Strangles

(Equine Distemper)

By Dr Jasleen Kaur
Assistant Professor
(Veterinary Medicine)
 Strangles

 Strangles derives from the enlarged retropharyngeal

LNs and guttural pouches causing respiratory distress
in severely affected equids.

 Highly contagious disease of the upper respiratory

tract of horses characterized by:
1. Severe inflammation of the upper respiratory tract
2. Abscessation in the adjacent lymph nodes.
 Etiology

 Streptococcus equi subspecies equi

 Gram-positive, capsulated ß-hemolytic Lancefied group C coccus
 Survival in the environment depends on temperature and humidity
 Susceptible to desiccation, extreme heat, and exposure to sunlight
 The organism can survive 7-9 week outside the Host.
 Epidemiology

1. Geographical distribution
 Worldwide.
 Outbreaks occur at any time of the year but mostly in cold, wet weather
 Movement of horses has more Influence on the occurrence of outbreaks than the climate.

2. Host range
 Horses, Donkeys and mules are the only species affected.
 All ages but common in young animals (1-5yr)
 Strong Immunity occurs immediately after an attack.
 With virulent Infection, repeated attacks may occur at intervals of about 6 months.
Contd..

3. Transmission :
 Highly contagious disease
a) Via fomites
b) Direct contact with infectious exudates
 Infection occurs by ingestion or by inhalation of droplet
 Prolonged carrier state in asymptomatic animals (at least 4 weeks after a clinical
attack).

4. Morbidity and mortality

 Morbidity as low as 10% and up to 100% in young animals with Inadequate shelter.
 Case fatality rate w/o treatment 9% but with Rx 1-2%.
 Pathogenesis

1.Binding to Cells
1.Streptococcus Ingestion or on the tonsillar
equi equi inhalation crypts + adjacent
lymphoid nodules

Enzymes and 1.Submandibular

Fever, Rhinitis and toxins release and
Pharyngitis (Streptokinase, retropharyngeal
Streptolysin S) lymph nodes

1. Suppuration Kidney, brain, liver, spleen, joints

2. After attack subsided, Purpura haemorrhagica due to sensitivity to streptococcal proteins.
 Clinical Findings
 Incubation: 3-14 days.
 Acute onset of fever (103°–106°F), anorexia, depression.
 A serous nasal discharge; mucoid to mucopurulent.
 Severe pharyngitis and laryngitis, difficult swallowing inspiratory respiratory noise.
 Rarely mild conjunctivitis.
 A soft, moist cough.
 Head may be extended to ease the pain in throat.
 Submandibular and pharyngeal lymphadenopathy with abscessation and rupture.
 Purulent nasal discharge.
 Metastatic infection in other organ systems.
 Contd..

 Metastatic Strangles (“Bastard Strangles") is characterized by abscessation

in other LN of the body, particularly LNs in abdomen &, less frequently, thorax.
 Metastatic Infections may occur in the CNS; results in suppurative meningitis
characterized clinically by
 Excitation, hyperesthesia, rigidity of the neck, and terminal paralysis.
 Abscesses in brain cause a variety of clinical signs, depending on location of
abscess, including severe depression, head pressing, abnormal gait, circling & fits.
 Metastatic infections of the ocular and extraocular structures, heart valves and
myocardium, Joints, bones, tendon sheaths, and veins may occur.
 Contd..

 An atypical form of strangles

1. Subclinical infection and a mild disease

2. Transient fever for 24-48 hours
3. A profuse nasal discharge and are anorexic
4. Sometimes moderate enlargement of the mandibular lymph nodes
5. Guttural pouch Empyema (filled with pus).
 Complications of Strangles

1. Bastard strangles
2. Purpura haemorrhagica
 Immune-mediated acute Inflammation of peripheral blood vessels that
occurs within 4 weeks of strangles, while the animal is convalescing.
 It results from the formation of immune complexes (ICs) between the
horse's antibodies and bacterial components.
 These ICs trapped in capillaries where they cause inflammation, visible in
m. m. as pinpoint hemorrhages.
 These hemorrhages lead to a widespread severe edema of the head,
limbs, and other parts of the body.
 Purpura can also be a complication of routine vaccination.
 Post-Mortem lesions

1. Caseous lymphadenopathy with rhinitis and pharyngitis,

pneumonia.
2. Metastatic infection in severe cases especially the liver, spleen,
lung, vessels and the peritoneum.
 Clinical Pathology

 Culture of S. equi from nasal and abscess discharges.

 PCR of nasal, pharyngeal or guttural pouch swabs.
 High serum antibody titer.
 Differential Diagnosis

 In the early stages of the disease it may confused with

1. Equine viral rhinopneumonitis
2. Equine viral arteritis
3. Equine influenza

 But in these disease there is usually no marked enlargement of the lymph nodes.
 Diagnosis

1. History and clinical signs.

2. Confirmation: by bacterial culture of exudate from abscesses or nasal swab
samples and isolation of S. equi.
3. CBC reveals neutrophilic leukocytosis and hyperfibrinogenemia.
4. PCR (DNA) for carrier state.
5. Complicated cases may require endoscopic examination of the upper
respiratory tract including the guttural pouches.
6. Ultrasonographic examination of the retropharyngeal area.
7. Radiographic examination of the skull to identify the location and extent of
retropharyngeal abscesses.
 Treatment
1. Antibiotic therapy
 Procaine penicillin G @ 22,000 IU/kg IM BID × 5d (min).
 Ampicillin, ceftiofur, erythromycin, rifampin, tetracycline, and
trimethoprim/sulfonamides also used.
2. Application of hot poultices to sites of lymphadenopathy to facilitate
maturation of abscesses, reduce swelling and provide pain relief.
3. Provision of Intravenous hydration in animals unable to drink.
4. NSAID e.g, phenylbutazone or flunixin meglumine can be administered
judiciously to reduce pain and fever and improve appetite in horses with
clinical disease.
5. Surgical drainage of mature abscesses
 Ruptured abscesses should be flushed with dilute (3-5 %) povidone-lodine
solution for several days until discharge ceases.
6. Tracheotomy may be required in horses with retropharyngeal
abscessation and pharyngeal compression.

Antimicrobial therapy Is controversial. Prolongs the course of disease by

delaying maturation of abscesses.
 Prevention
1. Vaccination
1. Commercial vaccine adm gradually Increasing doses 3 times at 10-14 days
Intervals- Immunity for 12 months.
2. PINNACLE® I.N. is the only two-dose modified-live vaccine developed to help
prevent strangles caused by S. equi.
3. Foals 2-12 months of age- vaccination with autogenous vaccine of whole cells
and acid extract of S. equi, 03 times at 10 d Interval- good protection.

2. Complications
1. Abscesses at subsequent IM Injection sites (live culture), submandibular
lymphadenopathy, serous nasal discharge, and purpura hemorrhagica.
 Control

1. Isolating affected horses (1 month) and cared by separate caregivers.

2. Temperature of all horses exposed to strangles should be obtained twice
daily, and horses developing fever should be isolated (and potentially
treated with penicillin).
3. Thorough cleaning and disinfection of equipments using chlorhexidine
gluconate or glutaraldehyde.
4. Control of flies.
5. Farriers, trainers, and vets should wear protective clothing or change
clothes prior to traveling to the next equine facility.
6. New entrant carefully scrutinized (nasopharyngeal culture) and
quarantined for 14-21 days. Two (-)ve nasal swab cultures should be
obtained during quarantine period.
7. Most horses continue to shed S equi for ~1 mo after recovery. Three
negative nasopharyngeal swabs, at intervals of 4–7 days, should be
obtained before release from quarantine, and the minimal isolation
period should be 1 mo.
8. Guttural pouch empyema used to identify persistent carriers.