respiratory system broken down into 3 Zones

Conductive zone: Nasal cavity, pharynx, trachea and bronchi Lined by ciliated epithelial cells and goblet cells Includes nasal turbinate's, Mucus blanket entraps particles Normal bacterial flora in the upper respiratory tract compete with potential pathogensTransitional zone: Bronchioles are lined with primarily by non-ciliated epithelium and Club cells that have the following properties: Secretion of surfactant Secretion of collectin and Detoxification Healthy bronchioles do not have goblet cells Goblet cell metaplasia may occur in chronic inflammatory conditionsGas exchange zone: Alveoli Air-blood barrier occurs between alveolar space and alveolar capillaries Intervening epithelium is thin and flattened T2 pneumocytes

Particulate removal

Nasal turbinates (conchae) are coiled - creates turbulent airflow- flings larger particles to mucosal surface (removed by sneezing +/- neutralised by Ab, phagocytosis)Tracheal bifurcation caused abrupt change in airflow direction - collide with mucosaAirways become narrower - tiniest particles eventually contact the mucosa because of lumen diameterAlveolar Macs phagocytose bacteria and matter than reach alveoli (most bacteria destroyed - Mycobacterium are resistant)

Damage and healing

Loss of ciliated epithelium (from viral infection) will cause:- stretching of adjacent cells to cover gap- regenerative hyperplasia to replace lost cells (initially with non-ciliated epi - impaired clearance)Impairment of respiratory defence mechanisms (viruses):- damage or kill mucosal cells (e.g. herpesvirus -> impairs mucociliary apparatus)- cause lymphocytolysis = immunosuppresion


inflammation of the mucous membranes of the nose

Serous Rhinitis

may result from mild irritants, type 1 allergies, cold air, or early viral infections - Serous discharge is oedema fluid (clear thin fluid)

Catarrhal rhinitis

Has progressed to include mucus production- increased activity or hyperplasia of goblet cells and mucous glands

Suppurative or mucopurulent Rhinitis

results from mucosal damage and primary or secondary bacterial/fungal infection- Strangles (streptococcus equi) in horses and chlamydiosis in cats (chlamydia felis) are examples of primary bacterial infections- Foreign bodies such as grass awns are common in dogs

Fungal Rhinitis

Nasal aspergillosis in dogs most often caused by growth of fungal hyphae of Aspergillus fumingatus-More common in dogs with long noses (labs, german shepperds)(German shepherds may develop systemic aspergillosis)

Common viral agents of conductive respiratory tract:

DOGS:- Canine distemper virus (paramyxoviridae, morbillivirus), Canine adenovirus T2, Parainfluenza VirusCattle:- Infectious bovine thinotracheitis (IBR, BHV-1), malignant catarrhal feverHorses:- Equine viral rhinopneumonitis (EHV-4), equine influenzaCats:- Feline Viral rhinotracheitis (herpesvirus), calcivurusPigs:- Swine influenza, pseudorabies

Hendra Virus

Henipah Virus (transmitted from bats to horses) SERIOUS ZOONOSIS- can infect both respiratory and CNS- Horses may present with respiratory signs (veterinarians can become infected without protective masks and goggles)- can cause meningoencephalitis- Nipah virus is related to hanipah

Atrophic rhinitis of pigs

Nasal infection with Bordatella bronchiseptica and toxigenic strain of Pasteurella multicoda (T D)- Damage osteoblasts to inhibit proper growth of nasal turbinate's- Stimulate osteoclasts to cause absorption of bone- Chronic changes in growing pigs result in crooked snouts, atrophied. Hypoplastic nasal turbinate's with correspondingly wide lumens in nasal passages§ Increased sneezing§ Decreased mechanical filtration of large particles -> secondary pneumonias

Guttural pouch disease

- Complication of strangles is empyema (filling space with pus)- Guttural pouch mycosis is associated with Aspergillus spp. - Fungal hyphae are antiinvasive - Internal carotid arteries pass through the median septum of each guttural pouch, may be breached by fungi - Massive nasal haemorrhage (epistaxis), thromboembolism with cerebral infarctsInfection and inflammaiton may also damage cranial and sympathetic nerves that pass through- leading to Horners syndrome = unilateral loss of sympathetic innervation to eye

Neoplasms of nasal passage and sinuses

Enzootic Nasal Tumour of sheep caused by retrovirusDogs may develop nasal carcinomas as well as sarcomas and lymphomas (Predispose to chronic rhinitis)Benign auditory polyps, nasopharyngeal polyps occur in cats - Extend from auditory tube into nasopharynx


loss of blood from the tissue that lines the inside of your nose- ethmoid haematoma may form in horses (blood-filled nasal polyp extending from ethmoid region of caudal nasal passage - highly vascular, similar to heamangioma)Epistaxis of any species may be secondary to trauma, FB, fungal infections etc.

Dorsal displacement of soft palate (DDSP)

Horses:- free edge of epiglottis normally rests upon caudodorsal aspect of soft palate when breathing- If epiglottis drops ventral to soft palate, this causes distortion of glottis and impairs breathing

Brachycephalic airway syndrome

Brachycephalic dogs, esp bulldogs, may have breathing problems associated with conformational defects- stenotic nares, elongation of soft palate, everted larungeal saccules- predispose to respiratory crisis and death - secondary to strong restraint, sedation or GA

Tracheal collapse

toy and miniature breedsunknown causenonproductive coughingchronic dry coughdifficulty breathing- dorsovental flattenin-wide, floppy dorsal tracheal membrane

Calf diphtheria

infectious laryngitis of cattle caused by Fusobacterium necrophorum - anaerobic bacteria of cattle that normally inhabits mucous membranes- reasons unknown, and the bacteria secrete a necrotizing toxin that causes epithelial necrosis, inflammation, and fibrin exudation

Kennel cough

infection of tracheobronchial epithelium with Canine Adenovirus type 2, Canine Parainfluenzavirus, and/or Bordetella bronchiseptica- anything that inflames the tracheo-bronchial tree will cause coughing


may cause chronic inflammation of the bronchi, sometimes with an eosinophilic component- cats (and other animals) may develop asthma- airway hyper-responsiveness (contraction of bronchiolar smooth muscle), eosinophilic bronchitis / bronchiolitis

Heaves in horses

Not asthma, but resembles asthma -> associated with exposure to allergens (dusty hay, cold climates)- Chronic recurrent constriction and inflammation of airways - Catarrhal and suppurative (goblet cell hyperplasia ++ mucous production and plugging)- airway constriction -> horse has prolonged forceful exhalations that include abdominal contraction -> lead to HEAVE LINE (external abdominal oblique hypertrophy)- COPD

Arachidonic acid metabolism (AA)

Degeneration and necrosis (hypoxia) ->Decrease O2 -> decreased ATP production -> decreased function of ATP dependent Ca2+ pump -> increase intracellular Ca2+ -> activation of calcium dependent enzymes in cytosol -> including activation of Phospholipase A -> cell membrane damage, blebbing, leakage CORTICOSTEROIDS BLOCK AA PRODUCTION

Lipoxygenase pathway

Occurs in neuts, and produces leukotrienesLTB4 = strong chemotactic propertyLTC4, LTD4 and LTE4 = induce classical symptoms of asthma§ Vasoconstriction, increased vascular permeability, and bronchospasm

cyclooxygenase pathway:

the cyclooxygenase pathway produces two prostaglandins that have opposing effects on plateletsProstacyclin (PGI2) = inhibits platelet aggregation and cause vasodilationThromboxane (TXA2) = promotes platelet aggregation and causes vasoconstriction- Also produced prostaglandins that cause vasodilation, pain and induce feverNSAIDS BLOCK COX


Collapse of pulmonary alveolar spaces, failure of alveolar spaces to expand- fetal atelectasis (lungs are natural state until born and takes first breath) -> Complete atelectasis in a dead neonate is indicative of stillbirth or suffocation during birth· Lung specimens will sink in formalinPartial atelectasis is indicative of weak, insufficient breathing attempts, pneumonia or insufficient pulmonary surfactantSurfactant produced late gestation and is essential to reduce surface tension between apposing alveolar wallsPremature delivery babies = less surfactant = more friction


inflammation of the lungs +/- bacterial infection

Cranioventral distribution of pneumonia

INHALED PATHOGENS:- bronchopneumonia- pneumonia affecting only right cranial lung may indicate aspiration pneumonia- R accessory bronchus breaches off trachea - first 'hole' for aspirated materials to travel down

Multifocal -> diffuse distribution of pneumonia

HAEMATOGENOUS SPREAD OF PATHOGEN- Diffuse pattern is referred to as interstitial pneumonia, whilst multifocal pattern of pneumonia may be referred to as embolic pattern

Dorsal inflammation of lung

pleuropneumonia of swine, caused by actinobacillus pleuropneumoniae

Caudal lung lobe pneumonia

WHEN SEEN IN ANIMALS -> SUSPECT LUNGWORM- Dictyocaulus filaria and other lungworms common in south Australian sheep


Most common pattern in ruminants and sheep (cranioventral)- most common cause of mortality in growing and finishing cattle and pigs- Initial infectious agent often VIRAL(bovine pestivirus (BVDV), parainfluenza (PI-3), bovine respiratory syncytial virus (BRSV), bovine rhinotracheitis (IBR))Viral damage of airway epithelium impairs mucociliary clearance and creates erosions, and lymphocytolysis may cause immunosuppression - Resident opportunistic bacteria or true bacterial pathogens can then more easily colonize the respiratory tractPasteurella multicoda is a common secondary infectious cause of bronchopneumonia in cattle, sheep and pig In cattle, mannheima haemolytica can be a primary pathogen, although usually follows viral infections- Secretes leukotoxin that kills neutrophils· Histologically, dying neuts have a stretched shape with a distorted nuclei = oat cells