Strangles or Equine Distemper

Strangles or Equine Distemper or Infectious adenitis is caused by Streptococcus equi subspecies equi in horses. It is an extremely contagious disease of horses, most commonly affecting foals.

The marked swelling of the retropharyngeal lymph nodes in throat causes “strangled breathe sounds” the disease is named “Strangles”. Prolonged carrier status noticed in asymptomatic animals.

The guttural pouches empyema causing respiratory distress in severely affected horses followed by death attributable to aspiration pneumonia.

Etiology

Strangles is caused by Streptococcus equi subspecies equi. It is an obligate, gram positive and cocco-bacillus organism.The organism expresses beta haemolysin around the colonies in blood agar. Similarities exists between the genome of S. equi and S. zooepidemicus. High virulent nature of the organism is due to the presence of M protein, hyaluronic acid capsule and leukocidine toxin.The mild atypical form of the disease is associated with non-capsulated variant of S. equi.

Epidemiology

Prevalence of infection

The disease has been widely distributed around the world. It is also recorded from Punjab and other places in India and Pakistan. The occurrence is highest in foals during February to the start of May compared to winter and summer seasons.

Predisposing factors

Sudden exposure to cold, high humidity, poor ventilation and severe stress are considered most important.

Source of infection

10-40% of recovered horses are carriers and hold the the organism in pharynx, guttural pouches for a long time. Discharges from nostrils, abscesses, contaminated grazing land, tracks, stalls, feed and water troughs, grooming kits, clothes of horses are sources of infection. Horses with guttural pouch empyema may excrete the organism for more than 3 years. About 25% of the recovered horses not immune and are susceptible to second cycle of infection. Over populated farms are at high risk.

Economic impact

Death of infected horses, time required and expenses incurred for treatment, aesthetic unpleasantness due to running noses and draining abscesses are responsible for economic losses.

Transmission

• Direct and indirect contact with fomites are important for infection. Inhalation also possible.
• Through skin wound from external environment.

Host affected

Horses, donkeys and mules around the world are susceptible. Morbidity rate is (20-100%) usually more in foals and yearlings than in adults. Age specific attack rates in foals 20-4o% and brood mares 20%. Case fatality rate is 10% in untreated and 1-2% in treated horses have been recorded.

Outbreaks occurs frequently in breeding farms, polo and race horses.

Pathogenesis

The virulence of the S.equi is due to the presence of surface M protein, a hyaluronic acid capsule and production of a leukocidine toxin.

Surface M protein

It is mainly known for three functions. Attachment to oral, nasal and pharyngeal tissues.

Entry into pharyngeal tonsils and associated lymphoid structures.

Prevention of host phagocytic activity by evading host immune response. There are two surface M proteins namely, SeM and Szpse. Of the two M protein, SeM is considered unique to S.equi which interfere with the action of c3b complements and therefore enhances the attachment of fibrinogen binding protein (Fbp) of the bacteria to host pharyngeal cells.

M protein avoid the phagocytic process by host neutrophils. Hyaluronic acid capsules resists against phagocytosis and increases pathogenesis.

Non-capsulated S.equi does not produce disease. On exposure the bacteria lodged in pharyngeal and tonsillar lymphoid tissues undergo rapid multiplication. The release of streptolysin O and streptokinase enzymes causes damage to tissues by directly injuring cell membranes and indirectly activating plasminogen leading to bacteraemia.Infiltration of neutrophils in lymphoid structures develops swelling and abscessation which causes disruption of lymph drainage and interfere with deglutition and respiration. Death due to pneumonia caused by aspiration, asphyxiation due to swelling secondary to upper airways and metastatic infection. Rarely death occurs due to purpura hemorrhagica in horses as sequlae to S.equi and is associated with high serum antibody titre to SeM. Metastatic infection or Bastard strangles It is a chronic illness eventually leading to death. Arise due to bacteraemia or extension of infection in lymphnodes.

Heart valves, brain, eyes, joints, tendons, sheath are affected. Meningitis, hyperaesthesia, rigidity of the neck and terminal paralysis.Abscess in brain leads to depression, head pressing, abdominal gait, circling and seizures.Purpura haemorrhagicaIt is a sequlae to S.equi infection. Two myopathic syndrome occurs in horses.

Muscle infarction

Due to immune mediated vasculitis, associated with purpura haemorrhagica with infarction in the gastrointestinal tract, skin and lungs.Rhabdomyolysis and subsequent muscle atrophy, stilted gait, elevated serum creatinin kinase, muscle derived enzymes due to cross reactivity of anti-SeM antibody with myosin.

Clinical Signs

Acute form

Incubation period is 1-3 weeks. Fever 103-105 ° F, sudden onset of anorexia, serous, copious and muco- purulent nasal discharge, abscessation of sub-mandibular, retropharyngeal lymphnode and guttural pouch develop.

Severe pharyngitis, laryngitis and mild conjunctivitis noticed.

Distinct enlargement of sub-mandibular lymphnode.

Pain in throat due to abscess, dysphagia, soft moist cough, extension of head. Hot, painful swelling of retropharyngeal lymphnode causes obstruction of oro-nasopharynx with respiratory distress which leads to death due to asphyxiation.

Affected nodes rupture and discharge thick creamy, white to yellow pus in 10 days. The course of the disease may be from 3 weeks to 3 months in severe cases.

Retropharyngeal lymphnode rupture and drain into guttural pouches leads to empyema and chondroids formation. In severe cases, pharyngeal, sub-maxillary, parotid and retrobulbar nodes have abscess and spread to local lymphatic vessels develops obstructive edema.

Atypical form

It is characterized by widespread sub-clinical infection. In which animals have transient fever, profuse nasal discharge.

Strangles in Burros Slow developing debilitated disease and have caseation and calcification of abdominal lymphnodes.

Chronic form (Metastatic infection or Bastard strangles) It is a chronic illness eventually leading to death. Arise due to bacteraemia or extension of infection in lymph nodes.

Heart valves, brain, eyes, joints, tendons, sheath are affected. Abscess in brain leads to depression, head pressing, abdominal gait, circling and seizures.

Complications

Suppurative necrotic bronchopneumonia, due to aspiration of pus from ruptured abscess in the upper airways / metastatic infection of lungs. Spreading of infection from RLN into guttural pouches due to rupture-uni/bilarteral nasal discharge.

Necropsy Findings

Suppuration of liver, spleen, lungs, pleura and peritoneum. Meningitis, hyperaesthesia, rigidity of the neck. Lesions in guttural pouch and  in various lymphnodes.

Diagnosis

• Isolation and identification organism.
• Using nasal swab collected and stained by a special Gram stain reveals S.equi as fluorescent purple color.
• A commercial test, measures the serum IgM antibody titer to SeM used to identify vaccination immunity.
• The test is not suitable in diagnosis of acute diseases.Serum antibody titre to SeM are very high (>1:12800) in horse with metastatic infection or purpura haemorrhagica. Detection of shedding S.equi DNA.
•  It is more specific than culture.Acute form: Leucocytosis with neutrophilia reaches the peak.
•  Hyper-fibrinogenaemia is a characteristic of both acute and chronic disease. Lucocytosis with a hyperproteinemia: Polyclonal gammaglobinemia is an important changes of metastatic and chronic abscessation.
• Hypoalbuminaemia.
• Affected animals may or may not have anaemia, it depends on haemolytic effect of streptolysin O and immune mediated hemolysis.

Sample Collection

Nasal, pharyngeal, guttural pouch dishcarge and abscess swabs from animals with active diseases and carrier state.

Differential Diagnosis

• Strangles
• Equine viral arteritis
• Equine viral rhinopneumonitis
• Equine influenza
• Equine rhinitis virus
• Equine adeno virus

Treatment

• Provide horses more comfort by feeding and watering.
• Perfect monitoring in order to avoid the development of secondary bacterial infection.
• Penicillin prevent recurrent and metastatic infection. For fever, anorexia, depression, purulent discharge,  Procaine penicillin G 22,000IU/kg bw by I/m for every 12 hours for 5 days is given.
• Tetracycline 6-7.5 mg/kg bw i/v for every 12-24hours. Sulphonamide-trimethoprim combination 15-30mg/kg orally or i/v every 12 hours may be effective but only be used if procaine penicillin administration is not possible.
• Guttural pouch empyema is flushed with sterile isotonic electrolyte solution (0.9% NaCl).
• Non-steroidal anti-inflammatory drugs (NASAIDs) and hot poultices to reduce swelling.

Prevention

Serum IgGb developed against SeM protein   can be used to prevent infection.Vaccination of mares 4-6weeks of gestation and foaling period by i/m.  

Genes HasA and HasB that are responsible for capsule formation and  its removal may increase the genetic stability of live vaccine strain (707-27) because they lack capsule and  become avirulent. It is only for intra nasal route for healthy horses not for infected horses and outbreak.

Control

• Isolation of infected horses.
• Colostrum fed foals are passively immune for 4 months.
• Majority of the horses develop solid immunity for 5 years.
• M Protein increases the concentration of serum opsonizing antibody but not offer resistance to natural exposure.
• Stop the movement of animals until outbreak is controlled.
• Establish whether clinically recovered horses are carriers.
• At least three nasopharyngeal swab or washing taken at weekly intervals from all recovered cases examined by culture to prove negative.
• Endoscopic examination of upper airways and guttural pouch.
• Eliminate S.equi by treating guttural pouch infection.
• Maintain strict hygiene.
• Topical application is effective for open infection.
• Tracheotomy for upper air ways obstruction.