My Veterinary Journal

I am now officially a third year vet student and loving life at the RVC’s Hawkshead campus in Hertfordshire. It’s a big change from London but the course content is a lot more clinical and exciting and it’s quite refreshing to be out in the countryside with London only 20 minutes away.

This post is to help outline the main reasons as to why an animal may be vomiting. When presented with a vomiting animal in practice it’s important to be able to narrow down different reasons and know what tests to do to reach a plausible diagnosis.

Firstly, it is vital to distinguish between vomiting and other similar presentations. One of these is regurgitation. Vomiting is an active process triggered by a part of the brain called the vomiting centre. It involves contractions of abdominal muscles and the stomach, along with closure of the glottis to prevent ‘breathing in’ the vomitus, which will most likely look partially digested and may even have a green tinge from bile in the alimentary tract. It is often preceded by a period of nausea in which hyper-salivation may occur, manifesting as repeated lip licking and swallowing.  Regurgitation on the other hand is a passive process in which food, probably looking less digested and covered in saliva, is passively ejected from the oesophagus with the aid of gravity. Gagging can occur in cases of regurgitation as well as vomiting. Regurgitation is caused by disorders often very different to those causing vomiting, and further diagnostic tests along with treatment will vary for each so it is important to distinguish between the two. Questions to ask the client if unsure include inquiring in to the appearance of the ‘thrown up’ food and whether the animal was contracting its abdomen. If you can’t reach a conclusion it is important to observe the animal yourself.

If you have distinguished that the patient is vomiting, the next step is to work out why. As mentioned before, vomiting is triggered by a ‘vomiting centre’ in the brain. This has a number of influences including toxins and chemicals in the blood, receptors in the gut and abdominal organs sensing inflammation, irritation and stretching and inputs form the brain such as smell, fear, motion sickness and taste.

Causes of vomiting can be divided in to primary gastrointestinal tract (GIT) problems and secondary GIT problems. Primary problems include those directly affecting the GIT (stomach, large and small intestines) and can be divided in to structural or functional causes. Secondary diseases involve organs and systems outside of the GIT including the pancreas, liver, brain and kidneys as well as endocrine systems, disorders of which can cause a build-up of toxins in the blood.

Primary causes of vomiting can further be divided in to gastric (stomach related) or non-gastric. Structural problems include a foreign body blockage, neoplasia, dietary indiscretion, parasites and infection. Functional problems refer to those affecting the movement of the gut, such as the muscles that move food along. Clues that help diagnose the cause as primary include if a foreign body can be palpated and if the vomiting is associated with diarrhoea.

Secondary causes of vomiting can be divided in to endocrine (relating to hormones), neural (triggered by the brain, be it motion sickness, a smell etc), and non-GI organs such as the kidney and liver. Quite often with secondary disease the clues are that the animal is obviously metabolically ill, for instance jaundice in the case of liver disease, and that vomiting is not related to when the animal eats.

It is important to hone down the cause of the vomiting in order to select the most appropriate treatment. It may be advised to run a blood and urine test on the animal to begin with (following a thorough physical exam to try and palpate foreign bodies/ inflamed organs). In an animal with secondary GI disease these blood tests are likely to highlight potential imbalances in minerals and toxins such as urea. Although less diagnostic in an animal with a primary cause of vomiting, the tests still give useful information on the clinical status of the patient, for instance if they are dehydrated.

If the cause is suspected to be primary, imaging is the next port of call, with radiography being a great way to get a better idea of what is causing the problem. Using contrast radiography is especially useful for spotting foreign body blockages. Ultrasound can also be very useful. Sometimes an operation called an exploratory laparotomy may occur, in which the vet surgically explores the GI tract to search for a cause. Remember for primary the cause could be something that recedes on its own, such as the dog eating the contents of a bin. This is much less likely with secondary disease.

The mention or sight of ragwort is a thing that can strike immediate fear in to any horse lover’s heart. I’m currently on the last of my pre-clinical placements at a stables and have been inspired to write a quick post about Ragwort poisoning.

Ragwort is a plant native to Britain and Europe. It is also found in the States however I believe it’s less of a problem across the pond (correct me if I’m wrong American readers!). It has characteristic yellow flowers and upright stems. It grows prolifically on grazing pastures and by the sides of roads.

Ragwort contains alkaloids, which means it can be poisonous to certain animals including horses, pigs and cattle. The alkaloids are metabolised to more harmful substances in the liver, leading to what can be debilitating liver disease and death. In horses it is thought to take 1-10% of the horse’s body weight in ragwort to be lethal. In its fresh form, ragwort has an unpleasant and bitter taste meaning horses won’t often choose to graze on it unless no other roughage is available. The toxins, however, are extremely stable and are still poisonous after drying. This means that if ragwort is incorporated in to hay, that hay can cause the horse serious problems when consumed. Dried ragwort loses its unpleasant taste and is hard to spot amongst the other dried plants, with this consumption being the most common cause of ragwort poisoning.

The effects of the toxins are thought to be cumulative in the liver meaning the disease can occur over an extended period of consumption. The effects can include necrosis of the liver, and lead to symptoms indicative of liver failure, including yellow mucous membranes, incoordination, photosensivity, apparent blindness, colic, depression and collapse. The effects are irreversible.

Diagnosis can include doing a blood test for liver enzymes or a biopsy of the liver looking for specific pathology. These are not definitive tests as the toxins produced by ragwort can also be produced by certain moulds also found in hay.

Control of ragwort and therefore prevention of poisoning is a tricky topic as the plant is a very important food source to many rare insect species. In the UK alone, thirty species of invertebrate use ragwort exclusively as their food source. Legislation in the UK and Ireland require land owners to control the growth of the plant, ensuring consideration of its spread especially if near grazing land. Control can be chemical or through uprooting and disposing of the plant.

As many of you are probably aware, over the past few weeks there has been an outbreak of babesiosis in the UK. I thought I’d make a quick post on what Babesia is and what it’s doing.

Babesia are parasites known as ‘protozoa’. These are single celled eukaryotic organisms. Babesia belong to a group of blood-bourne, tick transmitted protozoa known as piroplasms. Their life cycle consists of asexual and sexual multiplication within ticks. This can occur in the tick’s ovaries meaning the parasite enters the next generation of ticks causing a rapid spread. When the tick feeds, it transfers the parasite to the blood of the dog where it multiplies asexually in red blood cells forming two or four daughter cells that can be seen diagnostically in a blood smear with special stains. These daughter cells can disrupt the red blood cells, causing them to burst as the dog’s immune system tries to destroy the parasite. There are a variety of species, some being described as ‘small’ and others ‘large’ depending on the cell size. Some species are non-pathogenic, such as the large Babesia major, which may routinely be found in cattle blood smears without a worry. Others are pathogenic, such as Babesia divergens seen in cattle in the UK. This causes what is known as ‘red water fever’ as the bursting red blood cells result in haemoglobin in the urea.

The species of Babesia found to be responsible for the recent UK outbreak in dogs is the large Babesia canis. The tick vector is a tick known as Dermacantor which used to be confined to warmer parts of southern Europe and is rare in the UK. A variety of factors such as relaxations in the Pet Travel Scheme rules for treating dogs for ticks before they enter the UK, along with our mild winter allowing more ticks to survive, could be to blame for the outbreak.

Signs of a Babesia infection include weakness, lethargy, red urine, pale gums, fever and vomiting.

Reading reports from the 16th of March 2016, it appears that the outbreak was found in Essex, with 2 dogs dying from the parasitic infection and another three needing blood transfusions. None of these dogs had ever travelled outside the UK.

Babesia infections can cause immunity within the host relatively quickly. Cattle living in areas where the disease in endemic rarely show signs of disease as constant re-infection boosts their immunity. Here in the UK Babesia canis is not endemic, meaning dogs are completely naïve to the disease and have no immune protection from infection.

In order to infect the dog, the tick must have been feeding for at least 24 hours. To prevent infection, dog owners need to use tick medication that ensures it kills all ticks within this time frame for its entire duration. There are a range of tick preventing products out there so it is important to check that the product being used on your dogs sticks to this brief.

There is a worry that the infection will spread from Essex, especially due to the passing of the parasite from one generation of ticks to another. The Animal and Plant Health Agency are currently investing the outbreak. It appears that currently we are all being instructed to stay vigilant and ensure optimum tick control practices are being used by dog owners country-wide.

Toxocara canis is a roundworm harboured in almost all puppies. The adult worm can reach up to 18cm in length and live in the small intestine of the dog. Puppies with a small number of worms often show no symptoms, however large numbers can be fatal, causing a pot belly, diarrhoea, vomiting, weight loss and intestinal obstruction.

The worm infects all members of the ‘canid’ family including foxes and wolves.

It has a complicated life cycle that varies as the dog ages. In puppies up to 2 months of age, the infective egg is ingested and passes through the stomach in to the small intestine. Throughout this route the egg’s shell is digested and a larva released. This larva then burrows through the intestinal wall and through the hepatic portal system, reaching the liver. From here it enters the vena cava leading it to the heart where it then travels to the lungs and finally reaches the trachea. It then migrates up to the pharynx where it is swallowed back in to the intestines. Throughout this journey the larva undergoes a series of moults to reach its mature, adult form. This migratory route is typical of the ‘ascarid’ family of worms to which Toxocara canis belongs.

The adult then resides in the small intestine, producing eggs. The time frame from infection to egg production is 4-5 weeks. These eggs are tough and can survive in the environment for years. When the puppies are around 6 weeks of age, there tends to be a spontaneous expulsion of worms which can be a disgusting sight in their faeces!

In dogs older than 2 months, the worms take a different route. The eggs make their way through to the small intestine as with puppies and the larvae then penetrate the intestinal mucosa and enter the venous portal system to the liver, continuing their route to the heart. From here, they migrate to the lungs and then back to the heart. They then enter multiple tissues of the dog such as the liver, kidney and muscles where they reside in a ‘waiting state’.

Waiting for what? Well. In female dogs, the larvae are waiting for pregnancy. When the hormonal changes that come with pregnancy are detected, the larvae awaken and migrate to the placenta and mammary glands. Here they infect the puppies before they are born, and enter the milk ready to further infect the puppies at birth. Not all larvae are activated during a bitch’s first pregnancy, so infections of every litter are likely.

The ‘waiting’ larvae are around 0.5mm in length. If a male dogs becomes infected, he is a dead end host and no further infection occurs.

The worm’s life cycle is described as ‘direct’, as it only needs one host to complete its cycle. It can however have ‘paratenic’ hosts. This means a host, non-essential to the worm’s life cycle, in which no development happens. These include, rodents and birds. Eggs infect these hosts and develop in to ‘waiting’ larvae which reside in the tissue of the animal until it is eaten by a member of the canid family. Humans can also be paratenic hosts. The ‘waiting’ larvae in humans can cause serious pathogenic effects. The worm is associated with three disease syndromes in humans:

- Visceral larval migrans – this is where the larvae migrate though tissues and can cause inflammatory reactions, fever and asthma

- Ocular larval migrans – here the larvae migrate to the retina of the eye causing impaired vision

- Covert toxocarosis – this produces non-specific clinical signs

Around 55 cases of Toxocara canis infections in humans are diagnosed every year. Around 2.5% of British people are confirmed as seropositive for the infection, showing most cases are asymptomatic. Sadly it is mostly children who pick up the infection through playing in mud and sandpits infected with eggs from canine faeces.

Puppies, along with some adult dogs (and wildlife such as foxes), shed eggs in their faeces, constantly infecting the environment and making infection hard to control. Treatment tends to be regular worming of puppies from 2 weeks of age. Most treatments only to kill the adult worms, however this prevents the eggs from entering the environment, breaking the life cycle where possible. The ‘waiting’ larvae are very hard to kill and treatment involves dosing a pregnant bitch every day from day 40 of pregnancy until 2 days post whelping. This would costs the breeder £70-£75 per bitch, so it is clear why most breeders don’t opt in to this treatment.

The complicated, word-filled world of tumours and cancer can be a tricky one to wade in to. I thought I’d make a post outlining some of the basic definitions to help when things get wordy!

Starting with the basics, the word ‘tumour’ is a very broad and non-specific term used to describe a swelling. The word ‘neoplasm’ is also used. Oncology is the word to describe the clinical study of tumour characteristics/ development.

Neoplasia is the new, abnormal growth of tissue. A neoplasm is not necessarily cancerous or life-threatening, it’s just a term to describe a growth that’s not supposed to be there. Here are a few features of a neoplasm:

-Purposeless

-Uncontrolled growth

-Starts from a single mutated cell

-Growth continues even if inciting cause is taken away

-Cells have altered differentiation

-The rate of growth exceeds that of normal tissue

A neoplasm can be benign or malignant. Benign means a neoplasm that does not metastasise (oh here we go, another long word! This one means spread to other tissues in the body), resembles normal tissue under a microscope, has cells of a uniform size and shape, is often encapsulated and relatively easy to remove surgically.

A malignant neoplasm is bad news, another name for it being ‘cancer’. These tumours grow quickly and invade local tissue much like claws of a crab (hence the name cancer). The cells are often extremely undifferentiated and do not resemble normal tissue. They can spread by metastasis. Malignant neoplasms are a lot harder to remove surgically.

Most tumours stem from a single cell type. Epithelial cells and mesenchymal cells are the two main basic cell types of the body and tumour names reflect these.

A tumour name ending in the suffix –carcinoma or –sarcoma means malignancy. Carcinomas stem from cells of an epithelial origin, an example being squamous cell carcinomas. Sarcomas stem from cells of a mesenchymal origin, so an osteosarcoma would be a malignant cancer of bone tissue.  If the prefix ‘adeno’ is used, the tumour is in a gland, so a mammary adenocarcinoma is a malignant tumour of the mammary gland. Confusingly, a tumour name ending in the simpler prefix –oma refers to benign neoplasms. An example of this is lipoma, a functionless yet usually harmless growth of fatty tissue.

As always, there are exceptions! The word lymphoma is used to describe a malignant tumour of lymphoid tissue, with leukaemia the term used when the tumour affects circulating lymphoid cells. The term melanoma can be used to describe tumours of melanocyte cells, and these can be malignant. There are many other confusing exceptions too. These rules are just useful basic guidelines to help break down the confusing names often given to tumours.

I hope this has helped shed a little light on what some tumour-related terms mean! I’m going to end the post with a few examples to hopefully make things a bit more clear.

Pituitary adenoma – a benign, slow growing tumour of the pituitary gland. Remember ‘adeno’ means it is associated with a gland, and ‘oma’ on its own means the tumour is benign.

Gastric adenocarcinoma – a malignant tumour of the glands of the stomach. ‘Carcinoma’ means a malignant tumour epithelial cell origin. The ‘adeno’ again refers to glandular tissue. 

The stay apparatus in a horse has always confused me and today I decided to try and fix that. After a lot of concentration I think I’ve finally cracked it, so I am going to try and explain it while it’s still fresh! This post may be a little anatomy heavy so apologies for all the confusing words and terms. Today I am just focussing on the forelimb, the hindlimb has extra special features which I’ll write about another time.

The purpose of the mechanism is to allow the horse to rest while standing, without causing muscle fatigue. This enables them to conserve energy while standing while being ready to spring in to action should a threat arise. In order to do this the horse needs to use its muscles and tendons to overcome the joints’ ‘need’ to collapse when body weight is applied to them. Not only this, it needs to prevent muscles getting fatigued. I have annotated a picture of a forelimb sourced from here, with red arrows showing which way the joints ‘want’ to collapse due to body weight and the coloured lines showing parts of the mechanism I’ll mention throughout the post.

So firstly we have the issue of the shoulder wanting to flex. To prevent this, the horse has a specially adapted biceps brachii muscle. The muscle consists of a higher proportion of connective tissue to other animals. It also contains a thick band of fascia called the lacertus fibrosis. This tendinous band connects the tendon of the biceps brachii muscle to that of the extensor carpi radialis, which runs along the front of the limb all the way down to the metacarpal (cannon) bone. As the shoulder flexes under the body weight, the tendon of the biceps brachii muscle is stretched taught, forming an unbroken line through the lacertus fibrosis all the way down to the metacarpals. I have displayed this in the image as a green line.

This does not however, as you can see, prevent elbow flexion. Here, ligaments called collateral ligaments prevent flexion as they are placed behind the axis of the joint. These passively maintain the elbow in extension and an active counterforce is required to stretch them and allow flexion to occur. Think of it almost as a locking mechanism. I have drawn them in blue.

Next up is the carpal joint. This could either flex (go backward) or extend (go forward) under the force of body weight. In order to prevent flexion, you can see that the tension created in the biceps brachii muscle and continued by the lacertus fibrosis and extensor carpi radialis helps hold this joint in extension. Over extension of the carpal joint is prevented by the block shape of the bones along with a ligament called the palmar carpal ligament which runs behind the joint ensuring it doesn’t ‘bend forward’ too much.

Now, on to the fetlock. A different mechanism comes in to play here called the ‘suspensory apparatus’. This mechanism consists of a ligament called the suspensory ligament along with the sesamoid bones of the joint and associated sesamoidean ligaments. Sesamoid bones are small bones found within joints that help to prevent tendon wearing and increase their moment arms, the biggest example in the body being the knee cap (patella).

The suspensory ligament is actually part of a muscle called the interosseous muscle found in other animals. In a horse this muscle is entirely tendinous. I have drawn it as an orange line. It extends from the top of the metacarpals to the proximal sesamoid bone. This sesamoid bone is found at the joint between the metacarpals and digits. The suspensory ligament has extensor braches that run over the fetlock to the front of the limb to join the common extensor tendon. This connection helps relay tension from the extensor ligament to the suspensory ligament. The sesmoidean ligaments (drawn in purple) run from the proximal sesamoid bone to the distal (navicular) sesamoid bone and help stabilise the fetlock joint.

Superficial and deep digital flexor muscles have tendons that are also involved. These run along the back of the limb too and support the fetlock. The superficial digital flexor tendon has an accessory ligament that runs from the tendon to attach to the radius. This transfers tension from the tendon to the bone without reaching and fatiguing the muscle head. The deep digital flexor also has one of these tendons transferring tension to the cannon bone.

Beyond the fetlock joints are the pastern bones. These, as seen by the red arrows, ‘want’ to over extend. This is prevented by palmar ligaments and a ligament known as the straight sesmoidean ligament which support the joint.

Toxoplasma gondii. 7 syllables sure to strike fear in to any pregnant woman’s heart. I thought I’d do a little post today to summarise what toxoplasma actually is and how it affects us and the animals around us.

Toxoplasma gondii is a single celled parasite known as a protozoa. It has a complex lifecycle involving felines as its only final host. It does, however, have a vast array of ‘intermediate hosts’ thought to include virtually all warm blooded animals. It’s a very successful parasite infecting animals and humans worldwide. In France, 84% of people are thought to be infected.

Its lifecycle is as follows:

A cat becomes infected through consuming the raw meat of infected prey

The parasite infects the epithelial cells of the cat’s gut, sexually reproducing in these cells

Sexual reproduction produces oocysts which are shed in the cat’s faeces. The time period from consumption to shedding is around 3-10 days. Shedding only occurs for a few weeks before the cat’s immune system fights off the parasite, resulting in a persistent but non-shedding infection that can remain for life. After one infection it is highly unlikely the cat will get infected and shed again due to its raised immune response, however immunosuppression can result in subsequent shedding

These oocysts develop in the environment and after 1-5 days are developed enough to infect an intermediate host

Intermediate host ingests the oocysts through consumption of an item or fluid infected with cat faeces. Intestinal enzymes break down the oocyst wall releasing the parasite in to the gut

Acute asexual multiplication occurs in the intermediate host cells and the parasite is spread around the body in the blood

After around 2 weeks the host develops immunity but the infection enters a chronic phase as slow-growing forms of the parasite are ‘walled off’ into what is known as a cyst, protected from the immune system. These can remain infectious for months to years and can revert to the acute form if the host’s immune system becomes depressed (FIV, AIDs, canine distemper). They are often found in the brain and muscle.

This cyst-infected meat is consumed by the cat and the whole cycle begins again

Cats can also get infected by consuming oocysts from other cats, however they are a lot less susceptible to this than other intermediate hosts so a large number of oocysts would need to be consumed. To make it even more confusing, intermediate hosts can get infected via carnivorism/ scavenging when they consume meat infected with cysts (e.g. a human eating undercooked, infected pork). As well as this, transplacental transmission can occur in some host species during the acute phase of the infection (however this is not seen in dogs or cats). This creates a complex web of infection. The cysts are killed when meat is cooked.

Toxoplasmosis is most often asymptomatic, with flu-like symptoms possible during the acute phase. It can be fatal in immunosuppressed individuals, however this is rare. You may have heard the parasite’s name mentioned in relation to sheep. If a non-immune ewe is infected during pregnancy it can cause foetal death, reabsorption, abortion, mummified foetuses, still births and weak lambs, depending on when in pregnancy the ewe was infected. In cases of abortion, you can see tiny white spots on the placenta and foetal tissue. Diagnosis can be confirmed through stained impression smears or serological examination of the foetal fluid or blood from the ewe. Prevention in sheep includes a vaccine which primes the immune system to the parasite. Sheep are often infected from eating infected hay or concentrates, so keeping cats away from these can help reduce infection rates.

Toxoplasma is also a favourite in the press, who claim that it ‘controls our brains’ and causes abortions and deformities. Like in sheep, infection of a non-immune, pregnant mother can indeed cause deformities in her child. Does this mean we should all kill off our cats when expecting? Definitely not, and I’ll explain why.

As I stated earlier, infected cats will only shed for 2-3 weeks in their entire lifetime, unless immunologically supressed. To become infected by your cat, you would need to have never been infected before yourself (because if you have, your immune system is primed and ready to fight it off), your cat would have to be in the shedding phase and you’d have to ingest oocytes (that take 1-5 days to become infective, so changing the litter box daily can hugely reduce this risk).  If worried, a blood test to see if you’ve been previously exposed and a blood test in your cat to see if they’ve been previously exposed may put your mind at rest. Indoor cats are less likely to become infected if their only food is tinned or dried. Humans are much more likely to be exposed to the infection through handling and eating undercooked infected meat, soil infected with cat faeces and unwashed vegetables. If you’re a vet in the making and have been on a lambing placement, you may well have been asked if you’re pregnant. This is because being in contact with aborted material from sheep with toxoplasmosis is another way to contract the infection.

As for the ‘mind control’, it has been found that mice infected with toxoplasma are attracted to the smell of cat urine and a lot less frightened of cats than those without infection. This is an incredibly clever mechanism and probably one of the reasons the parasite is so wide-spread. In humans, when analysing the number of people who are involved in car accidents, it was found that a significantly high proportion were infected with toxoplasma gondii. It has been suggested that the parasite is responsible for making people more reckless and argumentative. Toxoplasma cysts in the brain could definitely be responsible for parts of your personality, however conclusions at the moment suggest that although the infection may have some effect, the brain and concept of ‘personality’ are so complex and involve so many factors that its overall influence seems negligible.  

I hope this made sense, it’s quite confusing to explain! I’ve drawn a quick diagram to try and demonstrate the different scenarios in which we could become infected. Enjoy!

I was lucky enough to shadow a vet this weekend at the RVC’s Beaumont Sainsbury Animal Hospital. At one point the nurses asked me to help them socialise a 2 month old macaw. This baby bird was absolutely stunning and amazingly cute, cheeky and intelligent. She had been admitted because the owner was struggling with the demanding feeding regime, resulting in damage to the bird’s crop through overfeeding. The nurse mentioned that the bird had, unrelatedly, been diagnosed with Avian Bornavirus, so I decided to do a bit of research to see how this virus would affect the life of my new little friend.

The bornavirus family affect a number of species, and are the cause of borna disease in mammals, which is a fatal disease of the nervous system. The disease was first recognised in 1885 however it was only in 2008 that Avian bornavirus was discovered in parrots. It is now thought to be the most common virus affecting companion parrots.

It is now strongly believed that Avian bornavirus is the cause of Proventircular Dilation Disease in parrots. This is where the nerves supplying the proventriculus, the glandular part of a bird’s digestive system found before the gizzard, as well as other parts of the digestive tract are damaged leading to weight loss, regurgitation, depression and the passing of whole seeds due to reduced gut motility. As well as this, other neurological signs can be seen such as head tremors, inability to perch and seizures. The proventriculus appears enlarged due to the back up of food accumulating here. It is not known exactly how, but the virus attracts the bird’s own immune cells towards its nerves, causing them to be destroyed through inflammation. This can occur in the nerve plexuses of the gut, or in the brain, spinal cord and heart to name a few others. The virus is thought to be transmitted through close contact and faeces.

Diagnosis is complicated. Until recently, getting the parrot to swallow barium then taking an x-ray was a good way of tracking the route of ingested food. By tracing the path of the barium, proventricular dilation could be spotted. Doing this alongside tests to eliminate other possible causes of the symptoms was usually enough. Looking at post-mortem tissue samples of infected birds under the microscope would show characteristic inflammatory tissue damage. Nowadays we can look for antibodies in the bird’s blood to see if it has been exposed to the virus. This however is again inconclusive as it doesn’t indicate whether the bird has fought off the virus and is healthy, or is still infected. You can also look for the virus itself using PCR to search for the viral RNA in samples from the blood, cloaca or a throat swab. This test is again inconclusive as the virus has a tendency to be shed intermittently, meaning it can ‘hide’ for periods of time within the body and not be detected.

Although there are strong ties to Avian bornavirus being the cause of Proventricular Dilation Disease, the majority of infected animals remain clinically healthy. These birds should be monitored for neurological and gastrointestinal signs of illness, receive regular veterinary checks and be fed a healthy, nutritious diet to ensure optimal health. The viral structure includes an envelope, making the virus unstable in the environment. It can be killed easily by bleach making disinfection of an area quite easy.

Treatment of Proventricular Dilation Disease includes non-steroidal anti-inflammatories to quell the damage caused by inflammatory cells.

Viruses and the immune systems of animals and humans have evolved alongside each other for millions of years, creating an ongoing and constantly developing selection pressure which can be to blame for their complexities. Looking at the ways in which viruses evade immune responses just goes to show how complex the interactions between viruses and our bodies really are. In this post I’m going to outline some of the methods viruses use.

Interferons: Cells infected with a virus secrete type 1 interferons. These are antiviral cytokines that cause neighbouring cells to express viral resistance genes. These genes reduce synthesis of viral protein and increase degradation of viral mRNA. They also upregulating the presentation of viral antigens on the cell surface; a way of displaying to the immune system that the cell is infected. Molecules called major histocompatibility complexes are used to do this, I’ll refer to them as MHC.

Pattern recognition receptors inside cells can detect viral double stranded RNA. Cell signalling mechanisms then lead to the expression of type 1 interferon genes and subsequent secretion of the interferons. Some viruses produce proteins that interfere with cell signalling to prevent interferon production. An example is Bovine Viral Diarrhoea Virus, a pestivirus. Other viruses target the interferon receptors of the neighbouring cells preventing the anti-viral response.

Immune privileged sites: Sites such as the eyes, brain, spinal cord and testes are referred to as ‘immune privileged’ as they have barriers protecting their cells from the blood, and hence white blood cells and antibodies, in the general circulation. This is to avoid damaging inflammation, as inflammation of any of these sites could easily lead to death or infertility, two states evolution wishes to avoid. Some viruses have evolved to evade immune detection by establishing themselves these sites, an example being Rabies virus.

Evasion of virus neutralising antibodies

When the cells of the immune system recognise a virus as foreign they can produce antibodies against them. The aim of these antibodies is to bind to surface receptors on the virus and prevent it from being able to attach to and enter its target cell. Antibodies cannot enter cells, so only attach viruses once they leave the cell to infect a new one.

Intracellular spread: Some viruses have evolved to avoid the phase of infection that requires it to leave the cell. Some do so by invading neighbouring cells by disrupting the cell membrane between them, forming an effect that can be seen under a microscope called a syncytium. This is where multiple cells have moulded in to one large, multinuclear cell. This can be seen in the lungs of cattle with parainfluenza type 3. Others, such as retroviruses, integrate their genome in to the cell’s genome and induce uncontrolled, neoplastic growth. Each cell division replicates the viral genome alongside it. If this is done in reproductive germ cells, the virus can be passed on to offspring. A fact that I find really cool is that many species have ancient viral DNA integrated in to their normal genome; remnants of infections their ancestors had millions of years ago. This is one issue to consider with organ transplants from one species to another, as the retroviruses may adapt and reactivate in new species.

Antigen decoys: As Ebola virus replicates it produces in large quantities a truncated, soluble version of one of its structural proteins. These are secreted from the cell before the virus exits, saturating the binding sites of surrounding antibodies meaning when the virus is released, less antibodies are available to bind and neutralise it. Other viruses express extremely immunogenic ‘decoy’ proteins on their surface which distract the immune response from the important proteins needed to bind to and enter cells. This means that while antibodies are produced, they are for non-important proteins and don’t effectively neutralise the virus.

Antigenic variation: Some viruses can change their genome, through mutation or gene exchange, leading to changes in their antigens and rendering antibodies previously produced against them useless. Antigenic drift is where the genes randomly mutate whereas antigenic shift is where two separate viruses exchange genetic information when they infect the same cell. This can make the synthesis of effective vaccines difficult, with an example being feline calicivirus, a major cause of cat flu.

Evasion of white blood cells

As well as producing antibodies to neutralise viruses, the body also contains cells that can target and kill infected cells. Antigen presentation is a key part in this immune response, using the previously mentioned MHC molecules to ‘show’ the immune system that the cell is infected. Cells called cytotoxic T lymphocytes can respond to the presented antigens, inducing apoptosis in the cell. Other cells called natural killer cells kill cells showing ‘symptoms’ of viral infection, with a major symptom being a reduced amount of MHC displayed on the surface of the cells.

Blocking antigen presentation: Some viruses have evolved to disrupt the antigen presenting pathway. When viral proteins are detected within a cell, it first breaks the protein down ready for presentation. The pathway includes transporters called TAP transporters which allow the passage of these broken down proteins in the endoplasmic reticulum ready to be combined with MHC for presentation. Some viruses block this transporter while others retain the MHC in the endoplasmic reticulum. Some highly evolved viruses can ‘push’ the newly synthesised MHC the wrong way through the TAP transporter in to the cytoplasm causing it to be degraded instead of presented. My lecturer pointed out that ‘these viruses understand immunology better than you do’. Although these methods are often effective, the reduced expression of MHC means that the infected cells are more susceptible to death by natural killer cells. Because of this, some viruses make fake MHC class 1 proteins to mask detection from natural killer cells.

Avoiding apoptosis: Finally, some viruses target phases of the killing response elicited by cells of the immune system. Methods include inhibiting the signalling responses of death receptors and producing analogues of anti-apoptosis proteins.

Hi there. It’s hard for me to recommend books as everyone has different learning styles and where I prefer books with large, labelled diagrams, others prefer a lot of text. If you’re looking for anatomy and physiology combined, I’d recommend Dyce’s Textbook of Veterinary Anatomy as a good starting point. It’s heavy on the anatomy and has a lot of text but the pictures are useful too. That includes all of the major veterinary species with large sections on dogs and horses. 

I love Pasquini’s ‘Anatomy of Domestic Animals’ because of his line drawings but it’s certainly not a style preferred by many and hardly touches on physiology at all. 

I don’t own any individual veterinary books on horses I’m afraid.

Hi there. The MRCVS is a great website for keeping up to date with recent veterinary news: http://mrcvs.co.uk/en/

The BBC news website/app is also useful if you look in the ‘animals’ and ‘agriculture’ sections. I also recommend ‘Farming Today’ podcasts which are uploaded daily on to the iTunes store for free.