3.3 Coughing in Horses 2

LRT: undifferentiated bacterial pneumonia causes & clinical signs

causes: strep zooepidemicus, also actinobacillus, klebsiella, staph aureus, bordetella, mycoplasma

clinical signs: auscultable changes, mild pyrexia, cough

undifferentiated bacterial pneumonia: diagnosis

history

clinical signs

mucopurulent exudate in trachea on endoscopy

bronchointerstitial pattern on radiography

BAL/tracheal aspirate neutrophils increased, degenerate, intracellular bacteria

undifferentiated bacterial pneumonia: treatment

-antibiotics (C&S, if not, ensure good against strep)
-rest
-dust free environment

URT & LRT: streptococcus equi equi (strangles)

gram positive

not normal inhabitant of URT

does not require viral infection for colonization

highly infectious, particularly weanlings & yearlings

equine specific

strangles: epidemiology

1-5 year olds

foals born from immune mares resistant for 3 months

morbidity 100%

mortality 10% without appropriate therapy

20% complication rate reported

immunity not lifelong (75% still immune after 3-4 years)

strangles: transmission

direct contact with nasal secretions or LN discharges, fomites, environment, only survives 1-3 days

asymptomatic chronic carriers-> guttural pouch, up to 56m

strangles: pathogenesis

incubation 3-14 days

recover over 2-3 weeks

nasal shedding continues for 2-3 weeks after disease

some horses for months or years (up to 10% become carriers)

3 clinical presentations: classic acute disease, atypical strangles, complications

classic acute disease: clinical signs

fever, depression, inappetence, lymphadenopathy

abscessation of mandibular, parotid, or retropharyngeal lymph nodes, rupture after 7-10 days

dyspnea & dysphagia if abscesses compress larynx or interferes with cranial nerve to pharynx

mucoid to purulent nasal discharge

cough

URT signs

atypical strangles: clinical signs

mild inflammation of URT

slight nasal discharge

cough

fever

self-limiting lymphadenopathy

probably dependent on bacterial strain & immunity & genotype of horses

importance of atypical strangles

looks like any other respiratory infection

samples not taken for culture

control & prevention not implemented

bacteria from atypical cases can cause classical strangle in others

strangles outbreaks with atypical cases usually go unrecognized until classical cases appear later

complications: internal abscessation

-intermittent colic
-pyrexia of unknown origin
-anorexia
-depression
-weight loss
-depends on site of abscess

complications: purpura hemorrhagica

-generalized vasculitis caused by type III HS reaction after 3-4 weeks
-1-2% of infected horses
-thrombosis of small arteries
-skin & muscle necrosis
-ventral & limb edema & petechial hemorrhages on mucous membranes
-death due to pneumonia, cardiac arrhythmia, renal failure, GI disorders

complications: guttural pouch empyema & chondroids

-purulent nasal discharge
-RP swelling
-dyspnea/dysphagia

strangles: diagnosis

clinical signs

leukocytosis, hyperfibrinogenemia/
high SAA

isolation (culture) or detection (PCR) of s. equi from LN pus, nasopharyngeal swab, GP lavage fluid

culture 3x of NP swab

guttural pouch lavage more sensitive than nasopharynx or nasal discharge swab

strangles: treatment (exposed, early signs, LN abscesses)

horses exposed to strangles: treat with penicillin, isolate from infected horses, will not become immune

horses with early clinical signs (rhinitis/pharyngitis phase): penicillin, may inhibit natural immunity so may contract disease again with continued exposure, general nursing, anti-pyretics, soft food

horses with LN abscesses: poulticing & draining of abscesses, antibiotics may prolong resolution of abscess, general nursing, anti-pyretics, soft foods

strangles: treatment (complications)

abdominal abscesses
diagnosis: US or rectal
treatment: long term antibiotics (penicillin +/- TMPS up to 6 weeks)

guttural pouch empyema +/- chondroids
diagnosis: endoscopy, radiography
treatment: drainage via pharyngeal openings or surgical drainage-> instill antibiotics

purpura hemorrhagica
diagnosis: skin biopsy
treatment: penicillin, dexamethasone or prednisolone, fluids, palliative measures (hydrotherapy, massage)

strangles: management of outbreaks

isolate premises, create 3 groups of horses

red: presumed infected, clinical signs, confirm resolution of disease once clinical signs have resolved (3x negative cultures or PCR of NP swabs, taken 7 days apart as shed intermittently or 1x negative GP washing)

amber: direct or indirect contact with red horse

green: no contact or clinical signs

amber & green: take temp daily, if pyrexic move to red group, screen using blood test for carriers (IgG vs 2 strep equi specific antigens- A & B, takes 2 weeks), if positive-> isolate & test via 1 CP lavage or 3 NP swabs, if positive, treat as carrier

strangles: carriers

identification & treatment
-endoscopic GP lavage
-retrieve chondroids via GP +/- surgery
-instill topical benzylpenicillin in gelatin
-repeat GP lavage & PCR after 2 weeks

strangles: prevention

modified live vaccine available in UK in 2005- withdrawn due to adverse reactions

new recombinant protein (strangvac)-> reduce clinical signs & number of URT LN abscesses

isolate new horses for 3-4 weeks + test for carrier status

rhodococcus equi

gram positive, pleomorphic coccobacillus

widespread in environment

survives in GIT of mares (no disease)

survives & multiples in GIT of foals (disease)

survives in GIT of earthworms (reservoir)

survives in soil for at least 12 months in hot dry conditions-> common in USA, Australia, & Ireland?

rhodococcus equi: epizootiology

spread via inhalation of soil/feces, also detected in exhaled air from infected foals

amplified with high risk management practices (concentrated facilities, dusty paddocks & stables, incomplete manure removal)

seasonal- late spring/summer-> high aerosol challenge & high number of susceptible foals

occurs sporadically & endemically

in endemic farms, morbidity 15-60%, mortality 1-12%

rhodococcus equi pneumonia

foals 1-6 months

inhalation of contaminated dust

scavenged by alveolar macrophages but not killed

destruction of macrophages-> pyogranulomatous response

bronchopneumonia with widespread abscess formation

rhodococcus equi pneumonia: clinical signs

anorexia, depression, fever, dyspnea, tachypnea, cough, varies from insidious to extremely acute onset, subacute form rare & may be found dead or with acute respiratory distress & pyrexia leading to death in 48 hours

rhodococcus equi: extrapulmonary signs

common: diarrhea, ulcerative enterotyphlocolitis, intra-abdominal abscesses, intra-abdominal lymphadenitis, immune-mediated synovitis

less common: bacteremia, cellulitis/lymphangitis, meningitis, IMHA, intracranial abscesses, osteomyelitis, peritonitis, pleuritis, septic arthritis/synovitis

often concurrent with pneumonia, can be found alone, can have >1 EP disorder concurrently, decreases prognosis

rhodococcus equi pneumonia: diagnosis

fibrinogen, neutrophilia, tracheal wash (culture, gram-stain cytology, PCR VapA gene), US, radiography (less sensitive than US), serology (not sensitive or specific enough), post mortem

rhodococcus equi pneumonia: treatment

total US abscess diameter <8cm & mild clinical signs=> 75% recover without treatment

do not treat if no clinical signs, WCC <20x10^9/L, abscess score <10cm

treat if mild signs & abscess score >10cm

treat if moderate to severe signs

rhodococcus equi treatment: antibiotic selection

clarithromycin OR azithromycin with rifampin

short & long term outcome better with clarithromycin

some clinicians no longer add rifampin, but still recommended to reduce resistance

treat until there is radiographic resolution of lesions & CBC & fibrinogen are normal->
4-12 weeks

treatment is expensive

4% resistance

rhodococcus equi: prevention via husbandry

difficult since pathogen shed in feces

increase ventilation & decrease dusty conditions

avoid dirt paddocks & crowding

rotate pastures to minimize grass destruction

vacuum or collect manure

isolate sick foals

rhodococcus equi: prevention via prophylaxis

hyperimmune plasma-> decreased farm incidence by 30-40% in some studies, no effect in others

will not prevent disease in every foal

optinal timing & dose not clear

surveillance mechanisms & environmental changes still necessary

prophylactic azithromycin not beneficial

no effective vaccine for mare or foal

rhodococcus equi: prevention via early diagnosis

daily observation by breeder

weekly vet exam: PE, US, WCC

WCC> 13x10^9/L= suspicious

>15x10^9/L= highly suspicious

parascaris equorum

not a major pathogen

eggs on ground from previous year's foal crop

can cause transient nasal discharge & cough as larvae migrate through lungs

diagnosis via FEC

treatment via anthelmintics