Difference between revisions of "Diseases of the nasal cavity and sinuses"
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==Clinical signs and locations of sinonasal pathology== | ==Clinical signs and locations of sinonasal pathology== | ||
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===Nasal discharge=== | ===Nasal discharge=== | ||
*Bilateral discharge: | *Bilateral discharge: | ||
Line 11: | Line 7: | ||
***Fungal infection | ***Fungal infection | ||
*Unilateral discharge: | *Unilateral discharge: | ||
− | **Lesion is cranial to nasal septum eg: nasal or sinus lesion; pharyngeal or guttaral pouch lesion in horses | + | **Lesion is cranial to nasal septum eg: nasal or sinus lesion; pharyngeal or guttaral pouch lesion in horses |
===Type of discharge=== | ===Type of discharge=== | ||
Line 66: | Line 62: | ||
**Bordered by glossopharyngeal, vagus, accessory and hypoglossal nerves; sympathetic trunk; internal and external carotid arteries | **Bordered by glossopharyngeal, vagus, accessory and hypoglossal nerves; sympathetic trunk; internal and external carotid arteries | ||
*Pathology | *Pathology | ||
− | **Mycotic infections eg: | + | **Mycotic infections eg: Aspergillus fumigatus |
− | ***Bacterial infections eg: | + | ***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) | **Tympany - associated with dysfunction of the pharyngotubal opening resulting from thickening (oedema, inflammation) or obstruction by a mucosal fold (eg: foals) | ||
Line 85: | Line 81: | ||
*Prevents dessication of the mucosal epithelium | *Prevents dessication of the mucosal epithelium | ||
*Contains antimicrobial substances | *Contains antimicrobial substances | ||
− | *Immunoglobulin - | + | *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 | *Lysosyme | ||
**Direct action on bacterial cell walls | **Direct action on bacterial cell walls | ||
Line 98: | Line 94: | ||
===Reflexes=== | ===Reflexes=== | ||
− | *Sneezing | + | ***Sneezing |
+ | ***Coughing | ||
==Pathology of the upper airways== | ==Pathology of the upper airways== | ||
− | + | *Developmental abnormalities | |
− | *Palatoschisis | + | **Palatoschisis |
− | *Nasal deviation | + | **Nasal deviation |
− | *All brachycephalic dog and cat breeds! | + | **All brachycephalic dog and cat breeds! |
− | **Esp. English Bulldogs - stenotic nares, wide/long soft palate, hypoplastic trachea | + | ***Esp. English Bulldogs - stenotic nares, wide/long soft palate, hypoplastic trachea |
− | + | *CIrculatory diseases | |
− | *Epistaxis | + | **Epistaxis |
− | **Haemorrhage from the nose | + | ***Haemorrhage from the nose |
− | **Causes | + | ***Causes |
− | ***Inflammation eg: ulcerative rhinitis | + | ****Inflammation eg: ulcerative rhinitis |
− | ***Neoplasia eg: infiltrating tumour, haemangioma | + | ****Neoplasia eg: infiltrating tumour, haemangioma |
− | ***Trauma | + | ****Trauma |
− | ***Clotting defects | + | ****Clotting defects |
− | **Horse: | + | ***Horse: |
− | ***Haemorrhagic nasal polyp | + | ****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. | + | *****'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. | + | *****Histology - multiple areas of acute to chronic haemorrhage within a fibrous tissue stroma. |
− | ***Exercise-induced pulmonary haemorrhage | + | ****Exercise-induced pulmonary haemorrhage |
− | + | *Inflammatory disease | |
− | + | **Inflammation in the URT can be classified on: | |
− | + | ***Location | |
− | *Inflammation in the URT can be classified on: | + | ****Nasal cavity - rhinitis |
− | **Location | + | ****Paranasal sinuses - sinusitis |
− | ***Nasal cavity - rhinitis | + | ****Guttural pouch and eustachian tube - eustachitis |
− | ***Paranasal sinuses - sinusitis | + | ****Pharynx - pharyngitis |
− | ***Guttural pouch and eustachian tube - eustachitis | ||
− | ***Pharynx - pharyngitis | ||
**Type | **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 | + | ***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) | ***Serous - transparent fluid exudate (acute inflammation) | ||
***Catarrhal - mucous exudation (acute to subacute inflammation) | ***Catarrhal - mucous exudation (acute to subacute inflammation) | ||
Line 145: | Line 140: | ||
***Irritant or allergens | ***Irritant or allergens | ||
***Neoplasia | ***Neoplasia | ||
− | + | ***Viral infections | |
− | + | ****Herpesviruses | |
− | *Bovine herpesvirus -1 | + | *****Bovine herpesvirus -1 |
− | **Causes Infectious bovine rhinotracheitis (IBR) | + | ******Causes Infectious bovine rhinotracheitis (IBR) |
− | **Highly infectious URT disease of cattle | + | ******Highly infectious URT disease of cattle |
− | **High morbidity, low mortality | + | ******High morbidity, low mortality |
− | **Aerosol transmission - requires close contact between animals | + | ******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 | + | ******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. | + | *******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. | + | *******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 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. | + | ******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 | + | ******Cause of abortion >5 months of gestation |
− | + | *****Cytomegaloviruses | |
− | + | ******Porcine cytomegalovirus | |
− | *Cytomegaloviruses | + | *******Causes Inclusion body rhinitis |
− | **Porcine cytomegalovirus | + | *******Disease of suckling piglets 1-5 wks of age |
− | ***Causes Inclusion body rhinitis | + | *******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) |
− | ****Disease of suckling piglets 1-5 wks of age | + | *******Morbitity high, mortality low |
− | ****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) | + | *******Histology: large basophilic intranuclear inclusion bodies in the nasal and sinus respiratory epithelium with lymphocytic infiltration of the mucosa. |
− | ****Morbitity high, mortality low | + | *******Can develop viraemic stage, with inclusions in other organs eg: renal tubular epithelium. Piglets can die during this phase. |
− | ****Histology: large basophilic intranuclear inclusion bodies in the nasal and sinus respiratory epithelium with lymphocytic infiltration of the mucosa. | + | *****Equine herpesvirus - 1, 4 |
− | ****Can develop viraemic stage, with inclusions in other organs eg: renal tubular epithelium. Piglets can die during this phase. | + | *****Feline herpesvirus -1 |
− | *Equine herpesvirus - 1, 4 | + | ******One of the causes of Feline viral rhinotracheitis |
− | *Feline herpesvirus -1 | + | ******Viruses and bacteria are involved in the complex. The most frequent aetiologic agent is FHV-1, and less frequently feline calicivirus and/or ''Chlamydophia psittac''i (NB: previously called Chlamydia psittaci var felis) |
− | **One of the causes of Feline viral rhinotracheitis | + | ******All three agents infect URT respiratory epithelium, although FHV-1 has the highest affinity for this epithelium |
− | ***Viruses and bacteria are involved in the complex. The most frequent aetiologic agent is FHV-1, and less frequently feline calicivirus and/or ''Chlamydophia | + | ******Feline calicivirus more frequently infects the oral mucosa -> ulcerative stomatitis |
− | ***All three agents infect URT respiratory epithelium, although FHV-1 has the highest affinity for this epithelium | + | ******C.psittaci more frequently infects the conjunctival epithelium -> chronic conjunctivitis |
− | ***Feline calicivirus more frequently infects the oral mucosa -> ulcerative stomatitis | + | ******Infection of the respiratory epithelium by FHV-1 results in a typical neutrophilic rhinitis with intraepitheial intranuclear eosinophilic inclusion bodies, with expected clinical signs |
− | ***C.psittaci more frequently infects the conjunctival epithelium -> chronic conjunctivitis | + | ******Resolution of clinical signs usually occurs by 7-14 days. |
− | ***Infection of the respiratory epithelium by FHV-1 results in a typical neutrophilic rhinitis with intraepitheial intranuclear eosinophilic inclusion bodies, with expected clinical signs | + | ******FHV-1 remains latent in the trigeminal ganglion, and can reactivate at times of stress. Can infect the cornea -> ulcerative keratitis. |
− | ***Resolution of clinical signs usually occurs by 7-14 days. | + | ******Occasional mortality in kitten or immunocompromised animals usually associated with secondary bacterial infection. |
− | ***FHV-1 remains latent in the trigeminal ganglion, and can reactivate at times of stress. Can infect the cornea -> ulcerative keratitis. | + | ***Bacterial infections |
− | ***Occasional mortality in kitten or immunocompromised animals usually associated with secondary bacterial infection. | + | ****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. |
− | **Atrophic rhinitis in pigs | + | *****Shortening and distortion of snout, secondary to nasal turbinate bone loss (histological evidence of osteolysis) |
− | **Pigs aged 4-12 weeks old show clinical signs | + | *****2 forms of the disease |
− | **Catarrhal nasal discharge (due to an acute rhinitis), sneezing, coughing, can progress to dyspnoea and anorexia. | + | ******'Progressive' atrophic rhinitis |
− | **Shortening and distortion of snout, secondary to nasal turbinate bone loss (histological evidence of osteolysis) | + | *******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) |
− | **2 forms of the disease | + | *******Turbinate bone atrophy is permanent and progressive |
− | ***'Progressive' atrophic rhinitis | + | ******'Non-progressive' atrophic rhinitis |
− | ****Due to infection of the nasal turbinates by P.multocida strains carrying the toxA gene that encodes for an osteolytic toxin. | + | *******Due to infection of the nasal turbinates by Bordatella bronchoseptica strains alone, that carry a gene that encodes for a dermonecrotic toxin. |
− | ****Turbinate bone atrophy is permanent and progressive | + | *******Turbinate bone can regenerate by the time of slaughter |
− | ***'Non-progressive' atrophic rhinitis | + | *****'Snuffles' in rabbits |
− | ****Due to infection of the nasal turbinates by | + | ******Most often P.multocida and/or B.bronchoseptica infection of the nasal mucosa |
− | ****Turbinate bone can regenerate by the time of slaughter | + | ******Clinical signs (nasal discharge, sneezing) result from an acute to chronic rhinitis. |
− | **'Snuffles' in rabbits | + | ****Streptococcus equi |
− | ****Most often | + | *****Streptococcus equi subsp. equi |
− | ****Clinical signs (nasal discharge, sneezing) result from an acute to chronic rhinitis. | + | *****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 | |
− | ***Cause of 'Strangles' in horses | + | *****Bacteraemia with abscess formation in other organs (eg: liver, kidneys) - Bastard Strangles! |
− | ***Infection with | + | ****Streptococcus equi subsp. zooepidemicus |
− | ***Organism remains viable in environment for months | + | *****Can infect the respiratory tract (nasal cavity, paranasal sinuses, trachea and bronchi/bronchioles) |
− | ***Possibility of other sources of infection - in pharynx of in-contact dogs? | + | **URT infection can be indistinguishable clinically from Strangles, but does not cause suppurative lymphadenitis (cf: S.equi subsp. equi) |
− | ***Colonisation of nasopharynx causing: | + | **Fungal infections |
− | ***Chronic purulent rhinitis, sinusitis, eustachitis | + | **Filamentous fungal organisms |
− | ***Can progress to development of nodular masses in the guttural pouch consisting of inspissated pus and viable bacteria (guttural pouch empyema) - 'carrier' state | + | **Aspergillus fumigatus |
− | ***Regional suppurative lymphadenitis - can rupture onto skin of neck | + | **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! |
− | ***Bacteraemia with abscess formation in other organs (eg: liver, kidneys) - Bastard Strangles! | + | **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. |
− | ***Can infect the respiratory tract (nasal cavity, paranasal sinuses, trachea and bronchi/bronchioles) | + | **Yeast-like fungal organisms |
− | + | **Cryptococcus neoformans | |
− | + | **Most commonly in cats and dogs | |
− | + | **Chronic granulomatous rhinitis | |
− | *Filamentous fungal organisms | + | **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' |
− | *Yeast-like fungal organisms | ||
− | ** | ||
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Revision as of 21:20, 29 November 2006
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
- Poor communication of frontal sinus in cats with nasal cavity
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)
- Mycotic infections eg: Aspergillus fumigatus
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
- Cilia beat in a caudal direction in nasal cavity
- Cilia beat in a 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
- Traps 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
- Haemorrhagic nasal polyp
- Epistaxis
- 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
- Location
- 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
- Causes 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
- Causes 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.
- Porcine cytomegalovirus
- Equine herpesvirus - 1, 4
- Feline herpesvirus -1
- One of the causes of 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.
- Bovine herpesvirus -1
- Herpesviruses
- 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
- 'Progressive' atrophic rhinitis
- '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)
- Pasturella multocida
- 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'
- Inflammation in the URT can be classified on: