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

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. </jats:sec

Amino acid changes in the spike protein of feline coronavirus correlate with systemic spread of virus from the intestine and not with feline infectious peritonitis

Recent evidence suggests that a mutation in the spike protein gene of feline coronavirus (FCoV), which results in an amino acid change from methionine to leucine at position 1058, may be associated with feline infectious peritonitis (FIP). Tissue and faecal samples collected post mortem from cats diagnosed with or without FIP were subjected to RNA extraction and quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR) to detect FCoV RNA. In cats with FIP, 95% of tissue, and 81% of faecal samples were PCR-positive, as opposed to 22% of tissue, and 60% of faecal samples in cats without FIP. Relative FCoV copy numbers were significantly higher in the cats with FIP, both in tissues (P < 0.001) and faeces (P = 0.02). PCR-positive samples underwent pyrosequencing encompassing position 1058 of the FCoV spike protein. This identified a methionine codon at position 1058, consistent with the shedding of an enteric form of FCoV, in 77% of the faecal samples from cats with FIP, and in 100% of the samples from cats without FIP. In contrast, 91% of the tissue samples from cats with FIP and 89% from cats without FIP had a leucine codon at position 1058, consistent with a systemic form of FCoV. These results suggest that the methionine to leucine substitution at position 1058 in the FCoV spike protein is indicative of systemic spread of FCoV from the intestine, rather than a virus with the potential to cause FIP

Protective Immunity against Infection with <i>Mycoplasma haemofelis</i>

Hemoplasmas are potentially zoonotic mycoplasmal pathogens, which are not consistently cleared by antibiotic therapy. Mycoplasma haemofelis is the most pathogenic feline hemoplasma species. The aim of this study was to determine how cats previously infected with M. haemofelis that had recovered reacted when rechallenged with M. haemofelis and to characterize the immune response following de novo M. haemofelis infection and rechallenge. Five specific-pathogen-free (SPF)-derived naive cats (group A) and five cats that had recovered from M. haemofelis infection (group B) were inoculated subcutaneously with M. haemofelis. Blood M. haemofelis loads were measured by quantitative PCR (qPCR), antibody response to heat shock protein 70 (DnaK) by enzyme-linked immunosorbent assay (ELISA), blood lymphocyte cell subtypes by flow cytometry, and cytokine mRNA levels by quantitative reverse transcriptase PCR. Group A cats all became infected with high bacterial loads and seroconverted, while group B cats were protected from reinfection, thus providing the unique opportunity to study the immunological parameters associated with this protective immune response against M. haemofelis. First, a strong humoral response to DnaK was only observed in group A, demonstrating that an antibody response to DnaK is not important for protective immunity. Second, proinflammatory cytokine interleukin-6 (IL-6) mRNA levels appeared to increase rapidly postinoculation in group B, indicating a possible role in protective immunity. Third, an increase in IL-12p35 and -p40 mRNA and decrease in the Th2/Th1 ratio observed in group A suggest that a Th1-type response is important in primary infection. This is the first study to demonstrate protective immunity against M. haemofelis reinfection, and it provides important information for potential future hemoplasma vaccine design

A molecular study of hemotropic mycoplasmas (hemoplasmas) in cats in Iran

BackgroundThree feline hemoplasma species are recognized: Mycoplasma haemofelis, Candidatus Mycoplasma haemominutum', and Candidatus Mycoplasma turicensis'. These species can cause anemia in cats and have a worldwide distribution. ObjectivesThere was no previous information on hemotropic mycoplasma spp in cats in Iran and the Middle East. Accordingly, we investigated the molecular presence, and clinical signs and hematological profile in cats infected with these microorganisms in Iranian cats. MethodsPolymerase chain reaction (PCR) assays and cytology were performed on 100 blood samples collected from Iranian Shorthair cats. ACBC and case history were also collected for each sample. ResultsBy PCR, 22 (22%; 14-30%, 95% CI) samples were positive. The prevalence of M haemofelis, Ca M haemominutum', and Ca M turicensis' was 63.63% (14/22), 54.54% (12/22), and 18.18% (4/22), respectively. Some double and triple co-infections were also found. Using PCR as the reference method, cytology had poor sensitivity (27%) and reasonable specificity (89.74%). Male cats were at a higher risk of infection (P=.001). Cats older than 8years were more frequently infected than the younger cats (P=.0018). Lower HCT (P=.018), RBC count (P=.028) and HGB concentration (P=.003) were also associated with hemoplasma PCR-positive status. ConclusionsBased on this study, the most prevalent feline hemoplasma species in Iranian cats was M haemofelis, but double and triple co-infections are also documented. Age and sex, as well as reduced RBC parameters, were predisposing factors for hemoplasma infection

Review and statistical analysis of clinical management of feline leishmaniosis caused by Leishmania infantum

There is limited information about feline leishmaniosis (FeL) management in clinical practice. Leishmania infantum is the species of Leishmania most frequently reported in both dogs and cats in countries of the Mediterranean region (henceforth 'Mediterranean countries'), Central and South America, and Iran. This study was conducted to provide veterinary clinicians with an updated overview of evidence-based information on leishmaniosis in cats. A review was performed using PubMed, Science Direct, Google Scholar and Web of Science. Case reports of FeL caused by L. infantum were sought for the period 1912 to 1 June 2021. Sixty-three case reports are included in this review. Fifty-nine out of the 63 cats were from Europe, mostly from Mediterranean countries (88.9%). Most of them were domestic short-haired cats (90%) with a mean age of 7.9 years, and had access to the outdoors (77.3%). Sixty-six percent of the cats had comorbidities, of which feline immunodeficiency virus infection was the most frequent (37.7%). Dermatological lesions (69.8%) was the most frequent clinical sign, and hyperproteinemia (46.3%) the most frequent clinicopathological abnormality. Serology was the most performed diagnostic method (76.2%) and was positive for 93.7% of cats. Medical treatment was applied in 71.4% of cats, and allopurinol was the most used drug (74.4%). Survival time was greater for treated cats (520 days; 71.4% of cats) than non-treated cats (210 days; 25.4%). The majority of the cats had comorbidities, of which feline immunodeficiency virus was the most frequent. Dermatological lesions were frequently reported, and systemic clinical signs and clinicopathological abnormalities were also common. Serology may be useful for the diagnosis of FeL in clinical practice, and a positive titer of ≥ 1/40 may be a useful cut-off for sick cats. The reported treatments and dosages varied, but there was a good clinical response and longer survival in most of the cats treated with allopurinol monotherapy

Genotyping coronaviruses associated with feline infectious peritonitis

Feline coronavirus (FCoV) infections are endemic among cats worldwide. The majority of infections are asymptomatic or result in only mild enteric disease. However, approximately 5 % of cases develop feline infectious peritonitis (FIP), a systemic disease that is a frequent cause of death in young cats. In this study, we report the complete coding genome sequences of six FCoVs: three from faecal samples from healthy cats and three from tissue lesion samples from cats with confirmed FIP. The six samples were obtained over a period of 8 weeks at a single-site cat rescue and rehoming centre in the UK. We found amino acid differences located at 44 positions across an alignment of the six virus translatomes and, at 21 of these positions, the differences fully or partially discriminated between the genomes derived from the faecal samples and the genomes derived from the tissue lesion samples. In this study, two amino acid differences fully discriminated the two classes of genomes: these were both located in the S2 domain of the virus surface glycoprotein gene. We also identified deletions in the 3c protein ORF of genomes from two of the FIP samples. Our results support previous studies that implicate S protein mutations in the pathogenesis of FIP