Flashcards in Respiratory Disease Horses Deck (47):
What type of pathogen is Strep equi equi?
G+ NOT commensal of URT
How does strep equi equi colonize resp tract?
Straight out, does not require previosu viral infection
What aged horses are commonly affected by strangles?
young weanlings 1-5yo (but can be any age)
Can foals inherit resistance?
foals born from immune mares resistant for 3 months
mornidity and mortality rates?
morbidity 100% mortality 10% with appropriate tx
is immunity long lasting?
No, not life long
only 75% still immune after 3-4yrs
How is strangles transmitted?
- 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
Incubation and shedding periods of strangles?
- incubation period 2-6d
- nasal shedding for 3-6 weks after clinical infection!!
- some horses shed asymptomatically for years
3 clnical presentations of strangles?
1. Classic acute disease
2. Atypical disease
Clinical signs of classic acute strangles
- 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
Clinical signs of atypical strangles
- mild inflam URT
- slight nasal discharge
- self limiting lymphadenopathy
== URT viruses
Why does atypical strangels occour?
- bacterial strain
- immunity of the horse
Why is atypucal strnagles so important/dangerous?
- 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
Clinical signs of complications asssociated with strangles?
> internal abscessation
- intermittent colic due to abdo LN spread
- PUO (pyrexia of unknown origin)
- 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
Diagnosis of strangles?
- clinical signs
- isolation (culture) or detection (PCR) of S. Equi from nasopharyngeal swab, LN, GP lavage
> culture 3x swabs weekly or 1x GP wash
Tx of strangles?
*depends on stage of disease*
Tx of a horse exposed to strangles?
> 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)
Tx of horse with mild strangles signs (rhinitis, pharyngitis)
> early clinical signs (rhinitis, pharyngitis)
- general nursing
- soft food
- NB. may inhibit natural immunity yand recontract disease if exposure continued
Tx of horses with strangles LN abscess
- poultice and drain abscesses
- ABx may prolong resolution
- general nursing
- soft food
Dx and Tx of horses with strangles complications? Prognosis?
> 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
Tx strangles carriers?
- 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
Management of a strangles outbreal?
- 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
Can blood tests be used to diagnose strangles?
- 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
How can strangles be prevented?
- 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
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
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
When is rhodococcus infection commonly seen?
- late spring/summer (^ aerosol challenge, ^ no. suscpetable foals)
What 2 forms of rhodococcus infection exist?
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
Clinical signs of respiratory rhodococcus infection?
- may be insidious or acute onset
- subacute form may be found dead or with acute respiratory distress and oyrexia
Diagnostic tests for respiratory rhodococcus?
- ^ fibrinogen
- trach wash (culture, G stain, PCR VapA gene)
- Rads/ultrasounds (peripheral lung abscesses only)
- NOT serology (poor sense and specificity)
Pathogenesis of intestinal rhodococcus? Prognosis?
- swallow sputum
- ulcerative enterocolitis
- mesenteric lymphadenitis
- abscess formation
- commonly seen in combination with respiratory form
> prognosis POOR
clinical signs of intestinal rhodococcus infection?
- weightloss/poor growth
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
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
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, $$$, worth a try if ongoing problem)
- no effective vaccine curreenlty available
How can R. Equi be diagnosied early?
- 2x weekly TPR to detect pyrexia
- monthly CBC and fibrinogen (WCC >15x10^9/L highly suspicious)
- rads/ultrasound for $$$ foals
> BUT detects subclinical disease.. would this deffo become clinical? Don't know.
Is parascaris equorum a major pathogen? pathogenesis? Dx? Tx?
- eggs on ground from last years foals
- can -> transient nasal discharge and cough as migrating through lungs
- Dx: FEC
- Tx: ivermectin, moxidectin
How pathogenic is equine rhinitis virus?
- controversial (isolated from asymptomatic horses and those with resp disease)
- can induce experimental infection
Which horses commonly affected by equine rhinitis virus?
- 60-80% horses have Ab titres by 5yo
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)
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
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
Clinical signs of EVA?
- oedema, pyrexia and conjunctivitis
- conjunctival oedema typical of this disease
Diagnosis of EVA?
- blood samples
- nasal swabs
> viral isolation, detectin of RNA by PCR
- paired serology
- can vaccinate seronegatvie breeding stallions (need pre-vax blood test) using modified live