In equids, it is most common in the first twelve months of life. Neonatal foals born to dams that are selenium-deficient often develop the condition. There are two forms: peracute, and subacute. The peracute form is characterized by recumbency, tachypnea, dyspnea, myalgia, cardiac arrhythmias, and rapid death.
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Peracute, alimentary and cutaneous clinical disease patterns have also been described. Death usually occurs within ten days. The mortality rate in symptomatic animals is 90 to 100 percent. Treatment is supportive only.
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Colitis X, equine colitis X or peracute toxemic colitis is a catchall term for various fatal forms of acute or peracute colitis found in horses, but particularly a fulminant colitis where clinical signs include sudden onset of severe diarrhea, abdominal pain, shock, and dehydration. Death is common, with 90% to 100% mortality, usually in less than 24 hours. The causative factor may be Clostridium difficile, but it also may be caused by other intestinal pathogens. Horses under stress appear to be more susceptible to developing colitis X, and like the condition pseudomembranous colitis in humans, an association with prior antibiotic use also exists.
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The peracute (very sudden and severe) form causes death within a few hours and treatment is of little avail. More commonly dogs suffer from the acute or subacute form. This is recognised by the dog being listless or lethargic, losing its appetite and running a temperature. If your dog is off its food, take a rectal temperature reading.
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Death is also common in deer with acute EHD, which is generally comparable to peracute EHD and is characterized by excessive salivation, nasal discharge, and hemorrhaging of the skin.(CFSPH 1996). Cattle that develop EHD typically have subclinical signs. These infections are less severe than the infections in deer, but they may still exhibit fever, oral ulcers, excessive salivation, lameness, and coronitis (inflammation of the coronary band in hoofed animal).
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One of the most common characteristics of deer with the chronic form of EHD is the sloughing or breaking of the hooves caused by growth interruptions. Deer with chronic EHD often become lame due to these hoof problems. Although they are ill for several weeks, they can eventually recover. Deer with the peracute form of the disease may go into shock 8–36 hours after the onset of symptoms, and are found lying dead.
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Newcastle disease was first identified in Java, Indonesia, in 1926, and in Newcastle-upon-Tyne, England, in 1927. However, it may have been prevalent as early as 1898, when a disease wiped out all the domestic fowl in northwest Scotland. The policy of slaughter ceased in England and Wales on 31 March 1963, except for the peracute form of Newcastle disease and for fowl plague. In Scotland the slaughter policy continued for all types of fowl pest.
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These tests may include a brain scan, cerebrospinal fluid examination, nerve conduction test (electromyography, or EMG), and an edrophonium chloride (Tensilon) test for myasthenia gravis. A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in peracute cases. Botulinum toxin can be detected by a variety of techniques, including enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests and mouse inoculation or feeding trials.
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Mortality in affected felid litters varies between 20 and 100%. Mortality of FPLV is 25–90% in domestic cats with the acute form of the disease and up to 100% in cats with peracute disease. In 2010, a retrospective study of 244 infected cats showed that "leukocyte and thrombocyte counts as well as serum albumin and potassium concentrations at presentation are prognostic indicators in cats with panleukopenia, whereas vaccination status, age, clinical signs, and housing conditions are not." A survival rate of about 50% has been reported with supportive therapies.
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To date, the precise causative factor has not been verified, and the disease has been attributed by various sources to viruses, parasites, bacteria, use of antibiotics and sulfonamides, and heavy metal poisoning. Other possible causes include peracute salmonellosis, clostridial enterocolitis, and endotoxemia. Clostridium difficile toxins isolated in the horse have a genotype like the current human "epidemic strain", which is associated with human C. difficile-associated disease of greater than historical severity. C. difficile can cause pseudomembranous colitis in humans, and in hospitalized patients who develop it, fulminant C. difficile colitis is a significant and increasing cause of death.
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Deer may become infected with peracute, acute, or chronic EHD infections. Deer can develop clinical signs in as little as 7 days after exposure and this is most constantly characterized by sudden onset of the disease. In general, deer infected with EHD lose their appetite, lose their fear of people, grow weak, show excessive salivation, develop a rapid pulse, have a rapid respiration rate, show signs of a fever which include lying in bodies of water to reduce their body temperature, become unconscious, and have a blue tongue from the lack of oxygen in the blood. The head and neck of infected deer may swell.
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Genes for the binary toxin were present, and toxin negative-regulator tcdC contained an 18-bp deletion. The individual animal studied in this case was diagnosed as having peracute typhlocolitis, with lesions and history typical of those attributed to colitis X. Use of antibiotics may also be associated with some forms of colitis-X. In humans, C. difficile is the most serious cause of antibiotic-associated diarrhea, often a result of eradication of the normal gut flora by antibiotics. In one equine study, colitis was induced after pretreatment with clindamycin and lincomycin, followed by intestinal content from horses which had died from naturally occurring idiopathic colitis.
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Horses are the most susceptible host with close to 90%The Merck Veterinary Manual – African Horse Sickness – Clinical Findings and Lesions mortality of those affected, followed by mules (50%) and donkeys (10%). African donkeys and zebras very rarely display clinical symptoms, despite high virus titres in blood, and are thought to be the natural reservoir of the virus. AHS manifests itself in four different forms: Pulmonary form The peracute form of the disease is characterized by high fever, depression, and respiratory symptoms. The clinically affected animal has trouble breathing, starts coughing frothy fluid from nostril and mouth, and shows signs of pulmonary edema within four days.
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