Conversatorio sobre el gusano barrenador en Ecosur 20 de Junio 2025 a las 11,00 hrs por Teams y redes sociales de Ecosur

 Para el link de Teams entra a ecosur.mx un día o unas horas antes.

Si puedo lo pondre aquí cuando lo tenga. 

Conversatorio "Impactos humanos en la bidiversidad y las enfermedades emergentes: experiencias de Mexico y Malasia" Mayo 26 5 pm

Kunjin virus vaccine in crocs might help to find better dengue & zika vaccines in humans

Awesome news!

We have to keep studing the health and immune system of crocs, mate!
:)

Kunjin virus vaccine in crocs might help to find better dengue & zika caccines in humans

Analysing ecological data book / Libro

Desde el famoso Zar de Bioestadistica o el muy bueno "Choosing and using statistics-a biologists guide" de Dytham, no habia vuelto a ver un librode análisis stadísticos que realmente me gustara.

Bueno eso terminó. Este libro "Analysing Ecological Data" de Zuur, Leno y Smith es lo mejor después del pan rebanado.

Fabuloso! No solo esta super completo y va desde exploración gráfica de los datos hasta análisis multivariados, sino que además todos los ejemplos son ecológicos/ambientales.

Super-recomendado!

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Since de infamous Zar-Biostatistical analisis and a few others, I haven't seen a statistical book that I really liked. Well, that just changed. This book of Zuur, Leno and Smith (Analysing Ecological Data, Springer) is totally amazing. Not only it covers it all from basic data exploration to complex multivariate analisis, but does so with ecological/environmental real-life examples. Awesome book, totally recomended. 

Human Diseases From Wildlife book / Libro Enfermedades Humanas de la Vida Silvestre

This is an excelent updated (2015) book on zoonoses as well as emerging and reemerging infectious diseases of humans as they are transmited from wildlife (and viceversa, that is antroponosis as well). Highly recommended.

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Un excelente libro actualizado (2015) sobre zoonosis y enfermedades infecciosas emergentes y reemergentes de humanos transmitidas por animales silvestres (y viceversa, es decir también cubre antroponósis). Altamente recomendado.

Why infectious disease research needs community ecology / Porqué la investigación de enfermedades infecciosas necesita de la ecología de comunidades

A very good paper on the link between community ecology & epidemiology / Un muy buen artículo tipo revisión del vínculo entre ecología de comunidades y epidemiología

http://science.sciencemag.org/content/349/6252/1259504.short

The PDF can be downloaded here / También pueden bajar el PDF completo aquí:

Download PDF (safe site)

Chikungunya es un virus, no un mosquito! (para los Campechanos)

Hace unos días, me entrevistaron unos reporteros de medios de Campeche sobre varias cosas, incluyendo la enfermedad del Chikungunya. Ya ha habido casos en Campeche y la población parece estar muy preocupada. Algo que me llamó la atención es que los reporteros (un hombre y una mujer) creían (equivocadamente) que el Chikungunya es un mosquito. No es así, es una enfermedad de nombre africano transmitida por un arbovirus. El nombre se refiere a la localidad en Africa donde fue descrito el virus por primera vez.

Después en la radio local, escuche a varias personas y otros reporteros refiriendose de nuevo quivocadamente al Chikungunya como si fuera "un mosquito nuevo". No es así. Lo transmiten los mismos mosquitos que el Dengue (Aedes spp).

One health book

Interesting book of the One Health approach. Downloadable for free / Interesante libro del concepto Ona Sola Salud, que se puede bajar aparentemente gratis para todos.

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One Health: The Human-Animal-Environment Interfaces in Emerging Infectious Diseases

The Concept and Examples of a One Health Approach

Editors:

• John S. Mackenzie,
• Martyn Jeggo,
• Peter Daszak,
• Juergen A. Richt

ISBN: 978-3-642-36888-2 (Print) 978-3-642-36889-9 (Online)

http://link.springer.com/book/10.1007%2F978-3-642-36889-9

Download Book 

Biodiversity may protect against spread of disease / La biodiversidad podría protegernos contra las enfermedades y su dispersión

An excelent paper entitled: Biodiversity decreases disease through predictable changes in host community competence was published in Nature by Pieter Johnson and col. This paper is probably the best scientifically speaking and the one that presents the strongest evidence for this somewhat controversial topic.
You can found the original paper here.

An excelent read about this paper can also be found here at the AAAS blog Quaia

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Un excelente artículo titulado: La Biodiversidad disminuye la enfermedad por medio de cambios predecibles en la competencia inmunológica de la comunidad de hospederos, fue publicado por Pieter Johnson y colaboradores en el último número de la revista Nature aquí. 

Este artículo es probablemente el mejor qua hay hasta ahora y el que presenta la evidencia científica más sólida sobre este tema un tanto controversial.

Pueden leer también una muy buena reseña de este artículo en el blog de la AAAS Quaia aquí

New tick-borne disease discovered / Nueva enfermedad transmitida por garrapatas

from Yale News here :

A new tick-borne infection that shares many similarities with Lyme disease has been discovered in 18 patients in southern New England and neighboring New York by researchers at the Yale Schools of Public Health and Medicine. The report is published in the Jan. 17 issue of the New England Journal of Medicine.
It is the first time that the disease — so new that it does not yet have a name — has been confirmed in humans in the United States.

Blood tests were used to detect evidence of infection by a bacterium that is found in deer ticks and is related to the one that causes Lyme disease. The researchers found positive results for the new infection in 21 percent of 14 patients with unexplained summertime febrile illness, 3 percent of 273 patients with Lyme disease or suspected Lyme disease, and 1 percent of 584 healthy people living in areas where Lyme disease is endemic.

Yale scientists discovered the bacterium, known as Borrelia miyamotoi, in deer ticks from Connecticut more than a decade ago. In 2011, they published the first evidence of human infection in Russian patients. The current study was designed to determine whether human infection occurs in the United States.

“While many symptoms are similar to Lyme disease, patients also may experience other symptoms, such as relapsing fever,” said Dr. Peter Krause, senior research scientist at the School of Public Health and primary author of the study. Although blood tests for Lyme disease will not detect infection with the B. miyamotoi bacterium, antibiotic treatment should be the same as for Lyme disease, Krause said. All patients in the study were from the Northeast, but researchers believe cases may occur in other areas of the country where Lyme disease is endemic because the bacterium has been found in about 2 percent of all ticks that transmit Lyme disease. “This is the first time we have found an infectious organism carried by ticks before we have recognized the disease in humans,” said Durland Fish, professor of epidemiology at the School of Public Health and the study’s senior author. “We usually discover new diseases during an epidemic and then try to figure out what is causing it.” Fish and his Yale colleagues specialize in tick-borne diseases with an emphasis on environmental surveillance for ticks and tick-borne pathogens.

Novel Polyomavirus associated with Brain Tumors in Free-Ranging Raccoons / Nuevo Polyomavirus asociado a tumores cerebrales de cancer en Mapaches

 Autopsy cross-section of an unaffected raccoon’s head (top) compared to an affected raccoon (below). Tumors have grown in the olfactory tract, extending into the frontal lobe and midbrain. Image: Dela Cruz et al./Emerging Infectious Diseases

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An amazing discovery of a new virus that causes cancer brain tumors in raccons as been published in the last issue of Emerging Infectious Diseases. Tumors and the new virus were found in 10 raccoons autopsied between March 2010 and May 2012. Nothing like that had been seen before in raccoons, in which tumors are very rare.
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Un increíble descubrimiento de un nuevo virus que causa tumores cerebrales en mapaches fue publicado en el último número de la revista Emerging Infectious Diseases. Tumores y el nuevo virus se encontraron en 10 mapaches a los que se realizó la necropsia entre Marzo de 2010 y Mayo de 2012. Nada parecido ha sido visto antes en mapaches, en los cuales los tumores cancerígenos son muy raros.

Click here to download the original paper from EIDs / Haz click para bajar el artículo original de EIDs

As biodiversity declines, tropical diseases may increase / En la medida que la biodiversidad disminuye, las enfemedades tropicales podrán aumentar

A brilliant recent article published in PLos Biology suggests -one more time- that as biodiversity declines, tropical diseases may increase its prevalence. The paper also questions other recent publications that claim to have found a relationship between latitudinal per capita income and tropical diseases in humans. Great lecture!
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Un excelente artículo en PLos Biology sugiere -una vez más- que en la medida que la biodiversidad disminuya, las enfermedades tropicales; como el dengue y la malaria, aumentarán, poniendo en entredicho la relación espúria que algunos artículos recientes han publicado sobre el gradiente latitudinal del ingreso per cápita y las enfermedades tropicales. Muy interesante lectura.

Bonds MH, Dobson AP, Keenan DC (2012) Disease Ecology, Biodiversity, and the Latitudinal Gradient in Income. PLoS Biol 10(12): e1001456. doi:10.1371/journal.pbio.1001456

The Advance of Ticks: New Areas, New Diseases, and a Weird Allergy to Meat

 The Advance of Ticks: New Areas, New Diseases, and a Weird Allergy to Meat

By Maryn McKenna at wyred.com

Following up on last week’s post about the advance of dengue: I’ve been keeping track of new news regarding other diseases transmitted by insects and arthropods, but haven’t had a chance to write them up. So here’s an end-of-year round-up. It’s not cheery (are my posts ever cheery?), but maybe it will prompt some New Year’s resolutions to wear repellents and long pants outdoors. These diseases are no fun.


The big player in tickborne illnesses is Lyme disease, and one of the most disputed issues within that condition is whether the infection can linger in a chronic form after treatment with antibiotics, and cause long-lasting symptoms. (This is separate from the problem of an unrecognized Lyme infection never being diagnosed or treated.) In one study in 2003, 10 percent of patients who got the standard treatment for Lyme still showed symptoms more than a year afterward; 4 percent showed symptoms at every follow-up visit; and 15 percent had a recurrence of the distinctive “bull’s eye” rash that is a diagnostic signal for Lyme. The team who did that 2003 study decided to look further into those recurrences, and their results were published in the New England Journal of Medicine last month.

They chose a small group (17 patients) who experienced rash recurrences at least a year, and sometimes many years, apart, and analyzed Lyme bacteria isolated from their skin or blood during each episode. (The  patients were enrolled in ongoing studies at New York Medical College, so years-earlier samples were available.) They analyzed a particular protein (outer-surface protein C, or ospC) that is expressed soon after infection takes place, and found that for any of the patients, the proteins were slightly different. Based on this, the researchers conclude that the patients they studied were not suffering from long-lasting infections and relapsing; instead, they were undergoing new infections — which happened to occur in the same time of year, and often on the same body part, as the original infection a year or more before.

At about the same time that paper was published, researchers attending the annual meeting of the American Society of Tropical Medicine and Hygiene in Atlanta were also discussing the spread of Lyme disease, along with the advance of less well-known tickborne illnesses.

In one presentation, researchers from the Yale schools of medicine and public health reported on the interplay between Lyme and the emerging illness babesiosis, which is also transmitted by ticks, and which spends part of its life cycle in the same rodent, the white-footed mouse. They found that when rodents are infected with both organisms (the Lyme disease bacterium Borrelia burgdorferei and the babesiosis parasite Babesia microti), the levels of Babesia rise higher in the mice’s blood than if they were infected only with babesiosis, and as a result the mice are more likely to transmit Babesia back to tick larvae. In other words, the Lyme bacterium somehow seemed to be intensifying babesiosis transmission.

That finding may explain, in part, why babesiosis is emerging so quickly, because the areas where the two diseases are common overlap. Another presentation by Yale researchers (this time with co-authors from Tufts University, the Connecticut Department of Public Health, and several private medical practices) described babesiosis’ rapid rise: In 2000, cases were reported in 30 towns in Connecticut; by 2008, it was in 85 towns. At least 10 percent of ticks caught in northern Connecticut now carry the parasite, a rate as high as Nantucket, where babesiosis was first spotted and dubbed “Nantucket fever” decades ago.
Because Lyme and babesiosis are northeastern diseases, the other tickborne illnesses in the United States tend to not get much attention. Researchers from the CDC, University of North Carolina and North Carolina State University who also attended ASTMH said that lack of awareness is causing some under-appreciated risks. Forest, parks and wildlife workers in North Carolina were scheduled to take part in a trial of clothing impregnated with tick repellent — but to give the study a baseline, they agreed to be tested for evidence of prior tickborne-illness infection. To everyone’s  surprise, almost one-quarter of the workers showed serologic evidence that they had already been infected with at least one of several tick-transmitted organisms. (The organisms were Rickettsia parkeri, Rickettsia rickettsii and Rickettsia amblyommii.).

In that study, the outdoor workers also submitted for study any ticks that bit them. The vast majority were the lone star tick (Amblyomma americanum), which is common in the Southeastern US; its range is increasing, which is troubling because that tick transmits a different illness, “Southern tick-associated rash illness” or STARI. (Despite the name, STARI infections have now been found as far north as New York.) But, it turns out, infections carried by that tick are not the only concern — and this last item is probably the strangest tick-related story of the bunch.

In a presentation at a different scientific meeting happening at the same time as ASTMH — the ACAAI, or American College of Allergy, Asthma and Immunology — researchers revealed that the bite of a lone star tick can induce antibodies to a sugar, galactose-alpha-1,3-galactose or alpha gal for short. The problem: That sugar is present in most red meat — beef, pork, and lamb — and also in products made from meat, including gelatin. Once that antibody has been created, the result is a serious, and rapidly worsening — in fact, potentially life-threatening — allergy to meat and meat products.

So, to sum up: The geographic ranges of different tick species are expanding. Diseases caused by ticks are becoming more common, and they are serious. People don’t understand the ways in which they might be at risk. And if you don’t take them seriously, and you get bitten by the wrong tick, you might have to give up meat for life. So on that resolutions list: maybe some socks and DEET?

What Ebola virus means to great apes / Lo que el virus del Ebola significa para los grandes simios

What Ebola virus means for primate populations

By Jonathan Ball Professor of Molecular Virology, University of Nottingham
BBC Nature News
 

For most, the mere mention of Ebola virus provokes abject fear - the archetypal blockbuster contagion - but just how dangerous is it to our ape cousins? A recent report highlighting possible Ebola virus infection in Indonesian orangutan populations provides a timely reminder of the threat to animal and human health that emerging virus infections pose.

Ebola virus was first described in the 1970s as the cause of deadly outbreaks of haemorrhagic fever in humans in the Democratic Republic of Congo and Sudan, and outbreaks continue to this day. Early studies of human epidemics showed they had been ignited by contact between hunters and animals - particularly gorillas and chimpanzees. Most significantly, these animals were dead and Ebola virus was the prime candidate for their deaths.

See how Ebola, bushmeat and pet trades affect gorillas
Watch orangutans being returned to the wild
Why has Africa's great ape habitat declined?

Population surveys of these great apes revealed a shocking truth. Massive declines in ape numbers had consistently accorded with Ebola virus outbreaks. In one study population in the Lossi Sanctuary in DR Congo, more than 90% of gorillas - an alarming 5,000 animals - were lost.

However, proving a definite link between virus infection and the great ape demise was not easy. In jungle environments dead animals are quickly dispersed by scavengers, or decay rapidly and become usurped by the thick forest undergrowth. But the repeated discovery of ape carcasses coincidental with human outbreaks was compelling evidence; that these corpses harboured Ebola virus was even more so. Maybe not the proverbial smoking gun, but incredibly persuasive evidence just the same.

But if the infection was so harmful to apes and caused so many deaths, it was unlikely that these animals were its natural reservoir. Viruses require large numbers of susceptible hosts to ensure continued spread and rapid wholesale killing is not conducive to this. Great apes - humans, gorillas and chimpanzees - are essentially dead-end hosts for these Ebola viruses.

Ebola virus infections 

• Ebola virus takes its name from the river in DR Congo near to the area where the first cases were described.
• There are five recognised species of Ebola virus: Sudan, Zaire, Ivory Coast, Bundibugyo located in Africa and Reston in the Philippines.
• All Ebola virus species cause fatal infections in non-human primates.
• The Zaire strain of virus is the most likely cause of the majority of gorilla and chimpanzee deaths.
• Clinical symptoms observed in wild animals dying during Ebola virus outbreaks include vomiting, diarrhoea, weight loss and bleeding from the nostrils.

Virus-hunters soon discovered that the most likely natural hosts for Ebola viruses were fruit bat species living in regions where outbreaks had occurred.

Great apes and bats, as well as Ebola virus, have co-existed for millennia, yet gorilla and chimpanzee population collapses seem a recent event.

Infection through interaction
As habitats are destroyed, great apes and a whole host of animals retreat into precious sanctuaries and protected parks. An inescapable irony is that these remaining bastions, supporting large populations of apes living cheek-to-cheek with bats, have probably aided the passage of this deadly virus.

And it's not just the infections carried by other animals that are a problem.
Great apes and humans share around 98% of their genetic material. This remarkable similarity means that these creatures are also susceptible to many human viruses: measles and a whole host of respiratory viruses, such as respiratory syncytial virus, human metapneumovirus and influenza, amongst many others.

Great ape encounters, through eco-tourism - a once-in-a-lifetime opportunity to get up-close to these mighty creatures, to see the "whites of their eyes" - is putting animals at risk. But this activity can also be a force for good. The great wealth generated provides incentive to secure the safety of these animals for generations to come.

 

Chimps and other primates are highly susceptible to human pathogens

So, conservationists find themselves stuck between an ecological rock and a hard place: damned if they try to support the remnants of these once widespread animals and equally damned if they don't.

Increased human interaction, through habitat encroachment or eco-tourism, is inevitable. So how can we mitigate the risks that this brings?
Understandably, great ape conservation is a highly emotive subject. If we are to secure the long-term survival of our closest relatives can we cling to the vestiges of non-interventionist strategies or do we need to be more proactive?

To one group of scientists the answer is simple: direct action, through a pioneering programme of vaccination, will be necessary to protect these primates from "natural" and human-wrought infection.

The VaccinApe project aims to take human vaccines and adapt them for use in wild apes: initially those at most risk from human disease, but ultimately protecting as many gorillas and chimpanzees as possible from a range of infections, including the deadly Ebola virus

Identifying Ebola virus
But what of the Indonesian orangutans: are we on the verge of a catastrophic Ebola virus-induced population collapse? To answer this key question we need to look at what the researchers did and understand what their data is telling us.
Dr Chairul Nidom and colleagues from Airlangga University, Surabaya, Indonesia, tested over 300 orangutan blood samples for the presence of antibodies that reacted with Ebola virus proteins.

The bat connection

 

• Ebola or Ebola-like virus infection is evident in bats in Africa, the Philippines, Spain and China.
• Ebola virus has been detected directly in three African species of fruit bat: the hammer-headed or big-lipped fruit bat (Hypsignathus monstrosus), Franquet's epauletted fruit bat (Epomops franqueti), and the little collared bat (Myonycteris torquata).
• Ebola virus-specific antibodies - a signature of past infection - have been detected in the Gambian epauletted fruit bat (Epomophorus gambianus), Veldkamp's dwarf epauletted fruit bat (Nanonycteris veldkampii) and the straw-coloured fruit bat (Eidolon helvum)
• The proportion of bats with evidence of current or past infection is very low - usually less than 5%.
• Geoffroy's rousette bats (Rousettus amplexicaudatus) in the Philippines were shown to harbour antibodies to Reston Ebola virus. This bat is widely distributed throughout south-east Asia including Indonesia.
• Ebola virus infection of bats is usually symptomless - this 'silent infection' is often a sign of extensive co-evolution between the virus and its host. However, the recent discovery of a novel Ebola virus in bats in Spain coincided with major die-offs of that particular bat in the region where the virus was found.
• Bats represent a unique mammalian virus reservoir - they can live in very large colonies, have a range of diets and are capable of flight - all of which aid virus transmission and spread.

Antibodies help defend the body from marauding viruses. They are produced by specialised white blood cells and each cell produces a unique type of antibody.

The virus and antibody interaction is specific: just like a lock and key. So the presence of antibodies to a particular virus is a tell-tale sign that we've seen it before, either through infection or by vaccination.

Around one-fifth of the orangutan samples tested by Dr Nidom contained antibodies that recognised Ebola virus proteins and 1% had antibodies to a related virus called Marburg virus. These animals had possibly been infected.
Antibodies are usually specific for their target, but non-specific or "sticky" antibodies do occur. Many of the study's orangutan samples reacted with proteins from different Ebola virus species. Could the data be explained by the presence of non-specific antibodies rather than past virus infection?

Possibly, but antibodies present in humans who recover from Ebola virus infection recognise many different strains just as the orangutan samples did.
These findings are tantalising, but only isolation of the virus or its genetic material will conclusively prove that this infection is happening. This will require large-scale screening of orangutans and other animals, such as bats, for the presence of virus. According to a recent review, finding Ebola virus in animals is a very rare event.

Sampling animals in the field is not easy, but extensive analysis of faeces - the approach that helped our understanding of a malaria parasite and HIV-like virus infection of African apes - may hold the key.

It would be no great surprise to discover another Ebola-like virus outside of Africa. The Reston species of Ebola virus originated from the Philippines, and Ebola-like viruses have been documented in bats in Spain and China. They appear ubiquitous. If confirmed, the discovery of Ebola virus infection in orangutans would not necessarily be their death knell nor automatically pose a serious risk to human health.

 The presence of antibodies in these animals shows that they successfully fought the virus infection and became immune. Perhaps other orangutans perished, but there is no evidence for this whilst Reston Ebola virus infection in humans often passes without symptoms.

Nor would Ebola virus spread easily through orangutan populations. Unlike their gregarious African counterparts, these are solitary animals that rarely meet.
Great ape populations are under unprecedented threat from illegal hunting and massive habitat loss. Ebola virus infections are turning the screw further on African gorillas and chimpanzees. But so far, the evidence suggests that orangutans have no worries on this score.

Let's hope it stays that way.

White-Nose Syndrome Bat Recovery May Present Challenges Similar to Those in Some Recovering AIDS Patients / Los murciélagos que se recuperan de WNS muestran signos respiratorios similares a los de los pacientes con SIDA

News release by: US Geological Survey here

White-Nose Syndrome Bat Recovery May Present Challenges Similar to Those in Some Recovering AIDS Patients

Bats recovering from white-nose syndrome show evidence of immune reconstitution inflammatory syndrome (IRIS), according to a hypothesis proposed by the U.S. Geological Survey and collaborators at National Institutes of Health. This condition was first described in HIV-AIDS patients and, if proven in bats surviving WNS, would be the first natural occurrence of IRIS ever observed. IRIS is a syndrome in which an organism's immune system, having been suppressed for a time, reactivates and, perceiving a serious infection around it, goes into overdrive resulting in severe inflammation and tissue damage in infected areas. In both human patients with HIV-AIDS and bats with WNS, the functioning of the immune system is severely reduced. For humans, this occurs when the HIV virus attacks the patient's white blood cells, and for bats, this occurs during normal hibernation. For both humans and bats, IRIS can be fatal. "The potential discovery of IRIS in bats infected with white-nose syndrome is incredibly significant in terms of understanding both the reasons for bat mortality and basic immune response," said USGS Director Marcia McNutt. "This discovery could also prove significant for studies on treatment for AIDS." IRIS was first described in humans with HIV-AIDS after patients with low counts of helper T lymphocytes, the type of white blood cells the HIV virus attacks, had increases in those cell numbers following treatment with antiretroviral therapy. In some patients, who had secondary bacterial or other opportunistic infections due to their suppressed immune system, their condition significantly worsened as the restoration in immune cell function resulted in an over-response to pre-existing infection and substantial damage to healthy tissue. In bats, IRIS might be a result of changes in immune system function during hibernation. During hibernation, all internal systems for the bats enter a reduced state, including the immune system, so as to conserve resources. This reduced immunity allows Geomyces destructans, the fungus that causes white-nose syndrome, to spread unchecked over the wings, muzzle, and ears of bats eroding through skin. If they survive the fungal infection through winter, when the bats emerge in the spring, they face a new challenge—intense inflammation at sites of infection with G. destructans. This inflammation in the wings can be so severe that it contributes to death. Scientists from the USGS National Wildlife Health Center and National Institutes of Health propose this sudden reversal of immune suppression in bats with WNS, accompanied by intense inflammation is a form of IRIS. Although never before observed outside a clinical setting, there is strong evidence that the inflammation observed in bats with WNS is IRIS. "We see strong similarities between human IRIS and the pathology associated with WNS , with potentially fatal outcome in bats," said USGS lead researcher Carol Meteyer. "We hope that these findings will stimulate more experimental studies that yield insight into the role of the immune response during IRIS in humans as well as hibernating bats." Even as the G. destructans fungus spreads throughout the bat's body, there is no obvious inflammation in response to this hibernation-dependent fungal skin infection. This lack of inflammatory cell response is consistent with hibernation-induced inhibition of immune cell activity as the body temperature of hibernating bats drops to ambient temperatures 35-50 degrees Fahrenheit (2-10 degrees Centigrade). In addition, inflammation is not seen until the bat"s body temperatures reach their active levels of 93-102 degrees Fahrenheit (34-39 degrees Centigrade). These temperature levels indicate that the bat’s internal systems have come back online, including the immune system. Only then is the inflammation observed, and only in areas where the G. destructans fungus has taken hold. This behavior is consistent with IRIS observed in human HIV-AIDS patients. The report, entitled "Pathology in euthermic bats with white nose syndrome suggests a natural manifestation of immune reconstitution inflammatory syndrome," is published in the November issue of the journal Virulence.

Crows spread infectious diseases caused by prions / Los cuervos dispersan enfermedades causadas por priones

Crows don't digest prions (vg. mad cows disease, cwd, scrapie) , may transport them to other locations / Los cuervos no digieren los priones (ejem. enfermedad de las vacas locas, cwd, scrapie) y pueden transportar las proteinas infecciosas a otras localidades

Crows fed on prion-infected brains from mice can transmit these infectious agents in their feces and may play a role in the geographic spread of diseases caused by prions, such as chronic wasting disease or scrapie.

...Kurt VerCauteren from the US Department of Agriculture (USDA) and other colleagues, shows that prions can pass through crows' digestive systems without being destroyed, and may be excreted intact after ingestion by the birds. According to the authors, their results demonstrate a potential role for the common crow in the spread of infectious diseases caused by prions.

Full open access article here: VerCauteren KC, et al. Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos). PLoS ONE, 2012; 7 (10): e45774.  DOI: 10.1371/journal.pone.0045774

The Armageddon virus?

Well I have to say it was taken from the Daily Mail so...but it is interesting though / Debo decir que fue tomado del super-amarillista periodico británico Daily Mail, así que...Pero la nota no deja de ser interesante.

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The Armageddon virus: Why experts fear a disease that leaps from animals to humans could devastate mankind in the next five years

By John Naish at Daily Mail.co.uk
 
PUBLISHED: 22:43 GMT, 14 October 2012 | UPDATED: 12:35 GMT, 15 October 2012

Armageddon: Scientists have warned that a global viral outbreak is inevitable within five years

The symptoms appear suddenly with a headache, high fever, joint pain, stomach pain and vomiting. As the illness progresses, patients can develop large areas of bruising and uncontrolled bleeding. In at least 30  per cent of cases, Crimean-Congo Viral Hemorrhagic Fever is fatal. And so it proved this month when a 38-year-old garage owner from Glasgow, who had been to his brother’s wedding in Afghanistan, became the UK’s first confirmed victim of the tick-borne viral illness when he died at the high-security infectious disease unit at London’s Royal Free Hospital. It is a disease widespread in domestic and wild animals in Africa and Asia — and one that has jumped the species barrier to infect humans with deadly effect. But the unnamed man’s death was not the only time recently a foreign virus had struck in this country for the first time.

Last month, a 49-year-old man entered London’s St Thomas’ hospital with a raging fever, severe cough and desperate difficulty in breathing. He bore all the hallmarks of the deadly Sars virus that killed nearly 1,000 people in 2003 — but blood tests quickly showed that this terrifyingly virulent infection was not Sars. Nor was it any other virus yet known to medical science. Worse still, the gasping, sweating patient was rapidly succumbing to kidney failure, a potentially lethal complication that had never before been seen in such a case.

As medical staff quarantined their critically-ill patient, fearful questions began to mount. The stricken man had recently come from Qatar in the Middle East. What on earth had he picked up there? Had he already infected others with it? Using the latest high-tech gene-scanning technique, scientists at the Health Protection Agency started to piece together clues from tissue samples taken from the Qatari patient, who was now hooked up to a life-support machine. The results were extraordinary. Yes, the virus is from the same family as Sars. But its make-up is completely new. It has come not from humans, but from animals. Its closest known relatives have been found in Asiatic bats. The investigators also discovered that the virus has already killed someone. Searches of global medical databases revealed the same mysterious virus lurking in samples taken from a 60-year-old man who had died in Saudi Arabia in July.

Potentially deadly: The man suffered from CCHF, a disease transmitted by ticks (pictured) which is especially common in East and West Africa

When the Health Protection Agency warned the world of this newly- emerging virus last month, it ignited a stark fear among medical experts. Could this be the next bird flu, or even the next ‘Spanish flu’ — the world’s biggest pandemic, which claimed between 50 million and 100 million lives across the globe from 1918 to 1919?. In all these outbreaks, the virus responsible came from an animal. Analysts now believe that the Spanish flu pandemic originated from a wild aquatic bird. The terrifying fact is that viruses that manage to jump to us from animals — called zoonoses — can wreak havoc because of their astonishing ability to catch us on the hop and spread rapidly through the population when we least expect it.   

One leading British virologist,  Professor John Oxford at Queen Mary Hospital, University of London, and a world authority on epidemics, warns that we must expect an animal-originated pandemic to hit the world within the next five years, with potentially cataclysmic effects on the human race. Such a contagion, he believes, will be a new strain of super-flu, a highly infectious virus that may originate in some far-flung backwater of Asia or Africa, and be contracted by one person from a wild animal or domestic beast, such as a chicken or pig.

By the time the first victim has succumbed to this unknown, unsuspected new illness, they will have spread it by coughs and sneezes to family, friends, and all those gathered anxiously around them. Thanks to our crowded, hyper-connected world, this doomsday virus will already have begun crossing the globe by air, rail, road and sea before even the best brains in medicine have begun to chisel at its genetic secrets. Before it even has a name, it will have started to cut its lethal swathe through the world’s population.

If this new virus follows the pattern of the pandemic of 1918-1919, it will cruelly reap mass harvests of young and fit people. They die because of something called a ‘cytokine storm’ — a vast overreaction of their strong and efficient immune systems that is prompted by the virus. This uncontrolled response burns them with a fever and wracks their bodies with nausea and massive fatigue. The hyper-activated immune system actually kills the person, rather than killing the super-virus. Professor Oxford bases his prediction on historical patterns. The past century has certainly provided us with many disturbing precedents. For example, the 2003 global outbreak of Sars, the severe acute respiratory syndrome that killed nearly 1,000 people, was transmitted to humans from Asian civet cats in China.

In November 2002, it first spread among people working at a live animal market in the southern Guangdong province, where civets were being sold.
Nowadays, the threat from such zoonoses is far greater than ever, thanks to modern technology and human population growth. Mass transport such as airliners can quickly fan outbreaks of newly- emerging zoonoses into deadly global wildfires.

The Sars virus was spread when a Chinese professor of respiratory medicine treating people with the syndrome fell ill when he travelled to Hong Kong, carrying the virus with him. By February 2003, it had covered the world by hitching easy lifts with airline passengers. Between March and July 2003, some 8,400 probable cases of Sars had been reported in 32 countries.

It is a similar story with H1N1 swine flu, the 2009 influenza pandemic that infected hundreds of millions throughout the world. It is now believed to have originated in herds of pigs in Mexico before infecting humans who boarded flights to myriad destinations.  Once these stowaway viruses get off the plane, they don’t have to learn a new language or new local customs.

Fears: Professor John Oxford at Queen Mary Hospital warns of a pandemic within the next five years

Genetically, we humans are not very diverse; an epidemic that can kill people in one part of the world can kill them in any other just as easily. On top of this, our risk of catching such deadly contagions from wild animals is growing massively, thanks to humankind’s relentless encroachment into the world’s jungles and rainforests, where we increasingly come into contact for the first time with unknown viral killers that have been evolving and incubating in wild creatures for millennia.

This month, an international research team announced it had identified an entirely new African virus that killed two teenagers in the Democratic Republic of the Congo in 2009. The virus induced acute hemorrhagic fever, which causes catastrophic widespread bleeding from the eyes, ears, nose and mouth, and can kill in days. A 15-year-old boy and a 13-year-old girl who attended the same school both fell ill suddenly and succumbed rapidly. A week after the girl’s death, a nurse who cared for her developed similar symptoms. He only narrowly survived. The new microbe is named Bas-Congo virus (BASV), after the province where its three victims lived. It belongs to a family of viruses known as rhabdoviruses, which includes rabies.

A report in the journal PLoS Pathogens says the virus probably originated in local wildlife and was passed to humans through  insect bites or some other as-yet unidentified means. There are plenty of other new viral candidates waiting in the wings, guts, breath and blood of animals around us. You can, for example, catch leprosy from armadillos, which carry the virus in their shells and are responsible for a third of leprosy cases in the U.S. Horses can transmit the Hendra virus, which can cause lethal respiratory and neurological disease in people.

In a new book that should give us all pause for thought, award-winning U.S. natural history writer David Quammen points to a host of animal-derived infections that now claim lives with unprecedented regularity. The trend can only get worse, he warns. Quammen highlights the Ebola fever virus, which first struck in Zaire in 1976. The virus’s power is terrifying, with fatality rates as high as 90 per cent. The latest mass outbreak of the virus, in the Congo last month, is reported to have killed 36 people out of 81 suspected cases.

According to Quammen, Ebola probably originated in bats. The bats then infected African apes, quite probably through the apes coming into contact with bat droppings. The virus then infected local hunters who had eaten the apes as bushmeat. Quammen believes a similar pattern occurred with the HIV virus, which probably originated in a single chimpanzee in Cameroon. Studies of the virus’s genes suggest it may have first evolved as early as 1908. It was not until the Sixties that it appeared in humans, in big African cities. By the Eighties, it was spreading by airlines to America. Since then, Aids has killed around 30 million people and infected another 33 million.

There is one mercy with Ebola and HIV. They cannot be transmitted by coughs and sneezes. ‘Ebola is transmissible from human to human through direct contact with bodily fluids. It can be stopped by preventing such contact,’ Quammen explains. ‘If HIV could be transmitted by air, you and I might already be dead. If the rabies virus — another zoonosis — could be transmitted by air, it would be the most horrific pathogen on the planet.’

Viruses such as Ebola have another limitation, on top of their method of transmission. They kill and incapacitate people too quickly. In order to spread into pandemics, zoonoses need their human hosts to be both infectious and alive for as long as possible, so that the virus can keep casting its deadly tentacles across the world’s population.

But there is one zoonosis that can do all the right (or wrong) things. It is our old adversary, flu. It is easily transmitted through the air, via sneezes and coughs. Sars can do this, too. But flu has a further advantage. As Quammen points out: ‘With Sars, symptoms tend to appear in a person before, rather than after, that person becomes highly infectious. 

Isolation: Unlike Sars the symptoms of this new disease may not be apparent before the spread of infection

‘That allowed many Sars cases to be recognised, hospitalised and placed in isolation before they hit their peak of infectivity. But with influenza and many other diseases, the order is reversed.’ Someone who has an infectious case of a new and potentially lethal strain of flu can be walking about innocently spluttering it over everyone around them for days before they become incapacitated. Such reasons lead Professor Oxford, a world authority on epidemics, to warn that a new global pandemic of animal-derived flu is inevitable. And, he says, the clock is ticking fast.

Professor Oxford’s warning is as stark as it is certain: ‘I think it is inevitable that we will have another big global outbreak of flu,’ he says. ‘We should plan for one emerging in 2017-2018.’ But are we adequately prepared to cope? Professor Oxford warns that vigilant surveillance is the only real answer that we have. ‘New flu strains are a day-to-day problem and we have to be very careful to keep on top of them,’ he says. ‘We now have scientific processes enabling us to quickly identify the genome of the virus behind a new illness, so that we know what we are dealing with. The best we can do after that is to develop and stockpile vaccines and antiviral drugs that can fight new strains that we see emerging.’ But the Professor is worried our politicians are not taking  this certainty of mass death seriously enough. Such laxity could come at a human cost so unprecedentedly high that it would amount to criminal negligence. The race against newly-emerging animal-derived diseases is one that we have to win every time. A pandemic virus needs to win only once and it could be the end of humankind.

Climate change will spread avian malaria north / El cambio climático dispersará la malaria aviar hacia el norte

Climate change to fuel northern spread of avian malaria, study finds

by: San Francisco State University communications

Researchers discover infected birds in Alaska, say global warming will send disease farther north

SAN FRANCISCO, Sept. 19. 2012 -- Malaria has been found in birds in parts of Alaska, and global climate change will drive it even farther north, according to a new study published today in the journal PLoS ONE.

The spread could prove devastating to arctic bird species that have never encountered the disease and thus have no resistance to it, said San Francisco State University Associate Professor of Biology Ravinder Sehgal, one of the study's co-authors. It may also help scientists understand the effects of climate change on the spread of human malaria, which is caused by a similar parasite.
Researchers examined blood samples from birds collected at four sites of varying latitude, with Anchorage as a southern point, Denali and Fairbanks as middle points and Coldfoot as a northern point,
roughly 600 miles north of Anchorage. They found infected birds in Anchorage and Fairbanks but not in Coldfoot. Using satellite imagery and other data, researchers were able to predict how environments will change due to global warming -- and where malaria parasites will be able to survive in the future. They found that by 2080, the disease will have spread north to Coldfoot and beyond. "Right now, there's no avian malaria above latitude 64 degrees, but in the future, with global warming, that will certainly change," Sehgal said. The northerly spread is alarming, he added, because there are species in the North American arctic that have never been exposed to the disease and may be highly susceptible to it.

 The study's lead author is Claire Loiseau, a former postdoctoral fellow in Sehgal's laboratory at SF State. Ryan Harrigan, a postdoctoral scholar at the University of California, Los Angeles, provided data modeling for the project. The research was funded by grants from the AXA Foundation and National Geographic.

Researchers are still unsure how the disease is being spread in Alaska and are currently collecting additional data to determine which mosquito species are transmitting the Plasmodium parasites that cause malaria.
The data may also indicate if and how malaria in humans will spread northward. Modern medicine makes it difficult to track the natural spread of the disease, Sehgal said, but monitoring birds may provide clues as to how global climate change may effect the spread of human malaria. "First evidence and predictions of Plasmodium transmission in Alaskan bird populations" was written by Claire Loiseau, Ryan J. Harrigan, Anthony K. Cornel, Sue L. Guers, Molly Dodge, Timothy Marzec, Jenny S. Carlson, Bruce Seppi and Ravinder N. M. Sehgal and published Sept. 19 in PLoS ONE.

H1N1 influenza in skunks from Vancouver / Influenza H1N1 en zorrillos de Vancouver

2009 influenza A (H1N1) in free ranging Vancouver skunks

by: Healthy Wildlife CCWHC blog

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Photo: donjd2 from Flickr

In January 2010, a fatal outbreak of influenza A 2009 H1N1 (swine flu) pneumonia in eight free ranging striped skunks which frequented a mink farm in the lower Fraser Valley was diagnosed by the Animal Health Centre in Abbotsford, British Columbia. This occurred during the worldwide pandemic of 2009 H1N1, and it was concluded that the skunks had most likely contracted the virus as a result of human exposure.  In March 2011, the Animal Health Centre again diagnosed fatal 2009 H1N1 pneumonia in a skunk that was found dead in a large public park in Vancouver.  City park workers reported that hand feeding skunks is a common practice by park visitors and it was presumed that the skunk had contracted the virus due to human exposure.

As a result of these findings, an influenza survey was initiated whereby dead skunks found by Vancouver city park workers are submitted to the Animal Health Centre for full necropsy and tested for influenza virus. To date, eight skunks have been analyzed. Seven skunks were found to have died from severe trauma. The cause of death could not be determined in the eighth skunk due to advanced decomposition. All of the eight submissions were negative for influenza virus.

Influenza virus infection of skunks has not been detected in surveys of wildlife conducted by other investigators. We hypothesize that influenza virus is highly virulent for skunks and thus, seemingly healthy skunks are not likely carriers of the disease.  If so, this would constitute a true anthroponotic disease: influenza virus passes from humans to skunks but not from skunks to humans. To minimize the potential for influenza exposure, human contact by way of hand feeding, petting or littering in areas frequented by skunks should be publicly discouraged, especially during influenza season.

Frogs, disease & climate change / Anfíbios, enfermedad y cambio climático

USF Study: Frogs Getting Sick from Climate Change

Project confirms cause-effect relationship between temperature fluctuations and disease-induced frog mortality / Proyecto confirma relación causa-efecto entre las fuctuaciones de temperatura y la mortalidad inducida por enfermedad en anfibios

Jason Rohr, USF associate professor of Integrative Biology, works in the field.

By Vickie Chachere

USF News

TAMPA, Fla. (Aug. 13, 2012) – Scientists studying the rapid decline of the world’s frog populations have suspected that fluctuating temperatures brought on by climate change might make frogs vulnerable to disease.

Now, a new study published in the prestigious journal Nature Climate Change confirms those suspicions, showing in laboratory and field tests that temperature fluctuations decrease frogs’ resistance to a pathogen implicated in global amphibian declines.

The study, conducted by scientists at the University of South Florida and Oakland University in Michigan, found that unpredictable temperature shifts temporarily decreased the frogs’ resistance to the deadly parasite, chytrid fungus. The study is a major step forward in shedding light on dramatic declines in the world’s frog population; scientists suspect climate change plays a role, but have been cautious in declaring it a cause of frog population declines without detailed experiments and more extensive data.

“In addition to increasing mean temperatures, global climate change is increasing climate variability, but few studies have considered how increased variability in temperature affects disease risk,” said Jason Rohr, a co-author of the study and an Associate Professor of Integrative Biology at USF.

“We hypothesized that temperature shifts associated with climate change would temporarily benefit parasites because they are smaller and have faster metabolisms than their ectothermic hosts and thus should acclimate more quickly to unpredictable temperature shifts.”

To test this hypothesis, Rohr and colleagues acclimated frogs to either 15 or 25 degrees Celsius in 80 independent incubators, switched half the frogs at each temperature to the other temperature, and then challenged the frogs with the chytrid fungus.  They found that frogs experiencing an unpredictable temperature shift, at either daily or monthly time scales, had greater chytrid fungal loads and fungal-induced mortality than frogs held at a constant temperature. The effect was particularly strong when temperatures unpredictably dropped.

Drops in temperature were also significant predictors of disease-associated frog extinctions in Latin America.  Furthermore, warmer years had larger drops in temperature and more extinctions than cooler years, providing a mechanistic link between global climate change and chytrid-related amphibian declines.

“This study provides an important step in understanding the role that climate change plays in amphibian declines, but we suspect that its implications will be even more far-reaching,” Rohr said.

“Temperature acclimation of host resistance to parasitism is almost certainly a widespread phenomenon, likely influencing invertebrate vectors of human diseases,” he added.  “Consequently, climatic variability and predictability might represent underappreciated links between climate change, disease, and biodiversity losses.”

Chytrid fungus kills frogs by causing the thickening of its skin, leading to electrolyte imbalance and dehydration. It has been implicated in the decline and extinction of numerous frog species worldwide. Scientists consider the disease to be one of the biggest threats to amphibian survival worldwide.

The study was conducted by Oakland University Assistant Professor Thomas Raffel, Rohr and USF Department of Integrative Biology postdoctoral researchers John M. Romansic and Matthew D. Venesky; and PhD candidates Neal Halstead and Taegan McMahon. The full text can be read here.