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Module 20: Global Vet Med > Equine Ubiquitous Infections - Strangles > Flashcards

Equine Ubiquitous Infections - Strangles Flashcards

1
Q

what is the bacteria that causes strangles

A

Streptococcus equi ss equi

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2
Q

how is strangles transmitted

A

direct contact with infected cause usually

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3
Q

what are the risk factors for strangles

A

Co-mingling, horse movement

Poor specific immunity

Asymptomatic carrier horses

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4
Q

what is the incubation period of strangles

A

3-4 days

depends on exposed dose may be much longer (3-14 days)

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5
Q

what is the pathogenesis of strangles

A

Nasopharyngeal mucosal hyperemia followed by intranodal abscessation

  • Spread to draining lymph nodes (hours)
  • Bacterial multiplication, PMNL infiltration
  • Lymphoid necrosis and lymphadenopathy

May be eventual LN rupture

  • Local complications in ~20% of cases
  • Purulent sinusitis, perioorbital abscessation, facial cellulitis
  • Cranial nerve damage: laryngeal paralysis, facial paralysis, Horner’s syndrome

Aspiration of nasopharyngeal exudate

Occasional pleuropneumonia

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6
Q

what is the first sign of strangles infection

A

pyrexia 39.9-40C

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7
Q

what are the subsequent clinical signs of strangles

A

Inappetence

  • Pharyngeal inflammation
  • Cranial nerve dysfunction

Lethargy

Nasal discharge (serious —> purulent)

Lymphadenopathy

May cough, often not

Mild signs only in horses with immunity

LN abscessation variable

Most cases much better by 3-5 days after start of clinical signs

May progress to LN rupture which prolongs course of disease

  • Skin
  • Guttural pouch

Retropharyngeal LN enlargement may compress dorsal pharynx

Stertorous breathing due to restricted airflow

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8
Q

what are less common clinical signs of strangles

A

Excessive retropharyngeal LN enlargement or guttural pouch distention

  • Increased pharyngeal compression

Reduced air movement at nostrils

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9
Q

when does bacterial shedding occur in uncomplicated cases and how long does it last

A

2-3d after fever onset

persists for 2-3 weeks in most animals

systemic + mucosal immune responses evident 2-3 weeks post infection

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10
Q

if the guttural pouch is infected how long does infection last

A

infection is usually cleared from guttural pouches within 6 weeks

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11
Q

what % of horses develop solid immunity after recovery from strangles

A

75%

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12
Q

how is strangles diagnosed in uncomplicated cases (5)

A
  1. Clinical signs
  2. Direct aspiration from LN and culture
  3. Nasal swab in media acceptable if discharging
  4. Nasopharyngeal swab required if no nasal discharge
  5. Saline lavage of guttural pouches
  • Culture/PCR has improved sensitivity
  • ELISA for antibody to specific cell wall antigen useful screening test — paired titres best at 3 weeks

***Note exposure vs. active infection!

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13
Q

if the culture is positive and the PCR is positive how do you interpret the results of a nasopharyngeal swab

A

the animal is infected

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14
Q

if the culture is positive and the PCR is negative how do you interpret the results of a nasopharyngeal swab

A

the animal is infected

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15
Q

if the culture is negative and the PCR is positive how do you interpret the results of a nasopharyngeal swab

A

animal is infected

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16
Q

if the culture is negative and the PCR is negative how do you interpret the results of a nasopharyngeal swab

A

animal is not infected?

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17
Q

what is the strangles blood test

A

Antibody production to two antigens

Measures the response using cutoff points

18
Q

how do you interprete ELISA

A

Paired serology requires re-testing of sample 2 against sample 1

Inter assay variation

  • Results and re-test +/- 0.3

Valid comparison ONLY between samples tested as pairs ex. A to A, B to B and C to C

First sample ideally taken 2 weeks after time of first exposure

19
Q

how are uncomplicated cases of strangles treated

A

Anti-inflammatories to reduce temperature

Hot packing of LNs to promote maturation

  • Lance and drain

Usually no antibiotics unless very unwell as may prolong duration

  • Penicillin G is antibiotic of choice >22,000 IU/kg
  • Reserved for refractory/severe cases only

OR

  • Use at first sign of pyrexia

Nursing care

  • Soft feeds
  • Management of abscessation
20
Q

what is purpura hemorrhagica

A

Leukocytoclastic vasculitis seen in 1-2% cases

circulating IgA and M protein immune complexes deposited on vessel walls

complement activation

  • Polymorphonuclear leukocytes (PMNL) recruitment and lysosomal enzyme damage to vessels, causing increased permeability
  • Commoner if higher antibody titres
  • If high at time of exposure more likely to develop this condition
  • Maximal at 2-4 weeks post infection
  • Delayed clinical manifestation
  • Ideally assay IgA prior to considering vaccination
21
Q

what are the clinical signs of purpura hemorrhagica

A

Petechial haemorrhages

Stiffness and reluctance to move

Edema of ventral abdomen, prepuce and legs

Hot, painful swelling, with sharp demarcation (‘stove pipe’ edema)

22
Q

how long does recovery take from purpura hemorrhagica

A

Recovery in 7-10 days or progression:

  • Widespread edema of head and respiratory tract with petechiation of mucus membranes
  • Skin necrosis with serum release
  • Progressive lung edema, neurological signs, death
  • Up to 50% mortality
23
Q

how is purpura hemorrhagica treated

A

Removal of antigenic stimulation

Penicillin (>25,000 IU/kg QID)

Corticosteroids if petechiation develops (prednisolone 0.5-2 mg/kg SID per os)

Wound care and bandaging of extremities

Hematinic agents may aid correction of chronic anemia

Intensive nursing

Guarded prognosis

  • Particularly for first 3 weeks after onset of clinical signs
24
Q

what is a possible sequela

A

disseminated abscessation or ‘bastard strangles’

25
Q

what is disseminated abscessation or bastard strangles

A

Mediastinal or mesenteric LN involvement most common

Compression of esophagus

Distention of jugular vessels, could rupture and cause pleural pneumonia

Liver, kidney, spleen, synovial membranes or brain may be involved

26
Q

what are the clinical signs of bastard strangles

A

Chronic weight loss

Recurrent colic

Adhesions

Recurrent peritonitis

CNS depression

May involve <10% cases

Clinical signs depend on site of involvement

27
Q

what can the guttural pouches become involved in infection

A

Inflammation of guttural pouch lining common

Purulent discharge from retropharyngeal LN into pouch may occu

28
Q

how long does guttural pouch empyema occur

A

Guttural pouch empyema mostly short lived

29
Q

what does guttural pouch empyema cause

A

Causes dysphagia and inspiratory stridor

Chronic empyema develops in up to 10% of animals

Eventual inspissation of pus —> chondroid formation

Asymptomatic carriers! Intermittent lifelong shedding

30
Q

how can a horse become a chronic shedder

A

chondroids in the guttural pouch

shedding intermittently from nasal mucosa

31
Q

how are guttural pouch emypemas treated

A

Drainage and lavage (water, saline, ringers) via indwelling Foley catheter or Mild guttural pouch catheter

Instillation of gelatin/penicillin G mixture:

  • Prolonged action

Systemic antibiotics:

  • Procaine penicillin >25,000 IU/kg IM BID
  • Oral TMPS 20mg/kg BID
  • Prolonged treatment required
32
Q

how are chondroids treated

A

Most chondroids can be removed via endoscope

  • Helical basket snap or simple snare

Multiple chondroids may require surgical removal

Standing approach possible

Site usually left open as contaminated wound

Subsequent lavage and treatment of pouch as for empyema

  • Culture/PCR required after minimum of 3 weeks to determine success of treatment
33
Q

what are important control points of strangles

A

Shedding does not start until 1-2d after pyrexia

Nasal shedding present for >2-3 weeks in most animals

Persistent guttural pouch infection may cause intermittent shedding for years

Incubation period variable depending on dose received

Mild disease only in previously recovered animals

34
Q

how would you control an outbreak of strangles

A
  1. Prompt isolation and ID of pathogen
  2. ID infected, exposed and unexposed horses
  3. Red, amber and green groups
  4. Quarantine
  5. Prevent horse movement on/off premise
  6. Strict hygiene principles
  7. Bacteriological screening of convalescing and exposed horses
  8. Investigate and treat carrier horses
  9. Vaccination?
35
Q

how effective is the stranlges vaccine

A

limited efficacy

36
Q

is it recommended to vaccine in the face of an outbreak

A

questionable

37
Q

when is recommended to vaccinate against strangles

A

Most appropriate for high-risk horses

Yards where isolation impossible

Yards with endemic Strangles

Booster intervals to be decided

38
Q

describe how you would vaccinate low risk, medium risk and high risk horses

A
39
Q

what are high risk horses for carrying strangles

A

New horse incubating disease

  • Especially from dealers premise

Recovered clinically but infectious

  • Subclinical S. equi carriers

Older horses with existing immunity

  • Milder disease syndrome

True long-term asymptomatic carriers

  • Guttural pouch empyema
  • Chondroids
  • Intermittent shedders
    • Metastatic involvement
  • Variant S. equi strains
40
Q

describe how you would control a strangles outbreak on a livery yard

A

Isolate new horses, ideally for 21 days

Look for signs of previous infection

  • Scarring, thickening over parotid region

Monitor for clinical signs

Consider blood sampling +/- swapping or scoping to pick up carrier cases

  • Then possible vaccination

Isolate any horse with a high temperature (temp 2x daily)

Confirmed cases are moved away from premises, subsequent samples are submitted for PCR/culture >6 weeks after clinical signs stopped

Carrier horses ID’d and isolated

All blood sample positive cases confirmed negative for shedding on guttural pouch endoscopy

Paired antibody titres collected from horses with original positive sample

Yard allowed to open 8 weeks after first case (no new clinical signs for >6 weeks, cessation of shedding, clearance of carrier horses)

Module 20: Global Vet Med (21 decks)

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