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CRH II > Equine Infectious Lower Respiratory Diseases > Flashcards

Equine Infectious Lower Respiratory Diseases Flashcards

1
Q

describe the physical exam for the equine resp tract

A
  1. does animal have a respiratory disease?
  2. is it upper or lower or both?
  3. is it non-infectious or infectious?
  4. what (if any) additional diagnostics are warranted?
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2
Q

describe the rebreathing exam

A
  1. listening for airflow in all fields
  2. abnormal sounds in lungs or trachea?
    -wheezes: often expiratory, trying to get air out
    -crackles:
  3. increased effort? coughing?
  4. recovery: should recover in 4-6 breaths
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3
Q

describe advantages and disadvantages of thoracic radiographs

A

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

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4
Q

describe pros and cons of thoracic ultrasound

A

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)

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5
Q

describe tracheal wash

A

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

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6
Q

describe bronchoalveolar lavage

A
  1. for generalized/diffuse disease
  2. samples distal small airways and alveoli
  3. cytology more representative than TTA
  4. NOT sterile
  5. BAL cytology:
    -70-95% alveolar macrophages
    - <5% degenerate neutrophils
    -nonreactive lymphocytes
    -eosinophils and mast cells VERY rare
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7
Q

GENERALLY describe equine viral respiratory diseases

A

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

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8
Q

describe equine influenza A

A
  1. MOST COMMON viral cause of severe URT epidemics in horses
    -40-60% of cases
  2. enveloped RNA virus: orthomyxoviridae
  3. antigenic determinants/envelope glycoproteins:
    -hemagglutinin (HA): binds to sialic acid on host cell
    -neuraminidase (NA): hydrolyzes sialic acid
  4. 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

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9
Q

describe antigenic drift and shift as relates to equine influenza A virus

A

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!!

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10
Q

describe disease characteristics of equine influenza A

A
  1. incubation period: 1-3 days
  2. aerosol spread:
    -adheres to epithelium, then replicates in and destroys respiratory epithelium, leading to dysfunction in mucociliary clearance
  3. infected horses shed virus for 4-10 days
  4. HIGH MORBIDITY (100%) but low mortality!
  5. clinical signs:
    -explosive dry cough
    -acute onset of fever (103-106)
    -serous nasal discharge
    -malaise, decreased appetite
    -stiffness, reluctance to move (myositis)
  6. diagnosis:
    -history and PE
    -nasal swab for PCR and antigen detection
    -viral isolation is difficult and slow
    -serology
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11
Q

describe complications associated with equine influenza A

A
  1. secondary bacteria pneumonia/pleuropneumonia
    -persistent clinical signs (>5 days) of fever, nasal discharge, abnormal lung sounds
  2. pleuritis/pericarditis
  3. myositis/myocarditis
  4. inflammatory airway disease (IAD)
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12
Q

describe treatment, recovery, and prevention of equine influenza A

A
  1. supportive and symptomatic
    -antimicrobial therapy: if secondary bacterial infection
    -antiviral medication not usually indicated
  2. recovery:
    -general rule: 1 week of rest per day of fever
    -minimum of 3 weeks of rest
    -NO forced exercise
  3. prevention: isolate new horses for 3 weeks
  4. immunity: protective immunity for 8-12 months after natural infection
  5. vaccination: risk based
    -intranasal and IM available
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13
Q

describe equine herpesviruses

A
  1. 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)

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14
Q

describe EHV-1 and EHV-4

A
  1. ubiquitous in the equine population
  2. enveloped DNA virus
  3. establishes latency
  4. up to 85% of horses carry EHV in latent stage
    -in trigeminal ganglia and lymphatic tissue
  5. 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
  6. non-neuopathogenic genotype and neuropathogenic genotypes
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15
Q

describe transmission, incubation, and shedding of EHV

A

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

  1. 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

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16
Q

describe epi triad factors of EHV

A

agent: strain, pathogenicity, replication

host: age, immune status, stress

environment: stocking density, fomites, stabling

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17
Q

describe EHV diagnosis

A
  1. qRT-PCR: detect viral DNA specific for EHV1 and EHV4
  2. sample collection:
    -nasal swab and EDTA anti-coagulated whole blood: dakron or cotton tip swab on viral transport medium
  3. serology cannot differentiate between EHV 1 and 4
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18
Q

describe EHV biosecurity after detecting a case

A
  1. don’t panic
  2. look at AAEP.org
  3. detect new cases
  4. separate and segregate
  5. clean and disinfect: people, equipment, environment
  6. communicate and REPORT
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19
Q

describe EHV treatment and prevention

A

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

20
Q

describe equine viral arteritis

A
  1. RNA virus in togaviridae family
  2. subclinical infection is common:
    -70-90% of standardbred horses are seropositive
    -is a rare cause of respiratory disease
  3. transmission:
    -inhalation of aerosolized respiratory tract secretions
    -venereal by infected stallion
  4. pathogenesis:
    -infection followed by replication in alveolar macrophages and bronchial LN, viremia by day 3 and then vascular lesions
21
Q

describe clinical signs and diagnosis of equine viral arteritis

A

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

22
Q

describe vaccination and indications for equine viral arteritis

A

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

23
Q

describe equine rhinitis virus

A
  1. 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
24
Q

describe adenovirus

A
  1. DNA adenoviridae- nonenveloped
  2. subclinical infection is common in immunocompetent
  3. may cause mild upper resp disease
  4. dx: nasal swab PCR
25
Q

describe strep equi ssp. equi

A
  1. host restricted bacteria of equids
  2. highly contagious
  3. NOT commensal
  4. upper respiratory tract infection
    -lymphadenopathy, nasal catarrhal
  5. pyogenic (pus) and pyrogenic (fever)!!
26
Q

describe strep equi ssp. equi epidemiology

A

2 populations

  1. young, naive: comingling horses at shows and auctions
  2. chronically infected; guttural pouch empyema/chondroids
27
Q

describe strep equi ssp. equi pathogenesis

A
  1. virulence!
    -constitutively expressed hyaluronic capsule: antiphagocytic
    -strep equi M protein: cell wall protein that binds fibrinogen and IgG, prevents complement mediated opsonization
  2. bacterial entry to the oral cavity/nasal passages
  3. 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
  4. 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
28
Q

describe disease course of strep equi ssp. equi

A

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

29
Q

describe diagnosis of strep equi ssp. equi

A
  1. culture and/or PCR
  2. sample:
    -purulent material
    -nasopharyngeal wash
    -guttural pouch lavage fluid
  3. serology (SeM) titer
30
Q

describe strep equi ssp. equi treatment

A
  1. supportive care:
    -NSAIDs
    -nutritional support
    -ensure airway!!
  2. guttural pouch lavage
  3. antibiotics?
    -for complicated cases only, beta lactams
31
Q

describe strep equi ssp. equi immunity

A
  1. 75% of infected horses develop protective immunity that lasts for approx 5 years
  2. antibodies (IgG) specific to surface proteins, including SeM protein
    -mucosal immunutyL IgA, IgGb specific to SeM
  3. foals:
    -ingest adequate colostrum
    -protected until weaning
32
Q

strep equi ssp. equi prevention

A
  1. isolate clinical cases and exposures
  2. monitor temperatures: fever develops prior to shedding
  3. clean and disinfect: equipment, environment, people
  4. persists for 2 MONTHS under some conditions!!
    -wood, glass, cool/warm conditions, organic material
33
Q

describe strep equi ssp. equi vaccination

A
  1. risk based vx
  2. recommended:
    -high risk (travel, pregnant mares)
  3. 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
34
Q

describe bastard strangles and purpura hemorrhagica

A
  1. infection beyond LNs of head
    -metastatic abscessation
    -hematogenous/lymphatic spread of bacteria
    -LNs, body cavity, sinus
  2. purpura hemorrhagica
    -aseptic necrotizing vasculitis
    -immune complex deposition (type III hypersensitivity)
    -affects blood vessel walls
35
Q

define bacterial pneumonia, lung abscesses, and pleuropneumonia

A

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

36
Q

describe pathophysiology of bacterial pneumonia

A
  1. 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

37
Q

describe epidemiology of bacterial pneumonia

A
  1. can affect any age, breed, sex, occupation
  2. risk factors:
    -long distance transport
    -strenuous exercise
    -viral respiratory infections
    -general anesthesia
    -immune status
  3. infections are usually polymicrobial!!!
38
Q

describe clinical signs of bacterial pneumonia

A
  1. none at rest (occult infection) OR
  2. fever, anorexia
  3. increased respiratory rate +/- increased effort
  4. nasal discharge: absent, mucopurulent, hemorrhagic
  5. halitosis
  6. cough: moist
  7. abnormal lung sounds
  8. pectoral edema
  9. pleurodynia

vary based on disease severity and duration!

39
Q

describe diagnosis of bacterial pneumonia

A
  1. history and PE
  2. minimum databse
  3. auscultation:
    -at rest or rebreathing
    -NO rebreathing if tachypneic/resp distress
  4. thoracic imaging
  5. transtracheal wash: cytology, aerobic and anaerobic culture and susceptibility
  6. thoracocentesis
40
Q

describe bacterial pneumonia treatment

A
  1. supportive care:
    -analgesia
    -IV fluids
    -nutritional support
    -intranasal oxygen
  2. broad spectrum antimicrobials:
    -empiric selection vs C&S
    -systemic +/- inhaled/nebulized: beta lactam AND gentamicin or enrofloxacin AND metronidazole
  3. duration: variable; weeks to months
41
Q

describe complications of bacterial pneumonia

A
  1. weight loss
  2. endotoxemia
  3. colitis (antimicrobials piss off the gut)
  4. jugular thrombophlebitis (long term catheter)
  5. penumothorax
  6. pleural abscess
  7. bronchopleural fistulas
  8. laminitis
  9. endocarditis
42
Q

describe prognosis of bacterial pneumonia

A

depends on:
-duration of clinical signs prior to treatment
-response to treatment
-secondary complications

45-90% survival rate
60% survivors return to race

43
Q

describe rhodococcus equi

A
  1. gram positive soil saprophyte
  2. intracellular pathogen: survives and replicates in pulmonary macrophages
44
Q

describe rhodococcus equi epidemiology

A
  1. worldwide distribution
  2. 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!!!!)
  3. occurs on farms in 3 patterns:
    -unaffected
    -sporadically affected
    -endemic
  4. morbidity: 5-20%, case fatality 4-30%
  5. year to year variation: complicates disease prevalence
45
Q

describe rhodococcus equi clinical signs

A
  1. often insidious, chronic progression
  2. peracute onset with sudden death
    -jumping around one day, down and out the next
  3. increased resp rate and effort
  4. coughing
  5. nasal discharge
  6. fever, malaise
  7. no effective prevention and no effective method of early detection
46
Q

describe rhodococcus equi diagnosis

A
  1. history: foal AND farm
  2. PE
  3. thoracic ultrasound and radiographs
  4. tracheal wash: cytology and culture
    -gold standard!
47
Q

describe treatment of clinical rhodococcus equi

A
  1. supportive care
    -oxygen therapy
    -anti-inflammatory
    -fluid/nutritional support
  2. 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

CRH II (53 decks)

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