Equine Diseases of the Northern Hemisphere Flashcards
what is the most important viral respiratory disease of equids
equine influenza A
how is equine influenza A transmitted
Direct/indirect contact, aerosols
is there a carrier state for equine influenza A
no carrier state
requires circulation
what is the incubation period of equine influenza A
1-5d
what type of virus is equine influenza A
RNA
H3N8 strain circulating
what is responsible for attachment of virus to host cells in equine influenza A
hemagglutinin
what breaks down mucus bonds in the resp mucous in equine influenza A
neuraminidase
allows access of virus to underlying epithelial cells
what is the role of hemagglutinin (HA) and neuraminidase (NA) in equine influenza A virus
they both undergo antigenic drift which alters the antigenicity
what are the subdividisions of eqiune influenza A
clade 1 and 2
what are the signs of equine influenza A
Typically URT signs, extreme pyrexia
- 39-40ºC
Lymphadenopathy
Nasal discharge
- Serous
Acute signs decrease after 7 days, with harsh cough for 3-4 weeks
Can result in secondary bacterial pneumonia
Swollen legs/vasculitis/myositis/myocarditis may occur
Life threatening dysrhythmias
- Should be evaluated for myocardial polypeptides, muscle enzyme before return to training
how is equine influenza A diagnosed
History, clinical signs, high morbidity rate
Viral isolation
- Useful for strain surveillance — vaccine implications
Paired serology
Rapid antigen detection tests (ELISA)
what is the morbidity and mortality rate of influenza A
High morbidity
High mortality rate in foals and elderly
Reduced morbidity with improved immune status (ex. prior infection/vaccine)
Age is predictor of disease risk
how long does immunity last post infection in equine influenza A
1 year
what are the risk factors of equine influenza A
Prolonged journey is risk factor for horses developing equine influenza in UK (ex. importation from Europe)
New horses should be quarantined for 4 weeks after arrival
AHT maintains map of confined cases, and strain types
Lapse of vaccination
Prior vaccination does not prevent but reduces severity
what are the vaccination requirements of equine influenza A
Essential to know strain of circulating virus
Maintain up-to-date vaccine reservoir
OIE supplies information on circulating strains
Vaccines for international market should contain both clade 1 and clade 2 viruses of the Florida sub lineage
ProteqFlu has both clade 1 and clade 2 strains
what are the compulory vaccine for equine influenza A
FEI:
- 1st vaccine at 4 months
- 2nd after 21-92 days
- 3rd after 150-215 days
- Thereafter 6 monthly booster required
BHA:
- As above, compulsory annual booster given on or prior to anniversary
Individual horse societies/events vary in rules
ProteqFlu vaccine
- Canary pox vector
how is equine influenza A treated
Symptomatic
Particularly severe in naive individuals
Prolonged rest, NSAIDs, fluid therapy if severe
- Post-viral syndrome and viral myocarditis relatively common
- Sufficient nursing and rest duration vital in recover
- May take 6 weeks for complete recovery to occur
Antibiotics may be required
- Secondary bacterial infections common
- May progress to interstitial pneumonia
- Disease of high morbidity, particularly if vaccination has lapsed
what are the diseases that equine herpesvirus causes
EHV1:
- Respiratory disease, abortion, neurological signs
EHV2:
- Respiratory disease, keratitis, conjunctivitis
EHV3:
- Coital exanthema
EHV4:
- Respiratory disease, (abortion)
EHV5: Respiratory disease
- Nodular pulmonary fibrosis?
what are the signs of equine herpesvirus respiratory tract infection
pyrexia (39-40C)
lymphadenopathy
URT signs but short duration
serous nasal discharge
what is the importance of EHV infections
common
performance limiting
contagious
spread from young to broodmares and neurotropic strains
abortion, neurological disease less common but high mortality
latent infections and recrudescence
why is important to know about the latency and recrudescence of EHV infections
disease prevetion
detection
disease transmission
how is EHV1 and 4 transmitted
Infection via inhalation or recrudescence of latent infection
Virus circulates in young horse population
Pregnant mares and visiting youngstock should be kept separate
Direct (nose to nose contact) or indirect (contaminated buckets, clothing, blankets contact with nasal discharges of infected horses)
Virus can travel via aerosol for short distances
Virus may also be transmitted by contact with aborted fetuses, placental fluids, or placentas form infected horses
what is the incubation period of EHV1 and 4
2-10 days
how long does shedding last of EHV1 and 4
up to 14d from onset of pyrexia
how is EHV1 and 4 controlled
3 week quarantine period of incoming horses
Separation of horses into suitable age groups
Consider vaccination to reduce circulating virus but does not prevent infection
how is EHV resp infection diagnosed
qPCR on fresh tracheal was specimen or nasopharyngeal swab
Serology not useful as virus is ubiquitous
May be useful to test several individuals
what is the disease progression of EHV resp infections
Self limiting in 3-7 days
May be secondary infections or vasculitis
Major risk due to abortion or neurological signs in susceptible individuals
Young animals should be quarantined for sufficient period to reduce likelihood of viral shedding
how are EHV resp infections treated
Symptomatic treatment only required
NSAIDs
Soft feed
Stable rest
Occasionally require treatment of vasculitis and limb edema, uveitis
Will remain carriers of infection and therefore concurrent disease or corticosteroids could induce recrudescence in future
what does rhodococcus equi infection affect
foals of 2-3 months most susceptible
waning colostral immunity
how is rhodococcus equi transmitted
Inhalation of contaminated dust
- Intestinal lesions due to contaminated sputum
- Parasites may introduce R. equi into tissues
- Hematogenous spread rare
Increase by crowding, poor ventilation, dust
how does rhodococcus equi become endemic on stud farms
Will have high burden in the soil and will spread to successive foal crops
May be a significant annual problem
A proportion of foals will harbour infection, develop pulmonary abscesses and then have natural regression of these abscesses
Others develop clinical signs and require treatment to prevent/reduce mortality
what is the pathogenesis of rhodoccocus equi infection
Survives intracellularly in macrophages (difficult for antibiotics to reach)
- Causes degeneration and necrosis of cells then further bacterial release
Polisaccaride capsule resists phagocytosis
VapA virulence factor
Exoenzyme virulence factors — phospholipase
what is the mortality and morbidity of rhodococcus equi
morbidity 10-15%
mortality >50%
what is the incubation period of rhodococcus equi
variable incubation period
clinical signs only apparent after few weeks
most presenting at 2-4 months old
what are the clinical signs of rhodococcus equi infection
initial pyrexia
Bronchopneumonia
- Polypnea, coughing, wheezing
- Abdominal effort, cyanosis
- May be nasal discharge, lacrimation
Ulcerative colitis +/- mesenteric LN abscess
- Weight loss, poor thrift, poor haircoat
- Low grade colic, lethargy and inappetance
Rarer clinical signs
- Polysynovitis, joint sepsis, or osteomyelitis
- Specific organ disruption ex. hepatic encephalopathy
- Uveitis and hypopyon
how is rhodococcus equi diagnosed
May be cultured from transtracheal aspirate (TTA) or blood
- Negative culture does not rule out infection as intracellular organism
Neutrophilia and high fibrinogen levels
Metabolic acidosis if struggling with oxygenation
Positive serology indicates exposure only
Usually clinical diagnosis made on evaluation of diagnostic imaging together with clinical pathology
- Cavitating abscesses may be present
- Compression of trachea may cause stertor
how is rhodococcus equi treated
Combination of erythromycin & rifampin most common
- Need a lipophilic antimicrobial to penetrate the immune cells
- Erythromycin may cause diarrhea, hyperthermia and tachypnea
Long term course of 4-9 weeks required
what is used to guide duration of therapy of rhodococcus equi infection
Ultrasonographic appearance and resolution of acute phase response used to guide duration of therapy in addition to clinical response
Consensus guidelines according to lesion classification (U/S)
what antibiotics may have greater efficacy in rhodococcus equi
Drug resistant R. equi huge problem in endemic areas (ex. Kentucky)
Newer macrolides have greater efficacy:
Azithromycin
Clarithromycin
Tulathromycin
what is the prognosis for racing of rhodococcus equi infections
Good for continued athletic function if recover
what is the intestinal presentation of rhodococcus equi infection
Settle in the abdomen in the lymph nodes
Failure to grow adequately
Diarrhea
May or may not be concurrent involvement of thorax
Difficult to treat, large abdominal abscesses and can adhere omentum and parts of bowel and major organs
how are rhodococcus equi infections treated
Old stud farms
Heavy population
Hot, dry, dust
Infected foals isolated
Early recognition:
- Observe foal lagging behind
- Measure WCC and fibrinogen
- Ultrasound screening repeated during first month of life
- Hyperimmune plasma at 48 hours and 3-4 weeks thought previously to decrease incidence but individual variation in susceptibility and strain pathogenicity
what is the causative agent of equine protozoal myeloencephalitis (EPM)
sarcocystis neurona
also incriminated – neopsora hughesi
where is equine protozoal myeloencephalitis (EPM) reported
USA
canada
france?
seroprevalence >>> disease
what are the risk factors for equine protozoal myeloencephalitis (EPM) infection
age (<1.5yo and >13)
season
presence of definitive hosts
watering/feeding management
adverse health events
what is the definitive host of equine protozoal myeloencephalitis (EPM)
opossum
fecal excretion of infective sporocysts onto pasture
what are the intermediate hosts of equine protozoal myeloencephalitis (EPM)
raccoon
armadillo
skunk
develop sarcosysts in muscle
what are the incidental hosts in equine protozoal myeloencephalitis (EPM) life cycle
horses
what does equine protozoal myeloencephalitis (EPM) cause in horses
multifocal distribution of lesions
expulsion of parasite –> asymptomatic
CNS lesions –> EPM
what are the clinical signs of equine protozoal myeloencephalitis (EPM)
Highly variable
Often insidious
Most have spinal cord lesions
- Ataxia & paresis often asymmetrical
5-10% have muscle atrophy
<5% have brain/brainstem lesions often persistent, but may wax and wane
- Inflammatory response to the cyst in the nervous tissue
Multifocal disease possible
EPM = differential for many chronic neurological disorders in endemic areas (herpes virus)
how is EPM diagnosed
Problematic due to widespread seroconversion
Relies on compatible signs and interpretation of relevant but non-definitive
Signalment, history, clinical signs
Exclusion of Ddx
Immunoblots (westner blot) — serum/CSF antibody ratio
- High sensitivity, low specificity
Response to treatment
how is EPM treated
Anti-protozoals
- Ponazuril (toltrazuril sulfone)
- Anti-coccidial, crosses BBB
- Prolonged course of medication required
- Sulphonamine-pyrimethamine
Ancillary therapy
- NSAIDs
- Corticosteroids/DMSO?
- Vitamin E
- Protect the myelin sheath
- Immuno-modulators
what is the % of horses that imrpove and relapse after EPM infection
60-70% improve
Relapse rate —> 10-20%
how is EPM prevented
difficult
aim to limit exposure of forage and pasture to definitive host
what is the causative agent of potomac horse fever
Neorickettsia risticii
how is potomac horse fever treated
Fluid therapy
- Colitis
Tetracyclines (doxycycline, OTC)
- 7 day course
Tetracyclines may correct pyrexia within 48 hours
how is potomac horse fever prevented
Vaccination highly successful in reducing incidence
Avoidance of risk factors
Stabling to avoid ingestion of infected trematodes at risk times of year
what type of bacteria causes equine monocytic ehrlichiosis (aka potomac horse fever)
neorickettsia risticii
intracellular gram negative coccus
where is equine monocytic ehrlichiosis (aka potomac horse fever) distributed
USA, canada, europe
what is the vector of equine monocytic ehrlichiosis (aka potomac horse fever)
Virgulate (rod shaped) trematode of freshwater snails
Methods of transmission is unknown
Possible ingestion of immature stages in aquatic insects
what is the pathogenesis of potomac horse fever
Infects monocytes
- Obligate intracellular organism
Predilection for colon tissue, macrophages, crypt cells, mast cells
- Loss of microvilli
- Reduced electrolyte transport
- Watery diarrhea
- Dose dependent effect
what is the prediliction site for potomac horse fever
colon tissue, macrophages, crypt cells, mast cells
what are the clinical signs of potomac horse fever
Typhlocolitis
- Biphasic fever (up to 41ºC)
- Edema
- Anorexia
- Diarrhea
- Endotoxemia
- Laminitis
Sub-clinical disease
Abortion
- Usually at 7 months
- Maladjusted foals
how is potomac horse fever diagnosed
history, signs
serology (IFAT or ELISA)
fecal PCR
what are ddx for diarrhea in young foals
Clostridium difficile
Rotavirus infection
Strongyloides westeri — high burdens (epg >2000) leads to diarrhea
Strongylus vulgaris — cause verminous arteritis and colic signs
Cryptosporidia — more likely to occur in more intensive stud farms
Giardia
Parascaris equorum becomes significant in foals >3 months
Antibiotic induced diarrhea also common as in adults
what are the viral causes of diarrhea in foals
rotavirus
what are the epidemiological features of rotavirus
highly contagious
short incubation period
rapid spread
what are the signs of rotavirus in foals
depressed and anorexic
what age does rotavirus affect
2 days to 6 months
how is rotavirus diagnosed
fecal antigen testing and electromicroscopy
what are ddx for rotaviral infection in foals
adenovirus
coronavirus
parvovirus
bacterial causes of diarrhea
what is the morbidity of rotavirus in foals
high
effective barrier nursing
disinfection required
vaccination in subsequent years
how is foal diarrhea treated
Fluid therapy most important
- IV or oral
- Electrolytes, glucose
- Hyperimmune plasma for Rotavirus infection
Intestinal protectants
- Bismuth subsalicyclate
- Activated charcoal
- Bio-sponge
Anti-ulcer therapy
Antibiotics if pyrexic with secondary infection
Probiotics
how is foal diarrhea prevented
Vaccination of mare at 8, 9, and 10 months of pregnancy to increase production of antibodies in colostrum to protect foals
what causes proliferative enteropathy of foals
lawsonia intracellularis
what age of horse does lawsonia intracellularis affect
weanlings
what type of bacteria is lawsonia intracellularis
obligate intracellular gram negative organism
where does lawsonia intracellularis invade
GI cyrpt cells
loss of villi and malabsorption
at what time are horses affected by lawsonia intracellularis
around time of loss of colostral antibody protection
4-7 months
what are the clinical signs of lawsonia intracellularis
Fever
Lethargy
Peripheral edema *
Diarrhea
Until final stages of condition
Colic
Weight loss
Profound hypoproteinemia
- Albumin falling to 10 g/l (ref 30-33 g/l) in some cases
- Foal may collapse due to hypotension
- Better prognosis with earlier diagnosis and treatment
how is l intracellularis diagnosed
Clinical signs and signalment
Extreme hypoalbuminemia
Fecal PCR
- Intermittent shedding
- Pool fecal samples or submit sequential samples for analysis
Serology
- Seroconversion in high proportion of adults, but seropositivity in foal with clinical signs is suggestive of active infection
US appearance of small intestine
- Cartwheel appearance
- Narrowed lumen
how is l intracellularis treated
Oxytetracycline
- 4-6 weeks required
- Doxycycline also effective
Colloidal oncotic support
- Hetastarch or plasma
Full recovery can be made with early diagnosis and sufficient duration of treatment
how is l intracellularis preveted
difficult
Wildlife reservoir
Vaccination of mares
Licensed equine vaccine
