Addison's Disease (Hypoadrenocorticism)
(2 votes)
Addison's disease is essentially the opposite of Cushing's disease, that is hypoadrenocorticism as opposed to hyperadrenocorticism. Primary hypoadrenocorticism (Addison's disease) results from a deficient production of glucocorticoid, mineralocorticoid or both due to bilateral destruction of all of the layers of the adrenal cortex.
Most cases of Addison's disease are thought to be idiopathic (unknown cause) but are probably immune mediated. Destruction of the adrenal cortex can also occur secondary to infections, tumors, ischemic necrosis, and the drug o,p'-DDD (used as treatment for Cushing's disease). There is no current evidence of a hereditary basis for primary hypoadrenocorticism (Addison's disease).
Secondary hypoadrenocorticism is associated with inadequate levels of circulating ACTH which results in a decreased level of adrenal glucocorticoids. Mineralocorticoids are not significantly affected. This is most commonly seen after abrupt withdrawal of long-term or high-dose corticosteriod therapy, but any lesion of the hypothalmus or the pituitary gland can cause decreased ACTH production.
Both types of hypoadrenocorticism are relatively uncommon in dogs with the highest incidence seen in young to middle age females. According to my current available references no breed predilection exists.
Early diagnosis is difficult since most of the clinical signs are present intermittently such as during stressful episodes. In the primary disease, as tissue destruction in the adrenal glands proceed the initial relative deficiency gives way to an absolute decrease in circulating cortisol level. Similarly in the secondary disease an early relative lack of ACTH becomes an absolute deficiency as the disease process progresses.
A presumptive diagnosis of hypoadrenocorticism can be made utilizing the following; history, physical examination, red cell counts and morphology, measures of kidney function (including urea nitrogen level, creatinine, urine specific gravity, and serum electrolyte levels), radiographic studies and electrocardiogram.
ACTH stimulation test is used in the definitive diagnosis of hypoadrenocorticism. While numerous protocols for ACTH stimulation tests have been published the following is in wide use:
- Patient fasted for 12 hours overnight in the hospital.
- Plasma sample for cortisol assay to determine basal level.
- ACTH injection
- Plasma sample taken 2 hours post-injection for cortisol assay.
Patients with either primary or secondary disease will show a sub-normal response to the ACTH administration. In most the resting or basal concentration of cortisol will be well below normal and the post injection value will be the same as or only slightly elevated from the basal level. In patients with primary disease there is no response due to lack of functional adrenal cortical tissue. In cases of secondary disease due to lack of ACTH there is no or minimal response since chronic ACTH deficiency results in atrophy of the adrenal cortex and the atrophied cells are not capable of responding to a single injection of ACTH.
Differentiation between primary and secondary disease can be done by either ACTH assays or repeating the ACTH stimulation test after several days of repeated ACTH injections. Most patients with primary disease will have significantly elevated ACTH level due to lack of negative feedback on the pituitary and continued unrestrained production of ACTH. ACTH determinations are somewhat difficult owing to rapid degradation in fresh whole blood samples. ACTH treatment over several days followed by another ACTH stimulation test can differentiate primary from secondary since the patient with primary disease will show the same pattern of response as with the initial test(low or minimal cortisol production) whereas the patient with secondary disease should be capable of responding to the ACTH injection after the atrophied cells have been stimulated into production by the repeated ACTH injections.
Since it is not particularly useful to specify a normal range of values for the ACTH stimulation test it is more relevant to test the response of the patient in terms of reference to the patients own baseline or resting values. The use of the test as a screening tool may have some value but would be subject to interpretation or the results, since subclinical disease may demonstrate a pretial or subnormal rels in cortisol levels that might well ball within what would be considered "normal".
The majority of dogs examined by researchers showed evidence for an immune mediated component to the primary disease, that is on histopathologic evaluation of the adrenal glands at necropsy, adrenal cortical tissue was found to be infiltrated by plasma cells, lymphocytes and replaced by fibrous connective tissue. This immune mediated atrophy was the most frequently observed lesion. This type of immune mediated disease process might in fact be genetically based but at present there is no evidence supporting this.
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Bloat (Gastric Dilatation and Volvulus)
Gastric Dilation-Volvulus (GDV), or bloat as it is commonly known, is a very serious and life-threatening condition, occurring suddenly and can kill in a matter of hours. Bloat usually occurs in two parts; first the stomach rapidly fills up with air, increasing pressure and causing compression of surrounding organs and shock. Secondly, filled with air the stomach can rotate on itself, pinching off the blood supply. The entire blood supply is disrupted and the dog's condition begins to deteriorate rapidly.
Which breeds are susceptible?
A definite link with the build of the dog has been recognised, and bloat is much more likely to occur in large, deep-chested breeds. Great Danes, Saint Bernard, Weimaraner, Irish Setter and Gordon Setter being among the breeds with the highest incidences, however and deep-chested breed is susceptible. It has been noticed that there is often a tendency for bloat to run in certain lines. Because bloat is correlated to the depth and width of the dog's chest, and genes from the parents determine these traits, if the parents are deep chested then it is most likely that their progeny will also have deep chests and thus be more susceptible to bloat. The problem has been known to occur in small dogs, but very rarely.
What causes bloat?
Bloat appears to be caused by a number of different and unknown reasons, and is usually a combination of events. Studies of the stomach gas that occurs, suggests that dilation occurs as a result of swallowing air. Whilst we normally burp to release excess air, for some reason these dogs are unable to release it.
What are the symptoms?
When gas first starts to accumulate in the stomach, the dog will appear slightly uncomfortable. The stomach then starts to dilate (gastric dilation) and the dog will become anxious and restless, often pacing, and the stomach may be swollen. He may also try to vomit, but will only bring up a white foam, no food.
The next stage is when the stomach twists (gastric volvulus) and the dog becomes extremely restless, whining and panting as well as salivating and trying to vomit every few minutes. He may go on to stand with his legs apart and hang his head down. The stomach is swollen and sounds hollow if tapped.
When the blood supply is cut off, organs become compressed and shock can begin to develop. The dog is unable to stand, or stands very shakily, with his legs apart. The stomach is very swollen and breathing is shallow.
The final stage is shock and heart failure develops, the dogs gums are white or blue and death is imminent.
How is it treated?
The best chance a dog has of surviving is immediate veterinary attention. Sadly, even with treatment, a large percentage of dogs still die, some survive surgery but then die of the shock after treatment.
Your veterinarian must relieve the pressure, decompressing either by using a stomach tube or inserting a large needle into the stomach to release the gas. The less time the pressure is on the stomach and organs the better the dog's chances of survival. Once the dog is stabile, x-rays are taken to determine whether a torsion is present. If it is, then surgery is performed to untwist the stomach, which is then stitched to the abdominal wall to prevent reoccurrence.
How is it prevented?
The cause of bloat is unknown and therefore it is near impossible to determine how to prevent it. Some suggestions are listed below, but there is no guarantee that these will help to prevent bloat occurring.
- Divide the day's ration into two or three meals a day, spacing them well apart.
- If feeding a dry food, ensure it is well soaked beforehand.
- If your dog has a tendency to eat very quickly, gulping his food down, try slowing him down by placing a very large smooth stone (too big to be swallowed) in the middle of the food bowl.
- If you have more than one dog and meal times are a competition to see who eats fastest then try feeding them in separate rooms.
- Put both the water and food bowls on a stand at head height, thus reducing the amount of air swallowed during eating or drinking.
- Do not allow your dog to drink large quantities of water at a time, especially after a meal.
- Avoid exercise for about two hours after a meal.
- Avoid feeding before or during stressful or exciting situations.
- Most important of all, ensure you know and can recognise the symptoms of bloat and act quickly by taking him to the vet immediately.
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Canine Hip Dysplasia
(1 vote)
Dysplasia literally means abnormal, so hip dysplasia literally translates as abnormal formation of the hip socket. The hip is a ball and socket joint, in a normal hip the ball fits snugly into the socket, forming a pivot point. Dogs which have a genetic predisposition for hip dysplasia are born with normal hips. However, as the dog grows, the structure of the hip joint becomes badly formed, and the ball no longer fits snugly into the socket and therefore does not rotate smoothly.
Although this problem is more common in larger breeds, smaller breed dogs and mongrels are not immune from it. Ultimately, the end result arthritis and a painful and crippling degenerative joint disease.
What are the Symptoms?
The severity of the symptoms obviously depends upon the degree of the dysplasia. More often than not the dog becomes lame and may be unwilling to run and play as much as he used to. He often starts to have trouble getting up or climbing stairs. If and older dog, he may perform a "bunny hop" when running, or walk with a "waddle" and become reluctant to exercise.
Diagnosis
There are many diseases which display the same symptoms as hip dysplasia, therefore the only true way to diagnose hip dysplasia is by a complete physical and neurological examination, and then x-ray of the hips.
What causes it?
Hip dysplasia is a multifactorial trait, which means that a number of different factors can contribute to it. However, hip dysplasia is basically a genetic trait and will not develop if the hereditary factor is not there to begin with.
The environment plays a large part in whether or not a dog will suffer from hip dysplasia.
Nutrition is the greatest contribution. Puppies should be kept lean and not fat, obviously a puppy which is carrying round too much weight will exacerbate any degeneration of the joint. Research has also shown that giving a diet too high in protein and calcium also exacerbates the condition. Rapid growth in a young puppy also contributes, and, in most cases, the rapid growth rate is directly related to feeding a high calorie diet to puppies. Over supplementation of calcium has likewise been shown to be a major factor in the development of skeletal disease in puppies.
Exercise is the other main contribution. Many people over-exercise young puppies, or give them the wrong type of exercise. The wrong type of exercise can include forced running for any distance and too much exercise on tarmac or other hard surfaces. Up to at least six months of age, exercise on hard surfaces should be kept at a minimum. Correct exercise for puppies includes running and playing in the garden or in a park, although games that involve jumping and very rough play should be avoided, and the puppy should be allowed to rest as soon as he has had enough and must not "over-do" it. Swimming is an excellent form of exercise which builds up the muscles without putting stress on the joints.
How is it treated?
The treatment depends a lot upon the severity of the hip dysplasia and the age of the dog concerned, and veterinary treatment must be sought.
Any dog with hip dysplasia should be kept fit and trim as any excess weight will obviously aggravate the condition, but good muscle tone will help to support the dog's weight. Swimming is an excellent form of exercise which builds up the muscle without stress to the joints.
Non-steroid anti-inflammatory drugs, such as aspirin and carprofen, can often help manage pain. Research has shown that
Vitamin C can also reduce the inflammation in the affected joints. Some people have also reported success with holistic medicines.
However, in some dogs the arthritis in the joint can become so painful that if cannot be controlled medically. When the pain becomes this bad, there are various surgical procedures which can be done to relieve the pain. Each procedure has its pros and cons, and different veterinary surgeons may have more experience, and therefore be more skilled, with a particular type of surgery.
One such procedure is called a femoral head osteotomy. This involves removing the head and neck of the femur so that the bone does not contact bone, and a fibrous scar tissue then forms a "false" joint. As the dog's muscles must be strong enough to support the dog's weight on the false joint, regular exercise is very important. Another surgical procedure is hip replacement. This is the same as the human hip replacement, the diseased joint is taken out and an artificial joint is inserted.
Can it be Prevented?
Hip dysplasia is an inherited disease with a polygenic (influenced by more than one gene) mode of inheritance. Total elimination of Canine Hip Dysplasia is an unrealistic goal, but by selectively breeding dogs with good hips, breeders can reduce the incidence of hip dysplasia. In this respect, the British Veterinary Association, along with The Kennel Club, run a scheme to test for hip dysplasia, which should aid the breeder when choosing breeding stock.
Nutrition and exercise factors have been discussed above, and we know that with the correct diet and exercise it is possible to ensure that the hip dysplasia is not expressed, causing lameness and pain. Each breed has different requirements, and advice on this should be sought from both the breeder and a veterinary surgeon.
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Canine Hip Scoring - Criteria
(1 vote)
The British Veterinary Association (BVA) and The Kennel Club in the UK (TKC) have joined together to run a hip scoring scheme for breeders, in order to test for canine hip dysplasia, the most common inherited joint problem of large breed dogs. This current system came into effect in 1984. Dogs are scored from the age of 12 months, and can only be scored once in their lifetime.The BVA/TKC publish a list of Breed Mean Scores (BMS) for each breed, together with the number of dogs tested to date and the range of scores achieved. It is then recommended that breeders ensure their breeding stock have scores which are well below the BMS. From an x-ray taken at the owner's vets, the BVA scores each of the hip joints: the norberg angle (0-6); subluxation (0-6); cranial acetabular edge (0-6); dorsal acetabular edge (0-6); cranial effective acetabular rim (0-6); acetabular fossa (0-6); caudal acetabular edge (0-5); femoral head and neck exostosis (0-6); femoral head recontouring (0-6), thus each hip can receive a maximum score of 53 and overall score of 106. The lower the score the better, so 0/0 would be perfect, while 53/53 would mean that the dog had no hips at all! Norberg Angle Measures two features; the degree of congruence between the FH and acetabulum and the length of the CrAE which gives a relative indication of acetabular depth. Subluxation Evaluation is based principally on the degree of congruence between the femoral had and acetabulum. The general 'fit' of these two components is assessed by the relationship between the FHC and the underlying image of the DAE; the configuration of the cranial joint space is also taken into account, particularly at the lower end of the scoring scale, when abnormalities are relatively minor. The cranial joint space is seen as a radiolucent shadow between the CrAE and adjacent cranial articular margin of the FH. For a zero score the FHC must be medial to the DAE and the cranial joint space uniformly narrow, with the curve of the CrAE eactly following that of the FH. Cranial Acetabular Edge Minor alterations in the shape, contour and possibly the length of the CrAE are generally believed to be indicators of poor articular congruence, while more severe changes are clearly consequences of chronic instability, abnormal marginal wear and remodelling of the joint. For a score of zero the CrAE should be convex, uniformly curved and match exactly the countour of the adjacent femoral head with no lateral or medial divergence of the cranial joint space. Dorsal Acetabular Edge On good quality radiographs, the DAE forms a well-defined density interface which traverses the fH almost vertically and extends a little beyond it cranially and caudally. The clarity with which it can be seen is highly variable. A minor change in the contour of the DAE, which is normal slightly curved, merits a score of 1, but small localised irregularities, seen only on radiographs of exceptionally high quality, are considered to be within normal limits. Higher scores are related to definitive pathological changes associated with degenerative joint disease (osteoarthritis), the smallest being minor exostosis, which is usually seen cranially. Cranial Effective Acetabular Rim The earliest detectable abnormalities of the CrEAR are either minor exostosis, usually in the form of a small, well-modelled osteophyte, or slight 'rounding off' of the junction between the CrAE and DAE, which may be seen in the presence of a non-biblabiated CrAE. Acetabular Fossa Detectable bone deposition in the AF is almost always associated with marked subluxation and the amount tends to increase in proportion with the increase in the other radiographic hallmarks of secondary degenerative joint disease (osteoarthritis). Objective numerical scoring of this criterion is difficult, but as changes are likely to be recorded only in dogs with a total score considerably higher than average, the importance of a high level of accuracy is diminished. Caudal Acetabular Edge The CaAE is the segment of the acetabulum which is subject to the widest range of normal radiographic variation. Radiographic abnormalities are scored between 0 and 5 and changes are due mainly to exostosis with signs of wear being apparent only in advanced cases. Femoral Head and Neck Exostosis The normal FH should have a smooth rounnnnndish profile, but the shape may vary considerably. Recontouring of the Femoral Head This criterion is used to record the extent to which the FH shape is altered as a consequence of instability. Thus scores are likely to be awarded only in cases in which secondary changes are well established, when remodelling occurs as a result of the combined effects of periarticular new bone formation and loss of subchondral bone following total destruction of articular cartilage. Scoring Criteria:
| Score | Norberg Angle | Subluxation | Cranial Acetabular Edge | Dorsal Acetabular Edge | Cranial Effective Acetabular Rim | Acetabular Fossa | Caudal Acetabular Edge | Femoral Head/Neck Exostosis | Femoral Head Recontouring | | 0 | +15 & over | Femoral head well centred in acetabulum | Even curve, parallel to femoral head throughout | DAE has slight curve | Sharp, clear-cut junction of DAE & CrAE | A fine bone line curves medial and caudal from caudal end of CrAE | Clean line | Smooth rounded profile | Nil | | 1 | +10 to +14 | Femoral head centre lies medial to DAE. Lateral or medial joint space increases slightly. | Lateral or medial 1/4 CrAE flat. Lateral or medial joint space diverges slightly | Loss of S-curve only in the presence of other dysplastic change | Indistinct junction of DAE and CrAE | Slight increase in bone desnity medial to AF. 'Fine line' hazy or lost | Small exostosis at lateral CaAE | Slight exostosis in 'ring form' and/or dense vertical bony line adjacent to trchanteric fossa ('Morgan line') | Femoral head does not fit in circle due to exostosis or bone loss | | 2 | =5 to +9 | Femoral head centre superimposed on DAE. Medial joint space increase obvious | CrAE flat throughout most of its length | Very small exostosis on cranial DAE | Very small exostosis or very small facet | Fine line lost in AF and ventral AE hazy due to new bone. Notch at CaAE clear | Small exostosis at lateral and medial CaAE | Slight exostosis visible on skyline and/or density on medial femoral head | Some bone loss and/or femoral head/neck ring of exostosis | | 3 | 0 to +4 | Femoral head centre just lateral to DAE. 1/2 femoral head within acetabulum | CrAE shows slight bilabiation | Obvious exostosis on DAE (especially cranially) and/or minor 'loss of edge' | Facet and/or small exostosis and/or slight bilabiation | Incomplete remodelling of acetabulum with medial face lateral to AF. Ventral AE lost. AF hazy. Notch irregular | Large exostosis and narrow notch at CaAE | Distinct exostosis in 'ring formation' | Obvious loss and distinct exostosis giving slight conical appearance | | 4 | -1 to -5 | Femoral head centre clearly lateral to DAE | 1/4 femoral head within acetabulum | CrAE shows moderate bilabiation | Exostosis well lateral to DAE and/or moderate 'loss of edge' | Obvious facet and/or obvious exostosis and/or moderate bilabiation | Marked exostosis and 'hooking' of lateral end of CaAE | Obvious complete collar of exostosis | Gross remodelling. Obvious bone loss and exostoosis gives mushroom appearance | | 5 | -6 to -10 | Femoral head centre well lateral to DAE. Femoral head just touches DAE | CrAE shows gross bilabiation | Marked exostosis all along DAE and/or gross 'loss of edge' | Gross exostosis and/or facet and/or gross bilabiation | Gross remodelling. Dense new bone throughout acetabulum. CaAE notch lost and AF obscurred | Gross distortion due to mass of new bone in acetabulum. Notch lost completely | Massive exostosis giving mushroom appearance | Very gross remodelling with marked bone loss and much new bone | | 6 | -11 and over | Complete pathological dislocation | Entire CrAE slopes cranially | Massive exostosis from cranial to caudal DAE | Complete remodelling of CrEAR. Massive exostosis and/or gross facet | Complete remodelling and new articular surface, well lateral to AF. Notch lost | Void | Massive exostosis and infill of trochanteric fossa and below femoral head | Femoral head improperly shaped due to maldevelopment or femoral head centre |
References: BVA/KC scoring scheme for control of hip dysplasia: interpretation of criteria; Christine Gibbs, BVSc, PhD, DVR, MRCVS
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Coprophagia
Coprophagia is the medical term for when a dog eats either its own faeces or that of another animal. There are three types of Coprophagia: Autocoprophagia eating its own faeces; Intraspecific Coprophagia eating faeces from within its own species (ie another dog); Interspecific Coprophagia eating faeces from another species (ie cat, deer, rabbit, horse, etc)
Interspecific Coprophagia is the most common version of this trait. The cause of this behaviour is not fully understood, these are some suggestions and theories
Attention-seeking behaviour: The owner reprimands the dog despite being a negative reaction it is attention, which is what the dog may crave.
Allelomimetic behaviour: The dog observes the owner picking up the faeces and learns from them to do so as well -- monkey see monkey do.
Genetic: the dog dates back to the Mesolithic period some 14000 years ago and fed off our middens and latrines therefore this was a staple diet.
Taste: taste may be a factor. It likes the, this is the likely mechanism in interspecific coprophagia such as eating cat faeces.
Maternal behaviour: A bitch with puppies has to stimulate the pups to toilet in the first 3 or 4 weeks. She then eats and drinks the resulting faeces/urine, therefore keeping the den clean and preventing the scent of the faeces from attracting predators. The pups see this and copy. Monkey see monkey do again.
It has also been suggested that eating faeces could be to aid digestion, in other words a probiotic which encourages healthy flora in the gut.
Some Treatments:
Forbid (TM)(R): A powder added to a dog's food. It is supposed to make the faeces taste bad (veterinary prescription only).
Deter (TM)(R): This is a pill given to a dog with its food. Like Forbid, Deter is supposed to make the faeces distasteful.
Some people put chilli sauce or mustard on the faeces in the hope that it will deter the dog. One of the best treatments is simply picking up the faeces. Lack of access can sometimes break the cycle.
Positive Reinforcement: This is the process of reinforcing another behaviour Instead When the dog is about to begin eating the faeces, the owner can then use a number of techniques and commands - "Leave it", "Off ", "No", etc.
Simple aversion therapy can be done by letting the dog approach the stool on a long lead. If he starts sniffing it, give a leash check with something like a Jingler or a noise aversion device such as training discs or a plastic bottle with pebbles can be rattled, these devises should be pre- programmed. If he passes by, then simply praise him.
Another technique that I have found can work extremely well is get one of the dog's or cat's faeces; allow it to dry a little. Go to your local joke shop and purchase a cap banger; this is a spring-loaded device that makes a bang when something is moved or lifted. Place the slightly dried faeces on the cap banger and await results. It works after about three bangs. Also great for counter surfing/food stealing which can of course be dangerous to a dog if it eats the wrong things.
If, as in the previous cure, the dog is "Autocoprophagic", i.e. eating own faeces, then a method that sometimes works is to feed your dog pineapple slices in its food. It apparently makes their faeces foul tasting. Not something even in the depth of scientific analysis do I intend to test for myself.
There are some health implications to coprophagia. It is merely a habit, which we see as vile and disgusting, but generally causes no real problems. However there is a risk ingesting internal parasites. This can happen if your dog eats the faeces of unfamiliar, infested dogs or cats or the faeces of wild life such as rabbit deer etc. If you worm the dogs regularly then the risk is far less, The fecal-oral route can also transmit some rather nasty canine viral diseases. Hepatitis and canine parvovirus are just two of these serious diseases. Fortunately, vaccinated dogs should be covered for these potentially fatal viruses.
I would also strongly recommend keeping the dog away from cat faeces because of the risk of organisms such as Toxoplasma gondii which can cause serious and sometimes fatal consequences including hepatitis, pneumonia, blindness, and severe neurological disorders. The intestinal phase of this nasty disease occurs only in cats (wild as well as domesticated) therefore transmission to dogs is by ingestion of oocysts (in cat faeces) or bradyzoites in raw or undercooked meat.
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Demodectic Mange
(1 vote)
One of the most difficult health problems a dog owner ever encounters is demodectic mange. This disease is caused by the presence of the mite Demodex Canis in the hair follicles of the dog in conjunction with an impaired or deficient immune system. The disease is thought to be caused by a genetic defect in the immune system.
Frequency
The disease is divided two ways: It is divided into juvenile and adult onset mange and into localized and generalized mange. The recent BTCA Health Survey found that almost 10% of Boston Terriers have had localized demodectic mange; 5% have had the generalized form. It is well established that the demodex mites are carried on almost all healthy dogs and spend their entire life in the hair follicles without causing problems for most dogs.
Demodectic mange in puppies
Demodectic mange is mainly a disease of young dogs that have poorly developed immune systems. The majority of puppies are immune to the mites and will display no ill effects from them. Most dogs will have mature immune systems by the time they are from 12 to 18 months of age and will "outgrow" the problem.
In the first hours of a puppy's life the demodex mites begin moving to the nursing puppies from the mother dog. These mites will lay eggs in the hair follicles which hatch and multiply. By the time a puppy is 4 to 6 months old he may be showing signs of hair loss around his face caused by the multiplication of the mites.
Diagnosis of demodectic mange
Diagnosis is always made with skin scrapings viewed under the microscope to identify the demodex mites.
Demodectic mange in older dogs
Older dogs with demodectic mange may have a serious underlying disease problem that interferes with a well functioning immune system. Cushings, cancer, hypothyroid and even diabetes have been thought to be associated with a predilection for this mange.
Localized demodectic mange
The differentiation of localized from generalized demodectic mange is based upon the severity of the infection. In cases where there are fewer than five spots of mange on a dog it is termed "localized"; more than 5 spots and the mange is termed "generalized" These spots usually occur on the face but may occur anywhere including the feet. A puppy with "localized" mange will usually be treated with the application of a gentle salve and the owner is encouraged to give supportive treatment that includes a high quality diet, possible addition of vitamins, and special baths. Miticidal treatment is not usually recommended as appropriate treatment for young dogs with localized demodectic mange, as most puppies (90%) will outgrow the problem as their immune systems mature.
Generalized demodectic mange
Generalized demodectic mange represents a totally different problem. With this disease symptoms can become severe, and in addition to substantial hair loss, there can be crusting, oozing, cracking and infection and inflammation of the skin. Some dogs can become very ill. Dogs with a substantial problem need immediate treatment of the skin as well as supportive treatment of the immune system. The first line of treatment is usually a miticide such as Amatraz. Sometimes the dog's coat is shaved and he will be given a series of dips with this medication. It is important to follow label instructions to avoid compli- cations for both dogs and humans. Your veterinarian will give you detailed instructions. Scrapings will be done again following the first series of dips. There is another treatment that is commonly used for demodectic mange that has not yet been approved by the FDA. It is the use of Ivermectin, the same medication that is used for heartworm prevention, but given in a much stronger dosage to kill the demodex mites. It is often continued for a month. Antibiotics may be used in conjunction as well as vitamin supplementation.
The dog may also be given further examination for any underlying disease. Most dogs will recover from generalized demodectic mange. A few will require life-long treatment. Dogs who receive miticidal treatment cannot be assumed cured until a final scraping is done 12 months after the last treatment. Most dogs that will relapse do so during the first 6 months.
Breeding Recommendations
Dr. Lowell Ackerman, a board certified canine dermatologist, advises against the breeding of animals with juvenile demodicosis. He says, "Animals that self cure have a much better prognosis than those requiring miticidal therapy".
Dr. Race Foster of Foster & Smith, Inc. says "Demodectic mange is not an inherited condition but the suppressed immune system that allows the puppy to be susceptible to the mites can be. Remember that all puppies receive the mites from their mother but only a few have ineffective immune systems and develop the mange. The sensitivity can be passed genetically through the generations. Individuals that have a history of demodectic mange, and their parents and siblings should not be bred. Through careful breeding most cases of generalized Demodicosis could be eliminated."
Dr. James M. Giffin and Dr. Liisa D. Carlson say in their book, Dog Owner's Home Veterinary Handbook, "Because of an inherited immune susceptibility, dogs that recover from demodectic mange should not be bred."
The University of California - Davis, Book of Dogs from the School of Veterinary Medicine says, "Because there is ample evidence indicating that juvenile-onset demodicosis has a heritable component, it has been recommended that dogs with generalized demodicosis be neutered (if that has not already been done) in order to prevent perpetuation of the underlying defect(s).
Canine dermatologists have a policy against treating dogs for generalized demodcicosis if they are to be used for breeding. They feel general acceptance of this policy will eventually eradicate the disease.
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Patella Luxation
Luxating means out of place, or dislocated. The patella is the equivalent to the human kneecap and part of the stifle structure, and therefore a luxating patella is a kneecap that moves out of its normal location. The patella normally moves up and down in a groove in the lower femur bone called the trochlear groove. In patella luxation the groove is often shallow and this shallow groove prevents the patella from sitting deeply, predisposing it to dislocation. A patella that is not stable but does not slip out of joint is said to be subluxating, while one that comes out of joint on its own is said to luxate.
There are two types of luxation, medial and lateral. Medial luxation is the most common and is where the patella dislocates to the inside of the knee. One knee can be more severely affected than the other. This type of luxation is mainly congenital (present at birth) and trauma is not usually associated with it.
With lateral luxation the patella dislocates to the outside of the knee. Lateral patellar luxation can be congenital or the result of trauma to the knee. In some cases the patella can luxate both medially and laterally. Again, this disorder can affect one or both knees and to varying degrees.
What are the Symptoms?
Signs of luxation may appear as early as weaning or may go undetected until later in life. Signs include intermittent rear leg lameness, often shifting from one leg to the other, and an inability to fully extend the stifle. The dog may frequently stop to stretch his rear leg behind him to allow the patella to pop back into its normal groove. Mildly affected animals can have a hopping or skipping action. This is due to the patella luxating while the dog is moving and by giving an extra hop or skip the dog extends its stifle and is often able to replace the patella until the next luxation, when the cycle repeats.
Diagnosis
A veterinarian can usually confirm diagnosis by manipulating the stifle joint and pushing the patella in and out of position. This can be done as early as 8 weeks of age to ensure that congenital patella luxation is not present before the puppy leaves for his new home. This type of examination is best left to the veterinarian, as an overzealous examination can stretch the ligaments.
The degree of patella luxation is graded from 1 to 4 depending on the relative ease with which the patella luxates.
Grade 1 is the mildest and grade 4 the most severe. With grades 1 and 2 patella luxation the dog may not show any symptoms and can be incidental findings in mature dogs who have never been lame. Grade 3 and 4 dogs are usually lame. Severe cases may develop abnormal growth of the long bones of the leg or a non-functional knee.
Grade 1: Occasional carrying of the leg is seen, often described as skipping or hopping, which may be transient, often returning to normal by itself. Your veterinarian may easily luxate the patella manually and return it to its normal position. Pain may be evident only when the knee cap is luxated.
Grade 2: The frequency of luxation increases, becoming more or less permanent. The dog will usually carry its leg, but will occasionally bear weight on it. When palpated by the veterinarian, a dry, crackling sensation (crepitation) may occur in the joint. A grade 2 luxation can increase in severity, and if not surgically treated, can develop into degenerative joint changes.
Grade 3: Permanent dislocation that occurs though weight bearing may still be possible, however the stance will appear somewhat crouching or bowlegged. Surgical intervention should not be delayed, especially if this is found in a young, growing dog. Rapid growth of abnormalities results in progressive deformities.
Grade 4: Permanent luxation, with the affected limb always being carried, creates a bowlegged / crouching stance. Early surgery is strongly recommended at this stage for bone deformities of the femur and tibia may occur.
What Causes It?
Patella luxation is strongly suspected of being inherited, but it can also be caused by trauma. When the luxation is from trauma, something has occurred that has caused the knee to be forced out of normal alignment. Usually the traumatic injury occurs when the dog's leg gets caught somehow and he struggles to pull free. Or during an overly enthusiastic playtime when the playmate grabs the foot and holds tight while the excited puppy tries to get away. Any other similar accident can permanently injure this small joint.
If the luxation is believed to be of a genetic nature, it is due to an abnormal development of the leg. The possible mode of inheritance is at present undetermined, but it is believed that it may be polygenic. This means that any number of genes may be involved, and that dogs are not "carriers" as such but it is merely an unfortunate specific combination of certain genes from the parents that produce patella luxation.
As with all polygenic traits, affected dogs should not be bred from as the risk of producing puppies with patella luxation would then be increased.
How is it treated?
Treatment is based on the severity of signs as well as the dog's age and weight, and ranges from rest (decreasing your pet's activity for 1-2 weeks) to surgical reconstruction of the knee joint.
Grade 1 luxations may respond well to anti-inflammatory therapy and restricted exercise. These may or may not progress to worsening grades.
Grades 2 through 4 luxations tend to require surgical corrections. The worse the luxations the more reconstructive surgery required to provide a functional joint.
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Understanding Laboratory Tests
(1 vote)
Have you ever received a copy of your dog's blood results and wondered what it all means? Below is a list of some of the major tests and vocabulary used in laboratory reports.
Veterinarians use a wide variety of tests to certify good health or indicate the presence of infection or disease. A Complete Blood Count or Full Blood Count shows the number and type of cells in the dog's blood. This standard test can identify conditions like anaemia and leukaemia, as well as diagnosing many infections. A Serum Chemistry Profile includes a variety of tests that examine the function of organs, such as the liver and thyroid. There can be a difference in clinical chemistry between different breeds. It is important to establish what is normal in your dog, as all animals will differ slightly. An abnormal reading may be normal for your dog. I have not shown the normal values as these can differ between the various laboratories; the normal range is usually shown beside each result on the lab report.
Red Blood Cells (RBC)
The Red Blood Cells are responsible for carrying oxygen and carbon dioxide throughout the body. Iron deficiency will lower RBC count. In a more reduced count, it may indicate haemorrhage, parasites, bone marrow disease, B-12 deficiency, folic acid deficiency or copper deficiency. A red blood cell lives for 120 days so anaemia of any kind other than haemorrhage indicates a long-standing problem.
Hematocrit (HCT) or Packed Cell Volume (PCV)
Provides information on the amount of red blood cells (RBC) present in the blood. Decreased levels means anaemia from haemorrhage, parasites, nutritional deficiencies or chronic disease process, such as liver disease, cancer, etc. Increased levels are often seen in dehydration.
Haemoglobin (Hb)
The essential oxygen carrier of the blood. Decreased levels indicate the presence of haemorrhage, anaemia, and iron deficiency. Increased levels indicate higher than normal concentrate of RBC, B-12 deficiency (because there are fewer cells).
Reticulocytes
Immature red blood cells. Decreased count is usually associated with anaemia. Increased count is associated with chronic haemorrhage or haemolytic anaemia.
Platelets (PLT)
Play an important role in blood clotting. Decrease in number occurs in bone marrow depression, vascular coagulation, systemic lupus, autoimmune haemolytic anaemia or severe haemorrhage. Increased number may occurs with fracture or blood vessel injury, or cancer.
MCV
This is a measurement of the average size of the Red Blood Cell. Elevated volumes can be due to B-12 folic acid deficiency and reduced volumes are from an iron deficiency.
White blood cells (WBC)
White blood cells are the body's primary means of fighting infection. Decreased levels may indicate an overwhelming infections (viruses), or drug or chemical poisoning. Increased levels indicate bacterial infection, emotional upsets and blood disorders.
Lymphocytes (L/M)
A white blood cell, which is formed in the lymphoid tissue. Lymphocytes produce immune bodies to overcome and protect against infection. These smooth, round white blood cells increase in number with chronic infection, recovery from acute infection or under active glands and decrease with stress, treatment with steroids and chemotherapy drugs.
Calcium (CA)
Diet, hormone levels and blood protein levels influence Blood calcium levels. Decreased levels indicate acute damage to the pancreas, deficiency of pancreatic enzymes or under active thyroid. Muscle twitches may occur in decreased level. Increased levels can be an indicator of certain types of tumours, thyroid or kidney disease. Also a high calcium level may indicate poor metabolism of fats and protein.
Phosphorus (PHOS)
Affected by diet, hormones and kidneys. Decreased levels may show overactive thyroid gland and malignancies, malnutrition and malabsorption. Increases with under active thyroid gland and kidney failure.
Electrolytes (Sodium, Potassium, Chloride)
The balance of these chemicals is vital to health. Abnormal levels can be life threatening. Electrolyte tests are important in evaluating vomiting, diarrhoea and cardiac symptoms.
Cholesterol (CHOL)
Decreased levels are found in an overactive thyroid gland, intestinal malabsorption. Elevated levels of cholesterol are seen in a variety of disorders including hypothyroidism and diseases of the liver, kidneys, cardiovascular, diabetes, stress.
Alanine aminotransferase (ALT)
An enzyme that becomes elevated with liver disease.
Alkaline Phosphatase (ALKP)
An enzyme produced by the biliary tract (liver). High levels indicate bone disease, liver disease or bile flow blockage.
Total Billirubin (TBIL)
A component of bile, bilirubin is secreted by the liver into the intestinal tract. High levels can lead to jaundice and indicate problems in the liver and bile duct.
Total Protein (TP)
Increases can indicate dehydration or blood or bone marrow cancer. Decreases indicate malnutrition, poor digestion, liver or kidney disease, bleeding or burns.
Globulins (GLOB)
Decreased levels may indicate problems with antibodies, immune-deficiency viruses or risk of infectious disease. Increased levels may indicate stress, dehydration or blood cancer, allergies, liver disease, heart disease, arthritis and diabetes.
Albumin (ALB)
Produced by the liver, reduced levels of this protein can point to chronic liver or kidney disease, or parasitic infections such as hookworm.
High levels indicate dehydration and loss of protein.
Blood Urea Nitrogen (BUN)
BUN is produced by the liver and excreted by the kidneys. Decreased levels are seen with low protein diets, liver insufficiency, and the use of anabolic steroid drugs. Increased levels indicate any condition that reduces the kidney's ability to filter body fluids in the body or which interferes with protein breakdown.
Creatinine (CREA)
Creatinine is a by-product of muscle metabolism and is excreted by the kidneys. Elevated levels can indicate kidney disease or urinary obstruction, muscle disease, arthritis, hyperthyroidism, and diabetes. An increased BUN and normal creatinine suggests an early or mild problem. An increased creatinine and increased BUN with elevated phosphorus may indicate a long-standing kidney disease.
Blood Glucose (GLU)
High levels can help diagnose diabetes and can indicate stress, excess of the hormone progesterone, an overactive adrenal gland. Low levels can indicate liver disease, tumours or abnormal growth on pancreas, or an under active adrenal gland.
Amylase (AMYL)
The pancreas produces and secrets amylase to aid in digestion. Elevated blood levels can indicate pancreatic and/or kidney disease.
Urinalysis
Colour The normal colour of urine is yellow to amber. Red is caused by blood. Dark yellow to brown with yellow foam is caused by bilirubin, reddish brown is caused by haemoglobin / myoglobin.
Transparency Normal urine is clear. Crystals, cells, blood, mucous, bacteria or casts, cause cloudy urine.
Gravity 1.007 - 1.029 Occurs with diabetes mellitus, insipidus, overactive adrenals, excessive thirst and pyometra. Over 1.040 occurs with high fever, dehydration, diabetes mellitus, vomiting, diarrhoea and severe haemorrhage.
PH Levels Urine should be 6.2-6.5, little on the acidic side.
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Vet Emergency
(2 votes)
When do you call the vet and when do you wait? Your dog isn't well, but the vets are closed until the next morning. Do you ring them for an emergency or will it wait until the morning?
The first thing you must do in any emergency is to keep calm. In a real emergency and if you are on your own, it is often better to call the vet immediately, rather than try administering first aid yourself, the quicker you call the vet, the quicker you can get professional help.
If you are in any doubt at all whether or not to call the emergency vet, it is far better to call and be advised. Never feel that you might be wasting their time!
Situations that should not wait until the morning are:
- The dog has difficulty in breathing and is distressed. This distress can be distinguished by posture, difficult or rapid breathing, gasping for air, whining/crying, or by change in the colour of the mucous membranes from a normal pink to blue.
- Any bleeding which can not be stopped by direct compression.
- Seizures or convulsions that recur in dogs not known to be epileptic.
- Most fractures. Some minor fractures can wait until morning, but this depends to some extent on the excitability of the patient. This warrants at least a call to the vet to confer on the advisability of waiting.
- Known ingestion of toxic substances.
- Allergic reactions. The need for emergency veterinary attention is not as clear cut. Excessive swelling around the facial area should be attended to immediately. Hives or welts deserve a call to the vet.
- Coma, or inability to respond to stimuli. Common in some small breeds of puppies due to hypoglycemia. Can occur in diabetics as well for the same reason.
- Any injury to the eye requires immediate attention. Since loss of vision can occur with injuries to the globe as well
as the cornea, examination can limit permanent damage. - Inability to urinate as evidenced by straining to urinate. Owner should be able to differentiate between staining to urinate and straining to defecate. If owner can not determine which is occurring than an examination should be done at once.
- Persistent vomiting/diarrhoea(especially bloody) can not always wait as electrolyte disturbances and dehydration can result.
- Symptoms of bloat in large, deep-chested dogs.
So now you have rung the emergency vet, what information should you have ready to tell them?
First of your entire name and, if you have to leave a message, your telephone number. If you have to leave a message and wait for the vet to call you back, remember to stay off the phone line!
You need to advise the vet that it is a dog and which breed, then the problem, clearly describing the symptoms and exact situation. What led you to be concerned? Have you administered first-aid or medications? If so, describe exactly what and when.
The dog's temperature is always useful if it can be obtained. Mucous membrane colour and CPR (capillary refill time) are very important. This is checked by pressing on the gums and noting how long it takes them to return to pink. Normal is almost immediately. Are there any current medical problems and what drugs is the dog taking? When were the last vaccinations given and what were they?
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