Difference between revisions of "Respiratory Viral Infections"

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*Some viruses are thought to induce modifications of the pulmonary defences by:
 
*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 [[Respiratory System General Introduction - Pathology#Mucociliary escalator|mucociliary clearance]]
 
**Damaging the upper respiratory tract, thereby facilitating bacterial attachment and colonisation, with reduced [[Respiratory System General Introduction - Pathology#Mucociliary escalator|mucociliary clearance]]
**Decreasing surfactant levels by destroying Type 2 pneu[[Monocytes]]
+
**Decreasing surfactant levels by destroying Type 2 pneu[[Monocytes|monocytes]]
 
**Impairing the phagocytic ability of alveolar macrophages
 
**Impairing the phagocytic ability of alveolar macrophages
  
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===African horse sickness===
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===[[African Horse Sickness]]===
[[Image:Lung oedema in African horse sickness.jpg|right|thumb|100px|<small><center>Lung oedema in African horse sickness (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]]
 
 
 
*Caused by [[Reoviridae|orbivirus]], family reoviridae
 
*Respiratory distress or cardiovascular failure
 
*Rapid death due to massive [[Lungs Circulatory - Pathology#Pulmonary oedema|pulmonary oedema]]
 
*[[Pleural Cavity & Membranes Degenerative - Pathology#Hydrothorax|Hydrothorax]] may also develop
 
*Large amounts of froth present in airways
 
  
 
===[[Hendra Virus]]===
 
===[[Hendra Virus]]===

Revision as of 12:03, 30 June 2010


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()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 Cats

Feline viral rhinotracheitis

Feline Calicivirus

In Horses

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

Equine rhinovirus

Equine influenza

Equine Rhinopneumonitis

Equine Viral Arteritis

Equine Adenovirus

African Horse Sickness

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