Equine Infectious Lower Respiratory Diseases Flashcards
describe the physical exam for the equine resp tract
- does animal have a respiratory disease?
- is it upper or lower or both?
- is it non-infectious or infectious?
- what (if any) additional diagnostics are warranted?
describe the rebreathing exam
- listening for airflow in all fields
- abnormal sounds in lungs or trachea?
-wheezes: often expiratory, trying to get air out
-crackles: - increased effort? coughing?
- recovery: should recover in 4-6 breaths
describe advantages and disadvantages of thoracic radiographs
advantages:
-can view deeper structures of chest: lungs, mediastinum, pleura, heart
disadvantages:
1. not very practical in field
2. could get non-diagnostic images in adults (less common in foals)
3. can only get lateral image
describe pros and cons of thoracic ultrasound
pros:
-easy to use in field
-quick and easy to perform
-eval of surface of lung
cons:
-aerated lung blocks deeper tissues (can only see surface of lungs)
describe tracheal wash
sample from trachea
-very sterile!
-sample coming from thoracic inlet
-better for infectious diseases
-sample represents ALL lung
-can perform a cytologic exam or a bacterial culture on the sample
describe bronchoalveolar lavage
- for generalized/diffuse disease
- samples distal small airways and alveoli
- cytology more representative than TTA
- NOT sterile
- BAL cytology:
-70-95% alveolar macrophages
- <5% degenerate neutrophils
-nonreactive lymphocytes
-eosinophils and mast cells VERY rare
GENERALLY describe equine viral respiratory diseases
clinical signs: fever, nasal discharge, and cough
diagnosis:
-viral isolation
-PCR
-serology: antibody detection; acute/convalescent
-antigen detection
-consider: turnaround time and cost!
diagnostic approach:
-PE
-rebreathing exam
-minimum database: lymphopenia (acute), +/- inflammatory leukogram
-resp diagnostics: imaging and sampling
-owner/barn manager: educate and isolate
describe equine influenza A
- MOST COMMON viral cause of severe URT epidemics in horses
-40-60% of cases - enveloped RNA virus: orthomyxoviridae
- antigenic determinants/envelope glycoproteins:
-hemagglutinin (HA): binds to sialic acid on host cell
-neuraminidase (NA): hydrolyzes sialic acid - H3N8 is the major subtype circulating in the equine population!!!!
-endemic in US with distinct sublineages that different vaccines target
-H3N7 thought to be extinct in equine population
-H5N1 NOT found in horses
describe antigenic drift and shift as relates to equine influenza A virus
antigenic drift:
-POINT mutation in HA or NA that results in viral escape of neutralizing antibodies from previous strains
-GRADUAL change
antigenic shift:
-two DISTINCT viruses infect the same host cell
-reassortment of genes results in novel virus
-occurs occasionally, spreads fast!!
describe disease characteristics of equine influenza A
- incubation period: 1-3 days
- aerosol spread:
-adheres to epithelium, then replicates in and destroys respiratory epithelium, leading to dysfunction in mucociliary clearance - infected horses shed virus for 4-10 days
- HIGH MORBIDITY (100%) but low mortality!
- clinical signs:
-explosive dry cough
-acute onset of fever (103-106)
-serous nasal discharge
-malaise, decreased appetite
-stiffness, reluctance to move (myositis) - diagnosis:
-history and PE
-nasal swab for PCR and antigen detection
-viral isolation is difficult and slow
-serology
describe complications associated with equine influenza A
- secondary bacteria pneumonia/pleuropneumonia
-persistent clinical signs (>5 days) of fever, nasal discharge, abnormal lung sounds - pleuritis/pericarditis
- myositis/myocarditis
- inflammatory airway disease (IAD)
describe treatment, recovery, and prevention of equine influenza A
- supportive and symptomatic
-antimicrobial therapy: if secondary bacterial infection
-antiviral medication not usually indicated - recovery:
-general rule: 1 week of rest per day of fever
-minimum of 3 weeks of rest
-NO forced exercise - prevention: isolate new horses for 3 weeks
- immunity: protective immunity for 8-12 months after natural infection
- vaccination: risk based
-intranasal and IM available
describe equine herpesviruses
- enveloped DNA virus: herpesviridae
-alpha herpesvirus:
–EHV-1: perinatal disease/death, RESPIRATORY DISEASE, abortion, neuro disease
–EHV-3: equine coital exanthema
–EHV-4 respiratory disease
-gamma herpesvirus:
–EHV2: mild resp signs, keratoconjunctivits
–EHV-5: equine multinodular pulmonary fibrosis (EMPF)
describe EHV-1 and EHV-4
- ubiquitous in the equine population
- enveloped DNA virus
- establishes latency
- up to 85% of horses carry EHV in latent stage
-in trigeminal ganglia and lymphatic tissue - do NOT persist in environment but ALWAYS present in horse population
-virus is NOT infectious in latent state; the latent virus that becomes reactivated is infectious - non-neuopathogenic genotype and neuropathogenic genotypes
describe transmission, incubation, and shedding of EHV
transmission:
1. viral recrudescence OR direct contact
-respiratory secretions can travel up to 35 feet
-shared feed/water
-nose-to-nose contact
-placenta or fetal fluids
- fomites: people, grooming, equipment, tack, crossties
incubation period:
<24 hr to 10 days, viral replication takes approx 20 hours
nasal shedding: 2-4 weeks post infection
describe epi triad factors of EHV
agent: strain, pathogenicity, replication
host: age, immune status, stress
environment: stocking density, fomites, stabling
describe EHV diagnosis
- qRT-PCR: detect viral DNA specific for EHV1 and EHV4
- sample collection:
-nasal swab and EDTA anti-coagulated whole blood: dakron or cotton tip swab on viral transport medium - serology cannot differentiate between EHV 1 and 4
describe EHV biosecurity after detecting a case
- don’t panic
- look at AAEP.org
- detect new cases
- separate and segregate
- clean and disinfect: people, equipment, environment
- communicate and REPORT
describe EHV treatment and prevention
treatment: like for influenza, supportive care, valacyclovir
prevention:
-vaccination! helps to reduce severity of clinical signs and reduce duration/magnitude of viral shedding
-does NOT prevent infection of establishment of latency
describe equine viral arteritis
- RNA virus in togaviridae family
- subclinical infection is common:
-70-90% of standardbred horses are seropositive
-is a rare cause of respiratory disease - transmission:
-inhalation of aerosolized respiratory tract secretions
-venereal by infected stallion - pathogenesis:
-infection followed by replication in alveolar macrophages and bronchial LN, viremia by day 3 and then vascular lesions
describe clinical signs and diagnosis of equine viral arteritis
clin signs:
1. fever, depression
2. nasal discharge, cough
3. conjunctivitis
4. edema of limbs, abdomen, mammary gland and scrotum
5. abortion (up to 70% of mares)
6. interstitial pneumonia and enteritis in young foals
stallions may be asymptomatic carriers
diagnosis:
1. viral isolation: nasal swab or whole lood
2. PCR: nasal swab or whole blood
describe vaccination and indications for equine viral arteritis
vaccination:
-does NOT prevent resp infection or viral shedding
-may help prevent abortion
-may help prevent development of carrier state in stallions
indications:
-seronegative mare being bred to carrier stallion
-prevent carrier state in seronegative stallion
-coordinated through state and USDA vet office
-transport of seropositive horses may be restricted
describe equine rhinitis virus
- rhinovirus A and B
-RNA virus in the picornaviridae family: nonenveloped
-clinical signs similar to other viruses
-nasal swab PCR
-vaccination against type A is available
describe adenovirus
- DNA adenoviridae- nonenveloped
- subclinical infection is common in immunocompetent
- may cause mild upper resp disease
- dx: nasal swab PCR
describe strep equi ssp. equi
- host restricted bacteria of equids
- highly contagious
- NOT commensal
- upper respiratory tract infection
-lymphadenopathy, nasal catarrhal - pyogenic (pus) and pyrogenic (fever)!!
describe strep equi ssp. equi epidemiology
2 populations
- young, naive: comingling horses at shows and auctions
- chronically infected; guttural pouch empyema/chondroids
describe strep equi ssp. equi pathogenesis
- virulence!
-constitutively expressed hyaluronic capsule: antiphagocytic
-strep equi M protein: cell wall protein that binds fibrinogen and IgG, prevents complement mediated opsonization - bacterial entry to the oral cavity/nasal passages
- access the host through pharyngeal/tonsil tissue
-bacterial surface antigens mediate entry into epithelial cells
-LNs draining to the pharynx colonized by bacteria
-neutrophils recruited but unsuccessful phagocytosis results in abscess formation - hyaluronic capsule allows bacteria to evade phagocytosis
-bacteria acquire iron
-bacteria release super antigens (mitogens) that induce T cells to elicit potent immune response without need for APCs
describe disease course of strep equi ssp. equi
exposure, then colonization, then fever for 3-14 days, followed by nasal shedding for 2-3 days
abscesses mature over 4-21 days
nasal shedding persists for 2-6 WEEKS
-nasal shedding in chronic guttural pouch infections can intermittently shed for years
describe diagnosis of strep equi ssp. equi
- culture and/or PCR
- sample:
-purulent material
-nasopharyngeal wash
-guttural pouch lavage fluid - serology (SeM) titer
describe strep equi ssp. equi treatment
- supportive care:
-NSAIDs
-nutritional support
-ensure airway!! - guttural pouch lavage
- antibiotics?
-for complicated cases only, beta lactams
describe strep equi ssp. equi immunity
- 75% of infected horses develop protective immunity that lasts for approx 5 years
- antibodies (IgG) specific to surface proteins, including SeM protein
-mucosal immunutyL IgA, IgGb specific to SeM - foals:
-ingest adequate colostrum
-protected until weaning
strep equi ssp. equi prevention
- isolate clinical cases and exposures
- monitor temperatures: fever develops prior to shedding
- clean and disinfect: equipment, environment, people
- persists for 2 MONTHS under some conditions!!
-wood, glass, cool/warm conditions, organic material
describe strep equi ssp. equi vaccination
- risk based vx
- recommended:
-high risk (travel, pregnant mares) - not recommended:
-clinical signs of disease following exposure
-outbreak with exposure
-prior infection within year
-SeM titer > 1:1,600
-not without some risk purpura hemorrhagica
describe bastard strangles and purpura hemorrhagica
- infection beyond LNs of head
-metastatic abscessation
-hematogenous/lymphatic spread of bacteria
-LNs, body cavity, sinus - purpura hemorrhagica
-aseptic necrotizing vasculitis
-immune complex deposition (type III hypersensitivity)
-affects blood vessel walls
define bacterial pneumonia, lung abscesses, and pleuropneumonia
bacterial pneumonia: inflammation of the lung caused by bacterial colonization and multiplication
lung abscess: localized, encapsulated regions of pulmonary necrosis, debris, and exudate
pleuropneumonia:
-microbial colonization of the lung, leading to development of pneumonia and/or lung abscesses
-extension to visceral pleura and pleural space
-development of parapneumonic effusion
describe pathophysiology of bacterial pneumonia
- occurs when pulmonary defense mechanisms are:
-overwhelmed: aspiration of oropharyngeal bacteria, pharyngeal/laryngeal dysfunction, esophageal obstruction/choke, general anesthesia, severe bacteremia
or suppressed: transport, exercise, viral infection, stress, poor ventilation, immunosuppressive drugs, immunologic disorders, systemic disease
describe epidemiology of bacterial pneumonia
- can affect any age, breed, sex, occupation
- risk factors:
-long distance transport
-strenuous exercise
-viral respiratory infections
-general anesthesia
-immune status - infections are usually polymicrobial!!!
describe clinical signs of bacterial pneumonia
- none at rest (occult infection) OR
- fever, anorexia
- increased respiratory rate +/- increased effort
- nasal discharge: absent, mucopurulent, hemorrhagic
- halitosis
- cough: moist
- abnormal lung sounds
- pectoral edema
- pleurodynia
vary based on disease severity and duration!
describe diagnosis of bacterial pneumonia
- history and PE
- minimum databse
- auscultation:
-at rest or rebreathing
-NO rebreathing if tachypneic/resp distress - thoracic imaging
- transtracheal wash: cytology, aerobic and anaerobic culture and susceptibility
- thoracocentesis
describe bacterial pneumonia treatment
- supportive care:
-analgesia
-IV fluids
-nutritional support
-intranasal oxygen - broad spectrum antimicrobials:
-empiric selection vs C&S
-systemic +/- inhaled/nebulized: beta lactam AND gentamicin or enrofloxacin AND metronidazole - duration: variable; weeks to months
describe complications of bacterial pneumonia
- weight loss
- endotoxemia
- colitis (antimicrobials piss off the gut)
- jugular thrombophlebitis (long term catheter)
- penumothorax
- pleural abscess
- bronchopleural fistulas
- laminitis
- endocarditis
describe prognosis of bacterial pneumonia
depends on:
-duration of clinical signs prior to treatment
-response to treatment
-secondary complications
45-90% survival rate
60% survivors return to race
describe rhodococcus equi
- gram positive soil saprophyte
- intracellular pathogen: survives and replicates in pulmonary macrophages
describe rhodococcus equi epidemiology
- worldwide distribution
- leading cause of MORBIDITY and MORTALITY in foals!!!
-prevalence of up to 50% on some farms
-most common age: 1-3 months
-most common cause of pneumonia in foals (second most common is streptococcus equi!!!!) - occurs on farms in 3 patterns:
-unaffected
-sporadically affected
-endemic - morbidity: 5-20%, case fatality 4-30%
- year to year variation: complicates disease prevalence
describe rhodococcus equi clinical signs
- often insidious, chronic progression
- peracute onset with sudden death
-jumping around one day, down and out the next - increased resp rate and effort
- coughing
- nasal discharge
- fever, malaise
- no effective prevention and no effective method of early detection
describe rhodococcus equi diagnosis
- history: foal AND farm
- PE
- thoracic ultrasound and radiographs
- tracheal wash: cytology and culture
-gold standard!
describe treatment of clinical rhodococcus equi
- supportive care
-oxygen therapy
-anti-inflammatory
-fluid/nutritional support - standard antimicrobial treatment:
-macrolide (erythromycin, azithromycin, clarithromycin) (az and clar more common) WITH
-rifampin
-macrolide resistance! is an issue :(
-treat until serial ultrasound exams show resolution of abscesses and clinical signs
