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Brucellosis
o Etiology
 Brucellosis abortus is a gram-negative coccobacillus
 Non-motile, aerobic and intracellular
 Causes supraspinatus bursitis (fistulous wither) most common manifestation
 Poll evil : supratlantal bursitis
 Organisms has a predilection for synovial structures
 Affects humans : B. malitniol???
 Zoonotic
 Organism has a predilection for synovial structures
 Affects all ages, breeds and genders
 Most infections are a result of contact with brucella positive cattle, especially
placental tissue and newborn calves
 Organism can survive in the environment for weeks
 Areas where B. Suis exists contact with infected pigs poses a threat to horses
 Route of infection is usually ingestion, however, inhalation or direct contact
through skin abrasions or mucous membranes (can get exposed during
reproductive manipulation—most common route of infection today for vets is
accidentally injection ourselves with strain 19 vaccine)
 Brucella abortus travels to the lymphatics and enters phagocytic cells leading to
granuloma formation
 Synonyms-bangs disease, undulant fever
 Cattle are the most common natural host for the organism, but it has been
isolated from horses, American bison, buffalo and yaks
 Most horses with brucellosis have a history of contact with infected cattle
o Clinical findings
 Predilection for the tendons, muscles, bones and joints
 Septic bursitis of the supraspinous bursa over the 2nd and 3rd dorsal vertebral
spinous processes (poll evil)
 Supraatlantal bursa over the 1st and 2nd cervical vertebrae (fistulous withers)
 In areas where the incidence of brucella abortus is low infection of the
bursa is usually the result of other organisms
 Osteomyelitis of the spinous processes
 Brucellosis is not an important organisms with regards to abortion in mares
o Fistulous withers
 Profuse serofibrinous exudates with varying degrees of necrosis
 Formation of fistulous tracts
 Early signs include pain, swelling, heat of the affected bursa, stiffness and
lethargy
 Once the bursa ruptures purulent exudates drains
 Several organisms may be cultured from the affected site including
staphylococcus aureus, streptococcus sp, actinomyces bovis
 Presenting complaint is usually a draining fistulous tract—gross picture of
abscess crap—tendency to put a drain in it—to treat you literally have to go in
and remove all then necrotic tissue, also need to do radiographs because this
could go down to the bone as well!!
o Diagnosis:
 Rise in titer in paired serum samples two weeks apart is considered diagnostic
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 High titer in conjunction with a history of exposure to infected cattle and clinical
signs of fistulous withers is also diagnostic (you do need to ask if there are cattle
present—important history question!! Make sure owner has his cattle tested as
well)
 Brucella sp is difficult to isolate via culture and sensitivity
 Plate agglutination test is more specific and sensitive than the card test for use
in cattle
 A titer of 1:50 or higher is considered positive
 Other tests (look up these other tests and be familiar with them!!!)
 Agglutination
 Compliment fixation
 Coombs
 Mercaptoethanol
 AGID
Therapy:
 State regulatory agencies must be notified of brucella positive animals
(reportable)
 Some states prohibit treatment of brucella positive animals-must be
euthanized-check local agency
 Lavage of fistulous tracts with antiseptic solutions
 Surgical resection of affected soft tissue and bone (ultrasound also helpful to
see if it affects soft tissue and bone)
 Systemic antibiotics—tetracyclines, streptomycin, chloramphenicol, some
sulfonamides
 Vaccination with strain 19 vaccine different injection regimens (some vets are
actually treating the disease by administering strain 19 and some do it once a
week for 3 weeks or 7 weeks or some do 3x a week for 3 weeks)
Public health concerns
 Brucella abortus is zoonotic
 Brucella infection is most frequently seen in slaughterhouse workers, vets,
farmers, dairymen, and travelers to endemic areas
 Infection in humans results in acute and subclinical dz characterized by malaise,
chills, myalgia, fatigue, arthralgia, weakness
 Fever is intermittent (undulant fever)
 Relapse is common in approx 10% of affected humans following successful tx
with antimicrobials (doxy for 28 days)
 Most infections are the result of accidental infection of strain 19 vaccine
Prevention
 Horses should not be housed or pastured with infected cattle
 Properly fitted tack will help reduce trauma to withers
 Effective parasite control to eliminate infection with onchocerca spp.
(onchocerca gutterosa—in equine nuchal and gastrosplenic ligament and
onchocerca cervicalis—in equine nuchal ligament and associated with a
dermatitis)—onchocerca species are brought in by intermediate hosts
 Effective fly control (simulean—black fly, hematobia—horn fly, culicoides—
gnats (no see-ums), musca—basic house fly)—not considered pathogenic but
when they do biopsies and culture and sensitivity they actually see onchocerca
species)
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African Horse Sickness
o Etiology
 Disease affecting the cardiopulmonary and respiratory systems
 Characterized by fever and edema
 Not reported in the U.S.
 Affects all species
 Disease most prevalent on the African continent
 Recent outbreaks in south Africa, Mozambique, and Zimbabwe
 Other countries reporting outbreaks are India, Jordan, turkey, Syria,
Iraq, Spain
 Caused by RNA virus orbivirus and vicerotropic
 Arthropod born disease primarily culicoides however ticks and mosquitoes may
carry the virus
 Virus affects the vascular endothelium resulting in edema
 Seasonal occurrence
 Spread to uninfected countries through import/export of infected horses
through transport of the insect vectors in aircraft or heavy winds
 After infection initial multiplication of the AHSV occurs in the regional lymph
nodes, followed by a primary viremia and dissemination of the virus to the
endothelial cells of the target organs
 In horses, viremia may last only 4-8 days but does not exceed 21 days
 Donkeys and zebras viremia may last up to 4 weeks
 Naïve animals like foals and horses never exposed usually develop the peracute
from of the disease
o Clinical signs:
 Fever
 Pulmonary edema-usually cause of death
 Frothy nasal discharge
 Edema of supraorbital fossa
 Colic subcutaneous edema of the neck
o Three presentations of the dz
 Dunkop or pulmonary form—peracute form of AHS
 Occurs in fully susceptible horses
 In endemic areas may affect foals who have lost their maternally
derived immunity
 Incubation period for pulmonary AHS is usually 3-4 days with rapid rise
in body temperature 104-106 F
 Characterized by rapidly progressive respiratory failure
 Respiratory rate may exceed 50 breaths per minute
 Dyspnea onset rapid and death usually occurs within 30 minutes to
hours onset
 Prognosis for dunkop is poor <55 survival rate
 Dikkop or cardiac form
 Incubation usually 5-7 days
 Fever 102-106 F that persists 3-4 days
 First sign is edema of supraorbital fossa
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Edema of the head and neck follow
Ventral edema and edema of the lower limbs absent
Milder form
Mortality is >50%
Death usually occurs in 4-8 days after onset of fever
If animal recovers swellings usually subside after 3-8 days
Complications
o Esophageal paralysis
o Equine piroplasmosis
 Mixed form
 Most common form of AHS, however rarely diagnosed clinically
 Death is usually due to cardiac failure
 Horse sickness fever
 Mild form of AHS
 Transient increased respiration, conjunctival edema
 Increased heart rate
 This form of AHS is usually associated with zebras and donkeys
Pathology
 Dunkop
 Diffuse severe subpleural and interlobular edema of the lungs
 Severe hydrothorax
 Trachea and bronchi usually large amounts of frothy fluid ****
 Petechia and ecchymoses present in trachea
 Dikkop
 Distinctly yellow edema of the subcutaneous tissue of the
subcutaneous and intramuscular connective tissues
 Severe edema around the nuchal ligament
 Severe hydrocardium
 Subpericardial petechiation and subendocardial ecchymoses over the
papillary muscles
 Mixed
 Lesions common to the cardiac and respiratory form are found in
animals that die from the mixed form of AHS
DDX
 EIA—serology
 Equyine biral arteritis—serology
 Purpura hemorrhagica—serology
 Equine peirplasmosis
 Anaplasmosis
 Congestive heart failure
 Requires lab testing to distinguish
Dx tests
 CBC/chem. Not applicable
 Thoracic radiographs evidence of pulmonary edema
 Thoracic u/s pleural effusion or pericardial effusion
 Definitive diagnosis—isolation of virus from whole blood or tissue or antibodies
to AHS virus in serum
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 PCR—gold standard
 Elisa
o Synonyms:
 AHS
o Zoonotic potential: possible accidental aerosol infection occurred in workers packing
mouse brain attenuated strands of AHS vaccine-neutropic strains have been removed
from vaccine
o Treatment
 No specific tx for AHS
 Usually fatal outcome
o Prevention
 Annual vaccination of horses in endemic areas in late winter early summer
 Horses with 3 or more courses of vaccination are usually well protected against
the virus
 Antibody acquired through colostral transfer determines the duration of passive
immunity—foals of vaccinated mares should not be vaccinated against AHS until
at least 6 most of age
 Stabling of susceptible horses before dusk until after sunrise
 Use of insecticides and insect repellants
 Control measure include:
 Delineation of the area of infection
 Strict movement controls within, into and out of the infected area
 Stabling all equids at least from dusk to dawn
 Insect control measures
 Tempe of all exposed animals for early detection
 Immediate vaccination of susceptible animals with attenuated
polyvalent vaccine
 Identification of vaccinated animals
 Notification of appropriate governmental agency (reportable)
 Strict adherence to guidelines establish by international animal health
code for horses imported form AHS-infected countries
o Housing animals in a vector protected quarantine facility for at
least 40 days
o Test for absence of AHS or demonstration of as table or
declining titers
Strangles
o Etiology
 Is highly contagious upper-respiratory infection with a low mortality rate
 90-95% infection—extremely contagious
 Is caused by bacteria—streptococcus equi-gram + cocci and usually appears on a
plate as pairs or in chains, it appears on blood agar plates in mucoid honey
colored colonies surrounded by a wide zone of beta hemolysis (since strep equi
and strep zoo are so close related there are a few characteristics that are
associated with equi that are not assoc with strep zoo—strep equi cannot
ferment lactose and sorbital!!!!
 Is contracted through environmental contamination, nasal discharge or direct
contact with an infected animal
o
 Virulence factors for strep equi include a nonantigenic hyaluronic acid capsule,
hyaluronidase, streptolysin S, streptokinase, immunoglobulin G, Fc-receptor
proteins, pyogenic exotoxins, petpidoglycan and antiphagocytic M protein
(SeM)
 Virulent isolates of strep equi are almost always encapsulated, producing
mucoid colonies
 The capsule appears to inhibit the ability of neutrophils to bind, ingest
and kill the organism
 It also facilitates the function of proteases and toxins within the
organism and is required for the function of SeM
 Streptokinase S is responsible for the beta-hemolysis observed with strep. Equi
 Stretpotkinase S binds to erythrocytes resulting in the formation of a
transmembrane pore and irreversible osmotic lysis of the cell
 Gram (+), coccoid, facilitative anaerobic, catalyse (-)
 Related S. zooepidemicus
 Beta-hemolytic
 Has an affinity for the guttural pouches
 Colonies appear mucoid, honey-colored with a wide zone of beta-hemolysis
 Colony morphology is identical to S. zooepidemicus
 S. equi is able to ferment lactose or sorbitol
 Virulence factors that make this bacteria capable of disease
 Hyaluronic acid
 Hyaluronidase
 Streptokinase S
 Responsible for beta-hemolysis
 Binds to the RBCs & causes a irreversible osmotic lysis of the cell
 Streptolysin S
 IgG
 FC receptor proteins
 Pyrogenic exotoxins – SePE-H, SePE-I, SePE-K, SePE-L
 Function by stimulating T-cells to proliferate & release pro-inflammatory
cytokines
 Causes neutophilia, hyperfibrinogenemia, & pyrexia
 Antiphagocytic M-protein – SeM
 Heat & acid resistant & is located on the Streptococcal surface
 Inhibits phagocytosis by binding fibrinogen & inhibiting deposition of C-3b
 Peptidoglycans
 Virulent types are heavily encapsulated
 Inhibits neutrophils to bind, ingest, & kill the organism
 Blocks access for C-3b, which is used for binding, & CR-1 (antibody) & FC
receptors on the phagocyte
 M proteins of streptococci are antiphagocytic
Transmission
 Purulent discharges from horse with active and recovering strangles are an
important source of new strep equi infections among susceptible horses
 Direct transmission refers to horse to horse contact
 Indirect transmission—occurs through the sharing of contaminated
housing, water sources, feeding or feeding utensils, twitches, tack ,
o
clothing footwear and equipment of handlers, caretakers, farriers and
veterinarians
 In apparent carrier horses: normal nasal secretions are the source of strep equi
infection
 A number of horses continue to harbor the organism for several weeks after
abatement of clinical signs. In most cases no detectable org can be cultured
after 4-6 wks post infection
 Horses that are fully recovered continue to shed S. equi for long periods of time
are referred to as long term subclinical carriers. They are source of infection for
susceptible animals
 The guttural pouches are the sites for continued infection in long-term
subclinical carriers
 The carrier state develops in approx 10% of affected animals
 Guttural pouch becomes infected in the early stages of dz, following rupture of
the adjacent retropharyngeal lymph nodes through floor of guttural pouch
 Chondroids formed after strangles may harbor S. equi
 In some animals, guttural pouch empyema with S. equi may persist without
clinical signs for months or years
Pathogenesis
 Strep equi enters through the mouth or nose and attaches to the cells of the
crypt of the lingual and palatine tonsils as well as to the follicular-associated
epithelium of the pharyngeal and tubal tonsils
 Translocation occurs within a few hours to the mandibular and suprapharyngeal
lymph nodes
 Although strangles affects the upper airways primarily, it may spread to other
regions via a hematogenous route or lymphatic channel
 Abscess formation in the lymph nodes of the thoracic and abdominal
regions
 Condition is referred to as “bastard strangles” (mesenteric lymph nodes
is more common presentation however it can go to thoracic lymph
nodes as well)
 Bacteremia occurs on days 6-12 in horses inoculated intranasally with strep equi
 First clinical sign of infection is a rapid increase in rectal temp to 103 F or
higher between days 3-14 **********
 Nasal shedding of the org begins after a latent period of 4-14 days and ceases
between 3 weeks and 7 weeks after resolution of clinical signs
 Some horses become persistent shedders
 Immunity to strep equi is acquired in approximately 75% of horses
following infection
 Older horses may have residual immunity to strep equi and develop a
mid form of the dz referred to as “catarrhal strangles”. They represent
a significant source of infection to younger animals.
 Colostrums from recovered mares provides sufficient protection for foals until
the time of weaning
 Several aspects of s equi pathogenesis are imp to consider when designing a
control/prevention program
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Shedding does not begin until 1-2 days after onset of pyrexia. New
cases can therefore be isolated before they transmit infection
Nasal shedding persists for 2-3 weeks in most animals. Persistent
guttural pouch infection may result in intermittent shedding for years
Field and experimental data support eh conclusion that disease severity
depends on the challenge load and duration
Symptoms:
 Ruptured submandibular lymph nodes
 High fever of 103-106F—may last from 3-14 days post infection
 Loss of appetite
 Moist cough
 Clear nasal discharge—later on it will develop yellow nasty mucopurulent
discharge
 Difficult breathing and swallowing (becomes a medical emergency—keep in
clinic because end up needing tracheotomy)
 Abscessed lymph nodes
 Depression
 Severe pharyngitis associated with dysphagia
 Laryngitis along with rhinitis may develop
 Nasal and ocular discharges—can be highly infective
 Submandibular and retropharyngeal lymph nodes become swollen and painful
4-7 days following infection
 Infected lymph nodes become hot swollen and enlarged and may either revert
to normal size or mature into abscesses and rupture
 Retropharyngeal lymph node swelling may not be seen externally they may
drain and rupture into guttural pouch causing empyema
 Severe swelling of the retropharyngeal lymph nodes may result in upper airway
obstruction. Other swelling may affect trachea at thoracic inlet
 Temporary laryngeal hemiplegia may develop due to retoropharyngeal or
cranial cervical lymphadenopathy
 Uncomplicated strangles can take 3-4 weeks to resolve most horses follow this
course
 Possible complications of strangles include: bastard strangles (most
common presentation of strangles complications), pupura
hemorrhagica, Vasculitis, myositis, glomerulonephritis (usually immune
mediated), myocarditis, agalactia in lactating mares
 Other complications
o Abdominal cavity result in abscess formation in mesenteric
lymph nodes leading to peritonitis
o Brain—vertebral abscesses and meningitis (rare)
o Kidney, spleen, and liver are other common sites for spread of
the organism
o Purpura hemorrhagica—aseptic necrotizing vascultiis character
by edema in petechial or ecchymotic hemorrhages
o Myositis-two types of myopathy assoc with exposure to strep
equi muscle infarction and rhabdomyolysis with progressive
atrophy
Diagnostics:
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 Culture and sensitivity of nasal swabs or pus aspirated from affected lymph
nodes remains the gold standard for detection of strep equi
 PCR-detects the DNA sequence of SeM. Does not distinguish between dead and
live organisms thus a positive result must be considered presumptive until
confirmed by culture
 Serology—it checks for the SeM virulent factors
 ELISA to detect internal abscesses of S. equi related purpura hemorrhagica
Prevention and Treatment:
 Isolate new horses for a month (make sure vax before coming on property)
 Isolate and avoid horses with upper-respiratory problems—don’t let horses
share water buckets!!
 Keep horse warm and dry (if infected)—stall needs adequate ventilation and
clean
 Feed infected horse soft foods—obviously if have pharyngitis it is more
palatable
 Use penicillin only if abscesses have not developed
Treatment
 3 options
 A. supportive care—provision of soft feed, hot packing swollen lymph
nodes to encourage rupture or lancing mature lymph nodes to facilitate
drainage. Draining abscesses should be flushed daily with a dilute 3%5% solution of betadine DO NOT USE THIS IN THE GUTTURAL POUCH
 Depressed animals may benefit from non-steroidals anti-inflammatory
therapy
 These animals will usually recover in 4-6 weeks
 B. treatment once an outbreak has started it is possible to delay the
onset of disease by taking the rectal temp of all exposed animals daily or
every other day and treating horses at the first sign of fever with
ceftiofur or penicillin
 Antibiotic therapy is contraindicated if lymphadenopathy (delays
abscess formation) is present
 Treated animals will not develop other clinical signs of strangles while
on treatment. However, immunity does not develop and once
monitoring and treatment discontinue these animals will develop
disease if environmental exposure persists
 Look up penicillin and naxcel dose!!!!!!
 Treatment C: cases of bastard strangles or cases of strangles where
swelling is so severe that upper respiratory tract is compromised
require special tx
o Antibiotics—penicillin, ceftiofur possibly 10-20 days (or
sulfonamide)
o Non-steroidal inflammatory
o Tracheotomy to relieve dyspnea
o Bastard strangles—thoracic or abdominal lymph nodes may
require long term antibiotic therapy 2-3 months with either
penicillin or ceftiofur. Alternative drug would be doxy 10mg/kg
bid PO
o
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Guttural pouch empyema—flushing and drainage or surgical
remove of chondroids. Concurrent antibiotics.
 SEE CHART IN NOTES (28-2)
 Tx healthy animals first if cleaning and treating—do sick animals last
 Do not bring any equipment from sick barn to clean barn
 If have several horses cluster them—put sick ones together so you don’t have
various sick animals all over in different spots on the premises
 If you suspect guttural pouch empyema or chondroids endoscopy is an
important diagnostic tool
o Controlling outbreaks:
o Cases may be treated following appropriate protocols once the
disease has run its course it is essential to identify potential
carrier animals and tx accordingly
 The standard recommendation for identifying carrier
animals is to test by PCR and culture at least 3
nasopharyngeal swabs or lavages at weekly intervals
(guttural pouch lavages are more likely to contain
infective orgs than nasopharyngeal swabs)
 Consistently negative animals should be returned to
clean areas
 Outwardly healthy animals with positive cultures should
have the guttural pouches endoscopically examined if
chondroids or empyema is found it should be treated
(the infection will not self cure)
o Stalls should be cleaned to remove all organic material from all
surfaces then disinfected with the appropriate compound
phenolic disinfectants are best. 10% povidone iodine is also
effective or stalls may be steam cleaned
o Pastures in which sick animals were held should not be sued for
at least 4 weeks
o Prevention:
 Vaccination two modified live vaccines available
 Pinnacle (fort dodge)-intranasal administration
 Equillis strepe (intervet)-submucosal administration in upper lip
 Both vaccines can cause abscess formation if given IM. Thus either no
other vaccines should be given in conjunction with the strangles vaccine
or all IM injections should be completed before administering strangles
vaccine
o Public health concerns:
 Cases of Strep equi infection have been reported in debilitated humans
 Animal handlers, veterinary personnel, caretakers and pathologist should avoid
unnecessary exposure especially oral and respiratory when coming into contact
with purulent material form infected horses.
Equine Infectious Anemia
o Etiology
 Swamp fever
 It is a viral disease
 Usually spread by cabinets—horse flies and deer flies
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Spreads by horse flies who bite an infected horse and then bite a healthy horse
Can result in fatality, usually within 30 days of contracting the disease
Can be carried by survivors
Lentivirus
Infectious disease of horses and other equids characterized by recurrent
episodes of fever, lethargy, inappetance, thrombocytopenia, anemia
 Closely related to FIV, HIV, CAEV and maybe visna virus
 Can cause persistent infection
 Antigenic variation and immune escape are major contributing factors to EIAV
persistence
Pathogenesis
 Effects horses, donkeys, mules, zebras
 Tabinids (horse and deer flies) stomoxys sp (stable flies are responsible or the
direct transmission of the virus from infected to non infected animals
 Iatrogenic transmission occurs through the use of contaminated hypodermic
needles, dental equipment, nasogastric tubes, instrumentation, semen and
blood or plasma transfusions
 Once infected the horse is infected for life
 EIAV infects cells of the monocyte/macrophage lineage and can be detected in
the liver, spleen, lymph nodes, lung, bone marrow, and circulation
 Foals born to positive dams are usually virus negative at birth but can become
infected by ingesting infected colostrums and milk
 Disease affects the hemic/lymphatic/immune systems, cardiovascular system,
hepatobilliary system, renal/urologic system and neurologic systems
 In North America the disease is more prevalent in the southeastern US,
northern swampy areas of Manitoba and Saskatchewan and Alberta and a very
narrow band in southern Quebec
 Virus constantly mutates and new disease attacks occur when a mutation arises
that successful in evading the hosts immune response producing a viremia
 Anemia and thrombocytopenia are the clinically consistent abnormalities noted
 Anemia I results from immune mediated destruction as viruses adhere
to red blood cells
 Anemia is non-regenerative or poorly regenerative
 Sideroleukocytes (iron containing leukocytes) may be seen in peripheral
blood
 Thrombocytopenia is the result of decreased production of platelets
and shortened platelet life span
Symptoms:
 High fever
 Labored breathing
 Pounding heartbeat
 Exhaustion
 Signs of anemia
Clinical signs:
Three clinical syndromes acute, chronic and in apparent
 Acute symptoms
 may be mild to severe (hemorrhage)
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Depression, anorexia, weakness, weight loss, fever, jaundice, petechial
hemorrhages, ventral and limb edema
 Affected animals are usually thrombocytopenic with sideroleukocytes
present in peripheral blood
 Initial attack is followed by death or recovery and the development of
the chronic or in apparent stage
 Chronic symptoms
 Associated with recurrent episodes of viral replication
 Signs similar to those seen with the acute phase however with less
severity
 Weight loss, anemia may become progressively worse
 During attacks of clinical disease, viremia is very high and the horse
blood is very infectious
 Inapparent Infection
 Most affected horses show no clinical signs but have increase globulins
 Viremia is low
 Affected horses often remain in apparent carriers for life
 Can act as reservoirs of infection
Differential diagnosis:
 Differential diagnosis depends on presenting clinical signs
 Anemia/thrombocytopenia
o Blood loss
o Red maple intoxication (tend to see thrombocytopenia due to a
toxin inside the red maple)
o Immune mediated thrombocytopenia/hemolytic anemia
(associated with other disease entities but there are toxins and
other disease states that cause this)
o Neoplasia
 Fever
o Viral bacteria, inflammatory diseases
o Neoplasia
 Weight loss
o Inadequate feed intake
o Dental abnormalities
o Parasitism
o Neoplasia
o Other chronic diseases
 Ventral edema
o Hypoalbuminemia
o Pleuropneumonia
o Vasculitis
o Neoplasia
o Protein-losing enteropathy
o Peritonitis
 Ataxia
o Wobblers syndrome
o EHV-1 Myeloencephalitis
o
o
o
o
o EPM
Diagnostics:
 Serologic testing—AGID (coggins testing) most widely used test—a federal
accredited vet must administer coggins test
 95% accuracy
 Acute infection produces detectable antibodies in 45 days
 ELISA testing more sensitive than AGID
 All horses testing positive with either test should be retested for confirmation
 If positive coggins run an ELISA and another Coggins three weeks later
 Reportable disease
Pathologic findings
 Horses that die during a febrile episode will commonly show the following on
necropsy:
 Splenomegaly
 Hepatomegaly
 Lymphadenopathy
 Mucosal and visceral hemorrhages
 Vessel thrombosis
 Ventral edema
 Accumulations of lymphocytes and macrophages in the periportal regions of the
liver, spleen, lymph nodes, adrenal glands, lungs and meninges
 Fatty degeneration of liver and hepatic cell necrosis
 Glomerulitis possibly
 In apparent carriers
 Necropsy findings are unremarkable
Treatment:
 None
 Euthanize the horse or have it permanently quarantined
 Prevent with coggins test which is a blood test determining disease carriers
 Test required to transport, show or sell a horse
 Test should be updated yearly
 Good nursing care during clinical episodes
 Blood transfusions in horses with severe anemia or thrombocytopenia
Prevention:
 Require coggins testing yearly
 Reportable disease
 Horses are either euthanized or must be quarantined away from non-infected
horses
 Slaughter or research facilities—USDA approved
 No public health risk
 Send coggins test results to OIE: Test results are valid for six months
 Any imported horses are mandatorily tested for coggins and must be coggins
negative
 Horses on racetracks should all have negative coggins tests
 If we are doing a quarantine period horses have to be isolated 200 yards
(600ft)—they figured the biting flies can and would only fly (600ft)—so if state

allows you to keep an EIA positive horse it has to be the this far away from the
other horses
o Fun Facts
 Since they initiated mandatory coggins test in 1972 seropositive horses in US
range from 5-20%--since they initiated this mandatory test it has gone down to
0-1%
 Reportable to OIE
West Nile Virus
o Etiology:
 Belongs to family flavivirus
 Genus flavivirus contain approximately 70 viruses that are transmitted by ticks
or mosquitoes
 Flavivirdae—WNV and JEV are single stranded RNA viruses
o Epidemiology:
 Vector-borne dzs with transmission occurring to avian and mammalian hosts
from blood-sucking mosquitoes
 Virus is either maintained or cycled between vectors and biologic amplification
occurs within the vector species
 Birds are best sentinel source (primary nonarthropod reservoir) (2 weeks before
you see it in horses you see it in birds usually)
 Horses and humans are “dead end” hosts and do not amplify the virus in
sufficient quantities to infect mosquitoes
 Additional modes of transmission include oral ingestion in both avian and
mammalian horses, oral and cloacal shedding in birds (Alligators have found to
have high titers for west nile and they actually do shed it)
 WNVF may be transmitted through contaminated blood transfusion or organ
transplantation if donors are viremic
 Vertical transmission has occurred through placenta and milk
 Spread and yearly occurrence of WNV coincides with the availability of vectors
and reservoir hosts with transmission potential
 Outbreaks are seasonal and reflect mosquito activity
 Culex sp of mosquito are considered the primary mosquito vector for WNV
 Northeastern USA-culex pipens
 Western USA-culex tarsalis
 Woutheastern USA-culex quinquefasciastus and Culex nigrapalpus
 Culex pipens and Culex salinarus are LIKELY THE MOST IMPORTANT
VECTORS IN TRANSMISSION OF WNV IN THE HORSE
o BOTH CULEX SP ARE VARIABLE FEEDERS (will feed off of horses,
dogs, cats anyone)
 Reservoir host is one in which a pathogen is amplified in vivo so that it can be
transmitted to a vector species
 High levels of viral amplification occur in many bird species especially
Passeriformes (songbirds) and charadriformes (shorebirds)
 The house sparrow is considered the most important amplifying host for
WNV

o
o
Crows are more competent vectors—they have a higher viremia and
mortality rate than sparrows-thus sparrows have a longer periods of
infectivity
 Gamebirds and parrots develop the lowest levels of viremia
 Corvids (crows) develop high viremia with very high mortality rates
 Corvid susceptibility to WNV is an important indication of local activity dead
birds counts are imp surveillance tool
 Occurrence in people and horses reflect vector activity
 Seasonal in temperate regions
 Year round in subtropical and tropical regions
 Intense virus activity in the U.S. begins in july with peak incidence in sept and
oct
 Older people are more susceptible to neuroinvasive dz from WNV and JEV. This
is true in horse also
 Men are more frequently affected than women
 In horses there is no breed or gender predilection
 Potential new hosts for WNV in NA include the gray squirrel, brown bat, eastern
chipmunk, eastern striped skunk, white tailed deer, brown bear
 Alligator have extremely high titers of viremia and may be important reservoir
 Cloacal shedding of virus has been demonstrated
 Dogs and cats have a natural infection
Pathogenesis:
 Initial WNV replication occurs in langerhans dendritic cell sand spread to lymph
nodes, monocytes, and blood stream and end up with viremia
 In bird the kidney and brain are predilection site
 In mammals the spleen and kidney affected before brain
 In horses virus in neurotropic and penetrates in CNS with little affect on other
organs
 Horses- some viral replication takes place in intestines
 In brain WNV stimulates inflammation causing clinical signs
 Neuro dz in horses show changes in mentation spinal cord abnormalities and
cranial nerve deficits of hindbrain
 Behavior changes may be related to viral infection of the thalamus,
medulla and pons
 WNV induced motor deficits are multifocal asymmetric and primarily
characterized by weakness and ataxia
 Ataxia and weakness can be due to problems in spinal cord and interruption of
motor tracts in hindgrain and loss of fine motor control
 WNV is also characterized by involuntary skin and muscle fasciculations, tremors
and hyperesthesia attributable to loss of fine motor control through infection of
the basal ganglia
 Two routes of neuroinvasion proposed:
 WNV causes a low level viremia, followed by replication in the lymph
nodes and entry into the CNS across the BBB
 Transaxonal transmission
Clinical signs:
o
o
o
o
o
o
 Approx 10% of infected horse show fever and neuro symptoms like ataxia head
pressing muscle fasciculations hyperesthesia depression and recumbency
 Illness typically lasts 1-3 weeks
 Many horses improve in 3-7 days of displaying clinical signs
 If the horse demonstrates signification improvement full recovery within 1-6
months can be expected in 90% of patients
Diagnostics:
 No pathognomonic signs distinguish WNV infection in horses from other CNS
disease
 Ancillary testing should include CBC/serum chemistry and CSF analysis
 Dead bird surveillance is one of the best predictors—usually give a 1-2 week
warning of first human or equine cases
 WNV specific IgM capture ELIZA test (MAC-ELIZA)
 4-fold change in paired neutralizing antibody titers is confirmatory of WNV
infection in non-vaccinated horses-plaque reduction neutralization test
 Postmortem detection of WNV
 PCR
 Culture of CNS tissues
 Immunohistochemistry
Diff Diagnoses:
 EEE, WEE (alphavirus infections)
 Rabies
 EPM
 EHV-1 neurologic dz
 Botulism
 Verminous meningoencephalomyelitis
 Leukoencephalomalacia
 Intoxication
 Hepatoencephalopathy
Pathology:
 Polioencephaloymyelitis (inflammation of gray matter)
 Hemorrhage
 Perivascular cuffing with mononuclear cells
 Lesions may extend from basal ganglia of cerebral cortex of the sacral spinal
cord
Treatment:
 Supportive
 Fluid therapy, anti-inflammatories, DMSO, anti-protozoals if in areas with
sarcocystis neurona and until EPM is ruled out
 Antibiotics for 2ndayr infection (recumbent horses get pneumonia)
 Tranquilization
 Keep horses quiet in deeply bedded stalls (large amounts of straw and hay
underneath to absorb and soak away moisture, sweat, urine)
Prognosis:
 In horses with clinical signs mortality is 20%-40%
 Death is likely in recumbent horses
 Non-vaccinated horses and older horses are greater risk of dying
Prevention:

 Vaccination—3 vaccines available
 Inactivated whole virus (killed) west nile innovator fort dodge
 Recombinant canarypox vaccine recomitek equine WNV merial (pulled
because horses developing dz from vax)
 Flavivirus chimera vaccine prevenile intervet/schering plough
 Killed vaccine prevents viremia in >90% of vaccinated horses vaccination
may or may not protect against mortality
 Recombinant canary pox vaccine gives better than 90% protection
against severe clinical signs and apparently complete protection against
mortality protection against viremia lasts up to a year
 Flavivirus chimera vaccine requires a single initial vax and provides
partial protection against dz as early as 10 days post vaccination.
Between 1-12 months post vaccination there is better than 90%
protection against severe signs and complete protection against viremia
or mortality
 In controlled comparative trial with horses experimentally challenged 12 months after being vaccinated all vaccines protected against death
and reduced the severity of signs
o Killed vaccine was significantly less effective than either live
vaccine in preventing clinical signs
o The flavivirus chimera vaccine was most effete in preventing
clinical signs (SHE WOULD USE THIS ONE)
 Mosquito control
 Stabling from dusk to dawn
 Use of smudge pots
 Mosquito repellants (deet and permethrin)
o Public health concerns:
 WNV is a zoonotic dz
 Infection can result from direct contact with infected tissue postmortem
Equine encephalomyelitis
o Etiology:
 Blind staggers or sleeping sickness
 Is an infectious disease affecting the horse’s brain
 Found in 3 forms
 Eastern
o Occurs most frequently
o Has highest mortality rate
 Western
 Venezuelan—central and south America and some part of Texas
 Caused by virus
 Carried by bird, reptiles and rodents
 Transmitted by mosquito from host to horse
 Occur from mid-summer to frost except for Venezuelan
 Venezuelan is most zoonotic
 EE, VEE, and WEE are encephalomyelitides that are present in North and South
America
 Considered arthropod borne viruses (arbovirus)




o
WEE, EEE and VEE are members of the alpha virus family-ss RNA enveloped
WEE, VEE and EEE are new world virus and only found in N and S America
All three viruses coexist in Argentina
Life cycle of equine alphaviruses involves transmission between birds or rodents
and mosquitoes
EEE
 Epidemiology:
 Wide geographic distribution from eastern Canada throughout the
Caribbean and Central and South America
 Primarily found in SE USA in all states east of the MS
 Most cases occur in Northern FL and the Carolinas
 No breed or sex predilection
 Younger and geriatric more at risk
 Occurrence of the human dz is sporadic (approx 10/year)
 In NA, EEE virus is perpetuated in a cycle b/w passerine birds and the
Culiseta melanura mosquito
 Birds do not develop the dz but a high level of viremia that allows
transmission of the virus to feeding mosquitoes (DON’T DIE)
 Culiseta melanura is not a mammalian feeder and is not responsible for
transmission between birds and mammalian hosts
 Several species of mosquitoes that feed on both birds and mammals act
as biologic vectors. Transmitting the disease to both horses, humans
and other vertebrae species.
 Culiseta melanura does not breed readily in south Florida or Caribbean
therefore it is not seen as an endemic disease in these areas
 Outbreaks in these areas can be attributed to influx on viremic
migratory birds to the area providing a source for secondary vectors
 EEE was first identified in Connecticut in 1937 following the intro of the
rink neck pheasant—since then disease has occurred in sparrows,
pigeons, chukar partridges, and pekin ducks
 Ss RNA, togaviridae, alphavirus
 Implicated in the exotic bird like emus and ostriches (causes fatal colitis)
 EEE has been the cause of disease outbreaks in swine and isolated cases
of cattle, sheep and non domestic ungulates
 Outbreaks of EEE in horses and or people are seen in mosquito infested
areas closest to swamps or poorly drained wetlands
 In temperate climates, infection builds during spring and summer in
mosquitoes and birds, leading to outbreaks in horses and humans in late
summer and early fall
 Symptoms:
 Noticeable five days after infection
 Beings with fever (103-104 or higher) and depression
 Becomes severe diarrhea, a drowsy appearance, no desire to move, self
mutilation, hyperexcitabilty, irritability, refusal of food and water,
uncoordination, head pressing, circling, paralysis and coma (these last
four usually mean dead horse)
 Results in fatality two to three days after first signs appear
o
 Clinical signs:
 No clinical signs, fever and transient viremia, fever and CNS signs
o CNS sings include blindness, head pressing, hyperexcitability,
depression
o Spinal cord lesions-ataxia weakness
o Incidental signs-colic like symptoms
o Mortality rate is high
 Pathology:
 Diffuse infiltration of the gray matter (polioencephalomyelitis) with
neutrophils, vasculitis, with thrombus formation (after two days get
polioencephalomyelitis)
 Diffuse bilaterally symmetrical changes within the spinal cordperivascular cuffing, gliosis and neuronal degeneration
 Visceral organs-mutlifocal areas of coagulative necrosis and vascular
changes in the heart and GI tract
 Hemorrhage
 Diagnostics:
 Geographic location SE part of us known hot spot for EEE
 Late season (late summer/early fall) with unusually high mosquito
population
 Horse has fever neurologic symptoms (febrile stage is short and easily
missed)
 Lab tests
o IgM capture ELISA for EEE antibody-if positive indicates
exposure for vaccination if vaccination should also contain IgM
antibody for WEE as most vaccines are multivalent
o Acute cases-hemagluttination inhibition
o Virus neutralization
o Seroconversion in paired serum samples collected 10 days apart
o Brain of dead horses can be tested using immunohistochemistry
or culture
 Treatment:
 Supportive
 No known antiviral drugs available for use
 Prevention:
 Vaccination yearly or twice a year in endemic areas
 Pregnant mares should be boostered 4-6 wks prior to foaling
 Vaccinate foals at 4 months then again at 10 months
 Much cheaper to vaccinate ($7) then to tx ($4000)
Western Equine Encephalitis (sleeping sickness)
 First described in 1930 active in North South and Central America
 Periodically cause large outbreaks of dz in horses and humans
 In NA occur in Midwestern areas—Texas to California and North to Montana,
North Dakota Saskatchewan and Manitoba
 Transmission:
 WEE is an arbovirus (arthropod borne) normally cycles between and
infects birds and several mosquito species particularly Culex tarsalis








Cx tarsalis is the primary vector that maintains WEE virus in cycle with
birds, especially nesting passerines
 Cx tarsalis population favored by a rapid inc in temp following a cool
wet spring
 This species ahs a predilection for irrigated fields as breeding grounds
 Other mosquito species become infected during summer and transmit
the virus to other birds and mammals—usually inapparent infections
 This results in the virus becoming established in other species of
mosquitoes with host preferences other than birds
 Horses infected with the WEE do not produce viremia high enough to
infect mosquitoes
 Infected mosquitoes develop chronic infections whereas bird develop a
severe viremia that lasts for less than a week
 Amplification occurs in the bird-mosquito cycle during warm months
and infection spills over into small mammals—rabbits and snakes
 Virus continues amplification in these species and infects mosquitoes
leading to human and horse infection
 Viremia in humans and horses is transiently and is usually gone before
clinical symptoms are seen
 SEE PICTURE OF AMPLIFICATION THAT SHE GAVE US IN NOTE PACKET
Clinical signs:
 Similar to those in EEE
 Depression ataxia weakness and recumbency in advanced cases
 Mortality rate lower
 Clinical course of dz is usually 2-14 days all horse affected with EEE die
horses with WEE and VEE are more likely to survive
Pathogenesis:
 Following the bite of an infected mosquito WEE, EEE or VEE the regional
lymph node is the site of viral replication
 Viruses cause encephalitis after hematogenous or neuronal spread
 Immunity after in apparent infection and clinical dz is long lasting in all
species
 Horses infected with EEE and WEE do not excrete infectious virus and
recovered animals are not persistently infected with virus
Diagnostics:
 Tissue culture
 PCR
 In living animals—measure anti-WEE IgM capture ELISA
Differential Diagnosis:
 Rabies, WNV, leukoencephalomalacia, hepatic encephalopathy
Treatment:
 Supportive-many horses who survive have residual neurologic deficits
Prevention:
 Vaccination
 Strict control of mosquitoes
 All equine cases should be reported to state health officials
Zoonotic potential:
o
o
WEE and EEE no virus amplification in affected horses—dead
end host
VEE
 Epidemiology:
 Responsible for outbreaks in humans and horses over large geographic
regions
 Two transmission cycles
o Enzootic cycle—centers around wild rodents (rates) that carry a
high infection rates and can develop viremia sufficiently large
enough to infect mosquitoes
 Culex cedecci is the most important vector for enzootic VEE
 It lives in tropical forests and swamps feeding on small forests mammals
 Activity for this mosquito peaks with high ambient temperatures and
rainfall
 Similar to EEE and WEE
 Togavirus, alphavirus
 Certain strains of the enzootic VEE virus I-E, II, and IV are low
pathogenicity for equids and do not result in high levels of viremia
 First recognized outbreak of VEE in equids occurred in 1935
 Outbreak in 1960 resulted in death of 50000-100000 equids and
affected roughly 25000 people
 Equine case fatality rate is approximately 90%
 High mortality rate
 Epizootic transmission
o Associated with variable equine mortality rates 20%-85%
o Efficient amplification of the virus in equids is the hallmark of
epizootic VEE
o Human disease has never been demonstrated in the absence of
equine disease
 All mammalian hosts are capable of developing a high titer viremia for
up to 5 days, but the horse I considered the most important host in
terms of vector capacity
 In contrast to WEE and EEE where the horse is not considered the major
source of virus for the vector
 In VEE epidemics, horses are the most important amplifiers of virus
activity
 Several sp. of mosquito are known to be naturally infected with the VEE
virus
 Virus has also been isolated form culicoides sp
 The majority of people affected with VEE develop signs within 1-4 days
 Most common symptoms are fever, chills, headache, muscle pain
 Neurologic symptoms may something develop in children
 Epizootics die out as infected mosquitoes decline—
o Death of natural amplifiers—equids
o Developing immunity of equids from infection or vaccination
o Use of insecticides
o
o

Various strains of VEE can be differentiated based on molecular
biology, serotype and pathogenicity for small mammals
Epizootic strains usually kill mice and guinea pigs whereas
enzootic strains may or may not kill small mammals
 Clinical Signs:
 Horses earliest sign is fever
 Nervous signs usually develop towards the end of the febrile period
o Include depression, droopy ears, aimless walking,
hyperexcitability, foot stomping, goose stepping, circling,
weakness, base wide stance, involuntary lateral recumbency,
and leg paddling
o Pregnant mares may abort
o Death usually occurs within 24-48 hours after the onset of
clinical signs
 Public health concerns:
 Alpha viruses are pathogenic for people but require a vector for
transmission to occur
 The horse does not develop a sufficient level of viremia in EEE and WEE
to act as reservoir or amplifying host for these viruses
 In VEE, the horse is considered the most important species for
amplification of the virus in epizootic VEE
o Control measures should include mosquito control, restricted
movement of horses, vaccination of all susceptible equids
o Blood and tissue from infected equids should be handled as
infectious biohazardous material
 Diagnostics:
 IgM antibody against VEE
 Virus culture of brain and spleen tissue
 Pathology:
 In horses the brain but not the spinal cord are commonly affected
 Perivascular cuffing with lymphocytes and macrophages, neuronal
death, gliosis
 Prevention:
 Vaccination with a live attenuated VEE vaccine
 Efficacy is reduced by prior vaccination with killed EEE, WEE vaccines
 Killed VEE vaccine is available in combination with EEE, and WEE vaccine
is effective
 Treatment and Prevention:
 Unknown cure
 Place horse in well-shaded padded area
 Force food and water into horse
 Can lead to mortality, results in mortality are extremely high
 Perform immunization and mosquito control
o Immunization lasts 6 months and needs to be repeated yearly
Potomac Horse Fever
o Diarrhea
o Can be associated with infectious and non infectious etiologies
o
o
o
o
o
o
o
o
In adult horses is usually associated with large colon and /or cecal dysfunction
May be associated with mild consequence and good prognosis or have a fatal
outcome
Usually classified as acute or chronic based on duration of clinical signs
Five mechanisms of diarrhea:
 Malabsorption—caused by a decrease n the absorptive capacity of the colon
 Secretory-caused by increase water and solute secretion
 Diarrhea cased by abnormal motility—decreased transit time
 Osmotic-caused by an increase in somatically active ingredient sin intestinal
lumen. Grain overload
 Diarrhea associated with increase blood to the lumen hydraulic pressure or
decrease plasma oncotic pressure, congestive heart failure and
hypoproteinemia
Synonyms:
 Shasta river crud
 Equine intestinal ehrlichiosis
 Equine monocytic ehrlichiosis ** (the one that Bellamy used to use)
 Equine ehrlichial colitis
Etiology:
 Neorickettisia ristici
 Gram negative coccus, organism tends to occupy one side of the cytoplasm
rather than being distributed symmetrically
 Organism found in membrane bound vaccule consisting primarily of
macrophages and glandular epithelial cells of equine intestine
 Org is rarely observed in peripheral blood monocytes
 N. risticii occurs in two forms
 singly
 In groups
Epidemiology:
 First recognized along Potomac river in 1979
 PHF is known to occur in 43 states and in 3 Canadian provinces, south
America, and Europe
 Disease typically occurs near freshwater streams, rivers and on irrigated
pastures usually during middle or late summer (may-nov)
 Neorickettsia are associated with certain trematode species: it appears that
disease transmission is by accidental ingestion of aquatic insect larvae
(Caddis flies, Mayflies) or freshwater snails (genus: Juga yrekaensis) which
contain the infective organism
Pathogenesis:
 After natural or experimental transmission, N. risticcii infects blood
monocytes
 It avoids the hosts’ defense mechanisms by inhibiting lysosomal fusion with
phagosomes (prevents phagocytosis)
 N. risitcii has an affinity for the intestinal wall especially the colon
 Colonic epithelial cells, mast cells, and tissue macrophages are the targets of
infection
 Lesions are confined to the gastrointestinal tract:
o
o
o
o
o
o
o
Resultant diarrhea is caused by loss of epithelial cell microvilli,
reduction in electrolyte transport and increase intracellular
cyclic adenosine monophosphate in infected intestinal cells
Clinical signs:
 Typically one or two horses per year on high risk pastures develop the
disease
 Disease is only seen when viable insect or snail vectors are present
 Clinical signs similar to salmonella
 Incubation period is approx 1-3 wks
 Initial presentation, depression, anorexia, high fever (102-107)
decreased barborgymi can be auscultated at this time
 Within 24-48 hours moderate to severe diarrhea seen
 Severe toxemia and dehydration may be seen
 Laminitis occurs approx 40% of affected animals
 Fatality rate are 5-30% and avg 10%
 Abortion may occur months after infection
Diagnostics:
 Serologic testing of acute and convalescent serum samples collected 10
days apart a 4 fold increase in titer is proof of infection
 PCR
 Provisional diagnosis is based on clinical signs and response to tetracycline
therapy (KEY METHOD)
 Culture of blood and feces from affected horses
Differential Diagnosis:
 Peritonitis, salmonellosis, clostridial diarrhea, intestinal ileus due to
obstruction or displacement
Pathologic findings:
 Distended large colon and cecum filled with watery contents
 Mucosal hyperemia and ulceration and areas of necrosis and hyperplasia of
lymphoid follicles and lymph nodes
 Changes in aborted fetuses are characteristic for PHF:
 Have increase volume of feces within the small and large intestine
 Liver discoloration
 Lymphohistiocytic enterocolitis
 Periportal hepatitis
 Lymphohistiocytic myocarditis
 Severe splenic inflammation characterized by lymphoid necrosis and
lymphohistiocytic infiltration
 N risticii can be recovered from bone marrow, spleen, lymph node ,
colon and liver
Treatment:
 IV administration of oxytetracycline (6.6-7 mg/kg SID or BID) for 4-5 days
 LOOK UP HOW TO TREAT WITH DOXYCYCLINE!
 Response to tx is usually seen in 24-72 hours of therapy-indicated by
decrease in temperature
 Supportive fluid and electrolyte therapy. Therapy to prevent laminitis
Prevention:

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
Natural infection results immunity up to 2 yrs
Limiting access to fresh water rivers and streams during peak periods
Reducing number of snails
Vaccination at least one month prior to PHF season
 Vaccine is inactivated, whole cell vaccine
 Vaccination series should include 2 injections administered 4 weeks apart
thereafter horse should be vaccinated at 4-6 month intervals
 Vaccine has been reported and is attributed to antigenic and genomic
differences among N. risticii isolates
 Vaccination does not prevent abortion
 No public health concerns—not zoonotic
Equine Protozoal Myeloencephalitis
 Disease caused by a protozoan affecting the muscles of the central nervous
tissue
 A neurological disease in equines of any age, sex or in any location throughout
the U.S.
 Is not communicable; horse is a dead-end host
 Is often consumed with lameness (lameness does not improve even with tx)
 EPM first identified 1964
 Initially attributed to toxoplasma-like organism
 Organism finally isolated and identified in 1991
 Sarcocystis neurona
 Commonly diagnoses neurological disease in US
 Most cases reported East of the MS river
 All breeds of horses are susceptible
 Most affected individuals are young to middle aged
 No sex predilection
 Serologic studies show high rate of exposure with only a small percentage of
horses showing clinical symptoms
 Clinical signs vary depending on the location of the parasite and lesions in the
nervous system
o Etiology:
 Sarcocystis neurona is most common etiologic agent, Neospora hughesi has
been implicated in some clinical cases
 Definitive host for S. neurona is opossum
 Opossum become infected through ingestion of mature sarcocysts containing
bradyzoites in tissues of intermediate hosts like the raccoon, nine banded
armadillo, domestic cat and sea otter
 Sarcocystis neurona has both sexual and asexual stages
 The sexual reproduction stage occur in the opossum
 Asexual reproduction and completion of natural cycle occur in intermediate
hosts
 Sporocysts passed in feces of opposums contaminate feed and water
 Horses consuming the contaminated feed and water become infected
o Pathogenesis:
 Horse is considered a “dead end” host and unable to transmit the disease to
another horse
o
o
o
o
 After ingestion of sporocysts from opossum feces, S. neurona replicates in the
equine intestinal epithelial cells
 Cell-associated parasitemia provides the parasites with access to visceral and
CNS tissues, where they undergo asexual reproduction
 After hematogenous spread, S. neurona may localize in any area from the
cerebrum to the spinal cord
 It is found in peripheral nerves
Symptoms:
 Horse is uncoordinated on one side
 Horse suffers from seizures, muscle atrophy (gluteals—can be bi or uni lateral),
and facial paralysis (indicated by droopy lip or atrophy of one half of the tongue)
 Infected horses may not show symptoms
Clinical signs:
 Organism causes localized inflammation
 Neurologic signs depend on the location and severity of the affected areas of
the CNS
 Ataxia
 Weakness
 Spasticity
 Dysmetria
 Onset of the disease may be acute or insidious. Signs may progress rapidly or
remain stable for several months.
 Asymmetrical muscle atrophy involving the gluteals and quadriceps muscles is
most common
 Cerebral signs are uncommon (seizures are uncommon)
 Depression
 Head tilt
 Facial paralysis
 Difficulty swallowing
 Dementia
 Initial spinal cord lesions may be confused with lameness (almost every neuro
exam has a lameness exam that occurs simultaneously because some of these
mimic each other)
Differential Diagnosis:
 Equine Degenerative Myopathy (MOST COMMON DIFFERENTIAL)
 Equine herpes encephalomyelitis-sporadic or herd problem, acute onset
followed by improvement
 Equine motor neuron disease-weight loss, trembling progressive (2nd most
common differential)
 Rabies-always consider, variable signs but particularly weakness, loss of
sensation, recumbency, fever, and death in 7 days
 Traumatic spinal cord injuries
Ancillary tests:
 CBC/Chem usually unremarkable
 CSF analysis usually normal (atlantoocciptial is supposedly more diagnostic than
the lumbosacral but it is more dangerous)
o
o
o
 Serology—helpful for ruling out viral or bacterial causes of CNS disease (helpful
to rule out sleeping sickness, west nile virus, and herpes)
Diagnosis:
 Based on ruling out other cause of CNS disease, lameness, observation or CNS
symptoms compatible with EPM and positive results of immunodiagnostic
testing
 Tests can be performed on either CSF or serum
 A serum sample positive for S. neurona indicates exposure to the
parasite but not necessarily active disease
 A positive CSF sample likely indicates CNS infection and active
production of antibodies
 Three types of tests available: (1. immunofluourescence (IFA)—thought
to be more accurate than western blot, 2. western blot—most labs runt
his test, 3. PCR—said to have high specificity and low sensitivity—PCR
for EPM is dependent on the presence of intact parasite DNA this
becomes problematic because we know EPM causes a very strong
inflammatory response which actually degrades the DNA—we could
have a horse that is positive for tissue biopsy of EPM but comes back
negative on PCR)
Pathology:
 Gross lesions of the brain seldom present
 Lesions more commonly present in the brainstem and spinal cord
 Gross lesion consist of multifocal areas of hemorrhage
 Microscopic lesions
 Hemorrhage
 Nonsuppurative inflammation
 Small areas of necrosis
 Perivascular cuffing with mononuclear cells (seen in all neuro infectious
dz)
 Giant cells, gitter cells and eosinophils may be seen in inflammatory foci
and in the meninges overlying the lesion
Treatment:
 Administer anti-protozoan drugs to kill the protozoan
 Practice anti-inflammatory therapy: about 60% of horses respond to therapy
 Use vitamin-E and folic acid supplements in treatment
 Antiprotozoal drugs
 Deroprim: First drug to successfully treat EPM were pyrimethamine and
sulfonamides. This combination interferes with the folate metabolism
of S. neurona
o Requires several months of treatment
o USDA approved drug combination rebalance
o Can cause anemia
o Fetal losses
o Fetal abnormalities of the neural tube
o Dosage 20mg/kg of the sulfadiazine and 1mg/kg of
pyrimethamine once daily
o Can cross BBB


Ponazuril is a triazinetrione (Marquis)
o Acts by inhibiting the respiratory enzymes of a S. neurona
o Dosage: 5mg/kg for 28 days
o Anti-coccidial activity against many parasites
o Toltrazuril is the parent drug, has activity on the mitochondria
and respiratory chain
o Able to cross the BBB
o Adverse affects include skin rashes, blisters on the skin and
nose, loose feces, and mild colic
 Nitazoxanide (Navigator) is a thiazolide antiparasitic agent with activity
against a wide variety of protozoa and helminthes
o Not used as widely because it has some severe adverse affects
o Navigator—IDEXX
o Rapidly metabolized in horses to the active metabolite,
acetylnitazoxanide
o Antiprotozoal activity is a result of interference with pyruvate
ferredoxin oxidoreductase enzyme-dependent electron transfer
reactions essential to anaerobic energy metabolism
o Approved for treatment of giardia and cryptosporidium
o Dosage 50mg/kg for 28 days
o Adverse effects include diarrhea, fever, depression, laminitis,
head and limb edema , increased water consumption
o Stallions are more prone to develop laminitis
 Prognosis:
 60% of affected horses show improvement of one neurological grade
 Mildly affected horses have a chance of complete recovery
 Relapses occur in about 10% of horses
 Prevention:
 Avoid feed contamination by opossums, intermediary hosts
 Remove spilled grains, cat food bird feed and carcasses of dead rodents
 Vaccine (fort dodge)
o Killed merozoites of S. neurona
o Received conditional approval by USDA
o Safety of vaccine established but not efficacious
o Vaccine no longer available (NOT EFFECTIVE)
Equine Influenza
o Equine influenza is endemic in horse population although Iceland and New Zealand are
currently free of the disease. Australia had their first outbreak in 2007
o It is most economically important contagious respiratory disease of the horse (CAN BE
UP TO 100% morbidity)
o All horses are susceptible with young horses (1-3 years) being the most often affected
o Affects the respiratory, musculoskeletal and cardiac systems (muscle and cardiac
involvement are rare)
o Etiology:
 Influenza A viruses are members of the orthomyxoviridae family-enveloped
viruses with segmented, ss negative sense RNA
o
o
o
o
 There are two very important glycoproteins associated with the influenza virus
*****
 HA-hemaglutinin-serves as the viral receptor-binding protein and is
responsible for fusion between the virion envelope and the host cell
o HA is the major target of the host immune response, it is also
responsible for the viruses ability to mutate (antigenic drift)—
why we can’t get rid of it
 NA-neuraminidase—facilitates the mobility of the influenza virus by
removing sialic acid residues from viral glycoproteins and infected cells,
thereby allowing the escape of the budding virus particles
 Equine influenza infections have been restricted to virus H7N7
(A/equine/1) and H3N8 (A/equine/2) subtypes.
Pathogenesis:
 Inhalation of aerosolized virus particles allows deposition of viral particles
throughout the respiratory tract
 The virus enters the epithelial cells lining the respiratory tract replicates and is
released into the airways
 Infected cells undergo apoptosis
 Rapid spread of virus causes desquamation and denudation of respiratory
epithelium and clumping of cilia
 This results in impaired mucocilliary clearance—this may persist for 4 weeks
post infection
 Secondary bacterial infection are common
Epidemiology:
 It is the most frequently diagnosed viral respiratory disease of horses
 Endemic in NA and Europe
 Outbreaks occur among large groups of susceptible horses, most often young
racehorses
 Prevalence of the disease is dependent on the age of the animals affected and
their previous exposure to the virus
 Morbidity may approach 100% during an outbreak
 Horses typically shed virus for 6-7 days post-infection
 Carrier states do not exist, however subclinical infection with shedding can
occur
 Two antigenically distinct but related influenza A viruses thac o-circulate in
horse populations in Europe and NA
Clinical signs:
 1-2 day incubation period
 Coughing, serous or mucopurulent nasal discharge especially in cases of
secondary bacterial infection
 Fever
 Anorexia, depression, limb edema, conjunctivitis, epiphora, submandibular
lymphadenopathy, muscle stiffness and soreness
Diagnostics:
 Based on classic clinical signs
 Virus isolation from nasopharyngeal swabs/washings-virus may be shed for up
to 10 days
 ELISA-Directigen Flu-A test-detect disease within 20-30 minutes-human test
o
o
o
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 Reverse transcriptase-PCR from nasopharyngeal swabs/washings
 Seroconversion-4 fold increase in antibody titer between acute and
convalescent samples taken 10-14 days apart
 HI, VN, SRH (single radial hemolysis)-best used to detect level of antibodymediated immunity provided by vaccination
Differential Diagnosis:
 EHV-1, EHV-4, EVA, Streptococcus equi sp
 The rapidity by which this disease spreads helps distinguish this respiratory
infection from other causes
 Coughing is less common in EHV, EVA and Streptococcal infections
 Lymphadenopathy associated with Strep equi infections is more marked than
that associated with Equine Influenza
Pathology:
 Pharyngitis, laryngitis, tracheitis
 Bronchitis, bronchiolitis
 Interstitial pneumonia, pulmonary congestion (hallmark), edema and
neutrophilic infiltration
 There is limited mortality associated with equine influenza
 Myocarditis is rare finding
 Neonatal infection can result in severe fatal bronchointerstitial pneumonia
(rare)
Treatment:
 Isolate infected animals to prevent spread
 Most affected animals recover from infection within 3 weeks
 Horses should be housed in well ventilated but protected shelters
 Stall rest is especially important until the respiratory epithelium have healed
(one week of rest for every day animal is febrile is rule of thumb)
 Early return to exercise is associate with delayed recovery and the development
of myocarditis
 Antiviral drugs: amantadine and rimantidine have been tried-inhibit viral
replication by blocking ion channel activity of the M2 protein
 Amantidine and rimantidine have antiviral action against all serotypes of
Influenza A virus.
 Amantidine has limited and variable bio-availability when administered to
equine patients orally
 IV administration at 10mg/kg q 8 hrs or 5mg/kg q4 hrs were much more
effective at giving high plasma levels of the drug
 Amantadine is associated with adverse CNS problems-seizures and acute death
 Rimantidine (30mg/kg q 12 hrs PO) is associated with higher plasma
concentrations, better bio-availability and no adverse effects
 Both drugs are associated with development of drug resistance
Prevention:
 Vaccination
 Killed influenza vaccines and MLV vaccines (administered intranasally)
 Following vaccination with MLV protection, it protected horses from
inhaled equine influenza virus

o
Killed vaccines maybe just as effective, however, some studies indicate
that killed products efficiency wanes in approximately 6-12 months
following vaccination
 Vaccination is recommended at 4-6 month intervals in susceptible
populations
 Vaccination can reduce morbidity but does not prevent the disease
 Restrict movement in and out of the premises at first sign of infection
 Isolation of new horses for a minimum of 4 weeks before introduction into the
general population
 Vaccinations should be completed at least 2-4 weeks prior to introduction to the
isolation facility
 Do not share grooming, cleaning or feeding supplies
 Take care of healthy animals prior to treating sick animals or have specific
personnel assigned to sick animals only
 Immunity up to 12 months occurs following natural infection
Public health concerns:
 Influenza A infects a wide variety of species including humans
 Equine influenza has not been shown to infect humans, however dogs have
been infected (racing greyhounds)
 Equine influenza may cause pregnant mares to abort
 Rhodococcus Equi
o
o
Etiology:
 Major cause of disease in foals 3 weeks to 6 months of age
 First described in horses in 1923
 Common clinical manifestation in pyogranulomatous pneumonia
 Infrequently may cause disease in adult horses-however usually associated with
immunosuppression
 Has been isolated from other species-dogs, cats, crocodiles, camelids
 Has been associated with humans infected with the HIV virus
 VERY ZOONOTIC!
 Formerly known as corynebacterium equi and mycobacterium equi
 Facultative intracellular organism
 Pleomorphic gram-positive organism with a rod-coccus life cycle
 Aerobic, nonmotile asporogenous partially acid-fast
 Favors a neutral pH 7-7.5 and the presence of horse feces (favors the volatile
fatty acid present in the feces)
 Virulent and non-virulent strains
 Virulent strains of R. equi are characterized by their ability to survive and
replicate inside macrophages
 There are 7 virulence associated proteins (Vaps A,C,D,E,F,G and H)-their precise
functions are unknown however Vap A is required for pathogenicity in foals
(most important the strain she wants us to be familiar with!)
 Look like chinese characters underneath the microscope
Epidemiology:
 Often associated with problem farms
 Foals kept in stables or moved to stables are more likely to contract the disease
o
o
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 Farms with large numbers of foaling mares or have dirt flooring in their stalls are
at an increased risk of disease
 The organism is widespread in soil samples and in the feces of equines
 Inhalation of dust particles containing virulent R. equi is the major route of
infection in foals!!
Pathogenesis:
 Inhalation of dust containing the organism is thought to be the major route of
infection
 Once inhaled the organism resided within the alveolar macrophages and
replicates-replication eventually kills the host cell
 Leading to a severe pyogranulomatous bronchopneumonia resulting from
necrosis and destruction of the lung parenchyma
 Intestinal forms of the disease include ulcerative colitis and abdominal
lymphadenitis
 GI forms of the disease are thought to be the result of foals swallowing infected
septum
 It can be found in the hip joint also on necropsy of foals
 R. equi may disseminate to other parts of the body causing septic arthritis,
vertebral body abscesses
 Immune-mediated polysynovitis, uveitis, hemolytic anemia, thrombocytopenia
are other manifestations of the organism
 Body systems that may be affected include-respiratory , GI, musculoskeletal,
hemic/lymphatic, immune, ophthalmic, renal, skin, nervous and hepatobiliary.
Clinical signs:
 Tends to affect young foals 1-6 months of age. MC with signs manifesting in
foals by 4 months of age
 Fever (high), cough, lethargy, depression, anorexia, poor weight gain, exercise
intolerance, diarrhea, joint effusion, and sudden death
 R. equi develops either chronically or in a subacute fashion-usually the early
signs of disease are missed
 A non-septic synovitis may be present in approximately 1/3 of all cases helps to
differentiate R. equi pneumonia from other pneumonias
 Hypopion is a common finding
 Abnormal lung sounds may not be detected until disease is well advanced
 When ausculatory changes are detectable they usually involve all parts of the
lung-generalized pathology
 Most bacterial pneumonias effect cranial ventral lung fields – this disease is
different in that it has a generalized pneumonia
Diagnosis:
 DDX
 Strep equi - Strangles
 Strep zooepidemicus
 Parasite migration (ascarids)
 Viral respiratory infections
 Lab tests
 CBC/Chem-CBC is characterized by leukocytosis with a mature
neutrophilia
o
o
 Hyperfibrinogenemia (normal = 100-400; infected = 1200-2300)
 Severely affected foals may have anemia and thrombocytopenia
 Auscultation
 BAL/Transtracheal wash
 AGID serology
 ELIZA serology for detection of antibody to cell surface R. equi antigen (ANTECH)
 SHI assays (synergistic hemolysis inhibition)
 PCR testing of BAL or transtracheal wash fluid (85%)
 Slow growing organism so may need to maintain culture for at least 72 hours
(control fever and support respiratory function in animals till results come back)
 Radiographic changes
 Increased interstitial density
 Dense patchy areas of alveolar pattern
 Consolidation
 Abscess formation (nodular densities)
 Ultrasonography
 Consolidation of lung parenchyma
 Pulmonary and intra-abdominal abscessation
 Serial screening device
Treatment:
 R. equi is an intracellular pathogen
 Only antibiotics that are capable of penetrating macrophages are effective
 Penicillin and gentamicin are INEFFECTIVE (foal on treatment regimen and has
not been effective – History)
 TMS and flouroquinolones (Baytril) are effective
 Macrolides in combination with rifampin is the drug regimen of choice
 Rifampin-erythromycin combinations (erythromycin estolate (best form
of erythromycin), erythromycin estolate or stearate 25mg/kg tid and
rifampin 5-10 mg/kg bid orally) (costs the client $2000-3000 to tx with
rifampin and erythromycin)
 Clarithryomycin-7.5mg/kg BID po along with rifampin-5-10 mg/kg BID
po is more effective than erythromycin-rifampin combination – treating
for less time (decreases cost)
 Azithromycin 10mg/kg SID (shorter tx times and far more effective)
 Minimize stress
 Restrict activity
 Turnout in small paddock – ventilation, high ammonia levels in stalls
 Good nursing care
 Do not move affected animals from an endemic farm to one with no history of
disease
Prevention:
 Prophylactic treatment of foals on endemic farms with hyperimmune plasma
does not consistently prevent disease or alter outcome
 Use of ultrasonography or radiography to detect and treat cases at an earlier
stage on problem farms (lesions show up earlier than clinical symptomology)
o
o
 Mares housed with foals treated with rifampin-erythromcyin combination are at
risk of developing a severe fatal colitis (associated with Clostridium difficile)
from ingestion of feces – need good feces removal
Pathology:
 Findings are related to the organ system involved
 Respiratory
o Multiple firm nodules separated by congested and partly
atelectic lung
o Military pyogranulomatous nodules
o Lesions are bilateral with concentration in the cranioventral
lung lobes
o Histologically lesions are predominately pyogranulomatouscellular influx into the alveolar spaces consisting largely of
macrophages and multinucleate giant cells
o Intact bacteria are often present within macrophages
o Necrosis involves the alveolar septa and pulmonary
parenchyema
 Intestinal tract
o Multifocal enterocolitis and typhlitis
o Peyer’s patches in the ileum and areas of lymphoidal tissue in
the cecum and colon
o Mesenteric and colonic lymph nodes may be enlarged with
caseonecrotic foci
o Histologically-pyogranulomatous inflammation of lymphoid
tissue with fibrinonecrotic ulceration of the overlying
epithelium
Public health concerns:
 Recognized as an opportunistic infection in immunocompromised humans
 HIV
 Organ transplant recipients
 Thought to be acquired via inhalation, inoculation into a wound or
ingestion (organism can live in soil so people don’t have to be around
horses)
 Organism has been isolated from every body site with pulmonary
involvement being the most common
 Treatment is with erythromycin, rifampin, vancomycin, ciprofloxacin,
impenem, aminoglycosides
 MORTALITY RATES
o 11% in immunocompetent individuals
o 50-55% in HIV-infected patients
o 20-25% In non-HIV infected immunocompromised individuals