines in fish that would feed other fish in the wild or feed humans (think anchovies and sardines, for example) directly (Aubin et al 2009, Ayer et al 2009, Mullon et al 2009, Pelletier et al 2009).

 

2. This new type of salmon and way of producing it will not likely produce a great many more jobs in the poorer countries that host these or any other modern aquaculture operations. Unemployment in the poorer countries where this type of aquacultured salmon (and any other type of aquacultured salmon) will not dramatically decrease, because operations such as these are  much efficient in their  use of manpower, particularly when compared to  the still large numbers of increasingly impoverished local traditional fisherfolk attempting to land ever diminishing catches.  This is not to say that the fewer workers in modern farmed fishing would not, in the long run, be better off, particularly if there was a requirement that these international aquaculture companies hire and train displaced local fisherfolk, instead of bringing in alien crews for permanent operations  (Adeel & Safriel 2008, Grigorakis et al 2010 ).

 

3. This new type of salmon and way of producing it will not likely increase the availability of low-cost, high-quality protein in the poorer countries that host these and any other modern aquaculture operations. Barring “set-aside-some for domestic use”  legislation in the countries in which these operations are set up, the local population will  probably not have greatly increased access to cheap salmon for their own consumption. The overwhelming share of farmed (and wild caught) salmon is sold on the international market as a cash crop to wealthy, highly developed countries like the US, and their consumers tend to buy the lowest priced salmon of comparable quality and freshness, regardless of which country was the source (Wozniak 2010).

 

Tony Stankus FSLA [email protected] Life Sciences Librarian, Science Coordinator & Professor

University of Arkansas Libraries MULN 233 E

365 North McIlroy Avenue

Fayetteville AR 72701-4002

Fax: 479-575-4592

Voice: 479-409-0021

Adeel, Zafar, and Uriel Safriel. 2008. Achieving sustainability by introducing alternative livelihoods. Sustainability Science 3 (1) (APR): 125-33.

Adhikari, S., L. Ghosh, S. P. Rai, and S. Ayyappan. 2009. Metal concentrations in water, sediment, and fish from sewage-fed aquaculture ponds of Kolkata, India. Environmental Monitoring and Assessment 159 (1-4) (DEC): 217-30.

Alderman, D. J. 2002. Trends in therapy and prophylaxis 1991-2001. Bulletin of the European Association of Fish Pathologists 22 (2): 117-25.

Aubin, J., E. Papatryphon, H. M. G. van der Werf, and S. Chatzifotis. 2009. Assessment of the environmental impact of carnivorous finfish production systems using life cycle assessment. Journal of Cleaner Production 17 (3): 354-61.

Ayer, Nathan, Raymond P. Cote, Peter H. Tyedmers, and J. H. Martin Willison. 2009. Sustainability of seafood production and consumption: An introduction to the special issue. Journal of Cleaner Production 17 (3): 321-4.

Bergh, Oivind. 2007. The dual myths of the healthy wild fish and the unhealthy farmed fish. Diseases of Aquatic Organisms 75 (2): 159-164.

Bernhisel-Broadbent, J, D Strause, and H A Sampson. 1992. Fish hypersensitivity. II: Clinical relevance of altered fish allergenicity caused by various preparation methods. The Journal Of Allergy And Clinical Immunology 90 ( 4 Pt 1): 622-629.

Boss, Donna L. 2009. College dining services tap into international street cuisines. Nation's Restaurant News 43 (27): 22.

Burridge, Les, Judith S. Weis, Felipe Cabello, Jaime Pizarro, and Katherine Bostick. 2010. Chemical use in salmon aquaculture: A review of current practices and possible environmental effects. Aquaculture 306 (1-4) (AUG 15): 7-23.

Cabello, F. C. 2006. Heavy use of prophylactic antibiotics in aquaculture: A growing problem for human and animal health and for the environment. Environmental Microbiology 8 (7) (JUL): 1137-44.

———. 2004. Antibiotics and aquaculture in Chile: Implications for human and animal health. Revista Medica De Chile 132 (8) (AUG): 1001-6.

Capone, D. G., D. P. Weston, V. Miller, and C. Shoemaker. 1996. Antibacterial residues in marine sediments and invertebrates following chemotherapy in aquaculture. Aquaculture 145 (1-4) (OCT 15): 55-75.

Cole, David W., Richard Cole, Steven J. Gaydos, Jon Gray, Greg Hyland, Mark L. Jacques, Nicole Powell-Dunford, Charu Sawhney, and William W. Au. 2009. Aquaculture: Environmental, toxicological, and health issues. International Journal of Hygiene and Environmental Health 212 (4) (JUL): 369-77.

Costello, Mark J. 2009. How sea lice from salmon farms may cause wild salmonid declines in Europe and North America and be a threat to fishes elsewhere. Proceedings of the Royal Society B-Biological Sciences 276 (1672) (OCT 7): 3385-94.

Cottee, Stephanie Yue, and Paul Petersan. 2009. Animal welfare and organic aquaculture in open systems. Journal of Agricultural & Environmental Ethics 22 (5) (OCT): 437-61.

Crozier, WW. 1993. Evidence of genetic interaction between escaped farmed salmon and wild Atlantic salmon (Salmo salar L.) in a Northern Irish river. Aquaculture 113, (1-2): 19-29.

Erkinaro, J., E. Niemelae, J-P Vaehae, CR Primmer, S. Broers, and E. Hassinen. 2010. Distribution and biological characteristics of escaped farmed salmon in a major subarctic wild salmon river: Implications for monitoring. Canadian Journal Of Fisheries And Aquatic Sciences/Journal Canadien Des Sciences Halieutiques Et Aquatiques 67, (1): 130-142.

FoodService Director. 2010. School District Dishes Up Sushi. FoodService Director  23(5): 8.

Foran, Jeffery A, David H Good, David O Carpenter, M Coreen Hamilton, Barbara A Knuth, and Steven J Schwager. 2005. Quantitative analysis of the benefits and risks of consuming farmed and wild salmon. The Journal Of Nutrition 135 (11): 2639-2643.

Fortt, Antonia, Felipe Cabello, and Alejandro Buschmann. 2007. Residues of tetracycline and quinolones in wild fish living around a salmon aquaculture center in Chile. Revista Chilena De Infectologia 24 (1) (FEB): 14-8.

Frazer, L. Neil. 2009. Sea-cage aquaculture, sea lice, and declines of wild fish. Conservation Biology 23 (3) (JUN): 599-607.

Grigorakis, Kriton. 2010. Ethical issues in aquaculture production. Journal of Agricultural & Environmental Ethics 23 (4) (AUG): 345-70.

Harel, Z, S Riggs, R Vaz, L White, and G Menzies. 2001. Omega-3 polyunsaturated fatty acids in adolescents: knowledge and consumption." The Journal Of Adolescent Health 28 (1): 10-15.

Hargrave, Barry T., Lisa I. Doucette, Kats Haya, Faron S. Friars, and Stephen M. Armstrong. 2008. A micro-dilution method for detecting oxytetracycline-resistant bacteria in marine sediments from salmon and mussel aquaculture sites and an urbanized harbour in Atlantic Canada. Marine Pollution Bulletin 56 (8) (AUG): 1439-45.

Herwig, R. P., J. P. Gray, and D. P. Weston. 1997. Antibacterial resistant bacteria in surficial sediments near salmon net-cage farms in Puget Sound, Washington. Aquaculture 149 (3-4) (MAR 31): 263-83.

Horrocks, L A, and Y K Yeo. 1999. Health benefits of docosahexaenoic acid (DHA). Pharmacological Research 40, (3): 211-225.

Lu, X. W., Z. Dang, and C. Yang. 2009. Preliminary investigation of chloramphenicol in fish, water and sediment from freshwater aquaculture pond. International Journal of Environmental Science and Technology 6 (4) (FAL): 597-604.

Mayor, Daniel J., Alain F. Zuur, Martin Solan, Graeme I. Paton, and Ken Killham. 2010. Factors affecting benthic impacts at Scottish fish farms. Environmental Science & Technology 44 (6) (MAR 15): 2079-84.

Meinertz, J. R., G. R. Stehly, and W. H. Gingerich. 1998. Liquid chromatographic determination of oxytetracycline in edible fish fillets from six species of fish. Journal of AOAC International 81 (4) (JUL-AUG): 702-8.

Mullon, C., J-F Mittaine, O. Thebaud, G. Peron, G. Merino, and M. Barange. 2009. Modeling the global fishmeal and fish oil markets. Natural Resource Modeling 22 (4) (NOV): 564-609.

Munoz, Ivan, Maria J. Martinez Bueno, Ana Agueera, and Amadeo R. Fernandez-Alba. 2010. Environmental and human health risk assessment of organic micro-pollutants occurring in a Spanish marine fish farm. Environmental Pollution 158 (5) (MAY): 1809-16.

Musclow, Sandy Lee. 2005. Impact Of Salmon Aquaculture On Sediment Chemistry And Mercury Loading. Master’s thesis. Montreal: McGill University.

National Fisheries Institute (2009). “Top 10 Consumed Seafoods,” http://www.aboutseafood.com/about/about-seafood/Top-10-Consumed-Seafoods

Naylor, Raymond L., Rebecca J. Goldburg, Harold Mooney, Malcolm Beveridge, Jason Clay, Carl Folke, Nils Kautsky, Jane Lubchenco, Jurgenne Primavera & Meryl Williams. 1998. Nature's subsidies to shrimp and salmon farming. Science 282 (5390): 883-887.

Ortega, C., O. Gimeno, V. Blanc, P. Cortes, S. Ania, and M. Llagostera. 2006. Antibiotic susceptibility of strains of Aeromonas salmonicida isolated from Spanish salmonids. Revue De Medecine Veterinaire 157 (8-9) (AUG): 410-4.

Pelletier, Nathan, Peter Tyedmers, Ulf Sonesson, Astrid Scholz, Friederike Ziegler, Anna Flysjo, Sarah Kruse, Beatriz Cancino, and Howard Silverman. 2009. Not all salmon are created equal: Life cycle assessment (LCA) of global salmon farming systems. Environmental Science & Technology 43 (23) (DEC 1): 8730-6.

Pitsios, Constantinos, Anastasia Dimitriou, Efthalia C Stefanaki, and Kalliopi Kontou-Fili. 2010. Anaphylaxis during skin testing with food allergens in children. European Journal Of Pediatrics 169 (5): 613-615.

Pollack, Andrew. 2010. Panel leans in favor of engineered salmon. The New York Times CLX (55170): B3.

Rivera-Ferre, Marta G. 2009. Can export-oriented aquaculture in developing countries be sustainable and promote sustainable development? The shrimp case. Journal of Agricultural & Environmental Ethics 22 (4) (AUG): 301-21.

Ruiz-Zarzuela, I., N. Halaihel, J. L. Balcazar, C. Ortega, D. Vendrell, T. Perez, J. L. Alonso, and I. de Blas. 2009. Effect of fish farming on the water quality of rivers in northeast Spain. Water Science and Technology 60 (3): 663-71.

Sapkota, Amir, Amy R. Sapkota, Margaret Kucharski, Janelle Burke, Shawn McKenzie, Polly Walker, and Robert Lawrence. 2008. Aquaculture practices and potential human health risks: Current knowledge and future priorities. Environment International 34 (8) (NOV): 1215-26.

Skaala, Oe, K. Glover, and V. Wennevik. 2006. Gene flow from escapes reduce survival in wild salmon populations. Fisken og Havet, Saernummer(2): 60-62.

Solensky, Roland. 2003. Resolution of fish allergy: A case report. Annals Of Allergy, Asthma & Immunology 91 (4): 411-412.

Soto, D., F. Jara, and C. Moreno. 2001. Escaped salmon in the inner seas, Southern Chile: Facing ecological and social conflicts. Ecological Applications 11, (6): 1750-1762

Thorstad, E.B., I.A. Fleming, P. McGinnity,  D. Soto, V. Wennevik & F. Whoriskey2008. Incidence and Impacts of Escaped Farmed Atlantic Salmon Salmo Salar In Nature. NINA Special Report 36. 110 pp.

U.S. Fish & Wildlife Service. 2010. Wildlife Species Information. Endangered Species:  Pacific Salmon, Oncorhynchus spp. http://www.fws.gov/species/species_accounts/bio_salm.html

Uusitalo, L., S. Kuikka, and A. Romakkaniemi. 2005. Estimation of Atlantic salmon smolt carrying capacity of rivers using expert knowledge. ICES Journal of Marine Science 62, (4) (Jun): 708-722

Vega, Mario H., Elizabeth T. Jara, and Mario B. Aranda. 2006. Monitoring the dose of florfenicol in medicated salmon feed by planar chromatography (HPTLC). JPC -Journal of Planar Chromatography-Modern TLC 19 (109) (MAY-JUN): 204-7.

Vizzini, Salvatrice, Cecilia Tramati, and Antonio Mazzola. 2010. Comparison of stable isotope composition and inorganic and organic contaminant levels in wild and farmed bluefin tuna, Thunnus thynnus, in the Mediterranean sea. Chemosphere 78 (10) (MAR): 1236-43.

Wolff, M. 2004. Use and misuse of antibiotics. time to evaluate it beyond humans. Revista Medica De Chile 132 (8) (AUG): 909-11.

Wozniak, Shawn. 2020. Has country of origin labeling influenced salmon consumption? Selected Paper prepared for presentation at the Southern Agricultural Economics Association Annual Meeting, Orlando, FL, February 6-9, 2010. http://ageconsearch.umn.edu/bitstream/56460/2/2010%20SAEA%20Wozniak.pdf

Wu, R. S. S. 1995. The environmental impact of marine fish culture: Towards a sustainable future. Marine Pollution Bulletin 31 (4-12) (APR-DEC): 159-66.

Ebola and Marburg: Two Closely Related, Highly Lethal Viruses that Cause Hemorrhagic Fever in Africa and May Still Be Being Sought By Terrorists and Rogue States To Weaponize and Attack Anywhere

Two of the most dreaded illnesses in the world are Ebola and Marburg. The names for these syndromes involves some medical geography;   in the first case, a river in Uganda (the Ebola) and in the second,  a city in Germany (Marburg),  where each of these hemorrhagic fevers was first detected in human patients.   

What is a hemorrhagic fever?

Hemorrhagic diseases are, by definition, characterized by profuse bleeding, internally or externally, and often both ways, and both Ebola and Marburg certainly qualify, although the panoply of other accompanying signs varies. (For a complete roster of possible symptoms, see Pittalis et al 2009 below )   Both Ebola and Marburg, are, however, in the early stages, primarily characterized by fever, exhaustion, and confusion in the patient. The hemorrhagic aspect is more obvious only in later stages.  Patients may develop dark-blister-like growths on their face and body where blood has pooled from broken capillaries.  They may then begin bleeding from the mouth, eyes, or ears. They almost always develop breakdowns in coagulation that leads to multiple sites of internal bleeding in a number of organs, leading further to localized tissue destruction. Eventually, the overall loss of sufficient internal blood supply can lead  to shock and death. Fortunately for the patients suffering, they often die only after they have gone into a coma.

How lethal are these two diseases?

While there are some less deadly strains (“Sudan” and “Bundibugyo” see Gupta et al 2010 below), Ebola and Marburg  kill off as high as 90% of infected patients, usually within three weeks of their contracting the responsible virus. The remaining patients of course, recover, although it is not always certain why they did so, when so many others have died.

From where did these diseases come?

They really both come from Africa, and all major outbreaks, and most individual cases, almost always are found there only, except  for patients  traveling to more developed countries seeking  diagnosis or treatment,  and medical researchers working with the virus in western countries. In addition to Uganda, Ebola has primarily broken out in Gabon, Sudan, and the Congo, with isolated cases elsewhere, including South Africa.  That Marburg is connected with a town in Germany has to do with laboratories there that make vaccines. (Two other European outbreaks  are based on similar circumstances.)  Lab workers  in Marburg  had routinely been importing  African green monkeys, but eventually unawares took in an infected  shipment which  gave this new disease to their handlers and research scientists.  Natural, as opposed to laboratory,  outbreaks of Marburg have occurred primarily  in Angola, Congo, Kenya, South Africa and Zimbabwe.

If this disease is so deadly, why hasn’t it already wiped out large portions of sub-Saharan Africa?

The disease breaks out most often in very isolated parts of the particular countries involved. There tends to be a steeply rising number of local cases for  several weeks to a few months, with a corresponding crescendo of deaths, and then a tapering off, with higher survival rates among later contractors of the virus. It is absolutely clear that quarantining patients and observing extreme measures to protect health providers, other patients and any family visitors, from contact with infective fluids, etc. is prudent and has done much to restrain the spread of outbreaks.  But Ebola and Marburg, often disappear altogether from a region as suddenly and unexpectedly as they erupted.

Avoidance strategies

Avoidance of Ebola and Marburg is much like avoiding running out of doors when there is a lightning storm.  It’s a very good idea, but of itself does not confer immunity. Avoidance does not seem to protect you from getting the disease unexpectedly elsewhere in sub-Saharan Africa, any more than avoiding one place where lightning has struck in the past will confer immunity to thunderbolts should a storm  break out elsewhere and you get caught there by surprise.

Where does the disease lurk, then, between outbreaks?

There is little doubt that these diseases persist in wild animals, where they do not necessarily make  all of their natural hosts fatally sick. Rodents, bats, and various small monkeys have been implicated as natural reservoirs (See for example Leroy et al 2009 below). By contrast, chimpanzees and gorillas are known to contract Marburg and Ebola, but seem to die off very quickly much like humans do in response to infection, so they do not seem to be a likely vector, except when their dead carcasses are eaten as bush meat by native peoples. (See Bermejo et al. 2006 below).   But those animals which do survive and harbor the virus, in  their feces, urine, saliva, blood, and perhaps other body parts or fluids apparently contaminate the food, water, or air that is taken in by nearby humans. While vermin eradication, particularly of rodents, is recommended as a possible preventive strategy to reduce the chances of a community developing an outbreak of Ebola or Marburg, there is not a great deal of evidence that reintroduction of vermin predators (such as the revival of cat ownership which had the effect of reducing rats with bubonic plague carrying fleas)  or even chemical extermination of pests  has stopped an ongoing outbreak, quite possibly because, with few exceptions, (such as an Angolan episode of Marburg)  they tend to be short term any way.   Current laboratory experiments in search of effective therapies generally use infected lab mice, rats, guinea pigs, or monkeys. Some of these experimental animals are more disease tolerant than others, and the point of using them is to see what contributes to that tolerance. Other laboratory animals are designed to get sick and die pretty much as a model for the human experience of these diseases. There is a peculiar case in the Philippines where a variant of Ebola called Ebola-Reston (after Reston, Virginia, where a shipment of crab-eating monkeys sent to a medical research lab was found to have Ebola) has infected pigs and pig farmers near Manila, but the pigs seem not to die off quickly, and the farmers do not get sick at all, despite the fact that blood tests show that  both animals and men have definitely had some sort of immune reaction indicating some level of infection (See Normile 2009 below).

What currently can be done for patients?

Patients are typically placed in medical isolation wards whenever possible, and given comfort care. They have fluid replacement, pain and fever reducers, but often do not get whole blood transfusions because these simply bleed out so rapidly.  

What do we know about the viruses responsible for Ebola and Marburg ?

The structure of both Ebola and Marburg viruses has been very well studied (See, for example, Hartman, Tower & Nichol 2010 or Noda et al 2010 below ) and they are  virtually identical, although they trigger slightly different immunological responses and have slightly different means of attacking cells (See Valmas et al 2010 below).  These viruses consist of a surprisingly long (for a virus) strand of RNA coated largely with lipids, with fairly short protein prongs alongside.  We can detect when and how they begin to penetrate cells (See Lipkin, Paacio & Briese 2009 or Tscherne, Manicassamy & Garcia-Sastre 2010  below ) and can now visualize how these  viruses bud (See Liu et al 2010, Mateo et al 2010 and Welsch et al 2010 below).  We have a pretty good idea of how  they evade the body’s immune defenses (See Basler & Amarasinghe 2009 and  Mohamadzadeh 2009 below ) yet provoke fevers that should otherwise have helped kill them off  nonetheless (See Okumura et al 2010 below), even as they induce immune cell death (See Bradfute et al 2010 below).

What are the current strategies for fighting Ebola and Marburg?

Vaccines seem to be the route of choice (See Bausch et al 2008 ,  Geisbert et al 2009, and Olinger et al 2009  below), in part because it does seem that the small percentage of survivors of  Ebola and Marburg have developed some immunological means of fighting off the remnant viruses (See Wauquier et al 2009 below) and this suggests that the right antigen triggers will generate a survival response similar to that of these patients. Nonetheless the Food and Drug Administration has relaxed the strict rules for claims of efficacy in humans by allowing initially for a greater reliance on animal models, largely because typical Ebola (and Marburg) outbreaks are extremely unpredictable and very often short-lived  and most often happen in poorly equipped remote jungle areas where  the numbers of patients fluctuate wildly and setting up rigid double-blind trials is simply unworkable (See Sullivan et al 2009 below).

Some vaccine prototypes are based on evoking natural immune responses to natural Ebola strains or  chemically altered Ebola mutants whose ability to replicate wildly and endanger the patient has  been tamed (See Halfmann et al 2009 and Prins et al 2010 below), although using specially tailored viruses more commonly associated with the common cold or flu also seems promising (See Bukreyev et al 2010 and Pratt et al 2010 below ).

Attacking proteins necessary for cellular invasion and/or replication is a common theme (See Hood et al 2010 below), as is disrupting RNAs making proteins using antisense morpholino  oligomers (See Swenson et al 2009 below) or microencapsulated “small interfering” RNA (Geisbert et al 2010) both of which block off key sites, while other approaches basically allow the viruses to enter some cells but then trap them there by halting the budding process (See Harty 2009 below).

Nightmare scenarios: Weaponization of Marburg and Ebola by the Soviets  and reported attempts by terrorists to acquire it

Several websites, including that of the highly respected Federation of American Scientists (http://www.fas.org/programs/bio/factsheets/ebola.html ) give credence to the notion that some form of the Ebola virus was developed as biological weapon of mass destruction by the Soviets, and  a book coauthored by a former Soviet bioweapons expert, Ken Alibek (see Alibek & Handelman 1999 below)  who is currently a well-respected  U.S. based bioterrorism medical expert (see Weinstein & Alibek 2003 below ) also documents the use of the Marburg virus in a similar context. Other credible websites assert that terrorists and doomsday religious cults, most notably the Japanese  group Aum Shinrikyo (http://www.globalsecurity.org/wmd/intro/bio_ebola.htm ) have sought to acquire and exploit hemorrhagic viruses. (They instead, released Sarin gas in an attack on the Tokyo subway system, killing 13, wounding 50, and temporarily blinding thousands.) Preparation for medical responses to the use of Ebola and Marburg in terrorist attacks is, alas, not taken as a matter of science fiction or television action and adventure thriller episodes any longer (see DuPuy & Schmaljohn 2009 and Goffman 2010 below).

 Tony Stankus, FSLA, [email protected] Professor, Life Sciences Librarian,  and Science Coordinator

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Alibek, Ken, and Stephen Handelman. 1999. Biohazard: the chilling true story of the largest covert biological weapons program in the world, told from the inside by the man who ran it. New York: Random House.

Aman, M. J., Michael S. Kinch, Kelly Warfield, Travis Warren, Abdul Yunus, Sven Enterlein, Eric Stavale, et al. 2009. Development of a broad-spectrum antiviral with activity against Ebola virus. Antiviral Research 83, (3) (09): 245-51.

Barrette, Roger W., Samia A. Metwally, Jessica M. Rowland, Lizhe Xu, Sherif R. Zaki, Stuart T. Nichol, Pierre E. Rollin, et al. 2009. Discovery of swine as a host for the Reston Ebolavirus. Science 325, (5937) (07/10): 204-6.

Basler, Christopher F., and Gaya K. Amarasinghe. 2009. Evasion of interferon responses by Ebola and Marburg viruses. Journal of Interferon & Cytokine Research  29, (9) (09): 511-20.

Bausch, D.G., A/G. Sprecher, B. Jeffs & P. Boumandouki. 2008. Treatment of Marburg and Ebola hemorrhagic fevers: A strategy for testing new drugs and vaccines under outbreak conditions. Antiviral Research 78 (1): 150-60.

Bermejo, M. J.D. Rodrieguez-Teijero, G. Illera, A. Barroso, C. Villa, & P.D. Walsh. 2006. Ebola outbreak kills 5,000 gorillas. Science 314: 1564.

Bhattacharyya, Suchita, Kelly L. Warfield, Gordon Ruthel, Sina Bavari, M. J. Aman, and Thomas J. Hope. 2010. Ebola virus uses clathrin-mediated endocytosis as an entry pathway. Virology 401, (1) (05/25): 18-28.

Bradfute, Steven B., Paul E. Swanson, Mark A. Smith, Eizo Watanabe, Jonathan E. McDunn, Richard S. Hotchkiss, and Sina Bavari. 2010. Mechanisms and consequences of Ebolavirus-induced lymphocyte apoptosis. Journal of Immunology 184, (1) (01/01): 327-35.

Bukreyev, Alexander A., Joshua M. Dinapoli, Lijuan Yang, Brian R. Murphy, and Peter L. Collins. 2010. Mucosal parainfluenza virus-vectored vaccine against Ebola virus replicates in the respiratory tract of vector-immune monkeys and is immunogenic. Virology 399, (2) (04/10): 290-8.

Dias, M. B., Leonardo Reyes-Gonzalez, Francisco M. Veloso, and Elizabeth A. Casman. 2010. Effects of the USA Patriot Act and the 2002 Bioterrorism Preparedness Act on select agent research in the United States. Proceedings of the National Academy of Sciences of the United States of America 107, (21) (05/25): 9556-61.

Douglas, Janet L., Jean K. Gustin, Kasinath Viswanathan, Mandana Mansouri, Ashlee V. Moses, and Klaus Früh. 2010. The great escape: Viral strategies to counter BST-2/tetherin. Plos Pathogens 6, (5): e1000913-.

Dupuy, Lesley C., and Connie S. Schmaljohn. 2009. DNA vaccines for biodefense. Expert Review of Vaccines 8, (12) (12): 1739-54.

Ebola Reston virus detected pigs in the Philippines. 2009. Euro Surveillance: Bulletin Européen Sur Les Maladies Transmissibles = European Communicable Disease Bulletin 14, (4) (01/29).

Feldmann, Heinz. 2010. Are we any closer to combating Ebola infections? Lancet 375, (9729) (05/29): 1850-2.

Geisbert, Thomas W., Joan B. Geisbert, Anders Leung, Kathleen Daddario-DiCaprio, Lisa E. Hensley, Allen Grolla, and Heinz Feldmann. 2009. Single-injection vaccine protects nonhuman primates against infection with Marburg virus and three species of Ebola virus. Journal of Virology 83, (14) (07): 7296-304.

Geisbert, Thomas W., Amy C. H. Lee, Marjorie Robbins, Joan B. Geisbert, Anna N. Honko, Vandana Sood, Joshua C. Johnson, et al. 2010. Postexposure protection of non-human primates against a lethal Ebola virus challenge with RNA interference: A proof-of-concept study. Lancet 375, (9729) (05/29): 1896-905.

Goffman, Thomas E. 2010. Bioterrorism: What might be walking into the ED? The American Journal of Emergency Medicine 28, (4) (05): 515-8.

Gupta, Manisha, Cynthia S. Goldsmith, Maureen G. Metcalfe, Christina F. Spipopoulou, and Pierre E. Rollin. 2010. Reduced virus replication, proinflammatory cytokine production, and delayed macrophage cell death in human PBMCs infected with the newly discovered Bundibugyo Ebolavirus relative to Zaire Ebolavirus. Virology 402, (1) (06/20): 203-8.

Halfmann, Peter, Hideki Ebihara, Andrea Marzi, Yasuko Hatta, Shinji Watanabe, M. Suresh, Gabriele Neumann, Heinz Feldmann, and Yoshihiro Kawaoka. 2009. Replication-deficient Ebolavirus as a vaccine candidate. Journal of Virology 83, (8) (04): 3810-5.

Hartman, Amy L., Jonathan S. Towner, and Stuart T. Nichol. 2010. Ebola and Marburg hemorrhagic fever. Clinics in Laboratory Medicine 30, (1) (03): 161-77.

Hartshorn, Kevan L. 2010. Role of surfactant protein A and D (SP-A and SP-D) in human antiviral host defense. Frontiers in Bioscience (Scholar Edition) 2, : 527-46.

Harty, R.N. 2009. No exit: Targeting the budding process to inhibit filovirus replication. Antiviral Research 81 (3): 189-97.

Hoenen, T., S. Jung, A. Herwig, A. Groseth, and S. Becker. 2010. Both matrix proteins of Ebola virus contribute to the regulation of viral genome replication and transcription. Virology 403, (1) (07/20): 56-66.

Hood, Chantelle L., Jonathan Abraham, Jeffrey C. Boyington, Kwanyee Leung, Peter D. Kwong, and Gary J. Nabel. 2010. Biochemical and structural characterization of cathepsin L-processed Ebola virus glycoprotein: Implications for viral entry and immunogenicity. Journal of Virology 84, (6) (03): 2972-82.

Leroy, Eric M., Alain Epelboin, Vital Mondonge, Xavier Pourrut, Jean-Paul Gonzalez, Jean Muyembe-Tamfum, and Pierre Formenty. 2009. Human Ebola outbreak resulting from direct exposure to fruit bats in Luebo, Democratic Republic of Congo, 2007. Vector Borne and Zoonotic Diseases (Larchmont, N.Y.) 9, (6) (12): 723-8.

Leung, Daisy W., Dominika Borek, Mina Farahbakhsh, Parameshwaran Ramanan, Jay C. Nix, Tianjiao Wang, Kathleen C. Prins, et al. 2010. Crystallization and preliminary X-ray analysis of Ebola VP35 interferon inhibitory domain mutant proteins. Acta Crystallographica.Section F, Structural Biology and Crystallization Communications 66, (06/01): 689-92.

Leung, Daisy W., Kathleen C. Prins, Dominika M. Borek, Mina Farahbakhsh, JoAnn M. Tufariello, Parameshwaran Ramanan, Jay C. Nix, et al. 2010. Structural basis for dsRNA recognition and interferon antagonism by Ebola VP35. Nature Structural & Molecular Biology 17, (2) (02): 165-72.

Lipkin, W. I., Gustavo Palacios, and Thomas Briese. 2009. Diagnostics and discovery in viral hemorrhagic fevers. Annals of the New York Academy of Sciences 1171 Suppl 1, (09): E6-E11.

Liu, Yuliang, Luis Cocka, Atsushi Okumura, Yong-An Zhang, J. O. Sunyer, and Ronald N. Harty. 2010. Conserved motifs within Ebola and Marburg virus VP40 proteins are important for stability, localization, and subsequent budding of virus-like particles. Journal of Virology 84, (5) (03): 2294-303.

Mateo, Mathieu, St Patrick Reid, Lawrence W. Leung, Christopher F. Basler, and Viktor E. Volchkov. 2010. Ebolavirus VP24 binding to karyopherins is required for inhibition of interferon signaling. Journal of Virology 84, (2) (01): 1169-75.

Mohamadzadeh, Mansour. 2009. Potential factors induced by filoviruses that lead to immune supression. Current Molecular Medicine 9, (2) (03): 174-85.

Noda, Takeshi, Kyoji Hagiwara, Hiroshi Sagara, and Yoshihiro Kawaoka. 2010. Characterization of the Ebola virus nucleoprotein-RNA complex. The Journal of General Virology 91, (06): 1478-83.

Normile, Dennis. 2009. Emerging infectious diseases. Scientists puzzle over Ebola-Reston virus in pigs. Science 323, (5913) (01/23): 451-.

Okumura, Atsushi, Paula M. Pitha, Akihiko Yoshimura, and Ronald N. Harty. 2010. Interaction between Ebola virus glycoprotein and host toll-like receptor 4 leads to induction of proinflammatory cytokines and SOCS1. Journal of Virology 84, (1) (01): 27-33.

Olinger Gene G., Julia E. Biggins, Vanessa R. Melanson, Victoria Wahl-Jensen Victoria,  Thomas W. Geisbert, and Lisa E. Hensley. 2009. Drug targets in infections with Ebola and Marburg viruses. Infectious Disorders Drug Targets 9, (2) (04): 191-200.

Pittalis, Silvia, Francesco Maria Fusco, Simone Lanini, Carla Nisii, Vincenzo Puro, Francesco Nicola Lauria, and Giuseppe Ippolito. 2009. Case definition for Ebola and Marburg haemorrhagic fevers: A complex challenge for epidemiologists and clinicians. The New Microbiologica: Official Journal of the Italian Society for Medical, Odontoiatric, and Clinical Microbiology (SIMMOC) 32, (4) (10): 359-67.

Pratt, William D., Danher Wang, Donald K. Nichols, Min Luo, Jan Woraratanadharm, John M. Dye, David H. Holman, and John Y. Dong. 2010. Protection of nonhuman primates against two species of Ebola virus infection with a single complex adenovirus vector. Clinical and Vaccine Immunology: CVI 17, (4) (04): 572-81.

Prins, Kathleen C., Sebastien Delpeut, Daisy W. Leung, Olivier Reynard, Valentina A. Volchkova, St Patrick Reid, Parameshwaran Ramanan, et al. 2010. Mutations abrogating VP35 interaction with double-stranded RNA render Ebola virus avirulent in guinea pigs. Journal of Virology 84, (6) (03): 3004-15.

Raabe, Vanessa N., Imaam Mutyaba, Paul Roddy, Julius J. Lutwama, Wenzel Geissler, and Matthias Borchert. 2010. Infection control during filoviral hemorrhagic fever outbreaks: Preferences of community members and health workers in Masindi, Uganda. Transactions of the Royal Society of Tropical Medicine and Hygiene 104, (1) (01): 48-50.

Shedlock, Devon J., Michael A. Bailey, Paul M. Popernack, James M. Cunningham, Dennis R. Burton, and Nancy J. Sullivan. 2010. Antibody-mediated neutralization of Ebola virus can occur by two distinct mechanisms. Virology 401, (2) (06/05): 228-35.

Stanwell-Smith, R. 2009. When nature turns cook: An epidemiological feast: Report of the John Snow Society Pumphandle Lecture 2009, delivered by Dr David Heymann. Public Health 123, (12) (12): 814-6.

Sullivan, Nancy J., Julie E. Martin, Barney S. Graham, and Gary J. Nabel. 2009. Correlates of protective immunity for Ebola vaccines: Implications for regulatory approval by the animal rule. Nature Reviews. Microbiology 7, (5) (05): 393-400.

Swenson, Dana L., Kelly L. Warfield, Travis K. Warren, Candace Lovejoy, Jed N. Hassinger, Gordon Ruthel, Robert E. Blouch, et al. 2009. Chemical modifications of antisense morpholino oligomers enhance their efficacy against Ebola virus infection. Antimicrobial Agents and Chemotherapy 53, (5) (05): 2089-99.

Trombley, Adrienne R., Leslie Wachter, Jeffrey Garrison, Valerie Buckley-Beason, Jordan Jahrling, Lisa E. Hensley, Randal J. Schoepp, et al. 2010. Comprehensive panel of real-time TaqMan polymerase chain reaction assays for detection and absolute quantification of filoviruses, arenaviruses, and New World hantaviruses. The American Journal of Tropical Medicine and Hygiene 82, (5) (05): 954-60.

Tscherne, Donna M., Balaji Manicassamy, and Adolfo García-Sastre. 2010. An enzymatic virus-like particle assay for sensitive detection of virus entry. Journal of Virological Methods 163, (2) (02): 336-43.

Urata, Shuzo, and Jiro Yasuda. 2010. Regulation of Marburg virus (MARV) budding by Nedd4.1: A different WW domain of Nedd4.1 is critical for binding to MARV and Ebola virus VP40. The Journal of General Virology 91, (01): 228-34.

Valmas, Charalampos, Melanie N. Grosch, Michael Schümann, Judith Olejnik, Osvaldo Martinez, Sonja M. Best, Verena Krähling, Christopher F. Basler, and Elke Mühlberger. 2010. Marburg virus evades interferon responses by a mechanism distinct from Ebola virus. Plos Pathogens 6, (1): e1000721-.

Wauquier, Nadia, Pierre Becquart, Clélia Gasquet, and Eric M. Leroy. 2009. Immunoglobulin G in Ebola outbreak survivors, Gabon. Emerging Infectious Diseases 15, (7) (07): 1136-7.

Weinstein, Raymond S., and Ken Alibek. 2003. Biological and chemical terrorism: a guide for healthcare providers and first responders. New York: Thieme Medical Pub.

Welsch, Sonja, Larissa Kolesnikova, Verena Krähling, James D. Riches, Stephan Becker, and John A. G. Briggs. 2010. Electron tomography reveals the steps in filovirus budding. Plos Pathogens 6, (4): e1000875-.