Inf. diseases II - Horses 2/2 Flashcards
Equine influenza is a contagious disease of horses, caused by Influenzavirus A, and is characterized by
acute respiratory disease.
Causative agent of Equine influenza.
genus, family, DNA-type
Agent: Influenzavirus A
genus Alphainfluenzavirus
Family Orthomyxoviridae
RNA virus
Subtypes of equine influenza virus.
Two subtypes
H7N7 (equine virus 1) – more historical
H3N8 (equine virus 2) (more common) – which has two lineages: Eurasian and American.
- Eurasian lineage is uncommon
- American lineage comprised of 3:
classical American lineage,
the Florida sublineage and
the South American sublineage.
The Florida sublineage widespread:
- Clade 1 predominant in North America
- Clade 2 in Europe
Equine influenza viruses appear to change more slowly than
human influenza A viruses or swine influenza viruses.
Equine influenza virus survival.
Survives on wet surfaces for 72h and dry surfaces for 48h.
Susceptible to a wide variety of disinfectants.
Host range of EIV?
More severe in?
equine influenza virus
horses and other Equidae
Disease may be more severe in donkeys and mules.
Humans might be susceptible but there is no evidence of recent natural infections.
Epidemiology of EIV.
Most common in fall and winter.
More common in younger horses (yearlings, ages 2-3 years).
Rare in foals (maternal immunity 3-6 months).
More severe cases seen in pregnant mares close to parturition.
Listed dz
Morbidity of EIV.
high (60-90%)
Mortality of EIV.
low (<1%)
Transmission of EIV.
Excretion: nasal discharge
Virus shedding 48h after exposure; shedding for 6-7 days.
Direct contact (droplets)
Aerosols
Fomites
Route: respiratory; Ocular too maybe.
IP of EIV
IP: 1-3 days
Clinical signs of EIV.
Acute respiratory disease:
Begins with high fever
Deep, dry, often paroxysmal cough; nasal discharge etc.
Complications: secondary bacterial infections
More rare: neurological signs, myocarditis
Animals with partial immunity – milder, atypical infection.
Young foals without maternal antibodies: severe viral pneumonia.
Recovery within 1-3 weeks
Up to 6 months in severely affected animals
Post mortem signs of EIV.
Lung consolidation and/or pneumonia.
Upper respiratory tract involvement alone in milder cases.
Material for diagnosis of EIV.
Nasal swabs
Lab analyses for diagnosis of EIV.
Virus isolation
PCR or antigens (ELISA)
Serology (ELISA, hemagglutination inhibition)
Tx of EIV.
Tx: supportive care and rest
ABs if secondary bacterial infections
Prevention & control of EIV.
Biosecurity measures to minimize the spread!
Vaccination – does not always prevent infections or viral shedding, but the dz is usually milder and virus shedding may be decreased.
Equine arteritis virus (EAV) is a contagious disease of equids, caused by arterivirus, and is characterized by
fever, vascular lesions and edema.
Causative agent of Equine arteritis.
genus, family, DNA type
Equine arteritis virus (EAV)
Genus Arterivirus,
family Arteriviridae
RNA virus
One serotype
Survival of EAV.
Can remain viable for 2-3 days in 37-38°C, and <75 days in 4-8°C.
Semen remains infectious after freezing!
Sensitive to sunlight and low humidity.
Readily inactivated by detergents, common disinfectants and lipid solvents.
Host range of Equine arteritis.
equids
Illness occurs mostly among horses and ponies.
Reported in horses, ponies, donkeys and zebras.
Epidemiology of Equine arteritis.
Reported in North and South America, Europe, Asia, Africa and Australia.
Common among horses in continental Europe.
Absent from Iceland and Japan.
In Europe, seroprevalence is particularly high among Warmbloods.
In U.S. – Standardbreds.
Notifiable dz
Morbidity & mortality of Equine arteritis.
Abortion rate varies: <10% - 60%
Deaths are rare in healthy adults; young foals more likely to die.
Transmission of EAV.
Venereal transmission
Aerosol transmission
Direct contact
Fomites
Route: venereal or respiratory
Excretion of EAV.
Excretion:
respiratory secretions;
urine and feces (during acute stage) and
in reproductive tract (acutely infected mares; acutely/chronically infected stallions), semen.
Stallions can become carriers! At which point virus is ONLY found in semen and in no other bodily fluids.
IP of EAV.
2 days to 2 weeks
Venereal transmission: infection occurs generally in one week.
Clinical signs of EAV.
Most cases asymptomatic. More severe in old or very young animals, and in horses that are immunocompromised or in poor condition.
Fever, depression, anorexia, limb edema (particularly hind limbs).
Dependent edema of the prepuce, scrotum, mammary gland and/or ventral body wall.
Also may be seen: conjunctivitis, photophobia, periorbital or supraorbital edema and rhinitis, urticaria.
Abortions and stillbirths in mares that were pregnant on exposure.
In stallions: temporary decrease in fertility, incl. reduced sperm quality and decreased libido.
In foals: fulminant infections with severe interstitial pneumonia and/or enteritis.
Post mortem signs of EAV.
Edema, congestion and hemorrhages of the subcutaneous tissues, visceral organs and LNs.
Clear, yellow fluid in peritoneal cavity, pleura and pericardium.
Foals: pulmonary edema, interstitial pneumonia, emphysema, splenic infarcts and enteritis.
In mares that abort: endometrium swollen and congested, can contain hemorrhages.
Aborted fetuses: partially autolyzed; excess fluid in the body cavities and signs of interlobular interstitial pneumonia.
Suspect EAV when
you observe fever, depression, edema, conjunctivitis, nasal discharges and abortions.
Material for diagnosis of EAV.
(equine arteritis virus)
Nasopharyngeal swabs
Conjunctival swabs
Blood
Semen
Tissue samples: cecum, colon, spleen and associated LNs, adrenal cortex.
Aborted fetuses,
Foals: lungs, liver, spleen
Lab analyses for diagnosis of EAV.
Virus isolation
Detection of antigens or nucleic acids with RT-PCR
Serology – ELISA
Histopathology
Detecting carriers:
Virus isolation from semen or breeding with two seronegative mares
Tx of EAV.
no specific Tx
Symptomatic and supportive care.
Prevention & control of EAV.
Isolation & quarantines.
Venereal transmission controlled by good management and vaccination.
Vaccination – prevents long term carriers (inoculated will shed virus for a time).
Carrier stallions: bred only to well vaccinated or naturally seropositive mares – same for semen use.
Excellent hygiene and decontamination of fomites.
Strangles is a highly contagious disease of horses, caused by Streptococcus equi subsp. equi, and is characterized by
infection of upper respiratory tract.
Causative agent of strangles.
gram positive bacterium
Streptococcus equi subsp. equi
also beta-hemolytic
Survival of Streptococcus equi subsp. equi.
Survives in the environment for <2 months
Host range of strangles.
horses, donkeys and mules
Epidemiology of strangles.
Worldwide distribution
More severe in young horses.
Majority of exposed horses develop immunity – lasts for ≥5 years.
Up to 10% of affected animals become carriers.
Morbidity of strangles.
high
Higher in young horses (foals and weanlings).
Mortality of strangles.
low
Case-fatality with Tx: 1-2%; without 9%
Death is usually due to pneumonia.
Transmission of strangles.
Excretion: nasal and abscess discharges.
Shedding begins 2-3 days after onset of fever, lasts for 2-6 weeks after the cessation of clinical signs.
Direct contact
Fomites
Route: via the mouth or nose mucous membranes
IP of strangles.
IP: 3-14 days
Clinical signs of strangles.
fever, Anorexia, listlessness, Nasal discharge (serous then, mucopurulent)
Lymphadenopathy (submandibular and retropharyngeal LNs)
Dysphagia, Dyspnea, stridor
Hyperemic nasal and ocular mucosa
Inconsistent cough
Other signs depend on specific tissue involvement (e.g. neurologic signs).
Complications in 20-30% of cases
E.g. chondroid formation within the guttural pouch, metastatic abscessation.
These Increase the case-fatality rate (<40%).
Post mortem signs of strangles.
Suppuration in internal organs – liver, spleen, lungs, pleura, peritoneum.
Material for diagnosis of strangles.
Nasal swabs
Nasal washes
Guttural pouch lavages
Aspirated pus
Lab analyses for diagnosis of strangles.
Culture
PCR
Serology (ELISA) - Does not distinguish between vaccine and infection response!
Tx of strangles.
ABs (penicillin)
Supportive care; NSAIDs
Long-term ABs if internal abscesses
In case of a strangles outbreak:
Restrict movement
Separate horses to affected, exposed and non-exposed groups.
Recovered and exposed horses should be evaluated for shedding before release from quarantine.
Compost manure and waste feed from infectious horses at an isolated location.
Contaminated pastures and paddocks should be rested for at least 4 weeks.
Prevention of strangles.
New arrivals should be isolated for 3 weeks and screened for S. equi.
Strict hygiene practices
Vaccination – new vaccine developed in Sweden.
Equine herpesvirus infection: rhinopneumonitis is a contagious disease of horses, caused by herpesvirus, and is characterized by
respiratory disease and abortions.
Causative agent of Equine herpesvirus infection: rhinopneumonitis.
genus
family
DNA type
Equine herpesvirus 1 and 4
(EHV-1 and EHV-4)
G.Varicellovirus
F.Herpesviridae
d/s DNA virus
EHV-1 causes what forms of disease?
EHV-4 causes what forms of disease?
EHV-1: abortions, sometimes respiratory dz,
specific strains cause neurologic disease called Equine herpesvirus myeloencephalopathy (EHM)
EHV-4 – respiratory dz, sometimes abortions
Survival of equine herpesvirus.
Survival in the environment 15-45 days.
Host range of equine herpesvirus.
horses, mules, donkeys
Epidemiology of equine herpesvirus.
Worldwide occurrence, ubiquitous.
Listed dz
80-90% of horses are latently infected with EHV-1 or EHV-4 by 2 years of age.
EHV-1 – protective immunity for only a few weeks to a few months.
Excretion of equine herpesvirus.
Excreted in nasopharyngeal excretions, aborted fetal and placental tissues and fluids.
Principal reservoir: latently infected horses.
Shedding virus for 6-10 days after onset of fever.
The neuropathic strain of EHV-1 produces a viremic load 10- to 100-fold higher than that of non-neuropathic strains.
Transmission of equine herpesvirus.
Direct contact
Aerosols
Fomites
Route in: respiratory, alimentary
IP of EHV.
IP: 1-10 days
Clinical signs of EHV: resp. dz.
Serous nasal discharge, Malaise, Pharyngitis,
Cough, Inappetence
Submandibular or retropharyngeal lymphadenopathy. Self-limiting dz.
Complications: bacterial pneumonia or pleuropneumonia
Abortions:
Abortion in the last third of pregnancy
No premonitory signs
Clinical signs of EHV myeloencephalopathy.
Neurologic disease that may vary in signs.
Mild incoordination, posterior paresis
Severe posterior paralysis with recumbency
Loss of bladder and tail function
Loss of skin sensation in the perineal and inguinal areas.
Quadriplegia
Death
Post mortem signs of EHV.
Foals: severe diffuse interstitial pneumonia, hepatitis with viral inclusion bodies and bone marrow depletion.
May have no gross lesions or only minimal evidence of hemorrhage in the meninges, brain, and spinal cord parenchyma.
Material for diagnosis of EHV.
Blood
Nasal swabs
Aborted fetuses: liver, lungs, adrenal and thymus samples.
Lab analyses for diagnosis of EHV.
Virus isolation
PCR
Serology – most available tests cannot differentiate between EHV-1 and EHV-4!
Histopathology
Tx of EHV.
symptomatic Tx
NSAIDs
Fluids if needed
Rest
Prevention of EHV.
Mares that abort should be isolated for minimum of 4 weeks and not mixed with pregnant mares for 56 days.
Good hygiene and biosecurity
Separate different age groups
Isolate pregnant mares from other horses
Disinfection
Pest and vector control
Vaccination
What is EHM?
Equine herpesvirus myeloencephalopathy (EHM)
a form of disease caused by specific strains of EHV-1.
(remember the typical form of disease from EHV-1 is abortions & sometimes respiratory dz)
