Theiler disease , also known as idiopathic acute hepatitis (IAHD), serum-associated hepatitis, serum sickness, and post-vaccinalis hepatitis, is a viral hepatitis that attacks the horse. This is one of the most common causes of acute hepatitis and liver failure in horses.
Video Theiler's disease
Signs and symptoms
There is a rapid onset of clinical signs over a period of 2-7 days, beginning with anorexia, lethargy, and hyperbilirubinemia (icterus and urine color changes). Signs of hepatic encephalopathy (ataxia, blindness, aggression, and coma) and fever may also occur. Other signs include photodermatitis, haemorrhagic diathesis, dependent edema, and colic. The reason for colic is unknown, but is thought to be caused by a rapid decline in liver size, and an increased risk of gastric impotence. Rarely, weight loss can occur.
Maps Theiler's disease
Cause
The latest theory is the result of a recent study which suggests it is caused by pegivirus, which is referred to as Theiler-related disease virus (TDAV). Eight horses who have received prophylactic antitoxin botulinum and developed subsequent signs of Theiler disease are subjected to tests for viral infection based on RNA sequencing techniques. When TDAV was found, the original source of the virus (antitoxin) was injected into 4 additional healthy horses, with one showing elevated liver enzymes and the fourth having an elevated TDAV level, suggesting that the virus could be spread by inoculation. Measuring the level of virus in infected horses has shown that the disease may become chronic, with some horses displaying low levels of the virus one year after the initial infection. All of the originally negative horses remain so, indicating that the virus is transmitted poorly horizontally.
However, not all horses tested positive for this virus show clinical signs, so additional contributing factors such as immune-mediated hypersensitivity or co-infection with other agents may be necessary to produce the disease.
Diagnosis
Currently it can only be done definitively through liver biopsy or post mortem examination. Given the isolation of virus causes it should be immediately possible to diagnose this with serology, polymerase chain reaction or viral culture. In necropsy, the liver will be small, flaccid, and "look like an eyelid". It has a stained surface of borders and bile. In microscopy there is a sign of centrilobular to midzonal hepatocellular necrosis and mild to moderate mononuclear infiltration. Can be mild to moderate bile duct proliferation. In radiology, the liver may shrink and it is difficult to visualize on ultrasound. Ascites may exist.
Lab test
The most distinctive features are increased levels of gamma glutamyl transferase (100-300 IU/L), aspartate transaminase (& gt; 1000 IU/L) and sorbitol dehydrogenase, with AST & gt; 4000 IU/L shows a poor prognosis. High levels of unconjugated and total bilirubin, and serum bile acid, can be seen. Moderate to severe acidosis, leukocytosis, polycythemia, increased creatinine kinase and hyperammonemia may be present, and haemolysis may occur in the later stages. Prothrombin (PT) time and partial thromboplastin time (PTT) are often extended. Subclinical horses can only show elevated liver enzymes without other clinical signs. Horses are rarely hypoglycemic, but blood glucose monitoring is ideal to show which horse can benefit from glucose treatment.
Differential diagnosis
It is quite spacious and includes
- acute hepatitis infection
- acute mycotoxicosis
- acute pyrrolizidine toxicosis
- hemolytic disease
- hepatotoxins
Treatment
Currently there is no special therapy. Intravenous fluid and hepatic encephalopathy treatment may be helpful. Increasing the level of branched chain amino acid diet and eating a low protein diet can help the signs of hepatic encephalopathy, which is often accomplished by feeding small amounts of grain and/or beetroot, and removing high protein feed ingredients such as alfalfa straw. Grazing on non-legum grass is acceptable if it is summer or autumn, although horses should only be allowed to eat at night to avoid photosensitization. Because of the risk of gastric impotence, the size of the stomach should be monitored.
Sedation is minimized and used only to control behavior that can cause injury to animals and to allow therapeutic procedures, and should involve tranquilizers other than benzodiazepines. Emphasizing animals should be avoided if possible. Plasma transfusion may be necessary if spontaneous bleeding occurs, to replace clotting factors. Antibiotics are sometimes prescribed to prevent bacterial translocation from the gut. Antioxidants such as vitamin E, vitamin B-complex, and acetylcysteine ​​can be given. High blood ammonia is often treated with oral neomycin, often simultaneously with lactulose, metronidazole and probiotics, to reduce the production and absorption of ammonia from the gastrointestinal tract.
Prognosis
This depends on the degree of hepatocellular necrosis that has occurred. Decreased SDH and prothrombin time along with increased appetite is the best positive predictive indicator of recovery. GGT can remain high for weeks even if the horse has recovered. Horses that survive more than a week and who continue to eat usually recover. Cases with rapid development of clinical signs, uncontrolled encephalopathy, haemorrhage or haemolysis have a poor prognosis. Horses that show clinical signs have a 50-90% mortality rate.
Epidemiology
This condition most often occurs after the administration of biological agents of horse origin such as antiserum originating from horses, and usually occurs 4-10 weeks after the incident. Diseases that have been vaccinated against the use of horse antiserum, which results in Theiler's subsequent disease, including: African horse disease, East and West Equine Encephalitis, Bacillus anthracis, tetanus antitoxin, Clostridium perfringens , Clostridium botulinum , Streptococcus equi subspecies equi , Equine influenza, Equine herpesvirus type 1, pregnant mare serum, and plasma. Though sporadic, it seems to be spreading somewhere, and there are outbreaks that occur on farms involving many horses for several months. In the Northern Hemisphere this is most common between August and November. This is seen almost exclusively in adult horses, and breast-feeding mothers given tetanus antitoxin post-foaling may be more susceptible.
History
The disease was described in 1919 by Arnold Theiler, a South African animal surgeon, after vaccinating horses against African horse disease using live virus vaccine and horse antiserum. This is then described in the United States after vaccinating horses for Eastern Equine Encephalitis, again using live virus vaccines and antiserum derived from horses. Since then it has been reported throughout North America and Europe.
References
Source of the article : Wikipedia
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