|
|
||
|
Home What is Headshaking? Symptoms & Checklist Causes Diagnosis & Treatment TCM Therapy Research Case Reports Contact |
||
| Home
|
Herpes Virus While nothing can be pinned down as to exactly why some horses develop headshaking and others do not, it is thought that horses which have been exposed to the EHV-1 virus are more at risk. With this theory, the herpes virus lies dormant in the horse's trigeminal ganglia, then with heat and stress created by i.e. direct sunlight or intense exercise, the virus becomes active again, this time affecting the central nervous system and producing the symptoms characterized by headshaking. Studies have proven that EHV-1 has a connection with headshaking. (Knottenbelt) IT IS NOT PROVEN and VERY UNLIKELY THAT VACCINATION WITH THE DEAD VIRUS VACCINE WILL CAUSE HS A lot of horses are herpes carriers but never will start with HS and a vaccination against herpes with the dead virus vaccine on top of it will not cause HS. That seems to be proven by virologists. The only known way to treat herpes is by
treating the immune system One article written by Annabel Ensor BVSc will give you the base information needed to understand the subject.
Equine Herpes Virus Infections in Horses Annabel Ensor BVSc, NZ In horses, herpes viruses are associated with a variety of diseases that range from relatively mild respiratory syndromes to abortion outbreaks on stud farms. Five serotypes of equine herpes virus have been identified (EHV1 → EHV5). The most commonly presented type of herpes virus infection in New Zealand is in the form of respiratory disease. This article will discuss the various equine diseases caused by EHV1 and EHV4. EHV1 and EHV4 are primarily respiratory pathogens and are remarkably common throughout the worlds horse population. Both viruses have the potential for causing widespread outbreaks of severe upper respiratory tract disease. EHV4 tends to be less virulent than EHV1. Respiratory disease commonly affects younger horses. Disease outbreaks are most likely between weaning and 2-3 years of age. Risk factors for such outbreaks of herpes virus respiratory disease include: overcrowding, heavy parasite burdens, poor nutritional state, climatic extremes, concurrent disease and mixing of animals from different social groups. Natural immunity is short lived therefore horses are commonly re-infected during their competitive careers e.g. racing, and showing. All herpes viruses have a unique characteristic; they can hide from the immune system so that it is impossible for the body to be totally rid of them. The viruses change their outer appearance and become latent in a secure area of the body e.g. lymph nodes of the respiratory tract (EHV1) and trigeminal nerve ganglia (EHV4). When the horse is stressed e.g. by weaning, transportation, fatigue; latent infections sometimes revert to a more active state and thus the infection is revived. Horses with latent infections excrete the virus during periods of disease reactivation and thus can act as carriers. In fact latent herpes virus can remain within a horse for its lifetime. It is important to note that reactivation of latent herpes viruses may occur without any clinical signs.
Infection occurs via inhalation of aerosols, by direct contact with infected horses or indirectly via contaminated equipment, feed and humans. Herpes viruses are relatively delicate therefore they do not survive for long in the environment. Herpes viruses are also very susceptible to destruction by common disinfectants. Close contact is thus an important feature of disease transmission. Disease transmission risk areas would include: stables and horses kept in high density grazing situations. Clinical signs are usually apparent 2-5 days following infection. The clinical signs of respiratory disease caused by herpes viruses include: fever, lethargy, anorexia, serous (clear) bilateral nasal discharge, pharyngitis, enlarged submandibular lymph nodes, watery eyes, pneumonitis and some horses may develop a cough. In the early stages of infection the nasal discharge is watery, free-trickling, inconspicuous and frequently goes unnoticed by handlers.
The clear secretions are laden with high numbers (titres) of infectious virus. As infection progresses, the nasal discharge becomes thicker and white in colour. These latter secretions often dry as crusts around the nostrils. Nasal discharge can become mucopurulent (thick, opaque and yellowish) with secondary bacterial infections e.g. Streptococcus equi ss zooepidemicus.
It is difficult to distinguish whether EHV1 or EHV4 is the causative agent, as the clinical signs caused by each serotype are very similar. Clinical signs and virus shedding are most intense during the first few days of infection. In uncomplicated cases of EHV induced respiratory disease, spontaneous resolution of clinical signs is usually complete by the end of the second week and recovery rates are good. However, secondary bacterial infections can prolong the disease and decrease the recovery rate. Diagnosis EHV4 is primarily a
respiratory tract pathogen, whereas EHV1 can cause
detrimental effects on other body systems. EHV1 can lead
to abortion, neonatal foal death, central nervous system disease (myeloencephalopathy),
severe lung disease, and eye disease. Perinatal Mortality Mares infected in late pregnancy
may give birth to weak foals that show signs of respiratory
distress, lethargy, and poor nursing ability. These foals usually
die within the first week of life. Large amounts of virus are shed
in the respiratory secretions of EHV1 infected foals,
thus they may be a major source of infection for other mares on the
property. Severe lung disease in young horses following EHV1 respiratory infections has been reported. It is termed "pulmonary vasculotropic EHV1 infection" and clinical signs include: a high fever, decreased feed intake, severe depression, and respiratory distress. Onset of clinical signs is sudden and sometimes horses may be found dead. Affected horses are found to have inflamed and damaged blood vessels throughout their body systems, especially within the lungs. Central nervous system The central nervous system (CNS) can become affected following EHV infection. Onset of neurological signs usually occurs within 6-10 days of the initial EHV1 infection. Neurological signs appear suddenly and are at their worst within 2-3 days of onset, generally they are non-progressive. Locomotor disturbances that vary from dragging a hind limb to complete quadriplegia can occur. Horses with mild signs have a relatively good chance of recovery. Horses that are recumbent (cannot stand) for longer than 2 days have a poor rate of survival. The picture below shows a horse with hind limb paralysis caused by EHV1.
Treatment Prevention Vaccination against EHV1 and EHV4 respiratory disease is recommended as part of a preventative herd-health programme for all horses at risk of becoming infected. An ideal vaccination protocol for at risk horses would be: two vaccinations spaced at 4-6 weeks apart just prior to weaning (5 months of age) with a booster every 6 months while the horse is exposed to periods of increased risk e.g. training, racing, competitions. Foals that are exposed to field infections or who have had insufficient colostrum can be vaccinated earlier than 5 months of age. Mares at stud (barren and pregnant) can be vaccinated as a management aid to prevent EHV induced abortions. Vaccination does not prevent respiratory infection however; it provides active immunisation and therefore decreases the severity of the clinical signs of respiratory disease caused by EHV1 and EHV4. Also, abortion may still occur in vaccinated mares but the risk of an abortion storm is greatly reduced. It is important to realise that some vaccinations protect horses against the respiratory form of the disease and against abortion while others only protect against respiratory disease. Your veterinarian will utilise a vaccine which best suits your horse.
|
|
|
All rights reserved Copyright ฉ Equis TCM 2009 Re-publishing or any use with permission only |
||
