MEDI107A: Equine Medicine
Bacterial Diseases in Horse
Jocelyn Miranda, DVM | June 30, 2023
I. STRANGLES (DISTEMPER)
● An infectious, contagious disease of equine characterized by
abscessation of the lymphoid tissues of the upper respiratory
tract
A. ETIOLOGY
● Causative Agent: Streptococcus equi, a Gram-positive,
capsulated, B-hemolytic, Lancefield group C coccus which is an
obligate parasite and a primary pathogen
→ Highly host-adapted affecting only horses, donkeys and
mules
B. PATHOGENESIS
● Highly contagious, produces high morbidity but low mortality
in susceptible animals
● Transmission is via fomites and direct contact with infectious
exudates (from nasopharyngeal area)
● Carrier animal is important source of infection and could
initiate outbreaks in premises previously free of the disease
● Organism is susceptible to desiccation, extreme heat and
exposure to sunlight
● Under favorable conditions, the organism can survive 4 weeks
outside of the host but under field conditions, do not survive 96
hours
C. CLINICAL FINDINGS
● Incubation period is 3 to 14 days
● First sign is fever of 39.4 to 41.1’C
● Mucoid to mucopurulent nasal discharge
● Depression
● Submandibular lymphadenopathy (infection of the lymph
nodes)
● Horses with involvement of the retropharyngeal lymph nodes
have difficulty in swallowing, inspiratory respiratory noise due
to compression of the dorsal pharyngeal wall, and extended
head and neck
● Animals with residual immunity develop atypical or catarrhal
form of the disease with mucoid nasal discharge, cough and
mild fever
METASTATIC STRANGLES (BASTARD STRANGLES)
● Characterized by abscessation in other lymph nodes
particularly those in the abdomen and less frequently in the
thorax
→ Most common cause of brain abscess in horses although it is
rare
DIAGNOSIS
● Bacterial culture of exudates from abscesses and nasal swab
samples
● CBC – neutrophilic leukocytosis and hyperfibrinogenemia
● Endoscopic examination of the upper respiratory tract
MEDI107A Fabello, Manuel, Palconit, Walker
● Ultrasonography of the retropharyngeal area
● X-ray of the skull to determine retropharyngeal abscessation
TREATMENT
● Keep environment warm, dry and dust free
● Warm compress will facilitate maturation of abscesses
● Facilitated drainage of mature abscesses will speed up
recovery
● Flush ruptured abscesses with 3 to 5% povidone-iodine until
discharge ceases
● NSAIDS to reduce pain and fever and improve appetite
● Tracheotomy for horses with retropharyngeal abscessation and
pharyngeal compression
● Antimicrobial therapy provides temporary relief from fever but
delays maturation of abscess; indicated in dyspnea, dysphagia,
prolonged high fever and severe lethargy or anorexia
→ Penicillin during early stage of infection , < 24 hours of
onset of fever will arrest abscess formation
→ Early antimicrobial treatment fails to mount protective
immune response rendering horses susceptible to infection
after cessation of treatment
→ Procaine penicillin at 22,000 IU/kg, IM, bid is the antibiotic of
choice
→ Untreated guttural pouch infection can lead to persistent
guttural pouch empyema
PREVENTION
● Post-exposure immunity produced after natural exposure to
the disease; local production of antibodies against
antiphagocytic M protein
● Vaccination with IM products that do not induce mucosal
immunity
● Intranasal live attenuated strain to elicit mucosal immunologic
response
→ Side effects:
▪ Abscess at site of IM injection
▪ submandibular lymphadenopathy
▪ serous nasal discharge and purpura hemorrhagica
CONTROL
● Isolate affected animals to be cared for by caretakers wearing
protective clothing
● Clean contaminated equipment with detergent and disinfect
with chlorhexidine gluconate or glutaraldehyde
● Control fly population
● Farriers, trainers and veterinarians should wear protective
clothing
● New animals should be quarantined for 14 to 21 days; 2
negative nasal swabs should be obtained
● Horses continue to shed organisms 1 months after recovery; 3
negative nasopharyngeal swabs at intervals of 4 to 7 days,
isolation for 1 month
→ Guttural pouch empyema source of infection in prolonged
carrier states
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 ● Generalized spasms disturb circulation and respiration
TETANUS (LOCK JAW) resulting to increased heart rate, rapid breathing, and
● Caused by specific neurotoxin produced by Clostridium tetani congestion of mucous membranes
● Almost all mammals are susceptible ● Sheep, goats, and pigs fall to the ground and exhibit
→ Dogs and cats relatively more resistant opisthotonus
→ Why are there animals not affected by Tetanus ● Temperature remains slightly above normal but may rise to
▪ Birds are quite resistant. 42-43 degrees Celcius toward end of fatal attack (bago
− Pag naglalaban yung mga manok, pag nahiwa ng tari mamatay)
ang isang manok, tinatahi lang ng karayom at sinulid ● Mortality = 80%
without anesthetic and anti-septic ● Convalescent period is about 2-6wks: protective immunity does
− The toxin needs affinity for the nervous tissue to be not develop after recovery
affected by Tetanus. Chickens do not have this ● In Horses
receptor. → Ears erect
→ Horses and lambs most sensitive of all species → Tail stiff and extended
→ Anterior nares dilated and third eyelid is prolapsed
ETIOLOGY AND PATHOGENESIS → Stiffness of the leg muscles causing “sawhorse” stance (See
● Caused by C. tetani picture below)
→ Aerobic organism with terminal, spherical spores, found in
the soil and intestinal tracts
● Introduced into the tissue through wounds that provide
suitable anaerobic environment
→ Long and narrow wounds are usually the type of wounds
being proliferated by C. tetani
→ Once multiplies, it releases toxins that produces the tetanus
● In lambs, often follows docking or castration
→ When animal is docked or castrated, pag-higa at sumayad
sa soil with organism = lamb gets infected
● Spores of the organism unable to grow in normal tissue and
circulating blood
→ Due to the presence of oxygen = organism will not survive
● Animals die when infected no matter how much antibiotics and
antibodies are given and presented, unless at an early stage.
● The toxin is absorbed by the PNS then gains access to the CNS Points to Note:
producing the tetanus. ● Why is rust associated with Tetanus
→ Organisms do not leave the wound as they will die when → Rust renders anaerobic
they travel to the normal tissue and circulating blood. ▪ Acted upon by water and oxygen by the environment,
→ NOTE: Only the toxin is absorbed. and iron = oxidative reaction
● Bacteria remain localized in necrotic tissue.
● Toxin is absorbed by the motor nerves and causes spasmodic, DIAGNOSIS
tonic contractions of voluntary muscles by interfering with the ● Clinical Signs and history of recent trauma
release of inhibitory neurotransmitter from presynaptic nerve → Hanapin yung sugat and clean with hydrogen peroxide
endings ▪ Will exhibit bubbles after applying hydrogen peroxide =
● Spasms oxygen release
→ When tetanus is present, spasms will occur. ● Confirmatory Diagnosis:
▪ Larynx, diaphragm, and intercostal muscles will be → Demonstration of toxin in serum of affected animal
spasmodic resulting to respiratory failure due to paralysis → Anaerobic culture and demonstration of bacteria from
of the diaphragm wound
− Diaphragm = major respiratory organ
TREATMENT AND CONTROL
o When exhale, diaphragm will go lower
o Inhalation: Diaphragm will elevate ● In early stages of disease: curariform agents (muscle relaxants),
CLINICAL FINDINGS tranquilizers, or barbiturate sedatives in conjunction with
300,000 IU of tetanus antitoxin
● Incubation Period: 10 to 14 days → Once toxin attaches to the nervous system, never na siya
→ There are instances that overnight, an individual will get maghihiwalay / irreversible
infected → Tetanus antitoxin = neutralize receptor site attached by
● Localized stiffness of masseter muscles, muscles of the neck, tetanus
hindlimbs and region of the infected wound which become → Muscle relaxants, tranquilizers or barbiturate = intended to
more pronounced relieve stiffness of muscles avoiding respiratory failure
● Tonic spasms and hyperaesthesia ● 300,000 IU of tetanus antitoxin into the subarachnoid space
● Difficulty in prehension and mastication = Lockjaw through the cistema magna
● Sweating is common
MEDI107A Bacterial Diseases in Horses 2 of 5
 → Subarachnoid space: space in the brain where the ● Similarity: Paralysis of the diaphragm = respiratory
subarachnoid fluid is found failure/system
→ Cisterna magna: cerebrospinal fluid (CSF) filled space
PATHOGENESIS
located in the posterior fossa dorsal to the medulla and
caudal to the cerebellum ● Found in soil and decaying plant or animal matter
● Draining and cleaning of wounds and administering penicillin ● Adult horses and foals less than 8 mos old are affected
or broad spectrum antibiotics ● Organism obtained by the animal contains toxin already =
→ Remove anaerobic condition pre-formed
→ Instill antibiotics → In comparison to tetanus, it is not pre-formed (wala pa yung
▪ Penicillin = treats gram+ organisms toxins pagka-obtain ng animal
● Place in quite, darkened stall box with feeding and watering CLINICAL SIGNS
devices
→ Hyperesthetic ● Clinical Signs
▪ Sensitive to sound and light when horse is paralyzed = → Impaired suckling
nanginginig pag may light and sound → Inability to swallow
● Sling for horses with difficulty in standing or rising ▪ No muscle tone
→ Sinasabat sa ceiling tapos yung hoof at least touching the → Decreased eyelid and tail tone and dilated pupils
ground; the weight should be on the feet but on the sling. ▪ Similar to tetanus
→ Respiratory paralysis
PREVENTION → In adults
● Active immunization with tetanus toxoid ▪ Many of same signs seen in foals
→ Vaccine against tetanus is toxoid ▪ Eventual muscle weakness, tremors and collapse
▪ Toxin infects the animal, thus you cannot administer the ▪ Respiratory paralysis → DEATH
toxin because it will develop tetanus = the toxin will be TREATMENT
detoxified by the toxoid
● Polyvalent equine antitoxin
− Usually treated with heat or chemicals
C. botulism has a lot of strains (A-F)
− Toxoid, it is not that virulent
→ To cover all strains, polyvalent vaccine strains are used
▪ Note: Toxin yung nakakamatay and not the organism
● Prevention
itself.
→ Vaccine recommended for endemic areas
→ Wound after immunization another toxoid
▪ Endemic: the disease is present
● If not previously immunized, give 1,500 - 3,000 IU of tetanus
antitoxin which provides protection for 2 weeks
CONTAGIOUS EQUINE METRITIS
→ When mares are unvaccinated before breeding, vaccinate
after giving birth with 1,500-3,000 because there is a ● Caused by Taylorella equigenitalis
possibility that the mare has a wound → Old name: Haemophilus equigenitaliS
● Transmission
→ When vaccinated, the antibodies induced by the toxoid will
● through direct breeding , AI and contact with
protect them = active immunity
contaminated items
● Toxoid given simultaneously with antitoxin and repeated in 30
days CLINICAL SIGNS
→ Anti toxin after 2 weeks is weared off by the horse ● Highly contagious, often asymptomatic though affected mares
● Yearly toxoid booster show mucoid vaginal discharge
● Mares vaccinated during last week of pregnancy ● Infertility or abortion in mares, no clinical signs in stallions
→ Stress = premature pregnancy → Infertility can last for one or more breeding cycles
▪ Foals will still survive kasi 1 week premature lang naman
● Foals at 5-8 weeks of age = high risk TREATMENT
→ Given antitoxin immediately after birth then every 2-3 ● Topical and systemic antibiotics
weeks until 3 months old then given anti-toxin ● Prevention
▪ 3 months of age = body is capable of producing → Clearance of stallion
antibodies ▪ Stallion allowed to undergo test breeding to negative
mares
BOTULISM ▪ Process takes 35 days to declare stallion negative
● Rare in horses but fatal ▪ Average to clear stallion takes 6-8 weeks
● Caused by toxins produced by Clostridium botulinum → Good hygiene practices
● Difference with Tetanus
→ Tetanus: affects CNS TYZZER’S DISEASE
▪ Release of glycine (neurotransmitter) = spasms ● Rare disease caused by Clostridium (Bacillus) piliforme
▪ Rigid paralysis (spasm - rigidity) ● Characterized by severe and peracute hepatitis affecting foals 1
→ Botulism: affects PNS to 6 weeks old
▪ Release of acetylcholine = transmission of impulses ● Foals infected by ingestion of spores from feces or environment
▪ Flacid paralysis

MEDI107A Bacterial Diseases in Horses 3 of 5

● Following colonization of intestinal tract, it infects the liver ● 2-year enzootic dual infection with Anaplasma
causing severe hepatic necrosis phagocytophilum cycle involving Ixodes ticks (hard ticks) and
mammals (deer and white-footed mouse)
CLINICAL SIGNS
● Ticks must be attached to mammal for at least 24 hours
● Foals simply found dead
CLINICAL SIGNS
● Weakness, lethargy, anorexia, dehydration, pyrexia, diarrhea,
tachycardia, tachypnea and icterus ● Low-grade fever
● Seizures, coma and death may rapidly ensue ● Stiffness and lameness in more than one limb
● Prognosis for foals poor and most affected foals found dead
TREATMENT
TREATMENT
● Tetracycline – 6.6 mg/kg IV every 24 hours for 1 week before
● IV fluids treatment w/ doxycycline
● Anti-inflammatories ● Doxycycline – 10 mg/kg PO every 12 hours for 1 month
● Antibiotics such as ampicillin and gentamicin ● Ceftiofur (4th gen antibiotic or advanced type) – 2-4 mg/kg IV or
● Parenteral nutrition IM every 12 hours
PREVENTION
PNEUMONIA IN FOALS
● Caused by Rhodococcus equi in foals ● Preventing tick exposure or prolonged attachment
● Also causes ulcerative enterocolitis, colonic-mesenteric ● Early antimicrobial treatment after exposure
lymphadenopathy, immune-mediated synovitis and uveitis, ● Vaccination
osteomyelitis, pyogranulomatous dermatitis, brain abscess,
immune mediated anemia and septic arthritis LEPTOSPIROSIS
● Inhalation of contaminated dust most important route for ● Caused by highly invasive Leptospira
pneumonic infection in foals → Leptospira interrogans serovar Pomona type kennewicki –
● Facultative intracellular parasites of monocytes and North America (skunk: most common maintenance host)
macrophages → Leptospira kirscheneri serovar Grippotyphosa strain duster –
CLINICAL SIGNS Western Europe
→ Leptospira kirschneri serovar Grippotyphosa strain moskva –
● Most common is suppurative bronchopneumonia with
Eastern Europe
extensive abscess formation and suppurative lymphadenitis
→ L. interrogans serovar Bratislava – host-adapted serovar of
● Early signs include slight increase in respiratory rate and mild
the horse
fever
● More commonly acute respiratory distress and high fever
(105-106’F or 40-41’C) CLINICAL SYNDROME
● Intestinal manifestations characterized by granulomatous or Syndrome - set of symptoms manifested at the same time
suppurative inflammation of Peyer’s patches and mesenteric or ● Reproductive Tract
colonic lymph nodes → Caused by L. interrogans serovar Pomona
TREATMENT → Responsible for most Leptospira abortions, but serovars
Grippotyphosa and Jardjo has also been reported
● Administration of erythromycin (25 mg/kg PO every 8 hours)
● Acute Renal Failure
and rifampin (5 mg/kg PO every 12 hours)
→ Caused by L . Pomona
→ Costly and labor intensive and can result to diarrhea and
→ Ever and acute renal failure; tubulointerstitial nephritis and
hyperthermia in treated foals
pyuria without visible bacteria
● Azithromycin (10 mg/kg PO every 24 hrs. for the first 5 days
● Recurrent Uveitis
then every other day and Clarithromycin (7.5 mg/kg PO every
→ Caused by L. interrogans serovar Pomona
12 hrs.)
→ Most common in equine: Equine recurrent uveitis (ERU) and
→ Used in combination with rifampin
immune-mediated keratitis
● Doxycycline (10 mg/kg PO every 12 hrs.)
→ IgG and IgA against Leptospira antigens cross-reacting w/
PREVENTION tissues of the lens, cornea, and retina
→ Live Leptospira organisms in the uveal tissue, aqueous and
● Husbandry – stocking density, proper ventilation, dust control
vitreous fluid of horses with recurrent uveitis
● Passive immunity – transfusion of hyperimmunized plasma 1L
→ Genetic factors in recurrent uveitis (Appaloosas genetically
during first 24 hrs. and 25 days later
predisposed)
● Chemoprophylaxis – development of superinfections, bacterial
→ ERU is the most common cause of blindness in horses
resistance and antimicrobial-induced colitis
TREATMENT
● Systemic administration of antimicrobials (for fever and acute
LYME DISEASE
renal failure) –
● Caused by Borrelia burgdorferi → Penicillin, ampicillin, cephalosporin, enrofloxacin,
Tetracycline, and doxycycline

MEDI107A Bacterial Diseases in Horses 4 of 5

● Fluid Therapy Corticosteroid and cyclosporine – temporary
relief
→ Vitrectomy – inoculation of gentamicin lavage (to wash off
organism)

SALMONELLA AND NOSOCOMIAL INFECTIONS

● Caused by Salmonella enterica sub spp. Enterica serotype
Typhimurium, Newport, Anatum, and Agona
CLINICAL SIGNS
● Enterocolitis
● Diarrhea
● Fever
● Leukopenia
● Danger of fecal shedding
TREATMENT
● Antimicrobial treatment
PREVENTION
● Cleaning and disinfecting of horse facilities.
● Temporarily close, empty wards and institute thorough,
intensive cleaning and disinfecting procedures.
● Strict traffic of humans and animals
● Adequate ventilation and distance between cases.

Points to Note:
● Salmonella
→ Not usually found in the normal flora unlike E. coli
→ Presence of salmonella indicates that the animal is really
sick

● Nosocomial Infections
→ Diseases acquired in hospitals or during the process of
receiving health care

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