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Respiratory > Equine strangles > Flashcards

Equine strangles Flashcards

1
Q

What causes strangles?

A

Streptococcus equi subspecies equi (gram positive, not a normal URT inhabitant, no prior viral infection required)

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2
Q

What age of horse tends to suffer with strangles?

A

weanlings and yearlings especially
Infection primarily aged 1-5 yo
Immune for first 3 months

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3
Q

What is the morbidity, mortality and complication rate with strangles?

A

Morbidity - 100%
Mortality - 10% (with appropriate therapy)
Complication - 20%

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4
Q

Outline immunity to strangles

A

Not lifelong but 75% still immune after 3-4 years

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5
Q

How is Strep equi equi transmitted?

A
  • 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)
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6
Q

Outline strangles pathogenesis

A

Incubation = 2-6 days
Recover over 2-3 weeks
Nasal shedding for 3-6 weeks after disease
Some shed asymptomatically for months-years

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7
Q

What are the 3 clinical presentations of strangles?

A
  • Classic acute disease
  • Atypical disease
  • Complications
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8
Q

CS - classic acute disease - 4

A
  • 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
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9
Q

CS - atypical strangles

A
  • only distinguishable from URT virus with further tests*
  • mild inflammation of URT
  • slight nasal discharge
  • cough
  • fever
  • self-limiting lymphadenopathy
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10
Q

Why is atypical strangles important?

A
  • 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)
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11
Q

CS - complications (strangles) 3

A

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).

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12
Q

What are chondroids?

A

Yellow lumps of inspissated pus that sits in GP and harbours bacteria therefore good source of infection.

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13
Q

List some other possible (less common) complications of strangles. 8

A
  • 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
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14
Q

Diagnosis - strangles

A

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

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15
Q

Tx - Strangles

A

Depends on disease stage

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16
Q

Tx - horse exposed to strangles

A
  • Penicillin until isolated from infected horses

- Will not become immune

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17
Q

Tx - horse with early CS (rhinitis/pharyngitis phase) - 4

A
  • Penicillin (may inhibit natural immunity so many contract the disease again with continued exposure)
  • General nursing
  • Anti-pyretics (NSAIDs)
  • Soft food
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18
Q

Tx - horse with LN abscesses - 5

A
  • Poulticing and drainage of abscesses
  • AB may prolong abscess resolution
  • General nursing
  • Anti-pyretics (NSAIDs)
  • Soft food
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19
Q

Tx - horse with complications

A

Depends on the specific complication:

  • Abdominal abscess
  • GP empyema and chondroids
  • Purpura haemorrhagica
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20
Q

Dx and Tx of abdominal abscesses as a complication of strangles

A

Dx - ultrasound or rectal

Tx - long term ABs (usually penicillin or trimethopri sulfa/rifampin) for up to 6 weeks

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21
Q

Define guttural pouch (GP) empyema. Cause?

A

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.

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22
Q

Dx and Tx of GP empyema and chondroids as a complication of strangles

A

Dx - endoscopy, radiography

Tx - drainage via the pharyngeal openings or surgical drainage (if inspissated), ABs

23
Q

Dx and Tx of purpura haemorrhagica as a complication of strangles

A

Dx - CS and skin biopsy
Tx - Penicillin, Dexamethasone or Prednisolone (to suppress hypersensitivity), analgesics (NSAIDs), fluids, palliative measures (hydrotherapy, massage).

24
Q

Prognosis - purpura haemorrhagica as a complication of strangles

A

Guarded

25
Q

How do you treat a carrier horse (strangles)?

A

Endoscopic GP lavage. Retrieve chondroids via surgical approach. Instil topical (Benzyl)penicillin in gelatin. Repeat GP lavage and PCR after 2 weeks.

26
Q

How should you manage an outbreak of strangles?
Which disinfectants?
How can you confirm resolution? 3

A
  • 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
27
Q

Describe the Strangles blood test

A
  • 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
28
Q

What does a positive response to the Strangles blood test indicate? 5

A
  • 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.
29
Q

How can Strangles be prevented? 2

A
  • MLV (reintroduced with less CS and LN abscessation associated with it)
  • Isolate new horses for 3-4 weeks, then test for carriers.
30
Q

What is Rhodococcus equi?

A

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

31
Q

Transmission - Rhodococcus equi

A

Inhalation of soil/faeces or exhaled air of infected foals.

32
Q

How common is R. equi?

A

Variation in strain pathogenicity –> sporadic to endemic presence.
Endemic farms = 15-60% morbidity (amplified with high risk management practices)

33
Q

When does R. equi infection occur?

A

Late spring/summer - coincides with high aerosol challenge and a high number of susceptible foals.

34
Q

What are the 2 main forms of Rhodococcus equi infection??

A

Respiratory and intestinal forms (intestinal form is the most common location of extra-respiratory tract R.equi).

35
Q

Describe the respiratory form of Rhodococcus equi

A
  • 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
36
Q

CS - respiratory form of R. equi.

A
  • anorexia, depression, fever, dyspnoea, tachypnoea, cough,
  • Variable onset (insidious to extremely acute, subacute possible with animal found dead or with acute resp distress + pyrexia)
37
Q

How can the respiratory form of R.equi be diagnosed? 6

A
  • 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
38
Q

Tx - Rhodococcus equi

A

AB selection

  • Traditionally Erythromycin and rifampin
  • Recently Clarithromycin OR azithromycin with rifampin in the treatment of R. equi
39
Q

Outline the use of Erythromycin and rifampin in the treatment of R. equi

A

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.
40
Q

Outline the use of Clarithromycin OR azithromycin with rifampin in the treatment of R. equi

A
  • 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
41
Q

What is a new theory regarding R.equi treatment?

A

75% foals with a total abscess diamter of 8cm and mild CS will recover without Tx and should be monitored weekly only

42
Q

Prevention - R.equi - 7

A
  • 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
43
Q

How can R.qui be diagnosed early?

A
  • 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)
44
Q

Describe Parascaris equorum:
CS
Dx
Tx

A
  • 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)
45
Q 
Describe Equine Rhinitis VIrus
Which horses
Immunity
CS
Dx
Tx
A
  • 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
46
Q

Outline Equine Viral Arteritis (EVA)

A

RNA arterivirus
NOTIFIABLE
- TRANSMISSION - venereal, contact with aborted foetuses and other products of parturition, direct contact in droplets
- RESERVOIR - stallions that are chronic shedders

47
Q

Epidemiology of EVA

A
  • no clinical outbreaks reported in TBs
  • UK outbreak in 1993
  • vaccination now required by most studs
48
Q 
Pathogenesis - EVA
Transmission
Incubation
Pathogenicity
Pathophysiology
A
  • 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.
49
Q

CS - EVA

A
  • 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
50
Q

Dx - EVA - 2

A
  • Blood samples, nasal swabs and semen for virus isolation or detection of viral RNA by PCR.
  • Serology - paired
51
Q

Tx - EVA

A

Symptomatic only

52
Q

Vaccination - EVA

A

Can vaccinate seronegative breeding stallions (need pre-vaccination blood test) using MLV and not this in passport

53
Q

Outline the code of practice in relation to EVA - 8

A
  • 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).

Respiratory (34 decks)

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