Posts Tagged ‘paper discussion’


Zoonotic diseases – causing more problems than illnesses/deaths alone

July 26, 2012 

@DiseaseMapper recently tweeted a link to a very interesting paper (which happily is also free to access so you can read it too – the link is here )

Why do I think this paper is so interesting?  Firstly, because it is a useful reminder that zoonotic infections (those that pass from animals to man and vice versa) do not just impact on our lives by causing us illness, and in the worst circumstance, death.  They have a massive economic impact as well.  In fact the paper reports that the estimated economic impact of zoonotic diseases from 1995-2008 was over 120 billion dollars.

There are many reasons for the economic burden of these diseases being so high: impact on tourism; impact on international trade agreements; impact on consumer consumption and behaviour; loss of farmed animals.  In many outbreaks the local economy is negatively impacted in multiple ways and obviously in poorer areas this can also secondarily affect people’s health.

The paper also goes on to speculate about why there should be a resurgence of zoonotic infections.  The authors split it into ‘Factors associated with human behaviour’; ‘Factors associated with pathogen characteristics’ and ‘Climate change and zoonotic resurgence’.  So, pinching their titles…

Factors associated with human behaviour

Here the authors split it down further:

Individual human practices – the authors use the example of ecotourism.  “urban citizens of the developed world who visit developing countries or rural areas of the developed world and engage in activities such as forest camping, river rafting, or bat cave exploring, are prone to zoonotic infections such as vector-borne rickettsioses, leptospirosis, and haemorrhagic fevers or lyssavirus-related illness, respectively“.  The authors also talk about how pet ownership, especially the increase in ownership of ‘exotic’ pets like reptiles is increasing people’s exposure to infections that previously they would never have been exposed to.

Socio-economic alterations – with an ever increasing global population there is an ever increasing demand for food, including meat.  It also means that as urban populations are expanding people are moving into previously uninhabited areas and so are being exposed to disease-causing agents that they had never been previously.

Political alterations – the authors talk about some countries with poorer veterinary surveillance or that have focal areas of zoonotic infections that previously were not having a global impact because they had strictly state-controlled economies but are now having a global impact because they have transitioned to allowing free  trade.  They also discuss the role that political disruption and upheaval can have on increasing the spread of zoonotic infections.

Scientific impacts – Part of the reason that we are recognising so many zoonotic infections is that we have got better at detecting them.  Infectious agents that we couldn’t have characterised decades ago can now be identified and classified.  Another scientific impact the authors mention is one that you will recognise if you are a regular reader of this blog: there have been many advances in medicine that allow us to live to an older age, but that have a negative impact on our immune system (for example, chemotherapy drugs can make us immunosuppressed; if you have an organ transplant you have to take immunosuppressing drugs, etc.)  This leaves a section of the population at a much higher risk of contracting any disease and so gives rise to some human infections with agents that would otherwise not normally infect humans.

Factors Associated with Pathogen Characteristics

The authors talk about how pathogens (disease causing organisms) that have a high genetic mutation rate (like flu viruses) can help them become zoonotic infections: in the authors’ words ” their enormous mutation rate is essentially a factory producing the species that are most potently pathogenic for humans

The authors also talk about how biodiversity can impact zoonotic disease transmission in this section (although, personally I’m not sure why it came into this section).  They talk about how sometimes wide diversity can reduce the spread of zoonotic agents because (if I am parsing this correctly) if there are many host animals that a vector (like a mosquito) can feed off there is less chance of it coming into contact with an animal that harbours the zoonotic agent – this is called the ‘dilution effect’.

Climate Change and Zoonotic Infection Resurgence

To quote from the paper: “Global warming is an ecological emergency, but its implications for human disease caused by infectious agents remains understudied“.  We do know some of the effects it could have – increases in temperature in previously colder countries leads to the spread of insects like mosquitoes – and the diseases they carry –  into those countries.  Climate change may also affect bird migration patterns and so may affect the exposure of birds to pathogens and also the exposure of us to them via the birds.

Finally the paper finishes with Projections for the Future. The authors point to 4 issues that “need urgent clarification and further attention“.

1) Recognition of the need for pre-emptive studies on the effects of massive or smaller developmental projects on local animal fauna and local zoonotic reservoirs

2) Recognition and enhancement of the health literacy of special populations that are at increased risk for the development of zoonotic infections (meaning that those patients on immunosuppressant drugs or who are immunosuppressed for other reasons should get more information about where they might encounter zoonotic infections and hw to avoid them.

3) Recognition of the major long-term burden induced by certain of these diseases with a chronic phase. There are some diseases that take a long time for any symptoms to show.  If a person has migrated from an area where the disease is relatively common to one where the disease is rare, the clinicians may be less likely to recognise the disease (or may recognise it at a later stage than if they were practicing in a country where the disease is common).  The authors recommend that clinicians “should be prepared to recognize the long history evolving in such patients and the extreme costs, mentioned in the introductory section, that will be passed on to the host countries”

4) Planning any intervention is difficult, for financial and scientific reasons. The burden of many of these diseases remains unrecognized… any zoonosis imposes a threat to the family as a unit—exposure is likely to be common for members of a household, particularly in agricultural settings, and animal loss (owing to the disease or state regulations for sick animals) may have a significant impact on the economy of the household, which is further worsened by the often observed inadequate access to appropriate medical treatment for the human patients themselves (imagine the scenario in any impoverished or conflict-active region of Africa or Asia). … ambitious eradication campaigns are not always feasible when all of the aforementioned issues have not been taken into account, and neither are successful elimination campaigns, as these may have temporary positive results but subsequent surveillance degeneration, leading to zoonotic resurgences, usually with some twists. (So basically we don’t really fully know the burden of most zoonotic diseases and rushing in there with eradication campaigns without considering all the other factors is not necessarily the best move.)

I think sometimes it can be really easy to think of zoonotic diseases as something one human gets from one animal, but this paper was a good reminder that these diseases can have a much broader impact.  It also had a useful discussion about why the number of zoonotic infections seemed to be increasing, but as it said (and as all papers say) there is still more work to be done in this area.

Image credit

All images were released under a creative commons licence (see links for details).  Thanks to Rugby471 for the dollar sign, to Wegmann for the tourist shot and to DROUET for the virus


Cascio A, Bosilkovski M, Rodriguez-Morales AJ, & Pappas G (2011). The socio-ecology of zoonotic infections. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases, 17 (3), 336-42 PMID: 21175957


Twitter Microbiology Journal Club #microtwjc

April 23, 2012

At the Society for General Microbiology’s Spring Conference in Dublin I attended a talk given by Natalie Silvey on Twitter Journal Club.

The Twitter Journal club (@twitjournalclub) was started in June 2011 and runs as a traditional journal club that discusses medically-related papers with the twist being it is all done by the medium of Twitter.

Having lurked at @twitjournalclub’s meetings a few times and listened to the talk at the SGM I thought it would be great if there was a microbiology journal club and I think others at the meeting thought so too. 

One month after the conference and there is no sign of one being set up so I figured I would get the ball rolling and give it a try…

Details will follow but what I really need are some willing volunteers to help me choose papers, run and moderate it.  It would also be good if people could help out putting transcripts together (I guess storify might be the easiest way of doing this?)

My plan is that we will run twice a month (edited for clarity!) as @twitjournalclub do (schedule to be decided depending on when volunteers can make it but will likely have a UK bias as that is where I am based) and ideally we would have at least a couple of moderators each time.  If there are enough people to help out it would mean that moderators would only have to be around once a month or perhaps less so it shouldn’t take over too much of our lives!  (My aim is for this to be fun and not just another work-related thing to occupy our precious time!)

If you are reading this and thinking it sounds like a good idea but you don’t have enough experience to volunteer – YOU DO!  I did barely any microbiology in my undergrad degree and I’m a second year PhD student – to be honest I feel like a bit of a fraud setting this up!  But my hope is that the volunteers are just there to steer the conversation/ask questions if it all goes a bit quiet.  Hopefully other, more experienced researchers will take part and they can help us out if we get stuck.  Hey – the worst that will happen is that we don’t understand something and so we will go away and find it out and learn something new.  Please don’t be put off helping out because of your level of experience.  ANYONE is welcome.

If you are interested and would like to help out please can you comment here/email me (link in the side bar)/talk to me on Twitter (@_zoonotica_).  It would also help if you could let me know what type of microbes you work with so I can try to make sure we have all areas covered.

For everyone else who can’t help out but would like to take part… watch this space and watch twitter #microtwjc


E Coli picture – Released into the public domain by Mattosaurus

Desk picture – Original picture by MZMcBride. Derivative work by Train2104.  Available at:


Sadly pet ownership comes with risks

March 13, 2012

Maryn McKenna over at SUPERBUG has got a post up discussing a recent paper (see below) that looked at 3 cases of (human) infection with Pasteurella multocida.  In all 3 cases it is thought that the patients involved caught the bacteria from nursing their sick pets.

Pasteurella multocida is a nasty species of bacteria and infection with it can very easily be fatal in humans.  Human cases are mostly associated with scratches and bites from cats and dogs (P. multocida can and does live happily in their mouths without causing any problems to them). However, in the cases published in the paper the transmission from animal to human seems to be effectively from mouth to mouth, rather than via injection through the skin as would happen with a bite.

It’s a very sad reminder that whilst pet ownership has many many benefits, we shouldn’t ignore the risks.


Paper Cited:

Myers EM, Ward SL, Myers JP. Life-threatening respiratory pasteurellosis associated with palliative pet care. Clin Infect Dis. 2012 Mar;54(6):e55-7. Epub 2012 Jan 11. DOI: 10.1093/cid/cir975 (May be behind paywall)


Photo by Adriano and released under a Creative Commons Attribution- Share Alike 3.0 Unported Licence


“Pig” MRSA – are the pigs really to blame?

February 23, 2012

Photo by Keith Weller

There is a strain of MRSA (methicillin-resistant Staphylococcus aureus) that has been tracked passing from pigs to humans.  It was always thought that the MRSA initially came from the pigs, but new research published in mBio (open access) suggests that pigs might not be the original source. 

Instead it looks like the strain may have originated in humans but been methicillin-susceptible.  It then at some point passed into pigs where it picked up some antibiotic resistance genes from other bacteria before then going back into humans (especially farm workers and others who have close contact with pigs) as a more dangerous strain.

Unfortunately antibiotic resistance is one of the problems we face when bugs (in the sense of pathogens, rather than insects!) can so easily share and swap their genetic material.

One of the co-authors on the paper, Tara Smith has written an interesting post about it over at her blog, Aetiology which is well worth a read.  (If you’re interested in antibiotic resistance, public health and epidemiology her blog is definitely one to add to your RSS feed.)


Bovine TB and badgers – why it all matters

January 17, 2012

I’ve been meaning to write about bovine TB for some time.  The news in December that there will be a badger cull trial in England has finally spurred me into actually doing so. 

Before I start I should mention that this post will not be about the political aspects of the cull decision.  Nor will it be about the scientific data that is being used to support and oppose the government’s plans.  I am not an expert in these areas and so do not feel competent enough to blog about the issues.  However, please feel free to discuss these things in the comments (please keep it polite and attack the argument rather than the person you disagree with).

What I want to write about today is why it is actually important to reduce the levels of bovine TB in our cattle and wildlife.  There is a good review article here (unfortunately behind a paywall) and it is from this that much of what will follow is taken.

Bovine tuberculosis (bTB) is caused by Mycobacterium bovis – a species closely related to Mycobacterium tuberculosis which is the most common cause of human TB. M. bovis can infect and potentially cause disease in most mammals, and is zoonotic (so can infect humans too).

Humans and Mycobacterium bovis

People can be infected by three main routes:

  1. Infected milk – this was the most common route before pasteurisation and is still a potential hazard in places where milk is not routinely pasteurised
  2. Inhalation of aerosolised infectious droplets – ie. when an infected cow with tuberculous lung disease breathes out there may well be droplets that carry the Mycobacterium.  Again, this was a reasonably common route historically.  The main group of people at risk from this route are farm workers.  (I was actually wondering whether this could potentially be a problem from places like children’s farms where more of the population could be exposed to infected animals.  I’ve not seen any information on it.  It’s probably not a problem at the moment but if the TB levels in the cattle herd keep increasing perhaps it could be in the future?)
  3. Infected meat – this is a very rare route of infection as gross signs of disease are easily spotted at meat inspection.

The World Health Organisation has this to say about bovine TB:

TB due to M. bovis often occupies sites other than the lungs (it is extra-pulmonary), but in many cases is clinically indistinguishable from M. tuberculosis infection. However, patients with M. bovis often do not respond to the drugs commonly used to treat TB, sometimes resulting in a fatal outcome.

In general there is a period of latency after exposure to the organism – in this period there are no clinical signs of disease.  Some (but not the majority) of latent infections will then go on to develop active disease which if not treated can be fatal.  This progression is more common if the person is immunosuppressed.

Cattle and Mycobacterium bovis

The picture in cattle is reasonably similar to that in humans.  Animals most commonly get infected via aerosolised droplets but there is the potential for calves to be infected via milk.  Some animals may never show signs of disease, in some the signs of disease may start off being quite vague (loss of appetite, weight loss) but cases can then develop into tuberculous lung disease.

Badgers and Mycobacterium bovis

Badgers, like cattle, are considered a “maintenance host” for bovine TB – the organism multiplies and infects the population from generation to generation and even if badgers never came into contact with any other possible Mycobacterium host the organism would still survive in the population. 

Again, some badgers may never show any signs of clinical disease but some may suffer from “florid disease” (as the paper by Gallagher and Clifton-Hadley – see below – beautifully describes it) including tuberculous lung disease and tuberculous lesions in other body sites.  That same paper proposes that it is those badgers with the most advanced disease that are the main reservoir of infection for other animals species such as cattle.

Other animals and Mycobacterium bovis

Some other species have also been proposed to act as maintenance hosts including deer and possibly goats.  Some species are thought to act as “spill-over” hosts (in these species the infection is self-limiting and they can be considered a “dead-end” host unless they happen to infect a maintenance host).  Currently considered as spill-over hosts are pigs, cats and dogs.  These animals may also show signs of disease (although again it can take a long time for disease to develop).

Importance in the UK

Because of milk pasteurisation and the control methods currently implemented in cattle the human cases of M. bovis are extremely rare.  This disease is much more of a problem in the developing world where these control mechanisms may not be in place. 

However, this does not mean the the disease should be forgotten about.

The incidence of the infection in cattle seems to be increasing (see the HPA link below) so there’s more chance of people coming into contact with it, if not directly from cattle, then from some of the spill-over hosts like cats and dogs. 

Another extremely important reason not to forget this disease is because the number of immunosuppressed people in the population is increasing (this includes people suffering from diseases like AIDs and also includes people on immunosuppressive drugs like chemotherapy) and as I mentioned before, this leads to greater chance of an infection becoming active and clinical symptoms developing. 

It may be (this is my speculation here) that in the future the most common picture for human infection (although it will still be extremely rare) will be an immunosuppressed person getting infected via a spill-over host like a pet cat or dog.


As I’ve discussed, this disease is not only bad for us but it is also bad for cattle, for badgers, and for many other animals should they become infected.  In the end, it is in all (and I’m including animals in this ‘all’) of our best interests to eradicate this disease from our country.

And this is generally accepted.  However, what still remains to argue about is “How?”


Badger picture: Made available by BadgerHero under a CC-BY 3.0 licence

Cow picture: Made available by CRV Arnhem under a CC-BY 3.0 licence

Further Information

World Organisation for Animal Health (OIE)‘s handout (NB: It is a PDF) on bovine TB

Defra’s policy statement on bovine TB control from December 2011  (also PDF)

Health Protection Agency information on bovine TB

Animal Health information on bovine TB

GALLAGHER, J. (2000). Tuberculosis in badgers; a review of the disease and its significance for other animals Research in Veterinary Science, 69 (3), 203-217 DOI: 10.1053/rvsc.2000.0422

de la Rua-Domenech, R. (2006). Human Mycobacterium bovis infection in the United Kingdom: Incidence, risks, control measures and review of the zoonotic aspects of bovine tuberculosis Tuberculosis, 86 (2), 77-109 DOI: 10.1016/


An unusual case of orf

July 18, 2011

Diseases don’t always behave exactly as we expect them too.  Sometimes, even when we think we’ve worked out most things about them, they can surprise us.

A case study published in Dermatology Online Journal – Orf parapoxvirus infection from a cat scratch by J Frandsen et al (see below for full ref) – is a nice example of this.

A Bit of Background

Electronmicrograph of orf virus

Orf (AKA ‘contagious pustular dermatitis’ or ‘ecythema contagiosum’)  is caused by a parapoxvirus infection.  (Parapoxviruses are double-stranded DNA viruses and other diseases caused by these viruses include bovine papular stomatitis and pseudocowpox).  The orf virus is found across the world and is carried by sheep and goats.  It is also zoonotic.

In sheep and goats the virus can cause disease at any time but generally causes the most problems in and just after the lambing season.  In infected animals it manifests as pustular, scabby lesions.  These scabs are full of virus.  A new animal becomes infected if it has damaged skin that comes into contact with the virus, usually via direct contact with an infected animal. 

We can become infected in exactly the same way and it is a known risk during the lambing season.  Luckily orf infection is generally self-limiting unless we/the animal are immunocompromised for some reason (e.g. already ill/taking immunosuppressant drugs etc.)

Sheep with orf scabs

However, transmission doesn’t always have to be via direct contact.  Transmission of the virus by fomites has also been reported including infection after contact with sheep fences or burrs in the sheep’s wool.

What’s interesting about this case report is that the sheep host is much further removed from the human case.

The Case Report

The authors of the paper report the case of a woman who presented herself to her ‘primary care physician’ (I’m guessing that’s the equivalent to my GP unless anyone else can tell me any differently) with an ulcerating blister in a region where she had been scratched by a stray kitten 4 weeks earlier.  She reported no contact with any sheep or goats and had not been in any fields where they were grazed but she did live near farmland with sheep on it.  She was treated with antibiotics but the lesion just got worse.

After being referred to specialist dermatologists she had a skin biopsy.  Under the microscope this biopsy was seen to have features that are characteristic of parapoxvirus infections – this included eosinophilic (pink staining) cytoplasmic (imagining a cell as a fried egg: in the egg white) inclusions for any budding histopathologists out there.  There were other differential diagnoses that could also fit this pattern, including milkers nodules, but the authors state that:

“Because milker’s nodules are smaller and less likely to ulcerate than orf, we assume our patient had orf “

The authors do point out that they couldn’t identify the specific viral type, however, what they had learnt from the biopsy was enough to allow them to prescribe topical treatment for the woman and the lesion healed up in 10 weeks.

What this means…

Now we can’t be totally sure that this case was caused by the orf virus but if it was that means that the kitten had presumably been wandering around a sheep farm, picked up the virus on its claws (possibly from scab material on the ground?) then trotted away from the farm and towards where this woman found it.  When it scratched the woman it effectively inoculated her with the virus and that is how it was able to get in. 

I would suspect that (prior to this case report at least) if you were a medic presented with this case, when a woman reports absolutely no contact with sheep, sheep pasture etc. that would move orf quite far down your differential diagnosis list.  This case reminds us that zoonotic diseases are not always transmitted the way we expect. 

They certainly keep medics and scientists on their toes!



With thanks to GrahamColm for the electron micrograph and Dnatheist for the sheep with orf images, both of which were licensed under Creative Commons Attribution-Share Alike unported 3.0 licence and with thanks to Evelyn Simak for the gorgeous photo of the lamb, licenced under Creative Commons Attribution-ShareAlike 2.0 generic licence.

Further information

Orf Infection in Sheep leaflet from the Moredun Research Institute

Information from the Health Protection Agency

Frandsen J, Enslow M, & Bowen AR (2011). Orf parapoxvirus infection from a cat scratch. Dermatology online journal, 17 (4) PMID: 21549084


A new zoonosis?

July 15, 2011

ResearchBlogging.orgIt’s been estimated that 3 out of every 4 emerging human diseases comes from animals and today has brought news of what has the potential to be another one. 


Scientists in California have published in PLoS Pathogens their research on: Cross-Species Transmission of a Novel Adenovirus Associated with a Fulminant Pneumonia Outbreak in a New World Monkey Colony (see below for the link)

The paper details an outbreak of disease in a New World titi monkey colony at the California National Primate Research Centre (CNPRC) in 2009.

In May of that year lots of the titi monkeys started to get sick – the symptoms were coughing, lethargy and signs of respiratory distress like tachypnoea (fast breathing) and abdominal breathing.   Gross pathology revealed the monkeys were getting pneumonia and in some cases hepatitis.  Of the monkeys that got sick 83% died or had to be put to sleep.

A figure from the paper showing clinical and epidemiological features of the infection.

(A) Map of the titi monkey cages situated in one quadrant of a building, showing the locations of asymptomatic, at-risk monkeys (brown or green), affected surviving monkeys (black), and monkeys who died from their illness (skeleton). 3 monkeys were moved into the building (arrows pointing down and to the left) and 4 monkeys out of the building (arrows pointing up and to the right) during the 3rd week of the outbreak. The upper left photograph shows an image of an adult male titi monkey and his infant. The upper right inset shows the location of the titi monkey cages relative to other rhesus monkey cages in the building. Asymptomatic monkeys with positive serum antibody titers to TMAdV 4 months after the outbreak are shown in green. (B) Epidemic curve of the outbreak, with the number of cases in blue and cumulative attack rate in red. (C) Anteroposterior chest radiograph of an affected titi monkey, showing bilateral basilar infiltrates and a prominent right middle lobe consolidation. (D) 1 – gross photograph of lungs at necropsy; the lungs failed to fully collapse upon opening the chest, and a single ~1.5 cm focus of dark red discoloration (hemorrhage) can be seen in the left caudal lobe. 2 – photomicrograph of H&E stained lung tissue showing a severe diffuse necrotizing bronchopneumonia characterized by the presence of hemorrhage and intranuclear inclusions (arrows). 3 – photomicrograph of H&E stained liver tissue showing a multifocal necrotizing hepatitis with numerous intranuclear inclusions (arrows). 4 – transmission electron micrograph of an affected lung alveolus (scale bar = 1 µm) filled with adenovirus-like particles (inset, scale bar = 0.1 µm).

Researchers took samples from the  sick and dead monkeys and tried to identify the cause of the disease.  One of the techniques they used was the ‘virochip’ which is a microarray containing ~19 000 probes derived from all of the viral species in GenBank (~2 500).

Typical microarray output

Basically the microarry works by having single stranded nucleotide ‘probe’ sequences bound to different areas of a solid base (e.g. in a grid format).  When a sample is added, nucleotide sequences complementary to the sequences on the microarray pair with them.  The microarry chip is washed, removing unbound sequences.  Fluorescence labelling of the sample nucleotide sequences allows researchers to see which of the probe sequences are now double stranded and the intensity of the fluorescence can be used to determine how strong the pairing is (effectively, what proportion of the bases in the sequence are paired).

The authors of this paper using this virochip in combination with their knowledge as to what groups of viruses cause pneumonia symptoms strongly suspected that the virus causing the outbreak was an adenovirus.

They then took the DNA sequences they had isolated from infected monkeys’ lungs, amplified a fragment of one of the genes and compared the sequence to other adenoviruses and found the viruses closest known relatives were an Old World vervet monkey adenovirus and the human species D adenoviruses.

They fully sequenced the virus and called it Titi Monkey Adenovirus (TMAdV).

They also did other cool work like growing it in a human cell line (although they couldn’t grow it in their monkey cell lines) and if you’re interested it’s definitely worth checking the paper out but what got me hooked on the story (other than the cute monkey pictures!) was the next bit…

One of the researchers reported becoming ill during the outbreak.  They suffered from a fever, chills, headaches and described it feeling like ‘a burning sensation in the lungs’.  Two of the researcher’s family members also had respiratory symptoms, although they were milder than the researcher’s.  The family members never had contact with the monkeys.  4 months after the oubtreak the researcher had neutralising antibodies against the virus in their serum and one of the family members had neutralising antibodies in their serum a year later.  None of the other researchers had any neutralising antibodies 4 months after the outbreak.  Interestingly they tested the serum from 81 random blood donors in the Western USA and found two individuals with weakly neutralising antibodies, suggesting they had also come into contact with the virus somehow.

But what do all these results mean?

The researchers suggest that the severity of the disease suggests that the monkeys were not the natural reservoir for the virus.  They don’t yet know what the reservoir is.

They also suggest that the virus spread from the monkeys to the researcher and not vice versa because:

  1. TMAdV’s closest relative is an Old World monkey adenovirus
  2. TMAdV can be picked up by PCR assays for human adenoviruses so if it was human in origin it would most likely have been identified before now
  3. GenBank contains loads more human adenoviruses than monkey viruses.  It is highly likely that there are a lot of primate adenoviruses we haven’t discovered yet.

but they do not rule out that it could have gone from the human to the monkeys.

A lot more work is now needed to learn more about the virus, its reservoir, and its potential to cross species barriers.

I will definitely be keeping an eye/ear out for more news of TMAdV…


 Single titi monkey:  Thanks to Tony Hisgett for releasing it under the Creative Commons Attribution 2.0 Generic Licence

DNA microarray: Thanks to Guillaume Paumier for releasing it under the Creative Commons Attribution-Share Alike 3.0 unported licence

Titi monkeys with tails intertwined: Thanks to Steven G Johnson for releasing it under the Creative Commons Attribution-Share Alike 3.0 unported licence


Wang, D. (2002). Microarray-based detection and genotyping of viral pathogens Proceedings of the National Academy of Sciences, 99 (24), 15687-15692 DOI: 10.1073/pnas.242579699

Chen, E., Yagi, S., Kelly, K., Mendoza, S., Maninger, N., Rosenthal, A., Spinner, A., Bales, K., Schnurr, D., Lerche, N., & Chiu, C. (2011). Cross-Species Transmission of a Novel Adenovirus Associated with a Fulminant Pneumonia Outbreak in a New World Monkey Colony PLoS Pathogens, 7 (7) DOI: 10.1371/journal.ppat.1002155