Equine Respiratory Bacterial Infection

Streptococcus Equi var Equi (Strangles)

Contagious equine rhinopharyngitis. 

Pathogen:

• Gram positive bacteria which forms chains.
• Catalase negative facultative anaeroble.
• Large mucoid colonies- B haemolytic.
• Lactose fermentation negative. 

M-Protein- antiphagocytic and promotes adhesion. M-protein antibody is protective. 

Host:

• Spread by direct contact and fomites.
• Spread in water and feed buckets.
• Recover= shed for months.
• Young/old/sick most affected.
• High morbidity and low mortality. 
• Good management and hygiene effective controls. 

Environment interactions can cause an increase in attack rate-

• Increased group size, movements, mixing, communal feeding and younger horses. Age related immunity due to previous exposure. 

1. Serous nasal discharge, fever and inappetence.
2. 2-3 days- mucopurulent discharge with added cough.
3. Next few days- abscess development in the submandibular and retropharyngeal lymph nodes. 
4. Abscesses rupture (2 week resolve), recovered horses may shed bacteria from the guttural pouch for between six weeks (usually) to six months.
5. Important to confirm free of infection before reintroduction. 

Complications

• Pharyngeal compression- tracheotomy required.
• Abscess rupture in the retropharyngeal lymph node drains into the guttural pouch and then normally into the pharynx to produce a mucopurulent discharge, however, if the pus cannot drain sufficiently it accumulates in the guttural pouch resulting in guttural pouch empyema. This requires flushing to remove and then feeding from the ground level to promote drainage.
• If empyema is not diagnosed within 1-2 months the pus thickens to form solid balls/chondroids. 
• Systemic spread results in abscess formation in the muscles, liver and kidney or lungs and may cause peritonitis. Difficult to treat 'bastard strangles.' 
• Purpura haemorrhagica- some horses develop an antibody antigen complex type three hypersensitivity that results in vasculitis and severe illness. Treated with corticosteroids. 

Diagnosis

• Positive culture.
• PCR.
• ELISA confirms exposure only.

To confirm a horse is free of infection (before mixing due to long shedding period):

• Nasal swabs- 3 negatives each week for 3 weeks (85%).
• Guttural pouch wash- 1 negative= 88% sure. 

Environment:

• Resistant- survives in pus for weeks. 
• Killed at 55 degrees for 30 mins.  Sensitive to many disinfectants. 
• Carriers significant- more so than environmental reservoir. 4 week survival in drinking water, 8 weeks in pus and 1 week if dessicated. Virkon disinfectant.
• Contagiousness of bacteria decreases with time.
• Direct droplet transmission and fomites important.

Control & Prevention:

• Isolation and barrier nurse.
• Reduce infection load.
• Increase air quality.
• 10% horses chronic carriers for one month at the end of clinical signs. Carrier status can persist for long periods (7 months).
• Predominantly guturral pouch persistence- endoscope abnormalities. 
• For carrier status- quarantine infected and recovered animals as they often shed bacteria for 3-6 weeks. Test before reintroduction, keep contact horses separate from clean and monitor their temperature daily for a fever onset. 
• Test using serum ELISA all new arrivals- detects all subclinical carriers. 2 week quarantine of all new horses even if negative ELISA (as tests for exposure only). Check temperature daily.
• Vaccination- modified live strangles vaccine Equlis Strep E. Administered submucosal injection. 3 months immunity results in reduction of signs/complications. 

Rhodococcus Equi

Supprative bronchopneumonia of foals between 1-4 months old.

Pathogen:

• Gram Positive pleomorphic rod.
• Aerobic soil saprophyte and normal GIT flora.
• Opportunistic pathogen due to low ab.

Variable virulence- challenge and immunity dependent and clinical strains tend to be more pathogenic than soil strains. 

• Free living/saprophytic/facultative pathogen 
• Lipid capsule- antibiotic implication.
• Intracellular- poor chemotaxis/immunogenicity.
• Infection between 2-4 weeks old. Colostral IgG not protective, requires cellular/humoral immunity and problem with encapsulated abscesses. 

Pathogenesis

1. Multiplies within alveolar macrophages and destroys them. 
2. Continual cycle of attraction and destruction- abscess formation. Slow progression. 10d- 3 week incubation period.
3. Destruction of lung alveoli- mediastinal lymphadenopathy/abscesses. 
4. Destruction of gut peyer's patches. 

Host:

• Acute young foal, chronic older foal.
• Acute- fever, anorexia, cough and nasal discharge.
• Chronic- cough, dyspnoea, weight loss, and exercise intolerance. 
• Large pulmonary abscess formation. 
• Occ diarrhoea.
• Long term affects and mortality in 8% cases. Reduces number of foals reaching racetrack but does not affect performance once there. 

Transmission:

• Inhalation- dust aerosol, cranial lung first and distribution may also suggest pyaemic spread to lung.
• Oral route- coprophagia. Swallowing organism from airway secretions. 
• Resistant to acid/alkali disinfectant. Survives in soil for up to 36 months.
• Survives in large colon of adults. Foal coprophagia. 
• Diagnosis often at chronic stage. 

Diagnosis:

• Clinical signs.
• Tracheal wash/culture/PCR.
• Radiography/ultrasound. 
• Must correlate culture with clinical design as healthy foals also have Rhodococcus Equi. 

Complications:

• Polyarthritis (immune) or septic arthritis.
• Granulomatous ulcerative enterocolitis and mesenteric lymphadenitis.
• Corneal oedema/anterior uveitis. 

Prevention & Control:

• Quarantine may work- environment pathogen by amplified by affected foals.
• Avoid crowding and remove foal faeces from pasture.
• Reduce dust- condition most common in dry dusty conditions.
• Examine foals twice a week until four weeks old.
• Hygiene.
• Plasma transfusion- 250-500ml hyperimmune plasma at birth. Repeat at 21 days. High effective. 
• Colostral IgG alone not protective. No vaccine.
• Early recognition and isolate.
• Pasture irrigation.