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The thyroid is a small, butterfly shaped gland located at the front of the neck. The thyroid produces the thyroid hormones, including the two major ones, namely the tri-iodothyronine (T3) and thyroxine (T4), which are essential for regulating the metabolic activities, growth, and several other body functions. The thyroid gland is divided into two halves or lobes, and is connected by a thin ‘bridge’ of thyroid tissue known as the isthmus. The thyroid is usually larger in women in comparison to men. The pituitary gland, which is situated at the bottom of the brain, and produces the thyroid-stimulating hormone (TSH), controls the functioning of the thyroid. TSH activates the thyroid to produce more thyroid hormones. Noted among the most widespread medical conditions, diseases of the thyroid gland are very common and affect millions of Americans. Thyroid disease occurs when the thyroid doesn't supply sufficient hormones required by the body to carry out its various functions properly. As the symptoms of thyroid are often noticed over a period of time, they are usually misdiagnosed. The three most common thyroid problems are the underactive thyroid, the overactive thyroid, and thyroid nodules. Overactive thyroid releases excessive thyroid hormone into the bloodstream, resulting in hyperthyroidism. Hyperthyroidism causes the body to use up energy more rapidly than it should, and chemical activities in the cells such as metabolism speeds up. In the case of underactive thyroid, the thyroid gland is attacked by the body's immune system. Thyroid Nodules is a condition that begins as a small swelling or lumps in the thyroid gland. Other thyroid problems include inflammation of the thyroid gland, enlargement of the thyroid gland, and thyroid cancer. In recent years, thyroid function tests have progressed significantly, allowing for diagnosis at an early stage, and better recovery rates than in the past. vimax penis enlargement testimonials plastic surgery penis enhancement penis enlagement surgery cost safe penile enlargment penis enlargement pill review semenax vigrx free penis enlagement video safe penile enlargment

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The causes can be physical or psychological. It is also possible for an initially physically led cause for impotence to attract psychological issues too. Physical Causes for Impotence or Erectile Dysfunction 1) Brain Damage If the head had suffered trauma and/or brain has been damaged, then there is a possibility that the signals required for a healthy erection will not occur and impotence will result. 2) Diabetes There is a higher possibility that someone with diabetes will suffer with impotence also. Conversely, and loss and or an inability to maintain an erection may be an indicator of diabetes. 3) Glandular Glandular issues and those connected to the thyroid may have an adverse effect on love-making and lead to erectile dysfunction. 4) Drugs Some drugs, both prescriptive and recreational may have side effects, one of which could be erectile dysfunction. Drugs that are prescribed for high-blood pressure may often be the cause of a loss of erection and therefore impotence. Some drugs prescribed for psychiatric conditions such as depression may also be a cause. 5) Injury to the Penis or Surrounding Area Sometimes damage, whether temporary or otherwise to the penis may lead to a temporary loss of erection or discomfort if the area is tender. Psychological Causes of Impotence – Erectile Dysfunction This refers to the way a man either thinks about what an erection and/or sex means to them or what they associate with the act of love-making. 1) Negative Conditioning A man may have learnt from parents or other persons of influence that sex is in some way wrong or bad or have some other negative connotations. In attempting to perform sex these influences may reduce arousal and replace it with negative feelings leading to a loss of erection and impotence. 2) Criticism A partner may have criticised a man either before after or during love-making. The next time the man makes love he may have that criticism on his mind. He will want to avoid being criticised again and may feel under pressure. The result of all this may be a loss of his erection. 3) Fear of Loss of Erection Sometimes a man loses his erection during love-making which is perfectly normal. If the man believes this is not supposed to happen he may feel under pressure to keep his erection throughout love-making. This leads to anxiety and anxiety does not help maintain an erection. 4) Alcohol Many men experience temporary impotence if they have been drinking excessively. This experience or memory may play on their minds and they may feel anxious during the next time they make love. Even though alcohol may not have been consumed on this subsequent occasion the man may lose his erection if this previous memory plays on his mind. 5) Partner or Marital Difficulties If there is an issue or problem in the relationship, this may well have an impact on love-making and the result may be temporary impotence. Unfortunately the partner may compound the issue by saying something like “you don’t love me anymore” after the man loses is erection. 6) Routine – Loss of Excitement In the majority of relationships the couple can settle down into a routine for love-making and one or both partners may lose interest because the initial excitement is no longer there. Each partner does the exact same thing during love-making and so it becomes more mechanical with less emotional input. If the sexual interest lessens impotence may result Impotence and Erectile Dysfunction Conclusion All of the above and more can lead to a fear of losing an erection. If the pattern is repeated during subsequent love-making this can have a negative and compounding impact on a man’s thoughts about making love. Often avoidance may be used as a strategy to cope. Unfortunately avoidance rarely resolves or releases a fear or impotence. vimax pillss inch top pennis enlargement pills free penis enlagement free penis enlargement tip pnis enlargement program penile girth enlargment guide to penile enlargement penis enlagement video cheap penis enhancement

Let me explain in simple sentences that exactly what and where is the G-spot located. G-spot also known as the Gräfenberg spot (it is named after German gynecologist Ernst Gräfenberg), is a small area located in female genital area behind the pubic bone and surrounding the urethra. It is the same as, or part of, the urethral sponge, the site of Skene's glands. Stimulation of the G-spot is said to promote a more vigorous and satisfying orgasm, and is possibly the cause of female ejaculation from the Skene's glands, contained in the urethral sponge. Such stimulation requires a somewhat opposite thrust to that required to obtain maximal clitoral stimulation via the penis, and is often referred to in the vernacular as "riding high". So the g-spot is the key to experience intense ecstatic sex. Whether you are male or female, it is simple techniques said that the g-spot unlocks the door to: • intense full body female orgasm • sacred amrita / female ejaculation • spiritual and tantric sex So even if you frequently experience orgasm, you may not know that there are many different types of orgasm: g spot orgasms, clitoral orgasms, squirting orgasms, and multiple orgasms. The shape of the penis determines which sexual positions best reach the G-spot. For instance, in missionary position intercourse, a penis that curves upward has a natural ability to exert more pressure on the front wall of the vagina. A man whose penis curves downwards, on the other hand, may find the doggy style position more suitable for stimulating the G-spot as the curve works against the front wall. There are far too many information that you can find online, both free and paid information. But for you to start experiencing the first stage of g-spot stimulation to orgasm, the stimulation of the G-spot through the use of a finger or tongue is possible through the combined pressure of pushing down on the clitoris while arcing the tongue or finger upwards in a beckoning motion. The finger or tongue must be approximately 1-3 inches inside the vagina for this to work. However, different individuals require different forms of stimulation. One of the fun side effects of this could be that you ejaculate for the first time. If you feel like you have to pee – you’re on the right track! The term 'G-spot' is also used by analogy as a slang term for the prostate gland in men. Yes, men have a g-spot too.The male g-spot which may be stimulated through anal play or by pressing on the perineum (skin directly beneath the scrotum). Similar to a woman’s g-spot, the important nerves for erection, orgasm and ejaculation converge at the male g spot and in the prostate and perineum area. This area also can provide intense and heightened pleasure, and is also the place where emotional and sexual issues are stored. A male orgasm that is stronger, longer, continuous and more explosive – often called a prostate orgasm - is all characteristic of stimulation to the male g spot. Rather than being an orgasm that is just located in your genitals or driven solely by your penis, a prostate orgasm becomes a whole-body phenomenon, and can offer you multiple orgasms as well as orgasms without ejaculation. herbal natural penile enlargement natural penis enlargement pills free penile enlargment technique buy penis enlagement pills penis enhancement photo does magna rx work guide to penis enargement penile enlargment excersizes cheap penis enhancement

If you’ve ever witnessed someone suffer a stroke, you understand the humbling nature of this disease. It can reduce the mightiest human being to an immobile, helpless creature. Impairment of crucial functions like speech, walking, and control of bowel and bladder can wrench control from the body in a moment. Even perpetually youthful TV personality Dick Clark was struck down by stroke at age 75, despite the outward appearance of perfect health. Clark’s stroke resulted in a six-week hospital stay and, judging from fragmented reports, significant disability. Stroke can be like a devastating fire that strikes without warning, leaving only smoldering rubble. Stroke can so ravage basic bodily functions that often all you can hope for is to regain a portion through rehabilitation. The disease process that underlies stroke requires decades—30 or 40 years—to develop. With that much lead time, why aren’t we better able to detect or stop this crippling disease? The truth is that we are able to predict many, if not most, strokes. Advances in imaging technology allow detection of atherosclerotic plaque that cause stroke years before it becomes a threat. Progress in deciphering the causes of stroke has also leapt forward. Unfortunately, your neighborhood physician still focuses on diagnosing the crisis rather than anticipating it. Physicians prefer to deal with catastrophes and are just not that interested in prevention. Most physicians ask: “Is it time to operate or not?” The medical community obsesses over procedures like carotid endarterectomy (surgical removal of plaque) or carotid stents. Even when a person is afforded the warnings of a “mini-stroke”, or transient ischemic attack (TIA), little more is done once it’s determined that surgery is not necessary—even though this person has high risk for future stroke (50% over 10 years). Let’s flip-flop this approach to stroke. Procedures represent a failure of prevention! Where do strokes come from? Stroke develops when some portion of the brain is deprived of blood. This usually results from a tiny bit of debris that dislodges from an atherosclerotic plaque along the walls of an artery (the same sort that accumulates in coronaries causing heart attack). The sources of debris have been a subject of controversy, but new imaging technologies have settled the question. Any blood vessel that leads from the heart to the brain can be a source. The two carotid arteries on both sides of your neck are a frequent source, as these arteries are prone to develop plaque. (Our discussion will be confined to what are called thromboembolic, or ischemic, strokes, i.e, strokes that occur from plaque that fragments, sending debris to the brain, and will not include the far less common hemorrhagic strokes due to rupture of small vessels in the brain, nor will we discuss atrial fibrillation and other heart causes of stroke. The thromboembolic strokes we discuss cause around 88% of all strokes.) Over the last 10 years, the aorta has been recognized as another important source of stroke. The aorta is the main artery of the body whose branches go to the head, arms, and legs. Atherosclerotic plaque is a live tissue that, through poor diet, inactivity, high cholesterol, overweight, etc., grows and becomes progressively more unstable. At some point, plaque fragments. Little bits break away, traveling to the brain. Fractured plaque also exposes its deeper structures to flowing blood, triggering blood clot formation, which in turn can also fragment and go to the brain. Atherosclerotic plaque is a prerequisite for the most common causes of stroke. If the majority of strokes originate from plaque, why not measure plaque to determine if you’re at risk for stroke? How can we easily, safely, and accurately measure plaque in the carotid arteries and aorta? And if plaque can be measured, can it be shrunk or inactivated to reduce or eliminate risk for stroke? How can plaque be measured? Just 20 years ago, the only practical method of identifying plaque in the carotids or aorta was through angiography, requiring catheters inserted into the body to inject x-ray dye. Angiography was impractical as a screening measure. CT scanning and magnetic resonance imaging (MRI) are emerging as exciting methods of imaging both carotids and aorta. Unfortunately, most centers and physicians are much more focused on the diagnostic uses of these technologies for people who have already suffered stroke or other catastrophe, and application of these devices for preventive uses is still evolving. One exception is when aortic calcification or aortic enlargement is incidentally noted on the increasingly popular CT heart scans; this is an important finding that can signal presence of aortic plaque. The one test that is widely available and can be performed in just about any center is carotid ultrasound. It’s simple, painless, and precise. Two basic observations can be made: 1. Plaque detection—Atherosclerotic plaque can be clearly visualized. If plaque blocks more than 70% of the diameter of the vessel, or if there are “soft” (unstable) elements in plaque, then stroke risk may be high enough to justify surgery or stents. However, if there are plaques that are less severe, substantial risk for stroke may still be present that can be reduced with preventive measures. 2. Carotid intimal-medial thickness—This is a measure of the thickness of the lining of the carotid artery in areas not involved by plaque, but often precedes the development of mature plaque. Carotid intimal-medial thickness also provides an index of body-wide potential for atherosclerotic plaque that can place you at risk for stroke. The aorta, for instance, cannot be well imaged by surface ultrasound but can still be a source for stroke. Increased carotid intimal-medial thickness and carotid plaque are closely associated with likelihood of aortic plaque. The Rotterdam Study of 4000 participants demonstrated that if carotid intimal-medial thickness is greater than normal (1.0 mm), then you can be at risk for stroke (and heart attack), even if no carotid plaques are detected. Carotid ultrasound is the one test you should consider that provides the most information with least effort. Ultrasound is harmless, painless, and can be obtained just about anywhere. Even if your doctor disagrees with your request for a carotid ultrasound, an increasing number of mobile services are popping up nationwide that make this test available for around $100. One important point: many scanners and interpreters will only report whether plaque is present or not. While this is important information, you should request that the carotid-intimal medial thickness be made as well. Not all centers can make this simple measure (because of software requirements), but it doesn’t hurt to try. Any amount of carotid plaque is reason to follow a preventive program, even if the plaque is insufficient to justify surgery. Can plaque be reduced? Can we shrink plaque in carotid arteries and aorta and thereby reduce, perhaps eliminate, these sources of stroke? That question is gaining momentum as effective therapies become available that pack real punch for reducing plaque. Study after study has now documented that plaque can be reduced and, with it, risk for stroke. Reduction in plaque of 10–20% is possible within a year or two. Let’s consider the most potent influences on carotid and aortic plaque growth that need to be considered in a plaque-reducing program. (I assume that you are a non-smoker—if you are a smoker, you first need to concentrate on quitting.) Hypertension Considerable experience documents the power of blood pressure-lowering for prevention of stroke. The most recently updated guidelines, the JNC–VII, recommends a blood pressure of 407 mg/dl heightens stroke risk six-fold. C-reactive protein (CRP) This measure of inflammation is proving to be a useful marker for identifying people at risk for stroke, with increased risk beginning at a level of 0.5 mg/l. High CRP also predicts more rapidly growing carotid plaque. Homocysteine Homocysteine is an important marker of increased likelihood of both carotid and aortic plaque, as well as stroke. In 1997, the European Concerted Action Project reported more than a doubling of stroke when homocysteine levels exceeded 12 mol/l. As homocysteine increases to 20 μmol/l, risk for stroke and heart attack increases an amazing 10-fold over that at a level of 9 μmol/l. Asymmetric dimethylarginine (ADMA) ADMA is recently discovered amino acid whose blood levels can skyrocket up to 10-fold in the presence of hypertension, metabolic syndrome, diabetes, high cholesterol and triglycerides, obesity, and high homocysteine levels. ADMA blocks the action of the amino acid, l-arginine. This mimicry reduces the availability of nitric oxide, a powerful dilator and protector of arteries. ADMA levels in the top 10% predict a six-fold heightened risk for future stroke, and ADMA levels in people with strokes are double that in other people. A carotid ultrasound study in 116 subjects showed that higher blood levels of ADMA are associated with more severe carotid plaque. Because of ADMA’s shared role across a variety of abnormal conditions, correction or blocking the action of ADMA has been suggested as a unique therapeutic tool to reduce stroke risk. Cholesterol Data suggest that lowering cholesterol with statin cholesterol-lowering drugs slows carotid plaque growth and reduce stroke risk approximately 22%. An interesting study from the Cardiovascular Institute at Mt. Sinai School of Medicine in New York using the precise measuring ability of MRI of the carotids and thoracic aorta showed an impressive 20% regression of plaque area with simvastatin (Zocor®) taken for two years. Although guidelines for cholesterol treatment recommend reduction of LDL cholesterol to 100 mg/dl in high-risk persons, a report from the Walter Reed Army Medical Center in Washington, DC, showed that carotid plaque was more effectively reduced when LDL cholesterol of 70 mg/dl or lower was achieved with statin cholesterol drugs. Lower LDL cholesterol may, therefore, be better. Treatment Strategies to Reduce Carotid and Aortic Plaque The essential question: How do we reduce carotid and aortic plaque? If we make this the focus of our efforts, many pieces begin to fall into place. If you’ve had any measure of carotid or aortic plaque such as a carotid ultrasound or aortic calcification on a CT heart scan, you know that you’re at increased risk for stroke. You also have a baseline for future comparison to gauge whether your program is working or not. Because most people have not one but several causes of carotid and aortic plaque, there is no one single treatment that effectively eliminates risk for stroke. Instead, most people require a comprehensive program of healthy diet, exercise, supplements, and medication when indicated. Here, we focus on the nutritional supplements that can be critical components of your plaque-reduction program. Fish oil Fish oil is a cornerstone of your stroke prevention program. Epidemiological observations suggest a strong relationship of fish intake and reduction of stroke risk. Carotid ultrasound studies demonstrate less carotid plaque with greater intakes of fish. A cleverly designed University of Southampton study made the fascinating observation that fish oil transforms the structure of carotid plaque. 150 people with severe carotid plaque scheduled for carotid endarterectomy (surgical removal of the plaque) were given fish oil, sunflower oil, or no treatment over several months while waiting for their procedure. (Delays in the British health system permitted this unique design.) Plaque was removed at surgery and examined. Participants taking fish oil had reduced inflammation in plaque and thicker tissue covering the fatty core, markers of more stable plaque. Those taking sunflower oil or no treatment had unstable plaques with greater inflammation and thinner, less sturdy covering tissue. This suggests that fish oil stabilizes carotid plaque, making it less likely to rupture and fragment. A standard capsule of fish oil (containing 300 mg of EPA + DHA) contains the same amount of omega-3s as a 3 oz serving of cod or halibut; three capsules (900 mg DHA + EPA) contain the equivalent of a serving of farm-raised salmon. The dose that seems to provide greatest protection from stroke, lowers triglycerides (that form abnormal lipoproteins; see above), and reduces fibrinogen, is four capsules per day (1200 mg EPA + DHA). Coenzyme Q10 (CoQ10) Although there are no data specifically addressing whether CoQ10 reduces plaque, it is a marvelously effective way to reduce blood pressure, one of the crucial factors causing carotid and aortic plaque growth. A pooled analysis of eight studies showed that, on average, CoQ10 in daily doses of 50–200 mg reduced systolic blood pressure by 16 mm Hg, diastolic pressure by 10 mm Hg. Data suggest that CoQ10 can reverse abnormal heart muscle thickening (hypertrophy), another manifestation of high blood pressure, strongly suggesting that CoQ10 has benefits beyond just reducing pressure. Supplements to correct the metabolic syndrome Weight loss is, without question, the most immediate and direct path to correction of this dangerous pre-diabetic condition. A drop of even 10–20 lbs yields improvements across the board: increased sensitivity to insulin, increased HDL, and reductions in triglycerides, CRP, fibrinogen, small LDL particles, and blood pressure. Diet and exercise are fundamental components of an effort to lose weight; low carbohydrate or reduced glycemic index diets (e.g., South Beach or Mediterranean) rich in fibers are clearly effective. Several supplements can amplify weight-reduction efforts and be useful adjuncts to your lifestyle program. Among them: White bean extract White bean extract blocks intestinal absorption of carbohydrates by 66%. 1500 mg twice a day with meals yields, on average, 3–7 lbs of weight loss in the first month of use. The only side-effect is excessive gas, due to unabsorbed starches. Glucomannan This unique fiber taken prior to meals absorbs many times its weight in water and thereby fills your stomach. You consequently take in less food. Most people lose around four lbs per month using 1500 mg prior to each meal. Interestingly, glucomannan also blunts the rise in blood sugar after meals, an effect that, by itself, may lead to weight loss. Be sure to take with plenty of water. DHEA This adrenal hormone is key to maintaining physical stamina, mood, muscle mass in men, and libido in women. A recent randomized, placebo-controlled study at Washington University in 56 subjects showed a 13% decline in abdominal fat (fat that drives resistance to insulin) measured by MRI with 50 mg of DHEA per day at bedtime, along with improved sugar control and lower insulin levels. Pectin, beta-glucan Pectin is the soluble fiber in citrus rinds, green vegetables, and apples, also available as a supplement. Beta-glucan is the soluble fiber of oats and is also available as a supplement. Both are wonderful fibers that provide feelings of fullness, lower cholesterol, slow release of sugars, and can yield modest weight reduction. A USC study in 573 subjects using carotid ultrasound showed that greater intake of healthy fibers like pectin and beta-glucan is associated with less carotid plaque growth. Folic acid, vitamins B6 and B12 Dr. Daniel Hackam at the Stroke Prevention and Atherosclerosis Research Centre in Ontario conducted a study using carotid ultrasound in 101 participants treated with folic acid 2.5 mg, vitamin B6 25 mg, and B12 250 mcg per day. Treatment resulted in plaque reduction, especially when homocysteine levels exceeded 14μmol/l at the start, compared to untreated participants who experienced substantial plaque growth. An attempt to clarify the role of homocysteine treatment was made through a National Institute of Health-sponsored study of stroke prevention. 3680 participants with a prior history of stroke were enrolled and given either a “low-dose” (20 mcg folic acid, 0.2 mg B6, 6 mcg B12) or a “high-dose” (2.5 mg folic acid, 25 mg B6, 400 mcg B12) regimen. Although starting homocysteine levels showed a graded association with stroke risk (higher homocysteine levels predicted greater stroke risk), the treatment groups experienced, on average, only a 2 μmol drop in homocysteine levels and no reduction in stroke risk over two years. The study investigators as well as critics have suggested that the study failed due to an insufficient treatment period and that the doses were too low. (The doses we use in our plaque reduction program are folic acid 2.5–5.0 mg, B6 50–100 mg, B12 1000–2500 mcg.) L-arginine L-arginine can be used to overpower the adverse effects of ADMA. L-arginine is emerging as an important carotid plaque-reversing tool. Early reports in animals showed that l-arginine completely halted growth of aortic plaque, and did so more effectively than lovastatin (a cholesterol-lowering drug). In humans, L-arginine reduces blood pressure, abnormal constriction of carotid and coronary arteries, blocks entry of inflammatory cells into plaque, increases sensitivity to insulin, and heightens exercise capacity. Following coronary angioplasty or stent placement, l-arginine results in up to 36% reduction in plaque growth. The average American takes in 5400 mg of l-arginine through food every day. Supplementing with doses of 3000–12,000 mg per day has proven useful to correct many of these phenomena. (We use a dose of 6000 mg of l-arginine powder, twice a day on an empty stomach, dissolved in water, for our plaque regression program.) Does this result in a reduction of stroke risk? The emerging data suggest that l-arginine is likely to exert a powerful plaque-reducing and stroke-preventing benefit, but we await more clinical trial data. Conclusion Reducing stroke risk by reversing carotid and aortic plaque is becoming an everyday reality, with better tools becoming available. To know whether you’re at risk, the best and most available imaging tool is carotid ultrasound, aiming to identify intimal-medial thickness >1.0 mm, or carotid plaque. Any degree of calcification of the aorta, such as on a CT heart scan, is another useful measure of risk. Treatment to reduce risk is multi-faceted but is based on examining all your sources of risk, including metabolic syndrome, small LDL, lipoprotein(a), and C-reactive protein. Fish oil is the one absolutely crucial ingredient in any stroke prevention program. Other supplements can be used in a targeted fashion, depending on the causes identified for your carotid or aortic plaque. Ideally, repeat scanning of your carotids should be done sometime after your program has begun to assess whether you’ve successfully achieved reversal of plaque growth. vimax penis enlargement pills product penile girth enlargment penile enlargement product natural penis enlagement pills safe penis enlargement penis enhancement herb vimax pillss inch online vigrx cheap penis enhancement

Rabies- Attacks the nervous system and causes encephalitis. The virus is transmitted in saliva from the bite of an infected animal. It usually takes two-eight weeks before the signs appear. However, it only takes about ten days before it's passable through saliva. The most common ways for an animal or human to be infected is by a bite from an animal who's infected – usually a skunk, fox, raccoon or bat. Cats are actually more at risk than dogs – because they put themselves more at risk that dogs. There are three stages to Rabies: Prodomal Stage- Lasts two-four days. Signs can include behavioral changes, fever, slow eye reflexes, and chewing at the bite of the site. The Paralytic Stage- Last two-four days. Signs of paralysis develop, usually beginning in the limb that was bitten. Paralysis of the throat or face causes a change in the bark. Drooling with typical foaming at the mouth, and a dropped jaw. Followed by depression, coma, and death from respiratory paralysis. Once clinical signs develop there is no treatment! If a pet has been bitten by a wild animal or known related rabid animal – if they've been vaccinated, re-vaccinate them and quarantine them for 90 days. If the pet has not been vaccinated, euthanize and submit tissue for rabies testing. If the owner is unwilling to euthanize the pet, it should be strictly quarantined for six months with vaccination one month prior to release. Distemper- Greatest single disease threat to the world's dog population. Distemper develops over a course of days. Canine distemper virus is fatal to 80% of the puppies and 50% of the adult dogs that contact it. Symptoms include congested lungs, nasal discharge, vomiting and diarrhea. As it progresses, it attacks the nervous system, often causing partial or complete paralysis and seizures. The disease is highly contagious. Dogs can get the virus through coming into contact with anything another dog infected, including through all secretions of the infected animal and very surprisingly, even through the air. Most distemper appear in dogs less than six months of age and in old dogs that have not been vaccinated. Once infected, there is no cure. Treatment is supportive -- fluids through I.V to prevent dehydration, and symptoms treated. Dogs who recover from distemper may have vision, nervous system problems, hardened foot pads and nose leathers, throughout their lives. In addition, puppies may also have mottled teeth from damage to developing enamel. Dogs should be vaccinated, and given boosters, to prevent this disease. Parvovirus- This disease can overwhelm a dog within hours of first symptoms and result in death within 48-72 hours. It is found through the world, it is highly contagious and attacks the intestinal tract, white blood cells, and sometimes the heart. It is spread with contact through feces of infected dogs. Parvovirus can be carried on shoes, crates, equipment or the hair and feet of infected dogs. Symptoms appear five-seven days after exposure and include depression, loss of appetite, vomiting, severe diarrhea. Feces are generally light gray, or yellow-gray, and may be streaked with blood. Puppies under six months are most susceptible to the disease. If the disease effects the heart, puppies can die within hours, weeks or even months. Doberman Pinschers and Rottweliers appear to be at a higher risk for parvo than other breeds. There is no treatment that cures the virus. Nursing care consists of replacing fluid, keeping the dog warm, controlling vomiting and diarrhea, and dosing with antibiotics to prevent secondary infections. Parvovirus can live for several months in an infected area, thorough cleaning of all surfaces is necessary to eradicate the disease. Household bleach is a very effective agent. Vaccination against parvo has dramatically reduced incidence of the disease. The vaccine protects the dog for several years. Infectious Canine Hepatitis- It is inhaled or ingested by the dog, enters the bloodstream, and targets the liver, kidneys, eyes, and the cells lining the inner surface of the blood vessels. Some cases barely show symptoms – puppies may show a slight fever or be slightly lethargic and recover quickly. Some cases are quick and deadly. They may also have tonsillitis, reddened mouth and eye membranes, colic, then shock and death. Sometimes all within 24 hours! The in-between manifestation of the disease is the one most commonly described. The early symptoms are similar to the other forms – some puppies recover within two weeks, others develop internal bleeding, central nervous system involvement, and liver disease. There is no cure, only supportive treatment. Vaccination lasts several years. Kennel Cough- This is a respiratory disease in dogs that covers the actions of several infectious agents, including Bordatella bronchiseptica, a bacteria, canine adenovirus 2, and canine parainfluenza virus. The parainfluenza virus is related to the canine distemper virus. Symptoms range from hacking cough to inflammation of the larynx, bronchial tubes and trachea. CAV-2 also produces pneumonia in ten-twenty percent of the affected dogs. They're highly contagious, especially in kennels or shelters where the canine immune systems are stressed. Good ventilation is necessary to prevent and spread diseases. A combined kennel cough vaccination contains CAV-2, parainfluenza, and Bordatella in one dose of nose drops. Symptoms are no more than a bad cold, vaccination is recommended if dogs are to be boarded, or will come into contact with a large numbers of dogs. Leptospirosis- This is a bacterial disease spread in the urine of wild and domestic animals and capable of causing illness in humans as well as dogs. Several species of the bacteria produce disease in dogs. Symptoms include lethargy, kidney inflammation, low-grade fever, vomiting, reddening of the mucous membranes, and conjunctiva, and blood clotting abnormalities. A more generalized form of the disease can cause elevated liver enzymes, jaundice, pneumonia, and intestinal inflammation. Chronic kidney problems can result. Antibiotic therapy is effective in fighting the bacterial invasion and supportive nursing (replenishment of fluids, administration of diuretics to flush the kidneys and prevent kidney failure, blood transfusions, if necessary) is required. Vaccinations are not recommended unless there is a disease in the area. The vaccines help to lessen the severity of the disease, but do not prevent it. It also may not be effective for more than six months. Puppies and small dogs can have adverse reactions to the vaccines. If there is a lepto outbreak occurring and veterinarians do recommend vaccination, dogs should be inoculated against all four strains of the disease, unless the particular strain is identified. Lyme Disease- Is a bacterial disease spread by ticks. Symptoms in dogs include lethargy, joint pain, lack of appetite, lymph node enlargement, and fever. Some dogs have antibodies to the disease, indicating they've been exposed, but they show no symptoms. Treatment is with antibiotic, Tetracycline. Vaccine is available, but is not widely recommended because the disease is self-limiting and protection is limited to no more than six months, following inoculation. Lyme disease is more serious for humans than for dogs. Coronavirus- This virus causes diarrhea and vomiting, and can be confused for parvo. The mode of infection is direct contact of an infected animal or its feces. Some dogs have antibodies but no symptoms, others lose their appetite, have smelly diarrhea, and are lethargic and dehydrated. Treatment involves replacing lost fluids and controlling vomiting and diarrhea. Vaccine is available, but not widely recommended. -Information taken from the American Veterinary Medical Association UC Davis Book of Dogs – By, Dr. Race Foster and Dr. Marty Smith (authors of the particular chapters).