Equine strangles Flashcards
What causes strangles?
Streptococcus equi subspecies equi (gram positive, not a normal URT inhabitant, no prior viral infection required)
What age of horse tends to suffer with strangles?
weanlings and yearlings especially
Infection primarily aged 1-5 yo
Immune for first 3 months
What is the morbidity, mortality and complication rate with strangles?
Morbidity - 100%
Mortality - 10% (with appropriate therapy)
Complication - 20%
Outline immunity to strangles
Not lifelong but 75% still immune after 3-4 years
How is Strep equi equi transmitted?
- Direct contact (nasal secretions or LN discharges)
- Fomites (survives in environment for 1-3 days)
- Asymptomatic chronic carriers (carried in the GP, shed intermittently for up to 56 months)
Outline strangles pathogenesis
Incubation = 2-6 days
Recover over 2-3 weeks
Nasal shedding for 3-6 weeks after disease
Some shed asymptomatically for months-years
What are the 3 clinical presentations of strangles?
- Classic acute disease
- Atypical disease
- Complications
CS - classic acute disease - 4
- Fever, depression, inappetance, cough, nasal discharge, - LN abscessation (mandibular, parotid or retropharyngeal LNs)) with rupture after 7-10 days.
- Dyspnoea and dysphagia if abscesses compress larynx or interferes with CN to pharynx
- Mucoid to purulent nasal discharge
CS - atypical strangles
- only distinguishable from URT virus with further tests*
- mild inflammation of URT
- slight nasal discharge
- cough
- fever
- self-limiting lymphadenopathy
Why is atypical strangles important?
- Doesn’t look like strangles, just looks like any other RT infection –> samples not taken and culture/prevention not implemented.
- Disease spread (can cause classical strangles in other animals)
CS - complications (strangles) 3
INTERNAL ABSCESSATION –> signs depending on abscess location, intermittent colic (commonest), PUO, anorexia, depression, weight loss
PURPURA HAEMORRHAGICA - generalised vasculitis due to a type 3 hypersensitivity reaction to bacteria, 1-2% infected horses get this, thrombosis of small arteries possible –> skin and mm necrosis. Ventral oedema, body swelling and petechial haemorrhage on MM. Death due to pneumonia, cardiac arrhythmia, renal failure, GI disorders.
OTHERS - GP empeyema and chondroids AND/OR retropharyngeal abscessation (these are the 2 commonest syndromes, others possible).
What are chondroids?
Yellow lumps of inspissated pus that sits in GP and harbours bacteria therefore good source of infection.
List some other possible (less common) complications of strangles. 8
- Laryngeal hemiplegia
- Horner’s syndrome
- Mammary gland abscess
- CNS abscess
- Endocarditis or myocarditis
- Agalactia
- Tracheal compression due to cranial mediastinal LN abscess
- Suppurative bronchopneumonia
- Myopathies
Diagnosis - strangles
Based on CS
Bloods - leukocytosis and hyperfibrinogenaemias
Isolation (culture) or PCR from LN
Nasopharyngeal swab
GP lavage fluid
Sensitivity: PCR> GP lavage fluid > nasopharyngeal swab
Tx - Strangles
Depends on disease stage
Tx - horse exposed to strangles
- Penicillin until isolated from infected horses
- Will not become immune
Tx - horse with early CS (rhinitis/pharyngitis phase) - 4
- Penicillin (may inhibit natural immunity so many contract the disease again with continued exposure)
- General nursing
- Anti-pyretics (NSAIDs)
- Soft food
Tx - horse with LN abscesses - 5
- Poulticing and drainage of abscesses
- AB may prolong abscess resolution
- General nursing
- Anti-pyretics (NSAIDs)
- Soft food
Tx - horse with complications
Depends on the specific complication:
- Abdominal abscess
- GP empyema and chondroids
- Purpura haemorrhagica
Dx and Tx of abdominal abscesses as a complication of strangles
Dx - ultrasound or rectal
Tx - long term ABs (usually penicillin or trimethopri sulfa/rifampin) for up to 6 weeks
Define guttural pouch (GP) empyema. Cause?
the accumulation of purulent, septic exudate in the guttural pouch. The infection usually develops subsequent to a bacterial (primarily Streptococcus spp) infection of the URT.
Dx and Tx of GP empyema and chondroids as a complication of strangles
Dx - endoscopy, radiography
Tx - drainage via the pharyngeal openings or surgical drainage (if inspissated), ABs
Dx and Tx of purpura haemorrhagica as a complication of strangles
Dx - CS and skin biopsy
Tx - Penicillin, Dexamethasone or Prednisolone (to suppress hypersensitivity), analgesics (NSAIDs), fluids, palliative measures (hydrotherapy, massage).
Prognosis - purpura haemorrhagica as a complication of strangles
Guarded
How do you treat a carrier horse (strangles)?
Endoscopic GP lavage. Retrieve chondroids via surgical approach. Instil topical (Benzyl)penicillin in gelatin. Repeat GP lavage and PCR after 2 weeks.
How should you manage an outbreak of strangles?
Which disinfectants?
How can you confirm resolution? 3
- Coordinated approach
- Isolate premises and horses with CS (wait at least 4 -weeks after signs resolve)
- Prevent movement of staff/equipment bw horses
- Phenolics to disinfect equipment and areas
- Iodophores and chlorhexidine to disinfect staff
- Confirm resolution using 3 negative cultures or PCR of nasopharyngeal swabs OR one negative GP wash
Describe the Strangles blood test
- Measure IgG against 2 specific Strep equi equi antigens (A and B).
- Takes 2 weeks from exposure to become positive
- Negative indicated horse not exposed
- Positive indicates one of several options
What does a positive response to the Strangles blood test indicate? 5
- strangles exposure and disease incubation
- acute phase strangles (horse may show CS)
- infection with strangles in previous 6 months without(/out) CS followed by full recovery
- Infection with strangles in past, with/out CS –> immunity to disease in face of recent exposure
- past infection with strangles which has resulted in the horse becoming a carrier.
How can Strangles be prevented? 2
- MLV (reintroduced with less CS and LN abscessation associated with it)
- Isolate new horses for 3-4 weeks, then test for carriers.
What is Rhodococcus equi?
Gram positive,
pleomorphic coccobacillus - widespread in environment
survive in GIT (mares and eathworms)
survives and multiples in GIT (foals)
soil survival of 12 months+ in hot, dry conditions
Transmission - Rhodococcus equi
Inhalation of soil/faeces or exhaled air of infected foals.
How common is R. equi?
Variation in strain pathogenicity –> sporadic to endemic presence.
Endemic farms = 15-60% morbidity (amplified with high risk management practices)
When does R. equi infection occur?
Late spring/summer - coincides with high aerosol challenge and a high number of susceptible foals.
What are the 2 main forms of Rhodococcus equi infection??
Respiratory and intestinal forms (intestinal form is the most common location of extra-respiratory tract R.equi).
Describe the respiratory form of Rhodococcus equi
- foal infected within first few days after birth
- CS at 1-6 months old
- disease due to overwhelming # of R. equi
- Bacteria scavenged by alveolar macrophages, not killed, macrophages destroyed –> pyogranulomatous response.
- bronchopneumonia with widespread abscess formation
- 50% cases have extra-pulomary sites of infection
CS - respiratory form of R. equi.
- anorexia, depression, fever, dyspnoea, tachypnoea, cough,
- Variable onset (insidious to extremely acute, subacute possible with animal found dead or with acute resp distress + pyrexia)
How can the respiratory form of R.equi be diagnosed? 6
- Bloods - high fibrinogen and neutrophilia
- Tracheal wash (lung) - culture, gram stain, PCR
- Radiography - detects abscesses
- Ultrasound (if abscess extends to periphery)
- Serology - not specific or sensitive enough
- PME - acute and subacute cases
Tx - Rhodococcus equi
AB selection
- Traditionally Erythromycin and rifampin
- Recently Clarithromycin OR azithromycin with rifampin in the treatment of R. equi
Outline the use of Erythromycin and rifampin in the treatment of R. equi
Organism sensitive and major differentials (strep and Pasteurella) are also sensitive.
- Combination therapy decreases resistance risk
- Complications - hyperthermia, tachycardia, increased liver enzymes (foals) and fatal colitis in dams.
Outline the use of Clarithromycin OR azithromycin with rifampin in the treatment of R. equi
- increasingly common, especially clarithromycin (short and long term outcome better)
- treat until radiographic resolution of lesions and CBC/fibrinogen are normal (4-12 weeks)
- expensive
- 4% resistance
What is a new theory regarding R.equi treatment?
75% foals with a total abscess diamter of 8cm and mild CS will recover without Tx and should be monitored weekly only
Prevention - R.equi - 7
- Difficult - organism shed in faeces
- Increase ventilation
- decrease dusty condition
- avoid dirt paddocks and overcrowding
- rotate pastures (minimise grass destruction)
- vacuum or collect manure
- isolate sick foals
- above measures reduce incidence by 30-40%
- optimal timing and dose unknown
- no effective vaccine currently
How can R.qui be diagnosed early?
- 2x week TPRs
- monthly CBC and fibrinogen - to ID sick animals (WCC >1310^9/L is suspicious and >1510^9/L is highly suspicious but not pathognomic
- Radiography/ultrasound to screen valuable foals and detect subclinical disease)
Describe Parascaris equorum:
CS
Dx
Tx
- minor pathogen
- eggs on ground from previous year’s foal crop
- CS - transient nasal discharge and cough as migrating throug lungs
- Dx = FEC
- Tx = anthelmintics (most routine preparations which include ivermectin or moxidectin will kill this)
Describe Equine Rhinitis VIrus Which horses Immunity CS Dx Tx
- role as pathogen is controversial
- isolated form asymptomatic and respiratory disease signs
- commonest in young horses
- 60-80% horses have Ab titres by 5 yo
- CS - subclinical or mild URT and LRT signs
- Dx - virus isolation from NP swab or BALF, serology
- Tx - symptomatic as no vaccine or anti-viral
Outline Equine Viral Arteritis (EVA)
RNA arterivirus
NOTIFIABLE
- TRANSMISSION - venereal, contact with aborted foetuses and other products of parturition, direct contact in droplets
- RESERVOIR - stallions that are chronic shedders
Epidemiology of EVA
- no clinical outbreaks reported in TBs
- UK outbreak in 1993
- vaccination now required by most studs
Pathogenesis - EVA Transmission Incubation Pathogenicity Pathophysiology
- TRANSMISSION - respiratory secretions, breeding or contact with aborted foetus/placenta
- INCUBATION - 3-14 days
- PATHOGENICITY - varies with strain
- PATHOPHYSIOLOGY - replicates in macrophages, travels to local LNs, followed by leucocyte-associated viraemia –> virus localises in endothelial cells, especially smaller arterioles and in epithelium of certian tissues (adrenals, seminiferous tubules, thyroid and liver) –> endothelial damage –> necrotising arteritis manifest as oedema and haemorrhage.
CS - EVA
- often none
- abortion and stillbirth (10-34 days following exposure, 3-10 months gestation)
- Fever, anorexia, oedema (limb, prepuce, scrotum, ventral, periorbital), lacrimation, conjunctivitis, nasal discharge, coughing
Dx - EVA - 2
- Blood samples, nasal swabs and semen for virus isolation or detection of viral RNA by PCR.
- Serology - paired
Tx - EVA
Symptomatic only
Vaccination - EVA
Can vaccinate seronegative breeding stallions (need pre-vaccination blood test) using MLV and not this in passport
Outline the code of practice in relation to EVA - 8
- Notifiable
- Stop all breeding
- Isolate and treat clinical cases
- Group in-contacts away from other horses on premises and obtain samples for virus isolation
- Screen all other horses on premises (paired serology)
- Test semen from ALL stallions. Monitor semen of positive stallions for persistence of shedding.
- Clean and disinfect
- Repeat testing until freedom from active infection is confirmed (i.e. declining Ab on serology and no virus isolated).
