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213 Cards in this Set

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  • Back
What are the 5 things required for efficient gas exchange?
Large volume of frequently changed air
Large area for diffusion
Warm, wet membrane
Enormous numbers of capillaries
Very thin capillary wall
What are the functions of the conductive system?
To heat, humidify and transport air to the lungs as quickly as possible.

Production of turbulent air flow to remove some inhaled particles.
Describe 'respiratory epithelium'.
Pseudostratified, ciliated columnar epithelium containing serous and mucus-secreting goblet cells
What is the transitional system?
Bronchioles - the section that connects the conductive and gaseous exchange systems. Distal bronchioles contain specialized secretory cells (Clara cells) which metabolize pulmonary toxins
Describe Type I pneumocytes.
Very delicate to facilitate gas exchange, but also susceptible to damage.
Describe Type II pneumocytes.
Cuboidal and secrete pulmonary surfactant (essential for alveolar expansion). Precursor cells for Type I pneumocytes should they be destroyed.
What is the function of BALT?
To sample the antigens dissolved in the mucus blanket.
What is another function of surfactant other than to reduce surface tension?
Acts as an opsonin for pulmonary macrophages.
What defense is employed against particles that do reach the alveoli?
Pulmonary macrophages.
What defense is used against blood-borne pathogens that reach the lungs?
Macrophages in pulmonary capillaries.
What are the 4 categories of inhibitors of respiratory defenses?
Toxic gases
Other (inc dehydration, stress, pulmonary oedema and anaesthesia)
How does a viral infectio predispose to secondary bacterial infection?
In health, the respiratory epithelium is resilient and prevents bacterial infection. Viral infection injures the epithelium, facilitating bacterial colonization.
Serous rhinitis...
Water nasal discharge.
Catarrhal rhinitis...
Produced through prolonged/severe damage to the respiratory epithelium producing ulceration and a hole in the mucus blanket. Goblet cells proliferate to fix it. Seen as a thick mucus discharge.
Purulent rhinitis...
Epithelial ulceration and disruption of the mucus blanket predisposes to bacterial infection. Seen as an opaque thick green exudate.
Fibrinonecrotic (aka diphtheritic) rhinitis...
Damage to blood vessels under the epithelium leads to fibrin leakage. Combines to form a pseudomembrane with dead cells. Seen as opaque discharge often containing blood.
Granulomatous rhinitis...
Discharge usually scarce, usually presents as polyp formation. Can be caused by fungal infection, TB, foreign bodies or allergies.
Sequellae to chronic bacterial sinusitis?
Osteomyelitis or meningitis.
Causative viruses of equine viral rhinitis?
EHV-4, rhinovirus, adenovirus and parainfluenza virus.
Describe the nature/duration of EVR
Mild, self-limiting
Causative bacteria of strangles?
Strep. equi.
What age group are at risk?
Young, naive horses.
How are they infected?
Inhalation with subsequent colonization of the nasopharyngeal mucosa.
What happens once the bacteria have colonized the mucosa?
They produce toxins which damage the epithelium, migrate to regional lymph nodes producing mandibular and retropharyngeal lymphangitis.
Describe the clinical signs.
Purulent rhinitis, conjunctivits and regional lymphadenopathy.
What sequellae of strangles may occur?
Bastard strangles (haematogenous bacteremia with abscessation and polyarthritis)
Purpura haemorrhagic (immune-complex vasculitis manifesting as haemorrhage or conversely DIC)
Guttural pouch empyema
Neurological signs (inc laryngeal hemiplegia, Horner's syndrome and facial n. paralysis)
What groups of horses are predisposed to progressive ethmoidal haematomas?
Older arabians and TBs
What is the presumed aetiology?
Begins as a minor haemorrhage between the resp. epithelium and the bone. The separation stimulates a chronic process which results in repeated haemorrhage. The developing haematoma may produce osteolysis of surrounding bone
Describe the clinical signs.
Mild epistaxis, coughing and later bone deformities.
Difficult to surgically remove and not often currative
Causative virus of IBR?
What other disease does BHV-1 cause?
Infectious pustular vulvovaginitis. Whether disease is respiratory or venereal depends on mode of transmission.
Mode of transmission of IBR?
Inhalation of respiratory droplets containing the virus.
What does the virus do once it's infected a resp. epithelial cell?
Replicates to produce daughter virions which are released by cell lysis. Mass cell lysis may produce severe ulceration and rhinitis/tracheitis.
What is really bad about IBR infections?
Predisposition to secondary bacterial infection (producing fibrinonecrotic rhinotracheitis)
Describe the gross lesions of IBR.
Ulceration and diphtheritic membrane formation in nasal cavity/trachea.
What specific bacterium takes advantage of IBR to produce lung infections?
Mannheimia haemolytica.
What characteristic feature of herpes virus enables period recrudescence in times of stress?
Ganglia latency.
What is the likely aetiology of bovine nasal granulomas?
Allergic, indicated by eosinophilia in the chronic nasal discharge.
Describe the gross lesions.
Pink polyps at the rostral nasal cavity. Chronic nasal discharge.
What is a common finding with bovine nasal granulomas?
Sticks and other things causing a necrotizing rhinitis.
How common is atrophic rhinitis in pigs in NZ, and what age groups is susceptible?
Affects around a third of all 5-8month old piglets.
Causative bacteria?
Bordetella bronchiseptica and Pasteurella multocida. Thought to require co-infection of both species.
What are the initial clinical signs prior to the onset of bone distortion?
Coughing and sneezing.
How does epiphora occur with atrophic rhinitis?
Blockage of the nasolacrimal duct due to nasal turbinate destruction.
How does the osteolysis of the turbinates occur?
Toxins produced by P. multocida inhibit osteoblasts and stimulate osteoclasts.
What factors make the disease worse?
Concurrent disease (inc inclusion body rhinitis) and anything else that is known to be immunosuppressive.
Causative virus of inclusion body rhinitis?
Herpes virus
What age group are susceptible?
Piglets less than 5 weeks usually.
Describe the infection and its clinical signs.
Typical viral rhinitis with serous progressing to catarrhal and then possibly purulent in the presence of bacterial infection. Coughing and sneezing usually self-limiting, although bronchopneumonia may sometimes occur.
Causative agent of canine fungal rhinitis?
Aspergillus fumigatus.
Clinical signs and gross lesions?
Unilateral purulent or haemorrhagic discharge. Greenish mats of fungal hyphae stuck on the nasal epithelium.
Histopath of fungal rhinitis?
Osteolysis and epithelial necrosis from fungal enzymes.
What must fungal rhinitis be differentiated from?
Nasal neoplasia, since both look clinically and radiographically similar.
Causative virus of feline viral rhinotracheitis?
Clinical signs?
Rhinitis and conjunctivits, sometimes progressing to lethargy and pyrexia.
What age group are predisposed?
Kittens around the time of maternal antibody decline.
What characteristic of herpes virus results in period shedding of virus in response to stress?
Ganglia latency
What bacterial infection does the condition predispose to?
Bronchopneumonia and bacterial sinusitis.
Describe bacterial sinusitis.
May result in turbinate lysis and permanent destruction of respiratory epithelium.
What are effects may be seen with an infection of FHV-1?
Ulcerative keratitis and abortion/still-birth if the queen is pregnant.
Describe feline calicivirus infection compared with herpes virus.
Lesions are very similar,but calicivirus may include a mild bronchiolitis and stomatitis and occasionally an acute self-limiting arthritis. Disease is usually transient except in secondary bacterial complications. When recovered cats enter a carrier state and become periodic shedders.
Causative agent of feline chlamydophilosis.
Chlamydophila psittaci (felis)
Describe feline chlamydia.
Mild transient infection that may result in bronchopneumonia.
Non-neoplastic tumours of the nasal cavity are also known as what?
Nasal polyps.
Where do polyps commonly develop in horses?
Ethmoidal region.
Where do polyps commonly develop in cats?
Nasopharynx or auditory tube.
What are common sequellae to feline auditory tube polyps?
Can extend into the middle ear and rupture the tympanic membrane. Tend to develop in younger cats and the aetiology isn't known but thought to be genetic or infectious. Benign and surgery is usually curative.
What other non-neoplastic tumour do horses develop?
Nasal cysts. Benign, but may be locally expansile resulting in deformation/destruction of surrounding bone.
Describe the aetiology of equine nasal cysts.
Originate as a nest of epithelium encased in bone. The epithelium is secretory, and the cyst enlarges as the secretion accumulates.
Which species have the highest incidence of nasal neoplasia?
What tissue malignancy is most common in this species?
Adenocarcinoma originating from respiratory epithelium.
Are nasal neoplasms in dogs generally benign or malignant?
Which breeds of dogs are predisposed to nasal neoplasia?
Long-nosed breeds inc. collies and German shepherds.
Describe the clinical signs of nasal neoplasia.
Unilateral epistaxis and chronic nasal discharge. May progress to mucopurulent discharge because these tumours commonly have secondary bacterial infections. Progression often results in nasal deformity.
Do these neoplasms often metastasize?
No, but are locally invasive and due to location they are difficult to excise.
What type of nasal neoplasm do cats and horses commonly develop?
SCC. Horses close to the nostril and cats in the sinuses.
Describe brachycephalic airway syndrome.
Stenotic external nares, excessively long soft palate may be combined with tracheal hypoplasia or collapsing trachea.
What developmental disease commonly occurs in horses and pigs?
Hypoplastic epiglottis.
What is the significance of the condition?
In horses it may become trapped leading to airway obstruction and subsequent exercise intolerance.
What are the causes of laryngeal oedema?
Any acute inflammatory reaction, but most often anaphylaxis.
What is the significance of laryngeal oedema?
May block the larynx and result in asphyxiation
Laryngitis can impair function and predispose to aspiration pneumonia.
What are the common causes of pharyngeal perforation?
Drenching accidents, stick, food, bite or collar injuries. Will lead to cellulitis and abscessation.
Why is guttural pouch disease very bad?
They have poor drainage (like sinuses) and are in close proximity to the internal carotid, a number of cranial nerves and the atlantooccipital joint.
Causative agent of guttural pouch mycosis.
Aspergillus fumigatus
Where do the spores come from?
Mouldy hay.
Describe the pathogenesis, clinical signs and gross lesions.
Necrosis of the guttural pouch mucosa with thick, adherent mats of fungal hyphae. If the necrosis occrus around the internal carotid artery it may weaken the wall leading to aneurysm or rupture. Clinical signs include dysphagia, Horner's syndrome or laryngeal hemiplegia may occur from damage to nerves.
Common cause of guttural pouch empyema.
Occurs after strangles, although any infection of the nasopharyn may result in an accumulation of pus in the guttural pouches.
Laryngeal necrobacillosis is known by which other names?
Calf diphtheria and necrotic laryngitis.
Which animals are likely to get it?
Sheep and cattle, pigs not so much.
What predisposing factor is required to allow the disease to occur?
Damage to the laryngeal cartilages which enables necrotizing bacteria to colonize.
Which bacterial species are associated with laryngeal necrobacillosis?
Fusobacterium necrophorum.
What happens once the bacteria have colonized the damaged laryngeal tissue?
They produce necrotizing toxins that result in an increasing area of necrosis.
How does the disease become fatal?
Inhalation of F. necrophorum into the lungs, toxaemia or sepsis.
Should the animal survive the acute episode to allow the larynx to heal by granulation tissue the lumpy cartilage will predispose to aspiration pneumonia.
What are common causes of laryngeal damage?
Drenching accidents, IBR or papular stomatitis in calves, contagious ecthyma in sheep and extremely rough forage.
Canine tracheobronchitis is more commonly known as what?
Kennel cough
What group of dogs does it commonly occur in?
Unvaccinated dogs which have sporadic contact with other dogs (such as when placed in a kennel facility)
Is it very contagious?
What agents are commonly responsible?
A variety including Bordetella bronchiseptica, CAV-2 and canine parainfluenza virus.
What other factors are needed to allow disease to occur?
Generally more than one inciting agent combined with stress, poor ventilation etc.
Where is the disease usually confined to?
Trachea and bronchi, although occasionally infection may predispose to secondary bronchopneumonia which may be fatal.
What are the 6 things that may alter the ventilation:perfusion ratio?
a) pulmonary collapse
b) pulmonary emphysema
c) pulmonary congestion
d) pulmonary haemorrhage
e) pulmonary oedema
f) pulmonary embolism
What are the 3 categories of pulmonary collapse?
Describe congenital collapse.
Occurs when new-born animals are unable to inflate their lungs. Commonly occurs because of aspiration of meconium (relaxation of the anal sphincter dt hypoxia releases meconium into the amniotic fluid). Foetal hypoxia can occur dt premature placental detachment or dystocia. Congenital collapse may also occur due to inadequate/abnormal sufactant. Alveoli aren't able to remain open. These animals may survive but hypoxia leading to retardation is an issue.
Describe compressive collapse.
Outside force on the lungs leads to collapse of the alveoli. May be pressure outside the body wall eg RTA or in the pleura eg pneumothorax, pyothorax, haemothorax etc or intrathoracic neoplasia.
Describe obstructive collapse.
The airway is blocked, trapping air in the alveoli which slowly collapse as the air is absorbed. May be blocked by oedema, foreign body, parasites, neoplasia or anaesthesia complications.
What is pulmonary emphysema due to?
Over-inflation of the alveoli.
Is it a primary or secondary disease process in animals?
Secondary - it's always due to something else.
What are the common causes of emphysema?
Bronchopneumonia of all causes and COPD in horses. Both result in increased inspiratory effort forcing excessive amounts of air into the lungs.
What are the 3 subclasses of pulmonary emphysema?
Alveolar, interstitial and bullous.
What commonly causes pulmonary congestion?
LSCHF, but may also be a normal post mortem change.
Describe the gross appearance and histo of pulmonary congestion.
Dark red in acute cases, more tan coloured in chronic cases. Hemosiderin filled pulmonary macrophages are seen on histo
What are common causes of pulmonary haemorrhage?
Trauma, anticoagulant toxicity, ruptured lung abscesses and exercise induced pulmonary haemorrhage in horses (EIPH)
What factors are thought to contribute to EIPH?
Alveolar hypoxia, pulmonary hypertension and laryngospasm.
What are some common causes of pulmonary oedema?
Haemodynamic, inc. vascular permeability, anaphylaxis, drug reactions, DIC and endotoxaemia.
What may lodge in the lungs to cause pulmonary embolism?
Neoplastic cells, sterile emboli from venous thrombolus or septic emboli.
What neoplasms commonly produce emboli which lodge in the lungs?
Canine osteosarcoma and haemangiosarcoma.
Why is it that pulmonary emboli in animals aren't often fatal?
The lungs have a collateral blood supply (unlike the kidneys and such which have an end arterial pattern). This compares with humans which commonly develop deep vein thrombosis which may lodge in the lungs.
What commonly produces septic emboli in the lungs?
Liver abscesses and right-sided endocarditis seed out into the lungs producing abscesses.
How do the bronchi/oles respond to injury?
Same way the nasal respiratory epithelium does - epithelial necrosis and ulceration. Initially serous exudate, progressing to catarrhal.
If the injury to the bronchi/oles is prolonged or severe what are 3 common sequellae?
a) squamous metaplasia (which isn't cilliated meaning the mucus blanket isn't propelled - bronchiectasis)
b) bronchiectasis is the outpouching of the bronchiole dt distension with mucus and the inflammation weakening the bronchiole wall. Appears grossly similar to pulmonary abscessation.
c) bronchiolitis obliterans - severe damage leads to necrotic epithelium convered by exudate which is infiltrated by fibroblast. Organization leads to contraction.
Describe alveolar repair.
Damage causes typeI pneumocyte necrosis - these slough into alveoli and combine with fluid leached from damaged capillaries. If the animal survives, typeII pneumocytes proliferate and may give the appearance of gland-like structure on histo. If the damage is severe and the basement membrane is eroded then the lungs heals by fibrosis.
What does the term pneumonia imply?
Terminal bronchiolar and/or alveolar involvement.
What is unique about inflammation of the lungs?
The alveoli can expand with inflammatory exudate.
What does the term 'consolidation' mean?
Alveoli distended with inflammatory cells, necrotic cell debris and fibrin
What are the 4 generic types of pneumonia?
Describe the distribution and gross appearance of bronchopneumonia.
Cranio-ventral consolidation - lungs are dark red, heavy and meaty.
Where is the initial site of inflammation in bronchopneumonia?
Terminal end of the bronchiole, and from there inflammation spreads up and down the respiratory tree.
Therefore, what is the source of causative agent?
Inhalation of bacteria and/or food (aspiration pneumonia).
What is the predominant cell type in bronchopneumonia?
If alveolar necrosis is severe what happens?
Damage to alveolar capillaries and leakage of fibrin which may extend through the pulmonary pleura (seen as yellow jelly adhesions)
This severe yellow jelly adhesions produce a pneumonia known as what?
What diseases characteristically produce pleuropneumonia?
Mannheimia haemolytica in cattle and sheep, Actinobacillus pleuropneumonia in pigs and gastric acid aspiration in all species.
Describe the distribution and gross appearance of interstitial pneumonia.
Firm texture and diffusely over-expanded (since inflammation in the alveolar wall prevents their collapse). Lungs do not collapse when throcic cavity is opened. Often pink and have rib imprints
What are the causative agents of interstitial pneumonia?
Blood-borne bacteria, virus, toxins and immune complexes. Viruses inc African horse sickness, Maedi-Visna and porcine reproductive, respiratory syndrome, FIP and certain other inhaled toxins.
What is the source of the causative agents?
Via the blood (NOT inhaled). Viruses that cause interstitial pneumonia enter the blood stream and infect the endothelial cells of the alveolar capillaries.
Do the majority of viruses causes interstitial pneumonia?
No, viruses usually infect respiratory epithelial cells and cause their effect by predisposing to bacterial bronchopneumonia.
What is the predominant cell type in interstitial pneumonia?
Lymphocytes and macrophages.
In certain toxicoses what unusual presentation occurs?
Marked necrosis can result in fibrin exudation and haemorrhage into the alveoli. Chronic interstitial pneumoina results in the deposition of fibrous tissue in the interstitium
Describe the distribution and gross appearance of embolic pneumonia.
Multifocal consolidation randomly distributed throughout the lung
What are the causative agents of embolic pneumonia?
Emboli from vegetative endocarditis of the right AV valve, bovine Mortierella wolfii abortion and canine osteosarcoma
What is the source of the causative agents?
Enter the lungs via emboli in the blood.
What is the predominant cell type in embolic pneumonia?
Depends on primary disease process (since embolic pneumonia is always secondary). Will be either neutrophils or neoplastic cells.
Describe the distribution and gross appearance of granulomatous pneumonia.
Multifocal areas of granulomatous inflammation randomly scattered in the lungs.
What are the causative agents of granulomatous pneumonia?
Fungi and higher bacteria inc Rhodococcosis in horses, Mycobacteriosis in all species and Cryptococcosis.
What is the source of the causative agents?
What is the predominant cell type in granulomatous pneumonia?
Epitheloid and multinucleat macrophages.
What are 2 congenital lung abnormalities?
Congenital melanosis in pigs and sheep.
Ciliary dyskinesia in dogs
Describe congential melanosis.
Incidental, but seen as dark lung pathces
Describe ciliary dyskinesia.
Mucus blanket can't be moved so affected dogs are predisposed to bacterial infection and chronic bronchitis
Describe the pulmonary manifestation of a metabolic disturbance.
Pulmonary calcification due to renal secondary hyperparathyroidism in dogs. Lungs have a firm, gritty texture. Not significant except to highlight renal status or indicate toxicosis.
What other conditions result in pulmonary calcification?
Rodenticide toxicity or plants containing vitamin D analogues. Mild calcification is considered a normal geriatric change.
What does aspiration pneumonia cause?
Bronchopneumonia if aspirated material is bland, or pleuropneumonia if caustic
What lung disease may result from Toxoplasmosis?
Interstitial pneumonia.
Equine viral rhinopneumonitis (EHV-4) usually causes rhinitis, how may it cause pneumonia?
Secondary predisposition to bacterial bronchopneumonia.
What other bacterial species is Rhodococcus equi similar to and why?
Because it has a capsule and lives inside macrophages.
What disease does R. equi produced?
Granulomatous pneumonia.
What age group of horses are at risk?
The young, old and sick (aka immunocompromised)
Describe the clinical presentation.
Variable, can range from acute pneumonia to chronic progressive disease.
What is a common sequel to the pneumonia and how does it occur?
Enterocolitis results from the bacteraemia localising in the intestine. Often severe and ulcerative with profuse diarrhoea. Zoonotic potential.
Describe the aetiology of COPD.
Considered to have an allergic basis. Previous sensitization to a number of things including virus particles, dust, toxins increases airway responsiveness and mild inflammation in the airways produces marked mucus secretion and airway contraction
How does lead to obstructive disease?
Excess mucus clogs the mucus blanket and leads to obstruction of the bronchiole. This requires the horse to increase respiratory effort.
What does the increased respiratory effort result in?
Increased intrathoracic pressure which may lead to pulmonary hypertension and cor pulmonale, and perhaps emphysema
What are the clinical signs of COPD?
Heave lines, recurrent respiratory distress, exercise intolerance and chronic cough.
What does histo look like?
Marked goblet cell hyperplasia, eosinophilic inflammation and bronchiolar narrowing.
What group of animals are susceptible to bovine enzootic pneumonia?
Calves less than 6 months old.
What are the predisposing factors necessary for the disease to occur?
Viruses inc. herpesvirus, parainfluenza virus, adenovirus, rhinovirus, reovirus and Mycoplasma spp as well as poor ventilation, stress, cold, crowding all play a part in weakening respiratory defences.
Which opportunistic species are responsible for the disease?
Pasturella multocida, Arcanobacter pyogenes, Haemophilus somnus and E. coli.
Describe the gross lesions of bovine enzootic pneumonia.
Characteristic bronchopneumonia - cranioventral consolidation and reddening. Incision of lesions may reveal suppurative exudate
Describe the histo lesions.
Neutrophils, necrotic debris and bacteria in bronchioles and alveoli. Sometimes a small amount of fibrin may be present.
If the pneumonia was caused by H. somnus, where else would lesions be seen?
In the brain (thromboembolic meningioencephalitis)and myocardium
Describe the morbidity/mortality of shipping fever compared with bovine enzootic pneumonia.
Shipping fever has a lower morbidity/high mortality.
What are the predisposing factors of shipping fever?
Most often shipping but can be induced by many other factors inc. weaning, mixing animals, fatigue, dehydration, cold, starvation and viral infection esp BHV-1). All these contribute to lower respiratory defences.
What bacterial species are responsible for the disease?
Mannheimia haemolytica or Pasteurella multocida.
Describe the pathogenesis of shipping fever.
Bacterial toxins produce necrosis of lung tissue, damaging blood vessels and enabling fibrin-rich fluid to leak through the pleura giving rise to pleuropneumonia. Toxins are also absorbed into the blood, and toxaemia is the common cause of death.
What are the clinical signs of shipping fever?
Depression, pyrexia and shallow coughing.
What are the gross and histo lesions seen?
Cranioventral consolidation with adherent fibrin overlying the pleura. Histo reveal necrosis, neutrophils and fibrin.
What are the toxins responsible for toxic pneumonia in NZ?
4-ipomeanol (mouldy kumara)and 3-methylindole (in pastures regrowing after silage making). 3-methylindolw is first metabolized to L-tryptophan prior to absorption in the rumen.
What happens once the toxins reach the blood after being absorbed from the rumen.
They are detoxified by Clara cells, which produced enormous amounts of free radicals in the process - these damage typeI pneumocytes.
What does this damage result in?
Alveolar and interstitial oedema, and since inflammation is centred on the alveolar interstitium and an interstitial pneumonia develops.
What are the gross, clinical and histo signs/lesions?
Animals develop dyspnoes 1-2 weeks post exposure. Gross exam reveals diffusely enlarged, rubbery lungs with rib imprints. Increased respiratory effort may lead to emphysema. Histo reveals interstitial oedema and fibrin in acute cases, with hyperplastic typeII pneumocytes in more chronic cases.
What is Mortierella wolfii infection associated with?
Feeding of contaminated silage, causing placentitis and abortion in cows.
How does the fungus get from the uterus to the lungs?
The contractions associated with abortion push fungi into the placental veins, which then lodge in the next capillary bed. They then grow in blood vessels there causing inflammation, necrosis and infarction.
What is odd about the type of pneumonia produced?
It should be embolic, but the disease is often so severe that the lungs appear diffusely affected, sometimes seen as haemorrhage and fibrin in the pleural cavity.
What does hist reveal?
Large quantities of oedema, fibrin and necrotic cell debris in the expanding interstitium and alveoli. Moderate numbers of neutrophils and macrophages may also be present.
Will Aspergillus also cause mycotic abortions?
Yes, but only M. wolfii causes pulmonary involvement.
Which group of animals are susceptible to ovine enzootic pneumonia?
Hoggets less than 1 year old.
What are the predisposing factors associated with ovine enzootic pneumonia?
Other viral infections inc. parainfluenza, adonevirus, reovirus, strees, mustering, dusty conditions, heat stress and dehydration.
What are the causative bacterial spp responsible for ovine enzootic pneumonia?
Mycoplasma ovipneumoniae and Pasteurella multocida.
What are the major clinical signs?
Coughing and decreased weight gain, but sheep very rarely die of the disease.
Describe the gross lesions associated with the disease.
Mild bronchopneumonia, sometimes progressing to small amounts of fibrin adherent to the pleura. The fibrous adhesions don't limit the clinical recovery of the animal, but will lead to carcass downgrading.
Describe the histo lesions.
Moderate numbers of neutrophils in bronchioles and a small expansion of the interstitium. Hyperplastic BALT is considered typical of Mycoplasma infection.
What predisposing factors are required for ovine fibrinous pneumonia?
Concurrent viral infection and stress etc etc.
What bacterial spp is responsible for disease?
Mannheimia haemolytica producing severe pulmonary necrosis and toxaemia.
Describe the gross lesions.
Marked cranioventral pleuropneumonia.
What other factors are required for occurance of porcine enzootic pneumonia?
Crowding, poor ventilation, humidity, cold, ammonia (anything that sufficiently compromises the respiratory defences). Death is rare unless secondary infection occurs.
What is the bacterial spp responsible for the disease?
Mycoplasma hyopneumoniae.
What bacterial spp are implicated in secondary bacterial infection?
Pasteurella multocida and Arcanobacter pyogenes.
What are the clinical signs?
Chronic cough and reduced growth rates.
What are the gross and histo lesions?
Typical bronchopneumonia, lesions are usually mild unless secondary infection occurs.
Neutrophils, necrotic cell debris and exudate distend alveoli. Mycoplasma typically produce BALT hyperplasia.
What is the causative bacterium of porcine pleuropneumonia?
Actinobacillus pleuropneumoniae
What is unique about this bacterium?
It can initiate pneumonia with respiratory defences still in full force - it doesn't require a whole host of other things to weaken the immune system.
What is unique about the nature of the pneumonia produced?
It has a caudodorsal distribution - unlike any other bronchopneumonia - even though the bacteria is inhaled.
What age group of pigs are susceptible?
Piglets between the ages of 2 and 5 months.
Describe the pathogenesis of porcine pleuropneumonia.
Necrosis of the alveolar and bronchiole leads to damage of capillaries and fibrin leakage through the pleura. Histo looks similar to bovine shipping fever and ovine acute fibrinous pneumonia.
What is the mode of transmission of canine distemper?
Inhalation of virions
What happens once its inhaled?
The virus localizes in the local lymphoid tissue, it replicates and from there it travels to multiple tissues inc. the URT and lungs.
How does distemper produce pneumonia?
The virus is immunosuppresive and so can predispose to pulmonary toxoplasmosis or secondary bacterial bronchopneumonia as well as being able to cause interstitial pneumonia directly.
What characteristic histo findings should be identified to make the diagnosis and where would they most likely be found?
Intracytoplasmic and intranuclear eosinophilic inclusions in the transitional epithelium of the renal pelvis and bladder.
What are the bacterial spp known to cause canine bacterial pneumonia?
Pasteurella multocida, Strep spp and E. coli. Almost always secondary due to aspiration pneumonia
What is paraquat?
Broad spectrum herbicide.
Describe the pathogenesis of paraquat toxicosis.
Paraquat is detoxified by Clara cells. In the process reactive metabolites and free radicals are formed. These cause necrosis of typeI pneumocytes and capillary endothelial cells. The initial damage leads to oedema, fibrin exudation and frank haemorrhage into the lungs. Should the animal survive, death occurs because of interstitial fibrosis (the basement membrane is damaged in the initial toxicity)
What is noted on PM?
Lungs are grossly distended and don't collapse when thoracic cavity is opened.