Respiratory

• Working rostral, down:

  1.      Conducting zone – the nasal cavity, larynx, pharynx, trachea and bronchi. Mucus and mucociliary clearance, antibodies and lysozyme act as defence mechanisms here.

  2.      Transitional zone – bronchioles. Defence mechanisms are clara cells, antibodies and lysozyme.

  3. Exchange zone – alveoli. Defence mechanisms are macrophages, surfactant and antibodies.
• The three main routes of invasion into the respiratory tract are aerogenous (via airways), haematogenous (via the blood) or transcoelomic (direct)
• Aerogenous invasion is when an infective agent reaches the lung as inhaled droplets, food particles or fluid. Particles larger than 10um are usually deposited above the larynx, with many small molecules interacting with the nasal cavity and nasopharynx. Hence, many viral and bacterial diseases initially replicate in the epithelium and lymphoid tissue of the URT, then spread into the LRT or systematically.

   

  As particle size decreases, they become more aerodynamic so are more likely to pass down the respiratory tract.
• The bronchiolar-alveolar junction is at particular risk for damage because airflow velocity drops due to the increased air space area. This gives pathogens time to settle by gravity.
• The pulmonary capillary bed is the largest in the body. Haematogenous lesions tend to localise in caudal lobes but if the challenge dose is high enough they will settle anywhere.
• transcoelomic invasion is Infection via extension from pleura or the mediastinum, or traumatic penetration of the chest wall (e.g. a bite ), diaphragm (e.g. traumatic reticulitis) or oesophagus (e.g. foreign body)
• The nasal cavity has some normal flora, which are variable but often gram positive. These prevent adherence by pathogenic (often gram negative) bacteria.
• Congestion and hyperaemia of the nasal cavity and sinuses:  

  Epistaxis: i.e. blood in nasal discharge – may originate from nose or lower respiratory tract

  Haemoptysis: blood in saliva or sputum

  Specific equine entity: progressive ethmoid haematoma- presents as chronic nasal bleeding in older horses. pedunculated mass in ethmoid region. Histologically the lesions contain many haemosiderophages. Grossly appears as a smooth lesion with a haemorrhagic surface.
• The nasal cavity receives far greater exposure than the rest of the RT as it is the first area of air passage. Rhinitis is inflammation of the nasal cavity. Inflammation of the sinuses is sinusitis.

  Rhinitis may be acute or chronic and can be caused by viruses, bacteria, fungi, allergens, toxins and trauma or foreign bodies

  Rhinitis can be serous, catarrhal, mucopurulent, fibrinous or granulomatous depending on which mucosal cells and protective processes are occurring
• Sinusitis is often a sequel to or is associated with rhinitis. Can also be caused by periodontal disease (extending into the maxillary sinus) and penetration of infection in dehorning wounds/ fractures (frontal sinus). Can also be caused by a diastema where a gap between the cheek teeth becomes impacted with food. Due to the poor drainage of the sinuses, purulent inflammation is likely to become chronic.
• Serous rhinitis is the Mildest form. Serous cells increase secretion (produces a watery, runny nose). Early stages of infectious disease, allergy or irritation.
• In catarrhal rhinitis goblet cells and mucous glands add to serous secretions. If this continues chronically it leads to goblet cell hyperplasia. Can contain white blood cells and exfoliated debris (mucopurulent)
• In Purulent or mucopurulent rhinitis there is thicker exudates with many more cells. Dominated by neutrophils
• in Fibrinous rhinitis there is an increase in vascular permeability allowing exudation of fibrinogen which coagulates to fibrin, forming a yellow mat on the affected surface. May be associated with underlying ulceration.
• Granulomatous rhinitis is A macrophage dominated reaction, either specific to pathogens (e.g. mycobacteria) or chronic allergic reaction.
• Bacterial rhinitis is usually secondary to viral, allergic, toxic or traumatic rhinitis.
• Chronic rhinitis occurs when there is failure to resolve acute rhinitis. Typically catarrhal or purulent.

  In chronic purulent rhinitis there may be extensive fibrosis of the lamina propria, atrophy of the nasal glands and squamous metaplasia in severe cases . This then further impairs local immune defences.

  Some cases see polypod thickening of the inflamed nasal mucosa (nasal polyps). These are round, often large with multiple protuberances into the nasal meatus. These are most common in horses, cats and sheep
• Atrophic rhinitis in pigs causes atrophy of the nasal turbinate bones, distorting the shape of the snout. It is caused by co-infection of the nasal mucosa with bordatella bronchiseptica and a toxin-producing strain of Pasteurella multiocida capsular type D.  The Bordetella appears to facilitate colonisation of nasal epithelium by the toxigenic Pasteurella.
• Strangles in caused by haemolytic streptococcus equi. The disease is characterised by suppurative rhinitis, pharyngitis and lymphadenitis (inflammation of Ln.) of the lnn. Of the head and neck which drain into the URT.

   

  These lymphnodes often rupture and discharge pus for 2-3 weeks after the onset of infection.
• Complications of strangles can occur via:

  • Metastatic abscesses – most often in the mesenteric and mediastinal lymph nodes. Less frequently other organs (e.g. liver and kidney) can become involved (bastard shingles)
  • Retropharyngeal lymph node abscesses can rupture into the guttural pouches causing guttural pouch empyema or chondroid formation
  • Purpura haemorrhagica: an acute vasculitis which causes urticaria (hives) and extensive oedema of the ventrum, head and distal limbs
• Mycotic (fungal) rhinitis is most commonly caused by aspergillus fumigatus in the dog (often also involves the frontal sinus) but it is rare in other species. Infection causes chronic necrotising inflammation with a friable exudate containing necrotic tissue and fungal hyphae (branching filaments) These lesions can destroy the turbinate bones and nasal septum.
• Cryptococcus neoformans causes a granulomatous rhinitis in cats, with sneezing, nasal discharge, nasal swelling and occasionally skin, ocular and CNS lesions. Formation of nodules or destructive masses which often result in facial swelling. In severe cases, extension from nasal cavity to involve skin and oral mucosa can occur.
• Neoplasia of the nasal cavity and sinuses is generally rare (but is more common in the dog). It can arise from any tissues in the region including glands or epithelia, cartilage, bones or CT. They are usually malignant and are secondarily infected, so distinguishing neoplasia from severe chronic inflammation can be difficult.

   

  Endemic ethmoid tumours which are found in ruminants arise from ethmoid epithelial tissue, invading locally – these are of retroviral origin
• Necrotic laryngitis (calf diphtheria) is a disease of the URT where plaques of fibrin form in the trachea, forming friable lesions which occupy space and debris can enter the lung.
• Laryngeal chondritis is a URT disease whith chronic suppuration within the arytenoid cartilages of the larynx. Results in swelling and occlusion of the lumen
• Viral disease of the larynx and teachea e.g. bovine rhinotracheitis and feline viral rhinotracheitis can cause thickening and fibrosis of the mucosa of the trachea. It is common to see secondary bacterial infection.
• In tracheal collapse the tracheal ligaments lose tension and there is dorsoventral tracheal flattening.
• Chronic bronchial irritation/ injury can result in :

  • Excess production of mucus as a result of goblet cell hyperplasia. (hypersecretion)
  • Replacement of ciliated epithelium by more resistant but relatively non-functional squamous epithelium. This is termed squamous metaplasia and clearly affects the effectiveness of mucociliary clearance.
  • Bronchiectasis – permanent dilation of bronchi as a result of accumulation of exudate in the lumen. This can cause partial rupture of the bronchial walls. Usually secondary to chronic bronchitis.
• Kennel cough (infectious tracheobronchitis) – characterised by persistent tracheobronchial inflammation. In severe cases there can be serous or mucopurulent rhinitis or cranioventral bronchopneumonia. Tonsils and retropharyngeal lymph nodes become enlarged. The major pathogen involved is bordatella bronchiseptica (but also parainfluenza or canine adenovirus)
• Chronic bronchitis in dogs – bronchial irritation and mucus hypersecretion causes a chronic cough. There is excess mucoid or mucopurulent exudate within the trachea and lower airways. The bronchial mucosa is thickened, hyperaemic and oedematous (consequence of increased size and number of mucus glands and extensive infiltration of the lamina propria by inflammatory cells.  There may be a coexistent bronchopneumonia. Another important feature is smooth muscle hypertrophy in pulmonary arteries - this can result in pulmonary hypertension leading to cor pulmonale.
• Bronchiectasis in cattle – permanent saccular or cylindrical dilation of the bronchi due to accumulation of exudate in the lumen. Usually occurs secondary to chronic bronchitis  where the bronchial wall is weakened.  Bronchiectasis has a classical appearance characterised by sac like nodules in the lungs which are filled with purulent exudate.
• Chronic bronchial irritation or inflammation causes stimulation of muscular hypertrophy in the walls of small arteries. This increases resistance in the pulmonary vasculature, leading to hypertrophy then dilation of the right ventricle. This is secondary to pulmonary hypertension (cor pulmonale)
• Bronchiolar epithelium is highly susceptible to injury for reasons thought to include:

  • Presence of Clara cells which contain oxidases that can locally generate metabolites that are toxic

  • Vulnerability to free radical damage.

   

  Bronchioles are much more prone to obstruct when inflamed than bronchi. In species with poor collateral ventilation in the lungs such as ruminants, when bronchioles obstruct lung tissue supplied by that bronchiole collapses (atelectasis) and becomes non functional.
• Bronchiolitis can occur:

  • As an extension of bronchitis or concurrently with bronchitis and pneumonia.

  • As a distinct entity e.g. certain viral infections; pulmonary toxicity.

   

  In severe cases when the exudate cannot be cleared, there is infiltration by fibroblasts leading to development of organised polyp-like masses within the bronchiolar lumen. This lesion is called bronchiolitis obliterans.
• Alveoli have extremely delicate structure, made up of type I pneumocytes. These cells are the most susceptible to injury.

  Irreversible injury results in sloughing of type I pneumocytes, but repair can proceed as long as the basement membrane remains intact. Repair occurs by type II pneumocyte division – these are larger, more cuboidal cells, so exchange capacity is reduced in repairing areas.  In severe, diffuse forms of alveolar injury, this process can be so spectacular that the affected tissue can take on the appearance of a gland - hence the term alveolar epithelialisation.
• Hyaline membranes are microscopic eosinophilic (pink) bands formed by the combination of pulmonary surfactant and plasma proteins which can leak into alveoli following type I pneumocyte injury or alterations in the blood-air barrier.
• Type II pneumocytes are the progenitor cells of type I and type II pneumocytes. They also produce surfactant which prevents alveolar collapse. The cover approximately 3% of septal surface.
• Pneumonia is defined as inflammation that takes place in the alveoli and their walls.
• Consolidation is defined as the altered texture of lung tissue (firmer) due to the accumulation of exudates
• Pneumonias are classified by the nature of the inflammatory process e.g. suppurative, granulomatous, the aetiological agent e.g. mycoplasma, and their pattern.