Background: Knowledge about primary hypoadrenocorticism coexisting with immune-mediated thyroiditis (Schmidt's syndrome) in dogs is limited. Objective: To evaluate thyroid function in dogs with naturally occurring hypoadrenocorticism before and during treatment. Animals: Sixty-six client-owned dogs. Methods: Measurement of canine thyroid stimulating hormone (cTSH), total thyroxine (T4), free thyroxine, and autoantibodies against thyroglobulin, T4, and total triiodothyronine. Results: Thirty-eight dogs were assessed before and 28 during treatment. Follow-up data were available for 24/38 and 17/28 dogs, with median follow-up duration of 3.8 years (range, <1.0-8.8 years) and 4 years (range, 1.1 weeks to 10.5 years), respectively. Canine thyroid stimulating hormone was above the reference range at the time of diagnosis of hypoadrenocorticism in 10 of 38 dogs but decreased into the reference range in 7 for which follow-up data was available. Hypothyroidism was confirmed in 5 dogs at a median age of 11 years (range, 7-15 years). In 4 dogs, the condition was diagnosed after a median treatment duration of 5.75 years (range, 2.6-10 years), while in 1 dog, the diagnosis was made concurrently. One dog had detectable thyroid autoantibodies. Conclusions and Clinical Relevance: Hypothyroidism occurs as a rare concurrent condition in dogs with hypoadrenocorticism, potentially at any phase of treatment. Close monitoring of cTSH levels in these dogs could be beneficial, as early changes might indicate the onset of hypothyroidism. The low prevalence of detectable thyroid autoantibodies suggests that nonimmune mechanisms might contribute to thyroid dysfunction.

Background: Salivary cortisol collected at home is a useful test to diagnose and monitor Cushing’s syndrome in humans. The main problem in dogs is to retrieve a sufficient amount of saliva. The aim of this study was to evaluate different salivary collection methods and compare their effects on volume, pH and cortisol concentration of saliva. Sixteen healthy Beagles were used in a 4 × 4 randomized crossover study with a washout period of 1 week between each of the following collection methods: 1. Salimetrics® cotton swab dipped in ginger powder (ginger group); 2. beef-flavored Salimetrics® (bouillon group); 3. Salivette® cotton swab with an enclosed treat (treat group); 4. plain Salimetrics® (control group). First, baseline saliva (plain cotton swab, S0) and, 2 min later, experimental saliva (according to group allocation above, SExp) were collected. Saliva was gathered by holding the swabs in the animal’s mouth for 2 min. After the cross-over study, another saliva sample was collected from all dogs by the ginger method, using a 30 s sampling time (30s-ginger method). Cortisol concentrations were measured by liquid chromatography tandem mass spectrometry. Results: All three stimulation methods increased saliva production significantly (S0 compared to SExp: ginger p = 0.0005; bouillon p = 0.009; treat p = 0.007). Only ginger stimulation, however, generated a significantly higher amount of saliva (SExp) compared to the control group (p = 0.00001; median (range) amount of saliva for SExp: ginger 1200 ul (600–1700), bouillon 650 ul (200–1900), treat 700 ul (300–1000), control 400 ul (0–1100)). The amount of saliva retrieved by the 30s-ginger method was still higher than that from the control group (p = 0.0004). Bouillon and treat stimulation led to decreased pH values (bouillon, p = 0.0028; treat, 0.0018). Excitement was higher in the ginger group (p = 0.01). Chewing was intensified in the ginger and treat group (ginger, p = 0.003; treat, 0.0009). The cortisol concentration SExp was higher compared to that of S0 in the ginger and treat group (p = 0.02, 0.003). The experimental cortisol concentrations (SExp) were not different between groups. Conclusions: The 30s-ginger method could prove useful in evaluating or monitoring dogs with Cushing’s syndrome, as sampling at home for 30 s by the owner seems feasible.

Feline infectious peritonitis (FIP) is a fatal but now treatable disease in cats caused by feline coronavirus (FCoV). This study prospectively investigated viral coinfections in 100 cats diagnosed with FIP and subsequently treated with oral GS-441524 (Bova UK) and their influence on outcome, focusing on viruses potentially associated with feline chronic gingivostomatitis (FCGS). Cats were tested for feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), feline calicivirus (FCV), feline herpesvirus (FHV), feline foamy virus (FFV), and feline gammaherpesvirus (FcaGHV1). Coinfections were identified at the following frequencies: FCV (27), FFV (22), FHV (6), FIV (4), FcaGHV1 (2), and FeLV (2, both progressive infections). FFV infection was significantly associated with FIV (p_F = 0.0021) and FHV (p_F = 0.0226) infection. FCGS was present in 25/97 cats with FCV infection being associated with FCGS (pF = 0.0032); no significant associa-tions were found for the other viruses and FCGS. The 42-day oral GS-441524 treatment’s success rate was 94% (five cats died, one relapsed). Coinfections did not significantly influence disease severity or treatment outcome, although the low number of cases for some pathogens warrants further investigation. However, advanced age was associated with treatment failure, potentially due to delayed diagnosis as FIP is considered to be less common in older individuals, or to age-related changes in immune function. In summary, viral coinfections, particularly with FCV, were common and should be considered in the clinical and hygienic management of cats with FIP.

Case summary: A 6-month-old male British Longhair cat presented with acute neurological signs, ocular changes, massive ascites and laboratory parameters consistent with feline infectious peritonitis (FIP). Systemic and neurological signs fully resolved with initial treatment (GS-441524; BOVA UK [15 mg/kg PO q24h for 42 days], levetiracetam [20 mg/kg q8h] and prednisolone [1 mg/kg q24h until day 21]). Lethargy and fever reappeared 17 days after treatment. Four days later, severe multifocal neurological signs re-emerged. High-field MRI revealed multifocal intra-axial and intramedullary lesions in the brainstem and cervical spinal cord, severe meningitis and generalised mild ventriculomegaly. Feline coronavirus (FCoV) RNA was detected in the cerebrospinal fluid by reverse transcription quantitative PCR (RT-qPCR). Abdominal effusion was absent. Serum alpha-1-acid glycoprotein (AGP) was again elevated. FIP re-emergence was suspected, and antiviral treatment was resumed. After 1 day of GS-441524 treatment (15 mg/kg PO q24h), severe hypoventilation developed, requiring intubation and mechanical ventilation for 1.5 days. Treatment was switched to remdesivir (16.7 mg/kg IV q24h, Veklury; Gilead) for 4 days. Oral GS-441524 was then reintroduced (10 mg/kg q12h) and continued until day 84. Treatment resulted in partial recovery with moderate ataxia and reduced left-sided menace response remaining 181 days after starting the second treatment. Relevance and novel information: This case illustrates the complexity of diagnosing and treating re-emerging FIP-associated neurological signs. AGP monitoring offers a promising non-invasive approach for early detection of relapse. By adapting short- and long-term antiviral treatment and providing intensive care, excellent long-term outcomes can be obtained for cats with severe relapsing FIP-related neurological signs.

Objectives: GS-441524 is effective against feline infectious peritonitis (FIP), but potential renal toxicity remains debated. Renal health was assessed in cats with FIP undergoing antiviral treatment. Methods: Cats with confirmed FIP (n = 80) receiving oral GS-441524 for 42 days were assessed before (day 1; D1), during (D7, D42), and after treatment (D84, D183). Assessments included urine specific gravity (USG), urine protein:creatinine ratio (UPC), urinary cystatin B (uCysB), urine protein electrophoresis, serum creatinine, urea and symmetric dimethylarginine (SDMA).The term potential renal dysfunction was used for cats fulfilling the following criteria: creatinine >140 µmol/l or SDMA ≥ 18 µg/dl and USG <1.035. Serum amyloid A (SAA) and alpha-1-acid glycoprotein (AGP) were assessed in serum, feline coronavirus (FCoV) RNA in blood and urine (D1–D42). Results: At baseline, 97.5% of cats had creatinine concentrations <140 µmol/l; by D183, 23.8% exceeded this threshold (D1–D183: PD <0.0001). Potential renal dysfunction criteria were met in 2.5% of cats at baseline and 8.8% at D183. In contrast, uCysB was increased in 83.8% of cats at D1 and declined during treatment (D1–D183: PD 100 ng/ml had higher UPC values (PMWU <0.0001). Most cats had elevated AGP and SAA at baseline, which normalised during treatment (D1–D42: PD 0.2) was present in 91.3% on D1 and 3.8% on D183; urine protein electrophoresis at D1 revealed predominantly tubular and mixed patterns. Urine was more frequently FCoV RNA-positive than blood on D1 (68.8%/61.3%), but not on D7 (16.3%/45.0%). Conclusions and relevance: Treatment reversed FIP-associated renal abnormalities and inflammation observed at baseline. A small subset of cats met criteria compatible with potential renal dysfunction during the study. Whether these findings reflect delayed FIP-related renal insults or adverse antiviral effects remains unknown but indicate that treatment should not be extended unnecessarily.

Feline infectious peritonitis (FIP) is caused by mutated feline coronaviruses. Immune-mediated hemolytic anemia (IMHA) arises due to immune-mediated erythrocyte destruction and can be non-associative or associative with diseases such as FIP. Records of cats with FIP were reviewed to find those with associative IMHA based on exclusion of other causes of anemia and a positive saline agglutination test and/or Coombs test. The inclusion criteria were met for 45 cats (26 (58%) cats with effusive and 19 (42%) with non-effusive FIP). Median hematocrit was 18% (interquartile range [IQR] 13–20). Anemia was non-regenerative in 36 (80%) cats and regenerative in 5 (11%) cats; 4 (9%) cats had no reticulocyte count available. Concurrent thrombocytopenia was present in 18 (40%) cats. All 45 cats were treated with nucleoside analogs, and 44 (98%) cats with glucocorticoids; in 5 (11%) cats, glucocorticoids were added after starting antiviral treatment due to persistent anemia. Median follow-up was 72 days (IQR 14–246); at the time of last follow-up 33 (73%) cats had survived while 12 (27%) had died or were euthanized. Of the 33 surviving cats, 17 achieved remission of both FIP and IMHA. In three cats, FIP remission was achieved, but IMHA relapsed; in one of these, IMHA relapsed twice. FIP relapsed without IMHA in two cats, and both FIP and IMHA relapsed in one cat. In 9 cats the antiviral and glucocorticoid treatment is still ongoing at the time of the publication. Although FIP is likely an uncommon cause of associative IMHA, as more cats with FIP are treated with antiviral therapy, it is important to consider IMHA as a possible cause of anemia in cats with FIP.