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Ask A Vet Online – Help, I’ve got a stuffy-nosed Pug!

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Natalie Kent asked:

My 8 year old pug has just been diagnosed with Pseudomonas in his nose. He's been having problems with his nose for about a year,   discharge, blocked up etc. Vet did a nose swab and found this bacteria. He's been on marbocyl antibiotics for 2 weeks and it's not       completely gone away, still a bit of discharge and a bit stuffy but vet refuses to give any more tablets, what else would you suggest?

Reply:

Hi Natalie, thanks for your question. Because of the conformation of their skull and nasal passages, Pugs are prone to a range of different breathing problems, and may suffer from recurrent nasal infections, so I’ll start by discussing the anatomy of the nasal passages and the defects Pugs typically suffer from. Pseudomonas is a particularly nasty bacterium that can be very difficult to treat effectively, so I’ll also talk about appropriate antibiotic therapy and the reasons why the symptoms may not have resolved. Finally, I’ll look at different ways forward for your dog.

What is the “normal” anatomy of a dog’s nose and airway? When a dog breathes in, the air flows through the nostrils (also known as the “nares”) into the nasal chambers. The left and right sides are separated by a dividing wall (the “nasal septum”) so what affects one side doesn’t always reach the other; and they are separated from the mouth by the bone of the hard palate (the ridged roof of the mouth). These chambers aren’t open – they are almost filled with scrolls or swirls of bone called the conchae (because they look a bit like sea shells), leaving only a narrow space in between for air to flow. This is important because even a small amount of fluid or swelling of the tissues here can make a dog very congested and uncomfortable. Behind these 2 chambers is a common space where left and right nasal chambers meet called the nasopharynx; the floor of this is made up of a strong muscular band called the soft palate. When breathing, the soft palate prevents food from entering the nasal passages. The air then flows through the larynx (voicebox), down the trachea (windpipe) and into the lungs. Opening out of the airways in the skull are the sinuses; these are hollow spaces inside the bone that make the head lighter and easier for the dog to carry around. There are 2 sets – on each side of the skull is a frontal sinus (in the forehead) and maxillary sinus (in the upper jaw, just above the tooth roots). So what’s different about pugs? Dogs can be divided into 3 different groups of breeds, based on their skull shape:
  • Dolichocephalic – dogs with long noses, e.g. Greyhounds
  • Mesocephalic (also known as mesaticephalic) – dogs with medium noses (most dogs, e.g. Labradors)
  • Brachycephalic – dogs with short noses (e.g. Pugs).
As one of the most extreme brachycephalic breeds, Pugs almost always suffer from some degree of Brachycephalic Airway Obstruction Syndrome. This is a condition caused by selective breeding over many generations for an abnormally short skull, and includes a range of conditions such as:
  • Nostril Stenosis – narrowing of the nostrils.
  • Elongated Soft Palate – over-long soft palate that blocks the airway.
  • Everted Laryngeal Saccules – folds of flesh that stick out into the voicebox, blocking airflow.
  • Hypoplastic Trachea – where the windpipe is a little too narrow.
These are all caused by excessive amounts of soft tissue – in the course of breeding for the modern Pug, we’ve been very successful in shrinking their bones, but not so much the soft tissues around them. As a result, Pugs have loads of extra folds of tissue in their nasal chambers and airways, making breathing a little more difficult. That’s all very interesting, but why did my dog get the infection in the first place? There are a number of possible reasons, but let’s start with the most obvious – with lots of extra soft tissue in their noses, all those little crevices, nooks and crannies are perfect for bacteria to find a home and start to grow! Other possible underlying causes include:
  • Foreign bodies – dogs are particularly prone to getting things stuck up their noses, like grass seeds or even bits of food.
  • Tooth infection – because the roots of some of the upper teeth are right next to the maxillary sinuses, an infection of the tooth can cause sinusitis and nasal infection.
  • Fungal infections – fairly rare in the UK, but they do occur.
  • Polyps – benign growths in the nasal chambers or pharynx.
  • Tumours – malignant growths of the airways.
These conditions aren’t uncommon in dogs, and often result in secondary bacterial infection. Once the infection is resolved, however, the symptoms may persist or recur because the underlying problem has not been addressed. What is Pseudomonas? Pseudomonas is a Gram Negative bacterium (meaning it has a double cell membrane as well as a cell wall) that commonly causes skin, ear and sometimes nasal infections. It is a very tough organism, and is prone to rapidly developing resistance to antibiotics. This means that in most cases, a prolonged (usually 2-6 weeks) course is required to ensure that it is completely eliminated. Exactly what antibiotic to use will depend on the results of the culture and sensitivity swab which your vet did – judging by what you’ve said, it would seem that this particular infection was susceptible to marbofloxacin (Marbocyl), a fluoroquinolone antibiotic commonly used against these bacteria. So why hasn’t the treatment worked? There are a number of possible reasons. Firstly, it may simply be that the course wasn’t long enough – however, your vet is right to be cautious about just handing out more antibiotics; overuse of antibiotics in animals or people is one of the main drivers of antibiotic resistance. A second possibility is that the course was long enough, but the Pseudomonas is now resistant to marbofloxacin; I’ve seen this happen before when treating these infections. You give an antibiotic that the bacterium is proven to be sensitive to, and within a week or two, the test results show that they have gained resistance to it. Alternatively, there may have been other bacteria on that nasal swab that didn’t show up because there were so many Pseudomonas. In that case, if they weren’t susceptible to marbofloxacin, they’ll still be there causing problems even once the Pseudomonas are all dead. Finally, and given the duration of the problems you’ve been having I’d say this is the most likely, there may be another underlying problem (such as a nasal polyp, a foreign body, dental disease, or even his nasal conformation and anatomy) that is causing the symptoms. OK, what should I do next? I think the most important thing is to find out what’s going on inside your dog’s nose right now. You know that some weeks ago there was a Pseudomonas infection; however, you’ve got no idea if that’s still the case and that treatment has failed (and if so, why); or if the symptoms are ongoing despite the successful treatment because the Pseudomonas were themselves only secondary to something else. The first step would be for your vet to repeat the nasal swab (if possible, using the same laboratory) and see how the results are different – what bacteria are growing there now, and what antibiotics they are susceptible to. The next thing to consider would be direct visualisation of the nasal chambers under anaesthetic; this usually involves rhinoscopy (putting a camera or endoscope up the nose) and/or retrograde visualisation (looking at the back of the nose with an endoscope or mirror) to see if there’s anything stuck there, or any masses or polyps growing. This isn’t always easy in pugs and may require referral to a specialist; however, your vet will be able to perform X-rays of the skull and nasal chambers, as often polyps and tumours are often clearly visible on an X-ray of this region. I think it’s very important for you to discuss your concerns with your vet, and talk about further diagnostics – you really need to sort out what’s going on in that nose to make him comfortable again and to hopefully avert any more serious consequences! All the best, I hope you can get this sorted out quickly. David Harris BVSc MRCVS
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Do I need to worry about “Alabama Rot”?

You may have read in the news recently of another cluster of dogs affected with the exotically named “Alabama Rot”. Also known as “Cutaneous and Renal Glomerular Vasculopathy” (CRGV), this condition is still poorly understood. As a result, there’s a lot of worry and speculation, and vets are receiving increasing numbers of panic-stricken phone-calls from dog owners! So, what do we actually know about CRGV? What is it? Firstly, let’s specify what it isn't – for example, despite excitable media reports, it isn't a “flesh eating bug”. Nor is it a “superbug” or a variant of the Ebola (or any other) virus. Technically speaking, it is a form of thrombotic microangiopathy, a condition where blood clots form in the small blood vessels in the body, blocking off blood supply. For some reason, the skin and the kidneys are most sensitive; without a blood supply, the tissue dies, causing ulcers on the skin, and failure of the kidneys. Is it a new disease?                                      Not exactly – it was first diagnosed in the United States in the 1980s. However, the first cases in the UK were detected in November 2012; since then, cases have been seen from across the country (there’s a map of confirmed and suspected cases here). It is most common in the winter and spring – most cases are detected between November and May. What causes it? No-one knows. It is probable that a bacterial toxin (i.e. a poison made by bacteria, that causes disease even in the absence of the bacteria themselves) is involved, perhaps from E. coli; however, this has not yet been confirmed, and tests for E. coli shigatoxin (one possible culprit) have proved negative. There is, however, no evidence that it is caused by a toxic plant, heavy metal poisoning, or genetics (although it was once thought that only Greyhounds and other sighthounds were predisposed, this is not now thought to be the case). It has been suggested that contaminated pet food may be involved, but this seems improbable – there just aren't enough affected dogs for that to be likely. So what are the symptoms? Initially, the first sign is an ulcer or wound, usually on the legs. They typically look like small, round sores and usually occur on the legs, but may also be found on the body, face or tongue. The lesions range from 5 to 50mm (1/5” – 2”) in diameter. 1-9 days later (usually about 3), affected dogs will usually suffer acute kidney failure. The symptoms are of increased thirst, changes in urination (increased amounts of dilute urine, or in more severe cases, reduction or absence of urine production). This is accompanied by lethargy, anorexia, vomiting, depression and often bad breath (which may smell metallic). Once clinical signs of renal failure occur, the prognosis for recovery is poor. Dogs that, for whatever reason, do not progress beyond the skin lesion stage have a better prognosis, assuming no further complications develop. Overall, half of the dogs affected will suffer abnormal bleeding (thrombocytopaenia); about a third may show some degree of jaundice (yellow gums and eyes); and one in five are anaemic (with pale gums and difficulty catching their breath). How do dogs get it? Firstly, it doesn't seem to be contagious from dog to dog, or to or from humans. The current thinking is that there is an environmental link – most cases are associated with walking in muddy woodlands, and it may be that there is a toxin in the mud that is absorbed by the dogs. How can it be avoided? As we don’t know the exact cause, avoidance is difficult. However, thorough washing of your dog’s coat after walking in woodland (especially if muddy… like everywhere this year!) is a sensible precaution that should reduce the risk. In addition, it is likely that certain places pose a higher risk than others; if there has been a case in your area, it is probably wise to avoid areas where the affected dog(s) were walked in the days before they were diagnosed. It’s also really important to check your dogs over regularly – not just for sores or ulcers, but also for cuts, ticks, mats of hair or other injuries. How do I know if my dog is affected? Fortunately, most dogs with skin lesions don't have CRGV! However, if your dog does have any strange or unexplained sores or wounds, it’s important to get them checked out by your vet – in the vast majority of cases, they’ll be able to demonstrate a far less worrying condition. They can also do blood tests to check for kidney problems – although as it is often several days before these show up, repeating the blood tests in 48 hours may be necessary. How can CRGV be treated? Unfortunately, there is no specific treatment. However, treatment of the skin ulcers will minimise the risk of secondary infection; and if kidney failure occurs or appears imminent, hospitalisation and intensive care will maximise the affected dog’s chance of survival. In some cases, referral to a specialist hospital may be suggested, to give your dog the best available care and therefore chance of recovery. How dangerous is it? As a rough estimate, the condition is fatal in 80-90% of cases. However, early diagnosis and treatment is thought to maximise the chances of survival. Fortunately, it is still a very rare disease – in the last three months, there have only been 4 cases (in Staffordshire, Hampshire, Greater London and Lancashire). If you are concerned your dog may be affected, contact your vet for advice – however, the majority of skin lesions and sores will be due to cuts, insect bites or grazes, and are nothing to worry about. It’s also important to remember that, even if your dog is affected, prompt diagnosis and rapid treatment gives them a much better chance of survival. For more information please visit Anderson Moores Veterinary Specialists who are taking the lead in treatment and advice on the condition.
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Grapes and raisins can kill dogs. Read this to find out how to keep your pet safe this Christmas.

Does your dog enjoy mince pies and Christmas cake? Beware: you could accidentally poison them.

For many people, it seems unbelievable that grapes and raisins can poison dogs. They're harmless to humans. We've all seen dogs occasionally eating foods containing raisins with no apparent ill effects. How can they suddenly be poisonous?

Why are grapes and raisins not always poisonous to dogs, and never poisonous to humans? First, like all poisons, the poisonous effect depends on the dose taken per kilogram of animal body weight. Large dogs can safely eat some raisins without problems. Secondly, the toxic ingredient in raisins seems only to be present intermittently, so a dog may eat raisins without problems on several occasions, then fall seriously ill the next time. What is the toxic ingredient in grapes and raisins? The actual toxic ingredient is still a mystery. The fact that grapes and raisins can be poisonous has only been deduced by circumstantial evidence, with many dogs developing acute renal failure for no obvious reason, with the only common factor being the previous ingestion of grapes or raisins. Samples of the fruit in such cases has been analysed, but a toxic agent has not yet been isolated. The best guess so far is that it is a water-soluble substance, and that it's in the flesh of the grape/raisin, but not the seed. One theory is that it is a mycotoxin (i.e. a poison produced by moulds or fungi on the grapes). The problem in dogs was first highlighted after a year with high levels of rainfall. This had led to damp grapes which were more likely to develop fungal growth. But why should humans be safe from this toxin? It's well known that cultured dog kidney cells in the laboratory are exquisitely sensitive to other types of mycotoxins. It makes logical sense that dog kidneys might also be more sensitive to damage by another mycotoxin, even its identity has yet to be established. So how much do owners need to worry about grape/raisin toxicity? If a terrier steals a mince pie, is a visit to the vet needed? If a Labrador has a slice of Christmas cake, do they need to be taken to the emergency vet? This is always a judgment that is not black and white. It seems sensible to look at the lowest recorded doses of grapes or raisins linked to acute renal failure in previous cases of poisoned dogs. This allows an estimate of the probable toxic dose depending on the animal's body weight. Grapes The lowest toxic dose is around 20g grapes per one kilogram of body weight. A typical grape weighs 2 – 5g, making a toxic dose is around 4 grapes per kg. So if a 5kg terrier eats 20 grapes, or a 30kg Labrador eats 120 grapes, there's a high chance of a serious problem, and veterinary intervention is definitely indicated. Raisins The lowest poisonous dose in confirmed cases has been around 3g/kg. An average raisin weighs around 0.5g, making a toxic dose approximately 6 raisins per kg. So if a 5kg terrier eats 30 raisins, or a 30kg Labrador eats 120 raisinsthey need to see the vet. Some studies have suggested that the toxic agent is neutralised by cooking, so cooked raisins (e.g. in pies and cakes) may not present such a high risk.

Important note

Please remember that the above doses mention quantities that have definitely caused serious kidney failure in the past. The decision on whether or not to take a pet to the vet is a personal decision, taken after balancing the possible risks. Many people prefer to take a conservative approach, to be as safe as possible. For example, if a dog has eaten even half of the above quantities, it may be safer to take them to the vet for “just in case” treatment.

What do vets do for dog that have eaten grapes/ raisins? 1) If ingestion has happened in the previous hour. This is the ideal situation: the vet can give an injection to cause the pet to vomit, emptying the stomach and removing the grapes/raisins before any toxic ingredients have had a chance to be absorbed into the bloodstream. 2) If ingestion has happened in the previous two days but the pet is still well Depending on the situation, vomiting may still be induced, activated charcoal may be given to limit absorption of the toxin, and intravenous fluids may be given to flush fluids through the kidneys in an attempt to minimise any damage. Blood and urine tests may be recommended to monitor kidney function. If the dog is well after three days, then the high risk period is over. 3) If ingestion has happened and the dog is unwell (e.g. vomiting, dull, inappetant) In such cases, the kidneys may have already been damaged by the toxin. Urine and blood tests will be carried out to assess the severity of the damage to the kidneys, and intensive care will be needed to save the pet's life, including high levels of intravenous fluids. The prognosis is guarded: unfortunately, some affected dogs die, despite the vet's best efforts.  Conclusion.
  • Keep grapes and raisins away from dogs.
  • If any dog eats them accidentally, phone your local vet (even if it's after-hours)
  • Tell your vet how many grapes/raisins were eaten along with the body weight of your pet.
  • Your vet will then advise you on the safest course of action.
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Ask A Vet Online – Help! The fleas are revolting…

flea-63043_1280 Anne Stafferton asked: This one is a bit boring really I've spent hundreds of pounds on flea stuff only for it not to work I breed cats so it's a nightmare I'm now combing them all every day to get fleas out any suggestions on what really really works Answer: Hi Anne, thanks for your question about fleas in cats. I know exactly what you mean – they can be a real nightmare to get under control! I’m going to answer your question by (briefly!) discussing the flea life-cycle and how it can be broken, and then talking about the specific treatments that are available. As a warning, on a blog like this I am legally obliged to use the generic names for all the drugs and medicines (otherwise I would get nasty letters from the Veterinary Medicines Directorate, the government department who regulate advertising of veterinary medicines). You can, however, look up any of the generic names for the active substances and “translate” them into brand names on the VMD’s Product Information Database. What are fleas? Fleas are a group of obligate ectoparasites – this means that they live on the outside of other animals, and cannot survive in any other way but by sucking the blood of their hosts. Once an adult flea lays her eggs, they fall onto the floor, the carpet, and into the cat’s bedding. Here they hatch into larvae, which live, hidden deep in the fabric, in the dust, and in cracks in floorboards etc. The larvae survive primarily by eating the faeces of adult fleas, which fall off the cat as the “black sand” we all know and hate! This material is semi-digested blood, and is very nutritious for the larvae. After their final moult, they turn into pupae (like the chrysalis of a butterfly but less pleasant) and there they stay, waiting for a chance to hatch. Pupae can remain dormant for months or years, and in this state they are more or less impervious to virtually any treatment we can use against them (although apparently repeated steam cleaning can kill them). When they detect air movement, heat, or increased carbon dioxide levels (all indicators that a cat, dog or human is close), they hatch and leap on board, to feed, breed and repeat the cycle. Traditionally, we think of fleas as being a spring and summer problem; however, with modern insulation and central heating, nowadays we see them all year round. The flea life cycle can only complete in a relatively warm environment, but we kindly provide them with a nice warm, comfy house to grow up in. So how do you break the cycle? There are a number of points at which the cycle is vulnerable – however, it’s important to remember that if the cats go outside (even briefly) they can pick up new fleas (deposited by other cats, dogs, foxes and even small mammals such as rodents). It only takes one amorous flea couple to reinfest a whole household… The adult fleas are actually pretty easy to kill – even old-fashioned drugs like fipronil will kill most of the adults present, and many of the newer medications are much more potent. The larvae need to cut their way out of their eggs (using a special “egg tooth” made of chitin); if their synthesis of chitin is impaired (e.g. by lufenuron) they cannot hatch. The larvae cannot develop into adults in the presence of juvenile hormone – if this is chemically supplied (as an Insect Growth Regulator, e.g. S-Methoprene), they cannot make the change into adults. The number of eggs, larvae and pupae in the house can also be reduced, by washing of fabrics (especially bedding) in hot (60C) soapy water. Although it won’t kill all of them, it will reduce the numbers and wash a lot away down the drain where they can’t hurt anyone! The pupae themselves are pretty much impervious to any treatment, but they can be “tricked” into coming out as adults, which are then much easier to kill. The common method is regular vacuuming – the air movement and heat trick the pupae into hatching; you won’t catch many in the cleaner, but once out, they are vulnerable to environmental insecticides. In fact, if you keep a “closed household”, with all the cats (and dogs if you have any) living indoors 24/7, it is theoretically possible to break the life cycle without treating the adults at all… but it will take a long time (the adults may live for 4-6 months) and you’re always at risk of a new introduction (in your clothes, for example). So how do I kill them? As you’ve found, there are a huge range of different flea control products on the market! Broadly speaking, these can be divided into 5 categories: Environmental insecticides: These are products used to spray the infested house, killing adults, sometimes eggs, and larvae. They will not kill pupae, but if applied rapidly after vacuuming, they can be very effective. Most products contain permethrin, which is toxic to cats – this means that you have to be careful using them, by treating rooms one at a time and shutting the cats out until they have ventilated. The cans will explain how long to leave it for on the label, or talk to your vet, before reintroducing the cats. On-cat environmental treatments: These are applied to, or administered to, the cat, to treat the environment, and rely on the fact that the larvae are eating the flea’s droppings. There are 3 particularly important ones:
  • Lufenuron – a chitin inhibitor, available as an oral liquid, a tablet, or an injection. Does not kill adults, but prevents larvae and pupae from hatching properly.
  • Pyriproxifen – an Insect Growth Regulator, available in some prescription-only fipronil products.
  • S-methoprene - another IGR, available in some prescription-only fipronil products.
  • Imidacloprid – an insecticide available as a spot-on that kills adults and larvae in the vicinity of the treated cat.
Over-the-counter adulticides (products that kill adult fleas only): These are of various effectiveness; most contain piperonyl butoxide or dimpylate (not very potent but pretty harmless) but there are still some on the market containing permethrin, which although effective is potentially lethal to cats. In general, if it is available over-the-counter without any regulation, it’s probably not that powerful. The most popular products in this group are the spot-ons containing fipronil, which is an older drug but still fairly effective. Some of these products are over the counter, and others are classified “NFA-VPS” (which means there are certain restrictions on their supply, but they still do not require a prescription) Contrary to popular opinion, there is no conclusive evidence that resistance of fleas to fipronil is widespread – however, fipronil containing products are water soluble (so may wash off if the cat gets wet) and are much less effective than the modern prescription-only products. The other commonly used active ingredient is imidacloprid, which is a different class of insecticide that is active against adult and against the larvae. Again, it doesn’t suit every cat but may be useful. There is also an interesting product available as a tablet containing nitenpyam, which is very effective at killing adults – but only lasts 24 hours after being given. It is best used to kill off the bulk of the adults when starting a flea control program. Prescription-only products: Fipronil-combos – spot-on products containing fipronil plus an Insect Growth Regulator, to treat the adults and the environment simultaneously. Last between 4 and 8 weeks, but the adulticide (killing of adults) effect tends to wear off after about 4-5 weeks. Flumethrin/Imidacloprid combo collar – this is a collar containing flumethrin (a form of permethrin that is safe for cats) and imidacloprid. It lasts about 6-8 months, and is very effective – if the cat will keep it on! Imidacloprid/Moxidectin combo – another spot-on, that treats a wide range of different parasites. Lasts about 4 weeks. Selamectin – a spot-on product, but one that is absorbed into the cats system so it cannot be washed off – very useful for outdoor cats! It also treats roundworms and both mange- and ear-mites, but does require the flea to bite before it works. Lasts about 4 weeks. Indoxacarb – Another spot-on, but one that is utterly inactive in the cat’s body, until it is “turned on” by a unique metabolic action inside the flea, and the larvae if repeated every 4 weeks. Spinosad – a tablet, given once a month, that is really effective against fleas, but does cause some cats to vomit; if given with food, however, it normally stays down - it does require the flea to bite, but kills very, very fast (in a few hours). Herbal and homeopathic remedies: Available, but no proven effectiveness. I have heard garlic recommended, but, sadly, in my experience it just doesn’t work and is potentially toxic to cats. There’s so much choice! What do I do? Bottom line – you’ll never control fleas if you only attack one stage of the life cycle. You need to kill the adults (and I’d recommend you talk to your vet about the more potent, modern, prescription products rather than rely on older and less powerful medications); however, you also need to decontaminate the environment, with regular vacuuming, insecticidal sprays, and good old fashioned washing and cleaning! If you’re still struggling to get on top of the situation, talk to your vet – not every product suits every cat, and it’s sometimes necessary to try several alternatives until you find the product, and the control methods, that suit your cats and their lifestyle. All the best – I hope you can rid your cats of their unwelcome visitors! David Harris BVSc MRCVS
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Ask a vet online – How often should my dogs get boosters?

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Karen Taylor asked: How often should our dogs be re-vaccinated (boosters)? Answer: Hi Karen, thanks for your question about booster vaccinations. This is an area that’s become quite controversial in the last few years, and there’s a lot of confusion about the subject. In addition, there’s a lot of very poor-quality information out there, so I’ll try to make this quite clear and obvious! To put it as simply as possible – see your vet every year for a health check, and discuss your vaccination strategy with them. For more detail... now read on! What are vaccinations? Put simply, a vaccination is a way of teaching your dog’s immune system how to recognise and defeat the micro-organism that causes an infectious disease, without the risks (of illness, potential long term health problems or death) inherent in a “natural” infection. This is achieved in one of three ways: 1)      A weakened form of the disease-causing organism. These are called “modified live” or “attenuated” vaccines, e.g. for Distemper and Parvovirus; the organism included is unable to multiply and/or cause clinical disease, but it is active enough to stimulate a strong immune response. Most modified live vaccines give a stronger and more long-lasting immune response than an inactivated vaccine; however, they aren’t suitable for every disease (because some organisms cannot be weakened enough to make them safe). 2)      An inactivated (“killed” or “dead”) form of the organism. These cannot ever cause disease, but allow the immune system to recognise the protein coat of the organism and therefore attack it next time. They may be used for particularly dangerous or unpredictable diseases such as Rabies or Leptospirosis, but don’t always give such long-lasting protection. 3)      Subunit vaccines, introducing part of the organism to teach the immune system what it “looks like”. For these, part of the protein coat of the target organism is replicated in a lab, and included in the vaccine; this means the immune response is really tightly targeted at one particular, vital, part of the organism. These are used, for example, in the Leishmania vaccine. There are 2 groups of vaccines – core and non-core. Core vaccines are those that should be given to every dog – they protect your dog and everyone else’s against dangerous, highly contagious and potentially fatal diseases. Non-core vaccines are those that are given to protect dogs that are particularly at risk of a specific condition because of their location, lifestyle, etc. The core vaccines that every dog should have are against:
  • Distemper.
  • Parvovirus.
  • Canine Infectious Hepatitis.
The vaccine against Leptospirosis is technically non-core; however, it is generally agreed that every dog in the UK is at risk of Lepto (which is spread by rat urine), and so it is treated as a core vaccine by most vets. The non-core (optional) vaccines available are:
  • Rabies (only necessary for pets travelling abroad).
  • Parainfluenza (one of the causes of kennel cough).
  • Kennel Cough (the bacterial sort, Bordetella bronchiseptica).
  • Lyme Disease (only necessary for dogs at high risk, e.g. gundogs, in high risk areas, e.g. the South West peninsula).
  • Leishmania (only necessary for dogs travelling to southern Europe).
  • Canine Coronavirus (only usually needed in breeding kennels).
If vaccines are so good, why do they need boosting? Because nothing lasts forever! Eventually, the immune system starts to “forget” how to handle a particular disease organism. Booster vaccines effectively remind the system and refresh the immunity. However, immunity to different diseases (and different types of vaccine, for that matter) lasts a variable amount of time, and that’s the problem. Some dogs will retain immunity for longer than others – unfortunately, there’s no easy way to tell which dogs are immune to what for how long. Is there any way to tell whether my dog actually needs a booster? Not really! The trouble is that although some vaccines operate by producing protective antibodies (e.g. Rabies), others rely on inducing a Cell Mediated Immune Response (immunity that doesn’t rely on antibodies in the blood, but circulating immune cells, e.g. T-lymphocytes and Natural Killer (NK) cells) – such as the Leishmania vaccine, which may not produce any antibodies at all. And most of them probably rely to some extent on both systems. It's easy to test the dog’s blood for antibodies (and there are some commercial companies that will do this and say “yes, high levels of antibody, so the dog is protected” or “no, not enough antibody, the dog needs to be vaccinated again”. However, this is not generally considered reliable, because:
  • The serological titre (level of antibodies in the blood) can only tell you how much antibody there is in the bloodstream at the specific time the test is done - it cannot tell you whether the levels will remain high for the following 12 months.
  • The link between antibody levels and protection isn't consistent - some dogs utilise other parts of the immune system (cell mediated immunity) – for example, dogs can be protected against Leptospirosis in the presence or absence of significant circulating antibody levels.
So how long does immunity actually last? How long the vaccine lasts depends on the exact formulation of the vaccine; at the time of writing, the three Core vaccines generally need boosting 1 year after the initial course, then every 3 years. Most Rabies vaccines needs boosting only every 3 years; and the others usually require annual boosters. To get a license for a vaccine, the manufacturer has to demonstrate that the product has a protective effect, however that is defined. For Core vaccines, they have to demonstrate onset and duration of immunity such as to fulfil the license claim to:
  • “Prevent mortality and clinical signs caused by canine distemper virus infection”.
  • “Reduce clinical signs of infectious hepatitis and viral excretion due to canine adenovirus type 1 infection”.
  • “Prevent mortality, clinical signs and viral excretion following canine parvovirus infection”.
If this cannot be demonstrated to the regulator (in the UK, the Veterinary Medicines Directorate - VMD), they won’t get a license for the product. This means that manufacturer’s recommendations for duration of immunity are those that will protect the vast majority of dogs for the quoted time (3 years or 12 months, depending on the vaccine). To make life a little more complex, any vet who uses a different vaccination interval, unless they can document a good clinical justification, is technically acting illegally by using the vaccine off-license (i.e. not as licensed by the manufacturer). This sort of behaviour tends to lead to unpleasant interviews with the VMD and has led to vets being struck off (although not, to my knowledge, for vaccine infringements as yet). Can over-vaccination harm my dog? There’s no reliable evidence that it can. In cats, every subcutaneous injection (of anything, even saline!) slightly increases the risk of an Injection Site Sarcoma, but despite a lot of scientists, vets and owners trying to find a link, there’s no evidence that it causes any problems in dogs. That said, absence of evidence is not necessarily evidence of absence, so a responsible approach would be to vaccinate as infrequently as the current evidence suggests is sufficient to provide protection – in other words: 1)      Get a health check for your dog at the vets every year. 2)      Follow the manufacturer’s recommendations (unless your vet has a particular clinical reason not to):
  1. Distemper, Parvo and Infectious Hepatitis – boosters every 3 years.
  2. Lepto – annual booster.
  3. Rabies – boost every 3 years.
  4. Other Non-core vaccines – usually every year.
  I hope that helps; this is a really controversial area in some quarters, but the evidence base for the current vaccination protocols is pretty secure, and it is what I’d advise you to follow. David Harris BVSc MRCVS
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