Lameness in HORSES
DISEASE
ETIOLOGY
Thrush
1. Fusobacterium
necrophorum
2. Unhygienic
conditions, lack
exercise, poor
foot care
Laminitis
1.
2.
3.
4.
Endometritis
Salmonellosis
Colitis X
Carbohydrate
overload
5. Excessive
trauma
6. Excessive
weight bearing
on single leg
7. Corticosteriod
– can induce
laminitis
HOST
TRANSMISSION &
PATHOGENESIS
PATHOGENESIS:
Circulating endotoxins
Initiate the peripheral
vascular response
Deprives the laminar
corium of blood supply
Sensitive laminae at the
junction of P3 and the
hoof
+ platelet aggregation,
microthrombosis,
perivascular edema,
arteriovenous shunting
Contagious
equine metritis
Taylorella
equigenitalis
- Gram negative
TRANS:
1. Mating
2. Fomites
CLINICAL SIGNS
1. Soft, spongy and
disintegrated frog
horn
2. Characteristic fetid
odor
3. Inflammation of
the coronet and
discharge of pus
from fissures
CLINICAL SIGNS:
ACUTE: all feet, common in
front feet
1. Shifts weight onto
the hind limb
2. Short strides
3. Recumbency is
common
4. Pain-prominent
over the sole
CHRONIC: individual limbs
(overweight horse)
1. Recurrent bouts of
variable lameness
2. Classic hoof wall
“rings”
LESIONS:
CHRONIC:
Dropped or flattened sole
with long toe
CLINICAL SIGNS:
MARES:
DIAGNOSIS
1. Clinical findings
2. Examination of the
sole
TREATMENT
AND CONTROL
1. Loose and
necrotic
material must
be pared
away
2. Antiseptic
products
3. Bandaging
1. Clinical signs
2. History
3. Radiologyconfirmation on
angulation of P3
1. Isolation of
organism
TREATMENT:
1. Stallioncleaning of
Lameness in HORSES
-
Epizootic
lymphagitis
Microaerophilic
Coccobacillus
Also called as
Contagious
Equine Metritis
organism
Histoplasma
farciminosum
- Dimorphic
fungus
Nature: mycelia
Tissues: yeast
Soil: saprophytic
3. Source for
outbreaks:
undetected
infected mares
and stallion
Host:
1. Horses
2. Donkeys
3. Mules
TRANS:
1. Wound infection
2. Bloodsucking
insects
PATHOGENESIS:
Entry into the wound
Subcutaneous tissue
(granuloma & ulcers)
Spreads thru lymphatic
vessels
Lymph nodes
1. Copious
mucopurulent
vaginal discharge
2. Chronically: no
signs
3. No conception
during infection
4. May infect foal
after birth
LESIONS:
1. Edema
2. Hyperemia of the
endometrium,
endocervix, vaginal
mucosa
3. Invasion of
neutrophils during
the acute stage
CLINICAL SIGNS:
1. Free movable
cutaneous nodules
2. Lymph nodes
enlarge and hard
-swabs from
endometrium
(Amies with
charcoal)
DIAGNOSIS:
1. Microscopic exudates and
biopsy specimens
2. Yeast form distends the
cytoplasm of macrophages
3. Serum agglutination titers
FORMS:
1. Cutaneous-most
common
2. Ophthalmic form –
less frequent
3. Respiratory form –
late development
of the cutaneous
form, UPR
DIFFERENTIAL:
1. Glanders
2. Strangles
3. Ulcerative
lymphagitis
4. Sporotrichosis
5. Histoplasmosis
penis with
chlorhexidine
surgical scrub
then applying
nitrofurazone
ointment
2. Mares rid
themselves
form the
infection
3. Treatment
and
elimination
from
breeding
programs
4. Strict import
regulations
TREATMENT:
1. No complete
satisfactory
treatment
2. Surgical
excision of
lesions
combined
with
antifungal
drugs
(amphotericin
B)
3. Parenteral
iodides
Lameness in HORSES
4. Asymptomatic
form-carriers
Glanders
Burkholderia malleiclose genetic and
antigenic relatedness
to Burkholderia
pseudomallei
HOST:
Primary –
1. Equids- horses,
donkey, mules
Secondary1. Human
2. Carnivores
TRANS:
1. Ingestion
-communal
watering troughs
2. Direct contact from
skin abrasions and
cutaneous form
PATHOGENESIS
Ingestions
Invasions of the intestinal
wall
Bacteremia or septicemia
LESIONS:
GROSS LESIONS:
1. Pyogranulomatous,
purulent discharge
of thickened
superficial
lymphatic vessels
2. Enlargement of
regional lymph
nodes
HISTOLOGY:
1. Large macrophages
-ovoid, double contoured
yeast-like cells are found
when gram-stained
CLINICAL SIGNS:
DIAGNOSIS:
ACUTE:
1. Mallein test –
1. High fever
injected
2. Cough
intradermally into
3. Nasal discharge
the lower eyelid
4. Nodules in skin of
with a tuberculin
lower limbs or
syringe
abdomen
2. CFT-most accurate
CHRONIC:
3. Culture – Strauss
3 major manifestations
reaction in guinea
1. Pulmonary-chronic
pigs (severe orchitis
pneumonia, couch,
and inflammation)
epistaxis
2. Skin-subcutaneous DIFFERENTIAL:
nodules which
1. Epizootic
lymphaginitis
TREATMENT:
1. Little
information
2. Sodium
sulfadiazineexperimental
CONTROL:
1. Complete
quarantine
2. Remove
mallein test
positive
3. Disinfection
program
Lameness in HORSES
Localized in lungs but skin
and nasal mucosa are
common
West Nile Fever
Flavivirus
- Less
pathogenic
than
Togaviridae
West Nile Virus
7 lineages:
1. Lineage 1 ( sl
1a, 1b, 1c
2. Lineage 2 –
people and
horses
3.
Equine
Alphavirus
encephalomyelitis Family: Togaviridae
Eastern equine
encephalitis virus –
most pathogenic
Host:
1. Horse- dead-end
host
TRANS:
1. Ticks
2. Wild birds
3. Mosquitoes i.e.
Culex spp.
HOST:
1. Horse
2. Human- dead-end
host
Normal cycle- bird
TRANS:
1. Mosquitoes
Culiseta melanura
(ornithophilic)-EEV
Culex tarsalis- WEEV
ulcerate and
discharge pus
3. Nasal-nodules
LESIONS:
Acute:
1. Petechial
hemorrhage
through the body
CHRONIC:
1. Lesions in lungs
-miliary nodules
-Ulcers in mucosa
of EPR
2. Nodules in skin and
subcutis
Clinical signs:
1. General loss of
apetite
2. Depression
3. Fever
4. Ataxia (stumbling
staggering wobbly
gait,
incoordination)
CLINICAL SIGNS:
Pathological diagnosis
1. No specific gross
lesion
Initial clinical signs include:
1. Fever
2. Ulcerative
lymphagitis
3. Sporotrichosis
4. Meliodosis
5. Other cause of
pneumonia
4. Restriction of
movement of
horses
DIAGNOSIS:
TREATMENT:
CONTROL:
1. Vaccine –
effective
2.
DIAGNOSIS:
Serology:
1. Detection of IgM
antibody – ELISA
2. Plaque Reduction
Neutralization (PRN)
TREATMENT:
NO SPECIFIC
TREATMENT
1. Supportive
care
Lameness in HORSES
1. North
American
variant (most
pathogenic)
2. South
American
variant
Western equine
encephalitis virus
2. Bridge vector birds
mammal EEV
Coquilletidia
perturbans
Aedes Canadensis
Aedes albopictus
Ochlerotatus spp.
Culex spp.
WEEV
Aedes melaniman
Aedes dorsalis
Aedes campestris
PATHOGENESIS:
Mosquito injects the agent
into the subcutaneous and
cutaneous tissues
Virus repli in non-neural
tissues
Virus binds to specific
tissue receptors 
endocytosis
Secondary viremia occurs
Viral migration into the
CNS (cerebral capillary
endothelial cells)
Cell-to-cell spread:
dendrites and axons
2. Anorexia
3. Depression
Severe cases:
1. Encephalitis
2. Altered mentation
3. Hypersensitivity to
stimuli
4. Involuntary muscle
movements
5. Impaired vision
6. Aimless wandering
LESIONS:
Microscopic:
1. Congestion of the
brain and
meninges
2. Multiple petechiae
on the viscerabirds
3. Severe
inflammation of
the gray matter
4. Neuronal
degeneration
5. Infiltration by
inflammatory cells,
gliosis
6. Perivascular
cuffing and
hemorrhages
test – differentiation
EEV, WEEV
3. Combination of both
4. Complement
fixation
5. Virus Isolation
- Brain tissue
- Liver
- Spleen
DIFFERENTIALL DIAGNOSIS:
1. Rabies
2. Borna disease
3. Japanese
encephalitis
4. Hepatic
encephalopathy
5. Botulism- doesn’t
cause cerebral signs
6. Yellow-star thistle
poisoning- exception
of fever
-anti-infla:
flunixin
meglumine
CONTROL:
1. Housing in
screened
barns
2. Clean water
tanks and
buckets
3. Vaccinationformalininactivated
Previously nonvaccinated adult
orses require 2
injections:
1. Temp
climatesannual with
4wk of the
start of
arbovirus
season
2. 2-3 times
yearly in very
active season
3. Mares- 3-4
wks yearly in
active
seasons
4. Foals-with
adequate
colostrum-
Lameness in HORSES
Japanese
encephalitis
Japanese encephalitis
flavivirus
-orient and south-east
asia
-all continents
Host:
1. Horses- incidental
host
2. Pigs – amplifiers
3. Birds (fam.
Ardeidae) – natural
maintenance
reservoir
4. Humans- dead-end
host
TRANS:
1. Mechanical:
Stomoxys
calcitrans
Chrysops sp.
Tabanus sp.
Culex
2. Intrauterine
infections –
abortion in 2 mos.
3. Use of
contaminated
surgical
instruments or
needles
PATHOGENESIS:
Primary entry
Infection of macrophages
Destruction of
macrophages and release
of virus
Production of antibodies
to antigenic
THREE SYNDROMIC
MANIFESTATIONS:
1. Transitory Type
Syndrome
2. Lethargic Type
Syndrome
3. Hyper excitable
Type Syndrome
CLINICAL FINDINGS:
Incubation 2-4 weeks
1. Anorexia
2. Depression
3. Profound
weakness
4. Loss of condition
5. Hyperesthesia
6. Blindness
7. Recovery at 3d – 3
wks
CLINICAL:
1. Virus isolation
- Brain
- Spinal cord
vacc at 5-6
mos of age
5. Foals to
nonvac
mares- vacc
at 3, 4, 6 mos
of age
TREATMENT:
NO SPECIFIC
TREATMENT
CONTROL:
1. Compulsory
identification
and testing
with
eradication of
infected
horses
DIFFERENTIAL DIAGNOSIS:
1. Other equine viral
encephalitides
- Western equine
encephalitis
- Eastern equine
encephalitis
- Venezuelan equine
encephalitis
CONTROL and
- Murray Valley
PREVENTION:
encephalitis
1. In-door
2. African horse
screens
sickness
2. Vector
3. Equine Herpes
control
myelencephalopathy
3. Immunization
4. Hepatic
of swines
5. Encephalopathy
6. Rabies
Lameness in HORSES
Formation of antigenantibody complexes, fever,
glomerulitis, anemia,
thrombocytopenia,
complement depletion
Hemolysis or phagocytosis
Temporary iron-deficient
erythropoiesis
App. Of new antigenic
variant of the virus and
commence of new cycle of
viral replication in
macrophages
Venezuelan
equine
encephalitis
Alphavirus
FAMILY: Togaviridae
Subtypes-highly
virulent for equine
I-A
I-B
I-C
Host:
TRANS:
CLINICAL SIGNS:
- Epizootic/epidemic
1. MosquitoHorse – more susceptible
1. Humans- dead end
epizootic/epidemic
1. Fever
host
2. Culex –
2. Anorexia
2. Horses & donkey –
enzootic/endemic
3. Depression
amplifiers
4. Flaccid lips
- Endemic/Enzootic PATHOGENESIS:
5. Incoordination
1. Rodents – natural
1. Inapparent
6. Blindness
reservoir
infection- mildest
7. Head pressing
form of a diease –
8. Circling
transient fever
9. Early nervous
2. Viremia- persist
signs:
throughout the
hypersensitivity to
course of dis
touch and sound
- Source for vector
transient
3. Virus- saliva and
excitement and
discharge
restless
DIAGNOSIS:
1. Virus isolation
- Fixation test
- Hemaglutination
inhibition
- Virus neutralization
- PCR
- ELISA
2. Serology
3. Demo of viral
nucleic acid
DIFFERENTIAL DIAGNOSIS:
1. Rabies
2. Botulism
3. Tetanus
TREATMENT:
1. Supportive
theraphy
CONTROL:
1. Vaccination
2. Quarantine of
infected
horses
3. Vector
control
measures
- Biological
control
- Chemical
control
Larvicide
Lameness in HORSES
INCUBATION: 1-5DAYS
Equine infectious
anemia
Lentivirus –RNA
FAMILY: Retroviriae
-related to human
feline
immunodeficiency
- Major group specific
antigen p26 antigen
-uses a reverse
transcriptase enzyme
to generate DNA which
infect into the host
Host:
-Horse family
TRANS:
1. Clinically infected
horse
2. Insect
3. Management
PATHOGENESIS:
Biting flies
Virus in spleen
Replication in mature
macrophages and
circulating monocytes
10. Stage of paralysis:
inability to hold
head
Humans – acute, mild,
systemic disease
1. Fever
2. Chills
3. Headache
4. Coughing
5. Vomiting
6. Diarrhea
PREGNANT woman:
1. Fatal encephalitis
2. Placental damage
3. Abortion/stillbirth
and congenital
disease
CLINICAL SIGNS:
ACUTE:
1. Anorexia
2. Depression
3. Profound
weakness
4. Fever
CHRONIC:
1. Jaundice
2. Ventral edema
3. Petechial
hemorrhages
4. Pallor of mucosa
5. Abortion
LESIONS:
4. Yellow-star
poisoning
5. Japanese
encephalitis
6. Borna disease
7. West nile
Encephalomyelitis
DIAGNOSIS:
1. Detection of major
antigen
2. Coggins Test
3. Competitive ELISA
DIFFERENTIAL DIAGNOSIS:
ACUTE STAGE:
1. Pupura
hemorrhagica
2. Babesiosis
3. Equine Granulocytic
ehrichiosis
4. Equine viral arteritis
5. Autoimmune
hemolytic anemia
6. Idiopathic
thrombocytopenia
Adulticide
4. Minimize
irrigation and
lawn watering
TREATMENT:
NO TREATMENT
1. Supportive
theraphy –
blood
transfusion
and
hematinic
drugs
CONTROL:
1. Identification
and slaughter
2. Testing of
new stock
3. Control insect
access
Lameness in HORSES
Destruction of
macrophage and release of
virus
Formation of VAC which
induced fever, glomerulitis
anemia and
thrombocytopenia
Viremia
1. Subcutaneous
edema
2. Jaundice
3. Petechial or
ecchymotic hemo
4. Enlargement of
spleen, liver, local
lymph nodes
5. Bone marros is
reddened
6. Pallor of mucosa
CHRONIC:
1. Metastatic
Streptococcus equi
infection
2. Inflammatory
disease
3. Neoplasia
4. Chronic hepatitis
4. Strict hygiene
during
vaccinating
and collecting
blood
Relapsed of clinical disease
Equine influenza
Influenza virus type A
Family:
Orthomyxoviridae
1. H7N7
2. H3N8
Death or survive and be
asymptomatic carriers
TRANS:
1. Interspecies
transmission
- Direct contact
- Personnel &
fomites
PATHOGENESIS:
The virus is inhaled
Attaches to respi epi cells
with its hema spikes
Fuses with the cell 
release into the cytoplasm
and replicates
Virions are releases from
the cell surface and infect
other cells or release to
the envi
CLINICAL SIGNS:
1. High fever
2. Serous nasal
discharge
3. Coughin
- dry, harsh, nonproductive
- moist and
productive
4. Depression
5. Anorexia
6. Weakness
DIAGNOSIS:
1. Strangles
(Streptococcus equi
infection)
2. Equine viral arteritis
(EVA)
3. Equine viral
rhinopneumonitis
4. Equine viral
rhinopneumonitis
Equine rhinitis virus
DIFFERENTIAL DIAGNOSIS:
1. Clinical signs
2. Virus isolation
3. Influenza A antigen
detection
4. Paired serum
samples
TREATMENT:
1. No specific
treatment
2. Supportive
care
CONTROL:
1. Quarantine
2. Vaccination
- Intranasal
modified cold
- Inactivated,
adjuvanted
3. Recombine
canarypox
vectored
vaccine
Lameness in HORSES
Equine
rhinopneumonitis
Equine Herpesvirus 4
(EHV-4)
FAMILY:
Alphaherpesvirus
-EHV-1 & EHV-4 show
antigenic cross
reactivity
Death of epi cells, infla,
edema, loss of protective
mucociliary clearance
TRANS:
1. Inhalation
-Direct
-indirect
PATHOGENESIS:
Inhalation
Binds & repli to the nasal
and nasopharyngeal
epithelium
Spread to the LRT and
lymph nodes
Viremia
Cell death & dev’t of
intranuclear inclusion
bodies in the respi tract
and its association
lymphoid tissues
Recovery latently
infected
CLINICAL SIGNS:
DIAGNOSIS:
1. Bilateral nasal
1. Nasopharyngeal
discharge
swab (nose and
2. Early stages: nasal
throat)
discharge is
2. Blood buffy coat
watery, freesample
trickling, clear
3. Virus detection
3. Progress to: thicker
- PCR
and mucilaginous,
- Isolation
whitish in color
4. Serological
containing infla
- Virus neutralization
leukocytes and
- Complement
desquamated respi
fixation test
epi cells
ELISA
4. Encrustation in the
nostrils
DIFFERENTIAL DIAGNOSIS:
5. Couging
1. Strangles
6. Pyrexia
2. Equine viral arteritis
7. Enlarge of
3. Equine influenza
submandibular and
4. Equine rhinitis virus
retropharyngeal LN
5. Equine adenovirus
8. Lethargy
9. Conjunctivitis with
mild ocular
discharge
LESIONS:
1. Hyperemis
2. Vesiculation
3. Ulceration of respi
epi
Lameness in HORSES
Equine vial
arteritis
Arterivirus
-small, envepoled
single stranded positive
snese RNA virus
HORSE – North and South
America, Europe, Africa,
Asia and Australia
TRANS:
1. Horizontal
2. Venereal
PATHOGENESIS:
Inhalation of virus
Bind to respi epi
Replication in alveolar
macrophages
Spread to bronchial lymph
nodes
Viremia
Infection epithelium,
mesothelium, smooth
muscle arteries and
uterine wall
Vascular injury
abortion
4. Multiple, tiny,
plum-colored foci
in lungs
CLINICAL SIGNS:
Adult
1. Edema
2. Congestion
3. Hemorrhage
- Necrosis and
hemorrhage in
several organs
Foal
1. Pulmonary edema
2. Accum of protein
rich fluid
3. Pregnant- abortion
in 3-10 mos
LESIONS:
1. Vasculitis
2. Vascular and
perivascular
edema
3. Lyphocytic
infiltration and
endothelial cell
hypertrophy
4. Fibroid necrosis
DIAGNOSIS:
1. Hematological
examination of adult
and foal –
leukopenia
2. Serological
conformation
- Virus neutralization
assay
- ELISA
3. Viral Isolation
4. Necropsy
DIFFERENTIAL:
1. Strangles
2. Equine viral
rhinopneumonitis
3. Equine viral
rhinopneumonitis
4. Leptospirosis
TREATMENT:
NO SPECIFIC
TREATMENT
1. Symptomatic
treatment
CONTROL:
1. Vaccination –
6-8 mos (colts
2. Isolation
3. Segregate
pregnanat
mares
4. Blood test all
stallions
5. Check semen
6. Vacc mares
againt EVA
atleast 3
weeks prior
to breeding
7. Vacc intact
males
between 6-12
mos.
Lameness in HORSES
Vesicular
stomatitis
Vesiculovirus
- Bullet-shaped
2 distinct serotypes:
1. New Jersey
2. Indiana
African Horse
Sickness
Orbivirus
- African Horse
Sickness virus
Virus endemic in:
1. South America
2. Central America
3. Parts of Mexico
Endemic:
1. Regions of Africa
(sub-Saharan)
TRANS:
1. Direct contact
2. Blood-feeding
insects
- Simulidae
- Lutzomyia :
endemic areas
TRANS:
1. Culiciodes spp.principal vectors of
allnine serotype
CLINICAL SIGNS:
1. Fever
2. Ptyalism
3. Loss of apetite
4. Lameness
LESIONS:
1. Vesicles in the oral
cavity
2. Ulcers and erosion
in the oral mucosa
3. Sloughing of the
epithelium of the
tongue
4. Lesions on the
mucocutaneous
junctions of the
lips
5. Coronitis with
erosion in the
coronary bands
6. Crusting lesions of
the muzzle, ventral
abdomen,
CLINICAL SIGNS:
Acute:
1. Death ~ 1wk
2. Dyspnea
3. Spasmodic
coughing
4. Dialted nostrils
5. Head extended
6. Congested
conjunctiva
DIAGNOSIS:
1. Presence of typical
signs
2. Antibody detection
3. Viral isolationvesicular fluid,
epithelial tags
4. ELISA
5. Virus neutralization
6. Complement
fixation test
DIFFERENTIAL:
1. FMD
2. Swine vesicular
exanthema
DIAGNOSIS:
1. Clinical signs and
lesions
2. RT-PCR
3. ELISA
TREATEMENT:
NO SPECIFIC
TREATMENT
1. Cleansing of
wounds
2. Management
3. Affected
animals
should be
isolated
ZOONOTIC RISK:
- Zoonotic, selflimiting
influenza luke
disease
TREATMENT:
NO SPECIFIC
TREATMENT
CONTROL:
1. Animal
movement
restriction
2. Husbandry
modification
Lameness in HORSES
7. Supraorbital fossa
edematous
8. Recovery- rare
Horse pox
Equine herpesvirus-3
- single
antigenic-type
- small and large
plaque variants
TRANS:
1. Venereal – primaty
- Probably acute
disease phase of
hed only in acute
ably transmitt
LESIONS:
1. Pulmonary edema
2. Distended lungs
3. Pleural effusions
4. Petechiae in
pericardium
5. Abdominal viscera
is distended
6. Pulmonary form –
dogs
7.
CLINICAL SIGNS:
1. Multiple, circular ,
red nodules on the
vulvar or vaginal
mucosa, clitoral
sinus, perineal skin
3. vaccination
DIAGNOSIS:
TREATMENT:
1. Clinical signs
1. Sexual rest,
2. Viral Identification
allow ulcers
3. Serum neutralization
to heal
4. Complement
2. Antibiotic
fixation tests.
ointments
3. During
acutephase:
breeding only
thru arti
insemination
4. Examine all
horses