Equine Lung Disease

Question 1

Equine herpes virus

1. Virus family
2. DNA/RNA?
3. Site affected and pathogenesis

Answer 1

1. Herpesviridae
2. Double stranded DNA
3. Infection of respiratory epithelial cells, some WBCs and endothelial cells. Can also end up in other areas of the body (cell associated viraemia). Can disseminate to secondary areas for replication e.g. uterus or spinal cord. Latency established.

Question 2

Equine herpes virus

1. Transmissing and source of infection
2. Incubation period
3. Epidemiology

Answer 2

1. Inhalation of aerosol or contact with infected fomites or reactivation from latency.
2. 2-10 days
3. Both EHV-1 and EHV-4 are endemic in horse populations worldwide

Question 3

Equine herpes virus

1. Prevalence of disease
2. Clinical Presentation
3. Diagnostic Procedures

Answer 3

1. The seroprevalence rates for EHV-1 and EHV-4 were reported to be between 8% and 85.2%
2. Fever, mild cough sometimes, nasal discharge, poor performance, abortion/sick neonatal foal, neurological disease if in CSF
3. Nasal swab or placenta or blood sample.

Blood sample – virus isolation in tissue culture, detection of antibodies in serum

Question 4

Equine herpes virus

1. Pathological lesions
2. Complications/sequelae
3. Treatment

Answer 4

1. Gross lesions of viral rhinopneumonitis are hyperemia and ulceration of the respiratory epithelium, and multiple, tiny, plum-colored foci in the lungs. Lung lesions are characterized by neutrophilic infiltration of the terminal bronchioles, peribronchiolar and perivascular mononuclear cell infiltration, and serofibrinous exudate in the alveoli.

Typical lesions in EHV-1 abortion include interlobular lung edema and pleural fluid; multifocal areas of hepatic necrosis; petechiation of the myocardium, adrenal gland, and spleen; and thymic necrosis. Horses with EHV-1–associated neurologic disease may have no gross lesions or only minimal evidence of hemorrhage in the meninges, brain, and spinal cord parenchyma. Histologically, lesions are discrete and comprise vasculitis with endothelial cell damage and perivascular cuffing, thrombus formation and hemorrhage, and in advanced cases, areas of malacia. Lesions may occur at any level of the brain or spinal cord

2. Secondary bacterial complications. Can cause abortion in pregnant mare and can cause neurological problems if it disseminates to spinal cord, although rare – as latency established
3. Rest athletic animals

Nursing

Anti-inflammatory medication

If ataxic if is at neurological stage, will need intensive nursing to ensure no pressure sores etc.

Question 5

Equine herpes virus

1. Vaccination?
2. Prevention?

Answer 5

1. Yes – stimulates antibody and cellular immunity as virus can get into cells and travel so it is important we have good cellular immunity
2. Good hygiene and PPE

Vaccinate

Quarantine new animals etc.

Monitor temperatures prior to traveling

Question 6

Equine influenza virus

1. Virus Family
2. DNA/RNA?
3. Site Affected and pathogenesis?

Answer 6

1. Influenza A
2. Negative sense ssRNA virus with segmented genome
3. Respiratory epithelial cells

Question 7

Equine Influenza virus

1. Transmisttion and source of infection
2. Incubation period
3. Epidemiology

Answer 7

1. Aerosol (infectious 1 mile away)

Fomites

2. 1-3 days
3. Global

Question 8

Equine Influenza Virus

1. Prevalence of disease
2. Clinical presentation
3. Diagnostic Procedures

Answer 8

1. Endemic
2. Fever, cough and nasal discharge (serous, may become mucopurulent –secondary bacterial infection)

Cough is harsh and dry –supposedly distinctive, actually quite a lot are

vaccinated and the first thing that gets suppressed is the clinical signs –horse

might not look ill, but may be shedding the virus
3. Nasal swab, really far up the nose!

–Detection of viral antigen (ELISA)

–Detection of virus genetic material =

RNA (RT-PCR)

–Virus isolation (usually in eggs)

Can take a while to do this

Serum samples (acute &

convalescent)

–Use for the detection of antibodies

(serology), typically done by:

• ELISA or
• Haemagglutination inhibition (HI)

4-fold increase in titre technique

Question 9

Equine Influenza Virus

1. Pathological lesions
2. Complications/Sequelae
3. Treatment

Answer 9

1. Destroys respiratory epithelial cilia
2. Onset of pneumonia
3. Nursing care and anti-inflammatory medication (might want to give antibiotics for secondary infection)

Question 10

Equine Influenza Virus

1. Vaccination
2. Prevention
3. Outbreak contol

Answer 10

1. Equine influenza vaccine
2. Equine influenza vaccine
3. Rapid ID of infected horses

Good isolation and quarantine – correct amount of time

Vaccinate

Treat symptoms

Good hygiene and PPE

Owner compliance

Question 11

Equine VIral Arteritis

1. Virus Family
2. DNA/RNA
3. Site affected and pathogenesis

Answer 11

1. Equarterivirinae
2. Positive-sense RNA genome
3. After respiratory exposure, EAV invades the upper and lower respiratory tract and multiplies in nasopharyngeal epithelium and tonsillar tissue and in bronchial and alveolar macrophages. Infected cells of the monocytic lineage and CD3+ T lymphocytes transport the virus to the regional lymph nodes, where it undergoes a further cycle of replication before being released into the bloodstream. The cell-associated viremia that follows ensures dissemination of EAV throughout the body. By day 6–8, the virus localizes in the vascular endothelium and medial myocytes of the smaller blood vessels, especially the arterioles, and causes a panvasculitis. It can also be found in the epithelium of certain tissues, particularly the adrenals, seminiferous tubules, thyroid, and liver

Question 12

Equine VIral Arteritis

1. Transmisttion and source of infection
2. Incubation period
3. Epidemiology

Answer 12

1. mating, artificial insemination, contact with aborted foetuses, on the breath of infected animals
2. 3-14 days
3. The epidemiology of EVA involves virus-, host-, and environment-related factors, including variability in pathogenicity among naturally occurring strains of the virus, modes of transmission, occurrence of the carrier state in stallions, and the nature of acquired immunity to infection. Outbreaks of EVA are most often linked to the movement of infected animals or the shipment of virus-contaminated semen. Frequently, viral transmission occurs with minimal if any detectable clinical signs in acutely infected equids

Question 13

Equine VIral Arteritis

1. Prevalence of disease
2. Clinical presentation
3. Diagnostic procedures

Answer 13

1. Worldwide
2. conjunctivitis (bloody tissue around the eye known as ‘pink eye’)

swelling of testicles or udder, also around eyes and lower legs

abortions (failed pregnancies in mares)

fever and runny nose

depression

lethargy and stiff movement
3. Because of the variability of symptoms, diagnosis is by laboratory testing. Blood samples, nasal swabs and semen can be used for isolation of the virus, detection of the viral RNA by polymerase chain reaction (PCR), and detection of antibodies by ELISA and virus neutralisation tests.

Question 14

Equine VIral Arteritis

1. Pathological lesions
2. Complications/Sequelae
3. Treatment

Answer 14

1. Vascular lesions include endothelial swelling and degeneration, neutrophilic infiltration, and necrosis of the tunica media of affected vessels. These lesions give rise to edema and hemorrhage, which are believed to result from activation of the proinflammatory cytokines IL-1 beta, IL-6, IL-8, and possibly TNF-α. Maximal vascular injury occurs by about day 10, after which lesions begin to resolve
2. Abortion
3. There is no specific antiviral treatment currently available for EVA. Aside from young foals, virtually all naturally affected horses make complete clinical recoveries. Symptomatic treatment (eg, antipyretic, anti-inflammatory, and diuretic drugs) is indicated only in severe cases, especially in stallions. Prompt symptomatic treatment of stallions with a high or prolonged fever and significant scrotal and preputial edema can reduce the likelihood of short-term subfertility. Good nursing care, adequate rest, and a gradual return to normal activity are indicated. There is no effective treatment for EVA-related cases of pneumonia or pneumoenteritis in foals. Because congenitally infected foals are very productive sources of EAV and their chances of survival are essentially nil, early euthanasia should be considered to minimize the risk of further spread of the virus to any susceptible contacts, especially pregnant mares and young foals

Question 15

Equine VIral Arteritis

1. Vaccination
2. Prevention
3. Outbreak control

Answer 15

1. Vaccine
2. isolation of new arrivals on a premises for 3–4 wk before allowing them to co-mingle with the resident equine population, maintenance of pregnant mares in small isolated groups, identification of carrier stallions, annual immunization of noncarrier breeding stallion populations, and vaccination of colts at 6–12 mo of age to minimize their risk of becoming carriers later in life. Carrier stallions should be managed separately and bred only to naturally seropositive mares or mares vaccinated against EVA. Because fresh-cooled or frozen semen can be an important source of EAV, it should be tested by a laboratory with appropriate diagnostic expertise to confirm its negative EAV status, especially if imported. When breeding a mare artificially with virus-infective semen, the same precautions apply as if breeding by live cover to a carrier stallion
3. Vaccinating horses and ponies against the disease - talk to your vet for advice

practising good biosecurity on your premises, especially if you’re involved in breeding

If you suspect equine viral arteritis, APHA vets will investigate.

If equine viral arteritis is confirmed the outbreak will be controlled in line with the contingency plan for exotic notifiable diseases.

Stallions suspected of having equine viral arteritis may be banned from use in breeding, along with semen from that stallion

Question 16

Define latency

Answer 16

• the state of existing but not yet being developed or manifest; concealment
• lying dormant or hidden until circumstances are suitable for development or manifestation.

Question 17

What is the clinical significance of latency of EHV 1 and 4?

Answer 17

• Can be reactivated during times of stress such as pregnancy and can cause abortion.
• Equine herpesvirus type 1 (EHV-1) is the herpesvirus associated with abortion. The virus has also been associated with perinatal foal death; rhinopneumonitis in foals, growing horses, and some adult horses; and encephalomyelitis in adult horses. The virus is distinct from EHV-4, which is the major cause of rhinopneumonitis in foals and is only rarely isolated from equine abortions
• Viral latency also occurs with EHV-1 infection, with periodic reactivation of latent virus resulting in asymptomatic shedding from the respiratory tract that may result in infection of in-contact horses

Question 18

What are the clinical features of Rhodoccuus equi infections?

Answer 18

• Cough, mild increase in RR, increase resp effort mild trahcela rattling, pulmonary crackling
• Occasional polysynovitis, diarrhoea
• Can get into joints and cause swellings

Question 19

What age group of horse are most frequently affected with Rhodococcus?

Answer 19

• Foals, 1-4 months old

Question 20

What is the route of transmission of Rhodococcus disease?

Answer 20

• Inhalation of air, faces, water, solid laden with bacterium
• Rarely detectable bacteraemia
• Faecal shedding

Question 21

What clinical and laboratory techniques can be used to confirm a diagnosis of Rhodococcus?

Answer 21

• Tracheobronchial wash/aspirate – bacteriology, cytology, PCR – DIAGNOSTIC
• Other things that can be done but aren’t necessarily diagnostic: CBC, US, radiography

Question 22

How would you treat a severely depressed animal that is tachypnoeic with severe respiratory distress where you suspect a diagnosis of R equi?

Answer 22

• Antibiotics (macrolide & rifampicin)
• Monitored via Ultrasound and CBC
• Passive transfer of hyperimmune plasma
• Supportive therapy includes provision of a clean, comfortable environment and highly palatable, dust-free feeds. Judicial IV fluid therapy and saline nebulization facilitates expectoration of pulmonary exudates. NSAIDs should be administered as needed to maintain rectal temperature <103.5°F (39.7°C). Nasal insufflation with oxygen is necessary in foals with severe respiratory compromise. Bronchodilator therapy may or may not improve arterial oxygenation. Prophylactic antiulcer medication is indicated in foals stressed by respiratory difficulty, pain, frequent handling, hospitalization, and transportation

Question 23

What species of parasites have a larval migration phase via the lungs

Answer 23

• Lungworm: pathogenesis
• Ingestion of L3 larvae from faeces / pasture, invasion of intestinal mucosa, migration to mesenteric LNs, moult L4 migrate via blood and lymph to lung capillaries > alveoli
• Adults lay eggs with L1 larvae which hatch & migrate up trachea
• Eggs / L1 coughed up & swallowed, pass through intestine then hatch in faeces

Question 24

What are the clinical signs of infection with these parasites?

Answer 24

• Adults hatch migrate to small bronchi, mucopurulent exudate, hyperplastic epithelium, lymphocytic infiltrate in lamina propria (alveolitis, bronchiolitis, bronchitis). Raised areas of over inflated pulmonary tissue
• Moderate to severe coughing (especially with exercise)

Question 25

How do you confirm a diagnosis with lungworm?

Answer 25

• First stage larval L1 in faeces (infrequent and few), tracheal wash for eggs, larvae and WBCs.
• Look for eggs and larvae basically