VETERINARY MEDICINE : PERISSODACTYLA

• Equidae
• Equus
• Equus subg. Asinus
• Equus asinus (ass, donkey) : Burkholderia mallei, Pongola virus


• Equus subg. Equus
• Equus caballus (horse) : Trichinella spiralis, Dermatophilus congolensis, Bacillus anthracis (equine outbreaks of this disease are usually secondary to infections in nearby livestock and/or wildlife and can involve tabanid flies, which is probably the case in this series, as the report indicates that the horses are penned in or near forest), Clostridium botulinum serotype B, Clostridium perfringens serotype C, Rickettsia rickettsii, Anaplasma phagocytophilum, Burkholderia mallei (glanders), Burkholderia pseudomallei, Leptospira interrogans, Streptococcus equi (strangles : yellow discharge from nostrils and eyes  that may resemble pus, swollen lymph nodes of the head and neck, difficulty in swallowing, and fever up to 106°F. The lymph nodes may swell and burst, thus spreading more bacteria. The horse may be lethargic and anorectic. Occasionally the abscess of the disease may spread to other organs of the body, even the neurological system, where it may be fatal. This dispersed form is sometimes called "bastard strangles."

Epidemiology : while usually seen in young horses, those of any age lacking immunity from prior infection or vaccination may contract it. Strangles seems to be sporadic throughout the USA. It is highly contagious, with a high morbidity and low mortality, but is seen essentially only in horses, donkeys and mules. 2005 Los Angeles, CA human "cases" may well be just coincident "colds" and such that are going around in a sympathetic species. But transmission of S. equi to humans from domestic animals has been reported and these streptococci cause infections very similar to those caused by group A streptococci (S. pyogenes) in humans ranging from pharyngitis to more invasive ones such as skin and soft tissue infections, pneumonia and sepsis.
Transmission of S. equi occurs through fomites and direct contact. The discharges (pus) from the nose and burst abscesses spread the disease. Objects such as water troughs, feed buckets, brushes, reins, and other equipment, if contaminated with infected pus, can also spread the disease. Horses can easily spread the disease for up to 8-10 months after they have recovered, even though they can appear clinically healthy and normal. Most horses will continue to shed S. equi for about a month following recovery. Therefore, 3 negative nasopharyngeal swabs at 4-7 day intervals should have been obtained before release from quarantine. Prolonged shedding for up to 18 months has been recorded.
Prevention : immunity from the disease is very short, and evidence suggests that as many as 25% of recovered horses do not mount an immune response. However, vaccination reduces the likelihood of disease, and in the face of disease reduces the severity as well as the number of animals that may be affected. Carrier animals are important for maintenance of the bacteria between outbreaks. Under ideal circumstances, the organism can survive outside the host for some 7-9 weeks. Thus paddocks and stables used by infected horses should be regarded as contaminated for some 2 months after outbreak resolution. Clinically affected horses should be physically separated from all other horses and cared for by a separate team of caregivers. The clinical attack rate can be reduced by 50% through the use of an intranasal live vaccine. While antibiotic therapy works, it is optimum to have the horse develop a protective immune response so that the infection does not reappear after cessation of treatment. Although it may not completely eliminate the disease, it will substantially reduce the seriousness of the disease. Horses that are moved form barn to barn between states and countries have a stressed immune system and may be more vulnerable to infection. Although most cases of strangles can be successfully treated, the treatment depends upon the stage the disease is in. Horse owners who know their horse will be in crowded situations such as racetrack barns or show barns should give consideration to vaccinating the horse at least 2 to 4 weeks prior to the situation. Horses need rest and should be isolated from other horses if they have the disease); Pongola virus; 2 subtypes of influenza A virus are known to cause equine influenza, namely :
• Influenzavirus A H₇N₇ (formerly known as A/equine 1) was isolated in Europe in 1956 and subsequently in the USA
• Influenzavirus A H₃N₈ (formerly known as A/equine 2) was isolated in 1963 in the USA and subsequently elsewhere in the world. It has been responsible for the majority of recent outbreaks and sequencing studies indicate that it has undergone only slight genetic drift since first isolation. Infection first occurred among naive horses in South Africa in December 1986. The virus was introduced following the importation of 6 horses from Wisconsin, USA. While the release of in-contact horses from quarantine 3 days after the arrival of these 6 horses played a role in the rapid spread of the disease in South Africa, other outbreaks of disease were associated with viral introduction by personnel or contaminated instruments^ref. During the outbreak, great concern was expressed about the potential effects that equine influenza could have on the large population of zebra (appx 50,000) that could not practically be vaccinated against the disease. However, this did not happen, and later serological evidence from zebras, as sentinels, lent support to the contention that equine influenza was not present in South Africa at the time of publication (1999). Unfortunately, this has recently changed. No influenza virus has been designated as specific to canines so far. In 1989 a severe outbreak of influenza A virus infection in horses in northeastern China was caused by a virus withe the same antigenicity as the prevalent equine influenza virus. However, it appeared to be a reassortant as its other genes were of avian origin.
=> fever and dry hacking cough. Horses become ill and are reluctant to eat or drink for several days but usually recover in 2 to 3 weeks. In fully susceptible animals, clinical signs include pyrexia, and a harsh dry cough followed by a mucopurulent nasal discharge. In partially immune vaccinated animals, one or more of these signs may be absent. The virus can be spread easily between horses through droplet, from nasal discharge, and from things like infected brushes. The disease is very contagious, with almost 100% infection rate in a population not previously exposed to the virus. Because it is a virus, there are no drugs that influence the outcome of the disease. Many horses develop secondary infections with bacteria which can lead to pneumonia and other problems.
Diagnosis of influenza virus infections is based on virus isolation from horses with acute respiratory illness, or on the demonstration of a
serological response to infection. Ideally, both methods are used. Infection may also be demonstrated by detection of viral antigen in respiratory secretions using an ELISA
Treatment consists of good nursing care and antibiotics, if necessary, to treat the secondary bacterial illness associated with the disease. Oral administration of oseltamivir phosphate (OP) in horses experimentally infected with equine influenza A virus (H₃N₈). 9 horses were divided into three horses each of control, treatment and prophylaxis groups. An administration protocol for the treatment group (2 mg/kg of body weight, twice a day for 5 days) was started immediately after the onset of pyrexia (above 38.9°C). An administration protocol for the prophylaxis group (2 mg/kg of body weight, once a day for 5 days) was started on a day before viral inoculation. In the treatment group, periods of virus excretion (mean days +/- standard deviation, 2.3 +/- 0.6) and pyrexia (2.0 +/- 0.0) were apparently shorter than those of the control group (6.0 +/- 0.0 and 8.0 +/- 1.0, respectively). In the prophylaxis group, although virus excretion and pyrexia were not prevented, the periods of virus excretion (5.0 +/- 0.0) and pyrexia (4.7 +/- 1.5) were shorter than those of the control group. Moreover, in the treatment and prophylaxis groups, bacterial counts of Streptococcus equi subsp. zooepidemicus known as the common pathogen of secondary bacterial pneumonia in bronchoalveolar lavage fluids collected seven days after inoculation were significantly fewer than that of the control group. The results indicated that the oral administration of OP to horses affected with equine influenza would contribute to reduce the magnitude of virus excretion, pyrexia and consequent secondary bacterial pneumonia^ref.
Prevention is still the key to dealing with this disease. Reasonably effective vaccines are available against the most important types of this virus, but horses need to be vaccinated 2-3 times per year to ensure their immune status.
Although these are not genuine human pathogens, humans can become infected with equine influenza virus subtypes. Such infections are unusual and subclinical, but may represent a potential biohazard to laboratory personnel. Both subtypes are generally included in commercial equine influenza vaccines. Information on the vaccines is available in Chapter 2.5.5 of the Manual of standards, Diagnostic Tests and Vaccines 2000 of the OIE and on the Equiflunet
These recommendations were made following a meeting, which was held on 1 Apr 2005, of the Expert Surveillance Panel on Equine Influenza Vaccines and relate to the composition of vaccines for 2005 and beyond.
• influenza activity in 2004 : outbreaks of equine influenza in Argentina, Canada, Croatia, Denmark, France, Germany, Greece, Hungary, Ireland, Italy, Sweden, the UK and the USA were reported during 2004. The outbreak that occurred during February and March in France was widespread and affected vaccinated as well as unvaccinated horses. All influenza activity was associated with H₃N₈ viruses. There were no reports of serological or virological evidence of H₇N₇ (equine-1) subtype viruses circulating in the equine population. Nevertheless, diagnostic laboratories should continue serological and virological monitoring and, when using PCR for rapid diagnosis, should ensure that primers specific for H₇N₇ virus as well as H₃N₈ virus are used^{ref1, ref2}.
• characteristics of recent isolates : all viruses characterized antigenically and/or genetically from Europe and North America during 2004 belonged to the "American" lineage. In hemagglutination inhibition (HI) tests using post-infection ferret antisera, all viruses isolated in Europe were most closely related to the A/eq/Newmarket/5/2003 reference strain, whereas viruses isolated in South Africa and the USA were more closely related to A/eq/South Africa/4/2003. Antigenic differences between the 2 geographically separate groups of viruses were, however, not consistently observed. The HA1 sequences of American lineage viruses isolated since 2003 in America, Europe and South Africa all fall within a single phylogenetic sub-group, previously referred to as the "Florida" lineage (Lai et al., 2001; 2004). The viruses isolated in America since 2003 (represented by A/eq/South Africa/4/2003 and A/eq/Ohio/2003) are characterized by 2 further amino acid changes in antigenic sites compared with the viruses isolated in Europe; these additional changes appear to contribute to greater antigenic drift from the A/eq/Newmarket/1/93-like viruses currently included in vaccines.
• recommendations for the composition of equine influenza vaccines : during the period January 2003 to April 2004, H₃N₈ viruses of the "American" lineage caused widespread outbreaks in Europe, with well-vaccinated horses frequently affected. These viruses, together with those responsible for recent outbreaks in South Africa and circulating in North America, were antigenically closely related to the currently recommended vaccine strains -- A/eq/South Africa/4/2003-like. No viruses belonging to the "European" lineage were characterized during 2004. The last isolation of a virus belonging to the "European" lineage was made in 2003. Nonetheless, the recommendation remains that a European lineage virus be included in vaccines, and monitoring for the circulation of European lineage viruses will continue. It is recommended that vaccines contain the following:
• a. an A/eq/South Africa/4/2003 (H₃N₈)-like virus (American lineage). A/eq/Ohio/2003 is as equally acceptable as A/eq/South Africa/4/2003.
• b. an A/eq/Newmarket/2/93 (H₃N₈)-like virus (European lineage). A/eq/Suffolk/89 and A/eq/Borlange/91, currently used vaccine strains, continue to be acceptable.
• reference reagents specific for the recommended European lineage vaccine strains are available for standardization of vaccine content by single radial diffusion (SRD) assay and can be obtained from the UK National Institute for Biological Standards and Control (NIBSC)^ref. Reagents for the new recommendation will be prepared at the earliest opportunity. 3 equine influenza horse antisera (anti-A/eq/Newmarket/77 [H₇N₇], anti-A/eq/Newmarket/1/93 [H₃N₈] and anti-A/eq/Newmarket/2/93 [H₃N₈]) are available as European Pharmacopoeia Biological Reference Preparations (EP BRPs) for serological testing of equine influenza vaccines by the single radial hemolysis assay. These antisera are also available from the OIE Reference Laboratory in Newmarket (UK) for use as primary standards in diagnostic serological testing. Pooled equine serum obtained post infection with A/eq/South Africa/4/2003 (H₃N₈) virus is currently the subject of an international collaborative study to establish this serum as an EP BRP/OIE primary standard to supersede the anti-A/eq/Newmarket/1/93 (H₃N₈) serum.
• SRD reference reagents: NIBSC, Blanche Lane, South Mimms, Potters Bar, Herts, EN6 3QG, UK Fax: +44 (0)1707 64.67.30 <enquiries@nibsc.ac.uk>
• EP BRPs for serological testing of equine influenza vaccines: European Directorate for the Quality of Medicines, BP 907, F-67029 Strasbourg Cedex, France
• OIE primary standards for diagnostic serological testing: Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk, CB8 7UU, UK Fax: +44 (0)8700 50.24.61 <info@aht.org.uk>
Japanese encephalitis virus (JEV); West Nile virus (WNV) (countries and dates of previous reports of WNV infection of horses are as follows:
• Morocco 1996, 2003
• Italy 1998
• USA 1999 - present (2006) : as the virus has become endemic in the USA morbidity in horses declined dramatically from > 10,000 cases in 2002 to < 1000 cases in 2005^ref
• France 2000, 2001, 2003
• Canada 2002 - present (2006)
• El Salvador 2003
• Mexico 2002 - 2003
• Puerto Rico 2004
• Cuba 2005
• Argentina ­ present 2006
• Russia (endemic) ­ present 2006 (Vopr Virusol. 2005 Nov-Dec;50(6):36-41. [West Nile virus infection of agricultural animals in the Astrakhan region, as evidenced by the 2001-2004 serological surveys; Article in Russian] Vasil'ev AV, Shchelkanov Miu, et al)
• Colombia 2004^ref
), EEEV, Venezuelan equine encephalitis virus (VEEV), Borna disease virus (Borna disease / enzootic encephalitis of horses / equine encephalitis : a fatal enzootic encephalitis of horses, cattle, and sheep; characteristics include tremor, lethargy, and flaccid paralysis), Western equine encephalomyelitis virus (WEEV), Vesicular stomatitis virus (VSV) (vesicular stomatitis (VS) is one of a group of clinically indistinguishable vesicular diseases of livestock which include foot and mouth disease (FMD), vesicular exanthema of swine, and swine vesicular disease. VS is transmitted by hematophagous insects such as Culicoides (sand flies) and Simuliidae (black flies), and occurs in tropical and subtropical North and South America)
• bites : rabies virus (rabies in equids (horses, mules, donkeys) is not rare. Like man, herbivores are dead-end victims of the infection; the vectors are carnivores or bats. Obviously, a rabid herbivore, though not a biter, might become a source of infection for those exposed to infected saliva. A unique mode of rabies spread among herbivores (the kudu antelope Tragelaphus strepsiceros) has been reported from Namibia (1977, 2002, 2006). These outbreaks provided an example of horizontal spread between individuals by means of non-bite transmission. The social behavior of kudu was believed to be the contributing factor, through the exposure of mouth lesions from the browsing of thorn bushes to the infected saliva. Domestic farm animals, particularly equids, in rabies-infected territories should be vaccinated. Horses should be vaccinated for rabies, unless in countries free of rabies. Most owners or associates of the owners often hand feed their animals and may be putting themselves at risk. Horses are naturally curious animals and will put their noses to skunks and other small animals, and may get bitten. Protecting them and yourself by vaccinating against rabies may be prudent)
• urine : Hendra virus (symptoms in horses include breathing difficulties, high fever and a blood-tinged foamy discharge from nose and mouth as the virus attacks blood vessels and causes pulmonary oedema)
Other diseases not transmissible to humans :
• Neorickettsia risticii (a.k.a. Ehrlichia risticii; equine monocytic ehrlichiosis / Potomac horse fever)
• African horse sickness (AHS) virus (AHSV)  an OIE List A disease, is an infectious but noncontagious viral disease affecting all species of equidae. 9 different serotypes of the virus have been described : all serotypes of AHS occur in eastern and southern Africa => at least 2 Culicoides species are the main insect vector : fever, hemorrhages in the mucous membranes, subacute, respiratory (large amounts of froth pouring out of the nasal passages and pulmonary edema), cardiac (intramuscular, gelatinous edema which can often be seen on the ligamentum nuchae of these horses), and mixed forms. Thus, the presentation is sometimes quite dramatic. Mortality > 75%. A vaccine with 2 separate injections is available, produced and available in South Africa, where it is endemic^{ref1, ref2, ref3}. AHS is not endemic in South Africa except for the subtropical North, and the virus moves a variable distance down to the temperate South each season. The distance moved depends on climatic factors favoring the vector and the immune status of the population. AHS appears to have become entrenched in the Eastern Cape possibly because of the large donkey population and the numerous zebras on the many game farms in which animals are kept. The virus circulates in a subclinical form. At the Reference laboratory in Onderstepoort, isolates of AHS serotypes 5, 7 and 2 have been recovered from 6 of the 9 provinces in South Africa. The following text appears on the package inserts, accompanying the attenuated AHS Onderstepoort vaccine: "Freeze-dried, polyvalent, live attenuated horsesickness virus strains for the prophylactic immunisation of horses, mules and donkeys against horsesickness. The vaccine is presented as 2 separate injections with different horsesickness virus types. First administer combination I and at least 3 weeks later combination II. Store the vaccine in a refrigerator at a temperature of 4 to 8 C. Do not use the vaccine after the expiry date printed on the bottle. Foals born of unvaccinated dams can be inoculated at any age, but foals of immune dams should not be vaccinated until they are at least 6 to 7 months old. Animals should preferably be immunised during early summer. Immunisation of mares should be avoided during the first 3 months of pregnancy. Annual immunisation is recommended. It takes up to 2-3 vaccinations for horses to become immune to all the serotypes in the vaccine. It is therefore important to combine vaccination with the control of the Culicoides midges which transmit the disease. Horses can be protected from midge bites by stabling them from dusk to dawn, using insect repellents and keeping animals away from low-lying vlei areas or other surface water during the day"^ref. According to OIE's Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (updated 23 Jul 2004), the attenuated Onderstepoort vaccine (Onderstepoort Biological Product Ltd.) is composed of 2 quadrivalent vaccines, constituted by mixing equal volumes of serotypes 1, 3, 4, 5 and 2, 6, 7, 8 respectively. AHSV serotype 5 was withdrawn from this vaccine. Immunity is known to persist for at least 4 years. However, in the light of possible interference between the individual serotypes in each quadrivalent vaccine, annual revaccination is advocated in enzootic regions. Vaccination with monovalent vaccine stimulates a practically lifelong immunity. There are 9 serotypes of AHS known to circulate in South Africa. Currently the live attenuated vaccine manufactured by Onderstepoort Biological Products (OBP) Ltd contains 7 of the serotypes, provided in 2 vaccine vials, administered 21 days apart. Although serotypes 5 and 9 are not included in the vaccine, some cross protection is provided from serotype 8 and 6 respectively present in bottle of the vaccine. Though AHS is not directly contagious, viraemic horses may introduce the virus into receptive areas during the vector's activity season, infecting the local culicoides population and, subsequently, local equines. This emphasizes the importance of full compliance to the applied animal movement restrictions, particularly during the late-summer and autumn months. AHS is known to be transmitted in South Africa by at least 2 culicoides species, namely C. imicola and C. bolitinos. C. imicola is the most common species, but in general prefers warmer, lower altitudes. This species breeds in saturated or wet soils containing a high level of organic material. C. imicola is also the main vector of another epizootic disease caused by an orbivirus, namely bluetongue (BT) of ruminants (predominantly sheep). C. bolitinos is a member of the Imicola complex of 7 species in South Africa. In 1998 it was implicated in an outbreak of AHS in the eastern Free State, South Africa, and also in the laboratory was shown to be susceptible to infection with AHS and BT viruses. This species is also widespread in the Afro-tropical regions and, like C. imicola, is known to feed on both cattle and horses. However, the breeding habitat of C. bolitinos is the dung of cattle, buffalo and wildebeest, which provides a stable and constant breeding microclimate for larval development. Hence, C. bolitinos is more abundant than C. imicola in areas with lower average temperatures, including cooler, mountainous regions. This was the case in 2003 in the Drakensberg mountains at an altitude of above 1500 metres, where many owners did not vaccinate and the disease had not been reported for at least 50 years : an outbreak of AHS serotype 2 was reported in 2003 . Experimentally, C. bolitinos was found to be a potential vector of AHS virus serotypes 3, 5, and 8^ref. The recording of AHS in the Western Cape Province^ref -- the only province in South Africa regarded as free from the disease -- in 2004 was followed by a 2-year ban by the EU on imports of horses from South Africa. The ban was due to elapse on 28 Mar 2006 : but on Apr 20, 2006 AHS was detected in the Worcester and Robertson districts of the Western Cape, 12 km (about 7.5 miles) from the premises where the area's 1st case of AHS in 2006 was reported on the border between the 2 districts. About 300 cases have been reported in KwaZulu-Natal (in the eastern part of the country)^ref. The earlier presence of the virus in Nigeria was reported in the following paper: Adeyefa CA & Hamblin C (1995). Continuing prevalence of African horse sickness in Nigeria. Rev Elev Med Vet Pays Trop. 95;48(1):31-3."Equine sera collected from 10 widely separated regions throughout Nigeria were tested for antibodies against African horse sickness viruses (AHSV) using [ELISA]. The animals sampled included imported, exotic horses, indigenous and locally cross-bred (local) horses and African donkeys. A high percentage of the sera (79.8%) were positive, confirming the continued prevalence of AHSV antibodies in Nigerian horses and donkeys"
• neonatal maladjustment syndrome : a disease of newborn foals, caused by perinatal hypoxia and characterized by behavioral disturbances such as inability to nurse, aimless wandering, apparent blindness, and uttering of a barklike sound; it may progress to convulsions, coma, and death. Affected foals are called barkers, dummies, or wanderers.
• white heifer disease / persistent hymen : a congenital condition of heifers, most commonly white ones of the Shorthorn breed, in which there is a rubberlike sheet of fibrous tissue and membrane partially or completely covering the posterior part of the vagina
• shaker foal syndrome : a type of botulism in young horses, accompanied by flaccid tetraparesis and inability to swallow, so that there is risk of aspiration pneumonia.
• wobbler syndrome / equine sensory ataxia / wobbles : in young horses, incoordination of the hind legs with a swaying gait progressing to stumbling, inability to walk, and sometimes paralysis; causes are varied and include stenosis of the spinal canal, malformation of the cervical vertebrae with demyelination, and inflammation of the cord
• grass disease or sickness : a usually fatal disease of horses occurring after they have been put to graze on grass, usually between May and July; characteristics include dysphagia, severe diarrhea, dehydration, interrupted peristalsis, and priapism. It was first observed in Scotland but has now spread across northern Europe and elsewhere
• Birdsville disease : poisoning of horses after eating either of the herbs Indigofera dominii or Indigofera linnaea; characteristics include abdominal pain, stiffness and incoordination, and discharges from the nose and eyes.
• blue nose disease : photosensitization of the face of a horse following ingestion of any of certain meadow plants; characteristics include blue discoloration of the muzzle, sloughing of nonpigmented skin, and frequently intense excitement.
• sleepy foal disease : a usually fatal type of equulosis affecting foals within the first three days of life, characterized by sudden onset and extreme prostration.
• navicular disease / podotrochlitis / podotrochlosis : necrotic inflammation of the navicular bone in horses, causing intermittent lameness
• Pictou disease : a type of seneciosis in horses and cattle in Nova Scotia
• equine herpesvirus 1 (EHV1) / equine abortion virus => equine rhinopneumonitis and immune-mediated vasculitis. It produces a febrile respiratory disease upon primary infection, which manifests as a fever of 39-42 C, neutropenia and lymphopenia, nasal and conjunctival serous discharge and congestion, malaise, pharyngitis, cough and inappetence. The resulting myeloencephalitis is believed to be secondary to the vasculitis. The neurological form of the disease may precede or follow the rhinopneumonitis or late-term abortion (in pregnant mares often in months 7 to 11 of pregnancy) aspect associated with this virus.
• equine herpesvirus 2 (EHV2) / equine rhinopneumonitis virus => respiratory disease
• equine herpesvirus 3 (EHV3) (subfamily Alphaherpesvirinae) => equine coital exanthema : a benign venereal disease of horses characterized by vesicles and ulcers on the external genitalia, and occasionally on the lips, nares, and conjunctiva, that heal within a few weeks.
• equine herpesvirus 4 (EHV4) (genus Varicellovirus) => equine viral rhinopneumonitis : a highly contagious disease of horses caused by a herpesvirus; characteristics include mild respiratory infection in young foals and abortion in mares exposed for the first time; in the latter it is called equine virus abortion. It produces a febrile respiratory disease upon primary infection, which manifests as a fever of 39-42°C, neutropenia and lymphopenia, nasal and conjunctival serous discharge and congestion, malaise, pharyngitis, cough and inappetence.
• equine herpesvirus 5 (EHV5)
EHV1 and EHV4 are most common. A type-specific ELISA can differentiate between EHV1 and EHV4. The fact that both viruses cause acute and recurrent respiratory disease that is commonly referred to as rhinopneumonitis means that, without laboratory confirmation, terminology for the viruses may continue to be ambiguous. Current EHV1/4 vaccines are not fully protective against disease, though clinical signs, duration of shedding, and quantity of virus shed can be reduced. The immunity inferred from the disease or the vaccine, are relatively short. Horses on the show or racing circuit are often vaccinated every 6 months. The risk of abortion and respiratory disease outbreaks are also reduced. We do not know whether vaccination may have a protective role in preventing EHV1 myeloencephalitis. As in the case of abortion, EHV1 vaccination may not be expected to provide 100% protection against EHV1 myeloencephalitis. In a major outbreak of EHV1 myeloencephalitis it was shown that in a group of 10 mares, 5 mares that did not develop myeloencephalitis were EHV1 antibody-positive, while of the 5 mares that did develop myeloencephalitis, 3 that were tested were either EHV1 antibody negative or had a rising EHV1 antibody titre^ref. The results of this study provide the first clue that specific EHV1 antibody negativity is a major risk factor in the development of myeloencephalitis and that -- accordingly, by analogy with a reduced incidence of abortion -- vaccination could reduce the incidence of myeloencephalitis in horses at risk^{ref1, ref2, ref3}. While this disease is not transmissible to humans or other animals, it is very contagious among horses and can cause them severe illness and death. It can be spread by close contact aerosol, or, in rarer cases, by organic materials on clothes or equipment. Contaminated feed or water may also spread the virus. Symptoms include fever, cough, runny nose or neurological signs, and typically appear within 21 days of potential exposure. Infection with equine herpesvirus is very common in the equine population, and most animals have neutralising antibody. Latent infection also occurs in at least 70% of horses; recrudescence, shedding and repeated infections during the horse's life are common. The precise reasons why the nervous form of equine herpesvirus is so rare are not known, but may include host and virus factors. Much current research is focused on sequence differences between paralytic and non-paralytic viruses. Older horses are more commonly affected with the nervous form -- this has been related to the usual presence of very high levels of circulating antibody and a circulating viraemia at the onset of nervous disease.
• equine rhinovirus
• equine adenovirus
most of these viruses produce rather mild signs, include a cough and nasal discharge.
• poll evil : an abscess behind the ears of a horse, caused by a dual infection of the supra-atlantal bursa by Brucella and Actinomyces; this condition is virtually identical to fistulous withers.
• fistulous withers : distention and rupture of the bursa in the withers region of horses, with suppuration; it is caused by a dual infection with Brucella species and Actinomyces species and is virtually identical to poll evil.
• Onchocerca cervicalis : a species found in the cervical ligament of horses and mules
• swamp cancer : a general term for several syndromes in horses consisting of skin or mucosal lesions with ulcers and granulomatous tissue on the head, trunk, or lower extremities
• cutaneous habronemiasis
• entomophthoromycosis : infection of the skin, oral mucosa, or nasal mucosa of horses by fungi of the order Entomophthorales, causing nodules or ulcerative granulomatous lesions. It is sometimes confused with cutaneous habronemiasis or pythiosis
• pythiosis / bursati / bursautee / hyphomycosis destruens equi / leeches / swamp cancer : infection by Pythium insidiosum, primarily affecting horses and mules but also seen in dogs and cattle, in India, Indonesia, Europe, and the southern United States; characteristics include formation of subcutaneous abscesses that enlarge until the overlying skin is destroyed, leaving large raw surfaces. It is often confused with cutaneous habronemiasis because of the close clinical similarity between the 2 conditions
• habronemiasis : infection with a nematode of the family Habronematidae. Habronema muscae and H. microstoma in the stomach sometimes cause a mild catarrhal type of gastritis. Draschia megastoma causes gastric habronemiasis. Any of these species can also cause cutaneous habronemiasis.
• cutaneous habronemiasis / bursautee / summer sores : a disease of horses in various parts of the world, including the southern United States, Brazil, India, and the Philippines, caused by skin infection with larvae of Habronema or Draschia species; cutaneous granulomas grow in size until the skin over and around them is destroyed, leaving a large raw surface. Because of the clinical similarity between cutaneous habronemiasis and pythiosis, the disorders are often confused
• gastric habronemiasis : infestation of the stomach wall of a horse with larvae of Draschia megastoma, which form large nodules filled with worms and necrotic material. Many affected horses do not show clinical signs, but they may die if the stomach wall is perforated
• purpura hemorrhagica : an acute, usually fatal disease of horses that may occur after a respiratory tract infection; characteristics include subcutaneous edema and petechiae around the head with tachycardia.
• mal de caderas : a fatal wasting trypanosomiasis associated with weakness, especially of the hindquarters, affecting chiefly South American horses, which is caused by Trypanosoma equinum, and transmitted by tabanid flies
• surra : trypanosomiasis of domestic animals caused by Trypanosoma evansi, usually transmitted by haematophagous tabanid flies. It occurs in East Asia, the Middle East, North Africa, southeast Asia (Indonesia and the Philippines), and Central and South America; in the latter regions it is usually seen in horses, is spread by vampire bats as well as flies, and is called murrina or derrengadera [Sp. “crookedness” or “lameness”]. Trypanosoma evansi has been reported to occur in a variety of hosts, the most economically important being horses, buffalo, and cattle; but it has also been reported from sheep and goats, pigs, dogs, cats, and a range of wild animals. Bactrian, elephants, and dromedary camels are known to be susceptible as well. Of these, horses are most severely affected. The clinical and haematological characteristics of infection is similar amongst the different species of host animals and includes a progressive anaemia, high temperature, marked depression, dullness, loss of condition, and in some cases, death. Reproductive wastage has been identified occasionally as a source of economic loss. There is a tendency to ascribe the occurrence of severe and often fatal disease to the horse and camel, and milder disease in cattle, but the range of susceptibility of the livestock and the variation in pathogenicity of the trypanosome strains is so great that this is an unrealistic view. The parasite does not affect humans
• equine or horse syphilis / dourine / covering disease : venereal trypanosomiasis affecting horses and asses in Africa, Asia, and certain regions of North and South America, caused by Trypanosoma equiperdum; characteristics include edematous swelling of the external genitalia, a mucopurulent discharge from the urethra or vagina, cutaneous plaques, and progressive emaciation and weakness
• equine viral arteritis (EVA) is a contagious viral disease of equids caused by equine arteritis virus (EAV), an RNA virus that is classified in the family Arteriviridae. The virus is found in horse populations in many countries world-wide. The disease was first recognized in the USA in an outbreak in Kentucky in 1984. Mortality is rare but economic losses can be significant. The economic impact includes decreased demand for carrier stallions as breeders, deaths in young foals, and abortions in 10-50% of susceptible mares. Equine arteritis virus is restricted to the Equidae. The prevalence of the virus can vary significantly among horse breeds; Standardbreds are particularly susceptible. Antibodies to equine viral arteritis have been found in most countries where testing has been done. Disease outbreaks are infrequent, but have been reported in the USA, Canada, Switzerland, Austria, the UK, and Poland^ref. EVA is included in the List B of the OIE, which are diseases of economic significance which should be reported annually from endemic countries, or as an emergency notification when recognized for the first time in a country; such is the current case in Argentina. The disease has been reported to the OIE, in the past, from Europe, Africa, North America, Australia and New Zealand, but not (yet?) from Asia and South America. EVA cannot be differentiated clinically from a number of other respiratory and systemic equine diseases. While laboratory-confirmed outbreaks of EVA have been infrequently reported in the past, the incidence of the disease appears to be on the increase.

Symptoms & signs : although many cases of EAV infection are subclinical, certain virus strains can cause disease of varying severity characterized principally by fever, depression, anorexia, dependent oedema, especially of the limbs, scrotum and prepuce in the stallion, conjunctivitis, an urticarial-type skin reaction, abortion and, rarely, a fulminating pneumonia or pneumo-enteritis in young foals. Apart from mortality in young foals, the case-fatality rate in outbreaks of EVA is very low. Affected horses almost invariably make complete clinical recoveries. A long-term carrier state can occur in a high percentage of infected stallions, but not in mares or nonbreeding horses. There is considerable evidence that short- and long-term carrier stallions shed EAV constantly in the semen but not in respiratory secretions or urine. International movements of horses, as well as their semen, is liable to testing and certification which are specified in chapter 2.5.10.1 of the International Animal Health Code^ref. According to OIE's Manual of Standards for Diagnostic Tests and Vaccines, stallions should first be serologically tested. Virus isolation should be attempted from the semen of stallions that are positive for antibodies to EVA and that do not have a satisfactory history of vaccination against EVA.
Transmission : the 2 most important routes are respiratory via the acutely infected horse and venereal via the acute or chronically infected stallion. Aerosol transmission is the principal means of spread of infection among horses closely congregated such as at racetracks, shows, and sales. Venereal transmission by an infected stallion is frequently responsible for dissemination of the virus on breeding farms. Indirect spread of the virus through contact with contaminated fomites (e.g., shanks, twitches, apparel, and personnel) is of minor significance during outbreaks. Congenital infection of foals due to exposure of mares late in gestation has been infrequently recorded. A significant percentage of stallions become carriers after exposure to the virus. These stallions transmit the virus venereally and play a major role in maintaining infection in horse populations from year to year. Attempts to establish the carrier state in mares, geldings, and sexually immature colts have been unsuccessful. No specific antiviral treatment is available.
Therapy : symptomatic treatment (antipyretic, anti-inflammatory, and diuretics) is indicated. Good nursing and rest with a gradual return to normal activity are desirable. There is no known medical means of eliminating the carrier state in the stallion.
Prevention : EVA can be prevented and controlled by sound management practices and selective use of a commercial, modified live virus vaccine. While the vaccine is both safe and immunogenic for stallions and non pregnant mares, it is not recommended for use in pregnant mares, or in foals < 6 weeks old. Prevention and control programs are aimed at curtailing dissemination of the infection. This minimizes the risk of virus-related abortions and helps prevent development of the carrier state in stallions.
• equine linear keratosis : ridges of hyperkeratotic hairless skin on the sides of the neck and chest of horses, with surface seborrhea; the etiology is unknown.
• scirrhous cord : chronic fibrous enlargement of the stump of the spermatic cord of a castrated horse caused by bacterial infection, with discharge of pus and sometimes formation of a tumorlike mass with numerous weeping sinuses
• capped elbow / shoe boil : a hygroma of the elbow or a hard, fibrous mass on the point of the elbow in horses or cattle
• capped hock : a hygromalike cyst or a thickening of the skin over the point of the calcaneus in the horse
• cribbing : a nervous habit of some horses consisting of grasping the manger or another object with the incisor teeth, arching the neck and making other peculiar head movements, and swallowing quantities of air; called also crib-biting and windsucking
• curby hock : a hock affected with curb.
• stringhalt / spring hock : myoclonus of the hind leg of a horse, causing a gait in which the leg is suddenly raised and then stamped on the ground
• bowed tendon : tendinitis of the flexor tendons in a horse, usually in the foreleg and due to strain from overwork; the tendons become enlarged and palpable.
• grain founder : laminitis in the horse with indigestion or an overloaded stomach, probably due to overeating that results in metabolic disturbance
• buttress foot / extensor process disease / pyramidal disease / low ring-bone : periostitis or ostitis in the region of the pyramidal process of the coffin bone of the horse, with fracture of the process, deformity of the hoof, and alteration of the normal angle of the joint
• pricked foot / nail prick : a condition in the horse in which the soft tissue of the foot has been punctured either by a horseshoe nail or by a nail or other object the animal has stepped on, causing pain and lameness. A nail that is near, but not into, the soft tissue may cause nail bind
• mare reproductive loss syndrome (MRLS) : in the Kentucky and surrounding states (and as far as north as Canada) outbreaks of 2001-2002, there was a strong association with the presence of unusually large numbers of eastern tent caterpillars (ETC) (Malacosoma americanum). This caterpillar tends to accumulate a cyanide compound. Consequently, the low oxygen tension of the developing fetus was affected by the even lower tension resulting from the presence of the cyanide compound in the mare's system. The syndrome was reproduced successfully : pregnant mares experimentally fed caterpillars typically aborted within several days. MRLS include late-term abortions, early-term fetal losses, pericarditis (heart problems), unilateral endophthalmitis (problem in only one eye), hyphema (blood in the eye) in foals, mouth ulcers, and laminitis. MRLS was first recognized as an outbreak of fetal deaths, foals born weak, and late-term abortions in Kentucky on Derby weekend (the first weekend in May) of 2001, but the outbreak was traced back to a start on 23 Apr 2001 of that year. All breeds were affected. Because of the high number of pregnant Thoroughbred mares in the area and the records kept on those horses, statistics on that breed reflect what was going on in the general horse industry. In 2001, there were 516 late-term abortions and 2998 early fetal losses in Kentucky's Thoroughbred industry alone. There also were about 60 cases of pericarditis and 50 cases of unilateral uveitis reported in Central Kentucky horses. > 30% of the anticipated 2002 thoroughbred foal crop in Kentucky was lost due MRLS. The economic cost to the state from losses suffered by all horse breeds was estimated at nearly USD 336 million. Where there are apple and cherry trees, there will be eastern tent caterpillars, although mid-Florida marks the far southern extreme of the ETC's distribution. They are common in North Florida and Georgia. It's been reported that the caterpillars have a 10-year cycle of high numbers, then nearly disappear for a time before building back up to high numbers. However, there is really no basis for that report. In one area it was 30 years between, or it could be 3 or 4 years. The large number seen in Kentucky (in 2001-2002) might never come back, especially since you cut down all the cherry trees (the ETC's favorite feeding/nesting site). The forest tent caterpillar has a general 8-10-year cycle, which is where the ETC report might have originated. You'll see a few nests one year, then a few more. So you get a warning. Entomologists at universities ought to keep track of that caterpillar since it has caused problems : if there were records kept, you could see the trends. In 2001 and 2002, there were unusually large numbers of ETC nests, but that changed dramatically between 2003 and 2005. An insect virus that kills tent caterpillars is likely the reason : a tent caterpillar baculovirus was isolated in 2003. This virus is rampant in Central Kentucky. 20-80% of the nests we collected in a 6-county region were infected (the virus kills the ETC) and 90% of the insects in affected nests had the virus. Researchers showed that the caterpillars cause tiny lesions in the mare's gastrointestinal (GI) tract and suspect that the lesions allow bacteria in the GI tract to enter and circulate in the mare's body to somehow reach the fetus, and ultimately cause abortion : the lesions were found to have tiny setae (caterpillar hairs) in them^ref. The highest levels of the types of streptococci that are routinely seen in MRLS were found in the mouth, with about 50% of the total isolated bacteria in the mare's mouth being MRLS-associated streptococcus. Although this same bacterial species was present in the lower GI, it was much less common. There are between 500 and 1000 different bacterial species with a total of between one and 100 trillion total bacteria in the GI tract : the numbers of the MRLS-associated streptococcus bacteria increased by about 10 times when mares were fed ETC. Using DNA fingerprinting, different strains of bacteria were found in different gut regions and discovered a 100% match between the suspect bacterial types found in the mouth of a mare and the bacteria that infected its fetus during MRLS. The bacteria causing MRLS is literally coming straight from the horse's mouth and is part of the normal (gut) flora of that animal. The obvious questions raised by this research are: Why are these particular bacteria involved? How and why do they get from the GI tract to the fetus? and Why doesn't antibiotic therapy work in treating these infections in mares? MRLS prevention (recommendations developed for Kentucky).
• primary preventive measures :
• minimize or eliminate exposure of pregnant mares to eastern tent caterpillars.
• keep pregnant horses away from wild cherry and apple trees.
• frequently mow pastures grazed by pregnant mares.
• offer hay to horses on pasture.
• secondary preventive measures :
• increase the grass-to-clover ratio in pastures.
• restrict time on pasture when a hard freeze is expected following a warm period.
• reduce exposure of pregnant mares to endophyte-infected tall fescue.
• other measures :
• mycotoxin binders have been fed by some farms. If mycotoxins are involved, this could help reduce risk. This decision should be made after discussions with a veterinarian and/or nutritionist.
• correct mineral imbalances. While this is always a good idea, there is a theory that mineral imbalances might be associated with MRLS. Again, discuss this with your farm's veterinarian and/or nutritionist.
• equine amnionitis and fetal loss (EAFL) is a similar entity in Australia. Abortions occurred in mid to late pregnancy without any illness in the mare. The most consistent pathologic change has been inflammation of the amnion and amniotic portion of the umbilical cord, and variable changes have been observed in the fetus. Cases do not have significant involvement of the outer placental membrane (chorion). Bacteria cultured from affected fetuses have included a range of organisms that normally live in soil, on plants, and in water, and that are not typically considered to be the cause of disease in animals (isolates include Microbacterium spp, Cellulosimicrobium spp, Athrobacter spp, and Curtobacterium spp). Similar cases of mare abortion have been reported occasionally from farms in New South Wales over the past several years, added Perkins, including instances in which small farms have had more than half of their pregnant mares abort. Perkins noted that pathology records from 2004 indicated that EAFL accounted for up to one third of all abortions in the Hunter Valley in 2004, in cases in which a fetus was found and submitted post mortem.
• lampas / palatitis : a swelling and hardening of the mucosa of the hard palate, immediately behind the upper incisors in horses
• contracted hoof, foot or heel : a condition in a horse's hoof in which it becomes dried out and reduced in size, which causes inadequate pressure on the frog and lameness
• ribbed or ringed hoof : a condition in which the wall of a horse's hoof is marked by ridges running parallel with the coronary margin.
• heaves : chronic obstructive pulmonary disease in equines, resulting from reduced elasticity and rupture of the elastic network of the respiratory bronchioles and pulmonary alveoli; characteristics include coughing, bronchitis, and labored respiration
• heave line : in an animal with heaves, a groove that appears along the costal arch during the forced contraction of abdominal muscles that follows the normal passive expiratory movement.
• equine babesiosis or piroplasmosis / biliary fever of horses / equine biliary fever : infection of horses or other equines transmitted by ticks of the genera Dermacentor, Hyalomma, or Rhipicephalus; characteristics include high fever, immobility, icterus, gastrointestinal disturbances, rapid emaciation, and dependent edema
• Babesia caballi : a species causing equine babesiosis in Africa and the former Soviet Union, transmitted by ticks of the genera Anocentor, Dermacentor, Hyalomma, and Rhipicephalus.
• Babesia equi : a species causing equine babesiosis in eastern Russia, Italy, Africa, India, and Brazil, transmitted by ticks of the genera Dermacentor, Rhipicephalus, and Hyalomma.
• contagious equine metritis is a venereally transmitted disease which can cause infertility.  It is associated with bacteria including Taylorella equigenitalis and spreads through direct transmission from mare to stallion or teaser and vice-versa. The disease is sporadically reported in Europe, Japan and Morocco. There were 14 cases in the UK in 1996 and 2 in 1997.  The UK was disease-free between 1998 and 2002. It was reported and subsequently eradicated in the United States in 1978. There was a small flurry of cases in 1998 associated with imported animals
• leukoencephalomalacia (ELM) is caused by fumonisins, a group of toxins produced by an endophytic mold found within the corn kernel. Typically, fumonisins are produced while the corn plant is growing in the field, but levels can also increase under improper storage conditions after harvest. Although > 10 types of fumonisins have been isolated and characterized, the most prevalent in contaminated corn is fumonisin B1 (FB1), which is believed to be the most toxic. The dangers from fumonisins are dose-related, and horses and rabbits are the most susceptible of the domestic species. Most of the investigated cases of fumonisin poisoning in horses have involved corn screenings (crushed kernels and other damaged grain material that was removed during the drying of corn by a local grain elevator^ref. For this reason, FDA recommends that corn screenings NOT be used in horse feed. Corn and feed containing corn also needs to be kept dry and protected from moisture when stored to prevent levels of fumonisins and other mold toxins from increasing. FDA recommends that corn and corn by-products used in horse feed should contain less than 5 parts per million (ppm) of fumonisins and comprise < 20 percent of the dry weight of the total ration. In November 2001, CVM and FDA's Center for Food Safety and Applied Nutrition jointly issued a final guidance for industry on fumonisin levels in human food and animal feeds^ref. Additional information about fumonisins^ref. Leukoencephalomalacia is extremely detrimental to horses and if not fatal, results in a debilitated animal that is normally euthanized. The portion of the corn responsible for the fumonisin can be seen in the feed when viewed under a microscopic, and the detrimental chemical can be detected by other analyses. Because of its appearance, the portion of the corn responsible for the disease is sometimes called 'bees wings.' Manufacturers that include corn screenings in their feed are liable for legal issues when horses either die or are euthanized. The corn screenings and fumonisin can be identified in the stomach contents of euthanized horses. Dry weather early in the season, followed by wet weather during silking of the corn plant, and insect infestation increase the extent of fungal infection of corn kernels.  In several countries, high levels of fumonisin in moldy corn have been suspected of causing esophageal cancer in humans

Web resources : EquiFluNet : Global Surveillance Network For Equine Influenza
• Equus subg. Hippotigris
• Equus burchellii (Burchell's common zebra)
• Equus zebra (mountain zebra)
• Equus zebra hartmannae
• Equus zebra zebra
Zebras are affected with anthrax but at rates significantly less than for many other grazing & browsing species, probably because they are mainly a savannah species in Africa. This open feeding pattern significantly reduces the probability of their finding and grazing a specific contaminated piece of ground. However the current rains indicate that they probably became infected via biting flies, e.g. tabanids, as the latter are frequently involved in anthrax epidemics when there have been rains. And these deaths can be wide spread as the female tabanid fly is a wandering feeder, having a number of blood meals before laying some eggs, then a few more meals, then some more egg laying. And they can fly 5-10 kms or further in all of this. Our experience in Texas in tabanid feeding areas is that the deaths are widely separated and can be singular, i.e. without any nearby deaths or sick animals. Wind spread from the QENP to the LMNP will not have occurred. If the 2 are linked --- and this can be checked through molecular typing --- it is probably through leap-frogging infections via biting flies or maybe the inter-park migration of incubating animals. A check on unexpected cattle deaths in herds associated with intervening villages may give a lead on this. That there were anthrax deaths in 2003 at Lake Mburo suggests a possible local contaminated site or two within the park. Grazing very close to the ground, as in droughts & hot weather, does present risks from soil ingestion. There is a common epidemiologic speculation that rains will 'float' the hydrophobic anthrax spores up into the grass mat from deeper down in the soil. While this may happen, there is as yet zero scientific evidence to support it. (If someone is willing to put up the money, a Texas ranch owner is willing to let others try it out on his ranch assuming that we first get permission from the TX Animal Health Commission .... ) Spores will survive longer in depressed areas which collect rain and thus stay moist longer in dry periods. Such places will also have grass long after dry areas have been grazed bare. One must hope that the Lake Mburo park rangers are burning these zebra carcasses. In a retrospective analysis of bison deaths in northern Canada it is patently clear that efficient carcass burning will effectively prevent cases in future years, while leaving carcasses only encourages future cases
• equine infectious anemia virus (EIAV) => equine infectious anemia (EIA) / swamp fever / slow fever / mountain fever / Coggins disease : anemia, intermittent fever, and severe weight loss. Members of the equidae family (horses, ponies, mules, and donkeys) are the only animals known to be affected by the virus. Once an animal becomes infected, it remains infected for life, regardless of the severity of the symptoms. There is no effective treatment. The virus enters the bloodstream, then invades the lymphocytes, where it reproduces until the cell bursts. Thus more virus is released into the blood, and the cycle repeats. The animal produces antibodies against the virus, but the antibody is not effective in eliminating the virus from the body. Furthermore, enough lymphocytes are destroyed over time to reduce the effectiveness of the immune system. When the animal reaches this stage, it usually succumbs to other bacterial or viral infection. The death rate of infected equidae varies from 30 to 70%, and is usually higher when the virus is introduced into a new geographical region. The anemia sometimes accompanying this disease is caused by the animal's immune system attacking the cells in the bone marrow responsible for producing red blood cells. The reasons for this are unknown. Transmission of EIA is by the exchange of certain bodily fluids, usually blood, from an infected to a noninfected animal. Insect bites are one mode of transmission. Horseflies, stable flies, and deer flies are blood feeders. The bite of these insects is painful and the animal often interrupts the insects' feeding, forcing them to relocate. Residual blood is often on the fly's mouth parts from an interrupted meal. If the fly moves from an infected to a noninfected animal, the virus may be introduced into the noninfected animal when the insect breaks the skin. The virus may be transmitted by mechanical means, such as instruments, hoof knives, needles (tattooing or bleeding), syringes, etc. Blood transfusions have also been implicated in transmitting the virus. Transplacental infection of the foal is possible if the levels of virus in the blood are high enough during gestation. About 10% of foals delivered from infected mares are infected at birth and remain virus carriers their entire life. Because of the presence of maternal antibodies to the virus in the mare's colostrum, foals born to infected mares will themselves be antibody-positive within 24 hours. Maternally acquired passive antibodies should be gone by 6 months of age. If the foal is infected at birth, its own antibodies will persist after 6 months. According to India's (2003) annual report to the OIE, the last year in which EIA occurred there was 1996. Until recently, EIA belonged to OIE's list B diseases, and had to be included in member-countries' annual reports. Following the recent amalgamation of lists A and B, it will have to be reported at least twice a year. Infected horses can remain viraemic carriers for life and will yield a positive serological result. Antibody response usually persists and antibody-positive animals older than 6 months are identified as virus carriers. The Coggins test for EIA made Leroy Coggins famous after he developed it in 1970. Testing represents a "tragedy of the commons" situation, as the animal can be healthy but be an inapparent carrier, the 1st sign of which is a positive test. Since many positive animals appear healthy, individual owners are reluctant to test their animals for fear of a positive test and euthanasia, since no treatment is effective.  If these carrier animals are not tested or at least quarantined in an insect-proof enclosure for life, they will transmit the disease after being bit by biting flies or mosquitoes. Testing is best for the population and the only way to rid a geographic area of the disease, but is not favored by owners, who fear the loss of their apparently -- but not truly --  healthy animals. During the 1st 3 months of 2005, Italy was the only EU country reporting EIA to the ADNS (Animal Disease Notification System): 2 cases, 8 Mar 2005. The disease was reported from Italy (Pavia) also, in July 2004. No other EU country reported the presence of EIA during 2004. According to OIE's data (last available annual report, 2003), 28 countries have reported the presence of the disease. EIA seems to be present in most countries of the American continent, in Australia and in south-east Europe, especially the Balkan countries^ref. EIA was first reported in the U.K. in 1976. The distribution of EIA is interesting in the sense that some countries (covering a wide area) in Europe are affected, while others have been free of the disease for decades.  For example, Denmark last saw EIA in 1928, Norway in 1975, Poland in 1960, Hungary in 1965, Spain in 1983 and U.K. in 1976.  On the other hand, the following countries have all reported the disease within the last 5 years: Ireland, Germany, France, Greece, Austria, Ukraine and Lithuania.  It is hard to discern a geographic pattern but that is what makes epidemiology so interesting. It is probably easier to list the European countries that have never reported EIA previously (according to OIE): Belgium, Czech Republic, Kosovo, Liechtenstein, Malta, Netherlands, Slovakia and Switzerland. All these countries should consider themselves lucky and congratulate themselves on the success of their disease control tactics, as EIA is not a trivial disease for the horse population. Identified in France in 1843 and first tentatively diagnosed in the USA in 1888, EIA has commanded a great deal of attention over the years. No vaccine or treatment exists for the disease. It is often difficult to differentiate from other fever-producing diseases, including anthrax, influenza, and equine encephalitis. EIA is significant historically because it is the first disease of horses proven to be caused by a "filterable virus" -- one that can survive a special laboratory filtering procedure and remain infectious. EIAV is the first lentivirus-induced disease proven to be transmitted by insects. And EIA is the first persistent virus for which antigenic drift was defined. (Antigenic drift is the virus' ability to change its form sufficiently so that it is no longer vulnerable to existing antibodies.) Finally, EIA is the first lentivirus-induced disease for which a diagnostic test was approved^ref.

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