Browsing by Author "Fu, Zhen Fang"
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- ItemEpidemiology of equine herpesvirus infections : a thesis presented in partial fulfilment of the requirement for the degree of Master of Philosophy in Veterinary Science at Massey University(Massey University, 1985) Fu, Zhen FangThe epidemiology of infections with equine herpesvirus (EHV) types 1 and 2 in foals on a Thoroughbred stud in New Zealand was investigated. As part of this study an ELISA test was developed to measure antibody titres to EHV-2 in equine sera. All the sera collected from the foals before the ingestion of colostrum were negative for antibodies to both EHV-1 and EHV-2. Soon after sucking, these foals had serum antibody levels against these two viruses similar to those of their dams. The maternally derived antibody to EHV-1 lasted for 3-4 months and antibody titres rose again at around weaning time. In contrast, passively acquired antibody to EHV-2 was rapidly supplemented by actively produced antibody. Serological evidence suggested that most of the foals (85%) became infected with EHV-1, and 25% were reinfected in their first ten months of life; however EHV-1 was not recovered either from these mares or their foals during the investigation period despite the large increase in antibody titres. Serological evidence of EHV-1 infection in foals indicated that this occurred around the time of weaning when the maternally derived antibody had declined to a level which was presumably unprotective. The clinical signs which developed after EHV-1 infection were very mild, the main symptom observed being a profuse nasal discharge usually lasting two or three days, occasionally with an elevation of body temperature. The source of EHV-1 infection in foals could not be determined and there was no evidence to suggest that their dams were infected with EHV-1 around the time when the foals became infected. However, a relationship between preinfection antibody titres (log 103) against EHV-1 and the viral infection was observed. In contrast, EHV-2 was isolated from all of the foals by 2 to 4 months of age. The virus infection persisted in these animals for 2 to 6 months and stimulated continuous production of antibody. As soon as the antibody level against EHV-2 reached a peak, the isolation of the virus decreased, and eventually EHV-2 was no longer isolated from these foals by 9 months of age. The foals possibly contracted EHV-2 infection from their dams since some of them excreted the virus around the time when EHV-2 was isolated from their foals. Clinical reactions at around the time of EHV-2 infection varied from foal to foal, ranging from subclinical to fever, mucopurulent nasal discharge and swollen submandibular lymph nodes. Two severely affected foals from which EHV-2 was isolated died of complications resulting from secondary bacteraemia. From these findings, an association between EHV-2 and the respiratory disease observed in these foals was postulated. However, the possible role of EHV-2 as a pathogen for young foals needs confirmation by further studies including experimental infection of gnotobiotic foals. A trail for evaluation of Pneumabort-K (an EHV-1 subtype 1 vaccine) was conducted in these foals. Animals inoculated with the vaccine at the age of 30 and 60 days failed to respond serologically to the immunization, and it was assumed that this was due to the intereference of the high levels of passively acquired antibody. Based on this observation, another EHV-1 vaccination procedure for foals commencing at 80-90 days was recommended.
- ItemEpidemiology of porcine rotaviral infections : a thesis presented in partial fulfilment of the requirements for the degree of Doctor of Philosophy in Veterinary Virology at Massey University(Massey University, 1988) Fu, Zhen FangThe epidemiology of porcine group A rotavirus was studied in commercial herds of pigs in New Zealand. A commercial enzyme-linked immunosorbent assay (ELISA) kit (Dakopatts, Copenhagen) was found to be highly sensitive (100%) and specific (96.8%) for the detection of group A rotavirus in pig faeces when compared to electron microscopy (EM). A highly sensitive and specific ELISA test for the measurement of antibody against group A rotavirus in pigs was also developed. Of 521 faecal samples collected from Massey University Piggery in a cross-sectional survey, 47 (9%) were positive for group A rotavirus by the ELISA test. Only sucking (19.3%) and weaner (14.4%) pigs were shedding rotavirus. Rotavirus was not detected in the faeces of fattener pigs (over two months old) or adult pigs including sows and boars. Three cohort studies revealed that all pigs became infected with group A rotavirus before they were 40 days of age and shed the virus for an average of eight days. Some of the piglets shed rotavirus a second time approximately 10 days after the first period of shedding. All piglets ceased to shed the virus by two months of age. Rotaviral shedding was associated with the occurrence of milk scours in sucking piglets. Diarrhoea in weaner pigs (post-weaning diarrhoea, PWD) was more closely associated with the presence of haemolytic E.coli than with rotavirus in faeces. Infection with group A rotavirus was transmitted from piglet to piglet and from litter to litter. In one cohort of 50 piglets from five litters, shedding of rotavirus was first detected in one litter, then in the second litter two days later, and finally in other litters of piglets. Over a period of 16 days, all piglets in the five litters were infected. Group A rotavirus was also detected in dust, faeces and effluent collected from the farrowing and weaner houses, and from a weaner house which had not been used for three months. Rotavirus was not detected in any of the sows (11) during the period of investigation. Neither was rotavirus detected in fattener pigs (from two months of age to the time of slaughter), nor in the environments where old pigs (fattener and sow houses) were housed. It was not therefore possible to confirm that adult pigs, especially sows, act as carriers for rotaviral infection of young piglets as has been suggested by other workers. All the piglets acquired maternal antirotaviral antibody from their dams and the levels of antibody in piglets' sera were comparable to those in the colostrum of their dams. The maternally-derived antibody was also detected in piglets' faeces. Antibody in sera and in faeces declined rapidly after birth. Rotaviral shedding commenced in each of the cohorts when the geometric mean ELISA antibody titre fell below 1/1600 (equivalent to serum neutralizing antibody titre of 1/8 to 1/16). However, this correlation between antibody titres and protection was not observed in individual litters. In each of the cohorts studied, rotaviral shedding was usually detected initially in one or two piglets of a litter. The infection then spread to other piglets within the same litter and, finally, to piglets of other litters in the same group. Onset of rotaviral infection in particular litters was related to their location in the farrowing unit rather than to the levels of antibody. The shedding pattern of group A rotavirus was studied further in another five New Zealand piggeries and was found to be similar to that observed at the Massey University Piggery. Faecal samples from these piggeries were analyzed by polyacrylamide gel electrophoresis (PAGE) and no common electrophoretype of group A rotavirus was found in these piggeries. More than one electrophoretype of group A rotavirus was detected in three of these piggeries. Faecal samples collected from Massey University Piggery were also analyzed by PAGE and it was found that rotaviruses detected during the first two years of the present investigation had identical electrophoretypes, but one isolate detected in the third year had a distinctively different pattern. Non-group A rotaviruses were also detected for the first time in New Zealand. Nine samples had an electrophoretic pattern similar to that of group C rotavirus and one was similar to that of group B rotavirus. One of the samples containing group C rotavirus was from two litters of piglets with diarrhoea at two to four days of age. In one of these piggeries, five electrophoretypes of rotaviruses representing three groups were detected. These observations indicate that rotaviral infections are important causes of milk scours in piglets, and are probably significant in exacerbating PWD. The epidemiology of rotaviral infections is complicated by a number of factors. These include the continuous transmission of virus from pig to pig and from litter to litter, the survival of the virus in the piggery environment, the incomplete protection afforded by maternally-derived antibody, and the simultaneous circulation of different strains and different groups of rotavirus in one piggery.