A 2-year-old 38.9-kg (85.58-lb) sexually intact male German Shepherd Dog was referred to the Veterinary Teaching Hospital at the University of Georgia because of a 4-month history of slowly progressive nasal swelling and nasal mucosa congestion. Beginning 1 month prior to the initial evaluation, the dog was incapable of breathing through its nostrils and frequently panted and sneezed. Despite treatment with antimicrobials (clindamycin and enrofloxacin) for 4 weeks prior to this initial evaluation, no improvement was observed. The owners had also noticed decreased appetite, but there was no obvious weight loss. The dog lived primarily outdoors and had never traveled outside the state of Georgia; its vaccination status was current, and it was regularly dewormed. No other previous health problems were known.
On physical examination, the dog was bright, alert, and responsive and excessive panting was evident. Rectal temperature was within reference limits. The dog's heart rhythm was regular (rate, 140 beats/min), although dyspnea, characterized by a loud stertorous breathing, prevented ideal auscultation of the lungs and heart. No nasal discharge was present at this time. The right and left mandibular lymph nodes were approximately 1.5 cm and 1 cm in diameter, respectively. The dorsal aspect of the nose was severely swollen, hard, and firm on palpation. The right side was more affected than the left. The mucous membranes in both nostrils were hyperemic, and severe tissue swelling was evident. The other findings of the physical examination were unremarkable.
The dog was hospitalized (day 1) for further examinations. Initial diagnostic tests included a CBC, serum biochemical analyses, urinalysis, and thoracic radiography. Results of the CBC included marked leukocytosis (26.8 × 103 WBCs/PL; reference range, 5.1 × 103 WBCs/PL to 13 × 103 WBCs/PL) with neutrophilia but no bands (18.22 × 103 neutrophils/PL; reference range, 2.9 × 103 neutrophils/PL to 12 × 103 neutrophils/PL), lymphocytosis (3.21 × 103 lymphocytes/ PL; reference range, 0.4 × 103 lymphocytes/PL to 2.9 × 103 lymphocytes/PL), monocytosis (2.14 × 103 monocytes/PL; reference range, 0.1 × 103 monocytes/PL to 1.3 × 103 monocytes/PL), and eosinophilia (3.21 × 103 eosinophils/PL; reference range, 0 to 1.3 × 103 eosinophils/PL); Hct was 44.3% (reference range, 35% to 57%). Mild thrombocytopenia (196 × 103 platelets/PL; reference range, 211 × 103 platelets/PL to 621 × 103 platelets/PL) was detected, but the platelet estimate on the blood smear was considered normal. No serum biochemical abnormalities were identified. Urinalysis revealed a urine specific gravity of 1.050, 1+ protein, and 2+ bilirubin.
No abnormalities were detected via thoracic radiography. A fine-needle aspirate specimen was collected from the right mandibular lymph node. Cytologic examination of the specimen revealed that the nucleated cells were mostly a mixture of small-, medium-, and large-sized lymphocytes with small lymphocytes predominating. Plasma cells were common. Low numbers of nondegenerated neutrophils, macrophages, and eosinophils and rare mast cells were observed. Microorganisms were not detected. Findings were compatible with lymphadenitis.
On day 2 of hospitalization, the dog was anesthetized and a nasal CT examination and rhinoscopy were performed. Results of a coagulation profile (assessments of prothrombin time, activated partial thromboplastin time, and thrombin time) and evaluation of buccal mucosal bleeding time performed prior to anticipated biopsy procedures were within reference limits.
Helical CTa images of the skull from the most rostral aspect of the nose to the most caudal aspect of the frontal sinuses were obtained with reconstructed 2.5-mm slices acquired before and after IV administration of 60 mL of contrast medium (iothalamate sodiumb). Poorly enhanced, hyperattenuated material was present bilaterally within the nasal cavity, from the alar fold to approximately the level of the second premolar teeth. There was also evidence of osteolysis of the horizontal part of the palatine bone and of the nasal and incisive bones. The remainder of the caudal aspect of the nasal cavity was unremarkable until the level of the cribriform plate of the ethmoid bone, where uniformly enhancing hyperattenuating material was observed in the right side, extending dorsally to the medial compartment of the frontal sinus and caudally to the right olfactory bulb of the brain with lysis of the internal surface of the right frontal bone (Figure 1). A small soft tissue density growth was present within the nasopharynx. There was no evidence of a foreign body. The findings were suggestive of a chronic inflammatory condition (eg, fungal infection or plasmacytic-lymphocytic inflammation) or, less likely, neoplasia. Rhinoscopy was performed by use of a 2.9-mm rigid cystoscopec and revealed bilaterally edematous, inflamed, and friable nasal mucosa (Figure 2). No fungal colonies were visible. Endoscopy of the nasopharynx was performed by use of a 6.0-mm flexible bronchoscope.d A soft tissue mass (approx 2 × 3 cm) with a hyperemic and slightly irregular surface was identified in the ventral region of the nasopharynx. These findings were consistent with severe rhinitis and nasopharyngitis. Multiple biopsy samples were obtained from both nasal passages and from the mass in the nasopharynx; specimens were submitted for histologic examination and fungal culture.
Because CT revealed contrast medium enhancement of the olfactory bulb, a CSF sample was obtained to investigate the possibility of CNS dissemination of the underlying disease. Clear and colorless CSF was obtained via cisternal puncture. Results of a Pandy test performed on the fluid sample were negative; further analysis revealed protein concentration of 17.4 mg/dL (reference range, 13 to 35 mg/dL), 4 WBCs/PL (reference range, 0 to 5 WBCs/PL), and 2,073 RBCs/PL (reference range, 0 to 30 RBCs/PL). Cytologic evaluation of the CSF revealed a moderate degree of blood contamination. No erythrophagocytosis or organisms (free or phagocytized) were observed. The WBCs were predominately neutrophils with a few monocytes and lymphocytes. This was interpreted as normal CSF with blood contamination. Unfortunately, no fungal culture or PCR analysis of the collected CSF was performed. A neurologic examination of the dog was undertaken on day 3 of hospitalization; results were considered normal.
Histopathologic findings for the tissues collected from the right nasal cavity and nasopharynx were similar. The lamina propria and submucosa were expanded by multifocal to coalescing granulomas of epithelioid macrophages that often had a central collection of neutrophils. Granulomas were surrounded by lymphocytes, plasma cells, and neutrophils. In the center of some granulomas and surrounded by neutrophils were 1 to several spherical yeast forms with lightly basophilic cytoplasm and a thick, double-contoured wall. The organisms stained with periodic acid–Schiff and Gomori methenamine silver stains and were compatible with Blastomyces dermatitidis. The histopathologic diagnosis was granulomatous to pyogranulomatous rhinitis and nasopharyngitis with intralesional Blastomyces-like yeast. There was a light growth (2 colonies) of B dermatitidis from tissue submitted for fungal culture.e A test for Blastomyces antigen (ELISA) in serum and urine or further PCR analysis of the biopsy specimens was not performed because results of histologic examination and fungal culture were indicative of blastomycosis. A diagnosis of nasal and nasopharyngeal blastomycosis was established, and oral administration of itraconazolef (5 mg/kg [2.27 mg/lb], q 12 h for 5 days and then q 24 h) was initiated.
Follow-up examinations were performed every month to reassess the swelling of the nose and to check for adverse effects of the antifungal treatment (eg, anorexia or hepatotoxicosis). The dog responded well to itraconazole administration. After 2 months, the nasal congestion was less severe and the external nasal swelling had substantially decreased to a small lump. A CBC revealed mild leukocytosis (17.4 × 103 WBCs/PL) with neutrophilia (13 × 103 neutrophils/PL) and monocytosis (1.6 × 103 monocytes/PL). The neutrophilia and monocytosis were attributed to ongoing inflammation. No abnormalities were detected via serum biochemical analyses. At this time, an ELISA was performed to detect Blastomyces antigeng in serum and urine and results were negative.
After 3 months of treatment, the nasal swelling had completely resolved, no abnormal airway sounds could be auscultated, and the dog was clinically normal. The dog was anesthetized, and rhinoscopyc,d was again performed to evaluate the nose and nasopharynx and to obtain biopsy samples to confirm resolution of the disease. The nasal cavity and nasopharynx appeared normal rhinoscopically. Histologic examination of tissue samples collected from the right nasal passage and pharynx revealed minimally hyperplastic mucosa. The lamina propria and submucosa were multifocally expanded by an infiltrate of a small number of macrophages, lymphocytes, and plasma cells. Sections stained with periodic acid–Schiff and Gomori methenamine silver stains were unremarkable. These findings were interpreted as chronic, mild lymphoplasmacytic rhinitis. Oral administration of itraconazole was continued for 2 months and then discontinued. Overall, itraconazole was administered for a total duration of 5 months. One year after discontinuation of the treatment, the dog was doing well and was without any clinical signs; its nose had no abnormalities on physical examination.
SOMATOM AR Star, Siemens AG, Munich, Germany.
Conray 400LM, Mallinkrodt Inc, St Louis, Mo.
Karl Storz GmbH & Co KG, Tuttlingen, Germany.
Olympus America Inc, Center Valley, Pa.
Infectious Diseases Laboratory, College of Veterinary Medicine, University of Georgia, Athens, Ga.
Sporanox, Ortho-McNeil Inc, Raritan, NJ.
MiraVista Diagnostics, Indianapolis, Ind.
Legendre AM. Blastomycosis. In: Greene CE, ed. Infectious diseases of the dog and cat. 3rd ed. St Louis: Saunders Elsevier, 2006;569–576.
Brömel C, Sykes JE. Epidemiology, diagnosis, and treatment of blastomycosis in dogs and cats. Clin Tech Small Anim Pract 2005;20:233–239.
Legendre AM, Walker M, Buyukmihci N, et al. Canine blastomycosis: a review of 47 clinical cases. J Am Vet Med Assoc 1981;178:1163–1168.
Schmiedt C, Kellum H, Legendre AM, et al. Cardiovascular involvement in 8 dogs with Blastomyces dermatitidis infection. J Vet Intern Med 2006;20:1351–1354.
Shurley JF, Legendre AM, Scalarone GM. Blastomyces dermatitidis antigen detection in urine specimens from dogs with blastomycosis using a competitive binding inhibition ELISA. Mycopathologia 2005;160:137–142.
Bialek R, Cirera AC, Herrmann T, et al. Nested PCR assays for detection of Blastomyces dermatitidis DNA in paraffin-embedded canine tissue. J Clin Microbiol 2003;41:205–208.
Ling FT, Wang D, Gerin-Lajoie J. Blastomycosis presenting as a locally invasive intranasal mass: case report and literature review. J Otolaryngol 2003;32:405–409.
Angtuaco EE, Angtuaco EJ, Glasier CM, et al. Nasopharyngeal and temporal bone blastomycosis: CT and MR findings. AJNR Am J Neuroradiol 1991;12:725–728.
Saito M, Sharp NJ, Munana K, et al. CT findings of intracranial blastomycosis in a dog. Vet Radiol Ultrasound 2002;43:16–21.
Legendre AM, Rohrbach BW, Toal RL, et al. Treatment of blastomycosis with itraconazole in 112 dogs. J Vet Intern Med 1996;10:365–371.