Treatment Terracycline works. Prevention A vaccine has been available since 1987.

1. Horse Diseases Equine encephalitesFive kinds of viruses kill horses, people and wild animals including birds.Horses are especially sensitive to all of these encephalitis viruses. The epidemiology of these mosquito-borne diseases is shockingly bad. One mistake after another and why? By following untested assumptions and accepting opinions as facts, and by lack of funds and interest. THOUSANDS of horses are killed by these viruses.

2. EtiologyThese mosquito-borne equine encephalites are caused by: 1/ Eastern Equine Encephalitis Virus: EEEV2/ Western Equine Encephalitis Virus: WEEV3/ St Louis Encephalitis Virus: SLEV4/ Venezuelan Equine Encephalitis Virus: VEE5/ West Nile Virus: WNV

3. DiagnosisDisorientation, pressing the forehead against a wall, fever and finally crashing into things are common symptoms shared by many encephalitic infections and also various hosts from rodents to humans. TreatmentGood nursing care is the only treatment.

4. PreventionA vaccine against EEE only is missing the point. We have a certain risk of infection by: 1/ EEEV, 2/ WEEV, 3/ SLEV, 4/ EEEV or 5/WNV. This risk—in some regions—is high enough to warrant a vaccination campaign. We need 5 and have 3: WEEV, EEEV & VEEV.

5. Regardless of vaccine progress, we are far behind in SURVEILLANCE AND VECTOR CONTROL of mosquito-borne diseases, which includes dengue (DEN 1-4). What should we vaccinate against and why do these pathogenic types and strains change from year to year and place to place? The epidemiologists went out to lunch and never came back. Surveillance is done by research motives not as necessary public health routine. Research might be after the outbreak, whereas routine surveillance is prognostic! We are ASSUMING virus amplifications in horses and not other hosts. Where & when?

6. Immunizing all the population COULD eradicate the pathogen.Here is a problem: The time is short between the warning and the vaccination application, and then the antibody response. But this is theory, since no warning system exists. Now you finally see why a tremendous or horrific CHAEMERA vaccine is needed for horses.THE VIRUS EPIDEMIC WILL RUN ITS NATURAL COURSE BEFORE VACCINATIONS CAN BE MADE. WHICH VIRUS WAS IT ?? There is nothing easy about this ! Did Virus X come from Colombia and Venezuela by hurricane?

7. Equine Infectious AnemiaEquine infectious anemia (EIA) is a highly contagious and potentially fatal viral disease for equines. EIAV is a retrovirus, containing genetic RNA material, which it uses to produce DNA. This DNA is then incorporated into the horse’s genenome. It’s really a case of Goodbye horse.When horses are exposed to EIAV, many may develop severe symptoms and die in 2-3 weeks. The initial fever may last less than 24 hours.

8. Federal regulations concerning interstate movement of horses and EIA are: “Any reactor to an official test shall be classified as infected with equine infectious anemia, and shall not be moved interstate unless: 1/ It is officially identified (officially identified by either a lip tattoo or a neck brand) and accompanied by a certificate . . . and 2/ It is moved interstate, for immediate slaughter or to a diagnostic or research facility . . . or

9. TransmissionHorse flies and deer flies mechanically transmit EIAV. Insect transmission of EIAV is dependent on the number and habits of the insects, the density of the horse population, the number of times the insect bites the same and other horses, the amount of blood transferred and the level of virus.

10. EtiologyEIA is caused by a retrovirus thereby it relates to the autoimmune deficiency syndrome (AIDS). Insects like horse flies can carry infected blood. In the US, 80 % of EIA is in the 9 southeastern states. Do these states make a valiant attempt to eradicate ? Of course not. Horses recovering are lifelong carriers.

11. DiagnosisThe first indication that a horse was exposed to and infected with EIAV may well be a positive result on a Coggins annual test.If the horse survives this first acute attack, it will develop permanent disease with:1/ Fever for an indeterminate period until the onset of another episode. 2/ Petechial hemorrhages-Minute blood-colored spots appear on the mucous membranes. 3/ Depression-The horse appears more or less dejected (head hangs low) and generally listless.

12. TreatmentNo treatment. Refer to AIDS.PreventionHorse quarantine and the Coggins test constitute the means of prevention. Positive horses are branded with 73ª on the left neck. Negative horses should have a certificate. ALL HORSES SHOULD BE COGGINS OR ELISA TESTED ANNUALLY. Otherwise ALL can—in the futre—be vaccinated (research not done !) in order to drive out—eradicate—EIA. But what is the risk, where ?

13. Equine InfluenzaEquine influenza is an acute respiratory disease of horses worldwide. Equine influenza is represented by 2 subtypes: 1/ Influenza A/ equine 2 and 2/ virus (H3 N8 ) which is an most important cause of respiratory diseases in horses, andInfluenza A/ equine 1 virus (H 7 N 7 ). Others are: A/equine/Miami/1/63 isolate are currently circulating in horse populations.

14. Three distinct types of influenza virus have been isolated from horses since 1956. These are represented by the following prototype strains: influenza A/ equine/Prague/1/56 (H7N7), influenza A/ equine/Miami/1/63 (H3N8), and influenza A/ equine/Jilin/1/89 (H3N8). Jilin is from China. Isolation of a H7N7 virus has only been reported twice since 1977. Racehorses from Miami, Florida (FL) and New Orleans, Louisiana (LA) returning to the north like New York (NY) say in March will routinely have outbreaks by the barn load as most are not vaccinated due to ignorance and tradition.

15. EtiologyEquine influ enza, type A, includes viruses infecting man, birds and swine. Type A influenza viruses are divided into subtypes according to the surface antigens, hemagglutinin and neuraminidase. Two subtypes are known to cause disease in equids (H7N7 or equi-1 and H3N8 or equi-2). These differ from the subtypes that cause infection in man (H1N1, H2N2 and H3N2). All the known subtypes (H1 to H15 and N1 to N9) have been isolated from aquatic birds that therefore seem to be natural reservoirs.

16. DiagnosisPoor performance, a hacking dry cough, depression, anorexia, fever, nasal discharge, enlarged and tender submandibular and retropharyngeal lymph nodes are notable symptoms. TreatmentWait a month without stressing the recovering horse. PreventionThere should be no trouble at all since good vaccines are available.

17. Potomac Horse Fever EtiologyPotomac horse fever (PHF)--equine monocytic ehlichiosis—is a worldwide disease associated with river valleys and caused by Ehrlichia risticii. See Int J Syst Bacteriol 1985, 35: 524-526. The life cycle of Ehrlichia risticii includes fluke larvas in snails and aquatic insects. For E. equi see Am J Vet Res 1975, 36: 85-88 and Int J Syst Bacteriol 1988, 38: 220-222.

18. Diagnosis Affected horses might develop diarrhea, fever and usually died unless treated promptly with tetracycline or similar antibiotics. The infected horse will go off his feed and develop fever. Low blood pressure and low blood counts develop. Intracellular bacteria will be seen in Giemsa blood smears. Severe diarrhea and painful colic may ensue. The horse may become severely dehydrated requiring IV fluids. It may founder. Infected mares may abort with inflammation of the placenta. Many horses test seropositive without signs of illness.

19. TreatmentTerracycline works.PreventionA vaccine has been available since 1987.

20. SarcocystosisAll mammals have Sarcocystis species or something close so the name equine protozoal myeloencephalitis is absurd. These coccidian genera of the phylum Apicomplexa are Besnoitia, Cystoisospora, Frenkelia, Hammondia, Neospora, Sarcocystis and Toxoplasma.Horses are simply hosts like many other mammals. Infections in raccoons or possums need not be different. Schizonts and merozoites, but no sarcocysts, are found in horses. Similar histopathologic lesions of S. neurona are seen in cats, mink, raccoons, skunks and so on.

21. EtiologyThe opposum (Didelphis virginiana) is the definitive host. The definitive host becomes infected by ingesting mature intramuscular cysts (with bradyzoites) from infected intermediate hosts. This stage can also be called merozoites. Bradyzoites penetrate the lamnia propria of the small intestine and form gametes. By sexually reproducing in the intestinal wall of the opossum, S. neurona produce fragile sporulated oocysts, which often rupture before being passed in the feces. Shedding of oocysts occurs for weeks to months. Sporocysts are not infectious to definitive hosts. Animals other than possums may be unknown final hosts.

22. DiagnosisAtaxia and incoordination can be present in one limb or all of the other limbs. Damage to lower motor neurons of the spinal cord or brainstem can result in muscle atrophy. Obscure lameness may be the only abnormality. Signs of cranial nerve dysfunction may be present in over 10% of EPM cases, including atrophy of the temporal masseter muscles, atrophy of the tongue, vestibular signs, facial nerve paralysis, laryngeal hemiplegia, and dysphagia.

23. TreatmentUsual treatment involves once daily oral administration of sulfadiazine (20 mg/kg) and pyrimethamine (1 mg/kg). Most treatment regimens very expensive. Diclazuril, a benzeacetonitrile coccidiostat for poultry, has anti-S. neurona activity. Toltrazuril and triazine are other coccidiostats. Ponazuril, another anticoccidial compound has a dosage regimen of 5 mg/kg body weight given orally, once per day, for 28 consecutive days. PreventionNo prevention is presented.