Posts Tagged ‘zoonosis’


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


Fish Pedicures and Zoonotic Diseases

July 10, 2012
As you can see the blog hiatus is over – it’s not that things have got a lot quieter (they haven’t), I’ve just missed blogging!  And what better way to get back into things than with a random anecdote…

When a friend asked if I would like a fish pedicure for my birthday my initial response was “Ewwww!”  It wasn’t at the thought of fish biting me per se (I’ve snorkelled and had wild fish do that – it’s not bad but it wasn’t something I found brilliantly therapeutic either). It was the thought that those fish had been nibbling on someone else’s feet before they nibbled on mine – surely that meant they could spread diseases to me?

Well having now had a look at what information is out there it turns out there aren’t many reported problems from these fish.   The Health Protection Agency in the UK produced a report called “Guidance on the management of the public health risks from fish pedicures”(PDF) that states:

On the basis of the evidence identified and the consensus view of experts, the risk of infection as a result of a fish pedicure is likely to be very low, but cannot be completely excluded.

The report also has a list of recommendations it says should further reduce the risk of disease transmission.

So maybe the pedicures are not such a bad idea then…

What I hadn’t considered, (and I really should have done), was that some of these fish could be being imported into the country already infected.

That’s what the scientists behind this letter in Emerging infectious Diseases found.

Large numbers of the toothless carp used in fish pedicures are imported weekly into the UK (generally from Indonesia and other countries in Asia) via Heathrow Airport.

In April last year there had been a disease outbreak among some imported fish and it turned out the bacteria killing them was most likely one called Streptococcus agalactiae.

To get an idea of how common it is for bacteria to be carried into the country by these fish, scientists from the Fish Health Inspectorate of the Centre for Environment, Fisheries & Aquaculture Science (that’s a mouthful and a half!) visited Heathrow Airport 5 times and sampled the fish being imported.

They found quite a range of bacteria on these fish and in their water, some of which did have the potential to infect people too. (Nice!)

The researchers say that these fish or the water they travel in could potentially be harmful to people, particularly those people with previously existing medical conditions like diabetes or who are immunosuppressed for some reason.  They do say however that if fish identified as disease-free were reared in controlled facilities this risk would probably be reduced so perhaps this is the way to go?

Another thing the researchers mention is that these controlled facilities should have “high standards of husbandry and welfare”.  I’m not aware of any studies looking at the welfare of these fish (please let me know if you know of one).  What we do know is that if the welfare of fish is bad then this can lead to poor fish health.  If the fish are unhealthy they are less able to fight off a pathogen (e.g. bacteria) so something that might ordinarily have caused no problems can instead go on to infect many fish and so multiply to really high numbers in the water, increasing the risk to anyone who puts their skin in the water.  (Not that protecting our own health is the only argument for making sure the welfare of these fish is good.)

So if the offer was made again for my next birthday (it’s in autumn – I am obviously not getting over-excited about it already…) would I take it up this year?

I don’t think so.  Not yet.  Not when so many of these fish are imported and we don’t fully know what they are carrying.  Just knowing there was a slight risk would mean I wasn’t very relaxed during my pedicure! :S


Released under a creative commons licence by jenny8lee


Verner-Jeffreys DW, Baker-Austin C, Pond MJ, Rimmer GSE, Kerr R, Stone D, Griffin R, White P, Stinton N, Denham K, Leigh J, Jones N, Longshaw M, & Feist SW (2012). Zoonotic Disease Pathogens in Fish Used for Pedicure Emerging Infectious Diseases DOI: 10.3201/eid1806.111782



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/


Using a parasite as a vaccine…

December 6, 2011

A group of researchers (see reference below) have been looking at a very interesting new method of vaccine delivery: using trypanosomes.

T. (megatrypanum) theileri  is found infecting cattle worldwide.  It is transmitted by flies and gains entry to the animal either through broken skin or via mucous membranes and once the animal is infected it tends to carry low numbers (~100 organisms/ml) of trypanosomes for the rest of its life. Although there is some evidence suggesting that infection with this organism has the potential to cause a drop in milk yield in some cattle the authors state that the “ubiquity of infection with this organism in cattle herds suggests that it has no significant impact on health or productivity in healthy animals”. 

Because of this apparent lack of pathogenicity and because the parasites persist for such a long time in the host the researchers thought they could potentially use the trypanosome to deliver antigens (molecules that will trigger an immune response) from other, more pathogenic organisms to the cattle, so effectively using it like a vaccine.

The researchers tested this by genetically modifying the trypanosome to produce Bd37 – an antigen from Babesia divergens (which causes a disease called “redwater fever” in cattle).  They engineered 3 different groups of trypanosomes.  The first expressed the Bd37 within themselves (intracellularly), the second expressed the Bd37 on their surface (extracellularly) and the third actively pumped out the Bd37 (secretory).  They then infected cattle with the trypanosomes.  After inoculation they took blood samples at regular timepoints to look for any antibody response.

All of the cattle became infected with the trypanosomes and they stayed infected for the entirety of the 12 week period of the trial.  The number of cattle that started to produce antibodies against Bd37 after infection were:

Intracellular group: 4/6

Extracellular group: 3/6

Secretory group: 5/5

The researchers also showed that those in the secretory group had significantly higher antibody levels than the other two groups.  The antibody levels of all animals that produced them continued to increase for 60 days and remained high for at least another 24 days (which was as long as they were measured for).

Finally the researchers compared the antibody levels achieved with the trypanosome method of delivery with a traditional vaccine delivery and they found that the antibody levels were “equivalent”.  (So this trypanosome delivery method is effectively providing as much protection as the traditional vaccine.)

If this method does not produce better antibody production than a standard vaccine why would you go to the bother of engineering these trypanosomes?  Well the researchers say that this method of delivery has several advantages:

  1. As trypanosomes can cross mucous membranes there is the possibility for vaccine delivery
  2. As the trypanosomes infect the host for a very long time, potentially for the rest of its life, they could potentially stimulate an immune response against a target antigen for this length of time, so providing immunity for a longer period than a traditional vaccine

Another advantage is that T. theileri is already non-disease causing in cattle.  Some vaccine delivery systems use attenuated bacteria such as Salmonella but these bacteria have the potential to revert to being disease-causing.  As T. theileri doesn’t cause disease this isn’t something the researchers need to worry about.

So all of this research is very promising and suggests that with more research trypanosomes could be used in the future to protect cattle from disease.

But I’ve tagged this as a ‘zoonosis’ post and so far only talked about cattle diseases.  What relevance does this have to human health? 

Blood smear from patient with African trypanosomiasis. Image taken by the US Centre for Disease Control and Prevention.

Human African Trypanosomiasis, also known as sleeping sickness is a fatal disease that occurs in sub-Saharan Africa.  It is caused by the trypanosomes Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense.  These trypanosomes are spread from person to person by the tsetse fly (it bites infected Person A, takes a blood meal which contains trypanosomes, flies off and then bites uninfected Person B, infecting them as it does so).  The main reservoir for T. brucei gambiense is the human population however cattle are an extremely important reservoir for T. brucei rhodesiense.

T. brucei rhodesiense (as you can tell by the name) is closely related to another trypanosome that infects cattle T. brucei brucei.  This trypanosome only infects cattle – it can’t infect humans because a substance called ApoL1 found in human serum kills it.

The researchers speculate (and it is currently only speculation) that if T. theileri was used to deliver a modified form of ApoL1 that killed T. brucei rhodesiense  this vaccine system could be used to dramatically reduce the cattle reservoir of this dangerous parasite.  There is a HUGE amount of work that needs to be done before this can even be trialled but it has the potential to make a great impact on human health. 

Watch this space!


The trypanosome image came from the paper (see below).

The blood smear image is available on Wikimedia Commons here

Further Reading

WHO information on Human African Trypanosomiasis

Mott, G., Wilson, R., Fernando, A., Robinson, A., MacGregor, P., Kennedy, D., Schaap, D., Matthews, J., & Matthews, K. (2011). Targeting Cattle-Borne Zoonoses and Cattle Pathogens Using a Novel Trypanosomatid-Based Delivery System PLoS Pathogens, 7 (10) DOI: 10.1371/journal.ppat.1002340



Darn it!

July 21, 2011

Not only is there a paper out discussing the characterisation of the latest E.coli bug (see posts here, here and here) but the use of badger culling to prevent bovine tuberculosis cases in cattle is also back in the news – all stuff I want to blog about but I MIGHT ACTUALLY HAVE SOME RESULTS!!! (only taken 9 months…) so I hope you’ll understand if posts on these topics are somewhat delayed!

Also – my blogroll is still out of date but thankfully those that have moved have got links on their old pages directing the reader to their new pages. 

I’ll post on twitter as usual when the next post is up (or you can subscribe/add the RSS feed).

*skips back to lab to check on experiment*