The Good Housekeeper: GBV-C Co-infection with HIV

I know that the study of infectious diseases seems grim. Bacteria are increasingly becoming antibiotic resistant, baby parasites nest in your brain and tuberculosis spreads to your toes. I get it – all this devotion to the study of what gruesome-thing-du-jour is in your blood and saliva isn’t sunshine, puppies and rainbows. So in the interests of maintaining public optimism, I offer you GBV-C, a virus that has been found to offer a protective, antiviral effect against HIV infection. Yes, that HIV.

GBV-C is a member of the Flaviviridae family of viruses; a truly distinguished and deadly lot that includes hepatitis C, yellow fever, West Nile virus, dengue and a slew of nasty encephalitis-causing viruses that roost in mosquitoes and ticks. GBV-C, however, appears to exist within the body as a benign, harmless infection. It provokes no identifiable clinical symptoms of disease and seems to be the black sheep of the noxious Flaviviridae family (2).

The one thing that makes this virus notable, even outstanding!, is that for those who are co-infected with HIV and GBV-C have been shown to live significantly longer than those without GBV-C (3). If HIV is an unwelcome houseguest in the human body, then infection with GBV-C is like waking up one day and unexpectedly finding a housekeeper doing the dirty dishes and containing the mess created by this destructive guest.

A model showing the morphology of the GBV-C virus. The human body’s antibody to the E2 envelope glycoprotein may assist in stymieing HIV infection. Source: the Physician Research Network. Click for source.

GBV-C is spread in ways similar to the transmission of HIV: through sex, birth and blood. Human infection with this virus is common, with 1–8% of healthy blood donors showing evidence of infection worldwide (1). So common in fact that isolated indigenous populations in Papua New Guinea have been found to harbor the virus (3). The global distribution and evolution of the major genotypes of this virus echoes human migration patterns, indicating that this is one old viral dude that’s been hitchhiking along with humans for millions of years (3).

GBV-C provides a beneficial, antiviral effect by stymieing HIV’s advances into immune cells and spurning its replication efforts in the body. It does so in a dizzying number of ways (reader beware: it’s gonna get molecular up in here). The infection stimulates messenger signals known as cytokines to activate a cellular response and consume HIV infected cells (otherwise known as the T helper 1 (Th1) cellular response system). The virus also encourages the innate immune response by boosting pathogen-fighting interferons; this innate response can be considered one of the “first responders” of the immune system as it responds to nearly every type of infection while also activating the more advanced components of the immune system to respond to any bacterial/viral/protozoal invaders.

GBV-C stops the human cells that HIV infects, CD4+ T cells, from killing themselves in the programmed-cell-death process known as apoptosis. Apoptosis is induced by HIV-infected T cells and can affect uninfected and infected cells alike; GBV-C protects these cells maintaining their population levels. This discovery is particularly noteworthy as a crash in the population of CD4+ T cells (“CD4+ counts”) is a hallmark of immune deficiency and disease progression from HIV to AIDS.

On the left, a T cell is covered in budding HIV virus particles and will soon undergo programmed-cell-death or apoptosis. On the right, a close-up of the budding virions. Infection with GBV-C may halt this process and prevent a population crash in the numbers of CD4+ cells. Image source: Roingeard P & Brand D (1998) Budding of Human Immunodeficiency Virus. N Engl J Med. 339(32). Click for source.

The GBV-C virus causes a decrease in the cellular presence of the receptors that HIV uses to gain entry into the cell (in science speak: there’s a down-regulation of the CCR5 and CXCR4 chemokine receptors); this is akin to temporarily removing the doors of your house to predators and thieves instead of just locking them shut. In addition, GBV-C infection seems to decrease the presentation of special “activation markers” on the surface of  T cells, interfering with signaling pathways that activate the production of T cells (2). Unfortunately, it’s not entirely clear what effect this “reduced immune activation” has on the immune system and whether this assists or hinders the immune system’s response to HIV infection. Certain proteins produced by GBV-C also inhibit HIV replication (1)(3).

Overall, co-infection with the two viruses leads to increased survival of HIV-infected patients and decreased mortality (1). Not too shabby! How it does this is largely uncertain – is it due to the presence of GBV-C virus particles (known as viremia) or the body’s response to GBV-C infection and its concomitant production of antibodies against the GBV-C virus (namely the anti–GBV-C envelope glycoprotein (E2) antibody)? The fact that 15-43% of HIV-positive people show active GBV-C infection and that another 31-55% show evidence of previous infection makes it difficult to disentangle these two questions (1). However, by all accounts, what we have here looks like a symbiotic relationship between GBV-C and humans.

Two researchers behind most of the work into GBV-C have suggested that this delightful house keeper may more accurately be called the “good boy virus”, a phrase that heartily captures its place in a HIV-positive body (2). The Flaviviridae family needs all the good PR it can get and this GBV-C do-gooder might be the trick.

Though it’s unlikely HIV physicians are going to start recommending GBV-C infection to HIV-infected patients anytime soon, the work of this benign virus has intriguing implications for future virology research. Study of the virus’s housekeeping efforts may yield new targets for anti-HIV medications and alternative avenues for future research. Perhaps this virus could even be genetically-modified to magnify its HIV-fighting ways and be employed as a form of HIV treatment? We already do the opposite of this with many virulent pathogens, using weak or killed viruses as vaccines, and there are physicians out there that advocate for the use of bacteria-killing viruses; using bacteriophages to fight stubborn infections was an especially popular treatment in Eastern Europe and the former Soviet Union in the 1950s (4). In the face of mounting antibiotic resistance across the globe, using do-gooder viruses like GBV-C may soon be the only option we have left.

Resources

The United State’s FDA does not screen donated blood for GBV-C. Dozens of studies have failed to find any link whatsoever between GBV-C infection and disease and, as such, an estimated 1000 Americans a day receive blood with GBV-C virions or antibodies (2). I covered blood screening for infectious diseases in this article here.

The Phage Therapy Center in the Republic of Georgia is the pioneer in providing bacteriophage treatment for a smorgasbord of bacterial infections.

A 2006 review looks at natural resistance to HIV in certain individuals, whether that be from GBV-C, the host immune response or host genetics. It’s free!

References
1. Xiang J et al. (2004) Inhibition of HIV-1 replication by GB virus C infection through increases in RANTES, MIP-1, MIP-1, and SDF-1. Lancet. 363(9426): 2040-6
2. Bhattarai N & Stapleton JT. (2012) GB virus C: the good boy virus? Trends Microbiol. 20(3):124-30
3. Polgreen PM et al. (2003) GB virus type C/hepatitis G virus: a non-pathogenic flavivirus associated with prolonged survival in HIV-infected individuals. Microbes Infect. 5(13): 1255–1261
4. Sulakvelidze A et al (2001) Bacteriophage Therapy. Antimicrob. Agents Chemother. 45(3): 649-659. Accessible here.

Polgreen, P., Xiang, J., Chang, Q., & Stapleton, J. (2003). GB virus type C/hepatitis G virus: a non-pathogenic flavivirus associated with prolonged survival in HIV-infected individuals Microbes and Infection, 5 (13), 1255-1261 DOI: 10.1016/j.micinf.2003.08.006

Baylisascariasis! The Tragic Parasitic Implications of Raccoons In Your Backyard

This article was published as a guest post on the blog of the Parents of Kids with Infectious Diseases (PKIDs) nonprofit on April 2, 2012. It can be visited here in an edited, shorter form. You can find out more about this great organization and their public health mission here.

The re-wilding or “greening” of urban and suburban spaces has been an indefatigable, faddy trend in urban planning for the past two decades. Urbanites like accessible parks and community gardens and food forests and stately trees and along with our car-filled cities. Hell, we name our streets after trees – spruce, elm, oak, pine and so on. These are the things we do to justify our shoddy recycling habits and not giving due care to our carbon footprint. Sustainability is the new mantra, screen-printed on our reusable grocery totes. So it can be troubling when we see the repercussions when we bring nature into the neighborhood and blur the line between urban comforts and rural charms. One of those manifestations can be rodents, coyotes, foxes, opossums, and raccoons joining the ‘hood.

And it works! Coyotes frequently visit the outskirts of cities. Bears drop by homes abutting forests in Colorado state. Rodents raid community gardens. Raccoons hang out in Central Park in NYC.

The omnivore raccoon (Procyon lotor). Image: John Biehler. Click for source.

Let’s talk raccoons. The bandit-style masking covering their faces, their insatiable curiosity, and nimble human-like hands has popularized them as mischievous varmints. Though their nocturnal habits tend to keep them out of the sights of most Americans, they can be unseemly guests with their destructive tendencies. All that these small mammals need is a permanent water source, a safely enclosed setting for their den and access to food. Luckily they can find all these things and more when living in suburbia and cities. Human dwellings and activities serve as both a den reservoir and food resource; we are nothing but extraordinarily generous, unwitting hosts.

They can eviscerate lawns in their search for earthworms and grubs, steal your invaluable rubbish from trash bins, suck dry bird feeders, and shred the ventilation ducts, sheetrock and insulation in attics. So cute! Aside from ruining the hard work you put into creating the perfect English garden or shingling your roof or whatever household chore has been on your to-do list for years, they also are host to diseases that really will, absolutely, positively kill you. Like rabies. And baylisascariasis.

Baylisascariasis describes the human infection with the raccoon roundworm Baylisascaris procyonis. The parasite is endemic in raccoons, with infection rates ranging from 72% to 100% (1)(2). If you live in a place with sidewalks, there are most certainly infected raccoons living in close proximity to you; B. procyonis is the pathogen hiding in your backyard (3). One of the larger parasitic worms out there, this big guy inhabits the intestinal tract of raccoons and produces thousands of eggs that are shed in the feces.

Typical raccoon latrines found in urban and suburban environments. (A) Latrine on a chimney ledge. (B) Large latrine in the crotch of an oak tree approximately 3.5 m (15 feet) above ground. (C) Large latrine, in use for years on a house roof. (D) Latrine site on the ground near downed timber and rocks in a suburban yard. (E) Latrine on a stump in a suburban park with plants sprouting from seeds in the scat. (F) Raccoon scat hidden in leaf litter in a suburban back yard.
Image and caption source: Roussere et al. See References for details.

Like humans, raccoons can be fastidious about their pooping habits. They make communal latrines that can be found on natural or artificially flat surfaces – at the bases of trees and in branch crotches, on woodpiles, along and on the top of fences, on roofs, attics, and sandboxes (2). This results in a condensing and localizing of the eggs in one specific spot, attracting foraging birds and small rodents to undigested seeds and the like, and successfully ensuring the continuation of the parasite’s life cycle as it infects and kills the intermediate host. The raccoon scavenges the dead, becomes infected with the larva and the parasite keeps marching on into life cycle infinity.

The life cycle of the raccoon roundworm Baylisascaris procyonis. Image: DPDx CDC. Click for source.

Raccoons sharing your living space, whether in the attic above you or in a nearby tree or under the porch, means that there’s a raccoon latrine near you; thankfully, they’ve kindly kept all their crap in one place unlike some roommates I’ve had the pleasure of co-habitating with. A 2009 survey checking out an area of suburban Chicago close to a marsh and forest preserve found that 51% of lawns had a raccoon latrine (4). This kind of work suggests that there’s a good chance of fecal contamination in many of our backyards, spaces that typically serve as children’s play areas. The uniqueness of the latrine itself – piles of feces with undigested seeds, berries and bones – can also attract curious toddlers. Alternatively, if raccoons occupy chimneys, infective feces can settle within and around fireplaces, contaminating the home.

How is that this random raccoon parasite can make it onto a child’s fingertips, aside from the obvious hand-to-mouth behavioral sequence most parents are familiar with? There are three major reasons. One is that the raccoon can defecate prodigious amounts of B. procyonis eggs, on the order of a million a day. The other is that the parasite’s egg is unbelievably hardy and damn near resistant to nearly all of our arsenals against eradicating grime, schmutz and filth. The egg has four shell layers and is resistant to high temperatures, strong acids and bases, oxidants and reductants, and protein-disrupting agents (2). Guys, that’s pretty much all we got in terms of dealing with dirty surfaces and buggies, and it’s resistant to all of them except for applying direct flames to the egg. And how often do you find yourself planning to incinerate your backyard, aside from Fourth of July celebrations? Lastly, the eggs are remarkably sticky, gluing themselves to available surfaces which may include toys littered in the backyard.

The large female (left) and male (right) adults of the Baylisascaris procyonis roundworm compared to a penny. Source: Roussere et al. See References for details.

Once hatched from the egg, the larva has a cruel propensity for the cranial region of their intermediate hosts and, as such, it’s carousing in the head and thoracic region has grim neurological implications. In fact, the parasite is the most common cause of larva migrans – larval worm migration in bodily tissues – in animals and can produce severe neurological larva migrans (NLM) in over 100 species of birds and animals (1). This can be a nasty worm and has heartily evolved and adapted to get into the raccoon anyway that it can.

That these alarmingly large adult worms produce sizable larva bodes also poorly for us humans. The immensity of these worms can cause significant tissue trauma, especially in young children with their small bodies. The most common diagnosis from infection is eosinophilic meningoencephalitis, in which the brain and spinal cord and the meninges membranes surrounding the two becomes enormously inflamed due to the larva activating a type of white blood cell known as an eosinophil.

Clinical symptoms can develop two to four weeks after initial infection (5). Usually children have been lethargic, feverish and a little “off” for a few weeks before being rushed to the emergency room with seizures, unsteady gait or abnormally regressive behavior. There is no commercial test to confirm antibodies to the infection, making it difficult to have an accurate diagnosis (6). Meningoencephalitis is an affliction that can be tough to track down the originating cause; there are numerous other larval worms to cross of the list before making a diagnosis (including Toxocara canis, Ascaris lumbricoides, as well as species of Angiostrongylus, Ancylostoma, Taenia and Echinococcus). The infection is not well known to many clinicians, outside of the infectious disease field, which can complicate proper treatment of the symptoms (6). In the emergency room, the most pressing need is to control the damaging inflammation, not figure out which worm is the culprit.

Children are more likely to suffer devastating effects of this reaction than that of adults due to their relatively smaller brains (2). Infection outcomes have been statistically grim – many of these young patients either suffer permanent neurological and ocular defects or death. A microbiology paper from 2005 puts it bluntly, “To date, all survivors have been left in a persistent vegetative state or with severe residual deficits”(1).

And the victims are mostly very young children, typically boys. Infants and toddlers are predisposed to learn about their world by oral contact and commonly engage in pica and geophagia (eating of dirt). These types of behaviors can also be demonstrated by older children with developmental disabilities, another important subset of patients that have become infected with the parasite (3). Overall, important risk factors for baylisascariasis infection include exposure to raccoon feces, pica or geophagia, age under 4 years, male gender, and intellectual development delay.

Thankfully, the number of cases is low but it’s hard to discern whether that’s attributable to an actually low incidence of disease or a lack of reporting. Many parents decline autopsies, the only true way to definitively identify a case of baylisascarisasis. I tracked down 22 cases that have been reported in the literature (1)(3)(6)(7)(8)(9). Subclinical infection may also occur – a Chicago study found that 8% of children showed antibodies to the parasite though none had ever shown symptoms of disease (10); baylisascariasis may be much more prevalent than we think.

A foreclosed home in Detroit taken over by nature. Photo is part of a series of "feral homes" in the city taken by photographer JD Griffioen. These properties compromise our ability to separate our urban landscapes from nature and invite wildlife into our neighborhoods. Image: James D. Griffioen.

Importantly, the numbers of reportable cases has been steadily rising in the past decade for unknown reasons, though I suspect that the greening of our surroundings and the increase in diagnosed autism cases, a medical situation that can predispose children to pica habits, may have something to do with it.  Most recently, adult B. procyonis worms have been detected in pet dogs (2). This worrisome finding suggests that cases could also rise further. There are few wild animals that live so freely along humans that are cable of transmitting such a ferociously nasty and fatal disease. Parents and communities should be made aware of the dangers of having such animals close by and should go to efforts to locate and remove any raccoon latrines within or near the home.

Bringing nature to the neighborhood isn’t always a deliberate process, like revitalizing our neighborhoods by putting in a park or planting some trees. Industrial decay, environmental catastrophes and housing foreclosures can transform our urban landscape into a more inviting setting for nature to recolonize our space. Bobcats have been found living in foreclosed homes, neighborhoods in New Orleans are literally turning into marshland, and feral animals prowl through Detroit. One of the benefits of living in a city, away from nature, is that the only animals we have to deal with are ourselves.

Resources

I stumbled upon one of the most fascinating fact-sheets I’ve ever encountered. It’s on raccoons. A quote: “They are constantly feeling around with their paws. Every glittering stone, every unusual object, every smelly tidbit catches their eye or nose and they will stop to inspect these objects with intense scrutiny.”

Just how does one clean a raccoon latrine?

A squirrel infected with the parasite exhibiting ataxia, loss of bodily movement control, a symptom of neurological larva migrans.

Curious about urban greening, re-wilding and planning initiatives bringing nature into the ‘hood? Here. Here. Here. Here. Here.

References

(1) Gavin PJ, Kazacos KR, and Shulman ST. (2005) Baylisascariasis. Clin Micro Rev. 18(4): 703-18
(2) Gilbert CE (Date unknown) Concern with Communicable (Infectious) Diseases of Raccoons. Epidemiology and Toxicology Institute, LLC.  Accessed online March 27, 2012.
(3) Hajek J et al. (2009) A child with raccoon roundworm meningoencephalitis: A pathogen emerging in your own backyard? Can J Infect Dis Med Microbiol. 20(4): e177 – e180
(4) Page K et al (2009) Letter: Backyard Raccoon Latrines and Risk for Baylisascaris procyonis Transmission to Humans.  Emerg Infect Dis. 15(9): 1530-1
(5) Park SY et al (2000) Raccoon Roundworm (Baylisascaris procyonis) Encephalitis: Case Report and Field Investigation Pediatrics. 106(4): E56
(6) Frank Sorvillo et al. (2002) Baylisascaris procyonis: An Emerging Helminthic Zoonosis. Emerg Infect Dis. 8(4): 355-9.
(7) Moertel CL et al. (2001) Eosinophil-Associated Inflammation and Elaboration of Eosinophil-Derived Proteins in 2 Children With Raccoon Roundworm (Baylisascaris procyonis) Encephalitis. Pediatrics. 108(5): E93.
(8) Haider S et al. (2012) Possible pet-associated baylisascariasis in child, Canada [letter]. Emerg Infect Dis. 18(2): 347-9. Accessible online.
(9) Kelly TG et al. (2012) Spinal cord involvement in a child with raccoon roundworm (Baylisascaris procyonis) meningoencephalitis. Pediatr Radiol 42(3):369-73. Epub 2011 Jun 1.
(10) Pai PJ et al. (2007) Full Recovery from Baylisascaris procyonis Eosinophilic Meningitis. Emerg Infect Dis. 13(6): 928-30

(Images 2 and 4) Roussere et al (2003) Raccoon Roundworm Eggs near Homes and Risk for Larva Migrans Disease, California Communities. Emerg Infect Dis. 9(12): 1516-22. Accessible here.

Roussere GP, Murray WJ, Raudenbush CB, Kutilek MJ, Levee DJ, & Kazacos KR (2003). Raccoon roundworm eggs near homes and risk for larva migrans disease, California communities. Emerging infectious diseases, 9 (12), 1516-22 PMID: 14720389

Chronicle of a Death Foretold: Human Sentinels for Disease Outbreaks

The bodies of dead crows were found littered through back yards, overgrown meadows, and public parks. We like to attach meanings to events, to craft symbols out of the mysterious and unknown. Birds, in particular, are favorite auguries of ours. These mass crow die-offs were an ugly, sinister sign – what could this mean, mass deaths of creatures customarily seen as living omens of death and the plague?

Unusual as it is, dead animals dropping from the sky isn’t uncommon. But the crows were different. In the summer of 1999, the massive die-off of Corvus brachyrhynchos heralded the entry of West Nile Virus (WNV) into the northeastern United States and its ensuing epidemic. Shortly after reports of clusters of dead crows crept into local health departments, news of a curious encephalitis sending many people to the emergency rooms in New York, New Jersey and Connecticut started popping up.

A flock of dead crows found in the state of Jharkhand, India in December of 2011. Crows can be susceptible to many avian viruses that threaten humans; in this case, these crows tested positive for H5N1 infection. Click for image source.

It is presumed that WNV had arrived from Israel, incubating in mosquito eggs hidden in rubber tires destined for transport to the United States. Local birds were soon infected by these foreign mosquitoes, then local mosquito populations acquired the virus by feeding on infected birds and soon the infection was introduced to Americans enjoying their summer outdoors. Now Americans had a novel type of sentinel, joining the sun, the sizzling barbecue and humid nights: when WNV sends people to emergency rooms around the country, we have unequivocal proof that summer has arrived.

Certain species of animals are sentinels for particular viral diseases; clusters of their deaths are red flags for emerging outbreaks and bioterrorism events that may soon spread to humans. The use of animals for this purpose can go beyond the canary in the coal mine, serving as bright flashes of information in uncertain times. Strangely acting horses can alert veterinarians to eastern equine encephalitis and Hendra virus, two very nasty viruses that are fatal to both humans and horses. Gorilla families hemorrhaging to death in Uganda can portend the emergence of Ebola in a nearby village. When pigs in Malaysia and Bangladesh are found coughing, slumped in mud, Nipah virus might soon make its leap into humans.

Depending on their profession, humans can be sentinels for outbreaks too. Many people ought to consider themselves lucky to work at a desk, rather than working face-to-face everyday with dozens of strangers or animals. When clusters of emergency room physicians and nurses, EMTs, or veterinarians multiply fall ill from odd illnesses, the CDC sits up and pays attention.

A local Red Cross group in Kikwit, Zaire in 1995 responding to the Ebola epidemic following the deaths of many hospital personnel. Click for image source.

In Zaire in 1995, entire teams of medical professionals, from hospital technicians to nurses to physicians, succumbed to the newly emerging Ebola virus; over 70% of the initial cases were nosocomial, hospital-borne infections among medical personnel (1). Since 1994, a series of sporadic outbreaks of the respiratory Hendra virus among horses have infected horse trainers and veterinarians in Australia, killing at least three people (2). The H1N1 pandemic in the spring of 2009 infected over 25% of medical professionals working in both the adult and pediatric emergency departments, significantly eclipsing the infection rates of other hospital departments (3). Most recently, the measles epidemic in New Zealand last fall spread to ambulance workers; a quarantine was implemented in one company to prevent spread to future patients and medical staff (4). An amplification of an infectious disease among medical professionals working on the front-lines of medical care is, unluckily, just another occupational hazard.

What other occupations might find themselves unintentionally waving this epidemiological flag? Flight attendants busily crossing the globe on international flights, handing out meager rations of peanuts to travelers. Bartenders and waitresses hurrying away in busy restaurants in major urban cities. Bushmeat hunters searching for wild game and loggers working in old-growth jungle and rain-forests, exposing themselves to fleeing animals and mosquitoes harboring unknown viruses. Hustling prostitutes. Teachers in elementary schools fending off the sticky hands of their students.

Hundreds of pigs culled during the Nipah epidemic in Malaysia in 1999. Image: BBC News Online. Click for image source.

This concept of human sentinels is crucial in light of the changing landscape of of diseases today – SARS, Nipah virus and Hendra virus are all diseases that have emerged as significant public health threats only in the past few decades. Zoonotic of origin, these guys love to flip back and forth between humans and wild and domestic animals in their natural transmission cycle. In a sense, outbreaks in certain occupations that traverse the line between the domesticated world and the wild can serve as a “yardstick” for measuring the health and stability of their surrounding ecosystem, an indicator of environmental disruption that encourages transmission of zoonotic diseases (5).

That wild and domestic animals may announce the onset of a zoonotic outbreak in humans is the very reason that public health agencies long for close working relationships between veterinarians and local health agencies. Shaping an effective disease surveillance program requires looking two-ways, at diseases and deaths in both humans and animals. Thankfully, we have a few existing groups that can pinpoint the origins of emerging diseases – the ProMed emails alerts of unusual disease incidences and outbreaks, the One Health initiative looks at human, animal and environmental health, along with the emerging viral research by the Global Viral Forecasting Initiative. Instead of looking to the skies for signs, we can take an interdisciplinary approach to disease surveillance by looking around us. Check out the resources below for some of the organizations doing just that.

RESOURCES

Automated Epidemiologic Geotemporal Integrated Surveillance System or AEGIS is a syndromic surveillance system for the Massachusetts Department of Public Health. It performs automated, real-time surveillance for bioterrorism and naturally occurring outbreaks.

The Global Viral Forecasting Initiative, brainchild of virologist extraordinaire Nathan Wolfe, is developing a global early warning system to prevent novel pandemics. By monitoring emerging viruses in humans and animals, the Initiative can molecularly track the development of novel zoonotic viruses. Super neat stuff.

Promed Mail sends email alerts on the latest infectious diseases and epidemics around the world.

The Global Avian Network for Surveillance or GAINS surveillance system has an electronic database of over 100,000 birds that monitors avian health worldwide, specifically the transmission of flu viruses among wild birds.

The Canary Database is an online database for biomedical research examining animals as sentinels of zoonotic, environmental, and toxic effects that are applicable to human health. It is pretty thorough and a great reference site. I’ve certainly had my fun tooling around on it.

Additionally, read this rather upsetting article from the Journal of Infectious Diseases describing the Ebola outbreak in Zaire and the difficulties in diagnosing the disease as, one by one, medical personnel died from the hemorrhagic fever.

REFERENCES

(1) Waterman T (1999) Ebola Zaire Outbreaks. Tara’s Ebola Site  [Accessed March 23, 2012]
(2) WHO (July 2009)  Hendra Virus Fact sheet N°329 WHO Media Centre [online] Available here. [Accessed Mar 20, 2012.]
(3) One News/NZN. (28/9/2011) Measles spreads to ambulance staff. ONE News/ NZN  [online] Available here. [Accessed Mar 20, 2012.]
(4) Santos CD, Bristow RB, Vorenkamp JV. (2010) Which health care workers were most affected during the spring 2009 H1N1 pandemic? Disaster Med Public Health Prep. 4(1):47-54
(5) Cook A, Jardine A and Weinstein P. (2004) Using Human Disease Outbreaks as a Guide to Multilevel Ecosystem Interventions. Environ Health Perspect. 112(11):  1143-46

Cook, A., Jardine, A., & Weinstein, P. (2004). Using Human Disease Outbreaks as a Guide to Multilevel Ecosystem Interventions Environmental Health Perspectives, 112 (11), 1143-1146 DOI: 10.1289/ehp.7122