Chapter 19 19.1 Investigation of infectious disease 19.2 Diagnosis of viral and bacterial infections 19.5 Equine viral arteritis (EVA) 19.7 Equine picornaviruses (rhinitis viruses) 19.8 Equine infectious anaemia (EIA) 19.9 African horse sickness (AHS) 19.15 Other equine viral infections 19.20 Proliferative enteropathy (Lawsonia intracellularis) 19.27 Equine granulocytic ehrlichiosis 19.28 Corynebacterium pseudotuberculosis 19.30 Other equine bacterial infections 19.32 Investigation of parasite-associated disease 19.33 Control strategies for equine parasite infections 19.43 Other equine parasitic infections 1. Is there an apparent increase in the incidence and/or prevalence of disease above the normal levels? To confirm that the apparent increase is real it is essential to know: • how new cases are being clinically defined. • if awareness of a condition has increased the level of reporting, rather than a true increase. • the rate of occurrence (i.e. incidence) and/or proportion of the group/population affected (i.e. prevalence) prior to the apparent increase. 2. If possible, confirm the diagnosis by appropriate additional tests. 3. Examine the distribution of cases within the group to establish ‘risk factors’. In particular: when did cases occur? e.g. post-weaning, at housing etc. where did cases occur? e.g. in a specific barn or pasture. • obtain rate of disease occurrence in different animal categories, e.g. in foals versus mares. • obtain detailed information from a sample of individuals within different animal categories, e.g. duration/severity of illness in young versus old. 4. On the basis of analysis of information in 1 to 3 hypothesize why the increase in disease occurred, e.g. introduction of an animal incubating disease; change in environmental temperatures etc. 5. The purpose of going through the processes of 1 to 4 is to use the findings to formulate a control strategy. Ideally this would be by identifying the cause(s) of an increase in disease and by removing it (them) to prevent further cases. Most often control is based on: • initiation of immediate control measures pending confirmation of diagnosis and other investigative tests. • isolation/segregation of affected cases (and those with known direct contact prior to intervention). • treatment of known cases would seem logical but is not always appropriate and requires specific knowledge of the disease/condition. • protect high risk groups, e.g. administer hyperimmune plasma to foals during rotavirus outbreak. • institute measures to prevent recurrence, e.g. establish quarantine protocol for new intake animals. 1. Virus isolation. Samples for isolation of viruses include swabs (e.g. conjunctival, nasal, nasopharyngeal etc.), body fluids (e.g. blood, semen, tracheal aspirates, etc.) and tissues. Samples often need to be obtained in the early stages of infection, and they should be collected into a special transport medium which contains antibiotics to prevent bacterial growth and proteins to stabilize the virus. The sample should be transported to the laboratory without delay, and may need to be kept at a low temperature (e.g. packed with ice). 2. Serology. A variety of serological tests is used to demonstrate serum antibodies. In many cases, the antibody titres present during the acute stage of the disease need to be compared with those in the convalescent stage 10 to 14 days later; a four-fold or greater increase in titre is generally considered significant. 3. Detection of viral antigens and nucleic acids. Viral antigens may be detected in blood, secretions, scrapings and tissues by a variety of immunodiagnostic techniques, such as immunofluorescence, immunoperoxidase staining, enzyme-linked immunosorbent assay (ELISA) and radioimmunoassay (RIA). Viral nucleic acids may be detected by techniques such as the polymerase chain reaction (PCR). These methods may provide a rapid diagnosis. Epidemiology: A major and economically important cause of acute respiratory disease throughout the world – with the exception of a small number of island nations, including New Zealand and Iceland. In North America and some parts of Europe the virus is enzootic with local outbreaks occurring regularly. Pathogenesis: Aerosolized virus is inhaled and deposits on the mucosa of the upper and lower respiratory tracts. The virus attaches to the epithelial cells and enters the cell cytoplasm where replication occurs. The epithelial lining of the entire respiratory tract is affected. Infected epithelial cells are damaged leading to inflammation, clumping of cilia and focal erosions. Mucociliary clearance mechanisms are impaired, and secondary bacterial infections are common, which can prolong the recovery period. • Cough (harsh, dry and hacking; sudden onset). • Pyrexia (up to 41.7°C, 107°F). • Enlargement and tenderness of submandibular lymph nodes. • Serous bilateral nasal discharge (becoming mucopurulent with secondary bacterial infections). • The severity of the disease is related to the virulence of the virus strain and the immune status of the horse at the time of exposure. In uncomplicated cases, recovery occurs in about 10–14 days, but coughing may persist for several weeks. • In some cases, secondary bacterial infection of the lower respiratory tract may give rise to bronchopneumonia with signs of dyspnoea, chest pain, reluctance to move (see Chapter 6). • In a minority of cases, myocarditis occurs causing tachycardia, arrhythmia and severe exercise intolerance. • Pregnant mares occasionally abort secondarily to pyrexia. • In partially immune or vaccinated horses, the clinical signs are usually mild, or the infection may be subclinical, but they can still shed virus and serve as a source of infection to other horses. Performance horses may demonstrate only exercise intolerance. 1. A presumptive diagnosis may be made on the basis of the clinical signs and rapid spread of disease, especially in unvaccinated horses; however, vaccinated horses may show few if any clinical signs, and laboratory analysis is required for diagnosis. • Anaemia, leucopenia and lymphopenia are seen early in the course of the infection (1–5 days). • Neutrophilia often occurs later as secondary bacterial infections arise. 3. Virus isolation from nasopharyngeal swabs. 4. Serology – acute and convalescent serum samples (taken 10 to 14 days apart) demonstrate antibody rise (haemagglutinin inhibition and single radial haemolysis). 5. Rapid immunological tests to detect viral antigens/nucleic acid include enzyme and fluorescent antibody tests, and real-time PCR. An immunoassay developed to detect human influenza (e.g. Directigen Flu-A and Espline) may also be used. Real-time PCR is considered to be very sensitive and provides a diagnosis within hours. 1. Complete rest for minimum of 3–4 weeks in clean, minimum-dust environment. 2. General nursing care and provision of palatable food. 3. Antibiotic (penicillin or trimethoprim/sulphonamide) treatment is necessary only if there is significant secondary bacterial infection. If bronchopneumonia is suspected, antibiotic selection should be based on culture of transtracheal aspirate. 4. Non-steroidal anti-inflammatory drugs (NSAIDs) such as phenylbutazone are helpful in horses with high fever, depression or muscle stiffness. 5. Immunostimulants, such as mycobacterial cell wall extracts, are reported to be beneficial. 6. Bronchodilators and mucolytics may be helpful in some cases. 1. Isolate infected horses as soon as possible (as soon as a temperature rise is identified). 2. Provide adequate ventilation and minimal dust conditions. 3. Avoid all contact between healthy and sick horses. 4. Cease exercise/training to minimize stress. 5. Maintain separate feeding, cleaning and grooming equipment, and personnel for sick horses. 1. Isolate new arrivals for 3 weeks. 2. Maintain adequate ventilation rates for all stabled horses, especially in barns. • Current vaccines contain both influenza subtypes as either inactivated whole virus or subunit viral antigens. • Manufacturers’ recommendations vary, but most advise two primary doses 3 to 6 weeks apart, followed by a booster dose 6 months later, a fourth dose after another 6 months and thence annually (or more frequently for high risk horses). Pathogenesis and epidemiology: Necrotizing vasculitis with ensuing hypoxia and malnutrition of tissues, including fetal tissues, placenta and central nervous system, is the basic underlying pathophysiological mechanism responsible for the clinical manifestations. Infection occurs by inhalation of virus in aerosols. The virus replicates in the epithelium of the upper and lower respiratory tracts and associated lymphoid tissue (resulting in lymphadenopathy especially in young horses). EHV1 appears to have evolved a number of mechanisms that allow it to evade the host’s immune defences. Systemic spread by a cell-associated viraemia can occur. Subsequent infection of endothelial cells may lead to vaculitis in the pulmonary, CNS and placental vasculature. A genetic mutation has been identified in the DNA polymerase of some EHV1 strains that appears to predispose to neurological disease. • The incubation period is 2 to 10 days. • Respiratory disease is commonest in young horses (up to 3 years). Older horses usually show mild or subclinical respiratory disease. • Pyrexia (up to 41.1°C, 106°F) (may be biphasic). • Serous nasal discharge (which becomes mucopurulent later). • Coughing (variable; mild or absent). Older horses show milder or subclinical disease – this may be associated with exercise intolerance or low-grade lower airway inflammation (see Chapter 6). Abortion (see Chapter 14).: Abortion may occur due to infection of the foetus and placenta after viraemia, or due to vasculitis in the maternal endometrium. It usually occurs in late gestation (7 to 11 months). The initial respiratory infection is often subclinical. Abortions due to EHV1 often occur as ‘red bag’ or premature placental separation deliveries. Neonatal disease (see Chapter 20).: Foals infected in utero may be affected by severe respiratory disease and are born ill and weak, dying within a few days. Alternatively, foals may appear normal at birth but develop severe illness after a few days. Pathologically, affected foals have necrotizing bronchopneumonia. Neurological disease (see Chapter 11).: Neurological disease is associated with vasculitis of spinal vessels and ischaemia of the cord. It may occur in association with or in the absence of respiratory disease or abortion. Onset of neurological signs may occur up to 8 days after an initial episode of fever. • Clinical signs vary in severity, but usually have a sudden, rapid onset, with maximal severity occurring within 48 hours: • Treatment of recumbent horses is difficult, and many cases require euthanasia due to complications of myositis, skin damage, pneumonia, etc. In general, horses that become recumbent for longer than 24 hours have a very poor prognosis. Some horses with severe neurological signs can recover completely whilst others may have residual defects. 1. Isolate incoming horses for 2–3 weeks. 3. Pregnant mares should be separated from young stock and ideally kept in small groups according to the gestational stage. 4. Horses showing clinical respiratory disease should be isolated. 5. Personnel handling infected horses should be isolated from healthy stock. 6. Bedding of infected horses should be burned. 7. Contaminated stable equipment/clothing should be disinfected. 8. Aborting mares should be kept and managed in isolation. The foetus and membranes are potential sources of infection and must be handled and disposed of carefully. 9. In cases of abortion, all mares due to foal in the same season should remain on the farm until they have foaled. Horses that leave the farm should not be allowed contact with pregnant mares. 10. In cases of neurological disease, infected horses should be isolated, and all horses on the premises should be confined until 3 weeks after the identification of the last new case. 11. Vaccination. EHV1 and 4 vaccines are available but provide only partial and short-lived immunity. However, repeated vaccination can reduce the severity of respiratory disease and reduce the incidence of abortions. Two initial doses given several weeks apart are followed by regular boosters at intervals varying between 3 months and 1 year (depending on specific vaccine). Unlike the recommendation for influenza, it is usually inappropriate to administer EHV1 and 4 vaccines to healthy, at-risk animals in face of an EHV outbreak. EHV4 causes respiratory disease indistinguishable from that caused by EHV1. • The pathogenesis, clinical signs, diagnosis, treatment, control and prevention are similar to those described for the respiratory form of EHV1. • EHV4 has been linked with sporadic abortions but has not been associated with abortion storms. It is not generally linked with neonatal disease or neurological disease. Epidemiology: EAV is widely distributed throughout the world, having been reported in North and South America, Europe, Africa, Asia, Australia and New Zealand. However, reports of clinically apparent EVA are relatively few, which is explained by a high prevalence of subclinical infection and confusion of the clinical disease with other viral infections such as influenza and rhinopneumonitis. Serological surveys indicate that the prevalence of infection varies widely between countries and between different breeds in the same country. Higher rates of infection are frequently found in Standardbreds and various Warmblood breeds. Pathogenesis: Although only one serotype of the virus has been isolated so far, there appear to be differences in antigenicity and pathogenicity among different isolates of the virus. The virus multiplies within alveolar macrophages and then passes to the bronchial lymph nodes. This is followed by viraemia and widespread distribution to many tissues. Vasculitis involving the small arteries occurs initially in the lungs and then in other tissues. Clinical signs: Infection may result in clinical disease or be subclinical. The clinical signs depend on the virus strain, viral dose, route of exposure, age and physical condition of the horse. The incubation period is usually 3–14 days. • Pyrexia (up to 41°C, 106°F) for 2–10 days. • Limb oedema (especially hind limbs). • Nasal or lacrimal discharge. • Periorbital/supraorbital oedema. • Ventral abdominal, scrotal, preputial or mammary oedema. • Vesicular-erosive stomatitis and hypersalivation. • Urticarial-type skin rash (especially over the head, neck and pectoral regions). • Abortion (any stage of gestation) – foetus usually partly autolysed. • Coughing, respiratory distress. Carrier state: A carrier state is established in 30–60% of infected stallions. The duration of the carrier state varies from several weeks to a lifetime. Carrier stallions shed the virus constantly in the semen. There is no effect on fertility. Mares do not become carriers of EVA. • Clinical signs – EVA cannot be diagnosed solely on the clinical signs, so laboratory confirmation is essential. • Haematology – leucopenia and lymphopenia. • Virus isolation or identification of viral antigens or PCR. To optimize the chances of virus detection, samples should be obtained as early as possible after the onset of fever. Prevention and control: Two vaccines are available (a modified live vaccine and an inactivated adjuvanted vaccine).The vaccines are safe and effective in stallions and non-pregnant mares. Prevention and control depend on management practices (as described for influenza and EHV1) and selective use of the vaccine, including vaccination of the at-risk stallion population. Stallions should be vaccinated annually at least 28 days before the onset of the next breeding season. Carrier stallions should be kept in isolation and bred only to seropositive mares. EAV is readily inactivated by heat, sunlight and many commonly used disinfectants. However, infectivity of the virus can be maintained for long periods of time below freezing temperature. Measures should be taken to prevent the spread of EAV in fresh or frozen semen used for AI. • Infection of foals may result in mild respiratory disease characterized by nasal discharge, coughing, conjunctivitis, pyrexia and occasionally diarrhoea. • Arabian foals affected by combined immunodeficiency syndrome (CID) (see Chapter 20) may develop severe, fatal, intersitial pneumonia (usually in conjunction with other pathogens). EIA virus (EIAV) is an equine-specific lentivirus of the retrovirus family, related to HIV-1. Epidemiology: The virus has been identified on all continents. In Europe, it is most prevalent in the northern and central regions, and in North America it is most prevalent in the Gulf Coast and northern wooded regions of Canada. Pathogenesis: EIAV replicates in macrophages in liver, spleen, lymph nodes, etc. High numbers of virus are released into the circulation, which causes pyrexia. Cell-mediated and humoral immune responses clear the virus from the blood, but the virus persists within tissue macrophages. Clinical signs: The clinical features are highly variable. Acute, subacute, chronic and subclinical syndromes are recognized. The severity of clinical signs varies according to the virulence of the strain of virus, the dose of virus, and the host response. Classical cases progress through acute, chronic and carrier phases. The acute syndrome is characterized by: The chronic phase is characterized by: Epidemiology: AHS is endemic in eastern and central Africa, but has spread elsewhere on a number of occasions, including Pakistan, the Middle East and Spain. Clinical signs: Four syndromes are recognized: 1. Peracute or pulmonary form. • Fever (up to 40.5°C, 105°F). • Congestion of mucous membranes. • Dyspnoea and tachypnoea (respiratory rate may exceed 50 breaths/minute). • Frothy blood-tinged nasal discharge (terminally). • Fever (up to 40.5°C, 105°F). • Congestion of mucous membranes. • Oedematous swellings of neck, chest, lumbar and pelvic areas. • Oedema of supraorbital fossa, eyelids, intermandibular space. • Petechial haemorrhages on tongue and conjunctivae. 3. Acute or mixed form (most common clinical form). • The initial clinical signs are similar to mild pulmonary form but then followed by oedematous swellings and effusions and death due to cardiac failure. • Endemic in central America and southern USA. • Affects horses and other livestock. • High morbidity and low mortality. • Virus-infected insects and plants are believed to be important means of transmission. Clinical signs: Although the disease starts with the formation of vesicles in the oral cavity and on the lips, the condition usually has progressed to the ulcerative phase by the time it is recognized by the owner.
Infectious diseases and parasitology
19.1 Investigation of infectious disease
19.2 Diagnosis of viral and bacterial infections
Diagnosis of viral infections
19.3 Equine influenza
The virus
19.4 The equine herpesviruses
Equine herpesvirus 1 (rhinopneumonitis)
Control of outbreaks and prevention
Equine herpesvirus 4 (rhinopneumonitis)
19.5 Equine viral arteritis (EVA)
The virus
19.6 Equine adenovirus
19.8 Equine infectious anaemia (EIA)
The virus
19.9 African horse sickness (AHS)
The virus
19.10 Vesicular stomatitis
The virus
