Aspergillus spp. are ubiquitous worldwide and found commonly in soil and decaying vegetation. Cases of FRS have been diagnosed in Australia, Europe, Japan, South America, and the United States.4–9 The taxonomy of Aspergillus species is complicated and is changing with the use of molecular techniques. There are hundreds of species in the genus Aspergillus as well as four major subgenera, each of which is comprised of two to six sections. Dogs with SNA are commonly infected with Aspergillus fumigatus while SOA is rare in dogs. In cats, several Aspergillus spp. cause FRS. Although A. fumigatus is the most common causative agent of SNA in cats, Aspergillus felis, Aspergillus ­flavus, Aspergillus lentulus, and Aspergillus niger have also been isolated from affected cats.^3,10 Aspergillus felis and Aspergillus udagawae most commonly cause the more invasive SOA, although some SOA cases are caused by Aspergillus wyomingensis.^3,5 Differences in species pathogenicity may play a significant role in the development and extent of clinical disease as well as antifungal drug susceptibility.⁴ The most common species that causes disseminated or focal non-FRS is unknown.

Aspergillus spp. branch dichotomously at 45-degree angles and form septate, nonpigmented hyphae that are about 3 to 8 μm in diameter, while spores are 2 to 3 μm in diameter. Infection can occur after exposure to ­contaminated soil or airborne pathogens.² Once inhaled, the organism invades respiratory epithelium. The ability to infect is related to both host and pathogen characteristics.

Since first reported in the 1980s, feline aspergillosis has been reported rarely; about 66% of the approximately 55 cases described in the literature were diagnosed in the past decade.⁵ Of 571 cats diagnosed with deep mycotic infections between 1952 and 1995, 7% had aspergillosis and only two were diagnosed with FRS.¹¹

Although Aspergillus species are found worldwide, cats living in Australia and the United States may be at the highest risk of infection as most cases have been diagnosed in those countries. There is no sex predisposition. Brachycephalic cats are predisposed with approximately one-third of FRS cases diagnosed in Himalayan, Persian, British Shorthair, Scottish Fold, and Ragdoll cats.3–5,12 Affected cats have ranged from 16 months to 13 years of age, with a median age of 5 to 6.5 years.^4,5

Invasive aspergillosis in people typically manifests as sinopulmonary disease in immunocompromised individuals. Dogs that develop SNA are rarely immunocompromised, while those with disseminated disease usually are.¹³ Cats with disseminated aspergillosis are more likely to have a comorbidity causing immunocompromise than those with FRS aspergillosis. In one study of nine cats diagnosed with otitis due to Aspergillus, eight had potential risk factors including diabetes mellitus, immunosuppressive drug therapy, and allergic dermatitis.¹⁴ Most cats diagnosed with SNA or SOA have tested negative for retrovirus infection and have no known comorbidities associated with decreased immune function.^15,16 In dogs, SNA has been associated with nasal trauma, foreign bodies, and neoplasia. It is not known if these comorbidities are risk factors in cats.

Historical findings are dependent on the location and duration of infection. Cats with FRS have a similar history to cats with other causes of upper respiratory tract disease (URTD), including viral infection. Sneezing or nasal discharge is common, although these signs may be absent in cats with SOA.4,15 Cats with disease other than rhinosinusitis due to aspergillosis have a variable history depending on the site of infection, but lethargy, depression, vomiting, and/or diarrhea are common. Signs may be present for a few days to several months prior to patient presentation.

Sinonasal aspergillosis has a similar clinical presentation in dogs and cats. Sino-orbital aspergillosis occurs when organisms invade the paranasal structures including the palate, cribriform plate, and orbit. Infection is associated commonly with retrobulbar granulomas.^4,15 Unlike dogs, where 99% of aspergillosis cases are SNA, in cats 65% are SOA.³

Currently, disseminated and focal non-FRS aspergillosis are diagnosed less frequently in cats than SNA and SOA, although disseminated disease was reported more commonly in cats in the past (1952 to 1995).¹¹ Dissemination is defined as active infection in two or more noncontiguous sites or hematogenous spread of infection. Focal invasive infection has been diagnosed in cats in the urinary bladder, lungs, and gastrointestinal (GI) tract.^5,11,17–19 A small number of cats have been diagnosed with otitis externa and/or media due to Aspergillus.¹⁴

Physical examination abnormalities at presentation in 23 cats with FRS included nasal discharge, stertor, fever, and mandibular lymphadenomegaly.⁴ Exophthalmos was present in all 17 cats with SOA and an oral mass or ulcer was diagnosed in 15. Epistaxis was rare. Ocular abnormalities included anterior uveitis, retinal tear, and optic nerve involvement; blindness may result.

There is little information concerning clinicopathologic abnormalities in cats with aspergillosis, although hyperglobulinemia may be the most common abnormality.4,15 Routine clinicopathologic test results may be within normal limits. Specific tests for the diagnosis of aspergillosis have been assessed. The accuracy of diagnosis using an agar gel immunodiffusion (AGID) assay and an indirect immunoglobulin G enzyme-linked immunosorbent assay (ELISA) for detection of antibodies was compared in cats with rhinosinusitis due to aspergillosis and cats with other causes of URTD.²⁰ The AGID assay had a sensitivity of 43% and specificity of 100%. Depending on the cutoff value used for diagnosis, the sensitivity of the ELISA was 90% to 100% and the specificity was 92% to 96%. Measurement of immunoglobulin A is less sensitive and specific for diagnosing aspergillosis.¹⁰ In one study, two cats with nasal cryptococcosis had false positive ELISA results for aspergillosis.²⁰ False positive results are clinically significant, as treatment and prognosis vary between the two mycotic infections. The ELISA test is best used as a screening test and positive ELISA results should be confirmed with organism detection.

Use of an ELISA assay to measure serum galactomannan, a component of the Aspergillus cell wall, is used to diagnose invasive aspergillosis in people. In a small number of cats, the test had a sensitivity of 23% and specificity of 78%; therefore, it is not recommended as a diagnostic tool.²¹ There is scant information concerning the use of antibody and antigen testing modalities in cats with aspergillosis other than the SNA and SOA forms.

Findings from computed tomography are well-characterized in cats with FRS and changes are dependent on the Aspergillus spp. involved.²² Aspergillus fumigatus infections are typically associated with changes limited to the sinus and nasal cavities. Abnormalities are similar to dogs with SNA, including granulomatous mass lesions (in the nasal cavity, sinuses, and nasopharynx), turbinate destruction, increased intranasal soft tissue attenuation, and sinus fluid. Cats infected with other species, including A. felis, have lesions that are more extensive. Abnormalities include masses (in the sinonasal, nasopharyngeal, retrobulbar, and orbital spaces) which have heterogeneous contrast enhancement with hypoattenuation centrally and peripheral rim enhancement. Other abnormalities include paranasal and orbital soft tissue attenuation, optic nerve involvement, and orbital boney lysis. Severe turbinate destruction is more common in SNA than SOA. Bone destruction is likely due to a proinflammatory response by the host as well as virulent fungal toxins, as occurs in people and dogs. Associated lymph nodes may be enlarged. Imaging results in cats with non-FRS infections are dependent on lesion location and severity.

Definitive diagnosis requires detection of the organism via cytology, histopathology, molecular techniques on tissue (fresh or formalin-fixed), or culture, although it is important to assess these results in the context of the clinical findings. For example, it is possible that Aspergillus might be cultured from a nasal swab when aspergillosis is not the cause of clinical signs.¹⁶

The sensitivity of diagnosis with cytology in cats has not been evaluated. In one study in dogs, cytology was diagnostic in 13% to 100% of cases.²³ Assessment of biopsy tissue imprint and nasal lesion brushing had the highest yield and nasal discharge cytology the lowest. Evaluation of nasal discharge for diagnosis is not recommended. False negative results may occur with cytology so use of multiple diagnostic modalities is recommended.¹⁵

Organisms may be seen histologically in concert with inflammation. The type of inflammation is variable; histiocytic, eosinophilic, neutrophilic, granulomatous, and/or plasmacytic inflammation have been identified in nasal mucosal biopsy samples. Granulomas are often comprised of central necrosis with fungal hyphae surrounded by primarily epithelioid macrophages and fewer numbers of mixed inflammatory cells. Fibrosis may be present. Special stains, including Grocott methenamine silver or periodic acid-Schiff (PAS), may maximize visualization of organisms.

Culture of samples is recommended, and culture of tissue or fungal plaques is preferable to nasal swabs or cytology samples. Although false negative results can occur, culture and susceptibility testing can guide therapy. Although there is a zoonotic risk of infection to laboratory personnel exposed to cultures of Aspergillus, it is minimal.

In people, due to growing resistance in invasive aspergillosis, itraconazole is not recommended as a first-line therapy and fluconazole has no activity against Aspergillus spp. Voriconazole has been considered first-line therapy for invasive aspergillosis and posaconazole is recommended in people that fail other therapies. Due to the emerging problem of A. fumigatus azole resistance, these recommendations may change over time.24,25

As there are no prospective studies assessing response to treatment in cats with aspergillosis, the treatment of choice is unknown. Multiple drugs have been used as monotherapy or in combination including itraconazole, posaconazole, voriconazole, amphotericin B, and terbinafine. There is limited information concerning the safety and efficacy of posaconazole and voriconazole in cats, but they may be preferred therapies. In one study of a small number of healthy cats, posaconazole was well tolerated when administered orally or intravenously.²⁶ Therapeutic serum drug levels are unknown in cats, but using data extrapolated from humans, the long half-life of oral posaconazole in cats allows for dosing every 24 to 48 hours. Cats administered a single oral 15 mg/kg loading dose followed by 7.5 mg/kg every 24 hours, or an oral 30 mg/kg loading dose followed by 15 mg/kg every 48 hours, achieved recommended trough levels of 0.5 to 0.7 μg/mL.

In many cats, Aspergillus spp. show in vitro resistance to one or more drugs. Resistance to fluconazole and/or flucytosine is common in multiple species of Aspergillus and resistance to itraconazole is on the rise.^2,4,15 Cross resistance in A. felis between itraconazole and posaconazole is more common than between itraconazole and voriconazole, although some isolates may be resistant to all three azole drugs. In two studies, the emerging Aspergillus spp. causing SOA were found to be resistant to itraconazole (3 of 13 cats), voriconazole (2 of 11 cats), and/or posaconazole (1 of 11 cats), but not to amphotericin B.^4,15 Patients with the less invasive SNA are more likely to respond to posaconazole and voriconazole due to differences in infecting species.⁴ The ideal duration of treatment is unknown and clinical relapse appears to be common.

In a study of five cats treated medically that achieved complete clinical remission, four had SNA and one had SOA.⁴ Fourteen other cats were either euthanized or failed treatment. In the surviving cats, therapy consisted of one to five antifungal drugs; cats that failed therapy with one drug responded to others. In addition, four cats had adjunctive therapy including rhinotomy and sinus trephination for surgical débridement of fungal plaques (with or without topical antifungal therapy). Little data concerning the benefits of surgery compared to medical management alone are available. The duration of medical treatment ranged from 7 to 16 months and the disease-free interval after discontinuation of oral antifungal therapy ranged from 7 to 50 months.

Based on the scant information available, the author recommends culturing plaques or tissue when aspergillosis is suspected. Susceptibility results are important in guiding therapy. Until results are available, administration of posaconazole with or without amphotericin B should be considered. If itraconazole is used, compounded formulations should be avoided as therapeutic levels may not be attained. Use of a brand name or generic formulation is recommended to decrease risk of treatment failure.²⁷ Thorough endoscopic or surgical débridement of plaques should be performed, based on the benefit seen in dogs with SNA.¹³ Client consent should be attained prior to use of posaconazole or voriconazole because these drugs are not labeled for use in cats in most countries and because there is a paucity of information concerning safety and efficacy. Voriconazole may be associated with GI complications, mydriasis, hind limb ataxia, and lethargy.^4,15

Of 17 cats treated for FRS in one study, 5 had complete clinical remission.⁴ Cats failing treatment were euthanized due to their disease. The prognosis for cats with non-FRS aspergillosis is unknown but is likely poor as well.

In the United States, the organism is endemic in the Mississippi, Missouri, and Ohio River valleys, and the mid-Atlantic states. Cats have been diagnosed with blastomycosis in Oklahoma, Tennessee, and Wisconsin.11,28 In dogs, blastomycosis has been diagnosed in New York, Wyoming, South Dakota, and Colorado.²⁹ In Canada, it is endemic in Quebec, Manitoba, Saskatchewan, and Ontario.³⁰ Blastomycosis has been reported in Africa, Central America, Europe, India, and Thailand.

In the environment, Blastomyces spp. exist in a mycelial form and reproduce sexually, producing infective spores. At body temperature, the spores transform into yeast and replicate asexually. Budding yeasts are 5 to 20 µm in diameter and have a thick, refractile, double-contoured cell wall. Soil is the likely source of infection for most patients. Infection occurs most commonly via inhalation of infective spores, which establish infection within the lungs. Blastomycosis disseminates via the lymphatics and hematogenously. Direct skin inoculation is rare.³¹

Dogs and people are most commonly infected. There are rare reports of other species developing blastomycosis, including the horse, lemur, kinkajou, and nondomestic cats.^32–35 Blastomycosis is rare in domestic cats and often fatal. In one study of 571 cats diagnosed with systemic mycosis, 41 (7.1%) were infected with B. dermatitidis.¹¹ In endemic areas, dogs are 100-fold more likely to develop blastomycosis than cats.³⁶ Over a 21-year period, blastomycosis was diagnosed in six cats in Saskatchewan and Manitoba (compared with 137 dogs)³⁰ and over a 24-year period, eight cats in Illinois were diagnosed with blastomycosis.³⁷

Risk factors and the epidemiology of blastomycosis are unknown in cats due to its rarity. As in dogs, exposure to endemic areas is likely the most important factor. Although soil is the most likely reservoir for Blastomyces spp., the source of infection in cats is unclear. Risk factors in dogs include exposure to sandy and acidic soil, decaying wood and vegetation, and animal waste, as well as living near water.38,39 In dogs, disturbing soil is associated with infection and precipitation may facilitate the release of infective spores.⁴⁰ People and dogs are most likely exposed to Blastomyces spp. on their own property, as there has been documentation of repeated cases occurring at the same location despite occupation by multiple families over time.

Blastomycosis can occur in cats living exclusively indoors.^36,37 It is difficult to determine the source of infection as the organism is rarely isolated from indoor environments of infected animals. One study analyzed 60 environmental samples obtained from four homes where blastomycosis was diagnosed in indoor cats and all were negative for B. dermatitidis.³⁶

A sex predisposition has been reported inconsistently; one study reported 69% of 36 infected cats were male.¹¹ Some breeds may be predisposed, including Siamese Abyssinian, Havana Brown, and Persian, but this is not supported in all reports.¹¹ Affected cats have ranged in age from 2 to 13 years, with a mean of 6 years and median of 4 years.^30,36,37 A history of immunosuppression is uncommon.^11,37

Physical examination findings are dependent on the location of infection. Blastomyces dermatitidis can infect many sites including the skin, lung, eye, kidney, central nervous system (CNS), GI tract, pleura, heart, liver, and spleen. Respiratory and dermatologic signs are common, and infection is frequently disseminated. Fever, respiratory signs (e.g., tachypnea, dyspnea, cough, changes in lung sounds) have been described. Skin lesions occur in 23% to 100% of infected cats and manifest as ulceration, draining tracts, nonulcerated dermal masses, and severe cellulitis.11,36,37,41 Ocular abnormalities may include retinal granulomas and detachment, chemosis, corneal edema, and uveitis. Neurologic abnormalities localizing to the CNS may be present. Duration of signs may vary from less than 1 week to 7 months.

Diagnosis of blastomycosis can be difficult in cats since there are no pathognomonic clinical manifestations. Little information concerning hematologic and biochemical abnormalities has been described. Abnormalities may include anemia, leukopenia, leukocytosis with left shift, monocytosis, hyperglobulinemia, hypoalbuminemia, hyper- and hypocalcemia, total and ionized hypercalcemia, and elevated calcitriol.37,41 However, clinicopathologic results may be normal.

Abnormalities are typically present on thoracic radiographs, even in cats with no respiratory abnormalities on physical examination. Abnormalities are variable and include a diffuse miliary or bronchial pattern, poorly defined soft tissue opacities with nodules or masses, alveolar lung consolidation, mediastinal masses, perihilar lymphadenomegaly, and pleural effusion (Figs. 37.1 and 37.2).^11,29,37

Serologic diagnosis via AGID for Blastomyces spp. antibodies was successful in one of four cats with confirmed infection in one study.11 An enzyme immunoassay that detects B. dermatitidis antigen in urine, serum, cerebrospinal fluid (CSF), and other fluids is available in the United States (MiraVista Diagnostics; https://miravistalabs.com). It has been validated in dogs. Urine testing is more sensitive than serum testing but testing both may provide the highest sensitivity. In dogs, specificity is lower than sensitivity as cross-reactions are commonly seen with histoplasmosis, paracoccidioidomycosis, penicilliosis; less frequently with coccidioidomycosis; and rarely with aspergillosis and possibly sporotrichosis. Sensitivity and specificity have not been assessed in cats.

Definitive diagnosis is often successful via cytologic or histologic confirmation of the organism. Pyogranulomatous inflammation is commonly seen associated with double-walled, broad-based, budding yeasts. Organisms have been detected in many sites, including skin, lung, lymph node, bronchoalveolar fluid, CSF, spleen, and brain. Culture of infected tissues or fluids is rarely performed due to the zoonotic potential. However, it is reasonable to culture infected tissue in patients that are refractory to treatment so that susceptibility information can be attained.

The most effective treatment for feline blastomycosis is unknown due to the rarity of the disease. Itraconazole is likely the first-line therapy in most cases, based on the response in dogs. Use of a brand name (e.g., Sporonox, Janssen Pharmaceuticals) or a generic formulation is recommended. In dogs and cats, compounded formulations are poorly bioavailable and treatment failure is a significant concern. The brand name Sporonox has a higher bioavailability than generic formulations, but both are thought to achieve therapeutic levels based on recommended dosages extrapolated from people.27 In cats, Sporonox solution is three times more bioavailable than the capsule formulation.⁴² Additionally, an oral solution of itraconazole approved for treatment of Microsporum canis in cats (Itrafungol, Elanco) is available in some countries and can be used to treat other fungal diseases.

Cats require a higher oral dosage of itraconazole (10 mg/kg/day) than dogs.

Gastric acid suppressants should not be administered with itraconazole as increased gastric pH decreases drug absorption.⁴³ Additionally, although administering food with the capsule formulation is recommended, the solution is best absorbed in a fasted patient. Where available, measurement of itraconazole blood levels is recommended in patients not responding to treatment (MiraVista Diagnostics; https://miravistalabs.com). Additionally, the dosage needed to attain therapeutic levels varies among patients. In some cats, a lower dosage might be effective, resulting in decreased drug cost. Additional protocols described for treatment of blastomycosis in cats include:

Clinical improvement typically occurs within 7 to 10 days of starting therapy, but resolution of radiographic abnormalities may take many months. Efficacy of the antigen test for monitoring treatment response is unknown. However, lack of decrease in the antigen value or an increase supports performing culture and susceptibility testing as well as changing therapy. Cats with presumed successful outcomes have been treated for 3 to 6 months,29 although the author treats for 1 to 2 months past clinical resolution and negative urine antigen levels. The prognosis for cats with blastomycosis is guarded to poor. Mortality rates range from 42% to 50%.³⁷

Coccidioidomycosis occurs primarily due to inhalation of infective arthrospores; less than 10 organisms can cause infection. Rarely, there have been suspect cases of dogs becoming infected after contacting fomites contaminated with arthrospores.44 Once inhaled, arthropsores spread to the lung alveoli. Increased temperature and carbon dioxide levels stimulate conversion of arthrospores into spherules. Mature spherules rupture and release up to 300 endospores. Each endospore can mature into a new spherule, leading to perpetuating of infection. After inhalation, it takes approximately 3 days for endospore formation, but clinical signs usually do not occur for at least 2 weeks. Infection may be disseminated or limited to skin.

As is typical of fungal disease, cell-mediated immunity is more effective in resolving coccidioidomycosis than is humoral immunity. Antibody formation typically occurs, but in dogs, it is more useful as a diagnostic aid than for identification of resolving infection. Although people that recover from coccidioidomycosis are considered immune to reinfection, recurrence or recrudescence in dogs and cats is common. It in unknown if this is due to premature discontinuation of treatment or to a lack of long-term immunity to Coccidioides.

Coccidioidomycosis occurs in a large variety of mammals but is rare in cats. In one study of 571 cats with deep mycotic infections, 53 (9.2%) were diagnosed with coccidioidomycosis over a greater than 40-year period.¹¹ Based on the increased number of human cases, the prevalence of feline coccidioidomycosis may also be increasing.⁴⁵

Other than living in or travel to endemic areas, risk factors for cats are unknown. Risk factors for coccidioidomycosis in people include human immunodeficiency virus infection, immunosuppressive drug therapy, diabetes mellitus, cardiopulmonary disease, and pregnancy.45 Infection has been reported in cats 1 to 17 years of age, with a mean age of 6.2 years and a median of 5 to 9 years.^11,28,46 There is no sex or breed predisposition. Retrovirus infection is not an obvious risk factor. In two studies, none of 29 cats and only 1 of 25 cats with coccidioidomycosis tested positive for feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), respectively.^44,46 Cats living strictly indoors may become infected.⁴⁴

Most cats have a history of living in or travel to endemic areas, even years prior to development of clinical signs. Historical clinical findings may be nonspecific and include lethargy, weight loss, and hyporexia. Other historical findings are dependent on the site of infection, including those related to the skin, lungs, and musculoskeletal system. Cats may only have a history of dermatologic disease, with no signs of systemic disease. Coccidioides spp. appear able to infect most tissues, including the pericardium and CNS. Duration of clinical signs ranges from 2 weeks to 1 year, with most cats having signs for <1 month prior to presentation.11,44,46

Physical examination abnormalities are dependent on the site of infection. In one retrospective study of 51 cases in Arizona, 61% had disseminated disease.⁴⁷ Dermatologic disease is present in >50% of cats.^11,46 Lesions are variable and include abscesses, dermatitis, chronic draining tracts, papules, pustules, and lingual ulceration. Regional lymphadenopathy may be present. Fever is the next most common physical examination abnormality reported followed by respiratory signs. Ocular abnormalities may include conjunctival masses, uveitis, chorioretinitis, retinal detachment, and periocular swelling.⁴⁸ Weight loss, lethargy, lameness, or neurologic abnormalities may also be present.

Routine laboratory findings are nonspecific and include nonregenerative anemia, neutrophilic leukocytosis with left shift, monocytosis, eosinophilia, hypoalbuminemia, and hyperglobulinemia. Routine imaging results are dependent on disease location, but osteomyelitis, interstitial pulmonary disease, and hilar lymphadenopathy have been reported.44,46

Multiple serologic methodologies have been used to measure Coccidioides spp. antibodies in cats. Most infected cats are seropositive when initially tested; the remaining become seropositive during the course of disease.^44,46 In one study, the median titer at diagnosis was 1:32 (range, 1:4 to >1:256).⁴⁷

Definitive diagnosis of coccidioidomycosis requires organism identification via cytology or histopathology. Pyogranulomatous inflammation is usually present. On unstained slides, the organism appears as a large (10 to 80 µm) round, double-walled structure containing endospores. Use of Wright, Papanicolaou (PAP), or PAS stain can make identification of the organism easier. With PAP stain, the capsular wall is refractile and purple–black, the cytoplasm is yellow, and the endospores are red–brown. When stained with PAS, the capsular wall is deep red to purple and the endospores are bright red. Inflammatory cells surrounding spherules may make them difficult to see. Histopathologic evaluation of infected tissues may reveal organisms in microabscesses of pyogranulomatous inflammation. Although spherules can be detected with routine hematoxylin and eosin (H and E) staining, they are easier to see with PAS or Grocott-Gomori methenamine silver stains.

There is rarely an indication to confirm infection via culture. The mycelial form, which grows on culture media, is zoonotic and testing should be done only at experienced reference laboratories.

Ketoconazole has been replaced by newer generations of azole antifungals and it is no longer recommended. In one study, two cats with Coccidioides spp. brain granulomas were successfully managed with surgical debulking and oral fluconazole therapy.49 The ideal duration of treatment is unknown, but many cats have been treated for 10 to 43 months.^46,49

In people with non-meningeal coccidioidomycosis, itraconazole and fluconazole are equally effective, although itraconazole may be more effective in management of skeletal lesions. Relapse rates may be higher with fluconazole therapy. Information concerning the use of posaconazole and voriconazole in people with coccidioidomycosis is sparse. Use of amphotericin B is recommended in people with severe pulmonary infections and may be beneficial in veterinary patients. Until evidence-based data becomes available, initiating therapy with itraconazole or fluconazole seems appropriate. Fluconazole is recommended in cases where CNS involvement is suspected, and amphotericin B may be considered in severe cases. Recrudescence months or years after discontinuation of therapy can occur.

In the retrospective study in Arizona, 40 of 46 cats treated with fluconazole responded well. Recurrent disease developed in 14 cats; all but one responded when therapy was reinstituted.⁴⁷ A reduction in serum antibody titer was associated with a favorable prognosis.