"No-one realises what we go through as Type 1s": A qualitative photo-elicitation study on coping with diabetes.

AIMS: Type 1 diabetes (T1D) has physical, emotional, and social consequences and little is known how adults cope with the condition long term. This research aimed to use a novel photo-elicitation technique to gain in-depth insight into the personal coping experiences of adults living with T1D. METHODS: In-depth photo elicitation interviews were employed to collect data and transcripts were analysed using thematic analysis. RESULTS: Participant-led data revealed an overarching theme of the relentlessness of the condition. Continuous self-management tasks infiltrated participants' lives and had a significant impact on coping experiences. A range of techniques and resources were used to cope including using alarms and reminders, diabetes technology, interpersonal relationships, supportive healthcare services and seeking a mind-body balance. CONCLUSIONS: Technology shows promise for easing the burden of the condition, expert-led online support would be of benefit, and peer support should be prioritised within interventions for adults with T1D.

'She's not obese, she's a normal 5-year-old and she keeps up with the other kids': families' reasons for not attending a family-based obesity management programme.

AIMS: To discover the reasons behind invited families' lack of engagement with a family-based childhood obesity programme in a deprived area. METHODS: Interviews were conducted with 10 families who were invited to join the programme, but declined to engage. There were two distinct subgroups of participants: those who had no interest in attending the programme and those who showed initial interest yet did not continue attending. The two subgroups were analyzed separately using inductive thematic analysis, and then compared. RESULTS: Analysis identified eight themes overall. For both groups, when the service was perceived to be not needed ('I didn't see how that would help'), the families disengaged with it. For both groups, this perception was partly related to the perceived appearance of their children: either that they were not obese ('I didn't think my son was overweight') or that they were growing into their size. There was also a similarity in both groups that they perceived that they were already following healthy lifestyles. In addition, several of the themes arising from the families who had no initial interest were related to the impact of the letter that parents received detailing the result of their child being weighed and measured at school. This angered parents ('I was disgusted'), and there was a feeling that the approach was too generic. CONCLUSION: This study identified a number of potential reasons behind why families may decline to engage with a childhood obesity programme in a deprived area. Across all families, if the programme was perceived as not needed, they would disengage. For those who did not engage at all, the initial communication of the child's body mass index (BMI) is crucial. Recommendations include taking a more personal and tailored approach for the initial communication and shifting the focus of the programmes onto healthier lifestyles.

Comparison of the viral proteins of canine parvovirus-2, mink enteritis virus and feline panleukopenia virus.

Canine parvovirus-2 (CPV-2), Mink enteritis virus (MEV) and feline panleukopenia virus (FPV) were produced using identical cell culture and purification techniques. The distributions of the haemagglutinating activity of the three different parvoviruses in a CsCl gradient were similar with haemagglutinating peaks identified at 1.48-1.49, 1.42, 1.36 and 1.30-1.31 g cm-3. The number and distribution of the viral proteins and the equivalent protein molecular weights are similar for all three viruses in SDS-polyacrylamide gels (10%). Four viral proteins were identified and their molecular weights were determined: protein A (77 500-79 500), protein B (63 000-63 500), protein C (61 500-63 000) and protein D (50 000-55 000). The viral protein D although reported for some other parvoviruses has not previously been demonstrated in CPV-2, MEV or FPV.

An unusual form of motor neuron disease following a cat bite.

A case of motor neuron disease with clinical and pathological resemblance to amyotrophic lateral sclerosis (ALS) in a woman who was severely bitten on the ankle by a cat is described. Weakness first appeared at the ankles and relentlessly advanced proximally, terminating in death from pulmonary failure in a year. A number of unusual features that are uncharacteristic of ALS were found that included a markedly elevated antinuclear antibody titre in the serum and the presence of prominent oligoclonal bands in the cerebrospinal fluid. The spinal cord showed loss of anterior horn cells and pyramidal degeneration that are characteristic of ALS, but an extraordinary finding was the presence of transmural granulomatous inflammation of numerous small and medium sized vessels, especially veins, in the subarachnoid space around the cord. There were also inflammatory changes in the brainstem and spinal cord consisting of microglial and astrocytic nodules and perivenous cuffing by mononuclear cells. Ill-defined hyaline eosinophilic cytoplasmic inclusions were seen in some remaining anterior horn cells. No viral particles were found by electron microscopy despite an extensive search. Virological studies were inconclusive but there is reason to believe that this patient's illness was caused by an as yet unidentified virus.

Feline calicivirus infection in kittens borne by cats persistently infected with the virus.

On the basis of repeated isolation of feline calicivirus (FCV) from oropharyngeal swabs four to eight months after exposure to FCV strain 255, four carrier queen cats were identified. These cats gave birth to 16 kittens. Litters were individually housed with their mothers until nine weeks of age and were monitored virologically and serologically from birth until 15 weeks old. All kittens became infected between three and nine weeks old and shed FCV consistently for periods of three to 11 weeks. Clinical signs of FCV were observed in 11 kittens but none developed severe respiratory disease. At the time of initial infection maternal antibody titres in the kittens ranged from 1:4 to 1:24. Within one to three weeks of infection titres began to rise. The results indicated that kittens of queen cats persistently infected with FCV frequently experience mild or subclinical immunising infections.

Pathogenesis of canine parvovirus-2 in dogs: haematology, serology and virus recovery.

The pathogenesis of canine parvovirus-2 (CPV-2) was studied in orally inoculated conventional dogs using haematological, serological and virological techniques. Virus was first isolated from mesenteric lymph nodes on day 2 after exposure, tonsil on day 3 and small intestine on day 3. Viraemia occurred subsequently and was present in most dogs on days 4 and 5 after exposure. CPV-2 could be isolated from all tissues during viraemia. Relative pyrexia, lymphopenia and neutropenia occurred on days 5, 6 and 7 after exposure, respectively. Virus excretion in faeces began in most dogs on day 4 and continued despite the appearance of neutralising serum antibody. Specific serum antibody, detected in some dogs as early as day 3 and in all dogs by day 7 after exposure, eliminated viraemia and inhibited virus isolation from tissues in cell culture.

Pathogenesis of canine parvovirus-2 in dogs: histopathology and antigen identification in tissues.

The pathogenesis of canine parvovirus-2 was studied in orally inoculated conventional dogs using histopathological and peroxidase anti-peroxidase staining techniques. Lymphoid necrosis and depletion of lymphocytes from lymphoid tissues were most notable on days 5 and 6 after exposure. Lymphocyte hyperplasia occurred following day 7. Epithelial cell changes in segments of the small intestine were more severe on days 6 to 9 after exposure in areas associated with Peyer's patches and in the upper segments of the small intestine. The lymphocyte was the primary infected cell. Virus infected cryptal epithelial cells were not detected until 24 hours after the identification of infected cells in lymphoid tissues on day 4 after exposure. The majority of virus infected epithelial cells were found in crypts intimately associated with or adjacent to Peyer's patches in the upper segments of the small intestine.

The pathology and sites of persistence associated with three different strains of feline calicivirus.

The pathology and sites of multiplication associated with three different strains of feline caliciviruses are described. The main pathological lesions were found in the tongue, soft palate and lungs and like the clinical signs were of mild nature. Virus multiplication was associated mainly with the tissues of the mouth and tonsils and in asymptomatic carrier animals the tonsil appeared to be preferred organ of viral persistence.

The clinical disease and patterns of excretion associated with three different strains of feline caliciviruses.

Three groups of cats were infected intranasally with three different feline calicivirus strains: A3, 68/40 and M8. Each strain produced a uniformly muld upper respiratory tract disease, with glossal ulceration being the most prominent clinical sign. Virus was most consistently isolated from the oro-pharyngeal region and, in non-euthanised animals, excretion continued long after clinical signs had disappeared. It is suggested that an asymptomatic phase of excretion may be a normal sequel to FCV infections.

Prevalence of bovine parvovirus infection in Ontario dairy cattle.

Studies were conducted to determine prevalence and dynamics of bovine parvovirus (BPV) infection. Dairy cows from 29 randomly selected herds in southwestern Ontario were tested twice, one year apart, for the presence of hemagglutination inhibition (HI) antibodies against BPV. Fifty-one percent of 1141 cows tested had BPV-HI titers > 1:32. One year later, the seroprevalence was 83% in 1131 cows from the same farms. The herd mean seroprevalence was 49% and 86% for the year-1 and year-2 samples, respectively. Evidence of BPV infection was found in 96% (27/28) of herds in year-1 and 100% of herds in year-2. A comparison of titers from 716 cows tested twice showed evidence of frequent BPV infection. Sixty-two percent of 326 animals selected in a systematic manner from 40 Guelph area dairy farms had BPV-HI titers > 1:32. The herd mean seroprevalence was 64% Two herds had no animals with titers above the critical titer (1:32) while in one-quarter of the herds all animals exceeded the critical titer.

Effect of orally administered ribavirin on experimental feline calicivirus infection in cats.

Ribavirin administered orally at 75 mg/kg/day in 3 divided doses for 10 days, beginning either 1 or 4 days, after aerosol exposure of cats to calicivirus strain 255, failed to have any beneficial effect on the clinical course of the disease or to reduce viral excretion. Indeed, there was enhanced severity of the clinicopathologic findings in the treated exposed group, due largely to hemorrhage resulting from profound thrombocytopenia. Other toxic effects included depression of red and white blood cells, increased alanine aminotransferase activity, icterus, and body weight loss. Toxic effects were largely reversed within 1 week of cessation of treatment.

In vitro antiviral efficacy of ribavirin against feline calicivirus, feline viral rhinotracheitis virus, and canine parainfluenza virus.

Ribavirin had marked in vitro activity against feline calcivirus, strain 255, and canine parainfluenza virus, but showed only slight antiviral effect on feline viral rhinotracheitis virus. Antiviral activity was manifested by partial to complete suppression of viral cytopathic effect and of viral replication, depending on concentration of ribavirin in the culture medium and dosage of viral inoculum. Concentrations of ribavirin as small as 3.2 microgram/ml and 1.0 microgram/ml showed some activity against feline calcivirus and canine parainfluenza virus, respectively.

Vaccination against feline viral rhinotracheitis in kittens with maternally derived feline viral rhinotracheitis antibodies.

The efficacy of a modified live-virus intranasal vaccine and a killed-virus adjuvanted parenteral vaccine in inducing protective immunity against feline viral rhinotracheitis (FVR) was evaluated in kittens with and without maternally derived FVR antibodies. The intranasal vaccine was given as a single dose to kittens 5 weeks old, and the parenteral vaccine was administered in 2 doses at 5 and 7 weeks of age. Seroconversion was delayed for 5 to 10 days in kittens with maternally derived antibodies, but occurred in all vaccinated kittens by 8 weeks of age. When virulent FVR virus was given, both vaccines provided satisfactory protection against disease but did not prevent infection. The results indicated that the modified live-virus intranasal vaccine or the killed-virus adjuvanted parenteral vaccine can be used successfully in kittens with residual maternally derived FVR antibodies.

Immunogenicity and safety of an inactivated vaccine for the prevention of rhinotracheitis, caliciviral disease, and panleukopenia in cats.

An inactivated vaccine for the prevention of feline viral rhinotracheitis (FVR), caliciviral disease, and panleukopenia has been developed. The efficacy of this vaccine for protection against FVR and caliciviral disease was assessed by vaccination of 41 cats and challenge of immunity with rrither FVR virus or feline calicivirus (FCV), strain 225. All vaccinates cats developed serum neutralizing (SN) antibody (mean SN50 1:45.5) to FVR virus, and 95% developed antibody (mean SN50 1:8.1) to FCV, strain 255. Following FVR challenge, the mean cumulative score of clinical signs was 1.1 for vaccinated cats versus 22.2 for controls. Following FCV challenge, the mean scores were 2.7 for vaccinated and 17.5 for controls. Immunogenicity of the panleukopenia fraction was demonstrated by the development of neutralizing antibody titers > 1:8 in all 21 vaccinates that were tested.

Antibody response to an inactivated vaccine for rhinotracheitis, caliciviral disease, and panleukopenia in nondomestic felids.

The efficacy of an inactivated vaccine for the prevention of feline viral rhinotracheitis (FVR), feline caliciviral disease (FCVD), and feline panleukopenia (FPL) was tested in 27 nondomestic adult felids from 7 species. The vaccine was given IM at the standard domestic cat dose in 19 animals and double this dose in 8 others. The animals were vaccinated either 1, 2, or 3 times. Serum-neutralization (SN) antibodies to FVR (mean SN titer, 23) developed in all 15 animals that were previously seronegative, and SN antibodies to FCVD (mean SN titer, 11) developed in 19 of 21 animals that were previously seronegative. There was no significant increase of SN antibody titers by doubling the vaccine dose or by administering a 3rd vaccination. The optimal response could be obtained by using the domestic cat vaccination protocol of a single dose given twice, 4 weeks apart. The critical evaluation of the SN antibody titer for FPL was complicated by preexisting titers to FPL from previous vaccinations, but in 23 animals the titers became higher, whereas they remained unchanged in only 4 animals. The persistence of the SN titers was evaluated 7 to 9 months later and found to be satisfactory for FVR (mean SN titer, 18) FCVD (mean SN titers, 43) and FPL (mean SN titer, 517). Enhanced persistence of titer could not be demonstrated by doubling the dose or administering a 3rd vaccination.

Suspected parvovirus infection in porcupines.

During a 142-day period, 6 porcupines died or were killed after becoming moribund. Three had severe acute necrotizing enteritis; two had acute necrotizing myocarditis, one with concurrent lymphocytic-plasmacytic enteritis; and one had chronic enteritis. Histologically, the acute necrotizing enteritis was characterized by villous fusion, blunting, and crypt dilatation. Many dilated crypts contained necrotic debris and were lined by flattened enterocytes. Acidophilic intranuclear inclusions were in colonic epithelial cells in one of these animals. The myocardial lesions consisted of degenerating shrunken myofibers, with infiltrating neutrophils and lymphocytes. Myofiber mineralization was evident in one animal. Though the histologic findings were indicative of parvovirus infection, electron microscopic, serologic, and virologic studies failed to demonstrate parvovirus as the etiologic agent.

Persistent viral infection. The carrier state.

A persistent viral infection is one in which the virus in a replicating or non-replicating form persists in the host beyond the normal recovery and elimination period for that particular viral infection. The clinical significance and mechanisms of persistence, when known, are discussed for the important viral infections of dogs and cats. Particular emphasis is given to feline viral rhinotracheitis, feline calicivirus, canine distemper, and feline leukemia.

Experimental induction of feline viral rhinotracheitis virus re-excretion in FVR-recovered cats.

The re-excretion of feline viral rhinotracheitis (FVR) virus (feline herpesvirus I) by FVR-recovered cats is recorded both spontaneously and following a variety of stimuli, namely, corticosteroid administration, change of housing, and parturition and lactation. At least 27 of 33 (82%) FVR-recovered cats studied were shown to be viral carriers. The carrier state was characterised by periods of viral latency interspersed with episodes of viral shedding. Administration of 0-75 mg dexamethasone trimethylacetate and 2-25 mg prednisolone on days 0,2 and 4 resulted in re-excretion after a mean lag period of 7-2 days in 22 of 32 (69%) FVR-recovered cats on a total of 31 of 57 (54%) occasions. Rehousing resulted in virus re-excretion after a mean lag period of 7-2 days in four of 22 (18%) cats tested on a total of six of 40 (15%) occasions. Apparently spontaneous shedding occurred on a total of 10 occasions in nine of 31 (29%) cats during a mean observation period of 8-8 months. Four of six FVR-recovered queens in a total of four of 10 litters (40%) shed virus within two to 10 weeks of parturition. Serum neutralising antibody titres were generally boosted at the time of first re-infection but afterwards remained essentially constant. Although 82% of cats in these studies were shown to be viral carriers, only 45% of cats shed virus spontaneously or as a result of the natural stress situations and it is postulted that these naturally excreting cats are of most significance epidemiologically.

Transmission of feline viral rhinotracheitis.

The transmission of feline viral rhinotracheitis (FVR) virus was investigated. Virus could be successfully transmitted between shedding carrier cats and unrelated susceptible kittens, but only if there was intimate contact between them. Studies on the transmission of FVR virus from carrier queens to their kittens showed that although four of 10 queens shed virus in the post partum period, a total of only four kittens from three litters developed a contact infection. All four kittens remained asymptomatic. Two shed for one day only and did not become carriers (as evidenced by corticosteroid treatment) and two shed for 15 days and 25 days and were subsequently shown to have become carriers. None of the remaining kittens tested shed virus. There was no evidence of in utero transmission between FVR-recovered queens and kittens. Passive antibody titres in kittens born to FVR-recovered queens declined to less than 1 in 4 in individual animals by two to 10 weeks of age. Mean titres calculated from a linear regression equation reached less than 1 in 4 and less than 1 in 2 by six and nine weeks of age, respectively. Experiments using a multistage liquid impinger demonstrated that FVR virus was unlikely to be transmitted between cats by aerosol and this was confirmed by the ability of a sentinel cat to withstand virus shedding from carriers over a six month period, although housed in the same air space.