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Respiratory > Respiratory Disease Horses > Flashcards

Respiratory Disease Horses Flashcards

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
Q

What type of bacteria is rhodococcus? SPread?

A
  • 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
Q

How pathogenic is rhodococcus?

A
  • 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
Q

When is rhodococcus infection commonly seen?

A
  • late spring/summer (^ aerosol challenge, ^ no. suscpetable foals)
28
Q

What 2 forms of rhodococcus infection exist?

A
  • respiratory

- intestinal

29
Q

Outline pathogenesis of respiratory rhodococcus infection

A
  • 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
Q

Clinical signs of respiratory rhodococcus infection?

A
  • 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
Q

Diagnostic tests for respiratory rhodococcus?

A
  • ^ fibrinogen
  • neutrophilia
  • trach wash (culture, G stain, PCR VapA gene)
  • Rads/ultrasounds (peripheral lung abscesses only)
  • NOT serology (poor sense and specificity)
32
Q

Pathogenesis of intestinal rhodococcus? Prognosis?

A
  • swallow sputum
  • ulcerative enterocolitis
  • mesenteric lymphadenitis
  • abscess formation
  • peritonitis
  • commonly seen in combination with respiratory form
    > prognosis POOR
33
Q

clinical signs of intestinal rhodococcus infection?

A
  • depression
  • fever
  • diarrhoea
  • colic
  • weightloss/poor growth
34
Q

Diagnosis of intestinal rhodococcus?

A
  • NOT ID of r. equi in the feaces (not diagnostic)
  • farm history
  • clinical signs
  • haematology (neutrophilia, hyperfibrinogenaemia, thrombocytosis)
    = PME definitive dx
35
Q

3 Tx protocols of rhodococcus equi infection?

A
  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
Q

Prevention of rhodococcus equi infection?

A
  • 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
Q

How can R. Equi be diagnosied early?

A
  • 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
Q

Is parascaris equorum a major pathogen? pathogenesis? Dx? Tx?

A
  • no
  • eggs on ground from last years foals
  • can -> transient nasal discharge and cough as migrating through lungs
  • Dx: FEC
  • Tx: ivermectin, moxidectin
39
Q

How pathogenic is equine rhinitis virus?

A
  • controversial (isolated from asymptomatic horses and those with resp disease)
  • can induce experimental infection
40
Q

Which horses commonly affected by equine rhinitis virus?

A

young horses

- 60-80% horses have Ab titres by 5yo

41
Q

Clinical signs of equine rhinitis virus? Diagnosis? Tx

A
  • 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
Q

Which respiratory disease is notifiable? Which population is this seen in? Prevention?

A
  • 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
Q

Pathogenesis of EVA?

A
  • 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
Q

Clinical signs of EVA?

A
  • none
  • abortion/stillbirth
  • oedema, pyrexia and conjunctivitis
  • conjunctival oedema typical of this disease
45
Q

Diagnosis of EVA?

A
  • blood samples
  • nasal swabs
  • semen
    > viral isolation, detectin of RNA by PCR
  • paired serology
46
Q

Tx EVA?

A
  • symptomatic

- can vaccinate seronegatvie breeding stallions (need pre-vax blood test) using modified live

47
Q

Code of practice for EVA?

A
  • 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

Respiratory (18 decks)

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