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Diseases of the nasal cavity and sinuses (view source)
Revision as of 20:36, 29 November 2006
, 20:36, 29 November 2006no edit summary
== Pathology of the nasal cavity and paranasal sinuses ==
===Clinical signs and locations of URT pathology===
**Nasal discharge
***Relation to choana?
****Caudal eg: pharyngeal lesion; LRT lesion in horses
***Bilateral discharge
****Cranial eg: nasal or sinus lesion; pharyngeal or guttaral pouch lesion in horses
***Unilateral discharge
****Nasal septum destruction
*****Neoplasia
****Fungal infection
**Type of discharge
**Serous
**Catarrhal
**Purrulent
**Haemorrhage
**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'
===Clinical signs and locations of URT pathology===
**Nasal discharge
***Relation to choana?
****Caudal eg: pharyngeal lesion; LRT lesion in horses
***Bilateral discharge
****Cranial eg: nasal or sinus lesion; pharyngeal or guttaral pouch lesion in horses
***Unilateral discharge
****Nasal septum destruction
*****Neoplasia
****Fungal infection
**Type of discharge
**Serous
**Catarrhal
**Purrulent
**Haemorrhage
**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'