When it comes to understanding animals and the diseases they have, contract, and carry there is no limits. From dogs and cats to livestock and exotics it is necessary to learn and understand diseases from metabolic to degenerative or idiopathic, Neoplastic diseases and Toxic poisonings, Congenital and Genetic diseases to Immune related diseases, and Infectious and Contagious diseases to Parasitic Infections. There is a world that one can get lost in when it comes to learning about theses things. Some diseases have been around for years while others are still being studied with new ones occurring today in the modern world. Along with these diseases it is important to study and understand what causes them, what signs to look for, what species to look for them in, how to treat them, and how to prevent them from happening, IF you can even prevent them. Some diseases and conditions have vaccines to help with prevention and some do not, while some diseases are zoonotic meaning that they can be transmitted from animal to human. While there are hundreds upon hundreds of diseases to be looked at, the ten researched below are the ones once prevalent among the veterinary technicians job in the clinic; Hip Dysplasia and Ethylene Glycol poisoning in dogs, Hyperthyroidism and Rabies in cats, Strangles and Equine Recurrent Uveitits in Horses, Cryptosporidium and Fasciola Hepatica in Ruminants and Swine, Idiopathic Epilepsy in Aviaries, and Lymphoma in Ferrets.
Hip Dysplasia in dogs is a congenial condition caused by a femur that does not fit correctly into the pelvic socket, or poorly developed muscles in the pelvic area. The causes of hip dysplasia are considered heritable, but new research conclusively suggests that environment also plays a role. Although to what degree is caused by genetics versus what portion is caused by environmental factors are a topic of debate. Environmental influences would include the canine being overweight, having an injury of the rear legs at a young age, overexertion on hip joint at a young age, ligament tear at a young age, repetitive motion on forming joint like jogging with puppy under the age of one year. As more studies are done we are learning more information that will help provide procedures to effectively reduce the occurrence of this condition as a dog ages. Studies have shown that in dogs, the problem almost always appears by the time the dog is 18 months old. The defect can be anywhere from mild to severely crippling, and can eventually cause severe osteoarthritis for that pet.
Hip Dysplasia is most common in medium to large pure bred dogs, such as Newfoundlands, German Shepherd Dogs, Labrador or Golden Retrievers, Rottweilers and Mastiffs, but also occurs in some smaller breeds such as Spaniels and Pugs and occasionally, although with usually with minor symptoms in cats; especially Siamese. Some cases of Hip Dysplasia are so mild there are no symptoms at all, but if your dog seems stiff or sore in the hips when getting up or moving around, if he seems hesitant to exercise, stand on his hind legs or even climb the stairs, or if he’s limping or what is called bunny-hopping, a visit to your vet is in definitely in order.
The classic diagnostic technique is with appropriate X-rays and hip scoring tests. These should be done at an appropriate age under a year old or when symptoms are first seen, and perhaps repeated at adulthood. If these are done too young they will not show anything and give a false negative prognosis. It is also common to X-ray the spine and legs, as well as the hips, where dysplasia is suspected, since soft tissues can be affected by the extra strain of a dysplastic hip, or there may be other undetected factors such as neurological issues like nerve damage involved. In diagnosing suspected dysplasia, the x-ray is used to evaluate the internal state of the joints is usually combined with an exam of the animal and how it moves, to confirm whether its quality of life is being affected. Evidence of lameness or abnormal hip or spine use, difficulty or reduced movement when running or navigating steps, are all evidence of a problem within the hips. Both aspects have to be taken into account since there can be serious pain with little X-ray evidence. There are several standardized systems for categorizing Hip Dysplasia, set out by respective reputable organizations like the Orthopedic Foundation for Animals/OFA, PennHIP, and British Veterinary Association/BVA. Some of these tests require manipulation of the hip joint into standard positions, in order to reveal their condition on an X-ray. Since the condition is known to a large degree inherited, the hip scores of parents should be professionally checked before buying a puppy from a breeder, and the hip scores of dogs should be checked before using them for breeding. Despite the fact that the condition is inherited, it can occasionally arise even to animals with impeccably hip scored parents due to the environmental indications mentioned above.
There is no complete cure for Hip Dysplasia, although there are many options to alleviate the clinical signs or make the pet more comfortable if found to have the disease. The aim of treatment is to enhance quality of life. Crucially, this is an congenital and degenerative condition and so will change during the life of an animal, so any treatment is subject to regular review or re-assessment if the symptoms appear to get worse or anything significantly changes. If the problem is relatively mild, then sometimes all that is needed to bring the symptoms under control are suitable medications to help the body deal better with inflammation, pain and joint wear. In many cases this is all that is needed for a long time.If the problem cannot be controlled with medications, then often surgery is considered. There are traditionally two types of surgery - those which reshape the joint to reduce pain or help movement, and full hip replacements for animals which completely replaces the damaged hip with an artificial joint, similar to human hip replacements.
Non-surgical interventions include three elements: weight control, exercise control, and medication.Canine massage may alleviate discomfort and help move lymph and nutrients through the system. Weight control is often the single most important thing that we can do to help a dog with arthritis, and consequentially reducing the dog's weight is enough to control all of the symptoms of arthritis in many dogs. Reasonable exercise stimulates cartilage growth and reduces degeneration but always remember that excessive exercise can do harm too, So it is important to find a happy medium for you and your dog. Regular long walks in early or mild dysplasia can help prevent the loss of muscle mass to the hips and legs. Medication can reduce pain and discomfort, and also reduce damaging inflammation. Some dogs can use non-steroidal anti-inflammatory drugs or NSAIDs which double as an anti-inflammatory and painkiller. Typical NSAIDs used for Hip Dysplasia in dogs are carprofen or Rimadyl and meloxicam or Metacam respectively, both of these are used to treat arthritis resulting from Hip Dysplasia. Other NSAIDs such as tepoxalin or Zubrin, and prednoleucotropin or "PLT", which is a combination of cinchophen and prednisolone, are sometimes tried but do not seem to have the best effects based on some studies that have been released. NSAIDs vary significantly between species as to their effect: a safe NSAID in one species may be unsafe in another. It is important to follow your veterinarians advice. A glucosamine supplement may also give the body additional raw materials used in joint repair. Most glucosamine supplements can take 3–4 weeks to start showing its effects, so the trial period for medication is usually at least 3–5 weeks. It is also common to try multiple anti-inflammatories over a further 4–6 week period, if necessary, since an animal will often respond to one type but fail to respond to another. If one anti-inflammatory does not work, a vet will often try one or two other brands for 2–3 weeks each, also in conjunction with ongoing glucosamine, before concluding that the condition does not seem responsive to medication. But as with any medications there are side effects that can occur and must be monitored for any pet who is on them long term. For example, Carprofen, and other anti-inflammatories in general, although very safe for most animals, can sometimes cause problems for other animals, and in a few rare cases even cause sudden death through liver toxicity. This is most commonly discussed with Carprofen but may be equally relevant with other anti-inflammatories. As a result it is often recommended to perform monthly, or at least every six months, some blood tests to confirm that the animal is not reacting adversely to the medications. These side effects are rare but worth being aware of, especially if long-term use is anticipated. This regimen or medications and blood work can usually be maintained for the long term, as long as it is effective in keeping the symptoms of Hip Dysplasia at bay. Some attempts have been made to treat the pain caused by arthritic changes through the use of laser therapy, in particular what is called class IV laser therapy. Well-controlled clinical trials are unfortunately lacking, and much of the evidence for these procedures remains anecdotal.
Sometimes if medications fail to maintain an adequate quality of life, surgical options may need to be considered. These may attempt to modify or repair the hip joint, in order to allow pain-free usage, or may in some cases completely replace it. Hip modification surgeries include excision arthroplasty, in which the head of the femur is removed and reshaped or replaced, and pelvic rotation, also known as triple pelvic osteotomy, or pubic symphodesis, where the hip socket is realigned, may be appropriate if done early enough at the start of Hip Dysplasia. These treatments can be very effective, but as a rule tend to become less effective for heavier animals because their ability to treat the problem becomes reduced if the joint has to handle more pressure in daily life. Pelvic rotation is also not as effective if arthritis has already developed to the point of being visible on X-rays. Femoral Head Ostectomy also called FHO, sometimes appropriate for smaller dogs and cats, is when the head of the femur is removed but not replaced. Instead of replacing it, the resulting scar tissue from the operation takes the place of the hip joint. In such surgeries like this, the weight of the animal must be kept down throughout its life in order to maintain mobility. FHO surgery is sometimes done only when other methods have failed, but it can also done initially when the joint connection is particularly troublesome or when arthritis is severe at the first signs of Hip Dysplasia. Hip modification surgeries such as these usually result in reduction of hip function in return for improved quality of life, pain control, and a reduction in future risk. Another surgery that may help with Hip Dysplasia would be a Hip replacement. Hip replacements have the highest rate of success, especially in severe cases, since it completely replaces the faulty joint. This surgery usually restores complete mobility if no other joints are affected, and also completely prevents recurrence. Hip replacement for dogs, can sometimes also be a preferred clinical option for serious Hip Dysplasia in animals over about 40–60 lb (18–27 kg), a weight that excludes certain other surgical treatments
Some other options for Hip Dysplasia that are under exploration include something called DARthroplasty, or Dorsal Acetabular Rim Arthroplasty, is a technique developed by Dr. Barclay Slocum and Theresa Devine Slocum where cortico-cancellous bone strips are taken from the iliac crest and are contoured over the femoral head and sutured to the dorsal hip joint capsule and packed with additional cancellous bone graft dorsally to eventually anchor to drill holes in the original dorsal acetabulum. The new "shelf" eventually becomes an extension of the original acetabulum, thereby providing support and eliminating subluxation of the hip joint. The joint capsule becomes the new joint surface. Another option is called Pubic symphysiodesis, also known as juvenile pubic symphysiodesis, or JPS, is a procedure for very young dogs that manipulates the way the pelvis grows to create a tighter hip. It involves cauterizing the growth plates of the pelvis, which in other words means that the part of the pelvis which would usually grow and spread in puppyhood, no longer does. To compensate, the rest of the pelvis grows outward, in a manner which enhances the socket of the hip and provides better support than that dog would have had naturally as it gorws up. Since it relies on growth in puppyhood, it has a very tight window for surgery which currently means no sooner than about 4 four months old and no later than about five months old. This is compatible with hip scoring of puppies at four months of age. Lastly there is an option called Capsular neurectomy which is a procedure in which the hip joint capsule is de-nerved to reduce pain in the affected hip. This allows the dog to exercise moderately with less pain. This prevents the leg muscles from weakening and causing disuse and also providing less support to the bad joint. An advantage to this is that both hips can be done at one surgery. This surgery should not prevent a future hip replacement, if a more complete fix is desired later on.
There are some things you can also do at home to keep your pet comfortable after showing signs of Hip Dysplasia. It is always good to talk to your vet about the following tips. Somethings you can do are to apply a warm water bottle for 15 minutes twice a day. Massage the muscles around his hip joints by gently rubbing it in a circular motion with your fingertips for ten minutes at the most. When doing this pay attention to your pets response. If massage seems to irritate your dog’s hip, don’t continue. Buffered aspirin may also take the pain away too, but speak with your veterinarian first about proper dosage, administration, and side effects as too much can cause a lot of issues for your pet. There are many newer prescription painkillers available as well to help keep your dog pain-free, but again, always consult your veterinarian first. Be sure to keep your dog out of damp, chilly weather as being cold can cause more discomfort in a pet with arthritis just like it does it people. Provide traction on slippery floors, as dogs with Hip Dysplasia often have a hard time on slippery floors, so lay carpet down, and if he needs to climb stairs or jump up into the car, a carpeted ramp will make it a lot easier on him or carry them and pick them up if possible instead of letting them jump. Also provide a firm, orthopedic bed for your dog to sleep on.
Canine Hip Dysplasia in its most serious forms can be prevented, and the life quality of dogs are improved if preventative measures related to early canine life is introduced. There's probably no better subject on evidence-based dog health care than the benefits and risks of early-age preventive measures for hip dysplasia. Because Hip Dysplasia is a congenital and developmental disease in which the hip joint fails to develop properly, determining both the genetic and environmental factors would help eliminate the disease through informed breeding and training practices. Although hip dysplasia is mostly a congenital condition, a recent doctoral research study by Randi Krontveit at the Norwegian School of Veterinary Science examined the role that environmental factors played in its development. Hip Dysplasia is a genetic disease. Dogs are not born with hip dysplasia, but puppies that are genetically predisposed to it may develop it in varying degrees. The severity of hip dysplasia has an effect on when the dogs show symptoms of this disease and on how long they tend to live. Through observations, Krontveit confirmed that varied exercise had a positive effect and dogs that exercised on a daily basis on a leash as well as running free in different types of terrain were free of symptoms longer than the dogs that were less active. Unfortunately, older puppies do not benefit in the same way from free exercise. Based on research, none of the exercise parameters registered seemed to have any effect on Hip Dysplasia risk after approximately three months of age. This means that preventive efforts probably are most effective before that age. Having said that, It is still recommend that genetically prone pups should be exercised regularly to strengthen musculature, but extensive jumping, running, stair use, and other activities like that, should be avoided until growth is completed at approximately one year of age for small to medium dogs. and two years of age in medium to large dogs.
Ethylene glycol poisoning is caused by the ingestion of ethylene glycol which is the primary ingredient in both automotive antifreeze and hydraulic brake fluid. Ethylene glycol should not be confused with propylene glycol which is a common food additive.
Ethylene glycol is a sweet-tasting, odorless liquid which is not only the active ingredient in antifreeze but can also be found, in lower concentrations, in some windshield de-icing agents, hydraulic brake fluid, motor oils, solvents, paints, film processing solutions, wood stains, inks, printer cartridges, and more. Ethylene glycol is so dangerous because dogs and cats are attracted to ethylene glycol by its sweet taste. Many animals will voluntarily drink ethylene glycol if antifreeze is spilled or leaks onto garage floors or driveways. Most intoxications are associated with ingestion of antifreeze. The widespread availability of antifreeze, its sweet taste and small minimum lethal dose, and the lack of public awareness of the toxicity like improper storage and disposal, can contribute to the frequency of this intoxication. In addition, antifreeze may be ingested by way of intentional poisoning or because it is the only available liquid in cold weather. Other sources of EG include some heat-exchange fluids used in solar collectors and ice-rink freezing equipment and some brake and transmission fluids. Cutaneous absorption from topical products that contain EG has been reported to cause toxicity in cats. EG intoxication occurs most commonly in temperate and cold climates because antifreeze is used both to decrease the freezing point and to increase the boiling point of radiator fluid. In colder climates, the incidence of EG intoxications is seasonal, with most cases occurring in the fall, winter, and early spring, when antifreeze is added to radiator fluid or when cooling systems are flushed. Ethylene glycol has a very narrow margin of safety which means that it only takes a tiny amount to result in severe poisoning. As little as one eighth of a teaspoon per pound of cat can result in fatalities in cats, while as little as half a teaspoon per pound of dog can result in fatalities in dogs. The minimum lethal dose of undiluted EG is 1.4 mL/kg body weight in cats, 4.4 mL/kg in dogs, 7–8 mL/kg in poultry, and 2–10 mL/kg in cattle. Younger animals may be more susceptible to fatalities.
All animals are susceptible to ethylene glycol also called EG toxicity, but it is most common in dogs and cats. Pigs ingesting EG are usually depressed, weak, and reluctant to move; knuckling, posterior ataxia, trembling, collapse, abdominal distention, pulmonary edema, and muffled heart sounds are common sequelae. Poultry may become drowsy, ataxic, dyspneic, and recumbent; torticollis, ruffled feathers, and watery droppings are also seen. Cattle may become depressed, tachypneic, and ataxic, and develop paraparesis or recumbency. Epistaxis and hemoglobinuria have also been seen in cattle that have ingested large doses of EG.
Common signs in dogs that you should watch out for with Ethylene Glycol poisoning depend on the time after poisoning. Early signs of EG poisoning are seen from thirty minutes to upwards of twelve hours after ingestion. These signs can include nausea an,d vomiting, mild to severe depression, wobbly, uncoordinated or a drunken like gait called ataxia or movement and knuckling. Twitching muscles, short, rapid movements of the eyeball, head tremors, decreased withdrawal reflexes and righting ability may also be seen along with increased urination and increased thirst called polyuria and polydipsia. Other symptoms often develop thirty-six to seventy-two hours after the ingestion of ethylene glycol. These symptoms are dependent on the amount of ethylene glycol ingested and these symptoms are almost always sudden or acute. Signs caused by ethylene glycol itself and its toxic metabolites are frequently fatal. Metabolites are substances produced by the body's chemical processes as it breaks down the ethylene glycol. Dogs will exhibit increasing depression, and tend to drink less but increased urination continues, which results in dehydration. Central nervous system signs lessen after approximately twelve hours but return later. Some may note severely low body temperature, and severe sluggishness or lethargy and can even go into a coma. Seizures, Lack of appetite or anorexia, vomiting, oral ulcers/sores on mouth, salivation or drooling may also occur and the kidneys are often swollen and painful.
To test for Ethylene Glycol poisoning some standard tests will be run including a urinalysis and complete blood test, which will be sent for laboratory analysis immediately. Your veterinarian may also use ultrasound to look at the liver and kidneys, which are often swollen in response to ethylene glycol ingestion. The best way to confirm ethylene glycol poisoning is by measuring the blood concentration of ethylene glycol. A test to determine the blood levels can be done at some veterinary diagnostic laboratories or even at human hospitals. This testing method is very accurate, but not always available in the middle of the night or in enough time for severe poisoning circumstances. In addition, a test kit that can be used in the veterinary clinic is available to detect the amount of ethylene glycol present in the bloodstream. However, these types of tests may not be as accurate, and false positives can be seen. For instance, certain agents other than ethylene glycol interact with the test, like propylene glycol, glycerol, mannitol, isopropyl alcohol, and sorbitol. Also, if this test kit is run too late, it may test falsely negative. In other words, since peak levels of ethylene glycol are detected in to the first one to six hours after ingestion of the toxin, it is important that this test kit be used early in the course of suspected poisonings. By as early as twenty-four hours after ingestion, insufficient ethylene glycol remains to allow detection on this blood test; however, the damage to your pet’s body from ethylene glycol has already occurred. Ultrasonography can also be helpful in detecting EG poisoning. Possible findings may be renal cortices, where the external layers of the kidneys become hyperechoic as a result of crystals. That is found when the external layers of the kidney respond to the sonographic sound waves with a denser echo than the surrounding areas because of the more solid nature of the crystal formation in the renal tissue.
It is imperative that you see a veterinarian immediately for proper treatment. When in doubt, you or your veterinarian can contact Pet Poison Helpline (800-213-6680) 24/7 for life-saving assistance in managing a poisoned patient before making it to your veterinarians office. If your veterinarian is able to examine and begin treating your dog in less than five hours from the time of ingestion, you may be able to avoid inpatient treatment. The treatment goal will be to prevent absorption of ethylene glycol into the body, to increase excretion or removal of the substance from the body, and to prevent the body from chemically processing the ethylene glycol into toxic compounds. Intravenous fluids or IV fluids will be given to correct and/or prevent dehydration, increase blood flow to the tissues, and to promote elimination of urine. This increases the possibility of eliminating the ethylene glycol from the body before it can do much damage. Treatment will be accompanied by administration of bicarbonate which is given slowly intravenously to correct metabolic acidosis which is a condition in which the pH of the body is too low.
If your dog develops excess levels of urea, a waste product of urine that is normally eliminated form the body, and other nitrogenous waste products in the blood and kidneys, failure of the kidneys can occur. This may be characterized by production of small amounts of urine in dogs, indicating that most of the ethylene glycol has been metabolized by the body. At that point there will be little benefit from treatment specifically designed for ethylene glycol poisoning. In this case, treating the symptoms becomes the goal. Correcting fluid, electrolytes, and acid–base disorders, promoting elimination of urine. Medications to induce production and elimination of urine may help, peritoneal dialysis may be used to hasten removal of the toxins from the body. Peritoneal dialysis is a type of dialysis in which fluids are delivered to the abdomen and the lining of the abdomen acts as a filter to remove waste products from the blood, after a certain amount of time, the fluids and waste products are removed from the abdomen. There is a possibility the dog may need extended treatment up to several weeks, before kidney function is fully reestablished. Blood work to monitor the kidneys, acid–base status, and urine output will be conducted daily for the first few days by a veterinarian. The doctor will also monitor urine pH to determine the response to treatment and adjust the treatment accordingly. If a dog is able to be treated promptly, before excess levels of urea and other nitrogenous waste products can enter the blood, there are usually no complications and recovery will progress sufficiently. It is all in the time it takes to get treatment.
There is no real prevention for EG poisoning except for the safe handling and keeping of the toxin. As a pet owner, you should be aware of the toxicity of ethylene glycol containing antifreeze and take precautions to safeguard your pets and other animals from potential sources of ethylene glycol. As much as possible, educate your family, social contacts and community about the hazards of ethylene glycol and how to protect animals. As most animals go outdoors, it is important to be aware of the surrounding environment. While you are walking your dog, it is good to make a habit of checking the neighborhood for spills, such as the type that would occur in driveways or curbside when someone refills the coolant/antifreeze chamber in a car's engine. Antifreeze is recognizable by its bright green coloring. Throwing a bucket of water over the puddle should be sufficient for dispersing the liquid and diluting it do that it does not cause harm to an animal that may come into contact with it. It is also possible to find antifreeze products that use propylene glycol rather than ethylene glycol as the active ingredient. Propylene glycol is relatively nontoxic, but should still be kept out of way of your pets.
Hyperthyroidism is the most common glandular disorder in cats. It is caused by an excessive concentration of circulating thyroxine which is a thyroid hormone better known as T4—in the bloodstream. Hyperthyroidism is one of the most common endocrine conditions affecting cats, especially older cats over the age of ten years old. Some veterinarians estimate that about five to ten percent of middle age to old aged cats will develop hyperthyroidism, and, due to factors that may include environmental exposures, that number is on the rise. Ferrets are often diagnosed with hyperthyroidism as well and also humans.
When your cat's thyroid glands are over producing the thyroxine hormone, every organ in its body is ultimately affected and there are numerous signs and changes in your cat that you should look out for. The cats kidneys, liver, muscles, heart, nervous and digestive system are all over-stimulated when there is an excess of thyroxine in the body. This leads to a number of physical changes you can see with your own eyes. Rarely does any one cat show all of the signs we associate with hyperthyroidism but rarely do they only have one symptom as well. The signs that do occur all begin very slowly. As time passes, they gradually become more severe. One of the most prevalent signs you will see is weight loss. It is also the most common complaint that takes hyperthyroid cats to the veterinarian and owners. These cats are lean in the extreme. Perceptive owners notice that although their cats are losing weight, their appetite is normal or increased. This is because the pet's metabolic rate has accelerated and it is using up food calories just as fast as it can consume them. Most hyperthyroid cats will eat more in order to meet their increased need for calories. You will hear them munching more and complaining when their food dish is empty. However, when they have reached the late stages of this disease, their general health deteriorates to the point that they don't have much appetite. Occasional cats have a form of this disease called apathetic or masked hyperthyroidism in which they appear listless and apathetic and disinterested in normal activities. Those cats may have less of an appetite than they once had. Many of these are late cases or cats with other coexisting illnesses. Many hyperthyroid cats are wired as if they were taking stimulants. They are overly restless or hyperactive, and they may be more cranky and aggressive. Some have disturbed sleep patterns. Many hyperthyroid cats will also appear unkempt. Some no longer groom themselves the way they used to while others over groom themselves to the point where their hair coat is thin or ragged and even missing in places. It is also very common for hyperthyroid cats to have an abnormally fast heart beat. Your cat's normal relaxed heart rate at home should be 140 to 200 beats per minute. Many cats with hyperthyroidism have heart rates of over 200 even when they are relaxed at home.
Increaded urination is also common occurrence in hyperthyroidism. Your cat's increased thirst is due to the increased thyroxine in its system. It's increased urine production is due to its increased water intake. There is still no known reason why some cats with hyperthyroidism vomit. It occurs in hyperthyroid humans as well. Perhaps it is due to the increased amounts of food they eat, or perhaps to the direct effects of their high thyroxine levels on stomach motility and portions of the brain. The increased level of thyroid hormone in hyperthyroid cats also causes their intestines to be more active. This is why many of these cats have bulky or loose stools. The odor of your cat's litter box may be considerably worse than it used to be. Cats that are hyperthyroid can also generate more body heat and may pant as they try to dissipate it. They are more sensitive to heat than they once were. If they get to a point in the disease where their heart is weakened, panting and difficulty breathing is more likely due to problems getting enough oxygen. In later stages of hyperthyroidism multiple factors often cause cats to become debilitated and weak. Muscle tremors, wasting, an anemic meow and generalized weakness can all be symptoms of advanced hyperthyroidism. Supplemental vitamin B-6 has helped somewhat with this problem in humans but is not well studied in cats. The high metabolic rate of hyperthyroid cats sometimes causes them to have a mildly elevated rectal temperature around 103 F, 39.4 C. One of the tall tell signs of hyperthyroid are lumps and nodules in the neck in the area of the thyroid glands. In healthy cats, the lobes of the thyroid gland cannot be felt with your fingers when you examine your cats neck. In hyperthyroid cat at least one lobe is often larger than it should be and can be clearly felt. You or your veterinarian may be able to detect this or small, pea-sized nodules, within the glands. Many older cats do have lumps in their thyroid glands but not all of them are hyperthyroid. If your veterinarian detects any mass in the thyroid area, it is prudent to run the T-4 test and a blood calcium level to assure that it is in fact hyperthyroidism. Some of these masses turn out to be located in the parathyroid glands that are adjacent to the thyroids. The parathyroid glands are involved in regulation of body calcium.
Diagnosis begins with a complete history and a physical exam. There are several different tests used to properly diagnose hyperthyroidism. The diagnostic path chosen will depend on the symptoms your cat has, and the availability of diagnostic tools your veterinarian has in the clinic. Your veterinarian will most likely do an exam and blood work first. Palpation of thyroid gland as stated above normally cannot be felt, or palpated, however with hyperthyroidism the gland typically enlarges in size and your veterinarian can palpate this during a physical exam. A CBC and Chemistry Panel of blood work will also be ran. These blood tests will evaluate various internal organ functions, including the heart, liver, kidneys, pancreas, metabolism, and electrolyte balance. The CBC is a measure of the amount and different kinds of red and white blood cells that are present in the body. Since hyperthyroidism can cause disruption of the function of several organ systems in the body, this blood test will measure and indicate if there is any significant dysfunction with the liver, pancreas, or kidneys. Cats with hyperthyroidism will generally have a higher red blood cell count. Another blood test called a Baseline T4, Total T4 or TT4 will determine the level of T4 thyroid hormone in the bloodstream. Cats that are experiencing hyperthyroidism will reveal a high level of T4 in the bloodstream. There are other conditions that can cause an increase of T4, such as kidney or heart disease, so if one of these is suspected after a positive T4 test, more definitive tests are run to confirm the diagnosis of hyperthyroidism.
A Baseline T3 test will determine the level of T3 thyroid hormone present in the bloodstream. T3 is another form of thyroid hormone produced by the thyroid gland, called Triiodothyronine. The T3 test is not a very reliable diagnostic tool for testing hyperthyroidism in cats because in 25 percent of hyperthyroid cats the T3 levels are not elevated. A Urinalysis may also been run and the results will reveal the function of your cat’s kidneys. Radiographs may show an enlarged, thickened heart muscle, accompanied by a cardiac ultrasound, both of which may show an enlarged, thickened heart muscle, a condition called hypertrophic cardiomyopathy, which is common among hyperthyroid cats.
Hyperthyroidism is not a condition you should ignore and it can be treated medically, surgically or even radiologically. I will discuss all of them. However, it is suggested you have your cat treated radiologically because cats treated that way do so much better than those treated medically and only a few cats are candidates for surgery.
Two closely related medications, methimazole, also called felimazole for cats, and carbimazole. Both are very effective in preventing excessive thyroid hormone production. Methimazole is relatively inexpensive. Unfortunately, every cat requires its own special dose and the difference between too high a dose, too low a dose and the right dose is small. So cats going this route run the larger expense of frequent thyroid hormone level checks to be sure the dose is working correctly. In most cats, dosing twice a day is required, but some dose frequency range from once to three times a day. It is safest if the cats dose is begun low and gradually increased until the desired effect is obtained.
Methimazole has an awful taste and cats usually hate it and sometimes vomit. The feline version, Felimazole tablets have a sugar coating that blocks the drug's taste. So if you cat is doing poorly when given generic or human methimazole, either try the coated veterinary tablets or have methimazole compounded as a transdermal ear cream. The problem with compounding is that there is a wide range in the effects of the cream depending on who prepared it. The medications can also have a number of serious side effects which include diarrhea, liver damage and bone marrow suppression. A few cats develop skin irritation while taking either drug. When side effects do not occur or resolve during the first three or four months of medication, cats generally do well for a number of years on either of those drugs. Some cats receive methimazole prior to thyroid surgery to improve their heart function and make them safer candidates for anesthesia, while others receive it prior to radio-iodine therapy to test the true efficiency of their kidneys. A low iodine diet is also helpful for a cat with hyperthyroidism. Iodine is necessary for a cat to produce the thyroid hormone. Cats gets the required iodine from the things they eat. When not enough iodine is present in its diet, it produces less of the hormones involved in hyperthyroidism. Hills Prescription Diets manufactures a a product called y/d, designed to lower your pet's thyroid hormone level by limiting the amount of iodine it consumes. There are some procedure options available if medications are not an option or do not help, the most commonly used is radioiodine therapy. Studies published in 2006 found that cats that were treated with radioactive iodine lived , on average, twice as long, about two to four years longer, as cats treated with just methimazole. This procedure is very safe. But because it involves the handling of radioactive materials, it is only performed at specialized veterinary centers. When the procedure is successful, and it generally is, the pet will need no further treatment or medications. In this procedure, a single injection of radioactive Iodine-131 is given to a cat subcutaneously or even intravenously. Occasionally, a second dose is required. Because iodine migrates to the cat's thyroid gland, the concentration of this special iodine there becomes great enough to kill the overactive cells that utilize iodine to produce thyroid hormone. Usually, enough normal and dormant cells are left to make all the thyroid hormone your cat will need in the future. Only about five percent of the cats treated will need daily, life-long supplemental thyroid hormone in pill form after the procedure. There have been no serious side effects reported from this procedure. It is not painful and the cat does not need to be anesthetized. However, the cat will need to stay at the hospital facility until the radiation that is released has subsided which is normally in one to two weeks. Radio-iodine is also the preferred treatment method for humans who are hyperthyroid. Occasional cats have misplaced thyroid tissue in other areas of their bodies which is called ectopic tissue. This treatment eliminates them as a potential problem as well.
Surgical removal of the diseased portions of your cat's thyroid glands is sometimes another option. But during the surgery, the difficult decision must be made as to how much of the glands to remove. There is no precise way to make this decision and if too much of the cat's thyroids are removed, the cat will become hypothyroid and need lifelong thyroid medications for that. If too little of the glands are removed, the cat will then remain hyperthyroid. Sometimes, it is appropriate to remove all of the thyroid. Cats usually have small islands of thyroid tissue scattered in other locations in their bodies that they can use. These ectopic thyroid cells can usually produce all the thyroid hormone the cat will need. But they can also lead to the re-appearance of hyperthyroidism months or even years later.
The thyroid glands are in a sensitive and very crowded location. If the adjoining parathyroid glands are injured during surgery, the cat may have trouble regulating its blood calcium and if nerves in the area are injured the cat may develop eye problems or voice changes. Most veterinarians will stabilize the cats with methimazole for a number of weeks prior to the surgery and some, remove a conservative amount of thyroid in a first operation and then monitor the cat's T-4 and blood calcium levels before deciding if a second surgery is required to remove even more. Even when performed by an experienced surgeon with excellent post-surgical monitoring, the fatality rate of this surgery can approach nearly ten percent. You can expect the cost of this surgery to be equal or more than radio-iodine therapy and to have less predictable results, it is normally a last resort.
There is no way to prevent hyperthyroidism, but early detection can prevent your cat from displaying severe symptoms.
The rabies virus is a single-stranded RNA virus of the genus Lyssavirus, which is in the family Rhabdoviridae. It is transmitted through the exchange of blood or saliva from an infected animal, and very rarely through breathing in the escaping gases from decomposing animal carcasses. Due to the zoonotic nature of this disease, any mammal who comes in contact with an infected animal can become infected with the rabies virus.
There are two forms of rabies, Paralytic and Furious. In the early symptom or prodomal stage of the rabies infection, a cat will show only mild signs of central nervous system or CNS abnormalities. This stage will only last from one to three days. Most cats will then progress to either the furious stage, the paralytic stage, or a combination of the two, while others succumb to the infection without displaying any major symptoms before dying. Furious rabies is characterized by extreme behavioral changes, including extreme aggression and attack behaviors. Paralytic rabies, also referred to as dumb rabies, is characterized by weakness and loss of coordination in the cat, followed by paralysis.
Rabies is a fast-moving virus. If it is not treated soon after the symptoms have begun, the prognosis is very poor. Therefore, if your cat has been in a fight with another animal, or has been bitten or scratched by another animal, or if you have any reason to suspect that your pet has come into contact with a rabid animal, even if your pet has been vaccinated against the virus, you must take your cat to a veterinarian for preventive care immediately. Some of the symptoms to watch for in your cat are pica, fever, seizures, paralysis, hydrophobia, the ats jaw is dropped, inability to swallow, muscular lack of coordination, unusual shyness or aggression, excessive excitability, constant irritability and changes in attitude and behavior, paralysis in the mandible and larynx, excessive and dripping salivation or hypersalivation, or even frothy saliva. Some cats will exhibit some of these symptoms all at once. If there is any chance of an infection it is important to contact your local veterinarians office.
Again, if you suspect your cat has rabies, call your veterinarian immediately. If it is safe to do so, cage, or otherwise subdue your cat, and take it to a veterinarian to be quarantined. If your pet is behaving viciously, or is trying to attack, and you feel you are at risk of being bitten or scratched, you must contact animal control to catch your cat for you. The last thing you want is to get scratched or bitten by an infected animal, whether it is your pet or not. If there is a chance your cat is infected your veterinarian will keep your cat quarantined in a locked cage for 10 days. This is the only acceptable method for confirming suspected rabies infection. Rabies can be confused with other conditions that cause aggressive behavior, so a laboratory blood analysis must be conducted to confirm the presence of the virus. However, blood testing for the virus is not veterinary procedure. The only diagnosis in the U.S. is done using a post-mortem direct fluorescence antibody test performed by a state-approved laboratory run by the USDA for rabies diagnosis. Your veterinarian will collect fluid samples if your cat dies while in quarantine, or if it begins showing progressive signs of rabies. If that is the case, your veterinarian may opt to put your cat to sleep by euthanize it humanely.
If your cat has been vaccinated against rabies, provide proof of vaccination to your veterinarian. If anyone came into contact with the cat's saliva, or were bitten by your cat, yourself included, advise them to contact a physician immediately for treatment. Unfortunately, rabies is always fatal for unvaccinated animals, usually occurring within seven to ten days from when the initial symptoms began. If a diagnosis of rabies is confirmed you will need to report the case to your local health department. An unvaccinated cat that is bitten or exposed to a known rabid animal must be quarantined for up to six months, or according to local and state regulations. You can visit the USDA website to find your states local laws on rabies quarantines and vaccinations. A vaccinated animal that has bitten or scratched a human, conversely, should be quarantined and monitored for at least 10 days.
Vaccination is the key to to prevention of rabies and in most areas of the country, it’s the law to vaccinate your pet. All companion felines should be kept regularly vaccinated by a veterinarian with a licensed rabies vaccine. Vaccinating your cat doesn’t just protect them from rabies but it also protects you and your cat if she bites someone. Some local ordinances require lengthy quarantines or even immediate euthanasia of pets who have bitten someone if the owner does not have proof of current vaccination. To further reduce the chances of your cat becoming infected with the rabies virus, ASPCA experts recommend keeping your pet indoors when at all possible and when unsupervised. The only non-adjuvanted rabies vaccine for cats is Purevax, manufactured by Merial. It is labeled for 1 year only so cats who receive this vaccination must be revaccinated annually, or once every year according to labeling. There is an killed rabies vaccine that is labeled for three years for dogs and cats but has been known to cause vaccine realted sarcomas in cats, but can still be used in cats that are hard to catch to bring to the vet every year. That way they are at least covered for three years without a trip to the vet.
Rabies is a severe, and often fatal, viral polioencephalitis. It also has zoonotic characteristics, and can therefore be transmitted to humans. However, it is only transmitted by the bite of a rabid animal. The virus is present in the saliva of the infected animal only for a limited time. If you are bitten by any animal that may be rabid, you should immediately wash the wound thoroughly with soap and water and seek the advice of a doctor without delay. Suspicious animals include all stray or feral dogs or cats and any wild animal, particularly if the animal is showing unusual behavior such as lack of fear of people, excessive salivation, or especially aggression. Post-exposure rabies treatment with serum or vaccine may be recommended and is very successful if given immediately after exposure for humans.
Strangles is a highly contagious and serious infection of horses and other equids caused by the bacterium, Streptococcus equi. The disease is characterized by severe inflammation of the mucosa of the head and throat, with extensive swelling and often rupture of the lymph nodes, which produces large amounts of thick, creamy pus. Strangles can effect all equids such as horses, donkeys, and zebras.
Susceptible horses develop strangles within three to fourteen days of exposure. Animals show typical signs of a generalized infectious process including but not limited to depression, inappetence, and fever. More typical of strangles, horses develop a nasal discharge, initially mucoid, rapidly thickening and purulent, a soft cough, and slight but painful swelling between the mandibles, with swelling of the submandibular lymph node following soon after. Horses are often seen positioning their heads low and extended, as to relieve the throat and lymph node pain. With the progression of the disease, abscesses develop in the submandibular or between the jaw bones and/or retropharyngeal lymph nodes which are at the back of the throat. The lymph nodes become hard and very painful, and may obstruct breathing hense the name "strangles". The lymph node abscesses will eventually burst or can be lanced open in seven to fourteen days, releasing a thick pus that is heavily contaminated with S. equi. The horse will usually rapidly recover once abscesses have ruptured and the pus has drained.
The main and often fatal complications of strangles appear after the infection is run its coarse. One complication is called Bastard strangles. This describes the dissemination of infection to unusual sites other than the lymph nodes draining in the throat. For example, abdominal or lung lymph nodes may develop abscesses and rupture, sometimes weeks or longer after the infection seems to have resolved. A brain abscess may rupture causing sudden death or a retropharyngeal lymph node abscess may burst in the throat and the pus will be inhaled into the lung and the horse can drown. Purpura haemorrhagica, which is an immune mediated acute inflammation of peripheral blood vessels that occurs within four weeks of strangles, while the animal is recovering. It results from the formation of immune complexes between the horse's antibodies and bacterial components. These immune complexes become trapped in capillaries where they can cause inflammation, visible in the mucous membranes as pinpoint haemorrhages. These haemorrhages lead to a widespread severe edema of the head, limbs, and other parts of the body. Purpura can also be a complication of routine vaccination for Strangles.
Some minor, non-fatal complications may also be seen after the infection. Post strangles myocarditis or inflammation of heart muscle, which may follow strangles in a small proportion of horses. An electrocardiogram or ECG can determine that a horse can return to heavy work or to training after an episode of strangles. Purulent cellulitis or inflammation of the subcutaneous tissue, which is an unusual occurrence where infection spreads locally in the subcutaneous tissue to the head. Laryngeal hemiplegia may also be seens, which involves paralysis of the throat muscles. It is commonly referred to as "roaring". The condition may follow abscessation of cervical lymph nodes. Anaemia or low red blood cell count, can occur during the recovery period because of immune-mediated lysis of red blood cells. Guttural pouch empyaema meaning it is filled with pus, which may be concurrent with classic strangles, or follow in the immediate recovery period. The two guttural pouches are large mucous sacs. They are present only in Equids and are situated between the base of the cranium dorsally and the pharynx ventrally. They open into the nasal pharynx and each has a capacity of about 300 mL. Persistent infection in the guttural pouch may lead to inspissation or drying of pus and, in some cases, the formation of a solid, stone-like, concretion called a chondroid. Animals that have persistent infection of the guttural pouches become the carriers, the major source of infection to spark outbreaks in susceptible horses with which they are mixed. Apart from the problem of long-term guttural pouch carriers, recovered horses may shed S. equi from their nose and in their saliva for up to 6 weeks following infection. Therefore, isolate all horses that have had strangles from susceptible animals for 6 weeks following infection.
The organism can be isolated from the nose or lymph nodes of affected animals, and is usually readily identified in the laboratory by simple sugar tests. Diagnosis can be confirmed by culturing pus from the nose, from abscessed lymph nodes or from the throat of clinically affected horses. Although S. equi isolates are thought to be genetically identical, isolates may vary in virulence and atypical isolates occur, which differ in their sugar tests from typical S. equi.
As with many streptococcal infections, penicillin or penicillin-derivative antibiotics are the most effective treatments. However, some authorities are of the opinion that use of antibiotics is contra-indicted once abscesses have begun to form, as they pre-dispose to lymphatic spread of the infection which causes so-called bastard strangles, and those have a much higher mortality rate. After an abscess has burst, it is very important to keep the wound clean. Use a diluted povidone-iodine solution has been used with good results to disinfect the open hole, flushing the inside with a syringe tipped catheter or with a teat cannula, followed by gentle scrubbing to keep the surrounding area clean.
Both intramuscular and intranasal vaccines are available to help prevent Strangles from occuring. Both a killed and a live vaccine are available for the control of strangles. The only killed vaccine currently available in Canada is StrepguardTM by Intervet. Killed vaccines, in general, are administered with an initial series of intramuscular injections followed by an annual booster. There may be adverse reactions at the injection site like marked pain, and even frank abscesses. Some animals have even developed purpura haemorrhagica following vaccination. The killed vaccines do not provide complete protection because they do not result in the local, nasopharyngeal antibodies thought to be important in protection, but they do reduce the severity of clinical illness should it occur.
More recently, a live, attenuated S. equi vaccine called PinnacleTM I.N. made by Fort Dodge, has been introduced as an intranasal vaccine for the prevention of strangles. The vaccine is administered twice, at an interval of one to two weeks. This approach to vaccination is intuitively more attractive than a killed, intramuscular vaccine since it produces the local antibodies necessary for protective immunity. Because the vaccine is a live but attenuated meaning it uses a low virulence organism S. equi, take care to avoid contamination of injections elsewhere in the horse. Concurrent injection of other vaccines has resulted in S. equi abscesses at these sites, presumably through inadvertent contamination. Therefore, it is strongly recommended to not administer other vaccines or injections at the same time as administering the intranasal vaccine and if it is a must be very careful about preventing contamination of injection sites. Other adverse reactions have also been reported. According to the manufacturer, adverse reactions occur at a frequency of about five for every ten thousand doses. These include submandibular and pharyngeal lymph node swellings, with or without abscesses, purpura haemorrhagica, which may be severe, and even bastard strangles. Since the live organism may persist in the nose, approaches to control that involve detection of carriers may not be effective in horses immunized with this vaccine. It is also recommended to isolate new horses for four to six weeks, and immediate isolation of infected horses, and disinfection of stalls, water buckets, feed troughs, and other equipment will help prevent the spread of strangles. As with any contagious disease, hand washing is a also a very simple and effective tool.
It is strongly recommended that all horses be included in a regular program of vaccination. It is particularly important that booster doses be given prior to periods of greater risk of infection, such as the breeding or performance season. Pregnant mares may be vaccinated up to two weeks before foaling, and consideration should be given to vaccinating high risk horses like brood mares, stallions, performance horses, pony club, racing, and eventing horses every six months.
Uveitis refers to inflammation of the uveal tract of the eye. The uveal tract consists of three components: the iris which is the colored portion of the eye responsible for opening and closing the pupil, the ciliary body that produces a watery fluid that maintains the shape of the eye, and the choroid which is the back portion of the eye responsible for supplying blood and nutrients. Equine recurrent uveitis or ERU is the term used for eye inflammation that recurs periodically in horses. Equine recurrent uveitis occurs to varying degrees among horses and may affect one, or both eyes. After a horse is affected, ERU recurs at varying intervals, each time causing additional ocular damage that leads to permanent changes in the internal structures of the eye.
Any injury to a horse's eye may result in the development of uveitis and subsequent ERU. The two most common causes of ocular injury are trauma and infectious diseases. Trauma to the eye may result from a blunt blow or by penetration of the globe or eyeball by a sharp object. Other common causes can include bacterial organisms like Leptospira, Brucella, and Streptococcus. Viral agents like Equine influenza, Equine viral arteritis, Parainfluenza type 3, Parasites such as Onchocerca, Strongylus, Toxoplasma, and other things like Endotoxemia, Tooth root abscesses, and Neoplasia. Regardless of the inciting cause, it is believed that the ERU is immune-mediated. This means that once the primary infection resolves, subsequent episodes of eye inflammation are the result of overaction of the horse's own immune system in response to active immune cells such as T-lymphocytes.
All animals can get Uveitits for multiple reasons but Equine Recurrent Uveitits is only seen in Equids such as Horses, Donkeys, and Zebras.
Clinical signs of active ERU include but are not limited to Photophobia or sensitivity to light, Blepharospasm or squinting, Corneal edema, Aqueous flare or small "floaters" in the front chamber of the eye, Hypopyon which is pus in the eye, Miosis or pupillary constriction. Other symptoms may be Vitreous haze which is a haze in the gel that fills the eyeball between the lens and the retina, and Chorioretinitis which is inflammation of the choroid and retina. Some signs of chronic ERU include Corneal edema, Iris fibrosis and hyperpigmentation, Posterior synechia or the adhesion of the iris to the capsule of the lens,
Corpora nigra degeneration which is an irregular body at the edge of the iris that shades the pupil, Miosis, Cataract formation, Vitreous degeneration and discoloration, and
Retinal degeneration.
The cornerstone of diagnosis is an accurate history, and a good clinical examination of the eye, in order to eliminate traumatic uveitis. Ultrasonography is a useful tool, as it can detect a thickened iris, but should only be used in the hands of an expert.
The diagnosis of ERU relies upon finding signs of inflammation within the front of the eye with no other detectable primary cause. Signs of active uveitis include pupil constriction, aqueous flare which is caused by protein in the aqueous humour, and hypopyon which is pus in the aqueous humour. Thorough examination of the entire eye to rule out any primary causes will result in a diagnosis of ERU. A detailed history from the owner may reveal mild episodes in the past, but this is not always the case. ERU is also one of the major causes of “blue eye”, or corneal adema. Inflammation inside the eye disrupts the endothelial water pumps that keep the cornea dehydrated, and therefore clear. When these pumps stop working, water floods into the cornea and disrupts the collagen fiber arrangement, turning it a pale blue color. More advanced techniques include measuring the pressure inside the eyeby using a small contraption called an Intra-Ocular Pressure also called an IOP. In the initial stage of a flare up, IOP will be reduced due to inflammation of the ciliary body, and decreased production of aqueous humour. Chronically IOP will be increased due to inflammatory debris obstructing the drainage of aqueous humour. In between active episodes of uveitis, ERU can still be diagnosed. The characteristic changes are darkening of the iris, shrinking of the granula iridica or the dark structures on the top of the iris, and butterfly lesions on the retina. Adhesions between the iris and other structures, typically the cornea or the lens, can also occur, this is known as anterior and posterior synechiae. These changes are not always present, and a horse with ERU may have a normal appearing eye.
Although there is no true cure for ERU, beacause it is an immune-mediated disease, treatment is often effective in controlling clinical signs and active episodes.
While a cure for equine recurrent uveitis or ERU, remains elusive, veterinarians have learned how to best control this devastating disease and are continuously working to unravel new treatment options. The main goals of therapy for ERU are to preserve vision and reduce and control ocular inflammation in an attempt to limit permanent damage to the eye. Therapy is directed at the allaying of symptoms and reducing ocular inflammation.
Because vision loss is a common long-term manifestation of ERU, initial therapy must be aggressive. In acute cases, treatment in the form of systemic and local therapy consisting of antibiotics, corticosteroids and anti-inflammatory drugs are used, many times simultaneously. Initial therapy is instituted for at least two weeks, and may be continued for an additional two weeks after the resolution of clinical signs. In severe cases, local subconjunctival injections of corticosteroids may be indicated as an adjunct to therapy. In most instances, a subpalpebral lavage catheter is placed to facilitate delivery of topical medications. Unfortunately, certain horses are never able to completely eliminate their uveitis and for these horses alternative forms of therapy must be considered.
Although traditional therapy may be used to control recurrent flare-ups, no therapy has proven to be a hundred percent effective in eliminating ERU. Some horses respond well to long-term topical and systemic therapy and are able to be managed in this fashion. Other horses, however, do not respond to traditional therapy and may experience recurrences of uveitis more frequently. Fortunately, studies investigating the use of an immunosuppressive drug known as cyclosporin are currently underway in an attempt to manage these horses. This treatment involves the ocular implantation of a cyclosporin delivery device, which requires general anesthesia.
Other management and prevention practices that are recommended include increasing insect and rodent control, and using a quality fly mask with ultraviolet protection. Decrease dust, change bedding, eliminate sharp objects from around the barn and pasture, eliminate low branches, decrease training and show schedule, and minimize trailer trips, avoid using hay nets, maintain proper hoof and dental care, as well as deworming and vaccination schedules, and ensure a proper diet for y our horses.
Cryptosporidiosis is caused by protozoan parasites of the genus cryptosporidium, in which there are thirteen valid species. Cryptosporidium is a microscopic parasite that causes the diarrheal disease cryptosporidiosis. Both the parasite and the disease are commonly known as "Crypto." There are many species of Cryptosporidium that infect humans and animals. One major species, C. parvum, infects both farm animals and humans. The parasite is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it very tolerant to chlorine disinfection.
C. parvum is not host-specific, and therefore can affect many different species; over fourty-five different species of animals including large mammals, including humans, cattle and sheep, small mammals like rodents, dogs, and cats, poultry, fish, and reptiles can become infected with C. parvum. It is common in young ruminants, particularly calves; it is also found in pigs and is very rarely seen in dogs, cats, and horses.
Cryptosporidium organisms have been isolated from the feces of dogs and cats. Infections appear to most commonly be subclinical, but may induce mild diarrhea. Cryptosporidium isolates from HIV patients have been specifically matched to isolates from dogs and cats and it is now considered that there is a dog-specific genotype called C. canis and a distinct feline genotype called C. felis, both of which can be infectious for humans. However, there are also studies showing no statistical association between human infections and dog or cat ownership. The domestic animal of most importance as a reservoir of Cryptosporidium parvum is clearly cattle. Neonatal calves are infected during the first days of life, leading to diarrhea. Nationally, in a study of 7,369 calves on 1,103 farms, oocysts were detected in the feces of calves on 59.1% of farms and from 22.4% of all calves tested. In a second study by Atwill, 92% of calves 7-21 days of age were shedding the organism in their feces. In a third study, rates of shedding among calves were lower, ranging from 0-13%, but the odds ratio for shedding was still higher for calves two to four months of age than in older cattle. Interestingly, the incidence of cryptosporidiosis in people in the U.K. dropped substantially during the foot and mouth disease outbreak in 2001. Clearly cattle may serve as a major source for environmental contamination with Cryptosporidium parvum. But is Cryptosporidium parvum DIRECTLY zoonotic from cattle to humans is the question. Infection has been well-documented among students and staff in veterinary school settings, suggesting direct infection from hospitalized animals.
On a broader scale, among people in WI, one study found that 44% of farmers vs. 24% of non-farming neighbors were seropositive. However, another study found a 60% seropositivity rate among the general population. Studies have also found high rates of seropositivity among horses, but few instances of clinical disease. Infection is particularly associated with diarrhea in severe combined immunodeficient Arabian foals. Pigs can be naturally and experimentally infected, but seldom show clinical signs. Llamas and alpacas can shed C. parvum. Cryptosporidium parvum has been isolated from subclinically infected guinea pigs. Birds and reptiles can also harbor Cryptosporidium spp. and suffer either gastrointestinal and often primarily manifest as regurgitation in reptiles, or respiratory disease, but with the exception of C. meleagridis from birds, these strains are rarely zoonotic. Deer have recently been shown to harbor a genotype of C. parvum that is infectious for humans, and Mice are infected with a gastric Cryptosporidium species called C. muris that can infect people, especially HIV patients.
Signs can range from a mild to inapparent infection to severe scouring. Death is an infrequent consequence. Infected, weaned and adult animals normally do not exhibit identifiable signs of disease, but will excrete oocysts that contaminate the environment. In calves, Cryptosporidiosis is one of the most common causes of diarrhea in calves. Calves one to three weeks old seem to be most susceptible. The mean incubation period in calves is approximately four days. C. pan/urn infections of cattle can cause mild to moderate yellowish, watery diarrhea with mucus which persists for several days regardless of treatment. Scouring may accompanied with varying degrees of dullness, anorexia, dehydration, fever and loss of condition. Less commonly, more severe disease with bloody diarrhea can occur perhaps especially with concurrent infections. Cryptosporidiosis rarely causes the acute dehydration, collapse and high mortality seen with enterotoxigenic Escherichia coll or rotavirus, which can occur at the same time.
C. andersoni Cryptosporidiosis affects the digestive glands of the abomasum of older calves and adult cattle destroying the microvilli of peptic glands, which may account for the elevated concentrations of plasma pepsinogen detected in infected hosts. Some infected animals exhibit reduced weight gain, but do not develop diarrhea and can excrete oocysts for several months. In lambs and goats, although outbreaks in lambs and kids are sporadic, mortality can be high. Lambs three to ten days and kids five to twenty-one days can be affected. Infected lambs and kids are depressed and reluctant to suck while the diarrhea lasts quite awhile. Very young lambs soon become dehydrated and die. In poor weather conditions, lambs may die of hypothermia first. The illness may last for up to ten days, and relapses after apparent recovery are very common.
Diagnosis of Cryptosporidiosis is based on the demonstration of oocysts in feces by conventional tinctorial stains, fluorescent/immunofluorescent stains or Cryptosporidium antigens in feces by enzyme-linked immunosorbent assay called ELISA.
C. parvum oocysts can be detected in fecal smears after fecal flotation in sucrose or zinc sulfate solutions. Because of their small size and transparency, the oocysts are easily overlooked in unstained wet mounted fecal sample; high-power magnification, preferably under phase-contrast illumination, should be used. Mature oocysts are four to five µm in diameter and contain four thin, flat, motile sporozoites. Fecal smears may be heat-fixed and stained by an acid-fast technique. The modified Ziehl-Neelsen is a simple and rapid procedure for large-scale routine diagnosis. Cryptosporidium oocysts stain red, whereas yeasts, which are about the same size and shape as the oocysts, stain with the blue or green counterstain. Oocysts are not shed continuously and repeated sampling may be necessary. Calves usually shed oocysts for a maximum of two weeks. Cryptosporidiosis can also be diagnosed or histologically confirmed in stained biopsy and necropsy specimens or fresh intestinal scrapings called haematoxylin and eosin. Other detection methods will be based on polymerase chain reaction called PCR directed to C. parvum DMA and on antigen-capture enzyme-linked immunosorbent assay ELISA or immunofluorescence assay or IFA, using monoclonal antibodies directed against antigens on the surface of the parasite.
There is no effective specific treatment; however, because the disease is self-limiting, supportive therapy, such as rehydration orally and parenterally, correction of acidosis, and maintenance of energy requirements, is usually sufficient. Halufiginone 60-125µg/kg once daily for seven days will protect against clinical disease and will markedly reduce oocyst excretion, but will allow some intestinal infection and thus development of immunity. Paromomycin sulfate 100mg/kg once daily for eleven consecutive days from the second day of age proved successful in preventing natural disease in goat kid's in a clinical field trial.
At present, no approved drugs are available for treating cryptosporidiosis in calves or humans. In addition, there is no a rigorously tested and accepted vaccine available. Therefore, prevention of cryptosporidiosis will depend on both blocking transmission of the parasite to susceptible neonatal farm animals and treating individuals if they become infected. High levels of hygiene are the best approach to control. Reducing the number of oocysts ingested may reduce the severity of infection and allow immunity to develop. Calves should be born in a clean environment and adequate amount of colostrums should be fed at an early age. Calf-to-calf contact should be prevented for at least the first two weeks of life, with strict hygiene at feeding. Diarrheic calves should always be isolated from healthy calves during the course of the diarrhea, and for several days after recovery. Great care must be taken during treatment to avoid mechanical transmission to other calves. The oocysts are resistant to most disinfectants but may be killed in the environment with five percent ammonia solution or desiccation. Because C. parvum has a wide host range, infection in other animal species on the premises should be considered. Flies, rats, mice, and other rodents should be controlled in calf-rearing houses and feed storage areas. Veterinarians and owners should take proper precautions when treating calves, lambs and kids with diarrhea. An infected person or animal sheds Cryptosporidium parasites in the stool. Millions of Crypto parasites can be released in a bowel movement from an infected human or animal. Shedding begins when the symptoms begin and can last for weeks after the symptoms stop. You can become infected after accidentally swallowing the parasite. Crypto may be found in soil, food, water, or surfaces that have been contaminated with the feces from infected humans or animals. Crypto is not spread by contact with blood but Crypto can be spread by putting something in your mouth or accidentally swallowing something that has come in contact with the stool of a person or animal infected with Crypto. By swallowing recreational water contaminated with Crypto. Recreational water can be contaminated with sewage or feces from humans or animals.
By swallowing water or beverages contaminated by stool from infected humans or animals.
By eating uncooked food contaminated with Crypto. All fruits and vegetables you plan to eat raw should be thoroughly washed with uncontaminated water. By touching your mouth with contaminated hands. Hands can become contaminated through a variety of activities, such as:touching surfaces like toys, bathroom fixtures, changing tables, and diaper pails that have been contaminated by stool from an infected person, changing diapers, caring for an infected person, and handling an infected cow or calf. Cleanliness is the only real way to prevent infection.
Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a parasitic flatworm of the class Trematoda, phylum Platyhelminthes that infects the livers of various mammals, including humans. The disease caused by liver flukes is called fasciolosis, fasciolasis, distomatosis or liver rot.
. F. hepatica is distributed worldwide, and causes great economic losses in sheep and cattle everywhere. It has been known as an important parasite of sheep and cattle for hundreds of years. Because of its size and economic importance, it has been the subject of many scientific investigations and may be the best known of any trematode species because of it.
F. Hepatica is one of the most abundant and damaging helminth parasites of grazing ruminants like sheep, goats, and cattle. In endemic regions a hundred percent of the animals can be infected at any given time. It is particularly harmful, even fatal for sheep to become infected. Incidence in a particular region depends strongly on ecologic and climatic conditions like habitats for intermediate hosts and wild mammals, overwintering of the parasites in the environment, and on livestock management practices like stock density, and grazing patterns. Horses and pigs kept outdoors can also be affected, but liver flukes are usually not a problem in housed pigs. Dogs and cats can be occasionally infected, especially in rural environments but it is very rare. The question commonly asked is if animals infected with Fasciola hepatica are contagious for humans. The answer is usually NOT, but it can happen. If livestock is infected with liver flukes, it is not directly contagious for humans, neither through contact, nor when consuming meat, milk,or blood of contaminated animals. It is also not spread through the feces, BUT experimental studies suggest that humans may be infected when consuming raw livers contaminated with juvenile liver flukes. The same applies to pets infected with liver flukes. Normally humans become infected through ingestion of water contaminated with infective cercariae not by ingesting adult flukes or their eggs.
Fasciolosis ranges in severity from a devastating disease in sheep to an asymptomatic infection in cattle. The course usually is determined by the number of metacercariae ingested over a short period. In sheep, acute fasciolosis occurs seasonally and is manifest by a distended, painful abdomen, anemia, and even sudden death. Deaths can occur within six weeks of infection. The acute syndrome must be differentiated from “black disease” which can manifest in the same way. In subacute disease, survival is longer , more around seven to ten weeks, even in cases with significant hepatic damage, but deaths occur due to hemorrhage and anemia. Chronic fasciolosis is seen in all seasons. Those signs include anemia, unthriftiness, submandibular edema, and reduced milk secretion, but even heavily infected cattle may show no clinical signs, although their immunity to other pathogens like Salmonella spp, may be reduced and reactions to the single intradermal test for tuberculosis may be modified. Heavy chronic infection is almost always fatal in infected sheep. Sheep do not appear to develop resistance to infection, and chronic liver damage is cumulative over several years. In cattle, there is evidence of reduced susceptibility after fibrosis of liver tissues and calcification of bile ducts.
Lesions can also sometimes be seen in infected animals. Immature, wandering flukes destroy liver tissue and cause hemorrhage. In acute fasciolosis, damage is extensive, the liver is enlarged and friable with fibrinous deposits on the capsule. Migratory tracts can be seen, and the surface has an uneven appearance. In chronic cases, cirrhosis develops. Mature flukes damage the bile ducts, which become enlarged, or even cystic, and have thickened, fibrosed walls. In cattle, the duct walls become greatly thickened and often calcified. Flukes may be found in aberrant sites, like the lungs and mixed infections with F magna can be seen in cattle. Tissue destruction by wandering flukes may create a microenvironment favorable to activation of clostridial spores.
Specific diagnosis depends on finding eggs in the stool. A false record can result when the patient has eaten infected liver and egg passes through the feces. Daily examination during a liver-free diet will unmask the false diagnosis. An enzyme-linked immunosorbent assay or ELISA test is available, as well. ELISA tests are available commercially and can detect anti-hepatica antibodies in serum and milk, but new ones especially intended for use on fecal samples are being developed. Plasma concentrations of γ-glutamyltransferase, which are increased with bile duct damage, are also helpful during the late maturation period when flukes are in the bile ducts. Only at necropsy, the nature of the liver damage is diagnostic. Adult flukes are readily seen in the bile ducts, and immature stages may be squeezed or teased from the cut surface.
Several drugs are available to treat infected ruminants, including triclabendazole, clorsulon for cattle and sheep only, albendazole, netobimin, closantel, rafoxanide, and oxyclozanide. Not all are approved in all countries, only clorsulon and albendazole are approved in the USA, and most have long withdrawal periods before slaughter if used in meat-producing animals and before milk from treated livestock can be used for human consumption. The timing of treatment is also important so that the pharmacokinetics of the drug used will result in the optimal removal of fluke. Each flukicide has varying efficacy against different ages of fluke. Traditionally, some treatments are determined by local epidemiologic factors and additional treatments by unusually suitable conditions for parasite multiplication. For example, in the Gulf Coast states of the USA, cattle should be treated before the fall rainy season and again in the late spring. In northwestern USA and in northern Europe, cattle should be treated at the end of the pasture season and, if not housed, again in late January or February. In European countries with large susceptible sheep populations, computerized prediction systems based on rainfall and temperature are used to determine the likely prevalence of F. hepatica infections. In areas where heavy infections are expected, sheep may require treatment in September or October, January or February, and again in April or May to reduce both the chances of acute or chronic infections and the output of fluke eggs for development of future disease.
Fasciola hepatica can infect virtually all mammal species, wild and domestic. Consequently it is almost impossible to eradicate it from a given property in endemic regions with favorable conditions. Therefore, where it is known to occur, preventive measures are a must to reduce the snail populations, the infection of pastures with infective stages, or the access to livestock to highly infested pastures. Vector snails are amphibious and live both in water like streams, lakes, pools, swamps, marshes, irrigation channels, ditches, ponds, and watering holes, as well in the humid vegetation around such places. These snails are enormously prolific and a single snail can produce more than 100,000 snails within one year. Whatever measures help keeping the pastures dry have to be encouraged. This can be done by ensuring an adequate drainage of fields, building watering points on solid ground, without puddles, and by making unavoidable ditches or channels less attractive to the snails. This can be done by making the borders steeper and/or cover them with concrete, eliminate the surrounding vegetation, and by drying them completely out periodically. Avoid even very small water points that support the snails, like hardened footprints of shoes or car tires If permanent humid environments cannot be eliminated, they have to be fenced to prevent livestock from grazing there. Rotational grazing is also highly recommended to diminish fluke infestations. Simultaneous grazing of sheep and cattle is not advisable. Alternate grazing of sheep and cattle, and sheep and horses, won't help, because liver flukes can infest all livestock. Livestock infected with liver flukes can develop a certain level of natural immunity and become resistant, especially cattle. Animals with chronic fasciolosis may recover spontaneously. However, such natural resistance is usually associated with hepatic fibrosis, like a partial impairment of the liver function that will certainly result in a reduced productivity. Keeping livestock healthy and well fed diminishes the harm caused by liver flukes and favors the development of the previously mentioned natural immunity. There are so far no vaccines against the common liver fluke and biological control of liver flukes like uding their natural enemies is so far not feasible.
Often we do not know exactly what triggers a seizure, when the cause cannot be determined, the condition is called idiopathic epilepsy or seizures. Some disorders leading to seizure may be primary such as tumors, infections such as bacterial, Chlamydophila, viral or even fungal, heat stroke, or trauma such as flying accidents. Secondary disorders include reproductive problems, metabolic disorders, nutritional deficiencies or imbalances and toxic events. seizures can be considered idiopathic, meaning that no other known cause can be determined for why seizures are occurring. Since the term "Idiopathic" means that there is no one known cause for the seizures, any animal or human can be diagnosed with Idopathic Epilepsy. Studies have shown that, Red-lored Amazons and peach-faced lovebirds are the species of aviaries most commonly diagnosed with idiopathic epilepsy.
The possible causes of seizures have to be understood and examined to rule them out as causes before a bird can be diagnosed with Idiopathic Epilepsy. Toxicities like heavy metal poisoning,, most often lead or zinc poisoning, are common in pet birds that chew on inappropriate items. Possible symptoms of heavy metal poisoning are green or bloody diarrhea, vomiting, depression, gastrointestinal stasis, intermittent lethargy, seizures, dysphagia, ataxia, increased thirst and urination, loss of balance, dehydration, weightloss, feather picking, and if left untreated even death. Exposure to pesticides can also lead to nonspecific signs of poisoning, including gastrointestinal problems, tremors, weakness, dyspnea, seizures or sudden death. Birds are especially susceptible to environmental toxins. Dehydration is another cause that is easy to fix. Once a bird is properly hydrated, the seizures usually stop. If not corrected, dehydration will lead to death. But keep in mind that the cause of the dehydration needs to be found, unless it obvious like a lack of water. But more often than not a dehydrated bird is suffering from an infection or some disease that causes the dehydration. Low blood sugar can also play a roll with symptoms like an increase in thirst and urination, weakness, collapse, and seizures.
Some birds particularly budgies are susceptible to stress seizures also referred to as cardiac racing syndrome and most of the time, they will come right out of it once they calm down. For birds that easily stress out, a stress-free environment should be created as much as possible, before any major change, some homeopathic remedy like the rescue remedy for pets might be indicated to help a pet deal with everyday stresses. Infectious diseases that may have neurological symptoms like PDD, Macaw Wasting Disease can also be apart of the seizures. Birds may show neurological signs such as seizures, and falling off perches. Aspergillosis / Aflatoxins show symptoms of nasal discharge, weight loss, diarrhea, flakey or delaminating beak, unstructured or frayed feathers, black-edged feathers on the outside of the wings, extreme itchiness, neurological problems including seizures. West Nile Virus may be suspect but only suspect if this disease has been identified in your area. This virus is transmitted by mosquitoes. Common symptoms of West Nile Virus are acute death, clinical signs involving the nervous system such as seizures, uncoordination, weight loss, diarrhea, intention tremors, difficulty walking or enteritis, or the infection may be unapparent. Infected birds can die or recover spontaneously with or without supportive care. End-stage liver disease can build up toxins in the bloodstream, resulting in central nervous systems signs, such as disorientation or seizures. Hyperthermia and heat exposure is when an overheated bird will begin panting, and with panting, will also begin getting dehydrated. If the bird's body temperature rises high enough, it will suffer a seizure and die. Metabolic diseases like hypocalcaemia, and hyperglycemia can also cause seizures. Another main reason we see seizures in birds is from a Vitamin D and Calcium Deficiency caused by a malfunctioning uropygial gland. Seizures occur, as the uropygial or oil gland produces vitamin D3 precursors that are spread into the feathers as the birds preen themselves. Upon exposure to ultraviolet light, the precursors will be converted to active D3, which will then be ingested when the birds preen themselves again. Therefore, it is important to also make sure that the gland is working properly.
Seizures may be mild to severe, partial or generalized, frequent or infrequent; and may involve twitching, paddling or convulsing. A bird may present a sudden, temporary loss of consciousness and control of motor function and it may appear disoriented and unable to perch. During a seizure, a bird may vocalize, lose consciousness, fall off its perch, flap its wings uncontrollably and stiffen its body. A partial seizure is characterized by a continuous twitching of a wing or leg. Fortunately, many birds will recover from a seizure and slowly regain their ability to control their movements and perch. There are three parts to any seizure. The initial phase is called the aura phase, and the bird may go through a period of altered behavior. The second phase is called ictus and is a period of disorientation, with an inability to coordinate the movements of the muscles. The bird will lose its grip and fall to the bottom of the cage. Often the body becomes stiff and the bird will jerk spastically. The bird may also defecate and vocalize. This phase usually lasts five to twenty seconds, but if you have never witnessed this before, it can be a frightening and seem like a much longer period of time has gone by. The third phase is called the post-ictal phase and lasts several minutes to hours. The bird will show a variable mount of exhaustion, lethargy, confusion, disorientation, agitation or restlessness.
A veterinarian familiar with birds will start with a complete history, weight and a physical examination. The diet will be evaluated for content and freshness, what supplements are being given, whether there are any possible deficiencies like vitamin D or calcium, and the possibility of contamination. There are a number of tests that can help your veterinarian determine the nature of your bird's problem. Each test provides another piece of the puzzle, and often many tests are needed to give more clarity. A complete blood count or CBC, gives important information about infections, dehydration, toxins and anemia. Blood chemistry tests are used to screen the liver, kidneys, and other body systems to help determine what system is being affected by disease. Specific infectious agents may be investigated using serology and DNA testing. X-rays may also be used to assess the bones, the size and the position of the internal organs, and to explore for the presence of foreign materials such as lead or zinc. Other tests that may be recommended are the EEG or electroencephalogram, MRI or Magnetic Resonance Imaging, and/or a CT or Computer Assisted Tomography. It is important to try to rule out a cause for the seizures before assuming that it is Idopathic Epilepsy so that the cause of the seizures can be treated if possible.
Specific treatments may then be implemented, based on the findings of the tests performed and the diagnosis made. The range of treatments varies depending on the specific problem and may include treating the underlying disease, modifying the diet, providing nutritional supplementation, and possibly hospitalizing the bird for supportive therapy like fluids and vitamins, plus an antibiotic, antiviral or antiparasitic medications as indicated. Sometimes the condition cannot be "cured", only managed and supported to improve the quality of life, that is when they diagnose Idopathic Epilepsy. When you notice your bird having a seizure the bird should be placed in a quiet dark box and taken to a veterinarian immediately. They will need supportive care, including a warm, quiet, safe environment, fluids, nutritional support, antibiotics, if appropriate, and anticonvulsants.
Diazepam or valium is used to temporarily stop the seizures. If the cause of the seizures can be found, treatment is generally directed specifically towards correcting the underlying problem. Lead and zinc toxicity, for example, may be treated by chelating drugs and removal, if possible, of the lead or zinc particles. Veterinarians who are presented with an African Grey exhibiting neurological signs and seizures may presumptuously treat him or her with intravenous calcium gluconate as well as with diazepam. Birds that are found to have epilepsy may be maintained on Phenobarbital to control and, hopefully, eliminate their seizures.
As of now there is no vaccine and no real way to prevent seizures in your bird or other pet, just like there is no way to prevent them in people. Proper nutrition, housing, and care is really the only way to help prevent them. And although humans can have Idiopathic Epilepsy it is not zoonotic as it is not contagious
Veterinarians have long suspected that lymphoma in ferrets might be caused by a virus. This is because certain lymphomas and leukemias in other animal species and humans are thought to be caused by virus as well. In 1995, veterinarians and researchers at MIT succeeded in transmitting lymphoma from one ferret to another with cell free extracts from an infected ferret. The presence of the enzyme, reverse transcriptase which is a calling card of the retrovirus group, made them suspect that the virus were replicating and playing a part in Ferret Lymphoma. Their studies also indicated that lymphoma may be only one end stage of a complex infectious viral disease.
All mammals have, as part of their immune system, white blood cells called lymphocytes. These cells move through the body through the blood and lymphatic systems. They reside in depositories called lymph nodes and are also found in the spleen, bone marrow and thymus gland. These cells sometime become cancerous. When they do, the tumors they form tend to be spread throughout the body, which is commonly known as lymphoma.
The adult form of lymphoma, called Adult Onset Lymphoma, usually occurs in ferrets over three years of age. The majority are five to seven years old when their decline in health is noticed. This form of lymphoma usually progresses very slowly. So the signs one sees usually depend on how long the problem has been present in your pet. Early in the disease, the signs can be easily overlooked. Some pets are brought to veterinarians because of vague signs like poor appetite, weight loss, and lethargy. Others are brought in because the owner has noticed firm swellings under the ferret’s chin or at the points of the shoulder and thigh. Animals that have had the condition for longer periods may come in with signs related to multiple or single organ failure. In these ferrets, the tumorous or cancerous cells have moved and invaded organs like the liver, kidneys and lungs. The spleen of these ferrets is usually also invaded by cancerous lymphocytes and can be many times it normal size. Lymphoma occurs less frequently in ferrets younger than two. When it does, it is called the juvenile form. When it occurs in these young pets, it produces a different set of symptoms that progress much faster. It is also referred to as the lymphoblastic form. This alludes to the fact that the cancerous lymphocytes seen in this type of lymphoma are less well developed and larger in size. Symptoms are variable depending upon the location and stage of tumor, but generally, they include loss of appetite or anorexia, weakness, lethargy, and weight loss. There are many other signs of lymphoma depending on where in the body it is effecting. Multicentric means there are possibly no signs in early stages, generalized, painless enlarged lymphs most common, may note distended abdomen, anorexia,weight loss, and depression may come along with the progression of the disease. Gastrointestinal signs would be anorexia, weight loss, lethargy, vomiting, diarrhea, abdominal discomfort, tarry stools, and an urgent desire to defecate. Mediastinal or mid-chest signs are seen most often in younger ferrets and include signs of anorexia, weight loss, drooling, labored breathing, regurgitation, exercise intolerance, coughing, and even difficulty swallowing. Cutaneous or skin signs would be solitary or multiple masses, lesions that may be pustular with thickening and crusting or even ulcerating. And the solitary form would depend on the location, spleen would show abdominal distention, and discomfort. Cancer in the area of the eyes would show facial deformity, and protrusion of the eyeball. Spinal cord cancer would show as a quickly progressing posterior partial paralysis and lymphoma in the kidneys would show as signs of kidney failure.
To properly diagnose Lymphoma in your ferret you will need to give your veterinarian a thorough history of your ferret's health and onset of symptoms. The history and details you provide may give your veterinarian clues as to which organs are being primarily affected. Knowing the starting point can make diagnosis that much easier to pinpoint. Once the initial history has been taken, your veterinarian will perform a complete physical examination on your ferret. Routine laboratory testing includes a complete blood count and urinalysis would probably be where they start. Diagnostic imaging, including X-rays and ultrasound, are often used to evaluate the size of regional lymph nodes. Your veterinarian may even recommend taking bone marrow samples, so that they can be sent to a veterinary pathologist for further evaluation and to determine the extent of disease.
Ferrets with the juvenile onset form of lymphoma decline rapidly despite treatment. No treatment plan is consistent in extending their lives. But ferrets with adult onset lymphoma have several treatment options. Depending on the age of the ferret, certain treatments may be better. Minimal Treatment may be best for older ferrets. Chronic lymphocytic leukemia in humans is not a painful condition. It is generally not treated for many years after it is diagnosed . Lymphoma, in ferrets does not appear to be a painful condition either. Some ferrets live happily for many years with the condition and eventually die from other unrelated conditions. As in people, when these cancerous cells eventually affect other organs, the result is primarily tiredness, and loss of body weight. So you may decide that no treatment is the right option for your pet, particularly if your ferret is an oldster in ferret years. Another option may be oral corticosteroids. Most adult onset lymphoma ferrets respond quite favorably to oral corticosteroid administration. The primary corticosteroid used for lymphoma in ferrets is prednisone. There is usually a significant improvement in the ferret’s general health once it begins receiving this medication. This improvement, however, does not usually last many months. Some veterinarians feel that lymphomas in ferrets that have been previously treated with corticosteroids are more difficult to keep in check with chemotherapy once they have returned. This has not yet been confirmed scientifically but something to keep in mind. Chemotherapy, with drugs developed for humans, is another option. They may prolong your ferret’s life, but they will not cure the Lymphoma. The treatment plans used in ferrets are ones that have been used successfully in dogs and cats with similar conditions. These are powerful drugs with multiple side effects. Original treatment plans required that they be given intravenously which is a difficult procedure in ferrets. At least one chemotherapy plan, developed at Tufts, allows some of the medications to be given under the skin or subcutaneously, and the rest orally. In this treatment plan, a combination of prednisone, cytarabine or Cytosar , cyclophosphamide, methotrexate, L-asparaginase, chlorambucil and procarbazine are used. More traditional treatments use cyclophosphamide, vincristine, asparaginase, doxorubicin and prednisone. Ferrets receiving any of these powerful medications need to be closely monitored for bad side effects. This can require frequent blood work and bone marrow examinations. Some ferrets tolerate the medications quite well. But some experience weakness, vomiting, lack of appetite and loss of their whiskers. If you chose chemotherapy consider yourself blessed if you gain another two to ten months time with your pet through these treatments. Please do not feel guilty if you elect not to try them as they can also be very expensive. Radiation is also occasionally used to treat Lymphoma in ferrets. As with many Lymphoma treatments, its benefits are difficult to judge. Some ferrets seem to improve after radiation treatment or when radiation is combined with oral medications. Because the progress of lymphoma is so variable, it is difficult to judge this treatment effectiveness. Many ferrets with lymphoma develop tremendously enlarged spleens. They only need removal if they are so large as to displace other organs in the abdomen to the extent that the pet’s general health suffers or when there is evidence that the enlarged spleen has ruptured and bled or may do so. There are innumerable unproven treatments for cancer in humans and pets like ferrets. They take advantage of our desperation to save the animals we love. Many ferret owners and some veterinarians who have exhausted scientifically proven treatments turn to alternative medicine. Before you go that route, ask yourself if you have exhausted everything that traditional veterinary medicine has to offer you and your ferret. Hope is an essential part of the human condition there is no harm in trying unproven therapy when you have no other options.
A permanent cure for Lymphoma is not possible. Perhaps in the future there may be such cures. The best you can hope for is more time with your pet. And as of now, there is nothing you can effectively do to limit the chances that your pet ferret will get lymphoma. But hopefully one day that will change.
So when it comes to understanding animals and the diseases they have, contract, and carry there is no limits but there is always a start. From dogs and cats to livestock and exotics it is necessary to learn and understand diseases from metabolic to degenerative or idiopathic, Neoplastic diseases and Toxic poisonings, Congenital and Genetic diseases to Immune related diseases, and Infectious and Contagious diseases to Parasitic Infections. There is no limit when comes to learning about theses things. Some diseases have been around for years while others are still being studied with new ones occurring today in the modern world. Along with these diseases it is important to study and understand what causes them, what signs to look for, what species to look for them in, how to treat them, and how to prevent them from happening, IF you can even prevent them.

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[->8] - http://www.ivis.org/proceedings/navc/2006/SAE/631.pdf?LA=1
[->9] - http://www.resteddoginn.ca/antifreeze.php
[->10] - http://www.abc.net.au/news/2012-05-01/race-club-downplays-strangles-impact/3982216