Equipped neuromuscular diagnostic laboratory
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- Mary Anne McPhail Dressurstuhl em Equine Sports Medicine
- Stress rhabdabdomiolysis (s)
- Ruinolysis recurring effort
- Polysaccharide memory myopathy Type 1 1
- Miopathy of polisaccharide memory type 2
- Myofibrile myopathy
- Glycogen branches
- Myosinas Heavy chains -Miopathy (Myhm)
- Seasonal grass myopathy
- Neuromuscular diseases related to vitamin E
- shaking chills
- McPhail's equine performance center
- Conflict of interests
- Atrophy
1. What is mysian heavy chains (MYHM)?
Power horses (American color, applicants, crosses) that have a specific genetic mutation in the geneMyh1It can develop a heavy chain myosin (MYMM) .MYMM shows two superimposed clinical syndromes, immune myositis taught (immunmiositis) and rabalolysis without distance.Myh1He encoded a specific muscle protein, which is found as a chain of heavy pider 1 in type muscle fibers 2 times; faster muscle fibers to get contracting. In a horsepower, more than 50% of the locomotor muscles consist of these fibersmuscle of the second plaque.Myh1It can lead to the immune system of the horse that attacks skeletal muscle (fiber) cells that contain mutated myosin protein. The trigger is required to activate the immune system and cause muscle diseases.
2. What is immune myositis (IM)?
Immunological myositis (IMM) is one of myhm.com.The immune system attacks the 2x type fibers in skeletal muscle cells along the back and back, which leads to a rapid loss of size and strength ofThe muscles (atrophy).
3. Oh, what is the cause of IMM?
This immune disease is caused by a loss of auto -Tolarance in the horse's immune system for a protein that is normally present in its own muscle cells.Myh1The mutation can be activated to perceive the type -2 muscle fibers as strange, which begins with a bodily process that has the white cell Celle that is supposed to destroy 2x muscle fibers. It is believed that certain infectious agents or possibly vaccines trigger "reaction. "" trigger.to give immunosimulants or after giving vaccines.
4. How often is IMSS?
Immune myositis is rare in horses with horses and the most common cause of rapid atrophy of the upper line in the district and horse painting.Myh1The mutation is approximately 7% of the horses in a quarterMyh1The mutation will really develop IMMS, but examined.
5. What are the clinical signs?
6. Are certain types of horses more susceptible to IMM than others?
Horses and colors are the main races affected byMyh1Mutation with the highest incidence in the combination and cutting of horses. They develop small children under 8 years or more than 17 years in the IMM.Myh1Mutation.
7. How is IM diagnosed?
History:The rooms of a horse tail with the last history of respiratory diseases or recently exposed to horses with respiratory diseases are a greater risk of developing IMM. RutinediagnosisS:Blood chemistry generally shows a chronic increase in serum creatine (CK) and Aspartatian saminase (AST) up to 10,000 U/L. Gene test:In the case of power, you can now find a final diagnosis of IMMS and MYMM this connection for the tests through genetic tests of the Veterinary Genetics Laboratory at the University of California, Davis.Siga:https://www.vgl.ucdavis.edu/services/horse/IMM.phpThe myopathy of the heavy myosin chain is inherited as a codominant characteristic. This means that a copy ofMyh1The mutation (heterozygotes) is sufficient for susceptible horses for the development of myopathy of the myosin chain.Cavalle with two copies (homozygot) seems to have more frequent and serious symptoms.
Registered results such as:
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N/n
There are no copies of the MyHM mutation. The horse does not have a greater susceptibility to real rabomialis or without cycling.
-
N/mine
1 copy of the MyMM mutation is available. The horse can be imm. The horse can deliver the mutation to 50% of the descendants.
-
Mi
2 copies of the MyMM mutation are available. The horse is in danger and can inum after infection or vaccination or not detailed rabbomiosis. Horses will change to all children.
Muskelbiopsie:Since genes are a pain -free form to create a normal diagnosis. The extensive infiltration of white blood cells and inflamed blood vessels, accompanied by regeneration and/or atrophied muscle fibers, are properties of IMM in the first weeks of atrophy.
8. What other diseases are immune?
9. How is it?
IMM is remarkably corticosteroid. The typical therapy consists of dexamethasone (0.05 mg/kg) for 3 days, followed by prednisolone (1 mg/kg for 7 to 10 days) .CBC) are analyzed and recommended if there is antibiotic therapy if there arehyperfibrinogemia or lymphadenopathy.
10. Are there management strategies that can help a horse with IMMS?
The horses that recover from the atrophy of the interition should feed with a high quality protein concentrate that is balanced for vitamins and minerals. At least 4-6 weeks for future vaccines to determine which vaccines the horse reacts. We do not recommend using the vaccineStrangulator for these horses because it seems to be a trigger for atrophy or muscle damage.
11. What is the prognosis of a horse with IMM?
Approximately 20% of heterozygous horses (my) forMyh1The mutation develops rapid atrophy. However, the IMS is generally dissolved without long -term consequences for heterozygotes. The appetite must be improved within 48 hours of steroid therapy.soon as you notice muscle atrophy. In some cases, you can remove in a muscle in a muscle. The solution and the return of muscle mass can take a long time. Some horses, especially those with two copies ofMyh1Mutation (homozygot my/my).), Especially within the first or two years of the initial presentation of IM, a recurrence of atrophy. Therefore, the latest study shows that 80% of homochigocos will probably develop a rapid rapid atrophy, which is serious and is less likely to recover from atrophy compared to heterozygous.
12. What is not -Radratal rhabdomyolysis?
Some horses with thatMyh1The mutation develops severe muscle damage that is not triggered by the movement. Sometimes, muscle atrophy shows signs of stiffness and possible swelling of the muscles along the back and the shells (AST) both indicators of muscle damage.
13. How does the mutation myH1 rhabdomyolysis cause?
The exact mechanism through which theMyh1The mutation caused by rabomiolysis is unknown. It can be a similar immune response, or mutation can change myosin interaction with actin during muscle contractions. In some cases, infection is developed with strangulation infection, especially to adjustthe infections of the bags when the rabalolysis develops.It does not matterAnd the type -2 -which -miosine that could explain this link. Cavalas cannot develop mymm -Rabbomisomisysis -Exkiales if they are exposed toAnaplasma phagocytophilum.
14. How often is not a rhabdomyolysis similar to MyHM?
No -Maltural Rabbomyolys for caused byMyh1The mutation is relatively rare.
15. What are the clinical signs?
16. Are certain more susceptible power groups?
Run in relation to a horsepower with theMyh1The mutation is more susceptible and homozygous horses for this mutation (mine) seem to have more serious symptoms than heterozygous horses (my/n).
17. How is an unwavering rhabdomyolysis diagnosed?
The Routine Diagnosis:Complete blood choice is required to determine if there is a simultaneous infection. An increase in white blood cells is observed with an increase in neutrophils and fibrinogen in an infection. Blood Chemistry:The creation of kinase values more than 50,000 U/L is diagnosed with MyHM.S. equiIt should be confirmed by the cultural chain reaction or polymerase (PCR) test. Genes test:In the case of power, the MYHM Veterinary Genetics Laboratory can now find a final diagnosis of MyHM. Signs of this link to the tests are made:https://www.vgl.ucdavis.edu/services/horse/IMM.php
Registered results such as:
-
N/n
There are no copies of the MyHM mutation. The horse does not have a greater susceptibility to real rabomialis or without cycling.
-
N/mine
1 copy of the MyMM mutation is available. The horse can be imm. The horse can deliver the mutation to 50% of the descendants.
-
Mi
2 copies of the MyMM mutation are available. The horse is in danger and can inum after infection or vaccination or not detailed rabbomiosis. Horses will change to all children.
Muskelbiopsie:Genetic test is the preferred diagnostic process. A muscular biopsy of the semi -membransus or semitendinous can be useful in horses with negativeMyh1Genetic tests to try to identify other causes of rabomiolysis not cycles. The characteristics of rabidyolysis include the swelling of muscle cells, the interruption of Sarkoplasm and the increase of large white blood cells (macrophages).
18. What other diseases may seem similar?
19. What is the treatment?
ForS. equiInfections, infected and antibiotic guttural bags are common treatments.
20. What is the prognosis?
The prognosis for a horse with undecided ruin is protected because the cases can be very serious, which leads to the difficulties to have difficulties after bedtime. Some horses will continue to develop muscle atrophy after indispensable rabomiologist.
21. How should I drive a horse with mymm mutation in the future?
Approximately 80% of heterozygous horses (my) forMyh1The mutation does not develop any sign of atrophy or muscle damage, and the vaccines do not seem to be a trigger. First we perform when vaccinating a mine/n my horse, which is only administered for 4-6 weeks using a distance. Small vaccines that areThe smallest as possible, for example, only tetanus (waiting for 4 to 6 weeks), only EEE, Wee and Vee (wait 4-6 weeks), only the western Nile (wait 4-6 weeks). Or atrophy is activatedmuscle, you can be sure to use these vaccines together next year. If the owners perceive atrophy after vaccination, there is a discussion with their risk or advantages for this vaccine. Owners must have quick access to prednisolone when atrophy began, after vaccines, flu vaccines/rhinos are a common immigrant as they areIt does not matterVaccines that are not normally recommended for horses that have MyHM mutation. References Finno CJ, giuliana g, perumbakka S., Williams ZJ, BORDBARI mh, Garder kl, Burns y, Pengbas S., Durward-Akhurst sa, Valberg SJ.A myh1 mutation sectibitility of the sensores de esquereto.https://doi.org/10.1186/s13395... Gianino GM, Valberg SJ, Perumbakkam S, Henry ML, Gardner K, Penedo C, Finno CJ.Previval of the E321G MyH1 variant for mediated immune myositis and does not exercise more rhabdabdomiis in the performance subgroups of the US rooms.sea 2019;33 (2): 897-901. Valberg SJ, Henry ML, Perumbakkam S, Gardner KL, Finno CJ.A E321G MYH1 Mutation is strongly connected to non -external rabbomiologists in the rooms.32 (5): 1718-1725 Lewis SS, Valberg SJ, Nielsen IL.2007.Inmune markers shamers. Hunyadi L, Sindman EA, Kass pH, Williams DC, Aleman M. 2017. Clinical effects and hospital hospital -Result of miyositis. Durward-Akhurst SA, Finno CJ, Barnes N., Shivers J., Guo Lt, et al.2016.Expression I and II of the main histocompatibility and lymphocytic subtypes in the PS muscle with immunamized myositis.