Listeria species in foods of animal origin.
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Animal Feed↗
Biomedical subjects
D J Hampson
Publications and source records attributed to D J Hampson.
Transfer of maternal antibody against group A rotavirus from sows to piglets and serological responses following natural infection.
An enzyme-linked immunosorbent assay (ELISA) was developed for the measurement of antirotaviral antibody in sera and faeces from pigs and used to study the dynamics of antirotaviral antibody responses in three cohorts of pigs. Piglets acquired antirotaviral antibody by sucking their dams soon after birth. Antirotaviral antibodies of IgA and IgG classes were detected in both colostrum and milk of all sows tested but IgM class antibodies were not. The antibody levels in colostrum were eight to 32 times higher than those in milk which was collected 18 days post partum. The levels of antibody in piglets' sera were comparable to those in colostrum but declined quickly to low levels by one month old. Maternal antibody was also detected in the faeces of piglets up to 18 days old. Natural rotavirus infection occurred in each of these cohorts when the geometric mean ELISA titres of maternal antibody in their sera declined to 1/1600 (by days 21, 25 and 30 for cohorts 1, 2 and 3, respectively). However, a positive correlation was not obtained between the levels of antirotaviral antibody and protection in individual litters within each of the cohort groups. In each of the cohorts, rotavirus infection usually occurred in one or two piglets first and then spread to other piglets in the same cohort. It is therefore suggested that maternally derived antibody is protective against rotavirus infection in piglets only for the first one or two weeks. Following natural infection with rotavirus, increases in serum antibodies were detected in two of the three cohorts by 20 to 30 days after the average time of onset of faecal shedding of virus.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Detection and survival of group A rotavirus in a piggery.
Samples of dust, faeces and effluent were collected from a piggery and examined for group A rotavirus, using a commercial ELISA test, electron microscopy and inoculation of MA-104 cells. Rotavirus antigen was demonstrated in samples collected from farrowing and weaner rooms but not from fattener and sow houses. Rotavirus antigen was also detected in samples collected from a weaner room which had been free of piglets for three months. A cytopathic porcine rotavirus (British isolate SW20/21) was kept at room temperature for four months; it survived with titres reduced by 2 log10. These observations suggest that the environment of commercial piggeries is an important source of rotaviral infection for young piglets.
Animals↗
Typing of Treponema hyodysenteriae by restriction endonuclease analysis.
Restriction endonuclease analysis (REA) was used to type eight well-characterised strains of Treponema hyodysenteriae originating from the U.K., Canada and the U.S.A., and 16 isolates from cases of swine dysentery in Western Australia (W.A.). Several of the W.A. isolates were also serotyped by the method of Baum and Joens (1979), and the two typing techniques were compared. REA typing was more discriminatory than serotyping, being able to distinguish strains within serotypes. The new technique was neither more difficult nor more time-consuming to perform than serotyping. Within the 16 W.A. isolates, three different REA patterns were identified, with common patterns found on different farms. The eight overseas strains had seven different REA patterns, all of which could be distinguished from the patterns of the W.A. isolates.
Animals↗
Proposed revisions to the serological typing system for Treponema hyodysenteriae.
Antisera were prepared in rabbits against seven well-characterized strains of Treponema hyodysenteriae of known serotype, and reacted in agarose gel double immunodiffusion tests (AGDP) with lipopolysaccharide (LPS) extracted from 18 Western Australian isolates of the organism. Eight isolates were provisionally typed by this method, but sera raised against one 'typed' and two 'untypable' local isolates reacted in an unexpected fashion with LPS from other local and type strains. Serum raised against the 'typed' local isolate reached with LPS from other previously untyped local isolates: this indicated the presence of more than one major LPS antigen amongst certain local isolates, and was confirmed by cross-absorption of sera. Sera raised against apparently untypable local isolates reacted with LPS from certain type organisms, thus suggesting the presence of complex antigenic relationships between LPS antigens. The serotyping system for T. hyodysenteriae which was proposed by Baum & Joens (1979) uses unabsorbed antisera and is made unworkable by these observations. Instead we propose placing organisms which share common LPS antigens into serogroups A to E, members of which are defined by their reactivity with unabsorbed sera raised against a type organism for the group. We suggest strains B78, WA1, B169, A1 and WA6 respectively as being the most suitable type organisms for the five serogroups identified so far. Isolates possessing additional unique LPS antigens can be regarded as serotypes within the serogroup. However the serotype of an isolate can only be established if antiserum is prepared against it, and this serum continues to react homologously after cross-absorption with bacteria from other serotypes within the serogroup.
Animals↗
Analysis of lipopolysaccharide antigens of Treponema hyodysenteriae.
Lipopolysaccharide (LPS) extracts obtained from Treponema hyodysenteriae of serogroups A, B, D and E, and from T. innocens were examined by SDS-polyacrylamide gel electrophoresis (SDS-PAGE), silver-staining, and immunoblotting with hyperimmune rabbit sera. All organisms possessed multiple LPS bands, but their position and number differed. Immunoblotting of LPS with grouping sera identified three or four major antigenic LPS components in the 10-42 kDa range in all organisms: these components were largely specific to each type-organism of a serogroup, and presumably represented group antigens. Although some minor cross-reactivity occurred between LPS from organisms in the different groups, this was insufficient to merit changes to the current LPS serogrouping system for T. hyodysenteriae. Besides this LPS 'complex', other higher-molecular-weight material which appeared to be a common component of the treponemes examined was present in low concentrations. Organisms with different serotypes within a serogroup apparently possessed common LPS bands, but also had unique LPS bands which may account for their serotype specificity. One 'untypable' organism lacked group-specific LPS and was thought to be a mutant of a group B organism. The loss of serogroup LPS by the isolate suggested that this material is an external component of the cell wall. The availability of an atypical organism lacking LPS components may facilitate further studies on the pathogenesis of swine dysentery.
Animals↗
Epidemiology of typical and atypical rotavirus infections in New Zealand pigs.
Polyacrylamide gel electrophoresis (PAGE) and enzyme-linked immunosorbent assay (ELISA) were employed to investigate the epidemiology of typical and atypical rotavirus infections in five piggeries. Of 152 faecal samples examined, 46 (30 per cent) were positive by ELISA for group A rotavirus. Rotaviruses with electrophoretic patterns resembling groups A, B and C were detected. At least two and up to five different rotavirus electrophoretypes (typical and/or atypical) were detected in each of the five piggeries. Out of 152 faecal samples examined, 28 (18 per cent) contained rotaviruses with group A electrophoretypes, 9 (6 per cent) with group C but only 1 with Group B. Six samples contained both group A and group C rotaviruses. No common electrophoretypes of group A or C rotaviruses were detected in these five piggeries. The PAGE technique was also used to analyze group A rotavirus isolated sequentially from another piggery over a three year period. A single electrophoretype was found during the first two years, but in the third year a different electrophoretype was detected.
Journal Article↗
Natural transmission of group A rotavirus within a pig population.
Five litters of piglets born within two days of each other, together with their dams, were investigated for faecal excretion of group A rotavirus antigen from birth to two months old. All the 50 piglets in these litters became infected with the virus between 19 and 35 days old. Rotavirus excretion was first seen in one litter which was housed with other litters not included in this study. Two days later, piglets of the second litter in another farrowing room began to excrete rotavirus, and then infection spread to the other three litters in the same room. Within each of these litters, one or two piglets were infected early and thereafter infection spread to other piglets. It took four to 10 days for rotavirus to infect every piglet within a litter, and 16 days in total before all piglets in the five litters were infected. No rotavirus antigen was demonstrated in faeces from sows during the investigation period.
Animals↗
Managemental influences on the selective proliferation of two strains of haemolytic Escherichia coli in weaned pigs.
In an experimental study on a piggery it was found that haemolytic Escherichia coli of O-serotypes 138 or 139 proliferated in the intestinal tracts of pigs following weaning, with E. coli of the O-138 type also being occasionally recovered from unweaned pigs, and once from a sow. Organisms of the O-138 type produced heat labile enterotoxin and their presence in weaned pigs was associated with the development of severe post-weaning diarrhoea. E. coli of O-139 type produced a vero cell cytotoxin and were associated with a milder diarrhoea in weaned pigs. Under various managemental circumstances the O-138 type E. coli almost invariably proliferated after weaning. The O-139 strain of E. coli did however proliferate rather than the O-138 strain following the movement of weaned pigs to new accommodation, after weaned pigs were returned to their sow and then weaning again 5 days later, and very occasionally in pigs weaned at 5 weeks of age. In all these cases earlier proliferation of the O-138 E. coli had been detected, suggesting that this may be a prerequisite for proliferation of the O-139 strain.
Animals↗
Pre-weaning supplementary feed and porcine post-weaning diarrhoea.
Attempts were made to induce an intestinal hypersensitivity response to weaner diet by feeding pigs with small quantities of this material before weaning. In two trials using different weaner diets piglets subjected to this regimen showed no significant differences in small intestinal structure, in ability to absorb xylose, in bodyweight gain, in incidence of diarrhoea or excretion of enteropathogens after weaning compared with pigs not given any of the diet before weaning, or fed with a different diet before weaning. When post-weaning diarrhoea occurred it was associated with an earlier, more prolonged and greater proliferation of enterotoxigenic Escherichia coli in the small intestines than occurred in healthy pigs after weaning. The greater proliferation in pigs which developed diarrhoea could not be attributed either to an excessive dietary intake after weaning, or to a specific proliferation of rotaviruses.
Animals↗
Investigation of the source of haemolytic Escherichia coli infecting weaned pigs.
Attempts were made to discover the source of strains of haemolytic Escherichia coli infecting weaned pigs on a piggery. The organisms were not detected in the faeces of sows in the farrowing house, or in the in the faeces or intestinal tracts of slaughtered bacon pigs or sows. Sows held in a quarantine unit, and their offspring born in the unit, did not excrete haemolytic E. coli until after they were returned to the piggery. The environment of the piggery was the most likely source of infection for weaned pigs, and routine cleaning and disinfection of the accommodation did not prevent infection. Unweaned pigs were however able to transfer haemolytic E. coli to a newly built, previously unused weaning house, and establish a cycle of infection.
Animals↗
The osmolality of caecal contents in piglets following weaning.
Pigs weaned for five days had caecal contents with significantly lower osmolalities than those of unweaned animals of the same age. Supplementation of a standard weaning diet with therapeutic levels of oxytetracycline to suppress the normal large intestinal microbial flora did not significantly further reduce osmolarity of caecal contents after weaning. This observation suggests that microbial activity in the large intestine may not be sufficiently developed by five days after weaning to have a major influence on absorptive processes at that site. Incomplete development of the large intestinal microflora may be one more factor which acts to predispose the young pig to diarrhoea after weaning.
Journal Article↗
Group A rotavirus excretion patterns in naturally infected pigs.
Cross-sectional and cohort studies were conducted in a piggery to investigate the excretion pattern of group A rotavirus in pigs. The cross-sectional survey revealed that 47 (9 per cent) of 521 pigs sampled were excreting rotavirus in the faeces. No rotavirus antigen was detected in the faeces of pigs either less than one week or over two months old. The prevalence of infection increased with age over the sucking period, and was greatest at five weeks old. Diarrhoea was observed in only eight (17 per cent) of the pigs excreting rotavirus. Sixteen piglets from four litters were selected and faecal samples collected daily from each animal from birth to two months old. All the piglets excreted group A rotavirus and the range of ages at which they first became infected was between 13 and 39 days. The average duration of excretion in individual piglets was 7.4 days. Ten of 13 sucking piglets which excreted rotavirus developed diarrhoea soon after it was first detected.
Animals↗
Porcine parvovirus infection in a commercial piggery.
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Letter↗
A comparison of serotyping, BRENDA-typing and incompatibility grouping, and toxin testing of haemolytic Escherichia coli isolated from piglets before and after weaning.
Before weaning, some young pigs in a research piggery excreted in their faeces a weakly haemolytic non-enterotoxigenic serotype of Escherichia Coli. After weaning, all of the pigs excreted strongly haemolytic Escherichia coli of known enteropathogenic serotypes (0-138 and 0-139). The 0-138 serotype produced vero cell toxin, whilst the 0-139 serotype elaborated heat labile enterotoxin. Haemolytic enterotoxigenic E. Coli were also recovered from three-week-old unweaned piglets with so-called ;milk scours; and from pigs with post-weaning diarrhoea on two local commercial piggeries. Selected haemolytic isolates were compared using serotyping, bacterial restriction endonuclease DNA analysis (BRENDA) and incompatibility grouping. The three typing methods divided most of the isolates into the same groupings; the exceptions were two isolates with the same BRENDA pattern and incompatibility group, but with different H-serotypes, and eleven isolates with the same serotype and BRENDA pattern but which showed differences in colony compatibility such that they were divided into five subgroups of a single incompatibility type.
Journal Article↗
Influence of creep feeding and weaning on brush border enzyme activities in the piglet small intestine.
The activities of the enterocyte brush border enzymes lactase (beta-D galactoside galactohydrolase, EC 3.2.1.23) and sucrase (sucrose alpha-D glucohydrolase, EC 3.2.1.48) were measured at set percentage lengths along the small intestines of 112 piglets killed between 21 and 32 days of age. The influences on these activities of consumption of creep feed and of weaning were recorded. Weaning at three weeks old resulted in large, rapid reductions in lactase activity at most sites along the small intestine; sucrase activity declined temporarily and then recovered. Minimum values were recorded about four to five days after weaning. Similar changes were observed whether or not creep feed was consumed before weaning. Continued consumption of creep feed by unweaned pigs over the 21 to 32 day period also produced small but significant reductions in lactase activities. The large loss of digestive enzyme activities at brush borders in weaned animals coincided with a reduced ability to absorb xylose and to checks in growth rate in otherwise healthy piglets.
Aging↗
Attempts to modify changes in the piglet small intestine after weaning.
The possible causes of changes in the piglet small intestine after weaning were investigated. Groups of piglets weaned at three weeks old were either given oral oxytetracycline daily, weaned on to a regularly fed sow-milk replacer or weaned on to specially formulated diets based on casein or hydrolysed casein as the protein source. After five days, changes in small intestinal structure and brush-border enzyme activities were compared with previous findings in weaned and unweaned animals of the same age. The presence of enterotoxigenic Escherichia coli and rota-viruses in the intestines and the occurrence of diarrhoea were also noted. Consumption of the diet based on hydrolysed casein resulted in significant modifications to crypt depth and brush border enzyme activity at sites between 50 and 75 per cent along the length of the small intestine. Possible reasons for this protective effect, which include the low level of antigenicity of the diet, are discussed in relation to normal intestinal changes after weaning.
Animals↗
Alterations in piglet small intestinal structure at weaning.
The small intestinal mucosa of 112 piglets aged between 21 and 32 days was examined to identify the effects on its structure of weaning and of consumption of creep food. In unweaned control pigs a gradual increase in crypt depth occurred with age, while villus height altered little. In contrast, weaned pigs showed a highly significant increase in crypt depth and an increase in the complexity of villus morphology with a dramatic reduction in villus height. Crypts elongated most in the distal small intestine, while the loss of villus height was greatest proximally. No inflammatory reaction was seen and the alterations were not influenced by consumption of creep food before weaning. This failed to support the hypothesis that hypersensitivity to dietary antigens is involved in the aetiology of such intestinal changes. The reduction in small intestinal absorptive area and the appearance of a less mature enterocyte population help to explain the increased susceptibility of the pig to diarrhoea and growth checks in the post-weaning period.
Aging↗