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.

Case summary A six-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, 42 days], levetiracetam [20 mg/kg q8h] and prednisolone [1 mg/kg q24h until Day 21 = D-21]). Lethargy and fever reappeared seventeen days after treatment. Four days later, severe multifocal neurological signs reemerged. 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 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 one 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 (Veklury, Gilead, 16.7 mg/kg IV q24h) for four days. Oral GS-441524 was then reintroduced (10 mg/kg q12h) and continued until D-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 noninvasive 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.