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Animal Disease Research Paper

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1 ) Rabies

Rabies is a viral disease causing inflammation of the brain ( encephalitis ). The virus is a member of the family Rhaboviridae. Worldwide, several variants of the virus have been identified, each associated with a single wild animal host that acts as a reservoir of infection for a particular geographic area. Although all warm -blooded vertebrates are susceptible, only mammals are important in the spread of rabies. In British Columbia, bats are the only reservoir of rabies. Records of bats submitted for rabies testing suggest that relatively few are infected, even among those submitted because they are behaving abnormally. Bats are valuable components of the natural ecosystem and many species are at risk in British Columbia. Other potential hosts of British Columbia include domestic dogs/cats, foxes, raccoons, skunks, wolves and coyotes. " Spill over " of rabies to terrestial mammals from bats has occurred in British Columbia, but rabies has never been maintained in wild populations of terrestrial mammals. Rabies should be suspected in any wild animal exhibiting any behavior considered " abnormal" including ; loss of fear or unusual friendliness, excitation or aggression, depression, incoordination, paralysis, convulsions or seizures, abnormal vocalizations, appearance of nocturnal creatures during the day, signs of choking or inability to drink or swallow food, drooling of saliva or frothing at the mouth. In Carnivores, evidence of having attacking prcupines. Bats, unlike mammals with rabies, may get sick and die before being observed or showing symptons typically found in other mammals Intact brain tissue is the key diagnotic tool in confirming rabies infection. If an animal is suspected of having rabies must be destroyed, it is important that it NOT be killed by gunshot to the head- other forms of euthanasia must be considered There is no treatment for rabies that can cure the disease once symptoms appear. Any treatment at that point involves managing symptoms and making the person comfortable (this is called supportive care). Death is almost certain once the rabies/ symptoms begin.
However, two decades ago, research scientists developed an extremely effective new rabies treatment regimen that provides protection from the disease when administered after an exposure (post-exposure prophylaxis). The treatment can also be used for protection before an exposure occurs (pre-exposure prophylaxis). Keeping rabies vaccinations up to date for all dogs, cats, and ferrets helps keep your pets from getting rabies, but it also provides a barrier of protection for you, if your animal is bitten by a rabid animal such as a bat. Seattle and King County regulations require that all dogs, cats and ferrets be vaccinated for rabies by 4 months of age and booster shots be kept current. Keeping pets under direct supervision so they do not come in contact with wild animals. Contacting a Veterinarian as soon as a pet is bitten also aids in the protection.Calling a local animal control agency to remove any stray animals from your neighborhood that may be unvaccinated and could be infected with rabies. Spaying or neuter your pets to help reduce the number of unwanted pets that may not be properly cared for or regularly vaccinated. 2) Giardia

Giardiasis is a major diarrheal disease found throughout the world. The flagellate protozoan Giardia intestinalis (previously known as G lamlia ), its causative agent, is the most commonly identified intestinal parasite in the United States and the most common protozoal intestinal parasite isolated worldwide. Infection is more common in children than in adults. Giardiasis is a chronic, intestinal protozoal infection that is seen worldwide in most domestic and wild mammals, many birds, and people. Infection is common in dogs and cats, occasional in ruminants, and rare in horses and pigs. The number of different species and the zoonotic potential of Giardia spp are controversial. There is circumstantial evidence that Giardia spp that infect domestic animals can infect people. It appears that some Giardiaspp isolates are infective to a variety of mammals, while others are more species specific. Wild animals may also be reservoirs. Giardia spp have been reported to be found in 1-39% of fecal samples from pet and shelter dogs and cats, with a higher rate of infection in younger animals. Many children and adults infected with Giardia Lamblia have no symptoms of giardiasis, even though they are infected and the parasite is present in their feces. These people can pass the infection to others. Diarrhea , usually lasting 7 to 10 days. It can last longer but can also get better within 2 to 4 days. There first may be a large amount of watery diarrhea followed later by greasy, foul-smelling stools that may float. This is a sign that fat is not being digested properly and instead is being passed from the body in the stool. Abdominal cramps or tenderness, Nausea and loss of appetite, Passing more gas or having more bloating than usual and Fatigue
People often do not seek treatment for these symptoms. In most cases, the symptoms gradually get better on their own. But if giardiasis is not treated during the first episode of symptoms, the illness may become a long-term (chronic) problem.
People with chronic giardiasis have bouts of diarrhea that come and go along with the other common symptoms of giardiasis. These episodes alternate between periods of constipation and normal bowel movements, and they last only a few days at a time. Because of this, many people do not seek treatment. Other symptoms of chronic giardiasis include:nLoose, soft, greasy stools (not always watery or liquid). Sometimes the stools may be foul-smelling or foamy and are often passed in small amounts. Discomfort in the abdomen or pit of the stomach that is often worse after a meal,Belly cramps, bloating, or pain,Passing more gas than usual, Persistent bad breath or belching that sometimes smells of sulfur, Occasional headaches, Weight loss and General feeling of discomfort or illness (malaise), weakness, or fatigue. The motile, piriform trophozoites are occasionally seen in saline smears of loose or watery feces. They should not be confused with trichomonads, which have a single rather than double nucleus, an undulating membrane, and no concave ventral surface. The oval cysts are best detected in feces concentrated by the zinc sulfate (specific gravity 1.18) flotation technique. Sodium chloride, sucrose, or sodium nitrate flotation media are too hypertonic and severely distort the cysts. Staining cysts with iodine aids identification. Because Giardia cysts are excreted intermittently, several fecal examinations should be performed if giardiasis is suspected; eg, 3 samples collected and examined over 3-5 days. About 70% of infected dogs can be identified with a single zinc sulfate flotation; 93% can be identified with 2. In dogs, duodenal aspiration for trophozoite detection is useful; however, in cats, Giardia spp are more prevalent in the mid to lower small intestine. An ELISA that detects Giardia antigen in the feces of dogs and cats is available, but field data on sensitivity and specificity are lacking. Metronidazole ( Flagyl ) is the most commonly used antibiotic for giardia infection. Side effects may include nausea and a metallic taste in the mouth. Don't drink alcohol while taking this medication. Tinidazole ( Tindamax ) works as well as metronidazole and has many of the same side effects, but it can be given in a single dose. Wash hands with soap and clean, running water for at least 20 seconds; rub your hands together to make a lather and be sure to scrub the backs of your hands, between your fingers, and under your nails also wash before and after eating food, Before and after caring for someone who is sick, Before and after treating a cut or wound, After using the toilet, After changing diapers or cleaning up a child who has used the toilet,After blowing your nose, coughing, or sneezing, After touching an animal or animal waste, After handling pet food or pet treats, After touching garbage, Help young children and other people you are caring for with handwashing as needed, Practicing good hygiene helps prevent the spread of disease.

3 ) Fescue toxicosis

Fescue is a hardy, popular, cool season perennial grass that can grow on a variety of soils in a variety of climates. It is grown on an estimated 35 million US acres. Equine Fescue toxicosis is caused when pregnant mares ea tall fescue that is infected with an endophyte fungus, Acremonium coenephialum. Both the mare and the foal can be affected when the mare eats endophyte-infected fescue.
A pasture seeded with fescue may look appetizing to a horse. All is not lost if your broodmare eats endophyte-infested fescue. The newborn foal can suffer greatly from the effects of fescue toxicosis. The range of fetal deaths in the last third of pregnacy for herds affected by fescue toxicity varies from 0 to100%. Generalized symptoms associated with foals born to mares grazing on endophyte-infected fecsue include Prolonged gestation, dystocia, abnormal foal maturation, weakness, starvation ( due to dam's agalactia ). Many Foals born to mares pastured on endophyte- infected fescue have reduced immunity, which makes them highly susceptible to infections. Normally, foals receive antibodies from the mare in the form of colostrum, consumed almost immediatley after birth. However, mares affected with fescue toxicosis are often agalactic, and so thier production of milk is limited or nonexistant. Thus, the newborn foal is not able to consume enough colostrum to have an adequate transfer of antibodies from the mother to the foal. The foal is at risck to contract a number of illnesses and infections. If a mare does not supply an adequate amount of milk or colostrum to the newborn foal, the foal should be given colostrum from a donor mare, or colostrum that is stored in a colostrum bank. If neither of these options is available, the foal should be given colostrum from another species of animal, followed by intravenous antibodies and a diet of supplemental milk. Cow or goat milk is often used, although additional sugar (in the form of dextrose) is added to more closely resemble the mare's milk. The best form of treating fescue toxicosis in horses is prevention. However, this is not always possible. Nonpregnant horses can safely graze on endophye-infected fescue pastures, as can broodmares during the second trimester of pregnancy. If a pregnant horse must graze on endophyte-infected fescue, there are pharmaceuticals available to help reduce the adverse effects. Some of the available drugs include: Domperidone ( which prevents ergovaline from inhibiting prolactin release and, hence, prevents agalactia. Perhenazine, and Reserpine are also drugs that can treat Fescue toxicosis. Fescue toxicosis is not unique to horses; it can affect any species of livestock that graze on endophyte-infected fescue. Some additonal sources of information on fescue toxicosis include

4) Hip Dysplasia

Hip dysplasia is considered to be a multifactorial condition. That means that several factors are involved in causing the condition to manifest.Cause is unknown but common in breech position or large fetal size. Hip dysplasia, characterized by an abnormal formation of the hip joint, occurs in many mammals. Both dogs and humans may fall victim to this disease, although it is far more prevalent in dogs. Hip dysplasia may affect any dog, whether it is male or female, small, medium or large sized. It is estimated however that more than 50 percent of some large breeds are affected, making it far more common in these animals than in smaller dogs. The disease seems to strike certain breeds particularly hard, including the Bernese Mountain Dog, Bloodhound, Boxer, Brittany Spaniel, Chesapeake Bay Retriever, English Setter, English Springer Spaniel, Golden Retriever, Gordon Setter, German Shepherd Dog, Labrador Retriever, Old English Sheep Dog, Standard Poodle, Rottweiler, St. Bernard, Welsh Springer Spaniel, and the Welsh Corgi. Large breeds with a low incidence of hip dysplasia include the Borzoi, Doberman Pinscher, Great Dane, Greyhound, Irish Wolfhound, and Siberian Husky. The earliest symptoms of hip dysplasia often begin to manifest themselves between the ages of four months and one year. This is not an “all or nothing” type disease, and the spectrum of symptoms ranges from practically nonexistent to severe crippling. Young dogs may have a wobbling, weaving, or waddling and unsteady gait. An effort is often made to draw the hind legs forward, placing more weight on the forelimbs and ultimately leading to an overdevelopment of the forequarters and an underdevelopment of the hindquarters. When running, afflicted dogs often move their hind legs together in a maneuver commonly termed “bunny hopping.” Dogs may exhibit an aversion to strenuous exercise, or may be sore after such activity. Stiffness is often at its worst in the morning, but dogs developing hip dysplasia will consistently have difficulty navigating stairs and rising from sitting or prone positions. A distinct clicking sound may occasionally be heard when the dog is walking or running. As is the case in humans, dogs have a varying tolerance for pain, and some animals may experience a change in temperament due to discomfort. Though physical examinations may be helpful, radiography and x-rays are the only means of reaching a definitive diagnosis of CHD.The goal of a physical examination is to determine hip joint laxity, or the degree of looseness in the joint. Looser hip joints are more likely to become dysplastic than are stable ones. Palpation of the hip joint and surrounding areas can provide an estimate of the laxity of the hip joint, but the measurements are subjective and not as definitive as x-rays. The traditional radiographic method is regulated by the Orthopedic Foundation for Animals (OFA). This organization upholds a standard based upon breed, age, and conformation information. Dogs are not eligible to be registered with the OFA until after 2 years of age. At this point they are examined according to OFA guidelines and graded on a 7-point scale from excellent conformation to severe hip dysplasia. Dogs with hip grades of excellent, good, or fair are eligible for OFA certification of dysplasia-free status. Positioning for the OFA test requires that the dog be sedated or anesthetized and positioned on his back with hind legs extended together nearly parallel to the tabletop. Researchers at Cornell University recently have developed a new test for canine hip dysplasia. Termed the dorsolateral subluxation (DLS) test, the procedure improves upon the OFA protocol by being more accurate at a younger age than the traditional test. While the OFA test is not accurate before 2 years of age, studies have shown the DLS test to be accurate as early as 8 months of age. The main difference between this new test and the old OFA method is the way in which the dog is positioned while being x-rayed. The OFA test places the hind limbs in a position that is not natural and may hide symptoms of hip dysplasia. The DLS test relies on a position much more similar to positioning normally found in a standing dog. Before the DLS x-ray examination may take place, a dog must be anesthetized or deeply sedated. It is then placed on its stomach on a foam rubber pad. There is a hole cut in the pad for the dog’s hind legs. The stifles (corresponding to a human knee joint) make contact with the x-ray table, and the dog’s femurs are nearly perpendicular to the table. Arranging the dog in a position that mimics its natural posture allows the x-ray to show with a high level of accuracy what the position of the hip joints is. In a normal hip joint, the head of the femur fits snugly into the joint socket, or acetabulum. In the dysplastic joint, the femoral head conforms poorly to the acetabulum. More space is evident between the bones. Displacement of the femoral head is the hallmark of the disease. Joints are evaluated using the DLS score. This measurement, expressed as a percent, is calculated from the radiograph and represents the percent of the femoral head covered by the acetabular rim. The greater the coverage, the higher the DLS score, and the healthier the hip joint. The DLS test, as with other diagnostic procedures, is carried out by your veterinarian.
Simple, practical measures may be enough to give comfort to dysplastic animals. Mild exercise such as walking, swimming, or slow running is beneficial, but excessive activity such as jumping and prolonged running should be avoided. Some analgesic and anti-inflammatory drugs can relieve the pain. Such medications do not however halt or reverse the progression of destructive changes in the joint. Injections and even oral administration of carbohydrate polysulfates have shown promise in increasing clinical use as a treatment for dysplastic dogs. These drugs can prevent pain and aid in normal remodeling to improve the contour of the hip joint. Although carbohydrate polysulfates do not cure hip dysplasia, many dogs receive at least some benefit from this treatment. Similarly, nutritional supplements have some proven benefits. Surgical procedures have been devised to treat dogs with chronic pain and lameness. Operations that can be performed in dogs with severe hip dysplasia include procedures that rearrange the bones of the pelvis or the femoral head to improve joint function. Removing or cutting the pectineus muscle near the pelvis often provides relief from pain. Creation of a false joint by removing the femoral head can relieve pain and restore mobility for a dog in some cases. Total replacement of the acetabulum and the femoral head by prosthesis has succeeded in a number of active dogs. The time of appearance and the rate of progression of hip dysplasia are influenced by the growth rate of individual dogs. Studies at the Baker Institute and elsewhere have shown that slowing growth during the early months of life can lessen the severity of hip dysplasia and even prevent it. One study followed two groups of susceptible pups from the time they were eight weeks old until their death. One group of pups was fed nearly 25 percent less food than the second, which were permitted to eat all they wanted of the same diet. Over the course of the 14 year study, data was collected regarding general longevity and the development of hip dysplasia. Not only did the dogs eating a restricted diet live significantly longer than their well-fed counterparts, they developed hip dysplasia at a much lower rate than did the second group. Further, for those dogs on a restricted diet who did develop hip dysplasia, the risk of developing osteoarthritis decreased by 57 percent. This study of course involved a diet restriction that is difficult to enforce for many pet owners. It would be desirable to use a less restrictive dietary regime that would confer many of the same benefits this more severe diet did.

5 ) Cushing's

Cushing’s disease is a slowly progressive condition that is a result of abnormally high levels of cortisol in the body. Although the disease can occur in any breed of horse, it is more common in Morgans and some pony breeds. It can occur in horses of both sexes and in animals of all ages; however, it seems to be more common in older animals. Although a relatively rare disease when compared to other horse diseases, Cushing's disease is showing up more often. One reason for this is because horses, like humans, are living longer due to advances in health care and nutrition. Cushing's disease can be found in humans, dogs, horses and other mammals. This disease is also known as pituitary pars intermedia dysfunction (PPID), hyperadrenocorticism, equine Cushing's disease (ECD) and Cushing's syndrome. Metabolic syndrome, also known as peripheral Cushing's syndrome, is a different ailment that has many of the same symptoms of Cushing's disease. Clinicians say it could be a factor in horses that develop Cushing's disease. Polydipsia (excessive thirst) and polyuria (excessive urination) are the first symptoms often noticed. Normal horses often drink from 6-10 gallons of water per day. A Cushing's affected horse might go through as much as 21 gallons of water a day. Because of muscle weakness and atrophy (shrinking), Cushing's disease also causes a swaybacked or potbellied appearance and a loss of muscle over the top line. The horse may experience an increased appetite without the corresponding weight gain. A history of chronic laminitis, often without any known cause, is a common sign. Another common sign that may be noticed by an owner is a change in the horse's coat. It fails to shed in the summer and becomes heavy, coarse, and wavy. Since cortisol regulates the immune system, a horse with Cushing's disease often suffers bouts of respiratory disease, skin infections, parasite infections, foot abscesses, mouth ulcers, and periodontal or dental disease. Wounds tend to heal slowly. Occasionally, a mare's estrous cycle will be abnormal or not occur at all. Some horses with Cushing's disease have become completely sterile. Mares may even produce milk despite not being pregnant. Having a horse that is lethargic and lacks energy is another sign of Cushing's disease. When a tumor is involved, it can swell and eventually put pressure on the hypothalamus and surrounding structures. The optic nerve is also nearby, and large tumors have been found to have put enough pressure on that nerve to cause blindness. Head tilting and dementia have also been the result of the larger tumors. Blood tests can reveal high blood sugar levels, high blood fats, anemia, reduced lymphocyte counts, and electrolyte imbalances. A CBC (complete blood count) will reveal if the horse is suffering from hyperglycemia (high blood sugar), which is often present in animals with Cushing's disease due to insulin resistance. The blood sugar levels of affected horses are over 120 mg per dl; sometimes they rise to over 300 mg per dl. A urinalysis can detect glucosuria and ketonuria (abnormally high levels of glucose and ketones in urine) and may prompt more specific hormone-related tests. When additional testing is done, the dexamethasone suppression test (DST) is commonly run. First, a blood sample is taken to establish a baseline on cortisol levels. Then, dexamethasone is administered and another blood test taken in 19-24 hours. Cortisol levels are normally elevated in horses with Cushing's disease. The ACTH stimulation test is another way of measuring cortisol levels in the blood. One unit of ACTH gel is given per kg of body weight. Cortisol levels are then measured 4 to 8 hours later. A diseased horse will show a four-fold rise in cortisol, whereas a normal horse will only show a two to three fold increase. However, it is important to note that recent research has cast a shadow on the accuracy of these tests, since there is such a wide range of "normal" hormone levels in horses. Furthermore, simply being off feed can throw hormone levels off by as much as 50 percent in some tests. Recently, other tests have been developed. One test combines the dexamethasone suppression test with a thyrotropin releasing hormone (TRH) stimulation test which results in a "spike" in cortisol levels. By measuring blood cortisol levels 3 hours after injecting dexamethasone and immediately following it with an injection of TRH, one can measure elevated cortisol levels just 30-45 minutes later. Another test measures pituitary peptides. It is supposedly very safe and avoids the use of dexamethasone (which may produce laminitis). If caught early, Cushing's disease is very treatable and the horse can enjoy several years of health. Horses with advanced cases of the disease are usually suffering symptoms from secondary afflictions and are harder to treat. It is important to also realize that the pituitary gland is inaccessible, so removing any tumor is not an option. Currently, two medications are often used to treat Cushing’s disease. One that seems to work the best is pergolide mesylate (Permax). Pergolide is a dopamine agonist originally used to treat Parkinson's disease in humans. At small dosages, smaller even that those used in humans, this drug can help without the high risk of laminitis that has formerly been connected to its use. The second drug that is sometimes used is Cyproheptadine. Cyproheptadine is a serotonin blocker that can be administered using a lower dose at first, with gradual increases until symptoms begin to improve. A simple way to determine improvement is monitoring the polyuria and polydipsia of the horse. As soon as the horse's drinking returns to normal levels, the dosage is at the right level for that horse. At that point, the other symptoms of Cushing’s disease have usually stopped as well. After a month of improvement, the dosage can be decreased slowly until it is at a maintenance level. Most horses with Cushing's are on medication for the rest of their lives. In addition to medication, horses with Cushing's disease need careful management of their health. A proper diet, vaccinations, deworming and dental care are important due to the cortisol’s ability to suppress the horse's immune system. They may also need special help in maintaining proper hoof health and body temperature, since laminitis and faulty thermoregulation are symptoms of Cushing's disease.

6 ) Hemangiosarcoma

Hemangiosarcoma is the most common primary tumor of the spleen in dogs. Less commonly it originates in the heart or subcutaneous tissues. Hemangiosarcoma leads to the formation of abnormal blood vessels which can rupture and bleed. It also commonly spreads to other places in the body (called metastasis). Diagnostic tests are recommended to determine which sites in the body are involved. These tests include Complete blood count (CBC), Serum biochemistry panel, Urinalysis (U/A), Thoracic radiographs, Abdominal sonogram and a Cardiac evaluation (echocardiogram ). Treatment of hemangiosarcoma is aimed at both removing the primary tumor with surgery and using systemic medication (chemotherapy) in an effort to delay or prevent metastasis. Doxorubicin is the drug of choice. It is given at 3-week intervals for a total of 4-6 treatments. There are also reports of a combination protocol consisting of vincristine + doxorubicin + cyclophosphamide (VAC). There is a biologic rationale for combination therapy over single-agent therapy, although the benefit of VAC over doxorubicin alone remains unclear for hemangiosarcoma (reported studies have included different populations of dogs, for example). Regardless, we recommend that the initial treatment be given with doxorubicin alone and if this is well tolerated, then consideration be given to adding the other two drugs. Also, due to the potential for cardiotoxicity with doxorubicin, we recommend follow-up cardiac evaluation, consisting of an echocardiogram and ECG, prior to the 4th treatment. Chemotherapy drugs work by targeting fast-growing cells and cancer cells divide faster and abnormally compared to normal cells. Because of this, chemotherapy preferentially destroys cancer and spares normal tissues. There is the potential for some normal tissues with rapid growth rates (intestinal lining, bone marrow, hair cells) to be transiently damaged by chemotherapy. However, our goal in treating cancer in animals is quality of life, so the dosages are lower than those used in people, and we do not normally see significant toxicity with chemotherapy. There is always some risk when a drug is given for the first time, and the oncologist will discuss what types of side effects may develop and what you should watch for. If the pet has no problems the first time they receive a drug, they should have no problems with subsequent treatments of that drug. If the pet experiences any side effects, we address them as needed and lower the dosage of the causative drug for future treatments to prevent recurrent problems. While the quality of life for dogs following surgery is generally very good, it is unfortunately not of long duration. Survival times following surgery alone for splenic hemangiosarcoma are approximately 2-3 months. With the addition of chemotherapy, survival times extend to approximately 5-7 months. Following completion of chemotherapy, or if chemotherapy is not pursued, metronomic therapy may be considered. Metronomic chemotherapy involves the administration of chronic oral low-dose chemotherapy (cyclophosphamide) in conjunction with other medications (carprofen or deracoxib and doxycycline). It is believed that this treatment approach may inhibit angiogenesis (new blood vessel growth) and thereby inhibit tumor growth. 7 ) Psittacosis

The causative agent is Chlamydia psittaci. This "microvarmit" is like a bacteria (in that it responds to antibiotics) as well as like a virus (in that it will grow only on a tissue culture, not on bacterial media). C. psittaci's ability to mystify us does not end with classification. It can cause disease in humans, other mammals and birds. It can kill a bird in 48 hours or it can survive in birds causing no outward sign of illness, for as long as 10 years. It can be explosively contagious or barely contagious. It can be destroyed by antibiotics easily or with incredible difficulty. It can be easy to diagnose or extremely frustrating. It can kill baby birds and cause no disease in their parents. It can live outside the body, as well as within. It can be easy to control or almost impossible. It causes massive flock outbreaks one year and none the next. The incubation period of psittacosis, as well as the degree of clinical illness, adds to our bewilderment. Just how a bird manifests its exposure to the disease depends on host susceptibility and the virulence (strength) of the strain.
Host susceptibility. Some birds, because of their genetic resistance, are less likely to become ill and, consequently, are more likely to develop into carriers. These include pigeons (one study suggests 70 to 90 percent of all wild pigeons are carriers), doves, budgerigars, cockatiels, cockatoos, herons, gulls, hawks, and approximately 100 additional sylvatic species. Other species, such as rosellas, lorikeets, neophemas, mynahs, canaries and some parrots have low natural resistance and are highly susceptible.
Young birds, due to the relatively incompetent immune systems, are subject to neonatal psittacosis with subsequent high mortality. Any factor that stresses a bird will lower its resistance and increase its potential susceptibility and mortality. Egg production, feeding young, weaning, poor management, overcrowding, concurrent infections and molting are just a few of the many things that stress birds. The individual power of any agent to infect is known as virulence. This power is subject to change, especially as it inoculates birds and is passed out in the stool. Since each gram of stool from diseased birds can infect 10,000 other birds, the agent's power to cause psittacosis becomes very pertinent. Transmission of C. psittaci is also unsettling. The organism is shed in the nasal secretions and in the stool from infected birds, recovering birds and carriers. Once outside the body, the organism can live for a long period of time, drying to form dust and infecting the susceptible hosts as they breathe. Fecal and oral contamination are especially significant in crowded conditions, as well as in nest boxes. As a general rule, inhaled Chlamydia will cause severe disease, while ingested Chlamydia will tend to develop into carriers. Transmission through the egg has been experimentally produced in ducks, but as a practical problem, is not documented in psittacines. The clinical symptoms can be variable, depending on the species infected, the virulence of the agent, the route of exposure and concurrent stresses. The "typical psittacotic bird" is ruffled, depressed, has labored breathing, nasal and ocular discharge, and is neither eating nor vocalizing. The appearance of lime-green or yellow droppings, especially when the urine component is discolored, is highly suggestive, although not diagnostic, of the malady. One form of psittacosis seen infrequently manifests central nervous system signs. Tremors, shaking, head twisting and convulsions may be the only symptoms you see. This clinical peculiarity has been recognized in Amazons, African greys and cockatoos. Cockatiels can develop a psittacosis syndrome that causes paralysis of the limbs, and usually dark, tarry stools. Additionally, cockatiels and neophemas (turquoisines, scarlet-chested parakeets) with low-grade infections may seem to have an eye disease resembling a sty. Diagnosis of chlamydiosis in birds is definitive only if the organism is identified, isolated or causes a predictable physiologic response. The identification of the organism is achieved by stains or a fluorescent antibody test. Treatment for parrot fever is now much more successful than it once was. Most veterinarians use tetracycline and its derivatives, mainly Vibramycin, to treat sick patients as well as carriers. The antibiotic can be given by intravenous or intramuscular injections, orally or mixed in proper ratios with palatable food. Calcium must be withheld - it binds the tetracycline. Blood levels of tetracycline can be enhanced by citric acid in the birds' drinking water. Patients in chlamydial crisis need intense, supportive care (heat, isolation, extremely clean conditions, absence from stress, etc.) as well as therapy for concurrent problems. Appropriate lactobacillus, as well as antifungal medications, are essential. Controlling avian psittacosis is best accomplished by keeping susceptible birds away from the infecting agent. Since this little "microvarmit" can remain infective for many months in dried excrement, cleanliness and disinfection are essential. The Chlamydia species is inactivated by quaternary ammonium compounds. These disinfectants should be used to clean cages and wet-mopped on surrounding areas. Eliminating drafts and spraying the area with disinfectants will help keep infectious feathers and dust to a minimum. Birds that have had the disease or are under treatment are fully susceptible to reinfection since the disease does not convey immunity. In wild birds, psittacosis is controlled naturally by the inability of sick birds to keep up with the flock. Additionally, infective droppings fall to the ground below the trees in which the birds perch. The clinical disease that we see in pets is promoted by confining, crowding, transporting, dietary changes, exposure to other infections and forced exposure to infective excrement.

8 ) Cryptosporidium

Cryptosporidiosis, also known as crypto, is a parasitic disease caused by Cryptosporidium, a protozoan parasite in the phylum Apicomplexa. It affects the intestines and is typically an acute short-term infection. It is spread through the fecal-oral route, often through contaminated water, the main symptom is self-limiting diarrhea in people with intact immune systems. In immunocompromised individuals, such as aids patients, the symptoms are particularly severe and often fatal.Cryptosporidium is the organism most commonly isolated in hiv positivenpatients presenting with diarrhea. Treatment is symptomatic, with fluid rehydration, electrolyte correction and management of any pain. Despite not being identified until 1976, it is one of the most common waterborne diseases and is found worldwide. The parasite is transmitted by environmentally hardy microbial cysts (oocysts) that, once ingested, exist in the small intestine and result in an infection of intestinal epithelial tissue. Infection is through contaminated material such as earth, water, uncooked or cross-contaminated food that has been in contact with the feces of an infected individual or animal. Contact must then be transferred to the mouth and swallowed. It is especially prevalent amongst those in regular contact with bodies of fresh water including recreational water such as swimming pools. Other potential sources include insufficiently treated water supplies, contaminated food, or exposure to feces. The high resistance of Cryptosporidium oocysts to disinfectants such as chlorine bleach enables them to survive for long periods and still remain infective.Some outbreaks have happened in day care related to diaper changes. Symptoms appear from two to ten days after infection, with an average of 7 days,and last for up to two weeks, or in some cases, up to one month.There are 3 possible forms of the illness in immunocompetent people. The disease can be asymptomatic or cause acute diarrhea or persistent diarrhea that can last for a few weeks. Diarrhea is usually watery with mucus. It is very rare to find blood or leukocytes in the diarrhea.As well as watery diarrhea, there is often stomach pains or cramps and a low fever. Other symptoms include nausea, vomiting, malabsorption and dehydration. The individuals who are asymptomatic (have no symptoms) are nevertheless infective, and thus can pass on the infection to others. Even after symptoms have finally subsided an individual is still infective for some weeks.Severe diseases, including pancreatitis, can occur.
Immunocompromised people, as well as very young or very old people, can develop a more severe form of cryptosporidiosis. There are 4 clinical presentations for patients with aids. 4% have no symptoms, 29% have a transient infection, 60% have chronic diarrhea, and 8% have a severe, cholera-like infection. With transient infections diarrhea ends within 2 months and Cryptosporidium is no longer found in the feces. Chronic diarrhea is diarrhea that lasts for 2 or more months. The most severe form results in the patients excreting at least 2 liters of watery diarrhea per day.They can lose up to 25 liters per day. AIDS patients can have up to 10 stools per day. They experience severe malabsorption and can have 10% weight loss. Many of them never completely eliminate Cryptosporidium from their bodies.When Cryptosporidium spreads beyond the intestine, as it can predominantly in patients with aids, it can reach the lungs, middle ear, pancreas, and stomach. Thus, one symptom is pain in the right upper quadrant. The parasite can infect the biliary tract, causing biliary cryptosporidiosis. This can result in cholecystitis and cholangitis. There are many diagnostic tests for Cryptosporidium. They include microscopy, staining, and detection of antibodies. Microscopy can help identify oocysts in fecal matter. To increase the chance of finding the oocysts, the diagnostician should inspect at least 3 stool samples. There are several techniques to concentrate either the stool sample or the oocysts. The modified formalin-ethyl acetate (FEA) concentration method concentrates the stool. Both the modified zinc sulfate centrifugal flotation technique and the Sheather’s sugar flotation procedure can concentrate the oocysts by causing them to float.Another form of microscopy is fluorescent microscopy done by staining with auramine.
Other staining techniques include acid-fast staining, which will stain the oocysts red. One type of acid-fast stain is the Kinyoun technique. Giemsa staining can also be performed. Part of the small intestine can be stained with hematoxylin and eosin (H & E), which will show oocysts attached to the epithelial cells. Detecting antigens is yet another way to diagnose the disease. This can be done with direct fluorescent antibody (DFA) techniques. It can also be achieved through indirect immunofluorescence assay. Enzyme-Linked ImmunoSorbent Assay (ELISA) also detects antigens.Polymerase chain reaction (PCR) is another way to diagnose cryptosporidiosis. It can even identify the specific species of Cryptosporidium. If the patient is thought to have biliary cryptosporidiosis, then an appropriate diagnostic technique is ultrasonography. If that returns normal results, the next step would be to perform endoscopic retrograde cholangiopancreatography. There is no reliable treatment for cryptosporidium enteritis; certain agents such as paromomycin, atovaquone, nitazoxanide,and azithromycin are sometimes used, but they usually have only temporary effects.
Treatment is primarily supportive. Fluids need to be replaced orally. A lactose-free diet should be taken as tolerated. In rare situations, intravenous fluids may be required. Antibiotics are not usually helpful, and are primarily reserved for persons with severe disease and a weak immune system. Sometimes relapses happen.

9 ) Myasthenia Gravis Myasthenia Gravis is a condition resulting from a deficiency of acetyl choline (ACh) receptors on the postsynaptic membrane resulting in a syndrome of muscle weakness. Both congenital and acquired forms of this condition occur in dogs, cats, and humans. To date, studies suggest the pathophysiology of these conditions are similar among these species. Acquired MG affects numerous breeds of dog older than 1 year of age. There appears to be a bimodal, age-related incidence, with peaks at 2-4 years and 9-13 years. Signs of muscular weakness may be focal with selective involvement of the esophageal, pharyngeal, and facial muscles, or diffuse, with signs of generalized muscle weakness. In one study it was estimated that one fourth of the canine patients presenting with idiopathic megaesophagus, had focal MG. Signs of generalized muscle weakness may vary considerably, ranging from some intolerance to exercise, which improves with rest, to acute tetraplegia. Patients with focal or generalized signs, and megaesophagus, often present with pneumonia secondary to aspiration. Evaluation of the thorax may reveal the presence of thymoma, which may be implicated in the etiology of this immune disorder. Recording of evoked muscle action potentials during repetitive nerve stimulation at 2-10 Hz may provide evidence of dysfunction of the neuromuscular junction. A decline in the amplitude of successive potentials (decremental response), provides a presumptive positive test for MG. A more sensitive repetitive stimulation test looking at single myofiber potentials can also be done. Variation in the single fiber potential (“jitter”) is much greater in affected animals with MG. Optimal therapeutic approaches for dogs or cats with acquired MG have not been established. One confounding factor in the assessment of treatments for acquired MG is the frequent occurrence of spontaneous remissions. Up to 87.7% of affected dogs will go into spontaneous remission at an average of 4 months after diagnosis (range: 1 to 18 months). Early and accurate diagnosis is an essential aspect for obtaining a good clinical outcome in most cases of acquired MG. Experienced clinical judgement and cooperative, dedicated owners also are essential considerations. Recognition of esophageal dilation and/or pharyngeal weakness prior to institution of therapy is mandatory. Maintenance of adequate hydration is essential in animals with acquired Myasthenia Gravis. Intravenous fluid therapy may be necessary in animals that regurgitate liquids. Special feeding procedures (e.g., feeding food and water from elevated feed bowls or holding an animal in a vertical position for AT LEAST 20 minutes after feeding), placement of a gastrotomy tube, and in some cases parenteral nutrition, must be considered. Construction of special chairs (“Bailey chair”) to aid in upright feeding can be invaluable.
Intensive care and ventilatory support may be required in animals with severe aspiration pneumonia or severe generalized weakness. Management of dysphagia and megaesophagus, with associated complications of aspiration pneumonia, regurgitation and esophagitis, is an essential consideration. Drugs that may improve esophageal motility (e.g., metoclopramide), increase lower esophageal sphincter tone (e.g., cisapride), or increase the pH of gastrointestinal contents (e.g., cimetidine or ranitidine) should be considered.Specific therapy for acquired Myasthenia Gravis is based on the severity of the disease in a specific animal. To facilitate treatment decisions, a classification system that addresses the heterogeneous and variable clinical signs of acquired Myasthenia Gravis has been introduced for use in dogs and cats : Group 1: Mild or focal MG, Group 2: Moderate generalized MG, and Group 3: Severe generalized or acute fulminating MG.

10 ) Gastric dilatation and volvulus ( GDV )

Gastric dilatation volvulus or bloat or a twisted stomach is a medical condition in which the stomach becomes overstretched by excessive gas content. It is also commonly referred to as torsion and gastric torsion when the stomach is also twisted. The word bloat is often used as a general term to cover gas distension of the stomach with or without twisting. The name comes from the Middle English blout, meaning soft or puffed, which is from the Old Norse blautr, meaning soft or soaked. Meteorism, its name derived from the writings of Hippocrates, is now rarely used in English. The condition occurs most commonly in domesticated animals, especially ruminants and certain dog breeds.
In dogs, gas accumulation in the stomach is usually associated with volvulus of the stomach, which prevents gas from escaping. Deep chestedbreeds are especially at risk. Mortality rates in dogs range from 10 to 60 percent, even with treatment. With surgery, the mortality rate is 15 to 33 percent. Bloat in dogs is likely caused by a multitude of factors, but in all cases the immediate prerequisite is a dysfunction of the sphincter between the esophagus and stomach and an obstruction of outflow through the pylorus, or a clog. Some of the more widely acknowledged factors for developing bloat include increased age, breed, having a deep and narrow chest, stress, eating foods such as kibble that expand in the stomach, overfeeding, too much water consumption in a small period of time; before or after exercise and other causes of gastrointestinal disease and distress. Studies have indicated that the risk of bloat in dogs perceived as happy by their owners is decreased, and increased in dogs perceived as fearful. This may be due to the physiological effects of the dog's personality on the function and motility of the gastrointestinal system. Alternatively perhaps the dogs become unhappy/uncomfortable as a consequence of the conditions that lead up to exhibiting bloat. Dogs with inflammatory bowel disease may be at an increased risk for bloat. One common recommendation in the past has been to raise the food bowl of the dog when it eats. However, studies have shown that this may actually increase the risk of bloat.Eating only once daily, and eating food consisting of particles less than 30 mm in size also may increase the risk of bloat. One study looking at the ingredients of dry dog food found that while neither grains, soy, nor animal proteins increased risk of bloat, foods containing an increased amount of added oils or fats do increase the risk, possibly due to delayed emptying of the stomach. As a general rule, bloat is of greatest risk to deep-chested dogs. The five breeds at greatest risk are Great Danes, Weimaraners, St. Bernards, Gordon Setters, and Irish Setters. In fact, the lifetime risk for a Great Dane to develop bloat has been estimated to be close to 37 percent. Standard Poodles are also at risk for this health problem, as are Irish Wolfhound, Doberman Pinschers, Rottweilers, German shorthaired pointer, German Shepherd Dogs and Rhodesian Ridgebacks. Basset Hounds have the greatest risk for dogs less than 23 kg/50 lbs. The stomach twists around the longitudinal axis of the digestive tract, also known as volvulus. Gas distension may occur prior to or after the stomach twists.The most common direction for rotation is clockwise, viewing the animal from behind. The stomach can rotate up to 360° in this direction and 90° counterclockwise. If the volvulus is greater than 180°, the esophagus is closed off, thereby preventing the animal from relieving the condition by belching or vomiting.The results of this distortion of normal anatomy and gas distension include hypotension (low blood pressure), decreased return of blood to the heart, ischemia (loss of blood supply) of the stomach, and shock. Pressure on the portal vein decreases blood flow to liver and decreases the ability of that organ to remove toxins and absorbed bacteria from the blood. At the other end of the stomach, the spleen may be damaged if the twisting interrupts its blood supply. If not quickly treated, bloat can lead to blood poisoning, peritonitis and death by toxic shock. Symptoms are not necessarily distinguishable from other kinds of distress. A dog might stand uncomfortably and seem to be in extreme discomfort for no apparent reason. Other possible symptoms include firm distension of the abdomen, weakness, depression, difficulty breathing, hypersalivation, and retching without vomiting. A high rate of dogs with bloat have cardiac arrhythmias (40 percent in one study). Chronic bloat may occur in dogs, symptoms of which include loss of appetite, vomiting and weight loss. A diagnosis of bloat is made by several factors. The breed and history will often give a significant suspicion of bloat, and the physical exam will often reveal the telltale sign of a distended abdomen with abdominal tympany. Shock is diagnosed by the presence of pale mucous membranes with poor capillary refill, increased heart rate, and poor pulse quality. X-rays (usually taken after decompression of the stomach if the dog is unstable) will show a stomach distended with gas. The pylorus, which normally is ventral and to the right of the body of the stomach, will be cranial to the body of the stomach and left of the midline, often separated on the x-ray by soft tissue and giving the appearance of a separate gas filled pocket (double bubble sign). At the first signs of bloat (restlessness and inability to sit or lie down comfortably) a dog owner can administer 1-2 tablets of Famotidine also known commercially as Pepcid down the dog's throat. Some vets recommend givingSimethicone during the early signs of a bloat emergency. A more invasive measure could include passing a tube down the dog's throat, as an emergencyfirst aid technique. This is not an easy task and cannot readily be improvised; some web sites document so-called bloat first aid kits and contain descriptions of the first aid a dog owner can provide at the time an attack of bloat is discovered.This is not a substitute for immediate veterinary treatment. There is risk of esophagus or stomach rupture if the tube is inserted too forcefully, or if the stomach is necrotic. Treatment usually involves resuscitation with intravenous fluid therapy, usually a combination of isotonic fluids and hypertonic saline or a colloidal solution such ashetastarch, and emergency surgery. The stomach is initially decompressed by passing a stomach tube, or if that is not possible, multiple trocars can be passed through the skin into the stomach to remove the gas, alternatively the trocars may be inserted directly into the stomach following anaesthesia in order to reduce the chances of infection. During surgery, the stomach is placed back into its correct position, the abdomen is examined for any devitalized tissue (especially the stomach and spleen). A partial gastrectomy may be necessary if there is any necrosis of the stomach wall. Recurrence of bloat attacks can be a problem, occurring in up to 80 percent of dogs treated medically only (without surgery).To prevent recurrence, at the same time the bloat is treated surgically, a right-side gastropexy is often performed, which by a variety of methods firmly attaches the stomach wall to the body wall, to prevent it from twisting inside the abdominal cavity in the future. While dogs that have had gastropexies still may develop gas distension of the stomach, there is a significant reduction in recurrence of gastric volvulus. One study showed that out of 136 dogs that had surgery for bloat, 4.3 percent of those that did have gastropexies had a recurrence, while 54.5 percent of those without the additional surgery recurred. Gastropexies are also performed prophylactically in dogs considered to be at high risk of bloat, including dogs with previous episodes of bloat or with gastrointestinal disease predisposing to bloat, and dogs with a first-order relative (parent or sibling) with a history of bloat.
Precautions that are likely to help prevent bloat include feeding small meals throughout the day instead of one big meal and not exercising immediately before or after a meal.

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...OF WILDLIFE MANAGEMENT SPECIAL PROJECT PROPOSAL TITLE: OPPORTUNISTIC SAMPLING AS A TOOL FOR SURVEILLANCE OF PARASITIC DISEASES IN WILD ANIMALS; A CASE OF MIKUMI NATONAL PARK STUDENT NAME: KIBONA, Juma A REG. NUMBER: WLM/D/11/T/0057 A SPECIAL PROJECT PROPOSAL SUBMITTED IN PARTIAL FULFILMENT OF THE REQUIREMENTS FOR THE BARCHELOR OF SCIENCE IN WILDLIFE MANAGEMENT FROM THE SOKOINE UNIVERSITY OF AGRICULTURE, MOROGORO – TANZANIA SUPERVISOR: Prof. E.K. BATAMUZI 2013/2014 0 Table of Contents 1.0 INTRODUCTION................................................................................................................................. 2 1.1 BACKGROUND OF INFORMATION ............................................................................................. 2 1.2 Statement of the Research Problem .................................................................................................... 4 1.3 OBJECTIVE ....................................................................................................................................... 6 1.3.0 General objective ............................................................................................................................. 6 1.3.1 Specific objectives ....................................................................................................................... 6 1.4 RESEARCH QUESTIONS...............................................................................................................

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