Diseases of the nasal cavity and sinuses

Clinical signs and locations of sinonasal pathology

• • Nasal discharge
    • Bilateral discharge:
      • Lesion is caudal to nasal septum eg: pharyngeal lesion; LRT lesion in horses
      • Lesion has resulted in nasal septum destruction
        • Neoplasia
        • Fungal infection
    • Unilateral discharge:
      • Lesion is cranial to nasal septum eg: nasal or sinus lesion; pharyngeal or guttaral pouch lesion in horses
  • Type of discharge
    • Serous
    • Catarrhal
    • Purrulent
    • Haemorrhage
  • Clinical signs
    • Sneezing - nasal
    • Facial swelling - nasal, pharyngeal
    • Pain - any location
    • Coughing - pharynx, larynx, trachea
    • Dyspnoea/altered air flow
    • Respiratory noise

Functional anatomy

• • Mucosa
  • Mucosal epithelium
  • Nares and epiglottis- stratified squamous
  • Nasal cavity, paranasal sinuses, larynx, trachea - pseudostratified, columnar, cilliated
  • Submucosa
  • Submucosal glands
  • Lymphoid tissue
  • Blood vessels, lymphatics and nerves
  • Very rich blood supply to nasal mucosa
  • Nasal chambers and turbinates
  • Scrolls of turbinate bone
  • Arrangements vary with species
  • Nasal septum
  • Full length of nasal chamber in horses
  • 2 openings into pharynx
  • Partial length in other species
  • Single opening into pharynx
  • Sinuses
  • Size, arrangement and number vary with species
  • Poorly developed in carnivores
  • Poor communication of frontal sinus in cats with nasal cavity
  • Predisposed to frontal sinus bacterial infections
  • Maxillary sinus opening very large - 'maxillary recess'
  • Maxillary sinus infections very uncommon in carnivores
  • Highly developed in horses
  • Slit-like, high openings in horses
  • Predisposed to bacterial infections
  • Cheek teeth embedded within the maxillary sinuses
  • Maxillary sinusitis secondary to tooth root abscesses
  • Guttural pouch
  • Horses
  • Diverticulum of the eustachian tube with a thin slit-like opening at the rostroventral aspect into the pharynx.
  • Mucous secretions drain out of the pouch when the horse lowers its head
  • Lined by respiratory epithelium
  • Bordered by glossopharyngeal, vagus, accessory and hypoglossal nerves; sympathetic trunk; internal and external carotid arteries
  • Pathology
  • Mycotic infections eg: Aspergillus fumigatus
  • Bacterial infections eg: Streptococcus equi var. equi ('Strangles') or S.equi var zooepidemicus
  • Tympany - associated with dysfunction of the pharyngotubal opening resulting from thickening (oedema, inflammation) or obstruction by a mucosal fold (eg: foals)

•*Defense mechanisms

• • Particle deposition
  • Coiled nature of turbinates promotes turbulent airflow and impaction of large particles >10 μm in diameter onto the nasal mucosa
  • Mucociliary escalator
  • Cilia on the respiratory epithelium beat in a co-ordinated manner
  • Caudal direction in nasal cavity
  • Cranial direction in trachea and lower airways
  • Mucus is swallowed when it reaches the nasopharynx
  • Constant movement reduces chances that pathogens can adhere to the respiratory epithelium
  • Mucus
  • Produced by the goblet cells of the respiratory epithelium and the submucosal glands
  • with contribution from lacrimal glands draining into the nose
  • Trap particles for transportation away and subsequent swallowing
  • Physical barrier against mucosal damage
  • Prevents dessication of the mucosal epithelium
  • Contains antimicrobial substances
  • Immunoglobulin - IgA
  • IgA produced by mucosal plasma cells
  • IgA can attach to specific pathogen antigens (viruses, bacteria) trapping them in the mucus for clearance
  • Lysosyme
  • Direct action on bacterial cell walls
  • Lactoferrin
  • Inhibits bacterial growth as sequesters iron, an essential co-factor for many bacteria
  • Commensal bacteria
  • The normal bacterial flora of the nasal cavity, pharynx, larynx and proximal portion of the trachea compete with potentially pathogenic bacteria and help to prevent their colonisation (competitive exclusion).
  • The airway environment distal to the mid-portion of the trachea is effectively sterile.
  • Reflexes
  • Sneezing
  • Coughing

•*Pathology of the upper airways

• • Developmental abnormalities
  • Palatoschisis
  • Nasal deviation
  • All brachycephalic dog and cat breeds!
  • Esp. English Bulldogs - stenotic nares, wide/long soft palate, hypoplastic trachea
  • CIrculatory diseases
  • Epistaxis
  • Haemorrhage from the nose
  • Causes
  • Inflammation eg: ulcerative rhinitis
  • Neoplasia eg: infiltrating tumour, haemangioma
  • Trauma
  • Clotting defects
  • Horse:
  • Haemorrhagic nasal polyp
  • 'Ethmoid haematoma', 'Progressive haematoma' - arise from the ethmoid region and can extend to fill the nasal cavity. They can be difficult to control as they can recur after surgery. Histology - multiple areas of acute to chronic haemorrhage within a fibrous tissue stroma.
  • Exercise-induced pulmonary haemorrhage ... see later lectures.
  • Inflammatory disease
  • Inflammation in the URT can be classified on:
  • Location
  • Nasal cavity - rhinitis
  • Paranasal sinuses - sinusitis
  • Guttural pouch and eustachian tube - eustachitis
  • Pharynx - pharyngitis
  • Type
  • Grossly many inflammatory processes (eg: response to viral or bacterial infection) in the URT will begin as a serous discharge, and then progress to a catarrhal exudate, and then to purulent/pseudomembranous/haemorrhagic as neutrophils are recruited
  • Serous - transparent fluid exudate (acute inflammation)
  • Catarrhal - mucous exudation (acute to subacute inflammation)
  • Pseudomembrnaous - fibrin exudation
  • Purulent - pus
  • Ulcerative
  • Haemorrhagic
  • Granulomatous (chronic inflammation)
  • Polypoid (chronic inflammation)
  • Timecourse
  • Acute, subacute, chronic
  • Causes
  • Infectious agent - viral, bacterial, fungal, parasitic
  • Trauma or foreign body (eg: grass seed)
  • Irritant or allergens
  • Neoplasia
  • Viral infections
  • Herpesviruses
  • Bovine herpesvirus -1
  • Infectious bovine rhinotracheitis (IBR)
  • Highly infectious URT disease of cattle
  • High morbidity, low mortality
  • Aerosol transmission - requires close contact between animals
  • BHV-1 infects the respiratory mucosal epithelial cells (intranuclear inclusion eosinophilic inclusion bodies)from nasal mucosa down to bronchioles
  • leading to neutrophilic inflammation of varying severity.... serous -> catarrhal -> purulent nasal discharge, sneezing, coughing.
  • with secondary bacterial infection (eg: Pasturella spp., Mycoplasma spp., Fusobacterium necrophorum) can lead to fibrinous to necrotizing inflammation; mucosal sloughing, ulceration... pyrexia, dyspnoea ... inhalation pneumonia... death.
  • Clinical signs include coughing, discharge, lacrimation, and increased respiratory rate.
  • Clinical disease most severe in young calves - can develop mucosal ulcerative lesions in the oesophagus and forestomachs and viraemia with multiorgan infection.
  • Cause of abortion >5 months of gestation
  • Cytomegaloviruses
  • Porcine cytomegalovirus
  • Inclusion body rhinitis
  • 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)
  • Morbitity high, mortality low
  • Histology: large basophilic intranuclear inclusion bodies in the nasal and sinus respiratory epithelium with lymphocytic infiltration of the mucosa.
  • Can develop viraemic stage, with inclusions in other organs eg: renal tubular epithelium. Piglets can die during this phase.
  • Equine herpesvirus - 1, 4
  • Feline herpesvirus -1
  • Feline viral rhinotracheitis
  • Viruses and bacteria are involved in the complex. The most frequent aetiologic agent is FHV-1, and less frequently feline calicivirus and/or Chlamydophia psittaci (NB: previously called Chlamydia psittaci var felis)
  • All three agents infect URT respiratory epithelium, although FHV-1 has the highest affinity for this epithelium
  • Feline calicivirus more frequently infects the oral mucosa -> ulcerative stomatitis
  • C.psittaci more frequently infects the conjunctival epithelium -> chronic conjunctivitis
  • Infection of the respiratory epithelium by FHV-1 results in a typical neutrophilic rhinitis with intraepitheial intranuclear eosinophilic inclusion bodies, with expected clinical signs
  • Resolution of clinical signs usually occurs by 7-14 days.
  • FHV-1 remains latent in the trigeminal ganglion, and can reactivate at times of stress. Can infect the cornea -> ulcerative keratitis.
  • Occasional mortality in kitten or immunocompromised animals usually associated with secondary bacterial infection.
  • Bacterial infections
  • Pasturella multocida
  • Atrophic rhinitis in pigs
  • Pigs aged 4-12 weeks old show clinical signs
  • Catarrhal nasal discharge (due to an acute rhinitis), sneezing, coughing, can progress to dyspnoea and anorexia.
  • Shortening and distortion of snout, secondary to nasal turbinate bone loss (histological evidence of osteolysis)
  • 2 forms of the disease
  • 'Progressive' atrophic rhinitis
  • Due to infection of the nasal turbinates by P.multocida strains carrying the toxA gene that encodes for an osteolytic toxin. P.multocida adheres poorly to mucous membranes, and therefore requires a predisposing nasal insult to assist colonisation eg: co-infection with B.bronchoseptica; or Porcine cytomegalovirus (inclusion body rhinitis)
  • Turbinate bone atrophy is permanent and progressive
  • 'Non-progressive' atrophic rhinitis
  • Due to infection of the nasal turbinates by Bordatella bronchoseptica strains alone, that carry a gene that encodes for a dermonecrotic toxin.
  • Turbinate bone can regenerate by the time of slaughter
  • 'Snuffles' in rabbits
  • Most often P.multocida and/or B.bronchoseptica infection of the nasal mucosa
  • Clinical signs (nasal discharge, sneezing) result from an acute to chronic rhinitis.
  • Streptococcus equi
  • Streptococcus equi subsp. equi
  • Cause of 'Strangles' in horses
  • Infection with Streptococcus equi occurs after contact with contaminated feed, water bowls or an infected carrier horse
  • Organism remains viable in environment for months
  • Possibility of other sources of infection - in pharynx of in-contact dogs?
  • Colonisation of nasopharynx causing:
  • Chronic purulent rhinitis, sinusitis, eustachitis
  • Can progress to development of nodular masses in the guttural pouch consisting of inspissated pus and viable bacteria (guttural pouch empyema) - 'carrier' state
  • Regional suppurative lymphadenitis - can rupture onto skin of neck
  • Bacteraemia with abscess formation in other organs (eg: liver, kidneys) - Bastard Strangles!
  • Streptococcus equi subsp. zooepidemicus
  • Can infect the respiratory tract (nasal cavity, paranasal sinuses, trachea and bronchi/bronchioles)
  • URT infection can be indistinguishable clinically from Strangles, but does not cause suppurative lymphadenitis (cf: S.equi subsp. equi)
  • Fungal infections
  • Filamentous fungal organisms
  • Aspergillus fumigatus
  • Guttural pouch infections in horses - fungal plaques form on the adventitia of the carotid arteries can lead to catastrophic haemorrhage following erosion of carotid arteries!
  • Nasal infection in dogs and cats - plaques develop on the nasal or paranasal sinus epithelium. Result in severe neutrophilic rhinitis/sinusitis. Can occur secondary to areas of mucosal compromise eg: adjacent to a space-occupying lesion.
  • Mucor spp.
  • Yeast-like fungal organisms
  • Cryptococcus neoformans
  • Most commonly in cats and dogs
  • Chronic granulomatous rhinitis
  • Can invade through adjacent structures, eg: through the cribiform plate into the brain! These cases therefore can present as a primary neurological disease.
  • Parasitic infections
  • Insecta
  • Oestrus ovis larvae in the nasal cavity of sheep and goats
  • 'Nasal bots'