Diagnosis of feline infectious peritonitis: Update on evidence supporting available tests

Abstract

Practical relevance: Feline coronavirus (FCoV) infection is very common in cats, usually causing only mild intestinal signs such as diarrhoea. Up to 10% of FCoV infections, however, result in the fatal disease feline infectious peritonitis (FIP). Clinical challenges: Obtaining a definitive diagnosis of FIP based on non-invasive approaches is difficult. Confirmation of the disease relies on finding appropriate cytological or histopathological changes in association with positive immunostaining for FCoV antigen. In FIP cases with effusions, cytology and immunostaining on effusion samples can be relatively easy to perform; otherwise obtaining diagnostic samples is more challenging and collection of biopsies from tissues with gross lesions is necessary. In the absence of a definitive diagnosis, a high index of suspicion of FIP may be obtained from the cat's signalment and history, combined with findings on clinical examination and laboratory test results. If largely consistent with FIP, these can be used as a basis for discussion with the owner about whether additional, more invasive, diagnostic tests are warranted. In some cases it may be that euthanasia is discussed as an alternative to pursuing a definitive diagnosis ante-mortem, especially if financial limitations exist or where there are concerns over a cat's ability to tolerate invasive diagnostic procedures. Ideally, the diagnosis should be confirmed in such patients from samples taken at post-mortem examination. Global importance: FIP occurs wherever FCoV infection is present in cats, which equates to most parts of the world. Evidence base: This review provides a comprehensive overview of how to approach the diagnosis of FIP, focusing on the tests available to the veterinary practitioner and recently published evidence supporting their use.

Figure 1

Schematic diagram of an FCoV particle. The spike protein binds to the feline receptor, mediating host cell entry. The feline receptor is known to be aminopeptidase N for type 2 FCoVs, but is, as yet, unknown for type 1 FCoVs. Modified with permission from Dr Emi Barker

Figure 2

Typical gross post-mortem findings in cases of FIP. Granulomatous lesions in organs or fibrinous plaques on the serosa of organs may be visible in the abdominal or thoracic cavity; tissues that are good to examine for these are the mesenteric lymph nodes, liver, spleen, kidneys and intestinal surfaces, as well as the peritoneal lining of the abdominal wall and diaphragm. In effusive cases, yellow sticky fluid can be visible in the pleural and/or peritoneal cavities, but the pericardium can also be checked for fluid

Figure 3

Examples of clinical signs seen in cases of FIP. Clinical signs are typically assigned to wet or dry FIP presentations, but there is much overlap between the two presentations and many signs are seen in both forms

Figure 4

Typical appearance of effusion seen in cases of FIP. Effusions tend to be clear, viscous and straw-yellow in colour

Figure 5

This is a positive Rivalta’s test as the drop has retained its shape with a connection to the surface of the liquid. A positive result indicates that the effusion being tested is an exudate, but is not specific for FIP

Figure 6

Schematic diagram of the FCoV genome. FCoV RT-PCR assays detect FCoV RNA. The section of the genome amplified by different RT-PCRs varies depending on the position of the primers used in the assays. As viral transcription starts at the 3’ end of the FCoV genome, with the production of multiple subgenomic RNAs at this 3’ end, PCR assays with primers located at the 3’ end of the genome (eg, in the M or N regions) will be susceptible to viral load overestimation as these will amplify these subgenomic RNAs, as well as the genomic RNA present in the FCoV. Conversely, PCR assays with primers located at the 5’ end of the genome (eg, the RNA polymerase) will amplify primarily genomic RNA and will be less prone to viral load overestimation. Assays directed at the 3’ end of the FCoV genome will tend to be more sensitive in detecting the presence of FCoV, due to their ability to amplify both subgenomic and genomic RNA. Coronaviruses, including FCoV, frequently undergo mutations and recombinations, meaning that PCRs designed to be specific for particular sequences may not amplify all FCoVs. PCRs can be designed to target conserved regions of the genome to minimise this, but elimination of FCoV sequence variability as a cause of non-amplification is impossible. Modified with permission from Dr Emi Barker