Respiratory Disease Horses Flashcards

(47 cards)

1
Q

What type of pathogen is Strep equi equi?

A

G+ NOT commensal of URT

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2
Q

How does strep equi equi colonize resp tract?

A

Straight out, does not require previosu viral infection

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3
Q

What aged horses are commonly affected by strangles?

A

young weanlings 1-5yo (but can be any age)

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4
Q

Can foals inherit resistance?

A

foals born from immune mares resistant for 3 months

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5
Q

mornidity and mortality rates?

A

morbidity 100% mortality 10% with appropriate tx

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6
Q

is immunity long lasting?

A

No, not life long

only 75% still immune after 3-4yrs

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7
Q

How is strangles transmitted?

A
  • direct contact or fomites (nasal secretions and LN discharge)
  • environment though only survives 1-3d
  • asymptomatic carriers up to 5-6months shedding from gutteral pouch
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8
Q

Incubation and shedding periods of strangles?

A
  • incubation period 2-6d
  • nasal shedding for 3-6 weks after clinical infection!!
  • some horses shed asymptomatically for years
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9
Q

3 clnical presentations of strangles?

A
  1. Classic acute disease
  2. Atypical disease
  3. Complications
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10
Q

Clinical signs of classic acute strangles

A
  • fever, depression, innappetance (SICK)
  • cough and nasal dischare (URTI)
  • abscessation of mandibular, parotid or retropharyngeal LNs with rupture ~ 1 week later
  • can -> dyspnoea and dysphagia if larynx compressed or pharyngeal cranial n. affected
  • mucoid to purulent nasal discharge
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11
Q

Clinical signs of atypical strangles

A
  • mild inflam URT
  • slight nasal discharge
  • cough
  • fever
  • self limiting lymphadenopathy
    == URT viruses
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12
Q

Why does atypical strangels occour?

A
  • bacterial strain

- immunity of the horse

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13
Q

Why is atypucal strnagles so important/dangerous?

A
  • doesn’t appear like strangles so samples not taken for culture and sense
  • control and prevention measures not implemented
  • disease spread cans till cause clinical disease in other animals
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14
Q

Clinical signs of complications asssociated with strangles?

A

> internal abscessation
- intermittent colic due to abdo LN spread
- PUO (pyrexia of unknown origin)
- anoriexia
- depression
- weight loss
purpura haemorrhagica
- generalised vasculitis (type 3 hypersensitivity)
- 1-2% infected horses
- thrombosis of small vessels (can -> necrosis skin and muscle)
- ventral oedema, body swelling and haemorrhage of mucous membranes
- death duye to pneumonia, cardiac arrhythmia, renal failure, GI disorders
other complications (anaemoia, GP empyema and chondroids, retropharyngeal abscessation, laryngeal hemiplegia, Horner’s syndrome, mammary abcess, CNA abscess, endo/myocarditis, agalactia, tracheal compression with cranial mediastinal LN abcess, supparative bronchopneumonia, myopathies

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15
Q

Diagnosis of strangles?

A
  • clinical signs
  • leucocytoisis
  • hyperfibrinogenaemia/SAA
  • isolation (culture) or detection (PCR) of S. Equi from nasopharyngeal swab, LN, GP lavage
    > culture 3x swabs weekly or 1x GP wash
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16
Q

Tx of strangles?

A

depends on stage of disease

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17
Q

Tx of a horse exposed to strangles?

A

> exposed horse

  • penicillin and isolate from infected (will not become immune for next outbreak)
  • wait and see (will build up immunity but may become worse)
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18
Q

Tx of horse with mild strangles signs (rhinitis, pharyngitis)

A

> early clinical signs (rhinitis, pharyngitis)

  • penicillin
  • general nursing
  • anti-pyretics
  • soft food
  • NB. may inhibit natural immunity yand recontract disease if exposure continued
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19
Q

Tx of horses with strangles LN abscess

A
  • poultice and drain abscesses
  • ABx may prolong resolution
  • general nursing
  • antipyretics
  • soft food
20
Q

Dx and Tx of horses with strangles complications? Prognosis?

A

> abdo abscess
- Dx U/S or rectal
- Tx long term Abx (penicillin or more likely TMPS/rifampin) for up to 6 weeks
GP empyema and chondroids
- Dx endoscopy, rads
- Tx drainage via pharyngeal openings, surgical draining if inspissated, ABx
Purpura haemorrhagica
- Dx clinical signs, skin biopsy
- Tx Penicillin, dexamoethosone or prednisolone, analgesics, NSAIDs, fluids, palliative measures (eg. hydrotherapy, massage)
- Prog guarded

21
Q

Tx strangles carriers?

A
  • endoscopic GP lavage (may be obvious pus or not viasable)
  • retrieve chondroids
  • instil topical penicillin with gelatin
  • repeat GP lavage and PCR after 2 weeks
22
Q

Management of a strangles outbreal?

A
  • isolate premises
  • isolate horses that have shown signs for MIN 4 weeks after resolution of signs
  • prevent movement of staff and equipment between cases
  • phenolics most effective disinfectant (equipment and areas
  • iodophores and chlorhexidine best for staff
  • confirm resolution of disease once clinical signs resolved (3 neg cultures or PCR of nasopharyngeal swabs1 week apart, 1 negative GP wash)
  • detect asymptomatic carriers same way or via blood test and treat
23
Q

Can blood tests be used to diagnose strangles?

A
  • 2 antigens
  • takes 2 weeks from exposure to become positive
  • if negative indicates hrose not exposed
  • If positive =
    = exposure and incubation
  • acute phase disease
  • infection previous 6 months followed by recovery
  • infection in the past resulting in immunity and recent challenge thus not presenting clinical signs
  • past infection and carier status
24
Q

How can strangles be prevented?

A
  • vax was introduced bt had serious problems
  • reintroduced, can v clinical signs and LN infection but does not completely prevent disease
  • isolate new horses for 3-4 weeks and test for carrier status
25
What type of bacteria is rhodococcus? SPread?
- g+, pleomorphic coccobacillus - widespread in environment - lives in GIT of mares and earthworms - survives and multiplies in GIT of foals - survives in soft soil HOT DRY conditions only for >12 months - spread via inhalation of soil/feaces and exhaled by infected foals
26
How pathogenic is rhodococcus?
- strain variation means can be sporadic or endemic - endemic famrs 15-60% morbidity - amplified with high risk practices eg. concentrated facilities, dusty paddocks, incomplete manure removal
27
When is rhodococcus infection commonly seen?
- late spring/summer (^ aerosol challenge, ^ no. suscpetable foals)
28
What 2 forms of rhodococcus infection exist?
- respiratory | - intestinal
29
Outline pathogenesis of respiratory rhodococcus infection
- infecteddays after birth - clinical signs 1-6 months later - bacteria scavenged by alveolar macrophages after inhalation but not killed - destruction of these macrogphages -> pyogranulomatous response - bronchopneumonia with widespread abscess formation - may have additional extrapulnoary sites of infection
30
Clinical signs of respiratory rhodococcus infection?
- anorexia - depression - fever - dyspnoea - tachypnoea - cough - may be insidious or acute onset - subacute form may be found dead or with acute respiratory distress and oyrexia
31
Diagnostic tests for respiratory rhodococcus?
- ^ fibrinogen - neutrophilia - trach wash (culture, G stain, PCR VapA gene) - Rads/ultrasounds (peripheral lung abscesses only) - NOT serology (poor sense and specificity)
32
Pathogenesis of intestinal rhodococcus? Prognosis?
- swallow sputum - ulcerative enterocolitis - mesenteric lymphadenitis - abscess formation - peritonitis - commonly seen in combination with respiratory form > prognosis POOR
33
clinical signs of intestinal rhodococcus infection?
- depression - fever - diarrhoea - colic - weightloss/poor growth
34
Diagnosis of intestinal rhodococcus?
- NOT ID of r. equi in the feaces (not diagnostic) - farm history - clinical signs - haematology (neutrophilia, hyperfibrinogenaemia, thrombocytosis) = PME definitive dx
35
3 Tx protocols of rhodococcus equi infection?
1. erythromycin and rifampin - organism sensitive for major ddx (pasteurella and streptococcus) - combo v resistnace formation * erythromycin -> complications: hyperthermia, tachycardia, ^ liver enzymes in foal - > FATAL COLITIS in dams (c. difficile) if licked off foal 2. clarithromycin or azithromycin +- rifampin - short and long term outcome bettwe with clarithromycin - tx until radiographic resolution of lesions and CBC/fibrinogen normal (~4-12 weeks) - Tx expensive 3. 75% foals with mild small abscesses recover without tx, monitor weekly may be fine
36
Prevention of rhodococcus equi infection?
- difficult as organism shed in feaces - ^ ventilation, v dust - avoid dirt paddocls and crowding/rotate pasture to minimize grass destruction etc. - isolate sick foals - Prophylaxis with hyperimmune plasma (not 100% effective, $$$, worth a try if ongoing problem) - no effective vaccine curreenlty available
37
How can R. Equi be diagnosied early?
- 2x weekly TPR to detect pyrexia - monthly CBC and fibrinogen (WCC >15x10^9/L highly suspicious) - rads/ultrasound for $$$ foals > BUT detects subclinical disease.. would this deffo become clinical? Don't know.
38
Is parascaris equorum a major pathogen? pathogenesis? Dx? Tx?
- no - eggs on ground from last years foals - can -> transient nasal discharge and cough as migrating through lungs - Dx: FEC - Tx: ivermectin, moxidectin
39
How pathogenic is equine rhinitis virus?
- controversial (isolated from asymptomatic horses and those with resp disease) - can induce experimental infection
40
Which horses commonly affected by equine rhinitis virus?
young horses | - 60-80% horses have Ab titres by 5yo
41
Clinical signs of equine rhinitis virus? Diagnosis? Tx
- subclinical or mild URT and LRT signs - Diagnosis by virus isolation from NP swabs or BALF serology (ddx herpes, influenza etc.) - Tx: symptomatic (no antivirals, no vax)
42
Which respiratory disease is notifiable? Which population is this seen in? Prevention?
- Equine Viral Arteritis - Venereal transmission by chronic shedding stallions between mares - AI can spread too - contact with aborted foetuses/products of parturition - direct contact resp tract or secretions - clnical disease in racing TBs not yet reported > prevention: vax required by most studs
43
Pathogenesis of EVA?
- spread via resp secretions, breeding or contact with parturition products - incubation 3-14d - variable pathogenicity of strains - replicates in macrophages, travels to local LNs - leucocyte associated viraemia -> endothelial damage -> necrotising arteritis -> oedema and haemorrhage endothelial cells esp small arterioles, epithelium of adrenals, seminiferous tubules, thyroid and liver
44
Clinical signs of EVA?
- none - abortion/stillbirth - oedema, pyrexia and conjunctivitis - conjunctival oedema typical of this disease
45
Diagnosis of EVA?
- blood samples - nasal swabs - semen > viral isolation, detectin of RNA by PCR - paired serology
46
Tx EVA?
- symptomatic | - can vaccinate seronegatvie breeding stallions (need pre-vax blood test) using modified live
47
Code of practice for EVA?
- NOIFIABLE! - stop all breeding - isolate and tx clinical cases - screen all horses serologically - test semen from all stallions - clean and disinfect - repeat testing until freedom from activeinfection confirmed (declining AB titre, no virus isolated) - monitor semen of +ve stallion for persistent shedding