2 - Infectious Diseases of Equine

1 EQUINE BACTERIAL DISEASES
1. Sporotrichosis 2. Glanders (Farcy and Malleus)

Definition
Non-contagious chronic infectious disease of equine, humans, and other acute or chronic highly fetal contagious disease of equine caused by Burkholderia mallei and
domestic animals, caused by Sporothrix schenckii, characterized by characterized by formation of fibro caseous ulcerating nodules in the upper respiratory tract, lungs
cutaneous nodules and ulcers on the limb with or without lymphangitis and skin
and lymphadenitis.
Etiology
Sporotrichosis is caused by Sporothrix schenckii Burkholderia mallei
Sporothrix schenckii is a dimorphic fungus, which form single walled, A Gram-negative rod in the family Burkholderiaceae. This organism was formerly known as
spherical, oval or cigar shape spores. It grows on Sabouraud dextrose Pseudomonas mallei.
agar. • It is Gram negative rod-shaped with rounded ends, non-spore forming, non-motile. It grows on
Predisposing factors: ordinary agar (blood or serum) or broth media at 37°C using glycerol as growth promoting.
Cutaneous wounds and presence of the animals in muddy unhygienic • It cannot survive outside the body of the host. It survives for 15-30 days in wet substances and
stables. water. It survives more than weeks in contaminated sables. It can be destroyed by heat (55°C
for 10 m), sunlight and disinfectants
Epidemiology
1- Distribution: S. schenckii can be found worldwide and present in 1- Distribution: Glanders is thought to be endemic in parts of the Middle East, Asia, Africa and
Egypt. South America. The disease is not reported in Egypt since 1928.
2- Animal susceptibility: Sporotrichosis occurs most often in horses. 2- Animal susceptibility: The major hosts for B. mallei are horses, mules and donkeys, but it has
Cases have also been seen in cats, dogs, rodents, cattle, goats, been reported in dogs, cats, goats, sheep and camels.
swine, mules, camels, non-human primates, birds, and various wild Occasional cases are seen in domesticated cats.
animals including foxes.
Cattle, pigs and birds are highly resistant to this disease.
3- Seasonal incidence: The disease increases during winter seasons.
Factors influencing susceptibility:
4- Transmission:
a. Badly fed animals and animals kept in poor environment, overcrowded stables are
Mode of transmission: more susceptible.
a. The pus discharged from the lesions of the infected animals is b. High incidence of the disease is observed in autumn and winter
the main source of contamination of beddings, grooming,
3- Mode of transmission:
utensils and other fomites.
a. Glanders is mainly transmitted by contact with skin exudates and respiratory secretions
b. Infection occurs through cutaneous wounds or abrasions either
from infected equids. Latently infected as well as clinically ill animals can spread the
by direct contact or indirect contact with contaminated
disease. Horses, mules and donkeys often become infected when they ingest B. mallei in
surroundings and fomites.
contaminated food or water. This organism can also be spread in aerosols, and by entry
through skin abrasions and mucous membranes.
b. Carnivores usually become infected when they eat contaminated meat.
Pathogenesis
1. The organism gain access through wounds and abrasions in the skin, 1. After infection occurs primary multiplication and lesions at point of entry,
invades the subcutaneous tissue causing nodular ulcerating lesions, 2. Then the organism passes to regional lymph nodes in which they propagate and via lymphatic
and then spreads through lymphatics. it reaches to blood causing septicemia (acute form) or bacteraemia (chronic form)
2. Finally, the nodules ulcerate and discharge pus. 3. Then localization of organism occurs in lung, other viscera as liver, spleen, nasal mucosae and
3. Inflammation of the lymph vessels and lymph nodes may be skin with formation of typical nodules (pyogranulomatous).
observed. 4. In lung the nodules result in bronchopneumonia and anoxic anoxia and finally death.
4. Involvement of bones and visceral organs with fetal termination is
rare, but has been reported in dogs and horses.
Clinical signs
• The disease has low morbidity, mortality and long course. Incubation Period varies from a few days to many months; two to six weeks is typical.
• Sporotrichosis may be grouped into 3 forms—lymphocutaneous, Morbidity and Mortality rate are high,.
cutaneous, and disseminated. Course of the disease from few days to up to 2 w in acute form while in chronic form is long
1. The Lymphocutaneous Form is the most common. extending for months.
a. Small, firm dermal to SC nodules, 1-3 cm in diameter, develop Acute form (Septicemia):
at the site of inoculation (usually about fetlock). 1. It is common in donkeys and mules, there are high fever, cough and unilateral thick
b. As infection ascends along the lymphatic vessels, cording and mucopurulent nasal discharge, which periodically are snorted from nostrils with labored
new nodules develop. respiration.
c. Lesions ulcerate and discharge a serohemorrhagic exudate. 2. Submaxillary lymph nodes are enlarged and painful (lymphadenitis of head and neck but less
d. Although systemic illness is not seen initially, chronic illness may than as in strangles).
result in fever, listlessness, and depression. 3. Rapidly spreading ulcers on nasal mucosa and nodules on skin of lower limb and abdomen.
2. The Cutaneous Form remains localized to the site of inoculation, 4. Death occurs due to septicemia.
although lesions may be multicentric. Chronic form (Bacteraemia): It is common in horses; signs are related to localization in one or more
3. Disseminated Sporotrichosis is rare but potentially fatal and may of the predilection sites:
develop with neglect of cutaneous and lymphocutaneous forms. 1. Pulmonary form.
Infection develops via hematogenous or tissue spread from the
2. Nasal form.
initial site of inoculation to the bone, lungs, liver, spleen, testes, GI
tract, or CNS. 3. Skin form (farcy).
Postmortem Lesion
There are no obvious lesions except cutaneous one. 1. Ulcers, nodules and/or stellate scars may be found in the nasal passages, trachea, pharynx
and larynx.
2. Gray nodules can also be found in other tissues, particularly the lung, liver, spleen and kidneys.
3. Glanders nodules are firm, round and approximately 1 cm. in diameter, with a caseous or
calcified center.
4. Catarrhal bronchopneumonia with enlarged bronchial lymph nodes may also be seen,
particularly in acute disease.
5. The lymph nodes may be enlarged, congested and/or fibrotic, and can contain abscesses.
6. Swollen lymphatics, with chains of nodules and ulcerated nodules, may be noted in the skin.
By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 1

Diagnosis
Field diagnosis: Field diagnosis:
• It depends on history, epidemiology and clinical signs of the disease. Depend on history, characteristic signs of nasal and cutaneous and ulcers on the extremities,
Laboratory diagnosis: corded lymphatic (lymphangitis) with lymphadenopathy beside Mallein test.
Samples: Pus, blood and serum sample.

Laboratory examinations: Mallein test
1. Direct microscopic examination of stained pus smear to detect It used to identify infected equids. In reactors
cigar shape spores. 1. marked eyelid swelling occurs 1 to 2 days after intrapalpebral injection of a protein fraction of
2. Isolation of the organism on Sabaurods Dextrose Agar and B. mallei.
identification of the organism from colony morphology and 2. Conjunctivitis occurs after administration in eye drops, and
biochemical reactions. 3. a firm, painful swelling with raised edges is seen within 24 hours after subcutaneous (nonocular)
3. FAT, it gives positive result with samples of infected animal. injection.
4. Animal inoculation, inoculation of mice I/P with pus material of 4. Positive reactions by any of these three routes are accompanied by fever.
infected animal, local lesion (granuloma) can be observed after 3 w 5. The subcutaneous Mallein test may interfere with future serologic testing, and the other two
of inoculation and peritoneal exudate contain cigar-shape fungi in routes of administration are generally preferred.
peritoneal cavity.
5. Serological test as latex agglutination test.
Laboratory diagnosis
a. Samples: Nasal discharge, nodular content from closed nodule, blood and paired serum
samples.
b. Laboratory examinations:
1. Examination of stained smear: B. mallei can be stained with methylene blue or Gram
stains, but the staining may be weak or irregular. Some authors report that this organism
stains best with Giemsa. B. malleus is a nonmotile, Gram negative, straight or slightly
curved rod.
2. Culture of the samples: B. mallei can be isolated on
1) Ordinary culture media including blood agar, but it grows slowly; a 48-hour incubation
is recommended.
2) On glycerol agar, a smooth, slightly cream-colored, moist, viscid confluent layer is
seen after a few days; this layer eventually becomes thicker, tougher, and darker
brown.
3. Serological tests: The most accurate and reliable tests in equids are complement fixation
and ELISA.
Agglutination and precipitin tests are unreliable for horses with chronic glanders and
animals in poor condition.
Serological tests cannot distinguish reactions to B. mallei from reactions to B. pseudomallei.
4. Laboratory animals’ inoculation (Strauss reaction): pus is injected I/P into male Guinea
pigs, it results in peritonitis and severe orchitis with inflammation of scrotal sac (edematous
and painful) which open discharging pus.
It is not highly specific for B. mallei.
It acts as an aid in diagnosis, other types of Actinobacillus, Pseudomonas aergnosa, C. ovis and
brucella. It should do with test Mallein or CFT.
Differential diagnosis
This disease may be misdiagnosed clinically with This disease may be misdiagnosed clinically with
• Glanders • Sporotrichosis
• Epizootic lymphangitis • Epizootic lymphangitis
• Ulcerative lymphangitis. • Ulcerative lymphangitis.
Treatment
1. Systemic treatment with iodides such as potassium iodide orally (0.5- Some antibiotics may be effective against glanders, but treatment is given only in endemic areas.
1 mg/kg, bw) as 1-2 dose daily for 7 days or sodium iodide I/V (40 Treatment is risky even in these regions, as infections can spread to humans and other animals,
mg/kg, bw) as 2-5 doses then one dose daily till cure. and treated animals can become asymptomatic carriers.
2. During treatment, the animal should be monitored for signs of iodide
toxicity—anorexia, vomiting, depression, muscle twitching,
hypothermia, cardiomyopathy, cardiovascular collapse, and death.
The dose of iodides may be stopped or reduced if signs of iodism
appear.
3. Local application of iodides daily to ulcers after evacuation of
contents.
Control
1. Early diagnosis, isolation and treatment of infected animals, 1. Animals that test positive for glanders are euthanized except in endemic areas.
2. Prophylactic treatment of all cutaneous wound and abrasions and 2. In an outbreak, the premises should be quarantined, thoroughly cleaned and disinfected.
Adequate hygiene to prevent spread of infection. 3. All contaminated bedding and food should be burned or buried, and equipment and other
fomites should be disinfected.
4. Carcasses should be burned or buried. Whenever possible, susceptible animals should be kept
away from contaminated premises for several months.
5. Quarantine on focus of infection for 6 months and during this period the clinical investigation
must be carried once a week and serologically examine one a month and testing by Mallein
every 3 m.
6. Imported horses should be tested by Mallein and CFT and kept in quarantine for at least 28 d.

Glanders Chronic form (Bacteremia)
Pulmonary form Nasal form Skin form (farcy)

1. Nodules and abscesses develop in the lungs. Some 1. Deep ulcers and nodules occur inside the nasal 1. The skin contains nodules (S/C pea-sized nodules of
infections are inapparent; others vary from mild passages, resulting in a thick, purulent, yellowish 1-2 cm in diameter, farcy buds along the course of
dyspnea to severe respiratory disease. discharge. lymphatic under the skin) that rupture and ulcerate,
2. In more severe cases, the clinical signs include 2. This discharge may be unilateral or bilateral, and discharging an oily, purulent
coughing, dyspnea, febrile episodes and can become bloody. 2. yellow exudate.
progressive debilitation. 3. Nasal perforation is possible. Healed ulcers become 3. The regional lymphatics and lymph nodes become
3. Diarrhea and polyuria may also be seen. star–shaped scars. chronically enlarged; the lymphatics are filled with
a purulent exudate. ◦ In addition, there may be
4. Discharges from pulmonary abscesses can spread 4. The regional (submaxillary) lymph nodes become
swelling of the joints and painful edema of the legs.
the infection to the upper respiratory tract. enlarged and indurated nodes (only one left or right
nodes and is cold and painless while in strangles 4. The nodules, ulcers and neighbouring lymph nodes
bilateral and become painful and hot), and may are connected by thickened lymphatic which can
suppurate and drain. be felt under skin (Rosary like).
5. The affected limb becomes marked swollen and
painful. The predilection site for cutaneous lesions is
the medial aspect of hock but can occurs on any
parts of the body.
6. Glanderous orchitis is a common symptom in males.
Chronic cases are usually ill for several months and
dying or become carrier.

3. Epizootic lymphangitis 4. Ulcerative lymphangitis
Definition
Equine blastomycosis, equine histoplasmosis, pseudoglanders or African glanders. Pseudotuberculosis or ulcerative cellulitis.
It is a chronic pyogranulomatous contagious disease of horse, caused by It is mildly contagious chronic infectious disease of equine, caused by C.
histoplasma farciminosum, characterized clinically by ulcerative, suppurative, pseudotuberculosis, characterized by lymphangitis of lower limb without involvement
spreading dermatitis and lymphangitis; however, other forms including pneumonia or of regional lymph nodes draining the affected part.
ulcerative conjunctivitis.
Etiology
• Epizootic lymphangitis results from infection by a dimorphic fungus, Histoplasma • C. Pseudotuberculosis or C. ovis alone or with other pyogenic infection cause
capsulatum var. farciminosum. similar lesions as Staph sp., Strept sp., C. equi and Pseudomonas. C. ovis is
• This organism has also been known as Histoplasma farciminosum. facultative intracellular, gram-positive rods, coccoid or filamentous, nonacid fast,
non-encapsulated, arranged in Chinese letter.
• It is yeast like cells with characteristic double wall capsule, large ovoid or lemon
shape refractile bodies and replicate by budding. • It survives long time in soil contaminated by pus, grow on media containing blood
or serum.
• It grows on Sabouraud dextrose agar and stain by Claudius stain.
• Virulence of the organism attributed to exotoxin and cell wall lipids where it resists
phagolysosomal disposal.
Epidemiology
1- Distribution: The disease is endemic in some countries in the Mediterranean 1- Distribution: The disease is worldwide distributed and present in Egypt.
region, and in parts of Africa and Asia and present in Egypt. 2- Animal susceptibility: Horses, donkeys and mules.
2- Animal susceptibility: Epizootic lymphangitis mainly affects horses, donkeys and 3- Mode of transmission:
mules. H. capsulatum var. farciminosum has also been reported in camels, cattle
• Pus is the main source of infection. The bacteria probably enter via skin wounds
and dogs.
including IM injections, arthropod vectors such as Habronema spp larva and
3- Mode of transmission: stable flies, and contact with fomites such as contaminated tack and grooming
• The source of the organisms can be the skin lesions and nasal and ocular equipment.
exudates of infected animals, or the soil. 4- Seasonal incidence: Autumn and summer
• Biting flies in the genera Musca and Stomoxys are thought to spread the
conjunctival form. Flies may also transmit the skin form mechanically when
they feed on lesions and exudates. Ticks might be involved in transmission. The
pulmonary form, which is rare, probably develops when an animal inhales the
organism
Pathogenesis
1. The fungus invades cutaneous abrasions or wounds result in formation of S/C 1. After infection of skin wounds or abrasion, C. ovis multiply and secrete exotoxins,
nodules which abscessed with discharging of thick creamy pus and then invade lymphatic vessels usually of hind limbs starting at fetlock with abscess
ulcerate and heal by scar. formation (papules or nodules) on the course of lymph vessels,
2. Spread of infection to adjacent lymphatic with formation of nodules along their 2. these progress toward inguinal region, abscess rupture result in ulcer and crust
course and adjacent lymph nodes are also abscessate. and formation of draining tracts, lymph nodes involvement is unusual swelling and
3. Hematogenous spread (yeast cells are present intracellular or extracellular pain of legs with lameness.
especially of macrophages) with visceral involvement may occurs which result in 3. Abscess formation in muscles of chest and caudal abdominal region may be
disturbance in general conditions of the animals. present.
4. Skin lesions are mainly present on head, neck, and limb (mainly hind one which is 4. Septicemia may result in abortion, renal abscess, debilitation and death.
more exposed to abrasions than forelimb).
Clinical signs
1. The Incubation Period is usually several weeks to 2 months. Morbidity is high and 1. IP is long
mortality is 10-15% 2. Morbidity and mortality are low
2. The most common form of epizootic lymphangitis affects the skin and 3. Course of the disease is 2-3w up to 12 m.
lymphatics. It often occurs on the extremities, chest wall, face and neck, but can
4. The hind legs from the hock downwards are the most common affected site. The
be seen wherever the organism is inoculated into a wound
affected leg becomes swollen, hot and slightly painful.
3. The first symptom is a painless, freely moveable S/C nodule, approximately 2 cm
5. These signs are usually associated with lameness (when lesions are in close proximity
in diameter. This nodule enlarges at portal of entry which rupture discharging
to joints) and development of nodules in the subcutaneous tissues especially
thick creamy pus with formation of indolent ulcer
around the fetlock.
4. The skin over the nodules may be fixed to the underlying tissues.
5. The surrounding skin is edematous at first, and later becomes thickened, hard
6. Lesions are of different sizes and may be large 5-7 cm in diameter. These lesions
and variably painful
may rupture discharging small amount of creamy green pus which may be blood-
6. The regional lymph nodes can be enlarged, but fever is uncommon. The stained. The ruptured lesions may heal within 2-3 weeks
infection also spreads along the lymphatics, causing cord–like thickening and
7. Occasionally, these lesions appear in other areas of the body such as inside the
further skin involvement
thighs, on the shoulders, or fore limbs. The lymphatic draining of the affected site
7. The lesion develops mainly on limbs especially hock but may present on the becomes enlarged and hard with the development of secondary ulcers
back, sides, vulva, scrotum, occasionally the lesion appear on nasal mucosa due
8. This disease has a tendency for the development of new lesions after the healing
to nibbling of the lesions on the limb and trunk but it lies just inside nostrils and do
of the old lesions.
not inovlve nasal septum.
8. Epizootic lymphangitis sometimes spreads to the underlying joints and results in
severe arthritis. Occasionally, there may be ulcerative conjunctivitis,
keratoconjunctivitis, a serous or purulent nasal discharge, or pneumonia
9. Sponatenous recovery can occurs and immunity is solid after attack but many
animals destroyed because of the chronic nature of the disease.
Postmortem Lesion
1. Areas of the skin and subcutaneous tissue are thickened
2. The regional lymph nodes may be enlarged and inflamed. Nodules in the skin
have a thick, fibrous capsule and the affected lymphatic vessels are usually
thickened or distended.
3. Both nodules and lymphatics contain purulent exudates.
4. The lungs, spleen, liver, testes and other internal organs may also contain nodules
and abscesses.

Diagnosis
A. Field diagnosis: signs as cutaneous nodules, lymphangitis and lymphadenitis with A. Field diagnosis: The disease can be suspected from history, clinical signs and
postmortem lesions. epidemiology of the disease
B. Laboratory diagnosis: B. Laboratory diagnosis:
• Samples: pus or exudate from lesions. Fungi die quickly in the samples if there is • Samples: Pus, blood and serum.
no antibiotic or refrigeration. Samples should be taken on solution contain 500 • Laboratory examinations:
iu/ml penicillin.
1) Direct microscopic examination of pus smear, the organism is short gram-
• Laboratory examination: positive diphtheroid Chinese letter.
1) Direct staining of smear: In a Gram–stained preparation, H. capsulatum is a 2) Isolation of the organism on blood agar, then the organism can be identifying
Gram positive, pleomorphic, ovoid to globose structure that is approximately by stained smear or biochemical tests.
2–5 µm in diameter.
3) Serological tests as toxin neutralization test, CFT and FAT.
2) Culture of the organism: H. capsulatum var farciminosum can be cultured on
a variety of fungal media as enriched Sabouraud dextrose agar with 2.5%
glycerol.
a. This organism grows as a mycelium at cooler temperatures.
b. These colonies grow slowly and develop in approximately 2 to 8
weeks at 26°C. They are dry, granular, wrinkled and grayish-white,
becoming brown as they age. Aerial forms are rare.
3) Serological tests include fluorescent antibody tests, enzyme–linked
immunosorbent assays (ELISA) and passive hemagglutination.
Differential diagnosis
This disease may be misdiagnosed clinically with This disease may be misdiagnosed clinically with
• Glanders 1. Sporotrichosis
• Sporotrichosis 2. Epizootic lymphangitis
• Ulcerative lymphangitis. 3. Ulcerative lymphangitis.
4. Pyoderma, abscesses, lymphangitis from other bacteria (eg, Staphylococcus
aureus, Rhodococcus equi, Streptococcus spp, or Dermatophilus sp),
5. Dermatophytosis
6. Equine cryptococcosis,
7. American blastomycosis
8. Onchocerciasis.
Treatment
Early cases (less severe cases) are cured by extensive excisions of affected parts • Prognosis is favorable. Nodules that do not affect deep tissue heal rapidly with
followed by local application of iodine or silver nitrate with parental injection of simple treatment within 1-2 weeks. After complete recovery, outbreaks of new
iodines preparation. nodules may develop.
Affected animals are showed extensive lesions are destroyed and buried is TTT:
advisable. 1. Abscesses are lanced and flushed with iodine solution. Large abscesses require
surgery.
2. Skin lesions and grossly contaminated limbs are scrubbed daily with an iodophor
shampoo.
3. Penicillin or trimethoprim-sulfa combinations have been given; however,
antimicrobial treatment may prolong the disease by delaying abscess maturation.
4. Phenylbutazone relieves pain and swelling. General supportive and nursing care is
indicated.
Control
1. Infected premises and equipment must be thoroughly cleaned and disinfected 1. It based on good hygiene in stables, careful disinfection of lower limb injuries or
(H. capsulatum can be inactivated by 1% sodium hypochlorite, glutaraldehyde, abrasions. Vaccination trials by bacterin-toxoid, fly and rodent control.
formaldehyde and phenolic disinfectants).
2. Bedding should be burned. Organisms in the soil may survive for long periods.
3. Early cases may be treated with sodium or potassium iodide, but the lesions may
later recur.
4. Vaccines are not widely available; however, live and inactivated vaccines have
been used in some endemic regions. There is no vaccine in Egypt.

5. Tetanus (Lock Jaw)
Definition
Acute highly fetal wound-infection toxemic disease of all animals and human which caused by the toxins of Clostridium tetani and characterized by an increased reflex excitability of the motor nerve centers with continuous spasmodic contraction of all
striated muscles and clinically by hyperesthesia tetany, convulsion and death.
Etiology
Tetanus is caused by exotoxins produced by Clostridium tetani. 3. It grows in blood agar producing colonies surrounded by complete zone of hemolysis after 24-48 hours.
1. C tetani, an anaerobe with terminal, spherical spores with typical drumstick appearance, is found in soil and intestinal 4. Spores can be killed by direct sunlight within 12 days, boiling water within 10-15 minutes, 30%hydrogen peroxide within 10
tracts. minutes.
2. It produces a number of toxins among them the most important are:
a. Neurotoxin or tetanospasmin: It is a protein in nature and responsible for the characteristic signs of tetanus.
b. Hemolysin or tetanolysin: It is a potent lethal toxin. It is responsible for the hemolysis around colonies on blood agar.
Epidemiology
1- Distribution: tetanus occurs in all parts of the world in all farm animals. It mainly appears as sporadic cases. In Egypt, it The portal of entry may be different according to the animal species such as:
commonly occurs in all farm animals 1. Horses: Puncture wounds of the hooves are common sites.
2- Animal susceptibility: Human and Solipeds (Horse, mules and donkeys) are the most susceptible followed by sheep, 2. Cattle: Introduction to the genital tract at the time of parturition is the usual portal of entry.
goats, pigs and cattle. Dogs and cats are rarely susceptible.
3. Sheep: following castration, shearing, docking, vaccinations, or injections of pharmaceuticals especially anthelmintics.
• Factors influencing susceptibility:
The portal of entry may be different according to the animal species such as:
• The disease may appear in all breeds, sexes and ages.
4. Neonatal born animals: tetanus occurs when there is infection in the umbilical cord associated with insanitary conditions
• The disease may appear any time of the year but outbreaks are common following castration, shearing, dehorning at parturition.
and other similar operations.
5. Pigs: pigs may be infected through umbilicus or through castration wounds.
3- Transmission:
• Wounds of internal organs such as teeth eruptions and injuries of intestinal mucosa due to worm infestations may give rise to
a. Source of infection: C. tetani organisms are commonly present in the feces of animals, especially horses, and in the soil infection (idiopathic tetanus).
contaminated by these feces.
• Moreover, spores may stay dormant in tissues for several months of even years until the conditions become favorable for
b. Mode of transmission: The portal of entry is usually through deep puncture wounds but the spores may lie dormant in the vegetation and proliferation of the organism and give rise to idiopathic tetanus (activated latent infection).
tissues for some time and produce clinical illness only when tissue conditions favor their proliferation.
Pathogenesis
1. The spores of C tetani are unable to grow in normal tissue or even in wounds if the tissue remains at the oxidation- 5. The toxin causes spasmodic, tonic contractions of the voluntary muscles by interfering with the release of
reduction potential of the circulating blood neurotransmitters from presynaptic nerve endings
2. Suitable conditions for multiplication occur 6. the excess is carried off by the lymph to the bloodstream and thus to the CNS, where it causes descending tetanus.
3. The bacteria remain localized in the necrotic tissue at the original site of infection and multiply. As bacterial cells undergo 7. Spasms affecting the larynx, diaphragm, and intercostal muscles lead to respiratory failure. Involvement of the autonomic
autolysis, the potent neurotoxin is released. nervous system results in cardiac arrhythmias, tachycardia, and hypertension.
4. The neurotoxin is absorbed by the motor nerves in the area and passes up the nerve tract to the spinal cord, where it
causes ascending tetanus
Clinical signs
Incubation Period: about 7-10 days after injuries but it may be 3 weeks or more in some cases 4. The animal may continue to eat and drink in the early stages but mastication is soon prevented by tetany of the masseter
• Tetanus usually appears as sporadic or individual cases muscles, and saliva may drool from the mouth. If food or water is taken, attempts at swallowing are followed by
regurgitation from the nose.
The mortality depends up on:
5. Constipation is usual and the urine is retained, the rectal temperature and pulse rate are within the normal range in the
1. Nature of the wound: deep badly soiled lacerated wound are accompanied with high mortality rate.
early stages but may rise later when muscular tone and activity are further increased.
2. The site of infection: wound near the head or neck are more dangerous than those of the trunk or hind limbs.
6. As the disease progresses, muscular tetany increases and the animal adopts a 'sawhorse' posture.
3. The incubation period (the infection doses): the shorter incubation period and higher mortality would be expected.
7. the hind limbs are stuck out stiffly behind and the forelegs forward. Sweating may be profuse and the temperature rises,
4. The adopted treatment: The course of the disease is different among and within the animal species. Generally, the often to 42°C. The convulsions are at first only stimulated by sound or touch but soon occur spontaneously.
duration of the fetal illness is usually 5-10 days in cattle and horse but sheep usually die in the third day.
8. finally, severe tetanic spasm during which respiration is arrested.
Clinical signs
9. Idiopathic tetanus, in which classical signs of tetanus occurs without wounds as in internal organs wounds as liver abscess
1. Initially, there is an increase in muscle stiffness, accompanied by muscle tremor. or intestinal erosion from parasites
2. There is trismus with restriction of jaw movements, prolapse of the third eyelid, an erect cartridge of the ears, retraction of 10. Ascending tetanus, this type occurs in not highly susceptible animals as dog and cat where only nerve trunk near the
the eyelids and dilation of the nostrils, and hyperesthesia with exaggerated responses to normal stimuli. toxigenic site absorb toxins to produce local muscular spasm
3. Stiffness of the hind limbs causing an unsteady, straddling gait, especially when backing or turning and the tail is held out 11. Desending tetanus, this type occurs in highly susceptible animal as equine and humans where toxins disseminated via
stiffly, (hump-like) vascular channels to nerve endings in areas far away from toxigenic site and toxin reach to CNS produce generlized
spasm begin from head to tail.

Prognosis
The prognosis is poor when the wound present near CNS, severe lacerated wound, high temperature, lock jaw, drenching pneumonia, idiopathic tetanus and signs rapidly progress.
Diagnosis
Field diagnosis: Tetanus can be diagnosed from the clinical signs which can be supported by history of non-vaccination, history of wound and recent obstetrical or surgical interference.
Laboratory diagnosis:
Samples: air-dried impression smears from spleen, wound site, culture swab from wound site in anaerobic transport media; spleen in sterile, leak proof container.
Laboratory examination:
a. Direct microscopic examination of the lesions smear by Gram stain: Demonstration of the characteristic drumstick spores is diagnostic. However, the results of this test are not satisfactory because the organism cannot be always demonstrated in
the wound.
b. Animal inoculation: It is the most reliable technique for the laboratory diagnosis of tetanus. Two groups of mice can be used. One group can be protected by subcutaneous inoculation of 750 IU/mouse of tetanus antitoxin two hours before
challenge. Both mice groups can be challenged by I/M inoculation in the hind leg with 0.25 ml of the supernatant of 48 hour cooked meat broth of the suspected sample. Rapid development of the clinical signs of tetanus in the non-protected
group indicates the presence of tetanus toxins.
Differential Diagnosis
Treatment
The main principles in the treatment of tetanus are to: 3. Relaxation of the muscle tetany:
1. Elimination of the causative agent: a. Relaxation of muscle to control the convulsions and avoid asphyxia can be done by administration of tranquillizers
a. Large doses of penicillin should be injected I/V as sodium benzyl penicillin 35,000 IU/kg followed after 12 hours by I/M such as Chlorpromazine (0.4-0.8 mg/kg body weight intravenously, 1.0 mg/kg BW intramuscularly, three or four times
inoculation of 2,000 IU/kg of procaine penicillin which should be repeated every 12 hours for 5-7 days. daily)
b. The wound (if found) should be treated by removal of necrotic tissue and irrigation with H2O2 or tincture of iodine then 4. Maintain hydration and nutrition
application of penicillin ointment. Treatment should be continued for 5 days and wound should be left opened. 5. Additional supportive treatment:
2. Neutralization of the unfixed toxin: a. Animal should be kept in dark quite well bedded place.
a. Administration of antitoxin for neutralization of unfixed neurotoxin in large doses during early stages has a great value b. If the animal is able to eat, soft laxative diet should be provided. In advanced cases, feeding through stomach tube
in the treatment. Very large doses of antitetanic serum (100,000 IU) should be injected I/V, I/M, and S/C every 12 or intravenous is necessary.
hours, respectively. Local inoculation of antitetanic serum around the wound is indicated c. In some cases, administration of enamas and catheterization may relieve the animal discomfort.
Control
1. Proper skin and surgical instrument disinfection for surgical procedures. 5. Foals from vaccinated mares should receive their first vaccination for tetanus at 6 months of age, followed by booster
2. Active immunization can be accomplished with tetanus toxoid vaccinations at 7 and 8 to 9 months of age. Tetanus vaccination should be repeated annually thereafter.
3. it should be treated with 1,500-3,000 IU or more of tetanus antitoxin, which usually provides passive protection for up to 2 6. Brood mares should be vaccinated annually 4 to 6 weeks before foaling to enhance the concentration of anti-tetanus
wk. Toxoid should be given simultaneously with the antitoxin and repeated in 30 days antibodies in their colostrum.
4. Foals from non-vaccinated mares should receive their first vaccination for tetanus (tetanus toxoid) between 3 and 4 7. Adult non-vaccinated horses or horses with unknown status should receive an initial series of 2 doses of tetanus toxoid
months of age. The second vaccination should be given between 4 and 5 months of age, followed by a third administered 3 to 6 weeks apart, followed by an annual booster.
vaccination between 5 and 6 months of age. 8. Adult vaccinated horses (those that have previously been vaccinated with the 2-dose regimen), should receive an
annual booster.

6. Strangles
Infectious Adenitis or Distemper
Def.
Acute contagious disease of equine (mainly young horses) caused by streptococcus equi
Characterized by
1. Inflammation of upper respiratory tract.
2. Abscessation of regional lymph nodes particularly submaxillary and pharyngeal lymph nodes.
3. Fever, anorexia.
Etiology
• Streptococcus equi subsp. equi (S. equi)
- GM +ve, non-motile and non-spore forming, coccobacillus, arranged in pairs or chains
- On blood agar → a zone of clear haemolysis (β haemolysis)
- Identified serologically according to Lancefield serologic grouping on basis of cell wall polysaccharides into Strept. equi Lancefield group C.
• It avoids destruction by neutrophiles through several virulence factors as capsule, antiphagocytic M-proteins and leukocidal toxins.
Predisposing factors:
1. Age, young ages are commonly infected due to low local immunity but adult can be infected if it they are not infected at young age.
2. Debility, fatigue and transportation.
3. Malnutrition and bad hygiene.
4. Stabled > outdoors animals.
5. Cold rain, or when there had been a hot or dry wind.
6. Concurrent infections as parainfluenza and debilitating disease.
Epidemiology
1- Distribution: worldwide and endemic in Egypt.
2- Animal Susceptibility: horse, donkey, mule of any age ( but youngs are more affected of 6 m to 2 y.) rarely over 5 y.
3- Transmission:
Source: Nasal, saliva and abscess discharge from infected animal
MOI
• Direct contact:
• Inhalation of infected droplets.
• Ingestion of contaminated food and water.
• Indirect: Contaminated fomites (utensils)
• Approximately 10-40% of horses that recover from the clinical disease has persistent infection of S. equi in the pharynx and guttural pouches for many months and are an
important source of infection (apparent carriers).
Pathogenesis
1. Following exposure of the oral and nasopharyngeal mucosal surfaces to S. equi, bacteria lodge in the pharyngeal and tonsillar lymphoid tissues →multiplication rapidly.
2. There is no evidence of colonization of mucosal surfaces, The binding of S. equi to pharyngeal cells is caused by fibrinogen binding proteins associated with M protein. The
resistance of S. equi to non-immune phagocytosis results in accumulation of large numbers of organisms surrounded by degenerating neutrophils.
3. Release of streptolysin S and streptokinase may contribute to tissue damage by directly injuring cell membranes and indirectly through activation of plasminogen,
Bacteraemia may occur.
4. Migration of neutrophils into lymph nodes causes swelling and abscessation.
5. Swelling of retropharyngeal lymph nodes may interfere with deglutition and respiration.
6. Nasal shedding of S. equi usually begins 4-7 days after infection, or 2 days after onset of fever, and persists for 2- 3 weeks in most horses but up to years in exceptional
horses.
7. Death is usually due to pneumonia caused by aspiration of infected material, although other causes of death include asphyxiation secondary to upper airway swelling
and impairment of organ function by metastatic infection.
8. Metastatic infection of the heart valves, brain, eyes, joints, and tendon sheaths or other vital organs may occur and cause a chronic illness and eventual death.
Clinical signs
IP →4-8 d
MB rate→ vary acc. to age, 10-50% and may reach to 80% MT rate→ low 3% Course→ 2-4 w.
A. Acute form: B. Bastard form C. Atypical or mild form (subclinical)

1. Diphasic fever (39.5-40.5°C), subside after 2-3 d • Means metastatic abscess formation in 1. Transient fever for 24-48 hrs.
and raise again when abscess in lymph node different internal organ, most commonly in 2. Anorexia.
developed. lungs, mesenteric L.Ns. Liver, spleen, kidneys,
3. Profuse nasal discharge.
2. Bilateral, serous nasal discharge which then and brain.
4. Moderate enlargement of the mandibular lymph nodes.
become copious and purulent. Signs depend on organ affected and severity of
3. Dyspnea (extension of head and neck due to infection but most commonly: D. Complication (immune mediated condition)
severe pharyngitis and laryngitis, dysphagia 1. Intermittent fever 1. Purpura Haemorrhagica:
4. Lymphadenopathy: Enlargement of 2. Chronic weight loss • Ag- Ab. complex causing vasculitis →S/C edema and
submandibular lymph nodes with painful 3. Sudden death due to rupture of abscesses petechial heamorrhage on serous mm and fever.
palpation into a body cavity • Occurrence:
5. Swelling of the retropharyngeal lymph nodes Metastasis to CNS: • Three weeks after acute disease.
may cause obstruction of the Oro- and
1. Excitation • Previously infected or vaccinated animal against
nasopharynx with subsequent respiratory distress
2. Hyperesthesia strangles.
and dysphagia.
3. Rigidity of the neck, and terminal 2. Post Strangles Myocarditis: due to M. protein react with heart
6. Death due to asphyxiation.
paralysis. myosin.
7. Rupture of lesion give thick creamy yellow pus.
4. Circling and abnormal gait 3. Post Strangles Anemia due to Ag- Ab. complex attachment to
RBCs and removal of them from circulation by RES.
5. Seizures
4. Guttural pouch empyema and sinusitis with dysphagia and
laryngeal hemiplegia.

P/M lesions
- Extensive suppuration in lymph nodes and internal organs particularly liver, spleen, lungs, pleura and peritoneum
Diagnosis:
Field diagnosis: history, epidemiology, clinical signs and PM

Laboratory Diagnosis:
Samples: Nasal discharge, pus, nasal swabs, blood and paired serum samples
Laboratory procedures:
• Direct microscopic examination of stained smear, the organism is Gram positive cocci exist in pair shapes.
• Isolation of organism on blood agar, and identification of the colony by staining or biochemical reaction. • Serological examination as passive hemagglutination test.
- • Animal inoculation as mice, pus inoculation will kill it in 2-4 days with evidence of acute septicemia
Treatment:
Isolation of infected animal and treat as soon as possible as following:

A. Medical treatment:
1. Penicillin (specific treatment)
a. 1st dose →combination of crystalline and procaine penicillin of 200 and 500 IU/kg BW respectively.
b. 2nd dose → procaine pencilling alone at 24 h intervals for 3-5 d.
2. Complications as Purpura Haemorrhagica treated by

a. Anti-inflammatory
b. Antihistaminic
c. Calcium therapy
d. Diuretics and blood transfusion.
B. Surgical treatment: Iodine or ichthyol ointment locally on enlarged nodes or hot fomentation to ripen the abscess with daily surgical dressing of the abscess after pus
evacuation.
C. Hygienic treatment: Rest of infected animal, provide soft palatable diet, clean separate water and food bucket and keep nostrils and muzzles clean with frequent
removal of discharges and washing with antiseptic.
Control
Proper management and hygiene:
1. Affected horse should be isolated for at least 6 weeks with strict hygienic control of all in contact workers and utensils.
2. Avoid contact of healthy animals with contaminated food, water.
3. Stalls and stable requirements should be cleaned and disinfected and the beddings should be burned.
4. Isolation of newly introduced animals for 2-3 weeks before introduction to the herd.
Vaccination (Vaccine is not available in Egypt)
1. Name: Strep. equi bacterin (Equibac II) and recently by M-protein extract vaccines (strepvax).
2. Animal: young foals at 12 weeks of age.
3. Dose: 3 successive doses at 3 weeks
Passive immunity from the immunized dams provides protection for foals in the early life till weaning.
7. Botryomycosis (Staphylococcosis)
Chronic granulomatous infectious disease of equine, caused by Staph. sp., characterized by development of granuloma commonly located on the limbs
Definition
near the point of elbow or scrotum (spermatic cord fistulae).
Aetiology Staph. sp is commonly isolated from the lesions. There are reports on isolation of Actinomyces viscous.
1- Distribution: The disease present where equine is raised.

Epidemiology 2- Animal susceptibility: Horses, donkeys and mules.
3- Mode of transmission: following trauma or contamination of cutaneous wounds as castration wounds.
Morbidity and mortality rates → low.

Cutaneous lesions
1. Papules, nodules (non-pruritic and non-healing), crusts and ulcers with formation of draining tracts.
2. Large solitary and resembles a tumor (may up to 10-20 cm in diameter)
Clinical signs 3. Rupture of nodules discharge pus which is sticky mucoid and yellow with whitish yellow seed or granules which is packed masses of staph. Sp.
4. On shoulder, neck, withers, ventral abdomen, udder, spermatic cord and limbs.
5. The lesion on spermatic cord causes scirrhous cord resulting in formation of chronic discharging sinus at scrotum with fibrosis and abscessation of
spermatic cord and testes.
6. metastasis of purulent lesions to internal organs as lung, liver, spleen and kidney may be occurs.
Field diagnosis: history, epidemiology and clinical pictures.

Laboratory diagnosis:
Samples: Pus, skin biopsy, blood and serum.
Diagnosis Laboratory examinations:
1. Direct microscopic examination of stained pus smear to detect staph sp.
2. Culture of pus samples.
3. Haematological and serological examinations.
Treatment Complete surgical excision of the lesion or local dressing of the lesions with prolonged course of systemic antibiotic.
1. Early diagnosis, isolation and treatment of infected animals.

Control 2. Prophylactic treatment of all cutaneous wound and abrasions.
3. Adequate hygiene to prevent spread of infection.

2 EQUINE VIRAL DISEASES
8. Equine African Horse Sickness (AHS)
Definition
It is a highly fatal, infectious, non-contagious insect borne disease of equines. Caused by African horse sickness virus (AHSV). The course is usually peracute to acute.
It is characterized clinically by:
1. Pyrexia.
2. Hemorrhages on the serosal surfaces of internal organs.
3. Edema in the subcutaneous tissues, lungs, pleura, and the internal cavities.
4. Rapid death.
Aetiology
African horse sickness virus is a member of the genus Orbivirus in the family Reoviridae.
• The virion is non-enveloped and consists of triple capsid structure.
• The core particle comprises two major proteins (VP3 and VP7) and three minor proteins (VP1, VP4, and VP6). These proteins make up the specific epitopes.
• The core particle is enclosed by the outer capsid, which is consisted of two proteins, VP2 and VP5. VP2 is the protein responsible for antigenic variation.
• The genome consists of 10 double-stranded ribonucleic acid (RNA) segments.
• Nine antigenically distinct serotypes are recognized with evidence of some cross immunity between strains.
Epidemiology
1- Distribution: The disease is endemic in Africa from Upper Egypt to South Africa. c. The disease prevalence is influenced by climatic (warm, moist climates) and
Some outbreaks were recorded in the Middle East and Southern Europe. other conditions that favor the breeding of Culicoides spp.
2- Animal susceptibility: d. Animals that have been infected with AHSV do not remain carriers of the
a. Horses are the most susceptible host (mortality of 70%-95%), followed by mules virus, which explains the failure of the disease to become established outside
(mortality of 50%-70%). tropical Africa, despite the occurrence of many outbreaks outside endemic
areas.
b. Horses of all breeds are equally susceptible to AHS. There is no difference
associated with age or sex of animals. 4- Transmission:
c. Most infections of donkeys and zebras are subclinical. A. Source of infection: The clinically affected horses are the major source of the
infection. The virus exists in all the body fluids and tissues of the affected
d. Dogs are the only other species that contract a fatal form of infection that is
horses from the onset of fever till recovery.
resulted from the ingestion of infected carcass of horses that have died from AHS.
The AHSV-9 has been isolated from the blood of stray dogs in Egypt. However, it is B. Mode of infection:
uncertain that dogs play any role in the spread or maintenance of AHSV • The virus is biologically transmitted by night flying midges such as Culicoides
because Culicoides spp. that transmit the infection do not feed on them. species and mosquitoes (Anopheles, Culex, and Aedes).
e. No other wildlife or domestic ruminants have been reported to play a • The disease is NOT transmitted by direct contact without insect vectors.
considerable role in the epidemiology of the disease. • The disease can be transmitted experimentally by intravenous or
f. Laboratory animals except rabbits are susceptible to the experimental infection, subcutaneous injections of infected blood.
especially mice and ferrets. 5- The economic importance of the disease:
3- Factors influencing susceptibility: • The disease causes high rate of mortalities.
a. The incidence of the disease increases during the season of the high activities of • AHS is one of the important and considerable diseases in international trade,
the insects. but movement can be accomplished safely by following appropriate
b. The AHSV is biologically transmitted by Culicoides spp., that have been shown to quarantine and testing procedures.
play an important role in Africa
Pathogenesis
1. After infection, the virus multiplies in the regional lymph nodes leading to a primary viremia.
2. The virus then disseminates to endothelial cells of target organs.
3. Effusions into body cavities and edematous changes of various tissues, as well as serosal and visceral hemorrhages, are consistent with endothelial cell damage.
4. Irrespective of serotype, the main targets for AHSV include heart, lung, and spleen.
5. However, the virus is present in most organs with high virus concentrations are found in the spleen, lungs, cecum, pharynx, and most lymph nodes.
6. Virus multiplication at these sites gives rise to a secondary viremia of variable duration.
Clinical Signs
A. Acute form (pulmonary or dunkop form): B. Subacute form (cardiac or dikkop form):
• The morbidity rate varies according to the number of insect vectors. • It is the common form in horses in enzootic areas.
• The mortality rate is upto 90%. • The IP is longer than the pulmonary form, usually 5 to 7 days.
• IP is about 2-5 days Mortality greater than 50%. Clinically, this form is characterized by:
• The Course of the disease is from few hours to 2 days. 1. Fever (39° C-41° C) that persists for 3 to 4 days.
• Prognosis with the dunkop form is extremely poor (<5% recover). 2. Bilateral bulging of edematous swelling overlying the supraorbital fossa, where the
• This is the most common form in fully susceptible horses, such as foals that lost their underlying adipose tissue becomes edematous and raises the skin well above the
colostral immunity or horses that never exposed to infection before. level of the zygomatic arch.
• In the diseased dogs, the pulmonary form is common. 3. The edema extends to the conjunctiva, eyelids, lips, cheeks, tongue (blue in color),
intermandibular space, and laryngeal region and may toward the chest.
Clinically, this form is characterized by:
4. These edematous swellings are doughy, painless, and cold.
1. High fever (40-41°C) over 1 or 2 days,
5. As the swellings increase, dyspnea and cyanosis may follow.
2. Conjunctivitis, and ocular discharges.
6. Petechial hemorrhages on the conjunctiva and on the ventral surface of the
3. Pulmonary edema, which results in rapidly progressive respiratory failure:
tongue are unfavorable prognostic signs that become evident shortly before
a. The respiratory rate may exceed 50 breaths per minute. death.
b. The animal stand with its forelegs spread apart, extended head, and 7. Animals may show signs of severe colic, repeatedly lie down, are restless when
dilated nostrils. standing, and frequently paw the ground.
c. Expiration is frequently forced, with the presence of abdominal heave lines. 8. Death usually occurs within 4 to 8 days after the onset of fever.
d. Paroxysmal coughing, often with frothy, serofibrinous fluid exuding from the 9. In horses that recover, paralysis of the esophagus may be a complication,
nostrils. especially in patients with severe edematous swellings of the head, resulting in
e. Profuse sweating is common. dysphagia.
f. Sudden onset of dyspnea, collapses and death occurs within 30 minutes to 10. Piroplasmosis is a common complication of AHS during recovery. In such horses,
a few hours of its appearance. icterus, anemia, and impaction are evident
4. The appetite of affected animals remains good despite the high fever and
respiratory distress.

8. Equine African Horse Sickness (AHS)
C. “Mixed” Form: D. Horse sickness Fever (mild form):
1. It is the most common form of AHS; however, it is rarely diagnosed clinically, but 1. It is the mildest form of AHS and is more common in donkeys.
is seen at necropsy of the majority of fatal cases of AHS in horses and mules. 2. The incubation period is between 5 and 9 days.
2. Both (pulmonary and cardiac) forms may develop in the same animal. 3. The temperature gradually rises over 4 to 5 days to 40° C then drop to normal, then
3. Initial pulmonary signs that are mild followed by edematous swelling and recovery.
effusions. 4. Some animals may be depressed with partial loss of appetite.
4. Death results from cardiac failure. 5. Transient congestion of the conjunctivae, slightly labored breathing, and increased
heart rate.
PM lesions
I- Acute form: II- Subacute form:
1. Edema of lungs and hydrothorax. 1. Marked hydropericardium.
2. The thoracic and abdominal lymph nodes may be enlarged. 2. Endocardial hemorrhage.
3. Hemorrhages may be found on the mucosal surface of the intestine. 3. Myocardial degeneration.
4. Anasarca, especially of the supraorbital fossa.
Diagnosis
I- Field diagnosis: based on history, clinical signs (dyspnea, edema of supraorbital fossa, subcutaneous edema of the head and neck, pulmonary and cardiac involvement,
and excess of pericardial and pleural fluids), and the epidemiology.
II- Laboratory diagnosis:
A. Specimens:
• For virus isolation and viral antigens detection: The blood of the febrile cases, slices from lungs, spleen, and lymph nodes collected at necropsy of dead animals.
B. Laboratory examinations:
1. Isolation and identification of the virus: Virus isolation is still the gold standard; however, both ELISA and polymerase chain reaction (PCR) can be used to detect AHSV
in blood and tissues. Primary virus isolation can be performed using a variety of cell cultures or by intracerebral inoculation of suckling mice. Cytopathic effects (CPE)
characterized by increased refractivity and detachment of cells.
2. Detection of the viral antibodies: CFT, FT, AGID, and NT are available for detection of the antibodies in the serum, but only NT is type specific.
Treatment
• This disease is a notifiable disease.
• There is no treatment has been described effective on the course of the disease.
• Only supportive and symptomatic treatment can be given.
Control
The control of this disease depends on:
a. Proper management and quarantine measures: b. Vaccination:

• Insect vectors should be controlled by the use of insect repellent, insecticides, and • Horses can be vaccinated with polyvalent modified live virus vaccine.
by keeping all equines in doors in insect proof stables especially at night. • All horses over 6 months should be vaccinated. The vaccine provides protection
• Strict +quarantine measures on the boundaries of the free area to minimize the within 21 days and full immunity is reached after 6 months and lasts for up to years.
entrance of infected horses or infected vectors. • In Egypt, polyvalent living attenuated vaccine is locally produced and used for
• Imported horses should be kept in quarantine for 60 days in insect-free places. vaccination of all equines in the Upper Egypt only.
• Foals born to immune mares acquire passive immunity by the ingestion of colostrum
for up to 4 to 6 months of life.
• Animals that survived after infection with one virus serotype produce protective
immunity against this serotype only, but they are susceptible to the other 8
serotypes.

9. West Nile Fever (WNF)
Definition
It is a Notifiable, Zoonotic, Vector-borne infection. Affects horses, humans, and several species of birds,
Caused by West Nile virus (WNV) that belongs to the family Flaviviridae.
Characterized by neurological illness which can be fatal.
Aetiology
• The infection is caused by West Nile Virus (WNV) that belongs to the family Flaviviridae and related to the viruses that cause St. Louis encephalitis, Japanese encephalitis,
and yellow fever.
• The WNV has an extremely broad host range. It replicates in birds, reptiles, amphibians, mammals, mosquitoes and ticks.
Epidemiology
1- Distribution: B. Mode of infection:
• The WNV is widespread. • Mosquitoes are infected when they bite infected bird, where it ingests the virus in
• It was first reported in 1937 in the West Nile region of Uganda and became blood. The mosquitoes are then spreading the virus from an infected bird to other
endemic in many African countries, as well as in the Middle East, European, birds and to other animals.
and Asian countries including Egypt. • In Egypt, Culex antennatus is the major mosquito species responsible for WNV
2- Animal susceptibility: transmission in the amplification cycle.
• Birds are the primary host. More than 300 bird species may act as vertebrate • Horses and human become infected when mosquito feed on infected birds then
hosts for WNV. bite horses or people; however, they are considered dead-end hosts because they
do not develop enough levels of virus in their bloodstream to spread the infection.
• Some bird species are more susceptible to the virus than others, especially the
crow. (Finding dead crows can be an indication for the presence of WNV)
• West Nile virus incidentally infects humans and equids (horses, donkeys, and
mules) that are considered as dead-end hosts that do not contribute to the
spread or amplification of the virus.
3- Factors influencing susceptibility:
• Majority of cases occurring in mid and late summer when the insect population
is the highest.
4- Transmission:
A. Source of infection:
• The main source of the infection is the infected insects (vectors or carriers).
• Birds are the reservoir of infection, and the infected migratory birds are thought
to play the major role in the spread of the virus in free areas.
Pathogenesis
After biting of the infected insect, virus goes to the blood stream.
Through the blood stream, the virus passes to the CNS, where it causes inflammation and pathological changes resulting in the nervous manifestations
Clinical Signs
• The IP is 2 to 14 days. 6. aimless wandering and circling
• In horses, some may be infected asymptomatically otherwise the clinical signs of 7. Convulsions.
the neurologic disease include: 8. Tremors of the face and neck muscles and inability to swallow.
1. loss of appetite and depression. 9. Periods of hyperexcitability
2. Ataxia, muscle twitching, 10. Coma and death may occur.
3. Weakness, usually in the hind limbs, Paralysis of one or more limbs 11. Fever has been seen in some but not all cases.
4. Impaired vision,
5. Head pressing, teeth grinding,
PM lesions
• The postmortem lesions are mainly restricted to the CNS.
• Limited to small multifocal areas of discoloration and hemorrhage in the spinal cord, brain stem, and midbrain with congested meninges.
Diagnosis
I- Field diagnosis:
The diagnosis can be made on the basis of history, clinical signs, and the seasonal incidence of the nervous manifestations.
Specimens: Blood, brain and spinal cord.
Isolation and identification of the virus: By inoculation of the suspected materials in tissue culture and confirmed by immunofluorescence or PCR.
Serological tests: Such as ELISA, NT, HI, and CFT.
Treatment
• There is no specific treatment, but animals or people affected may recover spontaneously
• Supportive and symptomatic therapy can be beneficial in reducing inflammation in the CNS and increasing the survival rate.
• Convulsions can be controlled by sedatives.
Control
Based on Vaccination, coupled with proper hygiene practices.
A. Proper management and hygiene:
1. Insect screens and topical repellents should be used on all susceptible animals specially during mosquito season.
2. Eliminate stagnant water to prevent mosquitoes from breeding.
3. Application of proper insect control program.
4. Carnivores should not be fed on WNF contaminated meat.
B. Vaccination:
1. It is considered an effective control measure.
2. Several commercial vaccines are available for horses.

10. Equine Encephalomyelitis
Definition
• Acute infectious arthropod borne viral disease of equines, Caused by a neurotropic virus.
• Characterized clinically by inflammation of the brain resulting in signs of CNS dysfunction such as:
Deranged consciousness, Motor irritation, Paralysis, & Moderate to high mortalities.
Aetiology
• The causative viral agent of this disease is Alphavirus genus, which belongs to Togaviridae family. It is neurotropic virus.
• There are 3 main strains of this virus:
1. Eastern Equine Encephalomyelitis virus (EEEV),
2. Western Equine Encephalomyelitis virus (WEEV),
3. Venezuelan Equine Encephalomyelitis virus (VEEV).
• These strains are immunologically distinct, and vary in their virulence, but produce quite similar types of diseases.
Epidemiology
1- Distribution: 4- Transmission:
• This disease is restricted to the Americans, USA, Canada, Venezuela, Brazil, and A. Source of infection: The main source of the infection is the infected insects.
Argentina. B. Mode of infection: The spread of this disease occurs by insect biting flies
2- Animal susceptibility: mainly mosquitoes (specially Aedes and Culex species) and by ticks, blood
• Domestic fowl and wild game birds are susceptible (unapparent infection). sucking bugs, and chicken nutes.
• Infections occur in horses, mules, donkeys, and possibly monk 5- The economic importance of the disease:
• Accidentally human may be infected. • High mortality rate.
• All laboratory animals, especially guinea pigs are susceptible. • The disease is zoonotic that can be transmitted to human.
3- Factors influencing susceptibility:

• Mostly occur in mid and late summer (high insect population).
Pathogenesis
• After biting of the infected insect, virus goes to the blood stream.
• Through the blood stream, the virus passes to the CNS, where it causes inflammation and pathological changes resulting in the nervous manifestations.
Clinical Signs
• IP ranges from 2 days to 3 weeks.
• The Morbidity Rate is low (depends on the insect population).
• The Mortality rate is about (75-100% in EEE), (10-40% in WEE), and (40-70% in VEE).
• The Course of the disease: 2 to 10 days.
• The clinical signs and lesions in horses infected with EEEV, WEEV, and VEEV are similar.
The disease is characterized by:
1. Fever (39-40°C) persists for 3-4 days (animal may show diphasic fever with EEEV and WEEV infection).
2. Anorexia and depression.
3. The nervous signs develop and appear at the peak of the fever or the peak of the second attack of the fever (in case of showing diphasic fever).
4. The early signs of nervous manifestations may include hypersensitivity, irritability, and aggressiveness.
5. Following, apparent blindness, head pressing or compulsive walking (usually in circles), facial paralysis, grinding of teeth, ataxia, and paresis of the trunk and limbs.
6. These signs are then followed by severe mental depression and the horse appears standing with its head down and its legs apart in a “sawhorse” stance.
7. The horse appears to be sleep, ears dropped, and chewed food may hang from the lips (the lay term of “sleeper” accurately describes this stage of the disease).
8. Finally, the horse becomes recumbent, has partial or complete pharyngeal paralysis, may convulse, becomes semi-comatose, and dies.
PM lesions
• The post-mortem lesions are mainly restricted to the CNS.
• The lesions include degeneration of the motor neurons, perivascular edema, and hemorrhage in the olfactory lobe.
• The greatest damage is in cerebral cortex, hypothalamus, and dorsal nucleus of the medulla.
Diagnosis
I- Field diagnosis: Based on history, clinical signs, and the seasonal incidence of the 2. Detection of the viral antibodies:
severe nervous manifestations in the endemic areas. • Several methods can be used such as ELISA, NT, HI, and CFT.
II- Laboratory diagnosis: • A definitive diagnosis is based on detection of at least four-fold increases in
Specimens: Blood, serum, brain stem, cerebrospinal fluid, and cerebrum. neutralization, complement-fixing, and hemagglutination-inhibiting
1. Isolation and identification of the virus: antibodies.
• The virus can be isolated by inoculation of the tissue suspension in 1-4 days • Higher antibody titers are found in CSF.
old mice that die within 3-8 days and the virus can be identified in their brain 3. Cross protection test: Used for differentiation between EEEV and WEEV by
by CFT & FAT. inoculation of the suspected materials and the antibodies in guinea pigs.
• Inculcation of the suspected materials in guinea pigs or chicken embryo.
Treatment
• There is no specific treatment.
• Supportive and symptomatic therapy can be beneficial in increasing the survival rate.
• Convulsions can be controlled by sedatives.
Control
Based on Vaccination, coupled with proper hygiene practices. B. Vaccination:
A. Proper management and hygiene: 1. Monovalent, bivalent, and trivalent formalin inactivated vaccines can be
1. The quarantine measures should be applied strictly. used.
2. The imported animals should be stabled in isolated place. 2. These vaccines are formalin inactivated tissue culture vaccines.
3. Application of proper insect control program. 3. The vaccination occurs by two doses with 7 days apart then booster dose
annually.
4. Horses’ movement during outbreak should be restricted.

11. Equine Viral Arteritis
Synonyms Viral arteritis, Equine arteritis, Epidemic cellulitis, Pinkeye, and Cellulitis Pinkeye Syndrome
Definition
• It is an acute contagious viral disease of equines caused by Arterivirus
• Characterized by Influenza-Abortion Syndrome and specific lesions in small arteries, interstitial pneumonia in very young foals.
Aetiology
• Arterivirus, RNA virus, belongs to family Togaviridae genus Pestivirus.
• This virus has a complement fixing antigen but does not cause hemagglutination.
• EVA virus grows well in primary equine, rabbit, and monkey cell lines.
• This virus resists freezing but not heat survives 75 days at 4°C between 2-3 days at 37°C and 20 - 30 minutes at 56°C.
• It is sensitive to the common disinfectants, Inactivated by lipid solvents (ether and chloroform).
Epidemiology
1- Distribution: 3- Transmission
• The disease has been reported in North America, Europe, and A. Source of infection:
some counters in Africa and Asia such as India. • The persistently infected carrier stallion serves as the natural reservoir that harbors EAV
• No cases have been reported in Japan and Australia. between breeding seasons.
2- Animal susceptibility: • The infected cases shed the virus in all discharges and secretions such as respiratory
• Horses are susceptible to natural infection. discharges, vaginal secretions, urine, feces, and semen.
• All ages and sexes of horse are susceptible. B. Mode of infection:

• Inhalation of the infective droplets, high titers of EAV are present 7-14 days during acute infc.
• Venereal transmission may occur from mares to stallions that remain carriers for long periods.
• Transplacental transmission may occur.
Pathogenesis
1. After inhalation, the virus infects pulmonary macrophages that transport the virus to bronchial lymph nodes (within 2 days) after aerosol infection, and then is
disseminated throughout the body through the circulation (viremia).
2. Vascular injury in EVA likely results from direct virus-mediated injury to the lining (endothelium) and walls of affected vessels.
3. Increased vascular permeability and leukocyte infiltration, lead to hemorrhage and edema around these vessels.
4. Severe septicemia and vascular damage especially in small arteries such as intestinal tract causing haemorrhagic enteritis, diarrhea, and abdominal pain.
5. Pulmonary edema and pleural effusion develop which manifested by severe dyspnea.
6. Abortion occurs due to severe necrotizing myometeritis (lethal fetal infection) that impairs progesterone synthesis, leading to fetal expulsion.
Clinical Signs
• The Incubation Period is usually 3-14 days and 3-4 days following venereal B. Acute form:
transmission. 1. Fever 39-41°C which persists for 1-5 days, anorexia, depression, stiffness in
• Morbidity Rate is high 70-90%. gait, rhinitis, conjunctivitis, and watery ocular and nasal discharges.
• Mortality Rate is low except in foals. 2. Edema can be observed in peri-orbital space, limbs, and ventral body wall.
• The Course of the disease is short 3-8 days. 3. Urticaria may develop in various locations on face, neck, and body.
• Most of infections are Clinically Unapparent or Subacute. 4. In pregnant mares, abortion may occur at any stage of pregnancy (during
A. Subacute form: It is the commonest form of the disease and characterized by the febrile reaction or shortly after).
1. Transient fever, anorexia, mild conjunctivitis, diarrhea, respiratory distress.

2. Edema in the legs and abdomen.
PM lesions
1. Congestion, edema, and hemorrhages in the subcutaneous tissues, lymph nodes, and visceral organs.
2. Thoracic and abdominal cavities may contain excess fluids.
3. In the aborted fetus, there is pulmonary emphysema, pulmonary and mediastinal edema, enteritis, and splenic hemorrhages.
Diagnosis
I- Field diagnosis: A presumptive diagnosis of EVA cannot be established on basis of field diagnosis
1. Specimens:
a. For virus isolation and viral antigens detection: Nasopharyngeal and conjunctival swabs, citrated blood samples for buffy coat separation, and semen should be
collected from the living cases as soon as possible after the onset of the disease.
b. For serological examinations: Paired serum samples should be collected form suspected animals. in the acute phase and convalescent phase
c. For Histopathological examinations: Samples from lungs, spleen, cecum, colon, and associated lymph nodes should be collected in neutral buffered formalin.
2. Laboratory examinations:
1. Isolation and identification of the virus: The virus can be isolated by inoculation of the suspected samples into primary equine cell cultures. The virus identification is
based on NT.
2. Detection of the viral antibodies: Fourfold increase of the antibody titer by NT, CFT, AGID, and ELISA confirm the diagnosis.
3. Serological examination, (VNT), evaluated (ELISAs) to detect 4-fold or greater increase in Acute and convalescent sera titer.
4. SNT is currently the OIE-approved gold standard for the detection of EAV in semen.
5. Reverse transcriptase–PCR assays is used for detection of the EAV nucleic acids in cell culture supernatants and clinical specimens.
6. Histopathological examinations: Histopathological examinations reveal evidence of panvasculitis especially in the small arteries.
Differential Diagnosis
The disease is confused with the following diseases:
1. Other respiratory tract infections of the horse (EHV-1, EHV-4, equine E.I, equine rhinitis A and B viruses, equine adenovirus), EIA, AHS, leptospirosis, purpura hemorrhagic.
2. Abortion differential diagnoses include EHV-1 (or rarely EHV-4), Equine herpesvirus-infected fetuses are expelled fresh and frequently have characteristic gross lesions,
whereas those infected with EAV are usually partially autolyzed and lack pathognomonic lesions.

11. Equine Viral Arteritis
Treatment
• Antibacterial drugs can be used to suppress or prevent secondary infection.
• Supportive and symptomatic treatments with non-steroidal anti-inflammatory drugs (NSAIDs), antipyretics, diuretics to reduce edema.
• Complete rest for 3-4 weeks help to improve the signs
Control
A. Proper management and hygiene: C. Vaccination
1. The suspected cases and their in-contact animals should be immediately isolated The modified living attenuated (MLV) vaccine is administered I/M to horses. MLV is
and kept under strict quarantine for 4 weeks. licensed for use in the United States and Canada for prevention of EAV infection.
2. The stables of the infected cases should be carefully cleaned and disinfected. 1. Live attenuated vaccines are commercially available.
3. Screening should be applied for detection of the EVA carrier stallions to avoid the 2. They are safe and effective for stallions and non-pregnant mares.
venereal spread among the breeding farms. 3. The MLV vaccine is not recommended to use in pregnant mares especially in the
4. Stalls and equipment on the affected premises should be disinfected with phenol, late stage of pregnancy or in foals less than 6 months of age.
chlorine, iodine. 4. Maternal antibodies to EAV disappear between 2-6 months of age, thus it is
B. Husbandry recommended that foals be vaccinated at 6 months of age.
1. Identification of persistently infected stallions. 5. Vaccinated stallions usually do not shed virus in either semen or urine.
2. Carrier stallions should be kept physically isolated and bred only to mares that are 6. Virus-neutralizing antibodies are induced within 5-8 days after MLV vaccination,
seropositive. and peak antibody titers are achieved by 7-14 DPV following vaccination
3. Mares should be kept isolated from other non-vaccinated or seronegative horses neutralizing antibodies will last for at least 2 years.
for 3 weeks after being bred to a shedding stallion or after insemination with
infective semen. To prevent contamination of collection equipment, teasers, and
premises with ejaculate because EAV can be transmitted to susceptible horses
by indirect aerosol contact.

12. Equine Infectious Anemia EIA (Swamp Fever, Typhoid Fever of horse)
Definition
• It is a contagious insect born disease of equine caused by virus, characterized by
1. Recurrent intermittent fever, depression, rapid loss of weight,
2. Anemia (may be transient or progressive),
3. Subcutaneous edema of lower part of the body and death.
• Infected horse can remain viremic carriers for life and will yield a positive serology
Aetiology
1. Equine Infectious Anemia Virus (EIAV), Lentivirus of family Retroviridae (single RNA),
2. There are a number of antigenically differ strains which have antigenic drift and vary in their antigenicity and virulence,
3. It grows on tissue culture and equine leukocytes,
4. It is easily destroyed by sunlight, persist for several months at room temperature in urine, feces, dried blood and serum.
5. The virus inactivated by sodium hydroxide, sodium hypochlorite, most of organic solvent and by heating at 58 c for 30.min.
Epidemiology
1- Geographical distribution: 3- Transmission
a. Most of the states of the United States, central and northern A. Source of infection:
parts of Europe. 1. The virus exists in all tissue secretions and excretions such as blood, urine, nasal and
b. Higher prevalence in regions with warm climates. eye discharges, and semen of the infected and carrier cases.
c. There are no reports on the disease in Egypt. 2. The virus may persist in the body for up to 18 years after infection.
2- Species affected: B. Mode of infection:
a. All breads and age groups of Equidae are susceptible, 1. Infection occurs Mechanically by biting insects as mosquitoes and horse flies
debilitated, and parasitized animals are highly susceptible. (Tabanus and Stomoxys), blood transfusion, and use of contaminated surgical
b. Less severe in donkeys and mules. instruments as hypodermic needles.
c. Experimentally, pigs and sheep are infected. 2. Intrauterine infection from mares to foals may occur.
3. Venereal transmission: The virus can be transmitted in semen of the infected stallions.
4. Oral infection by drinking of contaminated water, colostrum, or milk may also occur.
Pathogenesis
A. Infection
1. The virus infects macrophages, and most infected macrophages are detected in the spleen.
2. Viral replication occurs primarily in mature tissue macrophages that serve as the predominant source of the high titer viremia during acute infection.
B. Virus passes to blood streams and then localizes in spleen and liver
3. The spleen contains the highest level of replicating virus during acute infection, but other tissue sites of active infection include the liver, lymph nodes, bone marrow,
lung, adrenal gland, kidney, and brain.
C. Congestion then icterus, edema, and progressive anemia
4. The pathogenesis of anemia is multifactorial and includes immune-mediated erythrocyte destruction, as well as decreased erythropoiesis.
5. Early work indicated that erythrocyte life span is reduced to between 28 and 87 days (normal mean, 136 days)
Clinical Signs
The IP is 2-4 weeks. Morbidity rate is high up to 100% & Mortality Rate is about 50%. The Course is 3-6 weeks
A. Acute Form: B. Chronic Form: “Swamper”

1. Rapid onset of fever (over 40°C), depression, weakness, loss of condition, ataxia. 1. This form occurs as attacks with 1-3 months intervals.
2. Red-icteric mucous membranes. 2. The attack is characterized by severe anemia, weakness, and intermittent febrile
3. Edema of ventral abdomen, prepuce, and legs. attacks.
4. Rapid dehydration, droopy ears, and serous discharges from nose and eyes 3. Mucous membranes appear pale and icteric.
(nasal discharges may be haemorrhagic). 4. Pulse is weak and becomes fast with slight exercise.
5. Myocarditis (manifested by tachycardia and arrhythmia). 5. Offensive diarrhea associated with colic may occur.
6. Spleen is enlarged and can be detected by rectal palpation. 6. There are signs of marked blood-changes anemia as prolonged clotting time and
7. Pregnant mares may abort. serum is green-tinged.
8. Clinical episodes typically last 3 - 5 days, and the interval between episodes is 7. Pale mucous membranes, petchiation, icterus, and epistaxis associated with
variable, ranging from weeks to months, Infected horses appear normal between more severe haemolytic anemia and thrombocytopenia.
episodes. 8. Neurologic signs occasionally develop and can include ataxia and encephalitis.
9. Death may occur within 5-15 days in clots and 3-4 weeks in adults. These horses become inapparent carriers of the virus.
C. Subacute Form: D. Latent Form:

1. Conjunctiva is slight swollen and slightly icteric. 1. This form may become active at any time
2. Recurrent fever (attack occurs 2-3 times a month). 2. It is most dangerously in hard work, poor diet, parasitic infestations, or any
3. The Course of the disease in this form is 1-7 d (course of the attack). debilitating factor may aggravate the acute attack.
4. Death is usually due to exhaustion.
PM lesions
1. General anemia and emaciation with gelatinous atrophy of fatty tissues.
2. Subserous ecchymotic hemorrhages of abdominal cavity.
3. Thoracic and abdominal cavities are filled with fluids.
4. Hemorrhages in liver, spleen, and kidneys.
5. Pericarditis, interstitial pneumonia, and lymphadenitis.
6. Splenomegaly, hepatomegaly (spleen and liver are enlarged in size). Spleen usually appears blackish.
7. Cardiac degeneration and dilatation with epicardial hemorrhages.
8. In horses with neurologic disease, lesions include non-suppurative granulomatous meningitis, encephalitis, and plasmocytic-lymphocytic infiltration of the brain and spinal
cord.

12. Equine Infectious Anemia EIA (Swamp Fever, Typhoid Fever of horse)
Diagnosis
I- Field Diagnosis: The disease is difficult to be diagnosed based on clinical signs. The manifestations may be acute or chronic.
II- Laboratory Diagnosis:
A. Specimens:
1. For virus isolation and viral antigens detection: Citrated blood or sections from liver, kidneys, and spleen should be collected.
2. For serological examinations: Paired serum samples should be collected form the suspected animals. One sample should be collected early in the acute phase of
the infection and the other sample should be taken 2-3 weeks after the onset of the disease (convalescent phase).
3. For Histopathological examinations: Samples from spleen, liver, and kidneys should be collected in 10% formalin.
4. For hematological examinations: Blood samples should be collected on potassium oxalate for hemoglobin and PCV determination
B. Laboratory examinations: The laboratory diagnosis is based on isolation and identification of the virus.
1. Isolation and identification of the virus: The virus can be isolated by inoculation of the suspected samples into Equine Leukocytes Cell Culture.
2. Detection of the viral antibodies: Several serological examinations can be used for detection of the virus antibodies such as AGID (Coggin test) and competitive
ELISA. AGID is the only test, which identifies the clinical unapparent carriers.
3. Nested RT-PCR assays: allow detection of viral RNA in plasma from inapparent carriers.
4. Hematological examinations: Hematological examinations reveal decrease in Hb concentration and PCV value.
III- Differential diagnosis:
The disease is confused with all diseases characterized by anemia and edema as:
1. Purpura haemorrhagica.
2. Leptospirosis.
3. Sever strongylosis or fascioliasis, Dourine.
4. AHS.
Treatment
• Supportive therapy such as blood transfusion and hematinic drugs may facilitate the clinical recovery.
• Minimizing stress; and providing good nursing care, nonsteroidal anti- inflammatory drugs (NSAIDs), and hydrotherapy for dependent edema, and blood transfusion for
severe anemia and/or thrombocytopenia.
• Therefore, antimicrobial drugs may be indicated during febrile episodes to help prevent secondary bacterial infections.
Control
1. Any infected cases should be recorded and notification of the authority.
2. Test and slaughter policy: The clinically infected animals should be identified by Coggin test and destroyed.
3. Hygienically disposed all suspected materials such as contaminated food, water, semen, uterine fluid, and milk
4. The introduction of the infected cases to free areas should be restricted.
5. Animal vector control, especially for horse flies, deer flies, and stable flies, will minimize natural transmission of EIAV.
6. The swampy areas should be drained, and insects should be controlled by fly repellents and by using screened stables.
B. Vaccination:
Vaccines are available but are not in general use. Inactivated virus vaccines are safe.

13. Equine Viral Rhinopneumonitis (EVR)
Equine Viral Abortion - Equine Herpesvirus Infection - Equine Coital Exanthema
Definition
• EVR is an acute febrile contagious viral disease of equines, caused by equine herpesvirus.
• Characterized clinically by respiratory manifestations (rhino pneumonitis), abortion, and neonatal mortalities and encephalomyelitis.
Aetiology
• Equine Herpesvirus, DNA virus and belongs to Herpesviridae family.
• There are antigenic similarities to Bovine Herpesviruses (IBR/IPV)
a. EHV-1 is the cause of abortion, rhinopneumonitis, and perinatal mortalities and encephalomyelitis.
b. EHV-2 is the cause of mild respiratory disease.
c. EHV-3 is the cause of coital exanthema.
d. EHV-4 is the cause of rhinopneumonitis and rarely causes abortion.
• EHV-1 and EHV-4 are the most important among these viruses. Both neurotropic and lymphotropic.
• Herpesvirus can grow well in tissue culture such as fetal equine kidney or equine dermal cell lines production of CPE & intranuclear inclusion bodies
Epidemiology
1- Distribution:
EHV is widely distributed in North and South America, Europe, South Africa, Australia, and parts of Asia.
2- Animal susceptibility:
a. Natural outbreaks occur in horses & donkeys.
b. Recently the virus has been isolated from wild equines & wild ruminants with different clinical signs.
3- Transmission:
A. Source of infection:
a. The sources of infection are the diseased cases, latently infected animals, and animals in the incubation period.
b. The virus is shed in the Nasal Secretions for 2-3 weeks after infection and also in the uterine discharges.
B. Mode of infection:
• Direct horse-to-horse contact.
a. Aerosol/Inhalation of infective droplets.
b. Ingestion of food or water contaminated by nasal discharges, uterine discharges, and aborted fetus.
• Indirect transmission occurs through infected fomites.
4- Seasonal incidence: most commonly occurs in autumn &winter.
5- Economic importance: costs of veterinary care, also the longer-term, detrimental effects/poor performance on athletic performance.
Pathogenesis
A) Respiratory tract
1. Following inhalation, both EHV-1 and EHV-4 replicate in epithelium of the respiratory tract causing damage and necrosis of respiratory epithelium.
2. After 2-3 days, it passes to lymph nodes followed by viremia which may persist for 2 weeks
3. It localizes in organs such as uterus, lungs, and central nervous system causing necrosis, vesiculitis, and thrombus formation.
B) Uterus:
1. Infection of endothelial cells in the pregnant uterus causes a vasculitis that → affects small arteriolar branches in the glandular layer of the endometrium.
2. Most of abortion occurs at 7-11 m of gestation and both fetus and placenta are fresh.
3. Abortion is also caused by vascular lesions and thrombo- ischemia.
C) CNS: The pathogenesis of EHV-1 neurologic disease also involves vasculitis and thrombo-ischemia following endothelial cell infection.
Clinical Signs
IP is usually 2-10 days. The Morbidity Rate is high. the Mortality Rate is low. The Course of the Disease is 1-3 weeks
• Signs of upper respiratory tract infection are usually limited to young foals in breeding farms and mares showing only abortion without previous respiratory signs
A. Respiratory Form (in Young Foals): B. Abortion form (in Pregnant Mares):
• These viruses can cause severe lower respiratory tract disease (viral 1. The pregnant mares may express the respiratory form with the same clinical signs as in
pneumonitis) and can lead to secondary bacterial bronchopneumonia. foals, but a little mild.
1. The disease is characterized by mild fever (biphasic pyrexia) which persists 2. The respiratory manifestation may be followed by abortion in about 60-90% of the
for one week. pregnant mares after 2-16 weeks from the exposure to the virus.
2. Short dry cough which becomes moist later, dyspnea, rhinitis, conjunctivitis. 3. Abortion usually occurs between 8-11 months (the last Third) of pregnancy.
3. Ocular and Nasal Discharges: Watery which become mucopurulent later. 4. Mares often abort standing up, and the foal is usually expelled within the intact amnion
4. Slight enlargement of the throat lymph nodes. and may be expelled within the intact allantochorion.
1. Depending on the time of infection during pregnancy, some foals are stillborn, others
die soon after birth, and some are normal at birth, but become weak and die within 3
days of birth with signs of respiratory distress and severe mental depression (sleepy
foals).
C. Neonatal Foals: D. Encephalomyelitis form:

1. It is associated primarily with EHV-1 infection. 2. This form occurs in young foals.
2. Affected foals are born live but are sick at birth or become ill within 1 to 2 3. Neurologic signs such as rapid onset of ataxia followed by paresis and recumbence
days. then followed by death.
3. They show marked and rapidly progressive lower respiratory tract signs
(dyspnea and tachypnoea) caused by primary viral pneumonitis that leads
to respiratory distress, hypoxia, and death.
4. Secondary bacterial bronchopneumonia develops in foals that survive
more than 2 or 3 days. These foals may survive for 10 to 14 days but
eventually die from respiratory disease and other complications.

13. Equine Viral Rhinopneumonitis (EVR)
Equine Viral Abortion - Equine Herpesvirus Infection - Equine Coital Exanthema
PM lesions
1. Vasculitis in the CNS and fetal tissues and placenta
2. Rhinitis and pneumonitis.
3. Aborted fetus shows severe
a. Pulmonary congestion and focal hepatic necrosis.
b. Excessive fluid in the pleural cavity, bronchitis, pneumonitis, and slight icterus
Diagnosis
I- Field Diagnosis: The clinical diagnosis is based on
1. The clinical manifestations such as respiratory signs and
2. High incidence of abortion in the convalescent pregnant mares
3. The characteristics postmortem lesions.
A. Specimens:
1. For virus isolation: Nasopharyngeal secretions or swabs in suitable transport media on ice or at 4°C and citrated blood for buffy coat can be collected in early
stage of infection.
2. For serological examinations: Paired serum samples should be collected.
3. For Histopathological examinations: Samples from lungs, liver and lymph nodes should be collected in 10% formalin.
1. Isolation and identification of the virus: The virus can be isolated by inoculation of the suspected samples into the fetal equine kidney or equine dermal cell lines. The
isolated virus identified by FAT and NT.
2. Detection of the viral antigens: PCR and FAT can be used.
3. Detection of the viral antibodies: Fourfold increase of the antibody titer by NT, CFT, FAT, and ELISA confirm the diagnosis.
4. Histopathological examinations: Eosinophilic Intranuclear Inclusion Bodies in the endothelial and lymphoreticular cells.
5. Hematological findings transient leukopenia with lymphopenia in the first 7 - 10 days after infection, which is replaced by a leukocytosis with lymphocytosis up to
day 21 after infection.
III- Differential Diagnosis:
The disease should be differentiated from diseases causing respiratory o nervous signs and abortion as the following:
1. Strangles in which there are rhinitis and lymph nodes abscessation.
2. Equine Viral Arteritis, no lesion in aborted fetus and sever edema is present.
3. Purpura haemorrhagica, S/C edema of legs is severe.
4. All causes of Abortions in mares as Salmonellosis, or Strept. genitalium infection.
5. All agents causing Neurological Disease as protozoal encephalitis, brain trauma, arbovirus encephalitis, rabies and botulism.
Treatment
• Supportive and symptomatic therapy with complete rest during the acute febrile phase of the infection is indicated.
• Also, antibacterial therapy is recommended to minimize the secondary bacterial infection.
Control
1. The suspected cases and their in-contact animals should be immediately isolated and kept under strict quarantine.
2. Strict quarantine measures should be applied for the newly introduced animals.
3. Stables of the infected cases should be carefully cleaned and disinfected
4. Hygienic disposal of the aborted fetus and fetal membranes.
B. Vaccination:
1. Vaccination is the main protocol for control and prevention of this disease by using vaccines contain EHV-1 and EHV-4 either inactivated or modified live viruses.
2. Foals should be vaccinated at 3-4 months of age with booster dose after 2-3 months then annually.
14. Vesicular Stomatitis
Definition
Vesicular stomatitis (VS) is a viral disease of livestock that results in vesicles and ulcerations on the teats, oral mucosa, tongue, and coronary bands. All three main serotypes
of the VS virus can infect the horse.
Aetiology
• RNA Vesiculovirus – Family Rhabdoviridae – (Major serotypes: VSV-NJ and VSV-I)
• Affects horses, cattle, swine, camelids, humans – Sheep and goats resistant
• Closely resembles exotic vesicular diseases including FMD
Epidemiology
1- Geographic Distribution Human Transmission
• Western hemisphere – North, Central, and South America a. Direct contact – Infected tissues, vesicular fluid, saliva
• Emergence in eastern hemisphere? – 2009: Bahrain, Laos (suspected) – 2009: b. Insect bites – Blackfly, sandfly
Pakistan (limited regions) c. Aerosol – Laboratory settings
• Southwest U.S. – Outbreaks in warmer regions 3- Losses due to:
• Southeast U.S.: enzootic cycle a. Increased culling, increased mortality
2- Animal Transmission b. Reduced milk production
a. Vectors – Sandflies – Blackflies – Seasonal outbreaks c. Labor, medicine, veterinary costs
b. Direct contact – Infected animals – Contaminated objects.

14. Vesicular Stomatitis
Pathogenesis
Clinical Signs
• Incubation period – 3 to 5 days
• Fever and vesicles that resemble FMD.
• Morbidity – Range: 5 to 90% – Most animals seroconvert.
• Mortality – Higher in adults – Death rare in cattle and horses.
A. Horses severely affected
• Oral lesions; Drooling, chomping, mouth rubbing, lameness
• Coronary band lesions
B. Cattle, pigs
1. Vesicular lesions; Oral, mammary gland, coronary band, interdigital region
2. Usually isolated to one body area.
3. Salivation, lameness.
• Recover within 2 weeks
Foot & Mouth Disease Vesicular Stomatitis Swine Vesicular Disease Vesicular Exanthema of Swine
Clinical Signs All vesicular diseases produce a fever with vesicles that progress to erosions in the mouth, nares, muzzle, teats, and feet
by Species
Cattle Oral & hoof lesions, salivation, drooling, Vesicles in oral cavity, mammary Not affected Not affected
lameness, abortions, death in young animals, glands, coronary bands,
"panter"; Disease Indicators interdigital space
Pigs Severe hoof lesions, hoof sloughing, snout Same as cattle Severe signs in animals housed on Deeper lesions with granulation
vesicles, less severe oral lesions: Amplifying concrete; lameness, salivation, tissue formation on the feet
Hosts neurological signs, younger more
severe
Sheep & Goats Mild signs if any; Maintenance Hosts Rarely show signs Not affected Not affected
Horses, Not affected Most severe with oral and Not affected Not affected
Donkeys, coronary band vesicles, drooling,
Mules rub mouths on objects, lameness
PM lesions
Gross lesions Histopathology
– Erosive, ulcerative lesions – Degeneration of epithelial cells
– Oral cavity, nostrils, teats coronary band
Diagnosis
I- Clinical Diagnosis Samples should only be sent under secure conditions and to authorized laboratories
Vesicular diseases are clinically indistinguishable! But symptoms in horses are to prevent the spread of the disease.
suggestive – Salivation and lameness
VSV vs. FMD Virus isolation
– VSV less contagious Viral antigen detection
– VSV lesions generally found in one area of the body – Vesicular fluid or epithelium
II- Laboratory Diagnosis – ELISA, complement fixation, virus neutralization
Sampling Antibody tests
Before collecting or sending any samples, the proper authorities should be – Paired serum samples
contacted. – ELISA, complement fixation, virus neutralization
Treatment
• No specific treatment available.
• Supportive care:
– Fresh, clean water (Electrolytes if necessary)
– Soft feeds
• Antibiotics for secondary infection.
• Good prognosis.
• Production animals may suffer losses.
Control
Disinfection Vaccination Prevention
• Easily inactivated • Vaccines used in some endemic regions of Central, • Do not buy from positive herds for 3 months post-
– Area must be free of organic matter. South America. infection.
– Contact time of at least 10 minutes. • Vaccines may be available during an outbreak – • Avoid grazing at peak insect feeding hours.
Efficacy is unknown. • Segregation and isolation necessary for controlling
• Disinfectants
• Contact state veterinarian for availability information. spread.
– Phenolic, halogen-based disinfectants.
• Sanitation.
– Soda ash, 2% iodophores.
• Insect control programs.
– Chlorine dioxide, 1% chlorine bleach.
– 1% cresylic acid.
– Quaternary ammonium.

15. Equine Influenaza EI
Epizootic catarrh, Pinkeye, Infectious equine bronchitis, Laryngotracheobronchitis, and Equine cough
Definition
It is an acute contagious respiratory disease of equine, caused by influenza virus type A
Characterized clinically by severe cough, mild fever, conjunctivitis, serous to mucopurulent nasal discharges
Aetiology
1. Two antigenically distinct orthomyxoviruses are responsible for the disease (A/Equi/1 and A/Equi/2).
2. Both affect upper and lower respiratory tract of equine.
3. A/Equi/2 is more pneumotropic more severe clinical signs.
4. Antigenic drift has been reported in this virus
5. Equine influenza virus grows well in allantoic cavity of the embryonated chicken eggs and in different tissue cultures
6. It is stable and remains infective for 24-36 hours in aerosol
Epidemiology
1- Distribution:
• Equine influenza is widely distributed all over the world such as USA, Canada, UK, France, Germany, Africa, and Asia.
• Only few countries are free from infection such as Australia, Iceland, and New Zealand.
2- Animal susceptibility:
• All equine species are susceptible.
• Natural outbreaks are common in horses and mules.
• Some other equines may act as reservoir hosts.
• Outbreaks commonly occur in horses of 1-3 years of age.
3- Transmission:
A. Source of infection: The main source of infection is the infected horses that shed the virus in the nasal secretions and the expired air for up to 10 days.
B. Mode of infection: The infection occurs through inhalation of the infective droplets.
• The disease spreads mainly through coughing, respiratory droplets and through direct contact with infected subjects.
• Droplet transmission (droplets greater than 10 µm are capable of being projected over moderate distances by coughing), and airborne transmission (infectious
droplets less than 5 µm, capable of wide dissemination in confined environments & of reaching the lower respiratory tract of susceptible individuals) are common.
4- The economic importance of the disease:
a. Can put horses out of work for weeks
b. Potentially cause serious secondary infections.
c. Veterinary costs associated with diagnosis, treatment, care, and possible secondary infections.
d. Has a great importance in racing and sport horses because of explosive outbreaks, time off from training and competition due to layups and quarantines, and event
cancellations.
e. In the United States, EI is recorded as the second most common virus infect horses, following the equine herpesvirus. . Sahar A. Kandeel
Pathogenesis
1. After inhalation → virus multiplies in epithelial cells of respiratory mucosa especially in the upper part of respiratory tract.
2. The virus is binding to the receptors on the target cells located in upper respiratory tract after penetrating the mucus layer that forms a protective barrier over the cell
surface by the help of viral neuraminidase that destroy the mucous glycoproteins and removing decoy receptors present on mucins, cilia, and cellular glycocalyx (highly
charged layer of membrane attached to a cell membrane and act as a barrier between a cell and its surrounding).
3. Damage in cilia, hyperemia, edema, necrosis, and desquamation and erosion of the epithelial cells.
4. The horse expresses clinical signs of the typical viral respiratory disease.
5. This leads to damage in cilia, hyperemia, edema, necrosis, desquamation and erosion of the epithelial cells, and cell death.
6. The alveolar macrophages’ function is reduced as a result of the mucosal damage and secondary bacterial bronchopneumonia may develop.
Clinical Signs
• The IP is usually 1-3 days, Morbidity Rate is up to 100%, and Mortality Rate is 11. In severe infections, pneumonia is a common sequela (7-14 days after infection).
extremely low The Course of Disease is 1-3 weeks lung sounds increased in amplitude, and ultrasound demonstrate pulmonary
• Signs are typically seen 48 hours and sometimes as early as 24 hours, after exposure consolidation.
to infection. 12. Persistent respiratory disease can persist beyond 14 days after infection and is
mostly due to secondary bacterial infection.
Clinically, this form is characterized by:
13. Neonatal infection can be fatal, resulting in severe bronchial and interstitial
1. Sudden onset, rapid spread fever (39-41°C) which persists for 1-3 days, The fever
pneumonia.
may be biphasic with a second peak observed around day 7 after infection.
14. The infection in donkeys and mules is more severe than in horses and can result in
2. Short dry cough (becomes moist later), dyspnea, rhinitis, conjunctivitis,
mortality.
3. Watery ocular and nasal discharges (become muco-purulent later).
15. Subclinical disease with viral shedding may be common in previously vaccinated
4. Submaxillary lymph nodes may be painful in palpation with or without horses and is considered an important source of infection.
enlargement.
Complications
5. Variable degrees of dullness and horses become anorexic at the time of the
1. Bronchopneumonia.
initial pyrexia.
2. Edema of the legs.
6. Conjunctivitis with watery ocular discharges that may become muco-purulent.
3. Guttural pouch empyema.
7. The submaxillary lymph nodes may be painful in palpation with or without
enlargement. 4. Chronic pharyngitis, and abortion may occur.
8. Weight loss is recorded after influenza virus infection. 5. Myositis.
9. Dyspnea may be observed, 6. Rarely, cardiomyopathy may develop due to viral damage to the myocardium.
10. Clinical signs typically resolve in 1 to 2 weeks in uncomplicated cases, although 7. In rare cases neurologic disease may be observed.
coughing may persist for 21 days.
PM lesions
1. No specific lesions can be observed.
2. The mucosa of the respiratory tract is hyperemic or inflamed.
3. Sometimes, bronchopneumonia or lobular pneumonia may be found.

15. Equine Influenaza EI
Epizootic catarrh, Pinkeye, Infectious equine bronchitis, Laryngotracheobronchitis, and Equine cough
Diagnosis
I- Field Diagnosis:
• History, clinical signs (high morbidity, rapid fever, and cough), epidemiology (very rapid spread among horses)
A. Specimens:
1. For virus isolation & viral antigen detection: Nasopharyngeal swabs should be collected from the febrile horses during the early stage of the disease.
Swabs should be collected in sterile saline containing 25-50% sterile glycerol and transported on ice and should be examined within 48 hours.
2. For serological examinations: Paired serum samples should be collected from the suspected cases. One sample should be collected during the early acute phase
of the infection & the other should be collected 2-3 weeks later.
1. It depends on isolation and identification of the virus, detection of the viral antigens, and detection of specific antibodies.
2. Isolation and identification of the virus: EI virus can be isolated from the suspected nasopharyngeal swab suspension by cultivation on allantoic or amniotic sacs of
9-11 days old embryonated chicken eggs. The isolated virus can be identified by HA, HI, and CFT.
3. Detection of the viral antigens: Viral antigens detected by FA and ELISA
4. Detection of the viral antibodies: Fourfold increase of the antibodies titer by using HI confirm the diagnosis
III- Differential Diagnosis
1. Strangles: Strangles is caused by Streptococcus equi and It is more common among foals. serous to purulent nasal discharges, cranial lymphadenitis sometimes with
abscessation.
2. Equine viral arteritis: 70-90% morbidity rate, and some deaths. It is characterized by slight to moderate upper respiratory signs as serous nasal discharges and
occasionally cough may be developed. About 50-80% of pregnant mares may abort. Severe edema may be observed in ventral abdomen, legs, prepuce, scrotum,
and lungs. Enteritis and diarrhea may occur.
3. Equine viral rhinopneumonitis: Outbreak is rapid with delayed abortion. There are mild respiratory signs as serous to purulent nasal discharges with or without cough,
mild cranial lymphadenitis, and conjunctivitis. About 90% of pregnant mares may abort 13 months after the first attack.
4. Equine rhinovirus infection: Clinically, it is characterized by pharyngitis, pharyngeal lymphadenitis, serous to muco-purulent nasal discharges, and cough persists for 2-3
weeks.
Treatment
• Complete rest (stop work for a month) and good stable ventilation and hygiene.
• Suspected in-contact horses should be isolated and symptomatically treated.
• Intensive course of broad-spectrum antibiotics is helpful to control secondary
• Bacterial infections especially among foals.
• Antivirals can be used to reduce the virus spread. However it should be carefully used as it may result in the development of antiviral resistance among influenza A viruses,
which could reduce the effectiveness of treatment during outbreaks. There are two classes of influenza antiviral drugs are currently licensed for the prophylactic and
therapeutic use against influenza A virus in humans: the M2 ion channel blockers and the NA inhibitors. Hyperimmune serum is also helpful.
• Hyperimmune serum is also helpful.
Immunity
• There is no solid immunity against equine influenza.
• The recovered animals can be infected several times.
• There is no cross immunity between the strains of this virus.
Control
Proper management and hygiene:
• Premises in which equine influenza epidemics occur should be placed in quarantine for at least 4 weeks and similar restrictions should be applied to the stable men
handling the diseased horses.
• Cleaning and disinfection of the affected stables, transport vehicles, and equipment with phenol, chlorine, or quaternary ammonium products,
• good ventilation and dust control
• hygienic disposal of the contaminated feed stuffs and litter.
Vaccination:
• Vaccination can be applied by using adjuvanted bivalent inactivated vaccine containing A/Equi/1 and A/Equi/2 antigens.
• The vaccine is applied by intramuscular administration.
• The recommended vaccination program is vaccination of foals at 6 months of age with two doses with 1-3 months intervals then booster vaccination every 5-7 months.
• The vaccine performs immunity for 6 months.
• Severe physical exercise, training, and transportations should be avoided for 2-3 days after vaccination. Myocarditis or myositis is a common sequel if the horse is worked
hard following vaccination

3 EQUINE PARASITIC DISEASES
16. Equine piroplasmosis (EP) (Biliary fever.) 17. Dourine (Equine syphilis )
Definition
arasitic tick born disease of equines, caused by babesia spp and OR Theileria spp • It is an acute and chronic contagious parasitic disease of adult equine caused
characterized by fever, anemia, edema, jaundice and hemoglobinurea. by T. equiperdum characterized by edema & inflammation of genital tract and
cutaneous plaques and nervous signs or paralysis.
• The disease is sporadic in occurrence with spontaneous recovery or subclinical
infection
Aetiology
• The disease is caused by babesia caballi & previously designated as B. Equi (round, T. equiperdum
amoeboid or pear shape Or as maltese cross form), B. caballi large species resembles - Tissue parasite and rarely invades blood
to B. bigemina
• The only parasite that is not transmitted by invertebrate vector
• May present in blood in few or undetectable amount
• Trypanosomes are present in peripheral blood, cutaneous plaques & genital
secretions in low no.
• Can survive for years in vaginal mucosa & urethra
Epidemiology
1- Distribution: widespread present in Egypt. 1- Distribution: restricted mainly to Africa.
2- Animal susceptibility: 2- Animal susceptibility: Equines Donkey and mule more tolerant than horse
▪ Equines as horse, donkey, mules. Young one → least susceptible. 3- Transmission:
▪ Zebra act as carrier. a. Source: The parasites present in genital secretions as vaginal and urethral
3- Transmission: secretions and in dermal plaques.
1. Ticks (Dermacentor, Hyalomma & Rhipicephalus sp.) b. Mode:
▪ B. caballi →transovarian transmission. 1. Contact during coitus (Venereal)→ not in each copulation as
trypanosomes not continually present in genital tract throughout the
▪ T. equi trans-stadial transmission (from nymph to adults within a generation).
course of the disease.
▪ Both organisms →mechanical transmission (Contaminated by infective
2. Foals can be infected contamination of nasal or conjunctival mm by
blood as contaminated needle or surgical instruments).
secretions of dams.
2. Prenatal infection
4- Seasonal incidence: ↑ during breeding season
Pathogenesis
• T. Equi sporozoites inoculated into host after tick biting→invade lymphocyte → • Infection → parasite reach blood with replication → parasitaemia→
multiplication and development to schizont which rupture releasing merozoites → trypanosomes localized in S/C tissue (urticarial plaques), nervous system
invade erythrocytes changing to trophozoite which grow and multiply into pear (Paralysis) mucosa of vaginal mm & testicles (inflammation & edematous
shaped tetrad (Malatse cross) merozoites. swelling).
• B. Caballi sporozoites inoculated into host after tick biting→ Invade erythrocyte
→change to trophozoites which grow and divided to two round, or pear shaped
merozoites which release from erythrocytes after rupture invading new cells resulting
in haemolysis of erythrocytes.
Clinical signs
• I.P for Babesia → 12-19 day. D. Stage of Edema:
• I.P for Theileria→10-30 day. 1. Recurrent low-grade fever. Good appetite.
• M.T rate in free area →10-50 % while in endemic areas→very low. 2. Inflammation and edematous swellings of external genitalia with vulval
• T. equi is more pathogenic and tend to cause severe signs than babesia. edema which extended to udder and medial aspect of thigh
A. Peracute (rare): showing only dullness and death. 3. Mucous discharges (cloudy red-yellow purulent) come from genitalia.
B. Acute Form (common): 4. Occasionally vaginal mucosa is edematous, reddened & contain
ulceration (nodules, vesicles, and ulcers) with ↑sexual desire & frequent
1. Fever, anorexia, depression, reluctance to move and reduced appetite.
urination.
2. ↑ pulse and respiratory rate.
5. Enlargement of inguinal LN & abscessation of udder.
3. Congested (early), anaemic or icteric mucous mm (late stage).
6. The stallion has penile and preputial swelling with paraphimosis, and
4. Lateral recumbency. genitalia covered with vesicle, nodules and occasionally ulcers with selling
5. Edema of fetlock, head and ventral abdomen. of testicles and scrotum.
6. Anemia, hemoglobinurea, jaundice. 7. Lesions heal leaving area of depigmentation at genital tract, udder &
7. B. caballi cause persistent fever & anemia. perineum.
C. Chronic form → nonspecific illness with signs as: E. Stage of Urticarial: “Silver dollar plaques”
1. Mild inappetence. 1. Cutaneous eruption or edematous cutaneous plaques or urticarial

swellings.
2. Poor exercise tolerance.
2. On different parts of animal body.
3. Weight loss.
3. Up to 10 cm diameter and 1 cm thick contain serous fluid rich in
4. Transient fevers.
trypanosomes.
5. Enlarged spleen may be palpable on rectal examination.
4. Persist for 2:4 days and suddenly reappear on the other part of the body
6. Anemia can be minimal or absent in chronically infected horses.
F. Stage of Paralysis:
7. Chronically- infected donkeys show mild:
• It is the last stage and begins with facial ms paralysis) & extend to ms of back
a. Edematous swelling of distal part of limbs. & hind limb with incoordination, hyperesthesia, lameness, muscular atrophy,
b. Icterus and pale mucous mm. ataxia and finally complete paralysis with recumbency and death.
Chronic cases may survive for months and still carriers for about 4.y intravascular.
P/M lesions
1. Carcass emaciated. Anaemic or icteric 1. Carcass: emaciated and anaemic
2. Excessive fluid in serous cavity 2. Characteristic skin lesions
3. Bone marrow hyperplasia 3. Edematous swelling or S/C gelatinous exudate on genital organs as vulva,
4. Liver and spleen enlarged and congested with hepatic centre-lobular necrosis, but scrotum, and prepuce.
jaundice is more common and hemoglobinurea less frequent
5. Lung shows secondary infection (edema, emphysema, or pneumonia)
By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 23

16. Equine piroplasmosis (EP) (Biliary fever.) 17. Dourine (Equine syphilis )
Diagnosis
I- Field diagnosis: history, epidemiology, clinical signs, and PM I- Field diagnosis: history, epidemiology, clinical signs, and PM (Signs of
II- Laboratory diagnosis: development of characteristic external genital lesions in several mares served
by the same stallion
A. Samples:
1. Peripheral blood smears,
A. Samples:
2. Parts of organs as liver, spleen, and lungs
1. Skin lesion biopsy.
3. Blood & serum
2. Plaques fluid
B. Laboratory Procedures:
3. Vaginal or urethral secretions/ washings
1. Microscopic examination of stained blood films to detect characteristic
intraerythrocytic piroplasms during parasitaemia 4. Blood and serum
2. PCR B. Laboratory procedures:
3. Histopathology 1. Microscopic examination of stained blood film or smear by Giemsa

stain to detect intercellular flagellated Protozoan - It is rarely possible
4. Serodiagnosis as CFT, ELISA & IFAT, the last two tests considerd prescribed
due to trypanosomes are sparsely present extremely difficult to be
tests for international trade of equine.
found in blood, cutaneous plaques.
5. Estimation of bilirubin in serum & urine
2. Blood concentration techniques
6. Experimental inoculation of infective blood into susceptible horse.→Definitive
3. Lab. animal inoculation Rabbit I/M or intratesticular inj. with plaques fluid
but expensive and time-consuming method
or blood cause testicular edema
4. Hepatological studies: ↓ RBCs &↑ WBCs count
All causes of anemia and edema as
5. Serological tests: CFT IFAT, ELISA and agglutination test.
1. EIA
2. EVA
All causes of anemia, edema, urticarial and paralysis as
3. Purpura haemorrhagica
1. Coital exanthema
4. Trypanosomiasis
2. Herpes virus infection
5. Laminitis, colic, azoturia
3. Equine viral arteritis
4. Equine infectious anemia
Treatment
• T. equi is more resistant to therapy than B. caballi, • Suramin
• Imidocarb. (Imizol®) 2 mg/kg, b.w I /M • Berenil
• Supportive and symptomatic therapy
Control
Depend mainly on: Detection of infected stallion before breeding by CFT and positive one is castrated
• Avoid introduction of the disease (carrier and infected ticks) and discarded from breeding with prophylactic treatment of all breeding mare at
mating with Berenil
• Isolation of infected case and treatment by antiprotozoal drug as imidocarb
• Control of ticks and special care to prevent mechanical transmission
• There is no commercial vaccine yet available for use in field
18. Toxoplasmosis
Definition
Contagious disease of all worm-blooded animals species even human, caused by toxoplasma, characterized clinically by abortion and still births in ewes and in all species by
encephalitis, pneumonia and neonatal mortalities.
Aetiology
Toxoplasma gondii, intracellular protozoa
Attack most organs with predilection sites for reticulo-endothelial and central nervous system.
Epidemiology
1- Geographic distribution: Wide in distribution and present in Egypt
2- Species affected:
Cats are considered as final host while other animals (dogs, ruminants, equine, birds, rabbits, and humans) are act as intermediate host.
Decrease resistance of adult animals result in change of latent infection to clinical cases.
3- Mode of infection and transmission: Cats (final host) are infected by eating meat contain infective oocyst or by ingestion of feed contaminated by sporulated oocyst
while intermediate hosts are infected by the later route only.
4- Economic importance: Losses from abortion, neonatal mortalities, and zoonotic implications.
Life cycle and Pathogenesis

1. After ingestion of meat contain infective oocyst or feed contaminated with sporulated oocyst by final host or cats, the parasite pass a cycle as in coccidiosis in small
intestine (intestinal life cycle), where bradyzoites enter intestinal epithelium, multiply and differentiate to male and female gametes with formation of unpopulated oocyst
which are shedding in feces.
2. Sporulation occurs after several days under suitable conditions from humidity and temperature in environment.
3. Intermediate hosts are taking sporulated oocyst with contaminated food, since occurs extraintestinal life cycle where sporozoites penetrate intestinal wall and reach to
blood with occurrence of parasitaemia and change to tachyzoites which locate intracellular, multiply and invade any cells of the body resulting in cell rupture and
formation of tissue cyst of 10-50 um in diameter, these are formed in CNS, muscles and visceral organs as lung or liver.
4. Placenta and foetus in pregnant animals are invaded by tachyzoites resulting in placentitis, neonatal mortalities and abortion.
5. Foetus and placenta are most vulnerable tissues for toxoplasma in sheep resulting in abortion as main signs or fetal resorption, born dead fetus or macerated foetus or
born lamb infected congenitally by toxoplasmosis.
6. Also, prenatal infection may be occurring in pets. The parasite secretes powerful exotoxins resulting in granulomatous lesions.

18. Toxoplasmosis
Clinical Signs
A. Cattle: E. Dogs:
Fever – Dyspnea. 1. Occur mostly in dog less than one year.
Nervous signs as ataxia and hyperexcitability in early stage followed by lethargy. 2. Localised in resp., neuromuscular, gastrointestinal.
No or rare abortion to occurs but occurs still born or birth of weak calf which show 3. Characterised by fever, tonsilitis, diarrhea, vomiting.
fever, dyspnea, coughing, sneezing, nasal discharge, grinding of teeth, clonic 4. In old dog signs associated with neural and muscular affection as tremors,
convulsion, tremors of head and neck and death after 2-6 d. ataxia, paralysis, and stiffness.
B. Sheep: 5. Ocular lesion as retinitis and uveitis.
Systemic disease is rare as fever, dyspnea, generalized tremors, convulsion, F. Cats:
intermittent ataxia, and depression may precede abortion.
1) Prenatal toxoplasmosis
The common signs are Abortion and neonatal or prenatal death only, abortion
Still born kitten, kitten have enlarged abdomen because of enlarged live
occurs during last 4 w of pregnancy (late stage) in up to 50 %.
and ascites and encephalitis.
Full term lamb from affected ewe is born dead or alive but weak and die within 3-
2) Postnatal toxoplasmosis
4 d of birth.
a. Persistent or intermittent fever, dyspnea.
Lambs infected after birth are show signs of fever and dyspnea.
b. Hepatitis.
C. Goats:
c. Diarrhea, vomiting.
Systemic disease with a high fatality is more common especially in young goats.
d. Stiffness and lameness due to CNS involvement.
Neurological signs as convulsions, intermittent ataxia, blindness, and depression
may be precede abortion by several weeks. e. Retinitis and uveitis.
Abortion occurs nearly at 100 d of pregnancy, also still birth (mummified foetus) or
prenatal deaths occurs.
D. Equine: The protozoan result in progressive neurological signs as ataxia, circling,
paresis, and apparent blindness.
PM lesions
1. Multiple proliferative and necrotic granulomata are characteristic for toxoplasma
2. In cattle the lesion may be undergo calcifications, theses lesions present commonly in central nervous system, lymph nodes, liver, and lung.
3. In visceral involvement there are pneumonitis, hydrothorax, ascites, lymphadenitis, myositis, intestinal ulcer and necrotic foci in liver, spleen, and kidney.
4. In sheep involvement of uterine walls, placenta and foetus occurs and the lesions present in foetus as necrotic lesions in brain (microglial nodules), liver, lung and fetal
membrane contain gray, white areas in the cotyledon.
Diagnosis
I- Field Diagnosis: Signs of abortion, neonatal mortalities and nervous signs, history of frequent abortion in contact humans, post-mortem lesions and epidemiology of the
disease.
II- Laboratory diagnosis
A. Specimens: Placenta, uterine fluids, feces, peritoneal or thoracic fluids, brain, CSF, lung, liver, blood, and serum.
B. Laboratory procedures:
1. Serological test as CFT and dye test (methylene blue dye) or Sabin Field-man test, it is highly sensitive and specific for humans but not necessary for cat
toxoplasmosis or ELISA, PCR, Late agglutination test, indirect fluorescent test and indirect hemagglutination test.
2. Fecal examination, although cats are serologically show high incidence but oocyst in feces is low and cats shed oocyst for 1-2 w and following their first exposure
cats are usually not clinically ill during period of oocyst shedding.
3. Cytological examination, tachyzoites are detected in various body fluid during acute illness as in peritoneal or thoracic fluids.
4. CSF analysis, protein and leukocytes may be increase.
5. Radiograph on chest or abdomen.
6. Histopathology on brain or lung to see granulomatous necrotic lesions.
7. Toxoplasma isolation: by animals or cell culture inoculation. Mice inoculation by tissue emulsion (toxoplasma can be found in cells of most organs especially brain,
lungs, and diaphragm tissues), body fluids or by cleaned sporulated oocyst from feces, inject I/C or I/P or feeding of infected materials, oocyst detected in brain
of mice at 4-6 w post infection while tachyzoites can detect in peritoneal fluids at 4-6 d post infection.
8. Biochemical and haematological changes, there are hypoproteinemia, hypoalbuminemia, increase in GPT, GOT and CPK due to hepatic and muscular necrosis,
increase in serum bilirubin and leukopenia.
III- Differential Diagnosis:
All cases of abortion and still birth or pneumonia and nervous signs of sheep and cattle, Vit. A deficiency result in encephalopathy in newborns.
All cases of congenital defects as in vaccination by BT living attenuated vaccine, infection by akabne or BVD diseases.
Treatment
Drugs are not completely effective in killing the parasites,
Clindamycin is the drug of choice as 10-20 mg/kg, b/w for dogs, 12.5-25 mg/kg, b/w for cats every 8-12 h for 2 w orally or I/M,
Sulfonamides as Sulphadiazine, Sulphadimidine or Sulphamerazine or Tribrissen can be used for 1-2 w orally as dose every 24 h.
Control
• Avoid contact between pets especially cats and farm animals or avoid contamination of farm animal foods by cats feces.
• Protect humans food from contamination by pets feces (cats).
• Carcass of infected or suspected animals should be destroyed.
• Reduce incidence of cats infection to decrease oocyst shedding.
• This will decrease the incidence of the disease in farm animals by feeding of cats canned or commercially processed food and not eat raw meat products and avoid
eating of rodents, cockroaches or earthworms which act as mechanical vectors.
• Control of cockroaches, earthworm and rodents.

19. Habronemiasis 20. Strongylosis (Red Worm Disease) 21. Gastrophilus Infestation (Parasitic Bots)
Definition
Infectious parasitic disease of equine caused by Habronema sp., characterized clinically by Infectious parasitic disease of equines caused by Strongylus sp. Chronic infectious disease of equine caused by Gastrophilus sp. (Larvae, adult)
chronic catarrhal gastritis or gastric granuloma / or tumors, granulomatous cutaneous lesions characterized clinically by verminous arteritis, colic, lameness, diarrhea, characterized by chronic gastritis, loss of condition & ↓work performance.
(lower limbs abdomen, and glans penis) and conjunctival lesions. debility and anemia.
Aetiology
Habronema sp. Strongylus Sp.: Gastrophilus sp (larvae, adult ):
1. H. musca  Large strongylus as S. vulgaris, S. edentates and S equinus  G. Nasalis
2. H. majus  Small strongylus as Trichonema and Tridontophorus  G. Intestinalis→ the most important one
3. H. megastoma.  Adult worms live in large intestine (cecum and colon) & are blood  G. Inermis
4. All of them infest horse stomach (gastric granuloma) while most of cutanous lesions suckers and tissue feeder.  G. Haemorrhoidalis
attributed to H. megastoma
Epidemiology
1- Distribution: widespread in tropical and subtropical countries including Egypt 1- Distribution: wide distribution and present in Egypt 1- Distribution: wide distribution & present in Egypt
2- Animal Susceptibility: Equine of all ages but disease common in adult. 2- Animal susceptibility: Equines of all ages but young ages more 2- Animal susceptibility: all species of equine.
3- Seasonal incidence: More common in summer season. susceptible 3- Seasonal incidence: more common in summer season
4- Transmission: Ingestion of food and water containing dead flies with infective larva or 3- Seasonal incidence: no seasonal incidence. 4- Life cycle, mode of infection & Transmission:
deposition of the larvae on lips, wounds or around the eyes 4- Transmission: Ingestion of food or water contaminated by infective a. Bots fly put eggs on the animal hair and through 10 days hatch to larvae.
third larval stage (L3).
b. 1. migration from skin (legs, cheeks, lips) → 2. penetration of epidermis →
5- Economic importance: Losses from ↓ work performance and 3.licking
deaths of some diseased animals.
c. Reach buccal cavity where the larvae spend sometimes migrating in the tissue
Life cycle: of mouth & accumulate alongside the molar teeth resulting in mouth irritation.
d. Migration from mouth to stomach → larvae pass out in feces after 10:12 m of
infestation → moult and change to adult fly.
e. Some larvae may migrate to abnormal sites as brain, heart, lung.
N.B Stray larvae may found anywhere throughout the body as lungs causing pulmonary
habronemiasis.

Pathogenesis
1. H. megastoma larvae → gastric mucosal invasion → Mild chronic gastritis and in rare cases Larvae are most pathogenic resulting in arteritis and thrombosis
perforation of stomach wall with occurrence of local peritonitis and may involve spleen causing:
and intestine with formation of abscesses and constriction intestine. → Granulomatous 1. Partial or complete ischemia.
masses (tumors) formation which contain adult worms with a central orifice from which
2. Necrosis or gangrene.
eggs and larvae escape into gastric lumen.
3. Thickening of arterial wall.
2. H. maius and H. muscae: do not cause tumors but may penetrate stomach glands resulting
in catarrhal gastritis with production thick tenacious mucus and heavy worm burden may 4. Aneurysm, Intussusception.
cause stomach ulceration. 5. Bleeding due to rupture of intestinal wall nodules.
3. Conjunctival habronemiasis: is small granulomatous lesion (3:5 mm) on 3rd eye lid or eyelid 6. Verminous encephalitis.
skin with local irritation and profuse lacrimation. Adult worms are blood suckers (blood haemolysis due to toxins
4. Cutanous habronemiasis: habronema sp. Larvae deposited in wounds with local produced by the worm) & tissue feeders (intestinal ulceration).
inflammation and extensive granulation tissue with secondary bacterial infection.
Clinical signs
A. Gastric habronemiasis: Young foals show severe infestation & few deaths may occur within 3 1. GIT disturbance as variable appetite, pain on mastication, pale mm., emaciation,
1. Poor coat, variable appetite which is often depraved w. or more colic.
2. Large tumors may cause pyloric obstruction and gastric distension Clinical forms: 2. Shying, balking, head tossing and running due to fly annoyance during oviposition.
3. If perforation occurs →fever, depression, pain and heat on the left side just behind A. Intestinal form: 3. Marked debility
costal arch 1. Normal appetite or anorexia. 4. When the larvae present in rectum→ itching, ↑ frequency of defecation with
4. Mild to moderate colic acc. to intestinal stenosis. 2. Staring coat, weakness. straining and prolapse of rectum.
5. Marked anemia if spleen is involved 3. Pale or yellowish mm. 5. In severe cases death occurs after 6-8 w. from cachexia.
B. Cutaneous habronemiasis or summer sore: 4. Pendulous abdomen, hallow flank.

• Commence as pruritis and formation of rapid developing small papules or hard nodules 5. Profuse watery offensive feces (Small red worm may be seen in
with eroded scab covered centers with little discharge and some irritation. feces or on the hand after rectal palpation).
Lesion 6. Aneurysm of anterior mesenteric artery in form of firm pulsating
1. may increase up to 30 cm in diameter within few months swelling.
2. depressed center composed of coarse red granulation tissue covered with greyish 7. Intestinal wall nodules can be felt on rectal exam.
necrotic mm and raised, thickened edges B. Verminous colic form:
3. may regress in colder weather and recur in the following summer. 1. Repeated attacks of colic in adult horse which comes on
4. Confined to parts of the body where skin wounds or excoriation are most likely to occur during exercise due to presence of emboli in terminal branch
and where horses cannot remove the vector flies as on face below medial canthus of of mesenteric artery.
eye, middling of abdomen, prepuce and penis and less commonly on the legs, withers, 2. Colic may be intermittent, and the diseased animal may fall
fetlock or coronary bands. on the ground with muscular trembling and sweating.
C. Conjunctival habronemiasis: C. Paralysis of hind limb form:
1. Present on eye lids and may reach to 5 mm in diameter. 1. Thrombus in iliac artery in one or both limbs →intermittent
2. Conjunctivitis. lameness which comes on during exercise and disappear after
1-2 hrs. Of rest.
a. With small yellow necrotic mass about 1 mm in diameter under the conjunctiva.
2. The diseased animal standing with raised abducted limbs.
b. Soreness and lacrimation.
c. Not respond to bacterial conjunctivitis therapy.
P/M lesions
 Granulomatous lesions in eye, stomach, skin & occasionally lungs  Anaemic carcass 1. Presence of larvae in stomach cause marked congestion and swelling and
 Adult worm in wall of cecum & colon in form of small tumor like sometimes hemorrhage around point of attachment
nodules in size of lentil → some nodules may show small punctures 2. Edematous swelling of stomach and duodenum with formation of white deposits
through which worms escape into bowels. (necrotic epithelium) on mucosa.
 Patches of inflammation or necrosis in cecum and colon due to 3. Signs of commencing or complete perforation of gastric or intestinal wall.
the thrombus formed.

Diagnosis
I- Field diagnosis: I- Field Diagnosis: Depend on failure of young horses to grow Based on signs or direct inspection of eggs on the hairs in summer, larvae expulsion in
II- Laboratory diagnosis: properly, abnormal feces, anemia, lameness, colic, and less feces and on rectal examination larvae may be detected on rectal mucosa.
efficient performance of working horse. Rectal examination to
A. Sample:
detect thickening of anterior mesenteric arteries, intestinal nodules
• Biopsy or scrapings from cutaneous lesions and worms may appear as small reddish worm on the hands after
• Conjunctival smears or discharges examination
• Feces and blood. II- Laboratory diagnosis:
B. Procedures: A. Sample: Feces, blood, and serum.
1. Fecal examination for diagnosis of gastric form is difficult because larvae are not easy to B. Procedures:
be found in feces. 1. Fecal examination: The signs can be seen without eggs, fecal
2. Examination of skin biopsy or scrapings and conjunctival smears or discharges to detect egg count /gm feces (EPG) of 1500-2500 represent clinical signs.
the larvae 2. Arteriography on mesenteric or iliac arteries to see aneurysm.
3. Histopathology of cutaneous lesions has CT contain small yellow caseous areas up to 5 3. Hepatological examination: Anemia (↓RBCS, PCV, Hb. Conc.)
mm in diameter with marked local eosinophilia. with marked eosinophilia
III- Differential Diagnosis: 4. Serum changes: ↑ beta-globulin & ↓ albumin
1. Gastric form → Strongylus sp. or Gastrophilus infestation III- Differential Diagnosis:
2. Cutaneous form →Fungal granuloma or equine sarcoid. With disease causing diarrhea, anemia and debility as
3. Conjunctival form →Other eyes affection as histoplasmosis 1. Babesiosis
2. Ascariasis
3. Coccidiosis
4. Nutritional deficiency
5. Equine infectious anemia
Treatment
A. Gastric form • Rectal enema by soap and water or by vinegar and water for removal of larvae
1. Gastric lavage with 5-10 liters of 2 % sodium bicarbonate to remove excess mucus adhering on rectal mucosa.
Drug Dose
followed by carbon bisulfide 5 ml/ 45 kg, b/w, orally, this result in effective removal of H. • Oral medication by trichlorfon in dose of 40 mg/kg, b/w or systemic ivermectin as 0.2
musca and H. majus but H. megastoma residing in tumor are not affected 1. Piperazine highly effective as mg/kg, b/w S/C.
2. Trichlorphon may reduce infestation.  20-30 gm for horse • Gasterophilus spp are susceptible to ivermectin (0.2 mg/kg) S/C
B. Cutaneous form →not respond to standard wound treatments  20 gm for donkey
1. Application of 2:10% formaline or 10% chromic acid locally with trichlorphon 2. Banminth 12.5 mg/kg, b/w.
(Neguvan®) in dose of 25 mg/ kg bw IV in one liter dextrose for 2 doses with one week
interval 3. Ivermertin (eqvalan).
2. Ivermectin 4. Thibendazol 44ma/kg, b/w.

3. Surgical excision of skin lesion 5. Mebendazol 10 mg/kg, b/w.
C. Conjunctival form → systemic trichlorphon with local application of antibiotic anti-
6. Fenbendazol 30 mg/kg, btw.
inflammatory eye ointment.
7. Oxfenbendazol 10 mg/kg, b/w.
Control
Interruption of life cycle by Hygiene and sanitation of stables as 1. Destruction of larvae in feces
 careful disposal of horse manure 1. Disinfection. 2. Grooming of animals with clipping of hairs and burning it to remove the ova
 control of fly populations. 2. Regular or daily removal of manure. 3. Bathing the animals by 2% carbolic acid may destroy the parasite
In endemic areas all skin wounds should be early treated and protected from fly 3. Rotation of pasture. 4. Prophylactic treatment by available anthelmintic drug
4. Avoid overstocking.
5. Regular prophylactic treatments.

22. Filariasis
Filarial Dermatitis, Cutaneous stephano filariasis, Onchocerciasis, Dirofilariasis
Definition
Chronic parasitic arthropod born disease of domestic animal caused by filarial nematode and characterized by intramuscular, cutaneous and subcutaneous lesion.
Aetiology
1. Filarial dermatitis caused by Parafilaria bovicola and P. multipapillosa.
2. Cutaneous stephano filariasis caused by Stephanofilaria.
3. Onchocerciasis.
4. Dirofilariasis.
5. Dipetalonema or filaria evansi
Epidemiology
1- Geographic distribution: widespread in tropical and subtropical countries including Egypt.
2- Species affected: domestic, wild animal and human.
3- Transmission: biting arthropod.
4- Economic importance: Losses from abortion, neonatal mortalities, and zoonotic implications.
Life cycle and Pathogenesis

Adult worm in skin nodule → Pierce skin and lay egg on surface → Blood sucking fly (intermediate host) → Ingest egg or larvae during blood meal → Larvae developed to
infective form (microfilariae) → Infect animal during blood meal.
Filarial Dermatitis Onchocerciasis Dirofilariasis Dipetalonema or Filaria evansi
• P. Bovicola and P multipapillosa Caused by Onchocerca spp. Cause: Dirofilaria immitis infect • Infect camel and inhabit in
cause haemorrhagic dermatitis • Microfilaria in skin or subcutaneous lnn transmit by midges, sand, dog and cat mesenteric, pulmonary,
in cattle, buffaloes, and equine. or black fly. • Adult worm present in right spermatic, and genital blood
• Characterised by nodule in vertical, pulmonary artery and vessels or present as cyst in
• Nodules in subcutaneous tissue of brisket and lateral surface of
head, neck, wither, shoulder vena cava internal organs
thigh, free movable under skin.
and side. • Worm obstructs posterior vena • Characterized by emaciation,
• Misdiagnosed with bovine tuberculosis.
cava and cause acute orchitis, swollen of scrotum
Cutaneous stephano Filariasis In horse:
hepatic syndrome and and cardiac insufficiency
Cause: Stephanofilaria • O. cervicalis cause alopecia, pruritus especially ventral of sudden death
Characterized by skin lesion (3-5 abdomen, extend to forelegs, hind legs, face, neck and thorax
cm), exudative, haemorrhagic and inflammation in ligamentum nuchae through infection with
dermatitis adult worm
• O. Reticulata caused swelling and inflammation in suspensory
ligament of posterior part of canon (lameness)
Clinical Signs
PM lesions
Diagnosis
I- Field Diagnosis History, Clinical signs, Epidemiology, Laboratory diagnosis.
II- Laboratory diagnosis
A. Specimens: skin biopsy, skin scraping, tissue lesion, blood samples.
B. Laboratory procedures:
1. Detection of microfilaria in blood film after staining with Leishman or giemsa stain.
2. Knott or full borne technique: 1 ml of blood + 9 ml 2% formalin, centrifugation, sediment stained with MB.
3. Histopathological examination.
4. Serological test as ELISA.
5. Allergic cutaneous test.
Treatment
Surgical treatment: Two dose of Ivermectin with one week interval.
Control
1. Isolation of infected animal.
2. Treatment of infected animal.
3. Control of insect through using of insecticides.
Parasites and Parasitic Diseases of Respiratory System of Equine

1- Dictycallus arnfieldi.
5- Linguatula rhinaria or canine 6- Rhinotus purpureus or the

2- Echinococcus cysts: 3- Habronema sp. 4- Schistosoma nasalis
tongue worm nasal warble larvae,
• Occasionally found in lungs of • Fibrous peribronchiolar • Occasionally seen in nose of • Rare in horse nose or • Present in nose and paranasal
equine with no signs or rare nodules with very limited Indian horse and form paranasal sinus resulting in sinus sinuses and the larvae
respiratory signs and seen by respiratory signs. granuloma with mild stridor. snorting, head shaking and may reach to pharynx and
lung radiograph. nasal discharge. larynx with occurrence of
• Rear by trephining of the cough and airway stenosis.
affected sinus. • The worm may be diagnosed
by endoscopy and treat by
organophosphorus
compounds.

23. Equine Verminous Pneumonia
Definition
The disease is rare in equine with mild signs. Dictycallus (D) arnfieldi is the causative agent, it is more common in donkey than in horse. The life cycle is direct.
Diagnosis
I- Field Diagnosis: It depends on signs and postmortem lesions as discrete areas of overinflation surrounding inflamed bronchi which is blocked with worms and a greenish
mucus in addition of endoscopy to see the parasite in lung.
II- Laboratory Diagnosis: Examination of tracheal washings to detect eosinophilia, fecal examination for detection of embryonated eggs or larvae. The worm usually do not
mature in horses, therefore infection in horses cannot diagnosed by fecal exam.
III- Differential Diagnosis: It should be differentiated from all affection caused respiratory signs.
Treatment
• Thibenzole or mebendazole as 20 mg/kg. b/w for 5 d
• Fenbendazole 30 mg/kg b/w and ivermectin 200 ug/kg. b/w.
24. Equine cestodes 25. Equine Trematodes

Anoplocephala perfoliata is the main cestode affecting • Fascioliasis: Equine are less commonly infected and • Dicrocoelium dendriticum: The worms results in miliary
equine. are very resistant to infestation, it acts as a reservoir of and purulent hepatitis.
infestation for ruminants. • Gastrodiscus aegypticus: Live in small and large
• Orbated mites act as intermediate host and infection
occurs by accidental ingestion of infective stage in • Equine with heavy nematodes infestation and in poor intestine without occurrence of characteristic signs
these mites. condition more easily infested. but heavy infestation caused damage of intestinal
• Fecal exams show characteristic operculated mucosae.
Clinical signs:
Fasciola eggs. • Fecal examination shows oval operculated eggs of
• Catarrhal enteritis, diarrhea, colic, a dull coat,
• Recently Fasciola infestation was recorded among similar appearance to Fasciola eggs, but it is more
unthriftiness, anemia and intestinal obstruction,
different species of Equidae (horse, donkey and whitish. The worm is recorded in Egypt since long time.
perforation and peritonitis.
mules) in different province in Egypt.
Post-mortem lesions:
• Clinical signs: Signs of lowered performance, loss of
• There is catarrhal and haemorrhagic inflammation of
condition, diarrhea, severe chronic interstitial hepatitis
small intestine and the development of masses of
and cholangitis in heavily infested horses, mild colic,
granulation tissue around ulcerating lesions occur at
urticaria, edema and icterus.
sites of attachment to mucosa
• Treatment by
Diagnose in laboratory
• Rafoxanide as 3 mg/kg b/w.
• Detection of proglsegments as rice grain sized in
feces or detection of eggs with hexacanth embryos. • Niclofolan 300 mg / 75-100kg b/w
Control: by treatment with • Ivomic super.
• Niclosamide as 60-65 mg/ kg, b/w

• Pyrantel pamoate 12 mg/kg, b/w and control of
intermediate host
26. Mange in equine

Sarcoptic Mange Psoroptic mange Chorioptic mange (leg mange) Demodectic mange Trombiculiasis
Sarcoptic scabiei var equi is the Psoroptes equi produces lesions Chorioptes equi lesions start as a Demodex equi is rare in horses, Trombiculid mites can parasites
most severe type of mange in which start 1. Pruritic dermatitis affecting live in hair follicles and horses skin especially during late
horses. 1. Papules. the distal limbs around the sebaceous glands, there are summer and fall; the lesions
• There are small papules & foot and fetlock. 1. Patchy alopecia. appear as
2. Alopecia.
vesicles that later develop into 2. Papules are seen firstly. 2. Scaling or nodules. 1. Pruritic papules.
3. Thick haemorrhagic crusts.
crusts with intense pruritus, 2. Wheals.
4. Characteristic pruritus. 3. Followed by alopecia, The lesions appear on the face,
alopecia & skin folding
crusting and thickening of neck, shoulders, and forelimbs
• Lesions are present on head, • The lesions are present on
the skin. with absent of pruritus.
neck & shoulders and thickly hair regions as under
the fetlock and mane, at the In chronic cases
become generalized if there is
no treatment leading to base of the tail, under the Moist dermatitis of the fetlock
anorexia, emaciation, and chin, between hind legs and which confused with "greasy
general weakness. in the axillae. heel" in draft horses, signs are
• Psoroptes cuniculi may causes subsided in summer and recur
otitis externa with head with the return of cold weather.
shaking.
Diagnosis depend on signs, history, epidemiology and laboratory examination of skin scrapings
collected from the periphery of the lesions.
Treatment by
• Organophosphate insecticides or lime sulphur solution (spraying, washing or dipping), repeat at 12-
14. d for at least 3-4 times.
• Ivermectin 200 ug/kg, b/w, S/C can be used (it is important to treat all contact animals.
27. Equine Dermatomycosis

• T. equinum & T. mentagrophytes are the primary causes of ringworm in horses although M. gypseum, M. canis & T. verrucosum are also isolated from some cases
• Transmitted by direct contact or by grooming instrument
• The lesions appear as one or more patches of alopecia and erythema, scaling & crusting, most lesions are seen in the saddle and girth areas "girth itch", also may spread to
the axillary area, over the trunk and may be reached to neck, head and limb.
• Microsporum gypsum infect hair follicle result in formation of small foci of inflammation and suppuration with some irritation and itching.
• Treatment using Antimycotic agents as Miconazole or Clotrimazole preparations as local applications with isolation of infected horses and disinfection of premises and
grooming instruments.

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1 EQUINE BACTERIAL DISEASES

1. Sporotrichosis 2. Glanders (Farcy and Malleus)

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 1

Samples: Pus, blood and serum sample.

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 2

Pulmonary form Nasal form Skin form (farcy)

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 3

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 4

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 5

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 6

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 7

A. Acute form: B. Bastard form C. Atypical or mild form (subclinical)

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 8

Field diagnosis: history, epidemiology, clinical signs and PM

Isolation of infected animal and treat as soon as possible as following:

2. Complications as Purpura Haemorrhagica treated by

1- Distribution: The disease present where equine is raised.

Morbidity and mortality rates → low.

Field diagnosis: history, epidemiology and clinical pictures.

1. Early diagnosis, isolation and treatment of infected animals.

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 9

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 10

a. Proper management and quarantine measures: b. Vaccination:

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 11

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 12

• Accidentally human may be infected. • High mortality rate.

3- Factors influencing susceptibility:

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 13

• All ages and sexes of horse are susceptible. B. Mode of infection:

1. Transient fever, anorexia, mild conjunctivitis, diarrhea, respiratory distress.

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 14

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 15

A. Acute Form: B. Chronic Form: “Swamper”

C. Subacute Form: D. Latent Form:

4. Death is usually due to exhaustion.

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 16

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 17

C. Neonatal Foals: D. Encephalomyelitis form:

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 18

14. Vesicular Stomatitis

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 19

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 20

8. Weight loss is recorded after influenza virus infection. 5. Myositis.

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 21

By Mostafa Ahmed, BVSc., CPT. INFECTIOUS DISEASES OF EQUINE | 22

1. Ticks (Dermacentor, Hyalomma & Rhipicephalus sp.) b. Mode:

1. Mild inappetence. 1. Cutaneous eruption or edematous cutaneous plaques or urticarial

By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 23

2. PCR B. Laboratory procedures:

3. Histopathology 1. Microscopic examination of stained blood film or smear by Giemsa

Life cycle and Pathogenesis

By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 24

By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 25

By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 26

B. Cutaneous habronemiasis or summer sore: 4. Pendulous abdomen, hallow flank.

By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 27

2. Ivermectin 4. Thibendazol 44ma/kg, b/w.

By Samir Serag, BVSc. INFECTIOUS DISEASES OF EQUINE | 28

Life cycle and Pathogenesis