̽��ֱ�� of Cambridge - animal health

Scientists identify genes that make humans and Labradors more likely to become obese

jg533 — Thu, 06 Mar 2025 19:03:04 +0000

Researchers studying British Labrador retrievers have identified multiple genes associated with canine obesity and shown that these genes are also associated with obesity in humans.

̽��ֱ��dog gene found to be most strongly associated with obesity in Labradors is called DENND1B. Humans also carry the DENND1B gene, and the researchers found that this gene is also linked with obesity in people.

DENND1B was found to directly affect a brain pathway responsible for regulating the energy balance in the body, called the leptin melanocortin pathway.

An additional four genes associated with canine obesity, but which exert a smaller effect than DENND1B, were also mapped directly onto human genes.

“These genes are not immediately obvious targets for weight-loss drugs, because they control other key biological processes in the body that should not be interfered with.

But the results emphasise the importance of fundamental brain pathways in controlling appetite and body weight,” said Alyce McClellan in the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience, and joint first author of the report.

“We found that dogs at high genetic risk of obesity were more interested in food,” said Natalie Wallis in the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience, and joint first author of the report.

She added: “We measured how much dogs pestered their owners for food and whether they were fussy eaters. Dogs at high genetic risk of obesity showed signs of having higher appetite, as has also been shown for people at high genetic risk of obesity.”

̽��ֱ��study found that owners who strictly controlled their dogs’ diet and exercise managed to prevent even those with high genetic risk from becoming obese - but much more attention and effort was required.

Similarly, people at high genetic risk of developing obesity will not necessarily become obese, if they follow a strict diet and exercise regime - but they are more prone to weight gain.

As with human obesity, no single gene determined whether the dogs were prone to obesity; the net effect of multiple genetic variants determined whether dogs were at high or low risk.

̽��ֱ��results were published on 6 March in the journal 'Science'.

“Studying the dogs showed us something really powerful: owners of slim dogs are not morally superior. ̽��ֱ��same is true of slim people. If you have a high genetic risk of obesity, then when there’s lots of food available you’re prone to overeating and gaining weight unless you put a huge effort into not doing so,” said Dr Eleanor Raffan, a researcher in the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience who led the study.

She added: “By studying dogs we could measure their desire for food separately to the control owners exerted over their dog’s diet and exercise. In human studies, it’s harder to study how genetically driven appetite requires greater willpower to remain slim, as both are affecting the one person.”

̽��ֱ��current human obesity epidemic is mirrored by an obesity epidemic in dogs. About 40-60% of pet dogs are overweight or obese, which can lead to a range of health problems.

Dogs are a good model for studying human obesity: they develop obesity through similar environmental influences as humans, and because dogs within any given breed have a high degree of genetic similarity, their genes can be more easily linked to disease.

To get their results, the researchers recruited owners with pet dogs in which they measured body fat, scored ‘greediness’, and took a saliva sample for DNA. Then they analysed the genetics of each dog. By comparing the obesity status of the dog to its DNA, they could identify the genes linked to canine obesity.
Dogs carrying the genetic variant most associated with obesity, DENND1B, had around 8% more body fat than those without it.

̽��ֱ��researchers then examined whether the genes they identified were relevant to human obesity. They looked at both large population-based studies, and at cohorts of patients with severe, early onset obesity where single genetic changes are suspected to cause the weight gain.

̽��ֱ��researchers say owners can keep their dogs distracted from constant hunger by spreading out each daily food ration, for example by using puzzle feeders or scattering the food around the garden so it takes longer to eat, or by choosing a more satisfying nutrient composition for their pets.

Raffan said: “This work shows how similar dogs are to humans genetically. Studying the dogs meant we had reason to focus on this particular gene, which has led to a big advance in understanding how our own brain controls our eating behaviour and energy use.”

̽��ֱ��research was funded by Wellcome, the BBSRC, Dogs Trust, Morris Animal Foundation, MRC, France Genomique consortium, European Genomic Institute for Diabetes, French National Center for Precision Diabetic Medicine, Royal Society, NIHR, Botnar Foundation, Bernard Wolfe Health Neuroscience Endowment, Leducq Fondation, Kennel Club Charitable Trust.

Reference
Wallis, N J et al: ‘Canine genome-wide association study identifies DENND1B as an obesity gene in dogs and humans.’ Science, March 2025. DOI: 10.1126/science.ads2145

Researchers at the ̽��ֱ�� of Cambridge have discovered genes linked to obesity in both Labradors and humans. They say the effects can be over-ridden with a strict diet and exercise regime.

Dogs at high genetic risk of obesity showed signs of having higher appetite, as has also been shown for people at high genetic risk of obesity.

Natalie Wallis

James Barker on Unsplash

Labrador licking nose

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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AI algorithm accurately detects heart disease in dogs

sc604 — Tue, 29 Oct 2024 02:20:22 +0000

̽��ֱ��research team, led by the ̽��ֱ�� of Cambridge, adapted an algorithm originally designed for humans and found it could automatically detect and grade heart murmurs in dogs, based on audio recordings from digital stethoscopes. In tests, the algorithm detected heart murmurs with a sensitivity of 90%, a similar accuracy to expert cardiologists.

Heart murmurs are a key indicator of mitral valve disease, the most common heart condition in adult dogs. Roughly one in 30 dogs seen by a veterinarian has a heart murmur, although the prevalence is higher in small breed dogs and older dogs.

Since mitral valve disease and other heart conditions are so common in dogs, early detection is crucial as timely medication can extend their lives. ̽��ֱ��technology developed by the Cambridge team could offer an affordable and effective screening tool for primary care veterinarians, and improve quality of life for dogs. ̽��ֱ��results are reported in the Journal of Veterinary Internal Medicine.

“Heart disease in humans is a huge health issue, but in dogs it’s an even bigger problem,” said first author Dr Andrew McDonald from Cambridge’s Department of Engineering. “Most smaller dog breeds will have heart disease when they get older, but obviously dogs can’t communicate in the same way that humans can, so it’s up to primary care vets to detect heart disease early enough so it can be treated.”

Professor Anurag Agarwal, who led the research, is a specialist in acoustics and bioengineering. “As far as we’re aware, there are no existing databases of heart sounds in dogs, which is why we started out with a database of heart sounds in humans,” he said. “Mammalian hearts are fairly similar, and when things go wrong, they tend to go wrong in similar ways.”

̽��ֱ��researchers started with a database of heart sounds from about 1000 human patients and developed a machine learning algorithm to replicate whether a heart murmur had been detected by a cardiologist. They then adapted the algorithm so it could be used with heart sounds from dogs.

̽��ֱ��researchers gathered data from almost 800 dogs who were undergoing routine heart examination at four veterinary specialist centres in the UK. All dogs received a full physical examination and heart scan (echocardiogram) by a cardiologist to grade any heart murmurs and identify cardiac disease, and heart sounds were recorded using an electronic stethoscope. By an order of magnitude, this is the largest dataset of dog heart sounds ever created.

“Mitral valve disease mainly affects smaller dogs, but to test and improve our algorithm, we wanted to get data from dogs of all shapes, sizes and ages,” said co-author Professor Jose Novo Matos from Cambridge’s Department of Veterinary Medicine, a specialist in small animal cardiology. “ ̽��ֱ��more data we have to train it, the more useful our algorithm will be, both for vets and for dog owners.”

̽��ֱ��researchers fine-tuned the algorithm so it could both detect and grade heart murmurs based on the audio recordings, and differentiate between murmurs associated with mild disease and those reflecting advanced heart disease that required further treatment.

“Grading a heart murmur and determining whether the heart disease needs treatment requires a lot of experience, referral to a veterinary cardiologist, and expensive specialised heart scans,” said Novo Matos. “We want to empower general practitioners to detect heart disease and assess its severity to help owners make the best decisions for their dogs.”

Analysis of the algorithm’s performance found it agreed with the cardiologist’s assessment in over half of cases, and in 90% of cases, it was within a single grade of the cardiologist’s assessment. ̽��ֱ��researchers say this is a promising result, as it is common for there to be significant variability in how different vets grade heart murmurs.

“ ̽��ֱ��grade of heart murmur is a useful differentiator for determining next steps and treatments, and we’ve automated that process,” said McDonald. “For vets and nurses without as much stethoscope skill, and even those who are incredibly skilled with a stethoscope, we believe this algorithm could be a highly valuable tool.”

In humans with valve disease, the only treatment is surgery, but for dogs, effective medication is available. “Knowing when to medicate is so important, in order to give dogs the best quality of life possible for as long as possible,” said Agarwal. “We want to empower vets to help make those decisions.”

“So many people talk about AI as a threat to jobs, but for me, I see it as a tool that will make me a better cardiologist,” said Novo Matos. “We can’t perform heart scans on every dog in this country – we just don’t have enough time or specialists to screen every dog with a murmur. But tools like these could help vets and owners, so we can quickly identify those dogs who are most in need of treatment.”

̽��ֱ��research was supported in part by the Kennel Club Charitable Trust, the Medical Research Council, and Emmanuel College Cambridge.

Reference:
Andrew McDonald et al. ‘A machine learning algorithm to grade canine heart murmurs and stage preclinical myxomatous mitral valve disease.’ Journal of Veterinary Internal Medicine (2024). DOI: 10.1111/jvim.17224

Researchers have developed a machine learning algorithm to accurately detect heart murmurs in dogs, one of the main indicators of cardiac disease, which affects a large proportion of some smaller breeds such as King Charles Spaniels.

Jacqueline Garget

Huxley, a healthy volunteer Havanese, undergoes a physical examination at the Queen's Veterinary School Hospital, Cambridge.

Yes

New genetic test will eliminate a form of inherited blindness in dogs

jg533 — Sun, 21 Jul 2024 23:38:11 +0000

Progressive retinal atrophy (PRA) is a group of inherited diseases that causes progressive degeneration of the light sensitive cells at the back of the eye. Dogs with PRA have normal sight at birth, but by the age of four or five they will be totally blind. There is no treatment.

Now a team led by the ̽��ֱ�� of Cambridge has identified the genetic mutation that causes PRA in English Shepherd Dogs, and developed a DNA test for it. By identifying dogs carrying the disease before their eyesight starts to fail, this provides a tool to guide breeding decisions so the disease is not passed on to puppies.

Owners usually don’t realise their dog has PRA until it is middle-aged, by which time it might have bred, and passed on the faulty gene to its puppies. This has made it a difficult disease to control.

̽��ֱ��new discovery means that progressive retinal atrophy can now be completely eliminated from the English Shepherd Dog population very quickly.

̽��ֱ��results are published today in the journal Genes.

“Once the dog’s eyesight starts to fail there’s no treatment – it will end up totally blind,” said Katherine Stanbury, a researcher in the ̽��ֱ�� of Cambridge’s Department of Veterinary Medicine and first author of the report.

She added: “Now we have a DNA test, there’s no reason why another English Shepherd Dog ever needs to be born with this form of progressive retinal atrophy – it gives breeders a way of totally eliminating the disease.”

̽��ֱ��genetic mutation identified by the team is recessive, which means it only causes blindness if the English Shepherd Dog inherits two copies of it. If the dog only has one copy this makes it a carrier – it will not develop PRA but can pass the mutation on to its puppies. If two carriers are bred together, about one in four of the puppies will be affected with PRA.

Dogs breeds are very inbred, so many individuals are related – giving them a much higher chance of being affected by recessive diseases than humans.

̽��ֱ��team began the research after being contacted by a distraught owner of an English Shepherd Dog that had been recently diagnosed with PRA. ̽��ֱ��dog had been working as a search and rescue dog but had to retire due to visual deterioration that has resulted in total blindness. ̽��ֱ��researchers put out a call for DNA samples from other owners or breeders of this breed, and received samples from six English Shepherds with PRA and twenty without it. This was enough for them to pinpoint the genetic mutation responsible for PRA using whole genome sequencing.

̽��ֱ��team offers a commercial canine genetic testing service providing DNA tests to dog breeders to help them avoid breeding dogs that will develop inherited diseases. As part of this they will now offer a DNA test for Progressive Retinal Atrophy in English Shepherds. Anyone can buy a testing kit, costing just £48, to take a swab from inside their dog’s mouth and send it back for testing.

“An owner won't necessarily notice their dog has got anything wrong with its eyes until it starts bumping into the furniture. Unlike humans who will speak up if their sight isn’t right, dogs just have to get on with things,” said Dr Cathryn Mellersh in the ̽��ֱ�� of Cambridge’s Department of Veterinary Medicine, senior author of the report.

She added: “For the price of a decent bag of dog food people can now have their English Shepherd tested for Progressive Retinal Atrophy prior to breeding. It’s about prevention, rather than a cure, and it means a huge amount to the people who breed these dogs. They no longer need to worry about whether the puppies are going to be healthy or are going to develop this horrible disease in a few years’ time.”

̽��ֱ��English Shepherd is a breed of herding dog popular in the United States and is closely related to the Border Collie.

̽��ֱ��new discovery is the thirty-third genetic mutation causing an inherited disease in dogs that the team has found – twenty-three of which cause eye diseases. They say that the health and wellbeing of many dogs has been compromised because of how they have been bred by humans.

PRA occurs in many dog breeds including the English Shepherd Dog. And it is similar to a disease called retinitis pigmentosa in humans, which also causes blindness. ̽��ֱ��researchers say that their work with dogs could shed light on the human version of the disease and potentially identify targets for gene therapy in the future.

̽��ֱ��work was carried out in collaboration with Wisdom Panel, Mars Petcare, as part of the Consortium to Research Inherited Eye Diseases in Dogs (CRIEDD), with funding from the Dog’s Trust and the Kennel Club Charitable Trust.

Reference: Stanbury, K. et al, ‘Exonic SINE insertion in FAM161A is associated with autosomal recessive progressive retinal atrophy in the English Shepherd.’ July 2024.

FIND OUT MORE AND SUPPORT THIS RESEARCH

Cambridge scientists have identified the genetic mutation that causes progressive retinal atrophy in English Shepherd Dogs, which results in incurable blindness, and developed a genetic test to help eliminate the disease from future generations of the breed.

Now we have a DNA test, there’s no reason why another English Shepherd Dog ever needs to be born with this form of progressive retinal atrophy – it gives breeders a way of totally eliminating the disease.

Katherine Stanbury

English Shepherd puppy

Yes

Genetic mutation in a quarter of all Labradors hard-wires them for obesity

jg533 — Wed, 06 Mar 2024 19:06:36 +0000

This obesity-driving combination means that dog owners must be particularly strict with feeding and exercising their Labradors to keep them slim.

̽��ֱ��mutation is in a gene called POMC, which plays a critical role in hunger and energy use.

Around 25% of Labradors and 66% of flatcoated retriever dogs have the POMC mutation, which researchers previously showed causes increased interest in food and risk of obesity.

̽��ֱ��new study reveals how the mutation profoundly changes the way Labradors and flatcoated retrievers behave around food. It found that although they don’t need to eat more to feel full, they are hungrier in between meals.

In addition, dogs with the POMC mutation were found to use around 25% less energy at rest than dogs without it, meaning they don’t need to consume as many calories to maintain a healthy body weight.

“We found that a mutation in the POMC gene seems to make dogs hungrier. Affected dogs tend to overeat because they get hungry between meals more quickly than dogs without the mutation,” said Dr Eleanor Raffan, a researcher in the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience who led the study.

She added: “All owners of Labradors and flatcoated retrievers need to watch what they’re feeding these highly food-motivated dogs, to keep them a healthy weight. But dogs with this genetic mutation face a double whammy: they not only want to eat more, but also need fewer calories because they’re not burning them off as fast.”

̽��ֱ��POMC mutation was found to alter a pathway in the dogs’ brains associated with body weight regulation. ̽��ֱ��mutation triggers a starvation signal that tells their body to increase food intake and conserve energy, despite this being unnecessary.

̽��ֱ��results are published today in the journal Science Advances.

Raffan said: “People are often rude about the owners of fat dogs, blaming them for not properly managing their dogs’ diet and exercise. But we’ve shown that Labradors with this genetic mutation are looking for food all the time, trying to increase their energy intake. It’s very difficult to keep these dogs slim, but it can be done.”

̽��ֱ��researchers say owners can keep their retrievers distracted from this constant hunger by spreading out each daily food ration, for example by using puzzle feeders or scattering the food around the garden so it takes longer to eat.

In the study, 87 adult pet Labrador dogs - all a healthy weight or moderately overweight - took part in several tests including the ‘sausage in a box’ test.

First, the dogs were given a can of dogfood every 20 minutes until they chose not to eat any more. All ate huge amounts of food, but the dogs with the POMC mutation didn’t eat more than those without it. This showed that they all feel full with a similar amount of food.

Next, on a different day, the dogs were fed a standard amount of breakfast. Exactly three hours later they were offered a sausage in a box and their behaviour was recorded. ̽��ֱ��box was made of clear plastic with a perforated lid, so the dogs could see and smell the sausage, but couldn’t eat it.

̽��ֱ��researchers found that dogs with the POMC mutation tried significantly harder to get the sausage from the box than dogs without it, indicating greater hunger.

̽��ֱ��dogs were then allowed to sleep in a special chamber that measured the gases they breathed out. This revealed that dogs with the POMC mutation burn around 25% fewer calories than dogs without it.

̽��ֱ��POMC gene and the brain pathway it affects are similar in dogs and humans. ̽��ֱ��new findings are consistent with reports of extreme hunger in humans with POMC mutations, who tend to become obese at an early age and develop a host of clinical problems as a result.

Drugs currently in development for human obesity, underactive sexual desire and certain skin conditions target this brain pathway, so understanding it fully is important.

A mutation in the POMC gene in dogs prevents production of two chemical messengers in the dog brain, beta-melanocyte stimulating hormone (β-MSH) and beta-endorphin, but does not affect production of a third, alpha-melanocyte stimulating hormone (α-MSH).

Further laboratory studies by the team suggest that β-MSH and beta-endorphin are important in determining hunger and moderating energy use, and their role is independent of the presence of α-MSH. This challenges the previous belief, based on research in rats, that early onset human obesity due to POMC mutations is caused only by a lack of α-MSH. Rats don’t produce beta-melanocyte stimulating hormone, but humans and dogs produce both α- and β-MSH.

̽��ֱ��research was funded by ̽��ֱ��Dogs Trust and Wellcome.

Reference: Dittmann, M T et al: ‘Low resting metabolic rate and increased hunger due to β-MSH and β-endorphin deletion in a canine model.’ Science Advances, March 2024. DOI: 10.1126/sciadv.adj3823

New research finds around a quarter of Labrador retriever dogs face a double-whammy of feeling hungry all the time and burning fewer calories due to a genetic mutation.

Labradors with this genetic mutation are looking for food all the time, trying to increase their energy intake. It’s very difficult to keep these dogs slim, but it can be done.

Eleanor Raffan

A quarter of Labradors are hard-wired for obesity

Jane Goodall

Labrador retriever dog

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Evolution of two contagious cancers affecting Tasmanian devils underlines unpredictability of disease threat

cg605 — Thu, 20 Apr 2023 18:00:01 +0000

Transmissible cancers, which occur only rarely in the animal kingdom, are spread by the transfer of living cancer cells. In the case of Tasmanian devils, the cells are transferred through biting – a behaviour that is common in devils especially in fights over mates and food.

Tasmanian devils are susceptible to two fatal transmissible cancers called devil facial tumour 1 (DFT1) and devil facial tumour 2 (DFT2) that have caused rapid population decline in recent decades. ̽��ֱ��two cancers both manifest with disfiguring facial tumours.

In a new study, ̽��ֱ�� of Cambridge researchers, together with a global team of scientists from Europe, Australia and the United States, mapped the emergence and mutations of DFT1 and DFT2 and characterised these cancers’ ongoing evolution. ̽��ֱ��findings underline the continued threat that transmissible cancers pose to Tasmanian devils.

̽��ֱ��results are published today in the journal Science.

“ ̽��ֱ��incredible fact that Tasmanian devils have not one, but two, transmissible cancers, makes it possible to compare their evolution, and this gives us new insights into the key mechanisms involved,” said lead author Elizabeth Murchison, Professor of Comparative Oncology and Genetics at the Department of Veterinary Medicine, ̽��ֱ�� of Cambridge.

“By looking at the mutations that have accumulated in these cancers’ DNA, we can trace the origins and evolution of these diseases. Our results show that the two cancers arose through similar processes and that both have striking signals of ongoing evolution. It is difficult to predict how this continued cancer evolution will impact devils.”

̽��ֱ��researchers created an improved ‘reference genome’ – essentially a map of the entire DNA sequence – of the Tasmanian devil and compared this to DNA taken from 119 DFT1 and DFT2 tumours. DFT1 was first observed in 1996 in Tasmania’s northeast and is now widespread throughout Tasmania. DFT2, on the other hand, was first observed in 2014 and remains confined to a small area in Tasmania’s southeast. ̽��ֱ��scientists identified mutations in the tumours and used these to build ‘family trees’ of how the two cancers had each independently arisen and evolved over time.

By tracking mutations the researchers discovered that DFT2 acquired mutations about three times faster than DFT1. As mutations usually occur during cell division, the most likely explanation is that DFT2 is a faster growing cancer than DFT1, say the researchers, underlining the importance of DFT2 as a threat.

“DFT2 is still not widespread in the devil population, and very little is known about it. We were really startled to see just how quickly it was mutating, alerting us to what could be a very unpredictable threat to the devils in the long term,” said Maximilian Stammnitz, first author of the study.

̽��ֱ��team found that DFT1 arose in the 1980s, up to 14 years before it was first observed, whereas DFT2 emerged between 2009 and 2012, only shortly before it was detected.

Mapping the mutations revealed that DFT1 underwent an explosive transmission event shortly after it emerged. This involved a single infected devil transmitting its tumour to at least six recipient devils.

DFT1 has now spread throughout almost the entire devil population and has recently been reported in the far northwest of Tasmania, one of the few remaining disease-free regions of the state.

Researchers also identified for the first time an instance of DFT1 transmission between a mother and the young in her pouch. Additionally, they found that the incubation period – the time between infection and the emergence of symptoms – can in some cases be a year or more. These findings have important implications for conservation scientists working to protect the species.

“I come from Tasmania and love Tasmanian devils – they have a special place in my heart,” said Murchison. “Transmissible cancers pose an unprecedented and unpredictable threat to Tasmanian devils. This research highlights the continuing importance of monitoring and conservation programmes. It also gives us new insights into the evolutionary mechanisms operating in cancer more broadly, including in human cancers.”

̽��ֱ��research was funded by Wellcome, the Gates Cambridge Trust and Eric Guiler Tasmanian Devil Research Grants from the ̽��ֱ�� of Tasmania Foundation.

Reference: M. R. Stammnitz et al. ̽��ֱ��evolution of two transmissible cancers in Tasmanian devils, Science, DOI: 10.1126/science.abq6453

Scientists have traced the family trees of two transmissible cancers that affect Tasmanian devils and have pinpointed mutations which may drive growth of deadly diseases.

Transmissible cancers pose an unprecedented and unpredictable threat to Tasmanian devils.

Professor Elizabeth Murchison

Max Stammnitz

Tasmanian Devil

̽��ֱ��text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

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Researchers design AI system to assess pain levels in sheep

sc604 — Wed, 31 May 2017 23:02:29 +0000

̽��ֱ��researchers have developed an AI system which uses five different facial expressions to recognise whether a sheep is in pain, and estimate the severity of that pain. ̽��ֱ��results could be used to improve sheep welfare, and could be applied to other types of animals, such as rodents used in animal research, rabbits or horses.

Building on earlier work which teaches computers to recognise emotions and expressions in human faces, the system is able to detect the distinct parts of a sheep’s face and compare it with a standardised measurement tool developed by veterinarians for diagnosing pain. Their results will be presented today (1 June) at the 12th IEEE International Conference on Automatic Face and Gesture Recognition in Washington, DC.

Severe pain in sheep is associated with conditions such as foot rot, an extremely painful and contagious condition which causes the foot to rot away; or mastitis, an inflammation of the udder in ewes caused by injury or bacterial infection. Both of these conditions are common in large flocks, and early detection will lead to faster treatment and pain relief. Reliable and efficient pain assessment would also help with early diagnosis.

As is common with most animals, facial expressions in sheep are used to assess pain. In 2016, Dr Krista McLennan, a former postdoctoral researcher at the ̽��ֱ�� of Cambridge who is now a lecturer in animal behaviour at the ̽��ֱ�� of Chester, developed the Sheep Pain Facial Expression Scale (SPFES). ̽��ֱ��SPFES is a tool to measure pain levels based on facial expressions of sheep, and has been shown to recognise pain with high accuracy. However, training people to use the tool can be time-consuming and individual bias can lead to inconsistent scores.

In order to make the process of pain detection more accurate, the Cambridge researchers behind the current study used the SPFES as the basis of an AI system which uses machine learning techniques to estimate pain levels in sheep. Professor Peter Robinson, who led the research, normally focuses on teaching computers to recognise emotions in human faces, but a meeting with Dr McLennan got him interested in exploring whether a similar system could be developed for animals.

“There’s been much more study over the years with people,” said Robinson, of Cambridge’s Computer Laboratory. “But a lot of the earlier work on the faces of animals was actually done by Darwin, who argued that all humans and many animals show emotion through remarkably similar behaviours, so we thought there would likely be crossover between animals and our work in human faces.”

According to the SPFES, when a sheep is in pain, there are five main things which happen to their faces: their eyes narrow, their cheeks tighten, their ears fold forwards, their lips pull down and back, and their nostrils change from a U shape to a V shape. ̽��ֱ��SPFES then ranks these characteristics on a scale of one to 10 to measure the severity of the pain.

“ ̽��ֱ��interesting part is that you can see a clear analogy between these actions in the sheep’s faces and similar facial actions in humans when they are in pain – there is a similarity in terms of the muscles in their faces and in our faces,” said co-author Dr Marwa Mahmoud, a postdoctoral researcher in Robinson’s group. “However, it is difficult to ‘normalise’ a sheep’s face in a machine learning model. A sheep’s face is totally different in profile than looking straight on, and you can’t really tell a sheep how to pose.”

To train the model, the Cambridge researchers used a small dataset consisting of approximately 500 photographs of sheep, which had been gathered by veterinarians in the course of providing treatment. Yiting Lu, a Cambridge undergraduate in Engineering and co-author on the paper, trained the model by labelling the different parts of the sheep’s faces on each photograph and ranking their pain levels according to SPFES.

Early tests of the model showed that it was able to estimate pain levels with about 80% degree of accuracy, which means that the system is learning. While the results with still photographs have been successful, in order to make the system more robust, they require much larger datasets.

̽��ֱ��next plans for the system are to train it to detect and recognise sheep faces from moving images, and to train it to work when the sheep is in profile or not looking directly at the camera. Robinson says that if they are able to train the system well enough, a camera could be positioned at a water trough or other place where sheep congregate, and the system would be able to recognise any sheep which were in pain. ̽��ֱ��farmer would then be able to retrieve the affected sheep from the field and get it the necessary medical attention.

“I do a lot of walking in the countryside, and after working on this project, I now often find myself stopping to talk to the sheep and make sure they’re happy,” said Robinson.

Reference
Yuting Lu, Marwa Mahmoud and Peter Robinson. ‘Estimating sheep pain level using facial action unit detection.’ Paper presented to the IEEE International Conference on Automatic Face and Gesture Recognition, Washington, DC. 30 May – 3 June, 2017. http://www.fg2017.org/.

Inset image: Left: Localised facial landmarks; Right: Normalised sheep face marked with feature bounding boxes.

An artificial intelligence system designed by researchers at the ̽��ֱ�� of Cambridge is able to detect pain levels in sheep, which could aid in early diagnosis and treatment of common, but painful, conditions in animals.

You can see a clear analogy between these actions in the sheep’s faces and similar facial actions in humans when they are in pain.

Marwa Mahmoud

Sheep

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

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Opinion: How to save inbred, short-faced dogs such as pugs and bulldogs from poor health

Anonymous — Tue, 02 Aug 2016 14:23:06 +0000

Short-faced dogs such as pugs, bulldogs (known as English bulldogs in the US) and French bulldogs are among the cutest pets out there – they’re the very reverse of the wolves they descended from. Over the last few years these breeds have become increasingly common, partly thanks to advertising and their popularity among celebrities. In fact all three breeds are now in Britain’s top ten favourite dogs.

But these dogs are the result of an amazing transformation in appearance and temperament caused by selective breeding, which has come at quite a cost to the dogs' health. Around half of them have breathing problems that sometimes lead to overheating, exercise intolerance and sleep apnoea. Their large heads and narrow pelvises also cause problems in giving birth (forcing Caesarean sections for many if not most) and their skin folds can become infected. Their exposed eyes are also vulnerable to damage, with about 15% suffering prolapsed third eyelids and many having other types of eye damage. Quite a number of dogs in several of the breeds also succumb to back or hip problems.

So research geneticists have started to look at ways to reduce the intrinsic health problems of these breeds. A recent investigation of genetic variation in bulldogs showed that all the individuals examined had little genetic diversity in either paternal or maternal lines. ̽��ֱ��same was true for the diversity of some types of immune system genes, so that the ability of these bulldogs to respond to pathogens may be reduced, which may potentially also be connected to common allergies in this breed. ̽��ֱ��authors argued that the breed’s health could only be restored by breeding dogs with other breeds, rather than preserving the breed in its current closed state.

With colleagues including Jane Ladlow, Lajos Kalmar and Nai-chieh Liu, I have been doing both genetic and clinical analyses of bulldogs and other short-faced breeds. Working with breeders of bulldogs, we investigated the respiratory distress that many of these dogs suffer from. We started by developing a computer algorithm to interpret breathing traces taken from dogs at rest, allowing us to objectively identify the disease and quantify variation between individuals. This analysis, together with collection of DNA samples from the studied dogs, opened the way for accurate genetic analyses of the respiratory disease. On the way, we also gained information on the genetic health of the breeds we studied as a whole.

Our findings agree with those of the new study in suggesting that the best way of breeding back to a less extreme skull shape would be to introduce dogs from outside the current breed registers. This is likely to be true of many other aspects of conformation and temperament. And we would agree that the extreme changes in appearance (such as the excessive skin rolls in these breeds) do account for many of their disease problems.

An alternative to outbreeding?

Fortunately not all short-faced dogs suffer from the respiratory disorder and although our research is not yet complete, we now have pretty strong evidence that there are still multiple genetic variations between those that do and those that don’t. But we do not know whether this is also true for other aspects of conformation and appearance-related conditions.

A bulldog being assessed by respiratory trace recording in a barometric chamber. Traces from another dog on the right. Author provided

We believe that the swiftest way to remove these diseases would be to outbreed to a dog type that does not have the features that cause the health problems typical of these breeds.

Over the last few years groups such as the (now disbanded) Advisory Council on the Welfare Aspects of Dog Breeding, the RSPCA, a number of dog welfare charities and the Associate Parliamentary Group on Animal Welfare have offered a lot of advice about the health problems of these dogs in an attempt to reduce their popularity. Yet the kind of expensive advertising campaign that could really reach the public has been lacking.

An additional problem is that most breeders reject the introduction of genes from outside their breed. They fear the breed will “be contaminated”, that new diseases will be introduced and that the breed will lose its character or change in temperament. There appears to be no likelihood of legislation to compel breeders to outbreed on welfare grounds.

But with the help of our research it may be possible to breed for healthier dogs using the existing genetic variation within the breed (in addition to contributions from crosses outside the breed if necessary and if they can be made acceptable to breeders). If within-breed crosses to reduce disease do prove practical, this will probably be a slower route to reduce the disease burden for an individual offspring than an outcross-breed. However, the advantage is that within-breed crosses are likely to be widely accepted by dog breeders and so it may prove a quicker way of moving the whole population forward towards better breed health.

David Sargan, Senior Lecturer in Molecular Pathology at the Department of Veterinary Medicine, ̽��ֱ�� of Cambridge

This article was originally published on ̽��ֱ��Conversation. Read the original article.

̽��ֱ��opinions expressed in this article are those of the individual author(s) and do not represent the views of the ̽��ֱ�� of Cambridge.

David Sargan (Department of Veterinary Medicine) discusses the health implications of breeding the perfect pets.

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

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African Horse Sickness: mapping how a deadly disease might spread in the UK

amb206 — Sat, 25 May 2013 07:00:00 +0000

As its name suggests, African Horse Sickness (AHS) is associated with the continent of Africa, where it is feared as a deadly disease. It has long been assumed by British veterinarians and horse-owners that the disease, which is carried by midges, could not spread to cooler northern climates.

But researchers now think that its arrival in northern Europe could be only a matter of time – and perhaps more importantly, that it could spread if it did arrive.

A study undertaken by scientists at the ̽��ֱ�� of Cambridge Department of Veterinary Medicine, in collaboration with the Animal Health Trust and ̽��ֱ��Pirbright Institute, shows how dangerous it could be for the horse and pony population if AHS was introduced into the UK. ̽��ֱ��research also identified which regions would be worst hit at different times of the year.

This information could be vital to strategies for coping with an outbreak if it arrived. ̽��ֱ��study also emphasises the importance of the continued exclusion of the disease.

̽��ֱ��research was led by Dr Gianni Lo Iacono, a multidisciplinary scientist whose expertise lies in the mathematical modelling of a range of problems related to the interface between biology and physics. He worked with a team of colleagues from complementary fields including Professor James Wood, a renowned specialist in infectious diseases.

Most strikingly, East Anglia emerges from the study as the region that is most vulnerable to AHS spread which could occur if the disease was not identified early enough for action to be taken to contain it.

In Africa, the disease is spread by infected insects from species of midge known as Culicoides imicola, which carry the African Horse Sickness virus, an orbivirus of the family Reoviridae. Once a horse is infected by AHS, there is no treatment and no cure: the animal will have a high fever within 24 hours and most infected animals will be dead within 48 hours.

Other equidae, zebras and donkeys, are susceptible to AHS infection but do not have such severe disease. Infected zebras do not exhibit any apparent symptoms: as seemingly healthy animals they are potentially lethal carriers. Donkeys develop symptoms but can survive the disease.

First recorded references of AHS occurred in 1327 in Yemen, and in the mid-1600s following the introduction of horses to southern Africa. ̽��ֱ��disease was clearly identified by the British Army in South Africa 150 years ago when scores of cavalry horses perished in an epidemic.

Ever since, European horse owners have taken comfort from the fact that the disease could not strike in cooler countries. ̽��ֱ��British climate was considered too cold for the Culicoides imicola midges to survive. On top of this, the UK (and Europe more generally) has protective mechanisms in place that prohibit horses from Africa entering the country.

A growing number of veterinarians now believe that AHS can now arrive in the UK. Well-documented outbreaks were reported in Morocco (1965, 1989–1991), Spain (1987, 1988,1990) and Portugal (1989). ̽��ֱ��British climate is warming and global transportation of perishable fresh goods – such as flowers and vegetables – offers a possible route for infected midges to enter the country.

̽��ֱ��prospect of AHS brings sharply into focus the need for greater research into ways of preventing an incursion of AHS – and ways to cope in the event of an outbreak. “Our work demonstrates that there is no place for complacency about the ability of the virus to spread here,” said Professor Wood.

A greater understanding of AHS requires a multi-stranded approach covering the behaviour and life cycle of the midge and the geographical distribution and movement of horses, plus possible routes for infection to enter the country. Midge numbers and activity are highest during the warmer summer months, when the arrival of infection from overseas would be most serious.

In the UK, all horses have passports as a legal requirement but these documents record the owners’ address rather than the location where their animals are kept. If horses were mapped according to their owners address, London, for example, would emerge as the centre with the densest horse population. Clearly most horses owned by Londoners are kept outside the city, many of them within easy driving distance of their owners’ homes.

Correcting this issue posed problems. However, satellite data on land usage and a survey which recorded the distribution of distances between horses and their owners in different land-use settings (people live closer to their horses in rural areas than they do in urban areas) allowed the researchers to produce a more meaningful map of the risk of the disease. This showed that East Anglia is particularly vulnerable to an outbreak: not only is the region warm and dry, but it also has distinct clusters of horses, notably around Newmarket.

̽��ֱ��team has also investigated another important aspect of the disease: the possible 'dilution effect' that could be achieved through keeping animals not susceptible to the virus, such as cattle and sheep, close to horses.

Dr Lo Iacono explained: “In some communities in Africa people keep cattle or sheep near their houses in the belief that this will distract mosquitoes carrying malaria away from people. Some midges show apparent preference for cattle over sheep, so in South Africa deploying cattle to protect sheep from bluetongue (a similar disease to AHS in cattle and sheep) has been proposed as a way to control the disease. On the other hand, the presence of other species might well prove to be an added attraction for midges, exacerbating the threat to horses.”

̽��ֱ��research re-emphasises the importance of veterinary education to allow early disease identification, which can reduce the critically important reaction times to allow optimal control.

̽��ֱ��tools that Dr Lo Iacono has developed have potential applications in mapping and responding to the spread of other diseases, some of which are ecologically even more complex – such as Rift Valley Fever, a mosquito-borne disease that affects both humans and animals, causing a serious disease and in some cases death.

̽��ֱ��research provides a good example of how theoretical models can identify biological knowledge gaps (identifying midge biting preferences). This is now being taken forward in other studies.

‘Where are the horses? With the sheep or cows? Uncertain host location, vector-feeding preferences and the risk of African horse sickness transmission in Great Britain’ by Giovanni Lo Iacono, Charlotte Robin, Richard Newton, Simon Gubbins, and James Wood is published by the Journal of the Royal Society, Interface (2013) 20130194 doi:10 .1098/rsif.2013.0194

For more information on this story contact Alex Buxton, Office of Communications, ̽��ֱ�� of Cambridge amb206@admin.cam.ac.uk 01223 761673.

A disease lethal to horses, until now confined to hot countries, could arrive in the UK. New research creates a picture of its possible spread and pinpoints the area that would be worse hit.

Our work demonstrates that there is no place for complacency about the ability of the virus to spread here.

Professor James Wood

Mick Dolphin (Flickr Creative Commons)

Early morning, Newmarket

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