Amy Poland

Feline infectious peritonitis viruses arise by mutation from endemic feline enteric coronaviruses.

Abstract Feline infectious peritonitis virus (FIPV) strains from six cats and three different geographic areas were compared genetically with feline enteric coronavirus (FECV) isolates obtained from cats inhabiting the same environments. Sequence comparisons were made from 1.2- to 8.9-kb segments on the 3′ end of the genome. FECV/FIPV pairs from the same catteries or shelters were 97.3–99.5% related but were genetically distinct from FIPV and FECV strains obtained from cats living in geographically distinct environments. The high genetic similarity between FECVs and FIPVs from the same environment strongly suggested a common ancestry. Based on the presence of deletion mutations in the FIPVs and not in the FECVs, it was concluded that FIPVs evolved as mutants of FECVs. The mutations are deletions in the FIPVs and not insertions in the FECVs since similar sequences are present in other strains that have segregated earlier from a common ancestor. Therefore, the order of descent is from FECV to FIPV. Mutations unique to FIPVs were found in open reading frames (ORFs) 3c in 4 of 6 isolates and/or 7b in 3 of 6 isolates. When the study was extended to include 7 additional FIPV isolates, 11/13 of the FIPVs sequenced were found to have mutated 3c ORFs.

Common virus infections in cats, before and after being placed in shelters, with emphasis on feline enteric coronavirus

The purpose of this study was to determine the origin and subsequent spread of feline calicivirus (FCV), feline herpesvirus (FHV), and feline enteric coronavirus (FECV) in cats relinquished to shelters. FCV was isolated from the oral fauces of 11% of healthy cats upon entry, and isolation rates were highest for kittens (33%). FHV shedding was very low (4%) at the time of entry and occurred mainly in juveniles. FECV shedding was also common among newly relinquished cats (33%), especially older kittens and juveniles (90%). The subsequent spread of all three viruses was rapid and efficient in the shelter environment. Fifteen percent of cats were shedding FCV, 52% FHV, and 60% FECV after 1 week. More detailed studies were done with FECV shedding, which could be accurately quantitated. The amounts of FECV shed by infected cats ranged from 102 to 1016particles/swab of feces. FECV shedding was several logs higher in young kittens with primary infection than adult cats with primary infections. The mean levels of FECV shedding among adults were the same for primary and chronic infections. Although shelters were not the primary source of these viruses for many relinquished cats, factors intrinsic to the shelter environment were critical in amplifying shedding and spread to susceptible individuals. Extrinsic factors were especially important for the spread of FHV and FECV. FHV shedding rates increased from 4% to 50% in 1 weeks time. The speed and magnitude of the increase in FHV shedding suggested that there was reactivation of latent infections as well as acquisition of new infections. FECV shedding increased 10 to 1,000,000 fold in 1 week among cats that were already infected at entry, and more than one-half of initially negative cats were shedding FECV a week later. Feline calicivirus infection was the least likely to spread in the shelter. The infection rate only increased from 11 to 15% in 1 week.

An epizootic of highly virulent feline calicivirus disease in a hospital setting in New England.

This article reports an outbreak of 24 cases of an unusually virulent feline calicivirus (FCV) infection in a small animal hospital. The circumstances and disease signs were very similar to those recently described in an outbreak of FCV hemorrhagic disease in Northern California (Vet. Microbiol. 73 (2000) 281). The virus entered the facility through shelter cats showing upper respiratory signs. Affected cats manifested high fever, anorexia, labored respirations, oral ulceration, facial and limb edema, icterus, and pancreatitis. The infection spread rapidly among the patients by contaminated animal caretakers and hospital equipment. One case of fomite transmission from an employee to a housecat was documented. Prior vaccination, even with multiple doses of FCV-F9-based live calicivirus vaccine, was not protective. Affected cats often required extensive supportive care for 7–10 days, and the overall mortality from death and euthanasia was 32%. The strain of FCV responsible for this outbreak was genetically and serologically distinct from the FCV strain responsible for a similar epizootic and the FCV-F9 strain contained in most vaccines. Outbreaks of this type are being reported with increasing frequency, and are often associated with the practice of treating sick shelter cats in private practices. Similar to the present epizootic, outbreaks of FCV hemorrhagic disease have been self-limiting, but require prompt application of strict quarantine, isolation, personnel sanitation, and disinfection procedures.

Diagnostic features of clinical neurologic feline infectious peritonitis.

Feline infectious peritonitis (FIP) is a fatal Arthus‐type immune response of cats to infection with FIP virus, a mutant of the ubiquitous feline enteric coronavirus (FECV). The disease may occur systemically or in any single organ system, and primary neurologic disease is a common subset of such manifestations. We examined 16 domestic cats with clinical neurologic FIP and 8 control cats with nonneurologic FIP, with the intention of identifying the ante‐and postmortem diagnostic tests that most contribute to accurate diagnosis. Of the 16 cats with neurologic FIP, 15 were less than 2 years of age and all 16 originated from large multiplecat households. The most useful antemortem indicators of disease were positive anti‐coronavirus IgG titer in cerebrospinal fluid, high serum total protein concentration, and findings on magnetic resonance imaging suggesting periventricular contrast enhancement, ventricular dilatation, and hydrocephalus. Postmortem diagnosis was facilitated by FIP monoclonal antibody staining of affected tissue and coronavirus‐specific polymerase chain reaction. Most cats with neurologic and ocular forms of FIP had patchy, focal lesions, suggesting that recently developed technologies described in this report may be useful for evaluation of cats with suspected FIP.

Feline Coronavirus Serotypes 1 and 2: Seroprevalence and Association with Disease in Switzerland

ABSTRACT To determine the prevalence of antibodies to feline coronavirus (FCoV) serotypes 1 and 2 in Switzerland and their association with different disease manifestations, a serological study based on immunofluorescence tests was conducted with Swiss field cats using transmissible gastroenteritis virus (TGEV), FCoV type 1 and FCoV type 2 as antigens. A total of 639 serum samples collected in the context of different studies from naturally infected cats were tested. The current study revealed that, with an apparent prevalence of 83%, FCoV serotype 1 is the most prevalent serotype in Switzerland. FCoV type 1 viruses induced higher antibody titers than FCoV type 2, and were more frequently associated with clinical signs and/or feline infectious peritonitis. The antibody development in seven cats experimentally infected with FCoV type 1 revealed that, with progressing duration of infection, antibodies to FCoV type 1 significantly increased over those to FCoV type 2. There was a significant relationship between antibody titers against TGEV, FCoV 1, and FCoV 2 and TGEV antigen detected the highest proportion of seropositive cats. We conclude that a vaccine against FCoV should be based on FCoV type 1-related antigens and that for serodiagnosis of FCoV infection TGEV should be used to attain the highest diagnostic efficiency. When serology is used in addition to clinical signs, hematology, and clinical chemistry results as an aid to diagnose clinical FIP, TGEV shows a diagnostic efficiency equal to that of a FCoV antigen.

Ehrlichia spp. in cervids from California.

Blood samples from six mule deer (Odocoileus hemionus hemionus), 15 black-tailed deer (O. hemionus columbianus), and 29 elk (Cervus elaphus nannodes) were assayed for human monocytic and human granulocytic ehrlichiosis (HGE) by polymerase chain reaction (PCR), DNA sequencing, and serology to determine whether or not cervids are involved in the maintenance of these potential human pathogens in California (USA). The deer were sampled in August to October 1992–95. The 29 tule elk from Point Reyes National Seashore were sampled in August 1997. All deer were seronegative for antibodies to HGE/Ehrlichia equi, while the E. equi seroprevalence among elk was 17%. The 16S rDNA PCR prevalence in deer was 38% (in mule deer and black-tailed deer) for Ehrlichia-like sp. of white-tailed deer, 5% (one black-tailed deer only) for E. equi, and 0% for E. chaffeensis. The PCR prevalence in elk was 0% for Ehrlichia-like sp. of white-tailed deer, 31% for E. equi, and 0% for E. chaffeensis. The E. equi from two positive elk samples was successfully propagated in HL-60 cell cultures. DNA sequencing confirmed that the Ehrlichia-like sp. sequences from deer in California were closely related to sequences reported from white-tailed deer from Oklahoma and Georgia. The E. equi strain from deer and elk resembled other E. equi strains from California. These results suggest that cervids may be important in the natural maintenance of E. equi in California.

Disease outcome and cytokine responses in cats immunized with an avirulent feline infectious peritonitis virus (FIPV)-UCD1 and challenge-exposed with virulent FIPV-UCD8.

Eight cats were immunized with an avirulent strain of feline infectious peritonitis virus (FIPV)-UCD1, then challenge-exposed to a highly virulent cat passaged strain (FIPV-UCD8). Th1 and Th2 cytokine profiles in the peripheral blood mononuclear cells (PBMCs) were measured throughout in the experiment. No clinical signs of FIP were evident in the experimental cats after immunization. After challenge, the immunized cats demonstrated one of four clinical outcomes: (1) classical effusive FIP; (2) accelerated FIP; (3) non-effusive FIP, or (4) resistance to challenge. Only minor cytokine changes were observed following immunization, however, several cytokine changes occurred following challenge-exposure. The most noteworthy changes were in tumor necrosis factor-alpha (TNF-α) and interferon gamma (IFN-γ) levels. Our preliminary findings suggest that immunity against FIP is associated with TNF-α and IFN-γ response imbalance, with high TNF-α/low IFN-γ mRNA responses favouring disease and low TNF-α/high IFN-γ mRNA responses being indicative of immunity.

Virulent systemic feline calicivirus infection: local cytokine modulation and contribution of viral mutants.

Virulent systemic feline calicivirus (VS-FCV) is a novel, emerging pathogen with mortality up to 67% even in previously healthy adult cats; VS-FCV has resulted in at least six epidemics since 1998. Affected cats have systemic vascular compromise and hemorrhagic-fever like signs in part due to viral invasion of epithelium and endothelium, coupled with host cytokine responses. Affected skin tissues had, on average, 3.8 elevated cytokines compared with control tissue, with prominent upregulation in IL-10, TNF-α, and MIP-1α. Sequencing of most of the genomes of two VS-FCV strains documented patterns of virus relatedness and implicated changes in the capsid gene in the emerging phenotype, possibly through initiation of immune mechanisms manifest in the cytokine changes. Understanding the features contributing to the emergence of this disease is critical for management and prevention of this and similar outbreaks attributable to RNA viruses in animals and humans.