Respiratory Viral Infections

()Map CARDIORESPIRATORY SYSTEM (Map) 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 Virus

Canine Parainfluenza - 2

Infectious canine tracheitis

Canine Adenovirus 1

Canine Adenovirus 2

Canine Herpesvirus 1

Canine Respiratory Coronavirus

In Horses

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

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

In Cattle

Parainfluenza- 3

• Causative agent: parainfluenza- 3 virus (PI3)
• On its own causes rhinitis
• Often part of multi-aetiology disease complex (e.g. Enzootic pneumonia of calves), often followed by Pasteurella sp. obscuring viral origin
• Replicates in airway epithelial cells and results in an initial bronchitis -> bronchiolitis -> extension into alveoli, causing bronchointerstitial pneumonia
• Early stages may show intracytoplasmic inclusions
• The resulting exudate is predominantly neutrophilic
• Positive confirmation lies in a Fluorescent Antibody Test (FAT) to the specific virus on frozen sections of tissue

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

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

• As in cattle

Pulmonary adenomatosis

• See neoplasia

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

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)

• Caused by a porcine circovirus alone or in combination with porcine parvovirus
• May cause mild interstitial pneumonia, failure of lungs to collpse on opening the thoracic cavity
• Microscopically: thickening of alveolar wall due to type 2 pneumocyte hyperplasia