Showing posts with label Zoonotic. Show all posts
Showing posts with label Zoonotic. Show all posts

Monday, September 08, 2014

Mapping The Zoonotic Range Of Ebola Virus In Africa

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Mapping the zoonotic niche of Ebola virus disease in Africa

 

# 9050

 

In most cases, it is assumed the the index human infection in each of Africa’s Ebola outbreaks have come as the result of exposure to an infected animal, most commonly through the hunting, preparing, or consuming of bush meat. 

 

Bats are believed to be the primary host of the four known African species of Ebola (plus Marburg), but other mammals may serve as intermediate hosts as well.

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Today we’ve an open access study that attempts to map those geographic regions of Africa where Ebola virus transfer from animals to humans is most likely to occur.   This identifies areas where an index case might appear, but does not address where the virus could spread through human-to-human transmission.

 

 

Mapping the zoonotic niche of Ebola virus disease in Africa

David M Pigott, Nick Golding, Adrian Mylne, Zhi Huang, Andrew J Henry, Daniel J Weiss, Oliver J Brady, Moritz U G Kraemer, David L Smith, Catherine L Moyes, Samir Bhatt, Peter W Gething, Peter W Horby, Isaac I Bogoch, John S Brownstein, Sumiko R Mekaru, Andrew J Tatem, Kamran Khan, Simon I HayCorresponding Author

DOI: http://dx.doi.org/10.7554/eLife.04395 Published September 8, 2014 Cite as eLife 2014;10.7554/eLife.04395 Download PDF

Abstract

Ebola virus disease (EVD) is a complex zoonosis that is highly virulent in humans. The largest recorded outbreak of EVD is ongoing in West Africa, outside of its previously reported and predicted niche. We assembled location data on all recorded zoonotic transmission to humans and Ebola virus infection in bats and primates (1976-2014). Using species distribution models, these occurrence data were paired with environmental covariates to predict a zoonotic transmission niche covering 22 countries across Central and West Africa. Vegetation, elevation, temperature, evapotranspiration, and suspected reservoir bat distributions define this relationship. At-risk areas are inhabited by 22 million people; however, the rarity of human outbreaks emphasises the very low probability of transmission to humans. Increasing population sizes and international connectivity by air since the first detection of EVD in 1976 suggest that the dynamics of human-to-human secondary transmission in contemporary outbreaks will be very different to those of the past.

 

Of the 22 million people who live in `at-risk’ regions, the vast majority live in the DRC (formerly Zaire), which unsurprisingly is where the virus was first discovered in 1976, and the home to the most outbreaks.

 

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The authors talk about some of the factors behind the size and spread of Ebola outbreaks in recent years:


In all countries at risk we show  that since the discovery of EVD in 1976, urban and rural populations have increased and have become more interconnected both within and across national borders. During the last 40 years the increasing size and connectivity of these populations may have facilitated the subsequent spread of EVD outbreaks. These factors underline a change in the way in which EVD interacts with human populations.

 

They also argue that Ebola Virus Disease (EVD) is likely under reported in Africa.

 

The remote and isolated nature of Ebola zoonotic transmission events, paired with the relatively poor diagnostics and understanding of the disease transmission routes in early outbreaks, mean that underreporting of previous outbreaks is probable. An increasing understanding and description of a broader range of symptoms used in case definitions of EVD (Feldmann and Geisbert, 2011; Leroy et al.,  2000) also increase the possibility that past outbreaks may have been misattributed to different diseases (Tignor et al., 1993). This poor detectability of EVD also clearly limits capacity to accurately identify the locations and transmission routes of index cases (Baize et al., 2014; Heymann et al.,1980).

 

The entire 40 page PDF file is available for download, albeit in draft form. 

Sunday, July 13, 2014

Family Pets, Zoonoses & An Upcoming COCA Call

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The undisputed ruler of my house

 

# 8829

 

An oft-repeated factoid in this blog is that 70% of the infectious diseases plaguing humans began in other species, and then adapted to people. Most of these diseases only began to appear in humans after we – as a species – began to domesticate animals roughly 10,000 years ago (see The Third Epidemiological Transition).

 

That process continues to this day, with new zoonotic diseases emerging practically every year.  The list over just the past few years includes MERS-CoV, H7N9, H10N8, H6N1, Swine Variant Viruses, SFTS, and the Heartland Virus

 

All of which illustrates the importance of the `One Health Concept’, where human, animal, and environmental health are all viewed as being interconnected (see the One Health Initiative website). And while we watch these exotic emerging diseases coming from the wild (or agriculture) with concern, in truth, your next zoonotic disease exposure may just as easily come via your family pet.

 

This week, the media has been filled with reports of an exceedingly rare case of  Pneumonic plague found in a Colorado resident and pet dog, and while the chain of transmission in this case isn’t entirely clear, we’ve seen other cases where pets have picked up infected fleas and brought plague home with them.

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Credit CDC Plague fact sheet

 

Earlier this year, in Transmission Of Bovine TB From Felines To Humans – UK, we looked at a report on two rare human infections with M. bovis – both associated with an outbreak in cats – which likely became infected via contact (directly or indirectly) with badger setts (dens).


Although you are more likely to be infected from undercooked meat or unwashed fruits and vegetables than from your family pet, in Toxoplasmosis: Some Intriguing Para-Cites, we looked at the risks of zoonotic transmission from this fascinating parasite back in 2012.

 

And it will probably surprise a lot of my readers that every year about 200 people are infected with flea-borne typhus in the United States (mostly in California, Hawaii, or Texas), often brought home by a family pet.  This from the California Department of Public Health:

What animals can carry the typhus bacteria?

In the United States, rats, opossums, and other small mammals can carry the typhus bacteria. Rat fleas (Xenopsylla cheopis) and cat fleas (Ctenocephalides felis) are most commonly associated with disease transmission. Fleas may become infected when they feed on these animals and then can transmit the bacteria to humans, pet dogs, and cats.

 

And perhaps most infamously, a little over a decade ago – the United States experienced an unprecedented outbreak of Monkeypox  - when an animal distributor imported hundreds of small animals from Ghana, which in turn infected prairie dogs that were subsequently sold to the public (see 2003 MMWR Multistate Outbreak of Monkeypox --- Illinois, Indiana, and Wisconsin, 2003).

 

Although plague, typhus, TB, Monkeypox, and rabies infections are all possible (albeit rare) zoonotic infections, far more likely are the risks of contracting enteric (intestinal) infections from pathogens carried by animals - including household pets - such as Salmonella, E.coli, and Cryptosporidium. 

 

  • In June of 2012, in That Duck May Look Clean, But . . . , I wrote about a CDC investigation into an outbreak of Salmonella Montevideo involving 66 persons across 20 states linked to the handling of live poultry (baby chicks or ducklings or both) sold via mail-order hatcheries and  agricultural feed stores.
  • Similar warnings have gone out in the past regarding Human Salmonella Infections Linked to Small Turtles.  Like poultry, reptiles and amphibians can sometimes carry and spread the salmonella bacteria, which makes good hand hygiene particularly important after handling them.

 

All of which serves as a lead up to a CDC COCA Call, scheduled for next Thursday (July 17th), called:

 

Love the Pets, Not the Germs: CDC Update on Enteric Zoonoses 

Image of Continuing Education Credits abbreviation. = Free Continuing Education

Date:Thursday, July 17, 2014         Time: 2:00 – 3:00 PM (Eastern Time)

Participate by phone

Audio Bridge Line: 888-913-9971

Participant Code: 7400152

International number:212-547-0138

Participate by webinar

https://www.mymeetings.com/nc/join.php?i=PW7286673&p=7400152&t=c

Presenter(s)

Kara Jacobs Slifka, MD, MPH
Epidemic Intelligence Service Officer
Division of Foodborne, Waterborne, and Environmental Diseases
National Center for Emerging & Zoonotic Infectious Diseases
Centers for Disease Control and Prevention

Colin Basler, DVM, MPH
Epidemic Intelligence Service Officer
Division of Foodborne, Waterborne, and Environmental Diseases
National Center for Emerging & Zoonotic Infectious Diseases
Centers for Disease Control and Prevention

Overview

Enteric illnesses are common, costly, preventable, and increasingly attributable to animal contact. Animals provide many benefits to people; however, even clean and healthy animals may be responsible for spreading germs such as Salmonella, E.coli O157:H7, and Cryptosporidium, some of the frequent causes of diarrheal illness in children and adults. During this COCA call, clinicians will learn about enteric zoonoses, and the ‘One Health’ approach to helping patients prevent illness and maintain optimal health.

 

For more on family pets and zoonotic diseases you may wish to revisit:

 

Disease Transmission At The Human-Animal Interface

How Parrot Fever Changed Public Health In America

Friday, March 28, 2014

PHE: Transmission Of Bovine TB From Felines To Humans - UK

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# 8410

 

Readers with good memories will recall that back in 2010 I wrote a blog called Badgers? We Don’t Need No Stinkin’ Badgers!, that looked at a controversial plan to cull badgers in the UK in an attempt to reduce the wildlife reservoir of Mycobacterium bovis which is the cause of tuberculosis in cattle (known as bovine TB).

 

M. bovis is also capable of infecting humans (mainly through unpasteurized milk), although famers in contact with infected cattle are at risk as well.

 

In fact, of the three type of Tuberculosis bacteria (Mycobacterium bovis, M. avium, and M. tuberculosis – the most prevalent strain in humans), M. bovis has the largest host range – being capable of infecting just about all warm-blooded vertebrates.

 

Last year, a study appeared in the CDC’s EID Journal that attempted to estimate the global burden of M. bovis infection in humans (see Zoonotic Mycobacterium bovis–induced Tuberculosis in Humans), and found that while the number was small (roughly 1 per 100,000 pop.) - it was not insignificant – particularly in areas of the world where unpasteurized milk is still widely consumed.

 

DEFRA calls Bovine TB one of the biggest challenges facing UK cattle industry, and cites the following key facts:

    • 5.5 Million – total number of TB tests on cattle in England in 2011.
    • 28,000 – approximate number of cattle slaughtered for TB control in England in 2012.
    • 3,900 – approximate number of new TB incidents in 2012 (herds where at least one animal tests positive for bovine TB, when the herd had previously been TB free).
    • 11.5% of cattle herds in England were under cattle movement restrictions at some point in 2011 (the 2012 statistics will be published once additional quality assurance checks have been completed).
    • 23.6% of cattle herds in the South-West were under cattle movement restrictions at some point in 2011 (the 2012 statistics will be published once additional quality assurance checks have been completed).
    • £500 million – the amount it has cost the taxpayer to control the disease in England in the last 10 years.
    • £1 billion – estimated cost of TB control in England over the next decade without taking further action.
    • £34,000 – the average cost of a TB breakdown on a farm, of which around £12,000 falls to the farmer.

 

While many farmers see badgers as the primary source of their bovine TB woes, and blame them for reintroducing the disease into their herds each year, conservation and animal rights groups strongly disagree, and argue that the badger is the victim here.

 

They maintain that cow-to-cow transmission is the primary route of infection, and that badgers usually get the disease from cattle – not the other way around.

 

Four years, and a pilot culling program later, and the controversy still reigns. Recent media coverage has run the gamut from TB strategy about much more than badger culling – Paterson -Farmers Guardian to MPs vote overwhelmingly to halt badger cull in EnglandThe Guardian.

 

Adding a new dynamic to an already complex and contentious debate, yesterday Public Health England released a report on two rare human infections with M. bovis – both associated with an outbreak in cats – which likely became infected via contact (directly or indirectly) with badger setts (dens). 

 

The feline outbreak is described in a letter published in the BMJ’s Veterinary Journal called Mycobacterium bovis infection in cats by Nigel Gibbens, which prompted a full epidemiological investigation.  A brief excerpt:

 

BETWEEN December 2012 and March 2013, a veterinary practice in Newbury (west Berkshire) diagnosed nine cases of Mycobacterium bovis infection in domestic cats. In seven of those cases the diagnosis was confirmed by bacteriological culture. The nine affected cats belonged to different households and six of them resided within a 250 metre radius. The animals presented with mycobacterial disease of variable severity including anorexia, non-healing or discharging infected wounds, evidence of pneumonia and different degrees of lymphadenopathy. The latest information is that six of the cats have been euthanased or have died. The three surviving animals are undergoing treatment and are reported to be responding. At the time of writing, no new cases had been detected in local cats since March 2013.

 

PHE published the following press release on their website yesterday regarding the epidemiological investigation that turned up two probable cases where humans contracted M. bovis from cats.

 

Cases of TB in domestic cats and cat-to-human transmission: risk to public very low

Published 27 March 2014

Two people in England have developed tuberculosis after contact with a domestic cat infected with ‘Mycobacterium bovis’ (‘M. bovis’), Public Health England (PHE) and the Animal Health and Veterinary Laboratories Agency (AHVLA) have announced.’‘M. bovis’ is the bacterium that causes tuberculosis (TB) in cattle (bovine TB) and in other species.

Nine cases of ‘M. bovis’ infection in domestic cats in Berkshire and Hampshire were investigated by AHVLA and PHE during 2013. PHE offered TB screening to 39 people identified as having had contact with the infected cats as a precautionary measure. 24 contacts accepted screening. Following further investigations, a total of 2 cases of active TB and 2 cases of latent TB were identified. Latent TB means they had been exposed to TB at some point but they did not have active disease. Both cases of active TB disease have confirmed infection with ‘M. bovis’ and are responding to treatment.

There have been no further cases of TB in cats reported in Berkshire or Hampshire since March 2013. PHE has assessed the risk of transmission of ‘M. bovis’ from cats to humans as being very low.

Dr Dilys Morgan, head of gastrointestinal, emerging and zoonotic diseases department at PHE, said:

It’s important to remember that this was a very unusual cluster of TB in domestic cats. ‘M. bovis’ is still uncommon in cats - it mainly affects livestock animals. These are the first documented cases of cat-to-human transmission, and so although PHE has assessed the risk of people catching this infection from infected cats as being very low, we are recommending that household and close contacts of cats with confirmed ‘M. bovis’ infection should be assessed and receive public health advice.”

The findings of the animal health aspects of this investigation are published in The Veterinary Record today, 27 March 2014.

 

Molecular analysis at AHVLA showed that ‘M. bovis’ isolated from the infected cats and the human cases with active TB infection were indistinguishable, which indicates transmission of the bacterium from an infected cat. In the other cases of latent TB infection, it is not possible to confirm whether these were caused by ‘M. bovis’ or the source of their exposure.

 

Transmission of ‘M. bovis’ from infected animals to humans can occur by inhaling or ingesting bacteria shed by the animal or through contamination of unprotected cuts in the skin while handling infected animals or their carcasses.

 

Professor Noel Smith, Head of the Bovine TB Genotyping Group at AHVLA, said:

Testing of nearby herds revealed a small number of infected cattle with the same strain of ‘M. bovis’ as the cats. However, direct contact of the cats with these cattle was unlikely considering their roaming ranges. The most likely source of infection is infected wildlife, but cat-to-cat transmission cannot be ruled out.”

Cattle herds with confirmed cases of bovine TB in the area have all been placed under movement restrictions to prevent the spread of disease.

 

Local human and animal health professionals are remaining vigilant for the occurrence of any further cases of disease caused by ‘M. bovis’ in humans, cats or any other pet and livestock animal species.

(Continue . . . )

 

The PHE also released a HAIRS Risk Assessment, where they characterized the risk to public health as:

 

A Very low risk of transmission of M. bovis from cats to humans.

 

Although the risk of acquiring TB from a domestic cat in the UK is exceedingly low, and even less likely here in the United States, this report illustrates how animals – both wild and domestic – can carry and transmit zoonotic infections to humans.

 

This intersection of man and other species, and their sharing of viruses (zoonotic transmission), has increasingly been recognized as a driving factor in emerging infectious diseases, and even the creation of pandemics.

 

The age of emerging infectious diseases in humans really began in earnest about 10,000 years ago when humans began to domesticate – and live in close proximity to – other animals (see The Third Epidemiological Transition).

   

Measles probably evolved from canine distemper and/or the Rinderpest virus of cattle. Tuberculosis, which now infects 1/3rd of humanity, likely jumped from domesticated goats and cattle.  And influenza’s all seem to have an origin in waterfowl.

 

Other zoonotic nasties include Babesiosis, Borrelia (Lyme), Nipah, Hendra, Malaria, Hantavirus, Ebola, Leptospirosis, Q-Fever, bird flu . . . the list is long and growing.

 

Roughly 70% of the infectious diseases that afflict man today are believed to have begun in some other species, and new ones (think MERS-CoV, H7N9, H5N1, SFTS, etc. ) continue to show up each year. We live in an amazingly complex and interconnected world, where what happens in a live poultry market in China, a camel stable in Saudi Arabia, or a pig farm in Mexico can ultimately impact the health of people around the world.

 

So we watch these spillovers of diseases from animals to humans – no matter how rare, or small they may be – with considerable interest.

Monday, December 16, 2013

FAO: Surge In Animal Disease Increases Zoonotic Threats

Zoonotic Jump

 

# 8074

 

 

According to well respected anthropologist and researcher George Armelagos of Emory University, we are entering The Third Epidemiological Transition, which began in the late 1970s or early 1980s, and is hallmarked by newly emerging infectious diseases, re-emerging diseases carried over from the 2nd transition two hundred years ago, and a rise in antimicrobial resistant pathogens.

 

Over the past three decades, dozens of new – mostly zoonotic – diseases have been identified. Some have already had a major impact on humans (e.g. HIV, Lyme, XDR-TB), while others remain marginal threats, but may have tremendous potential for greater damage in the future. 

 

Which is why we pay so much attention to avian and swine flu viruses, emerging bat coronaviruses, and vector-borne diseases like Chikungunya, Dengue, CCHF, Nipah and SFTS. 

 

With an increasingly mobile global population now numbered over 7 billion, huge increases in the number of animals being raised for food consumption (often in environments conducive to the spread of diseases), and man’s continual encroachment into remote jungles and forests of the world - you have a huge potential to introduce new `exotic’ diseases to mankind.

 

Today the FAO has released a new 130 page report that calls for new, holistic approaches in dealing with animal disease threats, and warns that humanity faces increasing threats from zoonotic diseases.

Read the report

World Livestock 2013 (.pdf version)

E-book reader version

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3 minute Audio Interview with FAO Chief Veterinary Officer Juan Lubroth

 

For some more background on this report, the FAO published the following news story.

 

Surge in diseases of animal origin necessitates new approach to health - report

Focus on root causes and prevention needed

Photo: ©FAO/Sia Kambou

A poultry farm in Chad.

16 December 2013, Rome - Population growth, agricultural expansion, and the rise of globe-spanning food supply chains have dramatically altered how diseases emerge, jump species boundaries, and spread, according to an FAO report released today. A new, more holistic approach to managing disease threats at the animal-human-environment interface is needed, it argues.

Seventy percent of the new diseases that have emerged in humans over recent decades are of animal origin and, in part, directly related to the human quest for more animal-sourced food, according to the report, World Livestock 2013: Changing Disease Landscapes.

The ongoing expansion of agricultural lands into wild areas, coupled with a worldwide boom in livestock production, means that "livestock and wildlife are more in contact with each other, and we ourselves are more in contact with animals than ever before," said Ren Wang, FAO Assistant Director-General for Agriculture and Consumer Protection.

"What this means is that we cannot deal with human health, animal health, and ecosystem health in isolation from each other - we have to look at them together, and address the drivers of disease emergence, persistence and spread, rather than simply fighting back against diseases after they emerge," he added.

Multiple impacts of disease

FAO's new report provides a number of compelling reasons for taking a new tack on disease emergence.
Developing countries face a staggering burden of human, zoonotic and livestock diseases, it says, creating a major impediment to development and food safety. Recurrent epidemics in livestock affect food security, livelihoods, and national and local economies in poor and rich countries alike.

Meanwhile, food safety hazards and antibiotic resistance are on the increase worldwide.

Globalization and climate change are redistributing pathogens, vectors, and hosts, and pandemic risks to humans caused by pathogens of animal origin present a major concern.

(Continue . . .)

 

While the next pandemic could come from a wild bird in Asia, or the bushmeat trade out of Africa (see Bushmeat,`Wild Flavor’ & EIDs), the odds favor it coming from a commercial farm somewhere in the world where large numbers of animals intermingle, swap viruses, and come in daily contact with humans.

 

For a closer look at the risks of raising livestock, I heartily recommend Dr. Michael Greger’s free online book  Bird Flu: A Virus Of Our Own Hatching, and Helen Branswell’s terrific piece in SciAm  from late 2010 called Flu Factories.

Vast oceans and artificial geopolitical borders are no longer protection against the spread of diseases in our modern, interconnected world.

 

Which is why much more attention must be paid to global surveillance, international cooperation, and the immediate reporting of human and zoonotic disease outbreaks.

Friday, October 18, 2013

WER: Antigenic & Genetic Comparisons Of Zoonotic Flu Viruses And Development Of Vaccine Candidates

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Credit NIAID

 

 

# 7873

 

Influenza viruses are constantly changing, which is why seasonal flu vaccines must be adjusted nearly every year in an attempt to keep up with their evolution.  NIAID, part of the NIH, has a short (3 minute) video on Youtube that nicely illustrates how flu viruses change antigenically over time, and eventually mutate so that the current flu vaccine is no longer effective.

 

 

As you would expect, in the wild, avian and swine influenza viruses undergo similar changes.   

 

Small, incremental changes are called antigenic drift, and they occur more or less all of the time.   Most of these changes don’t convey any evolutionary advantage, and quickly disappear.  Occasionally, a `more biologically fit’  virus emerges, and blows away the competition.

 

More drastic changes can come by way of antigenic shift, also called reassortment. Shift occurs when one virus swap out chunks of their genetic code with gene segments from another virus.  While less common than drift, antigenic shift can quickly create a brand new `hybrid virus’.  One that can sometimes have pandemic potential.

 

For shift to happen, a host (human, swine, bird) must be infected by two influenza different viruses at the same time. 

reshuffle  

While successful reassortment is relatively rare, as any virologist will tell you . . . Shift happens.

 

H5N1 (aka `bird flu’) is not a single strain of influenza, but rather, a group of similar viruses sharing the same HA (hemagglutinin) and NA (neuraminidase) genes segments, that has continually evolved and mutated since its emergence in 1996.

You can see the evolution of the virus through 2011 in the chart below, starting with Clade 0, first detected in 1996.

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Over the years more than 20 genetically separate clades of the virus have emerged (not all continue to circulate), with many minor variants of each clade thrown in the mix. 

 

Different areas of the world have seen different clades set up residence, with clade 2.3.2 (and now 2.3.2.1) very common in South East Asia, clades 2.2.1 and 2.2 endemic in Egypt and clades 2.1.1, 2.1.2. and 2.1.3 circulating in Indonesia.

 

The problem is, vaccines based on older clades may not provide significant protection against infection with one of the newer clades.  So the World Health Organization, NIHCDC, the Vaccine Manufacturing community, and others are pitted in an ongoing `arms race’ against a constantly changing set of viruses.

 

And we now have more than just H5N1 to concern ourselves with.  There are multiple clades or variants of zoonotic H7N9, H9N2, H7N7, H3N2v, et. al. circulating around the world.  

 

The list is long, and it grows longer each year.

 

Which brings us to a long report today, that appears in the World Health Organization’s  Weekly Epidemiological Record (h/t @Ironorehopper)  One that looks at the strains of these zoonotic viruses that are currently circulating, and the development of candidate vaccine viruses against them.

 

Although I’ve posted some small excerpts below, I would recommend that you follow the link to read the report and its accompanying charts in their entirety:

 

 

Antigenic and genetic characteristics of zoonotic influenza viruses and development of candidate vaccine viruses for pandemic preparedness, September 2013


The development of representative candidate influenza vaccine viruses, coordinated by WHO, remains an essential component of the overall global strategy for pandemic preparedness. Comparisons of the candidate vaccine viruses with respect to antigenicity and their relationship to newly emerging viruses are ongoing and will be reported periodically by WHO.

(1) Influenza A(H5N1)

Since their re-emergence in 2003, highly pathogenic avian influenza A(H5N1) viruses have become enzootic in some countries and continue to cause outbreaks in poultry as well as sporadic human infections. The A(H5N1) viruses have diversified both genetically and antigenically leading to the need for multiple candidate vaccine viruses for pandemic preparedness purposes. This summary provides updates on the characterization of A(H5N1) viruses isolated from birds and humans, and the current status of the development of influenza A(H5N1) candidate vaccine viruses.

(Continue . . . )

 

Given its duration, and continued evolution, not surprisingly the WHO is proposing that 4 new H5N1 candidate vaccine viruses be developed.

 

Based on the available antigenic, genetic and epidemiologic data, A/duck/Bangladesh/19097/2013-like (clade 2.3.2.1), A/duck/Viet Nam/NCVD-1584/2012-like (clade 2.3.2.1) and A/Cambodia/W0526301/2012-like (clade 1.1) candidate vaccine viruses are proposed.

 

The WHO has previously selected candidate vaccine viruses for H3N2v, H9N2, H7N7, H7N3, and H7N9, and have not proposed work on any new vaccine strains for these flu types in this latest report.

Monday, July 15, 2013

Western Australia’s Equine Mystery

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Credit WA Horse Alert Brochure


# 7480

 

Overnight Crof picked up a report from ProMed Mail concerning Australia: Mysterious new horse disease may have been passed to humans with details provided by The Australian (full story behind a wall).

 

While still unidentified, the good news is that Hendra – a bat borne virus that occasionally infects horses (see Australia: Hendra Vaccine Hurdles) and has killed at least 4 people over the years – has been ruled out.

 

A quick look at Western Australia’s State Health Department website turned up nothing, but I was able to find the following statement (dated July 8th) on the WA Department of Agriculture & Food website.

 

Updated horse health information

The Department of Agriculture and Food is continuing to test samples to identify the cause of mouth papules (small, solid rounded lumps) in horses on three properties in the South-West. There have been horse or equipment movements identified as potential links between the affected properties.

 

The papules were reported by a private veterinarian attending to the horses. Testing has already ruled out the main virus of concern, vesicular stomatitis. Preliminary testing suggests the lumps might be a response to a viral infection. The department is continuing to work with the veterinary clinic involved to finalise a diagnosis.

 

The horses reported have mild signs and it is likely people examining normal healthy horses’ mouths may see small lumps that are not necessarily of concern. The black tongue reported on Facebook may be due to staining from treatment or feed and is not related to the condition.

 

The Department of Agriculture and Food reminds horse owners to contact their local veterinarian if they notice unusual signs in their horses.

 

There are no restrictions on horse movement in WA or on events. The department’s standard horse biosecurity recommendations are that only healthy horses should attend events and they should not share feed, water, or tack and equipment with other horses.

 

There have also been reports that some humans who have had contact with affected horses have developed similar lesions in their mouths, although they remain generally well. The Department of Health has been assisting with the investigation of these cases. At this stage, it is not clear if there is a relationship between the lesions reported in horses and people, and testing has not revealed a cause for the lesions in either horses or people.

 

The Department of Health advises that people handling affected horses should take general precautions, such as wearing disposable gloves and a face mask, and washing their hands well after contact with affected horses. If they are concerned about their health they should consult a general practitioner.

 

For more information about horse biosecurity, visit agric.wa.gov.au and search ‘horse alert’.

 

The earliest report I’ve been able to find on this outbreak was from June 26th, in the RWWA website.

 

Department of Agriculture and Food Horse Health Information

The Department of Agriculture and Food has taken samples to identify the cause of mouth papules (small solid rounded bumps) in horses on one property in the South West after being contacted by a private veterinarian attending to the horses.

 

Testing has already ruled out the main virus of concern, vesicular stomatitis, and further testing is underway to determine the cause of the papules.

 

The department reminds horse owners if they do notice unusual signs in their horses to contact their local veterinarian.

 

There are no restrictions on horse movement in WA. As generally recommended, horse owners should be mindful of horse biosecurity. Only take healthy horses to events and do not share feed, water, or tack and equipment with other horses.

 

While this may sound like a minor health concern (and it may very well turn out to be), Australia’s equine community is still reeling from a major outbreak of Equine Influenza in 2007, which infected 10,000 properties, and more than 76,000 horses.

 

Monetary loses were calculated at AUD$363 million ($100 million in direct response costs and $263 million in government ssistance to the horse industry) – Cite HORSE ALERT

 

For more on horse biosecurity concerns, you may be interested in the following 74 page brochure produced by various agencies of the Australian government.

 

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And in a slightly related story, back in 2010 I posted a fascinating article by Morens and Taubenberger: A New Look At The Panzootic of 1872 where they looked back at a wave of (presumably) equine influenza that swept across North American, infecting much of the horse population from Canada to Mexico – and killing up to 10%.

 

While the symptoms of this equine disease appear to be relatively mild in both horses and humans – over the past 30 years an estimated 70% of all emerging infectious diseases have originated from other animal species (see Woolhouse and Gowtage-Sequeria EID Journal 2005).

 

Which is why anytime what is perceived to be an animal disease jumps to humans, we tend to pay close attention.

Friday, May 24, 2013

Report: Saudis To Send Animal Samples To U.S. for MERS-CoV Testing

Coronavirus

Photo Credit NIAID

 


# 7316

 

 

A report from AFP this morning indicates that the Saudis have collected, and will now ship to labs in the United States, samples collected from a variety of animals that might be carriers of the emerging MERS Coronavirus.


First a link to the report, then I’ll be back with more.

 

Friday, 24 May 2013 KSA 16:23 - GMT 13:23

Saudi to send animal samples to U.S. in coronavirus probe

AFP, Geneva -

Saudi Arabia said Friday it would send samples taken from animals possibly infected with a deadly SARS-like virus to the United States for testing in a bid to find the source of disease.

 

The Saudi health ministry has “collected large samples from bats and other animals, including camels, sheep and cats,” said Saudi Deputy Health Minister Ziad Memish.

(continue . . . )

 

One of the keys to containing the MERS virus is determining from where, and how, it is spilling over into humans.  

 

Early on, bats have been suspected (see EID Journal: EMC/2012–related Coronaviruses in Bats and mBio: New Coronavirus Linked To Bats), since similar viruses have been detected in these winged mammals – but so far, no direct evidence of a primary animal host has been found.

 

There is also the possibility of multiple hosts species, or – perhaps more likely – a primary and one or more intermediate (or amplifying) host species (see mBio: Coronavirus Has An Affinity For Multiple Hosts).

 

 

At this point, the field of suspects is wide open, and nailing this down is of utmost importance. 

 

So this newfound willingness on the part of the Saudis to share more samples for testing would be a welcome move in the right direction.

Friday, February 22, 2013

Eurosurveillance: Contact Investigation Of NCoV Case Hospitalized In Germany

 

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Coronavirus – Credit CDC PHIL

 


# 6958

 

Yesterday the journal Eurosurveillance published a report on the numerous contacts of a patient from Qatar who last fall was treated for several weeks at a German lung clinic before being diagnosed as infected with the novel coronavirus (NCoV).

 

During this time scores of hospital personnel were potentially exposed. Despite taking few protective measures, none of these contacts appear to have become infected.

 

What makes this case a bit unique is the timing of this patient’s transfer to Germany, some 23 days after his symptoms first appeared. 

 

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While it is always perilous to base conclusions with such a limited dataset, this lack of secondary transmission late in the patient’s illness suggests a limit on the infectious period of a patient infected with NCoV.

 

Additionally, this patient’s interview turned up a possible zoonotic source of his viral infection.

 

It’s a long and detailed report, very much worth reading in its entirety. Below are the the link, abstract and some excerpts (slightly reformatted for readability), after which I’ll be back with more.

 

Contact investigation of a case of human novel coronavirus infection treated in a German hospital, October-November 2012

U Buchholz , M A Müller, A Nitsche, A Sanewski, N Wevering, T Bauer-Balci, F Bonin, C Drosten, B Schweiger, T Wolff, D Muth, B Meyer, S Buda, G Krause, L Schaade, W Haas

24 October 2012, a patient with acute respiratory distress syndrome of unknown origin and symptom onset on 5 October was transferred from Qatar to a specialist lung clinic in Germany.

 

Late diagnosis on 20 November of an infection with the novel Coronavirus (NCoV) resulted in potential exposure of a considerable number of healthcare workers.

 

Using a questionnaire we asked 123 identified contacts (120 hospital and three out-of-hospital contacts) about exposure to the patient. Eighty-five contacts provided blood for a serological test using a two-stage approach with an initial immunofluorescence assay as screening test, followed by recombinant immunofluorescence assays and a NCoV-specific serum neutralisation test.

 

Of 123 identified contacts nine had performed aerosol-generating procedures within the third or fourth week of illness, using personal protective equipment rarely or never, and two of these developed acute respiratory illness. Serology was negative for all nine. Further 76 hospital contacts also tested negative, including two sera initially reactive in the screening test.

 

The contact investigation ruled out transmission to contacts after illness day 20. Our two-stage approach for serological testing may be used as a template for similar situations.

<SNIP>

Patient interview

The patient reported to live in Doha, Qatar. He used to be a heavy smoker (2 to 3 packs of cigarettes per day), but denied smoking waterpipe or chewing qat.

 

Disease onset was rapid, with initial symptoms including fever (40 °C), cough, runny nose, and shortness of breath. Subjective weakness was pronounced. After the first two days of illness he improved a little but deteriorated again, and was finally admitted to hospital on day eight of illness because of increasing dyspnoea.

 

He reported no subjective symptoms of renal impairment such as foamy urine, reduced urine output, or back pain. He had not travelled and had no known contact with any other reported cases of NCoV infection.

 

The patient owned a camel and goat farm and reported a large number of casual contacts (approx. 50 persons per day) on a regular basis. He remembered that before his disease onset some goats were ill and had fever. He did not have direct contact with the goats or any other animals especially falcons or bats, but said he had eaten goat meat.

 

He also reported to have had contact with one of his animal caretakers who was ill with severe cough and was hospitalised. Other than the animal caretaker, he did not remember persons with severe respiratory illnesses in his wider or closer social environment.

 

 

We know the infectious period of viral diseases can vary widely, and is often dependent upon the age and the individual immune response of the host. Those with compromised immune systems often shed a virus longer than those with a more robust immune system.

 

The CDC’s general take on influenza’s infectivity is:

 

The Flu Is Contagious

Most healthy adults may be able to infect others beginning 1 day before symptoms develop and up to 5 to 7 days after becoming sick. Children may pass the virus for longer than 7 days. Symptoms start 1 to 4 days after the virus enters the body. That means that you may be able to pass on the flu to someone else before you know you are sick, as well as while you are sick. Some persons can be infected with the flu virus but have no symptoms. During this time, those persons may still spread the virus to others.

 

Norovirus, on the other hand, is most contagious during the first 72 hours of infection, but patients can still shed the virus in their stool for up to 2-weeks (see the CDC’s  Clinical Overview)

 

With the caveat that while this emerging NCoV is a coronavirus - it is not SARS  - in 2003 researchers found (unlike with influenza), those infected with the SARS virus did not appear to be contagious prior to developing symptoms.

 

The CDC’s SARS FAQ reads:

 

How long is a person with SARS infectious to others?

Available information suggests that persons with SARS are most likely to be contagious only when they have symptoms, such as fever or cough. Patients are most contagious during the second week of illness. However, as a precaution against spreading the disease, CDC recommends that persons with SARS limit their interactions outside the home (for example, by not going to work or to school) until 10 days after their fever has gone away and their respiratory (breathing) symptoms have gotten better.

 

This lack of asymptomatic (or presymptomatic) transmission of SARS virus made it easier to identify those infected, and made it possible to contain that outbreak.

 

In 2004 an EID Journal dispatch looked at how long the SARS coronavirus could be detected in a patient’s sputum and stool.

 

Long-term SARS Coronavirus Excretion from Patient Cohort, China

Wei Liu, Fang Tang, Arnaud Fontanet, Lin Zhan, Qiu-Min Zhao, Pan-He Zhang, Xiao-Ming Wu, Shu-Qing Zuo, Laurence Baril, Astrid Vabret, Zhong-Tao Xin, Yi-Ming Shao, Hong Yang, and Wu-Chun Cao

Abstract

This study investigated the long-term excretion of severe acute respiratory syndrome–associated coronavirus in sputum and stool specimens from 56 infected patients. The median (range) duration of virus excretion in sputa and stools was 21 (14–52) and 27 (16–126) days, respectively. Coexisting illness or conditions were associated with longer viral excretion in stools.

 

It should be noted that shedding enough virus to be detectable by today’s modern RT-PCR testing or virus culture, and being contagious and able to spread the virus, may be two entirely different propositions.

 

With just over a dozen laboratory confirmed cases of NCoV infection, we are still very early in the learning curve of this emerging virus. 

 

A limited contagious period is hardly unexpected, but this study does provide an important data point. We’ll need a larger sample size before researchers can quantify the typical infectious period for this virus.

 

The other intriguing aspect of this study is the possible (albeit, tenuous) link to goats as a zoonotic source of the virus. 

 

As the authors point out in their discussion (see below), this isn’t the first time that farm animal exposure has been mentioned in conjunction with NCoV.

 

During two interviews that the patient kindly agreed to, we explored a wide spectrum of factors that he might have been exposed to. Even though NCoV is genetically similar to bat coronaviruses [1,13,14], other animals may serve as (intermediate) host as well.

 

While our patient denied contact to bats, he remembered ill goats among the animals on his farm. Albarrak et al. reported that the first Saudi case was exposed to farm animals, but the first Qatari patient and the second Saudi patient were not [15]. Although our patient reported no direct contact with his animals, one animal caretaker working for him was ill with cough and might have been an intermediate link in the chain of infection.

 

Coronaviruses do infect ruminants such as goats [16] and thus goats could be considered as a possible source of origin for the novel virus, particularly in the geographical and cultural context of our patient.

 

 

So far, the number of known cases remains very small. Whether this virus has what it takes to present a larger public health concern has yet to be determined.

 

With scientists, doctors, and disease detectives hot on its trail, I fully expect we’ll know a good deal more about this emerging virus a month or two from now.

 

Stay tuned. 

Tuesday, January 08, 2013

EID Book Review - Spillover: Animal Infections and the Next Human Pandemic

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Link to book on Amazon (excerpts available online)

 


# 6834

 

In 2012, award winning author and Rhodes Scholar David Quammen published his 10th book on science, titled  Spillover: Animal Infections and the Next Human Pandemic. Quammen, whose first book was published in 1970, also has five books of fiction, along with many magazine articles in his resume.

 

Today, the CDC’s EID Journal has a short, but very complementary review of his book, Spillover.  I’d be remiss if I didn’t mention that reviews on Amazon have been superlative as well, and Spillover has made more than one Top 10 books of 2012 lists. 

 

First the EID review, then I’ll return with more.

Books and Media

Spillover: Animal Infection and the Next Human Pandemic

Article Contents

David Quammen
W.W. Norton & Company, Ltd., New York, New York, USA, 2012
ISBN: 978-0-393-06680-7
Pages: 487; Price: US $28.95

Spillover is a single event during which a pathogen from 1 species moves into another species; such movement can result in an outbreak. In 9 chapters, David Quammen chronicles various spillover events by using personal anecdotes and multiple stories to recount these events for the expert and novice alike. He frames the events within an ecologic sense of the pathogen, the host, and the increasing human population. He focuses recurrently on the NBO (next big one) and how, if HIV or Ebola virus were more easily transmissible, no one would remain to read his book.

 

Quammen’s analogies are superb. Instead of trying to turn the reader into a scientist with dry explanations, he uses analogies that have universal relevance. For viral morphology, Ebola and Hendra virions together would resemble a “capellini in a light sauce of capers.” Mathematical modeling can be appreciated in translation, just as Dostoevsky can be appreciated in translation instead of in the original Russian. Quammen compares combining specific antibodies with their virus to splashing holy water on a witch. Regarding airborne transmission, he says that pathogens can “waft into a nearby village as easily as the pleasant, autumnal smell of smoke from a pile of leaves.” Throughout the book, the subjects of human and animal diseases are “. . . strands of one braided cord.”

 

The last chapter, “It Depends,” is particularly sobering. If, in an ecologic sense, an outbreak is a rapid and explosive increase in the abundance of a particular species, then maybe humans are the current outbreak in the world. We have become a dense forest; tinder is dry; and the NBO is around the corner.

 

Who should read this book? Anyone interested in science can enjoy it—those who make their living at the bench, teach, or study—and anyone just looking for a good read.

Corrie BrownComments to Author

Author affiliation: Author affiliation: University of Georgia, Athens, Georgia, USA

 

 

Spillover also received a glowing endorsement from Ed Yong when he was at Discover Magazine (see Spillover, by David Quammen – a recommended read), and I can wholeheartedly recommend it myself.

 

For more on David’s book, and the threats posed by zoonotic disease spillovers, we turn to a Minnesota NPR radio interview recorded last September. It runs 30 minutes, and is well worth the time.

 

 

David Quammen on 'Spillover,' the next worldwide pandemic

11:20 AM, September 24, 2012

Friday, November 30, 2012

The Lancet: Zoonoses Series

 

 

# 6751

 

I’ve only just started to read them, but The Lancet has a three-part series today that looks at the ongoing, and increasing, threat from Zoonoses to global health.

 

Given the pedigree of some of these papers, I’m confident they will be worth your time to review them. The articles are free, but do require registration to view.

 

 

Zoonoses series

Zoonoses - Copyright: Science Photo Library Zoonoses have been responsible for some of the most devastating disease outbreaks in recent years, including HIV, Ebola, and SARS, and cause more than 60% of human infectious diseases worldwide. Despite their prominence, there are still major gaps in our understanding of how zoonoses spread and develop. This three part series highlights the threat from zoonotic infections; it discusses the ecology and evolution of zoonoses, and society’s response to these diseases, with a focus on the prediction and prevention of the next pandemic zoonosis.

Zoonoses

Published Nov 30, 2012

Executive summary

Zoonoses – pathogenic organisms such as bacteria or viruses which we share with animals – cause more than 60% of human infectious diseases, and have been responsible for some of the most devastating disease outbreaks in recent years, including HIV, Ebola, and SARS. However, despite their huge, and rising, impact on human health, there are still huge gaps in our understanding of how zoonoses spread and develop, which need to be urgently addressed if we are to be able to reduce the impact of the next zoonotic pandemic. In a new Lancet Series, leading experts discuss the ecology, drivers and dynamics of zoonoses, while also addressing how we might predict the next zoonotic pandemic, and reduce the potentially catastrophic human and economic cost of such an outbreak.

Comment

Emerging infectious diseases: the role of social sciences

Craig R Janes, Kitty K Corbett, James H Jones, James Trostle

Full Text | PDF

Series Papers

Ecology of zoonoses: natural and unnatural histories

William B Karesh, Andy Dobson, James O Lloyd-Smith, Juan Lubroth, Matthew A Dixon, Malcolm Bennett, Stephen Aldrich, Todd Harrington, Pierre Formenty, Elizabeth H Loh, Catherine C Machalaba, Mathew Jason Thomas, David L Heymann

Summary | Full Text | PDF

Drivers, dynamics, and control of emerging vector-borne zoonotic diseases

A Marm Kilpatrick, Sarah E Randolph

Summary | Full Text | PDF

Prediction and prevention of the next pandemic zoonosis

Stephen S Morse, Jonna AK Mazet, Mark Woolhouse, Colin R Parrish, Dennis Carroll, William B Karesh, Carlos Zambrana-Torrelio, W Ian Lipkin, Peter Daszak

Summary | Full Text | PDF

Friday, September 07, 2012

`Outlier’ Hantavirus Case Reported At Yosemite

 

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Yosemite High Sierra Campsite – Credit Yosemite National Park

 

# 6540

 

 

Although you are twice as likely to be killed by an errant bolt of lightning in the United States (average 54 deaths/year) than from infection with Hantavirus (roughly 20 deaths/year), the recent high profile outbreak at the campsites in Yosemite National Park has captured the public’s attention here, and around the world.

 

Hantavirus is an extremely rare rodent-carried virus that is transmitted to humans via their urine and feces. It causes a severe form of pneumonia called HPS (Hantavirus Pulmonary Syndrome) which is fatal in about 30% of the cases, but it is not transmissible from person to person.

 


Yesterday we learned that the number of cases in that cluster has increased to 8, with 3 fatalities. The latest death coming from a Charleston W.V. man who visited the park earlier this summer (see KCHD Investigating Hantavirus case).

 

The National Park Service has released a statement indicating that the 8th reported case is an `outlier’, as he did not stay in any of the 91 "signature tent cabins" in Curry Village where the other 7 cases were presumably exposed. 

 

Instead he backpacked and camped along park’s high country called the High Sierra Loop, which provides pre-setup tent camps along the route.

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Hantavirus in Yosemite

Information current as of September 7, 2012

(EXCERPTS)

The National Park Service has received confirmations from national and state public health agencies of HPS cases linked to eight individuals who stayed one night or more in Yosemite since June of this year. Three cases have resulted in fatality; the five remaining individuals are either improving or recovering. The confirmed cases include six individuals from California, one from Pennsylvania, and one from West Virginia. The types of hantavirus that cause HPS in the United States cannot be transmitted from one person to another.

 

Seven of the eight cases of HPS have been linked to the "Signature Tent Cabins" in Curry Village in Yosemite Valley. Those cabins have been closed and parties who stayed overnight since June 10 have been reached out to by the park or the operator of Curry Village, DNC Parks & Resorts at Yosemite, Inc.

 

The California Department of Public Health (CDPH) has advised the National Park Service that one of the eight confirmed cases of HPS stayed in multiple High Sierra Camps in Yosemite (a different area of the park than Curry Village) in July, and that the stay in the High Sierra Camps is the most likely source of that person's infection. This individual exhibited mild symptoms and is recovering.

 

 

You don’t, however, have to trek the high country of Yosemite National Park, or stay at Curry Village, to risk exposure to the Hantavirus.  As the chart below shows, while rare, this rodent borne disease has a wide range in the United States.

 

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Although Colorado, New Mexico, and Arizona are the nation’s hot spots for the virus, a few cases have been reported as far east as Florida the Eastern Seaboard.

 

The range of susceptible rodents (predominantly the deer mouse, but also the white footed mouse in the Northeast, and the cotton rat in the south) is such that some risk of exposure is possible practically anywhere in the country.

 

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Mash-up of CDC Data

 

Nonetheless, infection with HPS is rare in the United States. Still it makes sense to avoid exposure to the virus whenever possible, and so the CDC offers this advice:

 

 

Preventing Hantavirus Pulmonary Syndrome (HPS)

Eliminate or minimize contact with rodents in your home, workplace, or campsite. If rodents don't find that where you are is a good place for them to be, then you're less likely to come into contact with them. Seal up holes and gaps in your home or garage. Place traps in and around your home to decrease rodent infestation. Clean up any easy-to-get food.

 

Recent research results show that many people who became ill with HPS developed the disease after having been in frequent contact with rodents and/or their droppings around a home or a workplace. On the other hand, many people who became ill reported that they had not seen rodents or rodent droppings at all. Therefore, if you live in an area where the carrier rodents are known to live, try to keep your home, vacation place, workplace, or campsite clean.

 

For more information on how you can prevent rodent infestations, the following information is available on the CDC Rodents site:

Got Mice?

Person using caulk gun to seal holes on exterior of house

Seal Up!

Seal up holes inside and outside the home to keep rodents out.

person baiting a snap trap with peanut butter

Trap Up!

Trap rodents around the home to help reduce the population.

various food containers with properly sealed lids

Clean Up!

Avoid illness: Take precautions before and while cleaning rodent-infested areas.

 


And for more information, the CDC offers a   16 page PDF  on Hantavirus, which is available on their Hantavirus Main page.

 

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