Structural Diseases
Stenotic Nares and Brachycephalic Syndrome
Pathophysiology
Brachycephalic airway syndrome (BAS) is a congenital disorder resulting from primary conformational defects (stenotic nares or an elongated soft palate), which obstruct flow of air through the upper airways. Increased flow and pressure effects on the soft tissue structures of the larynx result in inflammation that leads to secondary findings of everted laryngeal saccules, thickening of the soft palate, and in the final stages, laryngeal collapse. In the bulldog, tracheal hypoplasia may be encountered as an additional component of BAS. BAS results from shortening of the nasal cavity and in some dogs (particularly Pugs) it can be accompanied by caudal protrusion of nasal turbinates into the nasopharynx (Figure 4.1), resulting in further obstruction of nasal airflow (Ginn et al. 2008).
History and signalment
Brachycephalic syndrome is common in bulldogs (English and French), Pugs, and Boston Terriers, and is also seen in Himalayan and Persian cats (Figure 4.2). Clinical signs include stertor, snoring or snuffling, gagging, exercise intolerance, respiratory difficulty, and collapse. Some dogs (particularly bulldogs) have vomiting or regurgitation due to concurrent gastroesophageal disease caused by reflux, inflammation, or an esophageal diverticulum (Poncet et al. 2005). Animals can be very young or aged (6 weeks to 14 years of age) when clinical signs require evaluation and correction.
Figure 4.1. Retroflex view of the choanae in a pug shows hyperemic and swollen turbinates that are bulging into the nasopharynx and contributing to upper airway obstruction.
Physical examination
Stenotic nares can be visualized on physical examination and must be compared to breed standards. Audible stertor is due to turbulent airflow through the nasal cavity, past everted saccules, or past an elongated soft palate. Stertor is often evident on inspiration and expiration. If laryngeal collapse is presence, stridor may be detected on inspiration with auscultation of the larynx. In dogs with tracheal hypoplasia, high-pitched inspiratory wheezes can sometimes be auscultated over the trachea. The remainder of the physical examination is usually within normal limits, although obesity often worsens the clinical presentation.
Figure 4.2. Stenotic nares in a brachycephalic cat.
Diagnostic findings
Cervical and thoracic radiographs are useful for subjective evaluation of the length and thickness of the soft palate and to assess tracheal size when tracheal hypoplasia is suspected. Two methods have been reported to evaluate tracheal size. One compares tracheal lumen diameter in the thoracic region to the third rib. A normal dimension is >3.0 (Suter 1984). In the second method, tracheal lumen diameter at the thoracic inlet is compared to the height of the thoracic inlet. The normal ratio in the bulldog is >0.127, in the non-bulldog brachycephalic is >0.160, and in the normal dog is >0.204 (Harvey and Fink 1982).
Documentation of soft palate elongation and assessment of laryngeal structures requires sedation for direct visualization, and because of anesthetic concerns with brachycephalic breeds, surgical correction should be planned at the time the diagnosis is confirmed. Normally, the soft palate should extend only 1–2 mm caudal to the tip of the epiglottis. In some cases, rostral retraction of the soft palate is required to assess the extent of elongation. Eversion of laryngeal saccules can be visualized as rounded and bulging soft tissue structures emerging from the ventral portion of the laryngeal aditus, just lateral to the vocal folds (Figure 4.3). Laryngeal collapse can be recognized as medial displacement of the arytenoid cartilages, possibly due to chronic weakening of the laryngeal abductor muscles or to some degree of chondromalacia (Figure 4.3). This condition must be distinguished from laryngeal paralysis, a disorder in which arytenoid cartilages do not abduct on inspiration but are normally positioned. Laryngeal collapse is designated grade 2 when the cuneiform processes are involved and grade 3 when the corniculate processes are collapsed. (Eversion of the laryngeal saccules is sometimes referred to as grade 1 laryngeal collapse.) If a flexible endoscope is available, a retroflex examination of the nasopharynx should be performed to document the presence of nasopharyngeal turbinates as these can lead to continued obstructed breathing following surgical correction of other lesions.
Figure 4.3. This laryngoscopic image is from a 9-year-old FS Cavalier King Charles Spaniel presented for chronic panting and syncope. Everted and edematous laryngeal saccules are evident ventrally in the image. Dorsal to the laryngeal aditus, the corniculate processes of the arytenoid are folding across midline, indicative of grade 3 laryngeal collapse.
Treatment
Weight reduction is essential to reduce the work of breathing in animals with brachycephalic syndrome, and when possible, this should be achieved prior to surgery to reduce complications associated with anesthesia. Stenotic nares and elongated soft palate are amenable to surgical resection with a scalpel or CO2 laser via wedge resection and staphylectomy, respectively. Excessive shortening of the soft palate is generally not recommended because this can result in nasal regurgitation, although some surgeons believe it is an appropriate technique. In some cases, saccular eversion will resolve when airflow has improved; however, in some dogs, chronic protrusion of the saccules results in irreversible hyperplasia that requires resection. Some surgeons elect to remove a single saccule initially to avoid mucosal apposition during the healing phase that could result in laryngeal stenosis. Others remove both saccules and place a temporary tracheostomy tube in case upper airway swelling results in obstruction. Currently, no specific treatment is available for laryngeal collapse, and the success of unilateral lateralization is relatively low. For dogs with severe stridor or respiratory distress, a permanent tracheostomy should be considered if weight loss and surgical correction of other lesions fail to alleviate respiratory difficulty. More aggressive therapy for brachycephalic syndrome includes laser resection of internal nasal turbinates.
The age at which this surgery should optimally be performed is unknown; however, it would seem wise to correct conformational disorders early in life to prevent development of secondary obstructive disease.
Prognosis
Surgical resection of upper airway obstruction is associated with an excellent outcome in the vast majority of cases. Perioperative mortality is low and postoperative complications of regurgitation or nasal discharge are generally mild. Dehiscence of the palatal repair is the most serious event encountered but occurs rarely. Animals that have concurrent gastroesophageal signs often have resolution or abolition of gastrointestinal signs following surgery (Poncet et al. 2006), although some may require continual use of prokinetic and acid reducing drugs.
Nasal Foreign Body
History and signalment
Foreign material can be aspirated directly into the nasal cavity through the nares or may lodge in the nasopharynx when the animal retches material from the oral cavity into the region above the palate. Animals with a nasal foreign body usually present with an acute onset of paroxysmal sneezing or reverse sneezing, nasal discharge, epistaxis, and pawing or rubbing at the face, although chronic signs can also be seen. Foreign bodies that are firmly lodged in the nasal cavity or in the nasopharynx can also result in chronic nasal discharge or halitosis.
Physical examination
Affected animals usually display unilateral mucopurulent or serosanguineous nasal discharge, and nasal airflow is preserved. In chronic cases, or if secondary nasal aspergillosis results, regional lymph node enlargement can be found.
Diagnosis and treatment
Animals are fully anesthetized for evaluation of the nasal cavity. Radiographs are usually recommended prior to examination of the nasal cavity to help guide removal of a radiodense foreign body; however, organic objects are usually not visible radiographically. In more chronic cases, secondary changes of increased fluid density or bony lysis can help locate the site of the foreign material.
Whenever possible, the caudal nasopharynx should be examined for a foreign body as well as both nasal cavities. If a flexible endoscope is not available, copious antegrade and retrograde flush of the nasal cavity can dislodge a foreign body (see Chapter 2). If the nasal cavity cannot be fully visualized with available equipment, gentle probing and retraction of alligator forceps can be successful in retrieving a foreign body. In rare instances an exploratory rhinotomy may be required. This is most likely when a large smooth foreign body (such as a stone) cannot be removed endoscopically. After foreign body retrieval, a broad-spectrum antibiotic is usually administered for 7 days to treat secondary infection.
Prognosis
In some cases, a foreign body can cause permanent damage to the nasal structures that allows development of secondary fungal rhinitis or results in chronic nasal discharge associated with alterations in turbinates and mucus production. In these cases, intermittent antibiotic therapy may be required to control clinical signs.
Tooth Root Abscess or Oronasal Fistula
History and signalment
Dental-related nasal disease usually affects the carnassial or canine tooth in older animals and results in unilateral mucopurulent to hemorrhagic nasal discharge. The animal may display difficulty or pain while eating or opening the mouth. Anorexia, drooling, and halitosis can be reported.
Physical examination
Unilateral nasal discharge should raise the suspicion of dental-related disease; however, it is important to note that the dental or gingival disease may not be obvious without an examination under anesthesia. Nasal airflow is preserved in animals with dental-related nasal disease. Oral or facial pain or swelling and regional lymphadenopathy can be found in some cases. With a carnassial tooth abscess, an expanding facial swelling may develop immediately below the eye on the affected side.
Diagnostic findings
Skull or dental radiographs highlighting the affected area can reveal bony loss surrounding a tooth root or a retained tooth root. In cases with chronic dental disease, destruction of turbinates can be seen on radiographs, computed tomography (CT), or rhinoscopy. Use of a periodontal probe to detect deep (>1 mm in the cat and >1–3 mm in the dog) periodontal pockets can identify occult tooth root disease.
Treatment
Effective treatment requires removal of the tooth and all roots. In some instances, bony curettage may be required or surgical debridement and closure of a fistula. A 7–10-day course of antibiotics (with a potentiated penicillin or clindamycin) is often used to treat secondary infection.
Prognosis
Generally nasal discharge resolves with tooth removal; however, as with a foreign body, alterations in turbinate structures can result in continued mucus production. Sequestration of a tooth root or a devitalized bony fragment must be ruled out in such cases.
Nasopharyngeal Stenosis
Pathophysiology
The opening to the caudal nasopharynx in dogs and cats is normally 1–2 cm across and can be greatly reduced or obliterated by a web of scar tissue. Nasopharyngeal stenosis (NPS) is thought to occur either as a congenital lesion in which the caudal opening of the choanae is malformed, or as an acquired lesion resulting from chronic inflammation in the caudal aspect of the nasal cavity that forms a cicatrix. Inflammation may result from chronic upper respiratory tract disease or from regurgitation of esophageal or gastric contents into the nasopharynx. The scar may be unilateral or extend across the entire choanae (Figure 4.4).
History and signalment
The predominant clinical feature of this disorder is obstruction of airflow through the nasal cavity. Stertorous respiration or snoring sounds are commonly reported. In some cases, this condition is preceded or accompanied by nasal discharge. When the deformation or scar is bilateral or circumferential, the animal will display mouth breathing because of an inability to breathe through the nose. It is usually nonprogressive and not associated with systemic disease, although inappetance has been reported in some cats.
Physical examination
The primary recognizable exam feature is a loud upper respiratory noise that may be stertorous (snoring) or stridorous. Respiratory difficulty is present on inspiration and there is a lack of nasal airflow that depends on the degree of stenosis. Respiratory distress occurs when the mouth is closed and nasal breathing is required.
Figure 4.4. Retroflex view of the choanae in a 17-year-old FS DSH presented for an 8-year history of difficulty breathing. In this case, stenosis of the nasopharynx reduces the diameter to less than a millimeter.
Diagnostic findings
Primary differential diagnoses include nasal obstruction due to neoplasia, a nasopharyngeal polyp, cryptococcosis (in the dog or cat), or aspergillosis (in the cat). NPS is most easily diagnosed using a flexible endoscope to obtain a view of the nasopharynx. Alternately, the obstruction can be appreciated by passing a 3–8-French catheter caudally through the ventral meatus into the oropharyngeal region. In the normal animal, this should pass easily into the pharynx; however, a stenosed region will block passage of the catheter. Tissue malformation in the choanal region can often be visualized on CT with sagittal reconstruction of the image.
Treatment
Treatment of this obstructive breathing disorder can be achieved by balloon dilation of the region under fluoroscopy or endoscopy, although several episodes may be required. Stent placement has also been successful in alleviating the obstruction (Berent et al. 2008). The membrane is too thick to be broken down manually or with a standard catheter. If surgery is contemplated, the approach to the caudal nasopharynx is through a midline incision in the soft palate. Iris scissors can be used to excise the nasopharyngeal membrane.
Prognosis
NPS represents a benign lesion; however, some owners report loss of appetite or lethargy related to nasal obstruction. In cats with concurrent rhinitis, it is unclear whether the presence of stenosis impacts clinical response to therapy.
Infectious Diseases
Acute Feline Upper Respiratory Tract Disease
Pathophysiology
The organisms most commonly implicated in infectious upper respiratory tract disease in kittens include feline herpes-virus 1 (FHV-1), feline calicivirus (FCV), Chlamydophila felis, Mycoplasma, and Bordetella. Other viruses may also be involved. Infection occurs via inhalation or via contact with mucosal membranes of the nose or ocular surface. Viral infection of the epithelial cells results in cell death and predisposes the respiratory tract to bacterial infection. However, the bacteria involved can also act as primary respiratory pathogens, and infection with bacteria alone can result in substantial clinical disease. Chlamydophila felis results in systemic infection although clinical signs may be manifest in the conjunctiva alone.
Viral infection is usually self-limiting with resolution of disease within 7–10 days. Viral shedding occurs within 1–3 days of infection and persists for up to 3 weeks, providing a constant source of virus in the environment. Both FHV-1 and FCV persist in the cat population as a carrier state and viral shedding can be reactivated during stressful periods. A virulent form of FCV has been associated with outbreaks of ulcerative lesions around the face, facial and forelimb edema, and fatal pneumonia with mortality rates of ~40% (Hurley et al. 2004).
History and signalment
Young kittens (2 weeks to 4 months old) are affected most commonly although older kittens and cats can develop signs of acute upper respiratory tract disease when exposed to high concentrations of pathogens in a shelter environment. Older cats are more severely affected by the virulent form of FCV, and any age cat may develop Chlamydophila conjunctivitis.
Physical examination
Sneezing and serous to mucoid oculo-nasal discharge are the classic findings in acute feline upper respiratory tract disease (FURTD). Fever and systemic signs of illness (lethargy and anorexia) are commonly seen. FHV-1 has a predilection for ocular infection, and conjunctival hyperemia and corneal disease are common. Tracheitis is also reported secondary to FHV-1 infection but signs are rarely observed clinically. FCV can cause lingual ulcers and pneumonia, while Chlamydophila is most likely to cause severe chemosis, which can be unilateral or bilateral.
Diagnostic findings
In general, FURTD is a clinical diagnosis. Testing is available through culture or polymerase chain reaction for FHV-1; however, the presence of virus does not correlate with disease (Maggs et al. 1999). The presence of FCV can be confirmed through virus isolation or reverse transcriptase PCR for the RNA virus, although positive tests are expected in chronic shedders, making it difficult to correlate the test result with disease activity. The virulent form of FCV is diagnosed based on clinical signs and physical examination.
Bacterial culture may be helpful in determining appropriate antibiotic therapy for Mycoplasma or Bordetella; however, this is rarely performed in the setting of acute upper respiratory tract disease. Diagnostic tests including virus isolation, bacterial culture, and PCR should be used in disease outbreaks that are associated with high morbidity or mortality to identify potential infecting organisms and institute appropriate control measures. These tests have also proven useful in providing details on the spread of organisms within confined populations. In a shelter study, shedding of FHV-1 was shown to increase from 4 to 52% after 1 week (Pedersen et al. 2004).
Treatment
Supportive care will aid in resolution of signs related to viral infection. The eyes and nose should be kept clear of exudate, hydration and adequate nutrition should be ensured, and animals should be kept in a warm environment. Steam inhalation to humidify inhaled air and use of lubricating eye ointment to manage virally mediated keratoconjunctivitis sicca can also improve overall health. Systemic antibiotic therapy is directed at control of secondary bacterial infection, and most antibiotics are efficacious, including amoxicillin–clavulanate and pradofloxacin, although if infection by Mycoplasma is documented, a quinolone or tetracycline drug would be recommended. Treatment of Chlamydophila requires at 4–6 weeks of therapy with doxycycline at 10 mg/kg/day.
Lysine has been recommended to reduce viral replication and decrease clinical signs associated with FHV-1 infection. However, dietary supplementation did not prove efficacious in a natural disease setting, (Maggs et al. 2007) and bolus administration of 250–500 mg PO BID is required to reduce viral replication.
A novel antiviral therapy for FCV that blocks virus synthesis by molecular interference with the initiation of translation was recently shown to reduce the severity of oral ulcers and reduce FCV shedding in an outbreak situation (Smith et al. 2008). Treatment also reduced mortality in an outbreak of virulent FCV, suggesting that this therapy could show promise in management of severe viral disease.
Prognosis
Most kittens survive an episode of acute upper respiratory infection. It is unclear whether severe infection at an early age plays a role in development of chronic rhinosinusitis. When disease is observed in a shelter or cattery situation, implementation of control measures with improved hygiene is needed. FHV-1 is labile in the environment and is readily killed by bleach or detergent; however, FCV can persist for up to 1 month and is more resistant to standard cleaning methods. Aerosolization is the prime method of infection, and isolation of sneezing or coughing cats can help limit spread. However, fomites can also spread disease, and general infection control should be stressed. Vaccination against upper respiratory viruses (FHV-1 and FCV) reduces clinical signs and may help limit spread of disease.
Cryptococcosis
Pathophysiology
Cryptococcus is a dimorphic fungus that exists in the yeast form in the animal. Various species enjoy a specific geographic distribution with Cryptococcus neoformans var. grubii found in bird guano worldwide, C. neoformans var. neoformans found primarily in bird guano in Europe, and Cryptococcus gattii localized primarily in Eucalyptus trees in Australia and numerous trees in Vancouver, Canada. Disease is thought to be spread primarily through inhalation with initial infection in the nasal cavity and subsequent spread to the nasopharynx or central nervous system, although direct inoculation causing skin infection may also occur.
History and signalment
Cryptococcal infection has been reported in all ages of animals, although young adults appear to be affected most often. Disease is reported much more commonly in cats than in dogs, with Siamese and Abyssinian cats overrepresented. Respiratory complaints include facial distortion, sneezing, chronic mucopurulent nasal discharge, and stertor. Lower respiratory infection occurs much less commonly, but signs of pneumonia may be present. Nonrespiratory complaints include nonhealing craterous skin lesions, blindness due to retinal detachment or optic neuritis, and central nervous system signs such as circling, seizures, ataxia, or vestibular disease.
Physical examination
The classic finding for nasal cryptococcosis is firm swelling along the dorsum of the nose. It can be central or unilateral, at the bridge of the nose or on the tip. In some cases, a mass can be seen protruding from the nose (Figure 4.5). Regional lymphadenopathy is not uncommon. In cases with lower respiratory tract disease, tachypnea may be noted and abnormal lung sounds may be found because of lobar consolidation. In some animals, ulcerated and craterous skin lesions are evident. Every cat suspected of cryptococcosis should have a thorough fundic examination to look for chorioretinitis. This inflammatory condition of the choroid and retina can appear as a hyporeflective, round to geographic, white to gray, sometimes raised fluffy lesion when active, or as a dark circular region on the retina when the lesion has scarred or healed.
Figure 4.5. This fleshy soft tissue mass protruding from the left naris was diagnosed as a cryptococcal granuloma.
Figure 4.6. Cytology of an impression smear from a nasal mass in a cat. Wright’s stain has been applied and reveals multiple 3–8 µm round organisms surrounded by a clear capsule ranging in size from 10 to 30 µm. Fungal culture was positive for C. gattii.
Diagnostic findings
Diagnosis involves identification of a fungal organism (5–8 µm in size) with a clear polysaccharide coat (~30 µm in diameter) in cytology of exudate, aspirates, impression smears, or a squash preparation of a biopsy specimen (Figure 4.6). Wright’s stain, Diff Quik, or iodine can be used. Because the fungal organism is so characteristic, cytologic examination of nasal smears from cats with chronic nasal discharge is warranted for quick differentiation of a fungal infection from other causes of nasal discharge, although nonencapsulated forms of Cryptococcus may confuse the diagnosis. Serology is recommended by using the latex capsular agglutination titer (LCAT), which offers a sensitive and specific method for diagnosis by detecting the cryptococcal antigen. A titer greater than 1:1 is positive, and the magnitude of the LCAT can be used to follow response to therapy.
Occasionally a fungal culture will be positive for Cryptococcus in the absence of clinical disease due to colonization of the nasal cavity without infection; however, in animals with signs consistent with disease, culture for cryptococcosis is recommended to determine the serotype of the organism involved. This will help establish the epidemiology of infection and can define the manifestations of disease and response to therapy for different strains. Depending on the clinical presentation and physical examination findings, chest radiographs or abdominal ultrasound should be performed to stage the disease. A complete blood count, chemistry profile, and urinalysis are performed to assess the general health of the animal and retroviral testing should be performed in the cat. Concurrent immunosuppressive disease due to FeLV may be associated with a worse prognosis for cure or control of disease, and FIV-infected cats may require longer duration of treatment.
Treatment
Cryptococcosis is typically treated with oral azole therapy, and prolonged therapy (4–12 months) should be anticipated (see Chapter 3). Itraconazole (50–100 mg/cat/day) is reportedly efficacious in approximately 50% cases of nasal cryptococcosis (Medleau et al. 1995) while fluconazole at a dose of 25–100 mg/cat PO BID resulted in cure of nasal cryptococcosis in 97% of cats, despite disseminated disease or concurrent FIV infection in up to 28% of cases (Malik et al. 1992). Duration of treatment required to achieve control of disease with fluconazole was significantly shorter than with itraconazole (4 versus 9 months) (O’Brien et al. 2006). Fluconazole is preferred if ocular involvement is documented because of better penetration of the blood ocular barrier, and if central nervous system involvement is suspected or confirmed based on physical examination, clinical signs, brain imaging, or CSF tap, fluconazole is used in combination with flucytosine because of improved efficacy in penetrating the blood–brain barrier. Posaconazole and voriconazole may also prove useful in management of cryptococcosis.
Terbinafine, a synthetic allylamine, can be employed in cats that do not respond appropriately to azole therapy or those that develop side effects while treated with azoles. It may be used alone or in combination with an azole.
Fungicidal treatment is needed in cases with severe cryptococcocis, and amphotericin B has proven effective in inducing remission. Subcutaneous administration of amphotericin B should be considered in animals that cannot tolerate oral medications. Nephrotoxicity is limited with this mode of administration, although cure of cryptococcosis can require a cumulative dose over 20 mg/kg (Malik et al. 1996).
Prognosis
The latex agglutination titer can be used to follow the course of disease and response to treatment. A twofold reduction in antigen titer per month is desired, although titers can be rechecked every 2–3 months rather than monthly. Treatment for cryptococcosis is continued until the latex agglutination titer to capsular antigen is >1:1. Cats with intranasal cryptococcosis have a slightly lower percentage of resolution of disease than those with cutaneous signs only, and central nervous system infection is the least responsive. Cats that fail to show a reduction in antigen titer over several months are less likely to achieve resolution of disease and may be resistant to the antifungal drug in use. In these cases, culture and susceptibility testing should be considered. Recurrence of cryptococcosis may occur months to years after apparent cure, and a relapse rate of 17% has been reported (O’Brien et al. 2006).
Canine Nasal Aspergillosis
Pathophysiology
Aspergillus is a branching septate mold that is ubiquitous in the environment. Nasal aspergillosis can result from infection with several different Aspergillus species, although infection with Aspergillus fumigatus is most common. Nasal aspergillosis occurs as a primary infection in healthy dogs, but the fungus can also colonize the nasal cavity and/or frontal sinuses following trauma, inhalation of a foreign body, or in conjunction with a neoplastic process. Aspergillus results in mucosal infection of the nasal cavity and/or sinuses with formation of fungal granulomas or plaque lesions. Toxins produced by the fungus and the local inflammatory response are likely responsible for the severe destruction and collapse of turbinates that occurs with infection. The nasal mucosa responds to infection by upregulation of proinflammatory cytokines (IL-6, IL-12, IL-18, and TNF-α) as well as the immunomodulatory cytokine IL-10, which may reduce tissue injury but also limit the host’s ability to clear the organism from the nose (Peeters et al. 2006).
History and signalment
Nasal aspergillosis is most commonly encountered in young to middle-aged dolicocephalic dogs. Animals tend to have a long-standing history (4–6 months) of purulent or hemorrhagic nasal discharge and sneezing. Dogs may become head-shy or exhibit pain. Recognition of neurologic signs such as seizures or obtundation suggests fungal invasion of the central nervous system through the cribriform plate.
Physical examination
Nasal discharge is commonly unilateral but can become bilateral with time when disease erodes through the septum. Dogs typically have preservation of nasal airflow because of marked turbinate destruction. Depigmentation of the nares with or without ulceration is found in approximately 40% of canine cases. Some dogs display marked facial or skull pain on palpation. Ipsilateral lymphadenopathy is found occasionally due to a reactive lymph node response; however, affected animals remain systemically healthy.
Diagnostic findings
A minimum database is typically unremarkable but may show evidence of chronic infection, with neutrophilia, monocytosis, and hyperglobinemia. An agar gel immunodiffusion test (AGID) using an Aspergillus antigen prepared from cultures of A. fumigatus, A. niger, and A. flavus has proven useful in confirming the clinical suspicion of aspergillosis in dogs. Positive AGID for Aspergillus spp. was highly suggestive of nasal aspergillosis in one study, with a positive predictive value of 94%; however, false-negative results were found in almost one-third of cases (Pomrantz et al. 2007).
In a recent study on cytologic diagnosis of aspergillosis, direct smear of nasal discharge or swab revealed fungal hyphae in a minority (<20%) of cases (De Lorenzi et al. 2006). Cytology of a swab or biopsy sample collected endoscopically was more likely (>90%) to demonstrate fungal spores. A recent study on the utility of fungal cultures in the diagnosis of canine nasal aspergillosis reported moderate sensitivity (77%) but high specificity (100%) (Pomrantz et al. 2007). It is important to note that in that study, the material submitted for culture was from a visualized fungal plaque and therefore, a low number of false-positive values would be expected. Fungal culture of nasal discharge has been associated with much lower sensitivity and specificity and is not recommended.
More definitive diagnosis and disease staging is obtained by finding the characteristic imaging findings with radiography or CT scan and with rhinoscopic detection of plaque lesions. Skull radiographs show variable degrees of turbinate lysis (unilateral or bilateral) and increased radiolucency (Figure 4.7). The majority of dogs (75% or more) have sinus involvement, and a frontal view of the skull should be included in the radiographic examination to look for a fungal granuloma in the sinus (Figure 4.7). In some cases, this might be the only location in which the granuloma can be identified (Johnson et al. 2006). CT scan is preferred for evaluation of dogs suspected of nasal aspergillosis. CT scans typically reveal unilateral loss of turbinate structures and may show granulomatous fungal lesions, particularly in the frontal sinus (Figure 4.8). The integrity of the cribriform plate can also be assessed, which aids in making the decision to use topical antifungal therapy (Figure 4.8). Dogs with destruction of the cribriform plate are more susceptible to central nervous system complications from edema or inflammation that results from contact of the vehicle and antifungal medication with the meninges.
Figure 4.7. Open mouth view (a) of the nasal cavity in a 2-year-old MC Golden Retriever presented for left-sided nasal discharge. Asymmetry is evident with lucency noted intranasally on the left side. An amorphous soft tissue density can be appreciated caudally. Turbinate structures on the right appear within normal limits. Frontal sinus image (b) of the same dog reveals a heterogeneous soft tissue density within the left frontal sinus. Sinuscopic examination and histopathology confirmed a fungal granuloma within the sinus.
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