Dog Parvo Symptoms

Radiation (ionizing photons, otherwise known as x-rays and gamma rays) interacts with water molecules to form highly reactive free radicals. These free radicals are responsible for breaking strong chemical bonds, most importantly in DNA, leading to eventual cellular destruction. This is summarized below:

• Chemical events resulting from the interaction of radiation with tissue
• Photon interaction with atom (most often with water molecule)
• Fast electron ejection
• Free radical formation
• Bond breakage and chemical changes

BIOLOGICAL EFFECT

While radiation can interact with any part of the cell, evidence garnered from cell death indicates the primary target is at the DNA level. The main goal of radiation therapy (and most cancer treatment modalities) is to eliminate tumor tissue while sparing as much of the normal surrounding tissues as possible in order to maintain normal body function. The basic principles of radiation therapy rely on the fact that different types of cells have different sensitivities to radiation.

In general, cell types can be divided into two main groups: fast proliferating cells and slowly or non-proliferating cells (the speed of proliferation mimes a cell’s DNA repair capability and thus its radiosensitivity). Radiation will randomly damage the DNA of either group, but fast proliferating cells are more sensitive to radiation (and chemotherapy) than slowly proliferating cells. Slowly proliferating cells spend more time in the G1 and synthesis phases of the cell cycle, allowing more repair time before mitosis (division of the cell). Cell death occurs at – but not before – mitosis if lethal radiation damage is present. Therefore, the clinical effect induced by radiation is a delayed effect.

Radiation damage can be divided into three types: lethal, sublethal, and potentially lethal damage. Lethal damage is non-repairable permanent damage. Sublethal damage is damage that can be repaired before cell division. If the cell is not saturated by sublethal damage and has sufficient time for repair, it will survive through mitosis. Potentially lethal damage is damage that might be repaired if the cell is in a certain favorable environment.

Most tumors consist of fast proliferating cells and are therefore quite radiosensitive. Normal tissues are divided into two general groups: early responding tissues, which consist of moderately to very fast proliferating cells; and late responding tissues, which usually consist of slowly to non-proliferating cells. The difference in sensitivity between tumor cells and normal tissues determines the likelihood of tumor control and of normal-tissue complications at various total dosages.

Various types of external beam (teletherapy) radiotherapy units are used in veterinary medicine. These units are usually categorized according to the radiation energy level produced:

Superficial units energy range from 50 to 150 kV
Orthovoltage units energy range from 200 to 300 kV
Supervoltage energy range from 500 to 1000 kV
Megavoltage units energy range > 1MV (includes Cobalt)

In human medicine, orthovoltage units have almost completely been replaced by electron radiotherapy, as have most superficial units. Ortho and megavoltage units are most commonly used in veterinary medicine. The use of megavoltage (which has many advantages over orthovoltage) units in veterinary medicine has made radiotherapy a more successful cancer treatment modality. The main advantages of the megavoltage energy radiation are summarized below:

Electron radiotherapy has become the treatment of choice for superficial lesions, because of its deeper-tissue sparing characteristics (a result of rapid dose fall-off). As with megavoltage photon radiation, electron radiotherapy also offers a relatively homogenous dose distribution with no bone preferential absorption. A large amount of power is necessary for electron radiotherapy and is therefore only available with megavoltage units producing at least 6 MV photon energy. These units are widely used in human medicine but, due to their extravagant cost, are only available at a few veterinary facilities in the United States.

Computer treatment planning has also permitted better tissue sparing by allowing dose calculations for multi-portal plans. By using multiple treatment ports, the superficial dose distribution is spread out over a larger area, thus decreasing the total dose to the skin. The dose to certain critical structures can be accurately calculated by the computer, and then divided among multiple portals while still adhering to the total desired dose. This results to better tumor control with a lower complication rate to the surrounding structures. This is particularly important in treating nasal and brain tumors where critical structures such as eyes and normal surrounding brain tissue are included in the treatment area. Because the dose distribution with orthovoltage and superficial radiotherapy is so unpredictable, accurate data cannot be entered into their computer programs for dose calculations. For this reason, treatment planning and dose calculations for orthovoltage and superficial radiotherapy cannot be done by computer with accuracy.

Cancer is one of the leading causes of pet deaths today. While modern veterinary medicine and technology has increased the life expectancy of animal companions, cancer is primarily a geriatric disease. Thus, the prevalence of cancer among animal companions has considerably increased, along with the veterinary and human treatments to combat it.

Medical and technological advances have been widely covered by the media, resulting in a more informed general public – many of whom seek advanced care for their pets. The human-animal bond can be quite impressive, and should be encouraged and cherished. We owe it to the public and our patients to offer the best quality care and most up-to-date medicine so that owners and their pets can benefit from it.

Currently, complete surgical resection (removal) is the most successful form of treatment for localized tumors. Unfortunately, in many cases, microscopic disease remains and further resection is limited by the tumor’s location or the owner’s fear of causing significant dysfunction or disfiguration. Adjuvant therapy (additional therapy to enhance the effectiveness of the primary medical treatment) is often necessary to maintain better tumor control. Chemotherapy, immunotherapy, biologic therapy, radiation therapy, thermotherapy and photodynamic therapy are all considered adjuvant therapies, and the optimal combination of these modalities depends on the individual case. Since tumors consist of aggressive cells, more combative approaches have resulted in increased success. Using modern medicine and research, some tumors can be beat, and many others can be controlled such that the pet’s quality of life is acceptable, to pet and owner alike, for a longer period of time.

The best chance to cure is the FIRST chance to cure. The key to success in oncology is to be aggressive. The key to achieving the best outcome is to be aggressive within reason – which means taking into consideration the owner’s concerns, the pet’s prognosis and any preexisting medical conditions.

Radiation therapy is not new to veterinary medicine, and publications on its use date back as far as the early 1900s (following closely behind Roentgen’s discovery of the x-ray in 1895). Using a growing knowledge of radiation physics and radiobiology, veterinary radiotherapy pioneers have perfected treatment protocols. The current use of higher energy radiation units, advanced computer treatment planning programs, and safer anesthetic agents that allow more frequent anesthesia, have all lead to an increased success in tumor control and the sparing of normal tissue, and a significantly decreased complication rate. Therefore, radiotherapy, as it is currently practiced, is an acceptable and effective cancer treatment that should be routinely considered as a potential therapy for localized tumors.

Fifth disease is a common viral infection that happens mostly in children. The symptoms of fifth disease are usually mild and go unnoticed. In fact, studies have shown that five to ten percent of children under age five and fifty percent of adults in the United States have had fifth disease, many without even knowing it.

Fifth disease is spread mainly by contact with the mucus of infected people usually through coughing or sneezing. The disease may also be spread from mother to child during pregnancy and rarely through transfusion of blood or blood products, such as platelets or serum. Minor outbreaks of fifth disease usually happen in the spring, possibly in local pre-schools, day care centers, or sometimes in an isolated case.

The main symptom of fifth disease in children is a blotchy, red rash that begins on the cheeks and within a day or two is followed by a pink lace-like pattern, which spreads to the exposed areas of the arms and legs. In the beginning, the facial rash may cause the child to have a characteristic slapped face appearance. The rash usually fades within seven to ten days, but may return over a one to three week period, if the child is exposed to sunlight or heat.

Fifth disease rarely happens in adults, but when it does, about one-fourth of adults who have fifth disease have no symptoms at all. Common symptoms of fifth disease in adults include:

• painful and swollen joints that may last from a few days to several months, and
• a rash that may be mistaken for the rash of rubella or scarlet fever.
• A very rare symptom for both children and adults is fever, which
• is usually very mild, if present at all, and usually comes before
• the rash. Fatigue may also happen prior to the rash appearing.

Fifth disease is usually diagnosed by a doctor from the person’s symptoms and from reports of outbreaks in the area.

Treatment is rarely needed, as a person with fifth disease usually does not show any symptoms that require treatment. The rash usually clears on its own within ten days. If a headache or joint pain occur, an aspirin substitute such as Tylenol or Panadol may be taken. Children and teenagers should not take aspirin as aspirin use in these age groups has been associated with a rare and serious liver and brain disorder called Reye’s syndrome.

Parents of children and persons with medical conditions are advised to read product labels carefully before taking any over-the-counter medication and consult a pharmacist if they have questions about use.

Serious problems associated with fifth disease rarely happen. However, some people may be at risk for these problems, including those whose health is weakened by other conditions such as:

• pregnancy,
• chronic blood disorders, including sickle cell disease, or
• immune system disorders.

If a pregnant woman gets fifth disease, the baby may be at risk for fetal anemia and death. However, birth defects do not happen as a result of infection with fifth disease during pregnancy.

People who have immune system problems are at risk of developing severe, chronic anemia from an infection of fifth disease. Symptoms of severe chronic anemia include:

• chronic fatigue,
• lack of energy,
• pale skin, and
• a low red blood cell count.

Anyone with this condition will remain contagious with fifth disease anywhere from a few months to years.

People in these three groups should call their doctor immediately if they suspect that they have been infected with fifth disease. For others not in these high risk groups, they may take care of their symptoms effectively and safely with home treatment.

To reduce the chances of getting fifth disease:

• wash hands often,
• don’t share eating utensils and drinking containers with an infected person, and
• avoid schools, day care centers, or hospitals during a known outbreak
• of fifth disease especially if you are pregnant, have a chronic
• blood disorder or an immune system problem.

 This is Louis story as kindly told by Denise & Roy Fisher.

We got Louis as a 3 year old through poodle rescue. He had been well cared for, but his owners circumstances had changed and they were finding it increasingly difficult to give him the level of care he deserved. They had already had to change his food because they found that cetain foods didn’t suit him, but at this point there was no reason to think he had anything but a slightly delicate stomach,until 8 months after we got him.

One evening he had his tea, had violent sickness & diarrhoea and just lay on his side in the garden with his breathing becoming increasingly shallow & his heart rate slowing. I was phoning the vet, and at one point Roy came to tell me it was too late, but a few minutes later Louis came to the kitchen door & shook himself as though nothing had been wrong. The illness was a complete mystery to the vets, there were no further problems until 6 months later.

Louis by then had survived several Addisonian crises and had an exploratory operation before Addison’s was diagnosed. His case was made more complicated by the fact he was still making small amounts of corticosteroids & still responded to the ACTH test. At first Addison’s was ruled out, Louis was 24″ at the shoulder and weighed only 3 stone. Due to sheer determination & efforts beyond the call of duty by one vet at our practice, who took a special interest in him, he was eventually diagnosed with Addison’s.

Louis was on steroids & other medication for the rest of his mostly healthy long life, until we sadly lost him aged 13 (he died of bladder cancer,completely unrelated to the Addisons).

The above story was taken from a web site run by Michelle Hargreaves. I believe the owner of the material would be happy for the story to be reproduced here.

Acquired Form of Myasthenia Gravis

The acquired form of myasthenia gravis is an immune-mediated disease caused by the production of antibodies directed against the proteins of acetylcholine receptors. These antibodies, mainly Ig G, cause accelerated breakdown of the receptors as well as blocking the acetylcholine binding sites. The result is severely reduced numbers of effective acetylcholine receptors in each neuromuscular junction. These antibodies also cause morphological changes in the neuromuscular junction, such as reduced folding of the postsynaptic membrane and a wider gap in the neuromuscular junction between the nerve and the muscle.

In a normal neuromuscular junction, acetylcholine effectively binds to the acetylcholine receptors which causes cation channels to open and produce successful muscle action potentials which stimulate muscle contraction. In animals with acquired myasthenia gravis, the nerves are functioning correctly and the normal amounts of acetylcholine are released, but the acetylcholine has troubles binding to its receptors. This may be due to lack of receptors from degradation or lack of available receptors that do not have antibodies already attached. If the amount of binding between acetylcholine and its receptors fall low, many muscle fibers will not have action potentials and therefore not contract and muscle weakness is produced. One of the main signs of acquired myasthenia gravis is progressive muscle weakness with exercise.

The reason muscle weakness gets worse with exercise is because with each repeating nerve impulse the amount of acetylcholine released usually declines. In this situation, not only is there a lack of receptors, there is also a decreasing amount of acetylcholine which decrease the chances even more of having acetylcholine binding to its receptors. Without binding of acetylcholine to its receptors there is no muscle action potential or muscle contraction.

Congenital Form of Myasthenia Gravis

The congenital form of myasthenia gravis is inherited as an autosomal recessive trait. The disease results from structural and functional abnormalities of nicotinic acetylcholine receptors. These abnormalities lead to insufficient amounts of the nicotinic acetylcholine receptors that function properly. Without sufficient numbers of functional nicotinic acetylcholine receptors, a muscle action potential cannot be triggered, and muscle contraction will not occur.

Canine Immune Mediated Disease Awareness, is an organisation that does what the title says, promotes the awareness of auto immune disease in dog’s. Jo Tucker is the lady at the helm of this organisation and has answered a lot of questions relating to Addisons.

C.I.M.D.A have funded and are circulating a survey undertaken by Sara M Gould BVetMed, CertSAM, MRCVS at The Queen’s Veterinary School Hospital , University of Cambridge. This survey is to investigate possible genetic susceptibility and possible triggering factors to auto-immune diseases in dogs. The more common examples (but still rare) are:

• ADDISON’S DISEASE
• AUTO-IMMUNE HAEMOLYTIC ANAEMIA
• IMMUNE-MEDIATED THROMBOCYTOPENIA
• HYPOTHYROIDISM
• IMMUNE-MEDIATED POLYARTHRITIS
• AUTO-IMMUNE SKIN DISEASES
• EXOCRINE PANCREATIC INSUFFICIENCY(EPI)

 

If your dog has suffered or is suffering from any auto-immune disease and you wish to help with this important survey or if you wish to know more about auto-immune diseases please contact C.I.M.DA, 73 Osidge Lane, Southgate, London N14 5JL. E-mail jo@cimda.fsnet.co.uk It will only cost you the price of a stamp and a little of your time to participate in the Cambridge University survey.

I personally cannot underestimate the suffering by dogs and humans alike that these diseases cause, so please help. There is a print out describing emergency treatment of Addisons Crises/Disease to be applied by vets. This information is supplied by Sara Gould BVetMed, DSAM,MRCVS. For help from other dog owners who have dogs with addisons & Auto-immune problems please e-mail Penel on the following e-mail address. CIMDAsupport-owner@yahoogroups.com

Autoimmune diseases occur when the immune system cannot discriminate between self and nonself. Anything that is foreign to the body is nonself. When an organism’s immune system is threatened by foreign particles such as cancer cells, viruses such as the flu virus, microorganism, and even tiny grass particles, an immune response is elicited. Anything that causes this immune response to occur is an antigen. When a immune response is triggered, the body produces antibodies to attack the antigens. Titer is the relative measure of the strength of an antiserum (serum with antibodies). If an antigen causes cancer, it is referred to as a pathogen. In a well functioning organism the immune system does not fight against its own components or self. The lack of immune response against self is termed tolerance. When the immune system loses its tolerance, it will attack its own components. When tolerance is lost, it is referred to as autoimmunity. Diseases that cause the body to act in this fashion are therefore called autoimmune diseases.

The Nerve Impulse (Action Potential)

Organisms respond to external stimuli. If the stimulus is stong enough, a nerve impulse occurs. The nerve impulse is an all-or-none event which depolarizes the membrane of the synaptic terminal of a nerve cell. The depolarization causes an increase in the calcium ion concentration. The calcium rushes into the nerve cell and causes synaptic vesicles, which contain the neurotransmitter acetylcholine, to fuse with the presynaptic membrane of the nerve and release the acetylcholine into the synaptic cleft. The synaptic cleft is the space that separates the presynaptic cell (nerve cell) from the postsynaptic cell (muscle cell) and is the location where the two cells communicate. When the synaptic cleft separates a nerve cell from a muscle cell it is referred to a neuromuscular junction. The acetylcholine then diffuses across the synaptic cleft to the acetylcholine receptors on the postsynaptic membrane of the muscle cell. The binding of acetylcholine to the acetylcholine receptors on the postsynaptic cell (muscle cell) triggers ion channels on the postsynaptic cell to open. The opening of these ion channels on the postsynaptic membrane of the muscle cell then stimulates the muscle cell to contract.

Ten days after my dog Eddie died from Addisons Disease, my neighbour Lynne’s 6 year old S Poodle, Kerry collapsed . Yes…. it was Addisonian Crises.

Lynne used the same vet as myself and the vet new exactly what Kerry was suffering from. Lynne attributes Kerry’s survival to Eddie’s recent passing. As without the new found knowledge that S Poodles are predisposed to Addisons, the vets may not have acted so swiftly with the correct diagnoses & treatment. Lynne is eternally grateful. With hindsight Lynne said she could now see that Kerry displayed many of the symptoms listed on the symptoms page for many years but the symptoms would come and go as true to the condition. This was my experience with Eddie also.

I thought I would also share this e-mail received on the 5th June 2002.

Hi there. Just wanted to send you a note and thank you. We went through almost exactly what you went through in the last few weeks with our poodle Abby. She also looks so much like that picture of Eddie it’s amazing. Anyway, when the pathologist suggested to test for Addisons our vet said that it wasn’t likely and not to think that that’s what it was or could be. Never having heard of the disease we came home (leaving our dying dog in a kennel at the vet with IV fluid) and looked it up on the net. My wife was in tears a few minutes later after finding your website first. We read the whole thing and phoned the vet that night and insisted that that’s what she had. It took them 4 days to test for it and get the results.

After one day of waiting I made the decision to go ahead and put her on the medication even though the vet had suggested “never to do that”. 3 days later she was so weak and could barely breathe, holding her head high in the air to try and get the short breathes she could manage. The vet told us she was suffering and we should put her to sleep. We wanted to give her one more day, knowing she was strong and only 3 1/2. We took her home with an IV bag hanging from the wall and about 4 hours later she was playing with her ball and the tail started wagging.

Two days later the vet discharged her and she has been fine and slowly gaining her weight back ever since. Words cannot express our deepest and sincere thanks and love we have for you for creating that web site and telling the world about your poor Eddie. We feel that Eddie’s life lives on in others and that you saved our dogs life. It’s pretty simple, without your web site our dog would be dead.

Thank you so much once again. Glen & Katrina BC Canada

When I feel sad at Eddie’s passing I draw comfort from knowing he has potentially saved the lives of others. All the kind words of condolance I received from people who read Eddie’s story at different locations on the web has also been a great help . May I take this time to thank you all for sharing your thoughts, stories & photos of your loveley dogs. I have been able to publish some of them, as you can see on Eddie’s tribute site. A heartfelt thankyou to you all.

The above story was taken from a web site run by Michelle Hargreaves. I believe the owner of the material would be happy for the story to be reproduced here.

In the presence of megaesophagus

If the animal has megaesophagus or aspiration pneumonia in conjunction with myasthenia gravis, the megaesophagus and aspiration pneumonia should receive the initial treatment since they have very poor prognosis.    Megaesophagus rarely responds to treatment.  The animals with megaesophagus or aspiration pneumonia should be fed in small quantities in an elevated position and remain standing for 5 to 10 minutes following eating.  In severe cases where regurgitation and aspiration are a very big problem, a percutaneous gastrostomy tube may be inserted for the delivery of nutrients, fluid, and medications.

If thymoma is present

If thymoma is present, thymectomy (thymus removal) is recommended.

 Anticholinesterase drugs

Both acquired and congenital forms of myasthenia gravis are treated with long-acting anticholinesterase drugs such as pyridostigmine bromide or neostigmine.  However, the number of feline species with congenital myasthenia gravis is too small to really comment on an effective treatment.  Anticholinesterase drugs inhibit enzymatic hydrolysis (breakdown) of acetylcholine at the neuromuscular junction.  The drug prolongs the interaction of acetylcholine with the acetylcholine receptors in the neuromuscular junction.

Dosage ranges

Pyridostigmine bromide:

    .5 – 3.0 mg/kg PO BID-TID

Neostigmine:

    .5 mg/kg PO BID-TID      (This is injectable neostigmine and is used if megaesophagus is present and oral drugs are not efficient.)

Corticosteroids

Corticosteroids are used for the treatment of animals with the acquired form of myasthenia gravis that do not respond well to anticholinesterase therapy.  These drugs are only recommended if aspiration pneumonia is not present.

Dosage ranges

Prednisone:

    start with 0.5 mg/kg/day and increased in 0.5 mg/kg/day increments every 2-4 days until a total of 2.0 mg/kg/day is reached 

Cytotoxic agents

Cytotoxic agents are generally given to thoseanimals that do not respond to corticosteroids. These agents are effective in suppressing the production of antibodies to acetylcholine receptors.

Dosage ranges

Azathioprine (Imuran):

                   
2mg/kg PO SID – QOD

Latin Abbreviations

SID  every day daily

BID  two times a day

TID  three times a day

QOD every other day

Other abbreviation

IM  intermuscular

IV  intervenous