Respiratory Viral Infections

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RESPIRATORY SYSTEM INFLAMMATION



In general

  • Some viruses are thought to induce modifications of the pulmonary defences by:
    • Damaging the upper respiratory tract, thereby facilitating bacterial attachment and colonisation, with reduced mucociliary clearance
    • Decreasing surfactant levels by destroying Type 2 pneuMonocytes
    • Impairing the phagocytic ability of alveolar macrophages


In Dogs

Canine distemper

  • Caused by a morbillivirus
  • Rhinitis
  • Although many organs can be affected by CDV, a relatively constant feature is the respiratory signs which occur in varying severity
  • A syndrome of catharral oculonasal discharge, pharyngitis and bronchitis is relatively common in the initial stages
  • Since one of the primary sites of action of this virus is lymphoid tissue, the resultant immunosuppression -> predisposition to secondary bacterial infection
  • May cause interstitial pneumonia where inclusions are found within alveolar macrophages
  • Gross pathology:
    • Oedematous lungs, diffuse interstitial pneumonia
  • Micro pathology:
    • Necrosis of pneumocytes, necrotising bronchiolitis, alveolar oedema, thickening of alveolar walls and type II pneumocyte hyperplasia


Parainfluenza- 2


Infectious canine tracheitis

Canine adenovirus

Adenovirus pneumonia (Image sourced from Bristol Biomed Image Archive with permission)

Canine herpes virus


Canine respiratory coronavirus

  • (CRCV)
  • Shown to be involved in an outbreak of disease in large kennels with rapidly changing population and high incidence of respiratory disease
  • Erles, K., Toomey, C. et al.(2003) "Detection of a group 2 coronavirus in dogs with canine infectious respiratory disease." Virology 310(2):216-223


In Cats

Feline viral rhinotracheitis

  • Caused by a herpesvirus
  • Tends to be more rhinitis than tracheitis, may extend to sinusitis
  • Feline herpesvirus -1
    • One of the causes of Feline viral rhinotracheitis
  • All three agents infect URT respiratory epithelium, although FHV-1 has the highest affinity for this epithelium
  • Feline calicivirus more frequently infects the oral mucosa -> ulcerative stomatitis
  • C.psittaci more frequently infects the conjunctival epithelium -> chronic conjunctivitis
  • Infection of the respiratory epithelium by FHV-1 results in a typical neutrophilic rhinitis with intraepitheial intranuclear eosinophilic inclusion bodies
  • Uncomplicated cases resolve in 2-3 weeks
  • FHV-1 remains latent in the trigeminal ganglion, and can reactivate at times of stress
  • Can infect the cornea -> ulcerative keratitis
  • Mortality may be high in young kittens, debilitated and immune-suppressed animals, usually associated with secondary bacterial infection.


Feline calicivirus

In Horses

Equine respiratory viruses Concept Map (Courtesy of B. Stanikova)

Equine rhinovirus

Equine influenza

Equine rhinopneumonitis

  • Causative agent: equine herpesvirus type 1 and type 4
  • Primary viral lesions in nasal mucosa and lungs
  • Mild, transient bronchointerstitial pneumonia
  • Latent infection acting as a reservoir
  • Sites of latency: bronchial lymph nodes and trigeminal ganglia
  • Replicates in upper respiratory tract epithelium
  • Disseminated to lower respiratory tract
  • Transported to other organs in T-lymphocytes - viraemia up to 3 weeks
  • Vasculitis, abortion
  • May be accompanied by secondary bacterial infection


Equine viral arteritis (EVA)

  • Causative agent: equine arterivirus
  • Rhinitis, peripheral oedema, bronchitis/bronchiolitis, conjunctivitis, periorbital oedema
  • Replicates in macrophages and endothelial cells
  • Disseminates via the circulatory system causing necrotising arteritis
  • Interstitial pneumonia
  • Transmitted by respiratory and venereal routes through direct contact with infected horse or its secretions
  • Stallion are a reservoir of infection as they are chronic shedders


Equine adenovirus

Adenovirus in equine lung (Image sourced from Bristol Biomed Image Archive with permission)
  • Adenoviridae
  • May cause necrotising bronchiolitis in immune-deficient foals (Arabian foals)
  • Grossly:
    • Atelectasis and consolidation of lobules in cranioventral region
    • Mucopurulent exudate in airways
  • Histologically:
    • Severe bronchiolitis, necrotising -> proliferative
    • Bronchiolar obstruction by sloughed debri and neutrophils -> alveolar atelectasis
  • May lead to secondary bacterial infections


African horse sickness

Lung oedema in African horse sickness (Image sourced from Bristol Biomed Image Archive with permission)
  • Caused by orbivirus, family reoviridae
  • Respiratory distress or cardiovascular failure
  • Rapid death due to massive pulmonary oedema
  • Hydrothorax may also develop
  • Large amounts of froth present in airways

Hendra Virus

In Cattle

Infectious bovine rhinotracheitis (IBR)

Parainfluenza- 3


Bovine adenovirus

Respiratory syncytial virus

  • Causative agent Respiratory syncytial virus (RSV), synonym: bovine RSV (BRSV)
  • Outbreaks of RSV associated disease usually occur associated with winter housing
  • Gross pathology in severe cases
    • Cranioventral atelectasis and consolidation
    • Interstitial emphysema
      • More prominent in the caudal lung lobes
      • Results from bronchoconstriction which results in airway obstruction - this constriction is thought to arise from mast cell degranulation and histamine release
  • Histologically
    • Acute bronchiolitis, characteristic of the bronchiolar response is the formation of syncytial giant cells (formed by proliferating bronchiolar epithelial cells which may contain intracytoplasmic inclusion bodies), alveolar epithelium sometimes affected
    • Obstruction of bronchioles by exudate - these may later become obliterated by the fibrous tissue of organisation
  • May contribute to Enzootic pneumonia of calves

Bovine rhinovirus

In Sheep

Maedi Visna

  • Caused by a retrovirus
  • The respiratory from of the disease caused by maedi-visna virus (Maedi) is also called lymphoid interstitial pneumonia
  • Transmitted by close contact and via milk
  • The pulmonary lesions develop very slowly hence this disease is uncommon in sheep < 2 years old
  • Increased respiratory rate upon exertion, loss of weight
  • Remains in Monocytes and macrophages
  • Gross findings
    • Severe interstitial pneumonia
    • Lungs fail to collapse properly on opening the chest and can weigh more than twice the normal weight
    • Impressions of the ribs remain on the visceral pleura
    • Lungs are a mottled grey/ tan colour - the lesions can vary from irregular grey speckling to homogeneous grey consolidation
    • Rubbery in consistence
    • Diaphragmatic lobes most affected
    • Associated bronchial and mediastinal lymph nodes are often enlarged
  • Histologically
    • Major features are extensive lymphoid proliferation around perivascular, peribronchial and peribronchiolar sheaths associated with pulmonary lymphatics
    • Many of these areas contain germinal centres and smooth muscle hyperplasia (in walls of terminal bronchioles and alveoli)


Parainfluenza -3


Pulmonary adenomatosis


In Goats

Caprine Arthritis-Encephalitis (CAE)

  • Caused by retrovirus (lentivirus) similar to Maedi Visna in sheep described above
  • Two forms:
    • Non-suppurative leukoencephalomyelitis in young goats and kids
    • Chronic, non-suppurative arthritis-synovitis in adult goats
  • Also causes interstitial pneumonia which tends to be obscured by other clinical signs
  • Gross pathology:
    • Mainly caudal lobes
    • Lungs are firm, grey-pink with grey-white focal lesions on cut surface
  • Micro pathology:
    • Thickened alveolar wall
    • Lymphocyte infiltration and type II pneumocyte hyperplasia
  • Can be confused with or coexisting with Parasitic pneumonia


In Pigs

Inclusion body rhinitis

Inclusion body rhinitis (Image sourced from Bristol Biomed Image Archive with permission)
  • Herpesviridae, porcine cytomegalovirus
  • Disease of suckling piglets 1-5 wks of age
  • Clinical signs: those associated with acute/subacute rhinitis (ie: serous nasal discharge, progressing to catarrhal or purulent discharge with time and secondary bacterial infections; sneezing; pyrexia), fever in young piglets (3-8wks old)
  • May progress to sinusitis, otitis media or pneumonia
  • Morbitity high, mortality low
  • Gross pathology - catarrhal discharge becoming purulent (secondary infection)
  • Histology:
    • Large basophilic intranuclear inclusion bodies in the surface and subepithelium of nasal and sinus glandular epithelium with lymphocytic infiltration of the mucosa
    • Bursting of nucleus with cell necrosis and sloughing of necrotic epithelium
  • Can develop viraemic stage, with inclusions and focal necrotising lesions in other organs eg: renal tubular epithelium
    • Usually younger piglets, can die during this phase
  • Usually resolves if uncomplicated but rhinitis may persist if secondary infection is present
  • May persist in pulmonary macrophages


Swine influenza

Porcine reproductive and respiratory syndrome

  • The syndrome is caused by a small enveloped RNA virus which belongs to the new Arteriviridae group
  • Replicates in and destroys macrophages and endothelial cells causing vasculitis -> viraemia -> virus shedding (nasal secretions, faeces)
  • Clinical signs: respiratory and reproductive failure, weaned pigs, tachypnoea, eyelid oedema, conjunctivitis
  • Moderate to severe interstitial pneumonia in the cranial lobe
  • Superimposed bacterial infections are common
  • Infectious disease in swine that emerged 10 years ago
  • Today, PRRS is endemic in many if not all the pig-producing countries


Postweaning multisystemic wasting syndrome (PMWS)


Porcine respiratory coronavirus