Development of post-weaning diarrhoea in piglets. Relation to presence of Escherichia coli strains and rotavirus

Weaning of piglets complicated with an exposure to pathogenic strains of Escherichia coli was scrutinized in two sets. The first set comprised 20 animals representing two litters and the second set included 30 animals from five litters. The piglets were either left as controls or exposed to one or three pathogenic strains of E. coli. Aiming to simulate a natural exposure the challenge strains were spread on the floor of the pens at weaning. In addition the pigs experienced several non-infectious stress factors commonly occurring at that occasion. Some groups were given adrenocorticotropic hormone (ACTH), aiming to simulate a stressful weaning. The balance and the composition of the faecal coliform populations, measured by a metabolic fingerprinting method, was disturbed among all animals following weaning. This disturbance was more pronounced and lasted longer among piglets exposed to pathogenic strains of E. coli. All piglets exposed to pathogenic E. coli shed these strains in faeces. Diarrhoea was induced in the groups exposed to E. coli, but not among the control animals. Pigs not treated with ACTH and subjected to a single pathogenic strain of E. coli became infected but did not develop diarrhoea unless if coinciding with shed of rotavirus. Control pigs excreting rotavirus had no diarrhoea. Diarrhoea was most frequent in the groups exposed to three pathogenic strains of E. coli, and in these groups diarrhoea was seen in the absence of rotavirus. ACTH administration amplified the clinical signs. The litter of origin influenced the development of post-weaning diarrhoea.     

Quantitative analysis of the gastrointestinal flora in the piglet prior and after weaning with special reference to the pathogenesis of Coli-enterotoxemia]

The gastro-intestinal flora of clinically intact piglets on an industrialised sow unit was investigated prior to weaning (n = 12) and after weaning (n = 12). The age of the former group was 23 to 36 days and that of the latter between six and eleven days. While enormous proliferation of haemolysing E. coli was recorded from the anterior portion of the small intestine in the post-weaning group, weaning, quite, generally, was found to have only little impact upon the gastrointestinal flora of piglet. More particularly were there no indicators to the effect that post-weaning proliferation of enteropathogenic strains was favoured by any correlation whatsover between E. coli and other bacterial species or between different types of E. coli. Other factors of possible importance to the pathogenesis of coli-enterotoxaemia are discussed with reference to literature.     

Development of Post‐weaning Diarrhoea in Piglets. Relation to Presence of Escherichia coli Strains and Rotavirus

Weaning of piglets complicated with an exposure to pathogenic strains of Escherichia coli was scrutinized in two sets. The first set comprised 20 animals representing two litters and the second set included 30 animals from five litters. The piglets were either left as controls or exposed to one or three pathogenic strains of E. coli. Aiming to simulate a natural exposure the challenge strains were spread on the floor of the pens at weaning. In addition the pigs experienced several non‐infectious stress factors commonly occurring at that occasion. Some groups were given adrenocorticotropic hormone (ACTH), aiming to simulate a stressful weaning. The balance and the composition of the faecal coliform populations, measured by a metabolic fingerprinting method, was disturbed among all animals following weaning. This disturbance was more pronounced and lasted longer among piglets exposed to pathogenic strains of E. coli. All piglets exposed to pathogenic E. coli shed these strains in faeces. Diarrhoea was induced in the groups exposed to E. coli, but not among the control animals. Pigs not treated with ACTH and subjected to a single pathogenic strain of E. coli became infected but did not develop diarrhoea unless if coinciding with shed of rotavirus. Control pigs excreting rotavirus had no diarrhoea. Diarrhoea was most frequent in the groups exposed to three pathogenic strains of E. coli, and in these groups diarrhoea was seen in the absence of rotavirus. ACTH administration amplified the clinical signs. The litter of origin influenced the development of post‐weaning diarrhoea.     

Preliminary investigations of the distribution of Escherichia coli O149 in sows, piglets, and their environment

Little is known about the sources and kinetics of enterotoxigenic Escherichia coli colonization in pigs during the pre-and post-weaning period. In this study, farrowing pens, sows, and piglets were tested for the presence of E. coli O149 by real-time polymerase chain reaction (PCR) after bacterial culture pre-enrichment on 2 farms, one with a history of post-weaning diarrhea (problem farm - PF) and the other without such a history (non-problem farm - NPF). Unlike those on the PF, the sows from the NPF did not carry E. coli O149 before parturition, although they were colonized to frequencies similar to animals on the PF soon afterwards. Most piglets from the NPF were colonized within a week after birth, whereas only a small proportion of those on the PF were colonized during that period. No difference was observed in the frequency of piglet colonization at the 2 farms either at weaning or during the following week. Post-weaning diarrhea (PWD), which is caused by enterotoxigenic E. coli (ETEC), is a multifactorial disease. The presence of ETEC alone is not always sufficient for the disease to develop. Many other factors are considered to be associated with the occurrence of PWD, including feed type (1,2), feeding regimen (1,3,4), the presence of other infectious agents (3,5), weaning age, and weight (6). Weaning, which is considered to be a major physiological and psychological stress factor, is critical for the disease to occur (7). Although piglets are already colonized with ETEC before weaning (4,8), on many farms, clinical disease occurs only after weaning (1). Both sows (9,10) and the environment (6) could be possible sources of infection for piglets, but results from previous studies have not resolved this issue because of the low sensitivity of ETEC detection methods. This study provides preliminary data based on a sensitive detection method for E. coli O149 in pigs and their environment. The results demonstrate the potential of real-time PCR for future studies on this topic.     

The effect of dietary spray-dried porcine plasma on clinical response in weaned piglets challenged with a pathogenic Escherichia coli.

Weaned piglets were used to determine the effect of dietary spray-dried porcine plasma (SDPP) on the clinical response to an infection with a pathogenic Escherichia coli (E. coli) O139:K82 LT(-). The piglets were divided into two groups of 10 animals each. One group was fed the control diet containing soybean(meal) plus whey powder. The test piglets were fed a diet with 8% SDPP. Piglets were orally infected with the challenge strain on days 6 and 7 after weaning. The experimental period lasted 14 days after which the piglets were euthanised and necropsied. Faecal samples were collected daily for bacteriological analysis. Segments of jejunum, caecum and rectum were removed for bacteriological analysis post mortem. Feed intake and weight gain, faecal and condition scores and body temperature were measured daily. In the control and SDPP groups, 6 and 7 piglets died from diarrhoea. The average daily feed intake (ADFI) and average daily gain (ADG) were substantially higher in the SDPP group than in the control group. SDPP-fed piglets generally had a more favourable faecal score and a healthier appearance than did the control piglets. The faecal excretion of E. coli O139:K82 was similar for control and test piglets. There were no diet effects on the E. coli O139:K82 counts at different sites of the intestine. In this experiment, the inclusion of SDPP at an economically acceptable percentage in the diet could not prevent piglet losses due to challenge with a pathogenic E. coli, but improvements of ADG, ADFI and faecal and condition scores were achieved.     

In vivo and in vitro colonization patterns of AIDA-I-positive Escherichia coli isolates from piglets with diarrhea.

Transmission electron microscopy (TEM) was used to characterize the colonization patterns of 3 pathogenic Escherichia coli strains: PD58 and PD149 of the AIDA-I/STb/EAST1 pathotype, serogroup O: ND (not determined), and PD31 of the LT/STb/EAST1 pathotype, serogroup O149. These strains were isolated from diseased piglets and caused diarrhea in experimentally inoculated, newborn, colostrum-deprived pigs. In this study, intestinal tissues from newborn pigs experimentally infected with a high inoculum (20 ml containing 10(10) cfu) were harvested and examined for bacterial colonization using light microscopy. A nonaqueous perfluorocarbon fixation method was used to preserve the glycocalyx of the microvillus border in tissues collected for TEM. Transmission electron micrographs revealed that E. coli strain PD149 displayed long flexible fimbria-like structures that intimately attached the bacteria both to the microvillus border of the upper colon and to adjacent bacteria. In vitro, this strain demonstrated the localized adherence pattern to HEp-2 cells characteristic of enteroaggregative E. coli (EAggEC). Both PD58 and PD31 strains colonized the upper colon through the formation of a biofilm, also characteristic of EAggEC. Strains PD58 and PD31 adhered poorly to HEp-2 cells in vitro, although these demonstrated a colonization pattern suggestive of diffuse and aggregative adherence, respectively. These findings suggest that strains PD58 and PD149, expressing the AIDA-I, factor and strain PD31 represents hybrid pathotypes of diarrheagenic E. coli and that they probably cause diarrhea in piglets through differing mechanisms.     

Age-dependent competition of porcine enterotoxigenic E. coli (ETEC) with different fimbria genes - short communication

To investigate the association of pathogenic Escherichia coli fimbrial adhesins with the development of diarrhoea in piglets of different age groups and to test their relative competitiveness, piglets were orally inoculated with a mixture of E. coli strains harbouring F4, F5, F6, F18 and F41 fimbrial genes. A total of 537 E. coli strains with haemolytic activity were isolated from 36 diarrhoeic piglets. The F4 fimbrial gene was observed in 98.5%, 97.6% and 80.6% strains carrying fimbrial genes isolated from diarrhoeic piglets that were infected at 1, 3 and 5 weeks of age, respectively. These data demonstrate that F4 fimbriae are highly associated with diarrhoea in piglets of all age groups. Interestingly, the F18 fimbrial gene was observed in 2.4% and 25.4% strains carrying fimbrial genes isolated from the 3- and 5-week-old groups, respectively, which confirms that F18 fimbriae are associated with diarrhoea in piglets from late stages of suckling to post-weaning, and are more related to diarrhoea in weaned than in unweaned piglets.     

Experimental models of porcine post-weaning colibacillosis and their relationship to post-weaning diarrhoea and digestive disorders as encountered in the field

The aim of this study was to develop a reliable model system of porcine post-weaning colibacillosis, and in doing so to assess the primary relationship of enterotoxigenic Escherichia coli to post-weaning diarrhoea and digestive disorders as encountered in the field. Six sequential experiments were carried out using 168 SPF piglets weaned into an optimal controlled environment at 28 days of age. The piglets were allocated to 23 treatment groups, 17 of which were inoculated either orally or intragastrically with enterotoxigenic strains of E. coli (LT+, STI+, STII+) possessing adhesive factors including K88 (F4). The piglets were challenged either once (Day 4 post-weaning) or on several days post-weaning, with the challenge load for each inoculation varying from 10(8) to 10(12) CFU.Overall 14.5% of inoculated pigs developed severe illness and died: these had lesions in their digestive tracts typical of colibacillosis. Diarrhoea occurred on at least 1 day in 50% of inoculated pigs, but was transient (1.7 days on average), appeared very soon after challenge (sometimes within half a day), and was accompanied by signs of depression and low weight gain. Generally a prompt recovery then occurred. In the second 2 weeks post-inoculation daily weight gain reached the same level in most inoculated groups of pigs as in the uninoculated controls. Only a small number of pigs developed a chronic enteritis lasting several days, as is typically observed in field cases. Diarrhoea was more common in the piglets that were tested adhesive positive to the K88 fimbriae receptor, but the disorders were no more severe in these animals. The response of all pigs depended primarily on the inoculum used, and especially on the challenge load. Although enterotoxigenic E. coli are clearly important in the aetiology of post-weaning diarrhoea, other factors are also required for the production of the chronic post-weaning digestive disorders and ill-thrift that are commonly encountered in commercial piggeries.     

Aspects on feed related prophylactic measures aiming to prevent post weaning diarrhoea in pigs

The ability of feed related measures to prevent or reduce post weaning diarrhoea (PWD) was examined in a split litter study including 30 pigs from 6 litters allotted into 5 groups. Four groups were exposed to 3 pathogenic strains of E. coli via the environment at weaning. Three of them were given zinc oxide, lactose+fibres or non-pathogenic strains of E. coil as probiotics. The challenged and the unchallenged control groups were given a standard creep feed. Diarrhoea was observed in all challenged groups but not among uninfected animals, and the incidence of diarrhoea was lower in the group given nonpathogenic E. coli compared to all other challenged groups. The severity of PWD also differed between litters. When corrected for mortality due to PWD, a decreased incidence of diarrhoea was also seen in the groups given zinc oxide or lactose+fibres. The dominating serotype of E. coil within faecal samples varied from day to day, also among diarrhoeic pigs, indicating that diarrhoea was not induced by one single serotype alone. The diversity of the faecal coliform populations decreased in all piglets during the first week post weaning, coinciding with an increased similarity between these populations among pigs in the challenged groups. This indicated an influence of the challenge strains, which ceased during the second week. The group given lactose+fibres was least affected with respect to these parameters. In conclusion feed related measures may alleviate symptoms of PWD.     

Escherichia coli post-weaning diarrhoea occurrence in piglets with monitored exposure to creep feed

The objective of the study was to investigate the effect of offering supplementary creep feed to piglets during the suckling period on the faecal shedding of haemolytic Escherichia coli bacteria and occurrence of spontaneous post-weaning diarrhoea 0-5 days after weaning. Supplementary creep feed was offered to half of the piglets in 12 litters, from 2 weeks of age until weaning at 4 weeks, and the individual feed contact was recorded by direct observations. It was found that diarrhoea occurrence was associated with faecal shedding of haemolytic E. coli bacteria (p=0.003), specifically E. coli O149 (p=0.004). Occurrence of diarrhoea and faecal shedding of haemolytic E. coli was not associated with creep feeding per se. However, the faecal E. coli O149 shedding occurred significantly less often in piglets that were offered creep feed in the suckling period but only showed limited interest in the feed (i.e. contacted the feed less than or equal to the median level of contact) compared to piglets that had frequent creep feed contact or piglets that had not had access to creep feed at all (p=0.015). Correspondingly, the diarrhoea occurrence tended to be lower in these piglets (p=0.081). Piglets with low creep feed contact during the suckling period ate the same total amount of feed during the 5 days after weaning, however, they ate less feed on days 0-2 after weaning compared to the piglets with frequent creep feed contact and non-creep fed piglets. It is suggested that intestinal function associated with a voluntary low creep feed contact during the suckling period leads to decreased feed intake just after weaning, and thus reduces the intestinal proliferation of E. coli O149 in these piglets.     

Verification of the protective effect of a toxoid vaccine against edema disease of weaned piglets in an infection model

105 piglets (56 vaccinated and 49 control animals) were utilized in 6 consecutive experiments. Each used litter was divided randomly into vaccine and control animals. One week prior to weaning each of the 56 piglets of the vaccine groups received 5 mg of nonpurified toxin treated with glutaraldehyd subcutaneously whereas to the remaining 49 control animals an extract of apathogenic E. coli was administered. During the first 12 hours post weaning each of the 105 piglets was challenged perorally with 10(10) cfu of edema principle toxin producing germs of E. coli serogroup O 139. 23 animals of the control groups (46.9%) and one animal of vaccine groups (1.8%) died due to the infection between days four and five post challenge. These control animals showed classical clinical symptoms as well as pathological findings typical for edema disease. In contrast, such findings as mentioned before could not be observed in the vaccinated piglets. The remaining part of the control animals and eight of those vaccinated ones exhibited edema disease symptoms. The vaccinated animals have shed the challenge strain one to three days, while the survivals of control groups shed those germs for two to six days. The vaccinated piglets showed a better growth rate than the remaining control animals. Presented data suggest that our toxoid immunizing procedure can be used successfully against edema disease of swine.     

苏太仔猪FUT1基因M307位点多态性与F18大肠杆菌抗病相关性的体外鉴定

采用PCR-RFLP方法检测了江苏苏太断奶仔猪FUT1基因M307位点等位基因多态性分布,在所检的49头仔猪中,GG基因型个体16头,AG基因型19头,AA基因型14头。在此基础上,制备上述不同基因型个体仔猪小肠上皮细胞,分别与表达F18ab菌毛的野生型大肠杆菌、表达F18ac菌毛含fed操纵子全基因的重组大肠杆菌和V型系统表面分泌表达F18abFedF亚单位的重组大肠杆菌进行体外黏附试验和黏附抑制试验。研究结果表明:FUT1基因M307位点中GG型和AG型仔猪小肠上皮细胞均能黏附上述3种大肠杆菌,而AA型个体小肠上皮细胞则不能黏附。将上述3种大肠杆菌分别与抗F18ab菌毛高免血清、F18ac菌毛高免血清及抗F18abFedF亚单位单因子血清作用后,则失去黏附仔猪肠上皮细胞能力。上述结果对苏太猪从体外试验上证明了FUT1基因M307位点多态性与断奶仔猪腹泻和水肿病存在着直接的相关性。     

Active oral immunization of suckling piglets to prevent colonization after weaning by enterotoxigenic Escherichia coli with fimbriae F18

Immunoprophylaxis of porcine oedema disease and post-weaning diarrhoea caused by strains of Escherichia coli expressing fimbriae F18 is an unsolved problem. The study was designed to examine whether vaccination with a live F18ac vaccine of unweaned pigs born to sows with F18ac antibody in the colostrum requires preformed fimbriae in the vaccine, and whether protection against the heterologous fimbrial variant F18ab is induced as well. Genetically susceptible pigs were vaccinated orally on three consecutive days, beginning 10 days before weaning with 10(11) CFU of an F18ac culture. Challenge with a dose of 10(7) CFU of E. coli F18 on three consecutive days was initiated 9 or 11 days after weaning. Eighteen pigs given the fimbriated F18ac vaccine and challenged with a strain of the homologous fimbrial variant were protected against colonization; mean faecal viable counts of the challenge strain were >3 log10 lower than those from the 17 non-vaccinated control pigs. The vaccinated pigs developed a significant rise of F18ac IgA serum antibodies. The 23 pigs which had received the non-fimbriated vaccine showed no significant protection and exhibited much lower serum F18ac IgA ELISA reactivities. Eighteen pigs vaccinated with the fimbriated F18ac and challenged with an F18ab strain had faecal viable counts nearly as high as those from 16 non-vaccinated control pigs. It is concluded that only oral vaccines having preformed fimbriae induce protection limited to the homologous fimbrial variant.     

Experimental colonization of piglets and gilts with systemic strains of Haemophilus parasuis and Streptococcus suis to prevent disease.

Haemophilus parasuis and Streptococcus suis are both major causes of losses during the nursery period, especially in herds using the segregated early weaning system. In this system, only a few piglets may be colonized with the herd's prevalent systemic strain, which results in infection of naive penmates late in the nursery. In view of these factors, the objectives of this study were: (1) to evaluate the early colonization of piglets with the farm's prevalent systemic strain of H. parasuis and S. suis as an alternative method for disease prevention; and (2) to evaluate 2 different protocols for experimental colonization: direct colonization of piglets and colonization of piglets through nose-to-nose contact with inoculated sows. Haemophilus parasuis and S. suis isolates recovered from diseased nursery pigs were characterized by the rep-PCR technique and the herd's prevalent strains were used for colonization. Piglets in the experimentally colonized groups were inoculated at 5 days of age by the oral route using a spray pump. Sows were colonized at 2 weeks prior to farrowing using a similar protocol. Although both colonization protocols were successful in getting the piglets colonized, direct inoculation of 5-day-old piglets with the herd's systemic strains of H. parasuis and S. suis tended to be more effective in reducing the morbidity and the mortality than the colonization of piglets by nose-to-nose contact with inoculated sows.     

Isolation,Identification and Drug Resistance Analysis of Interstinal Pathogenic Escherichia coli and Salmonella Isolated from Diarrhea Piglets

In order to find out the serotype, resistant phenotype and genotype of Escherichia coli (E. coli) and Salmonella in piglets, this study collected 128 samples of diarrhea piglets from seven large-scale pig farms in five cities in Guizhou province, and the E. coli and Salmonella were isolated and identified. The pathogenicity of the strain was identified by animal test. The drug resistance of the main pathogen was tested by drug susceptibility paper. The resistance gene of each pathogen was detected by PCR. The drug resistance and genotype correlation of the bacterial were analyzed. The results showed that 78 strains of pathogenic E. coli and 21 strains of Salmonella were isolated and identified in this study. The serotypes of pathogenic E. coli were predominantly O138 and O87. Salmonella Typhimurium and Salmonella Enteritidis were predominant serotypes. The susceptibility test showed that the resistant strains of 78 strains of E. coli were more than 80% resistant to β-lactams and more than 40% for other antibacterials. The resistance rate of 21 strains of Salmonella to aminoglycosides was more than 50% and more than 20% to other types of antibacterials; 12 and 10 kinds of drug resistance-related genes of E. coli and Salmonella were detected, respectively; The coincidence rate of resistant genotype and phenotype of two kinds of bacteria were above 60%, and both were multiple drug resistance. This study provided a theoretical basis for comprehensive prevention and control of piglets diarrhea.     

腹泻仔猪肠道致病性大肠埃希氏菌和沙门氏菌的分离鉴定与耐药性研究

为探明仔猪细菌性腹泻肠道致病性大肠埃希氏菌和沙门氏菌流行的血清型、耐药表型及耐药基因型,本试验采集了贵州省5个地（州）市7个规模化养猪场的128份腹泻仔猪肠道样本,并对采集的样本进行了大肠埃希氏菌和沙门氏菌分离与鉴定,通过动物试验鉴定菌株的致病性,利用血清学方法鉴定其血清型,并通过药敏纸片法对主要致病菌进行耐药性研究,采用PCR技术检测各致病菌株耐药相关基因,分析细菌耐药表型和耐药基因型相关性。结果显示,本研究共分离鉴定到78株致病性大肠埃希氏菌与21株沙门氏菌,致病性大肠埃希氏菌血清型以O138、O87为主,沙门氏菌血清型以鼠伤寒沙门氏菌、肠炎沙门氏菌居多;药敏试验结果表明,本试验分离到的78株致病性大肠埃希氏菌对β-内酰胺类药物耐药率达80%以上,对其他种类的抗菌药耐药率均超过40%,分离鉴定的21株沙门氏菌对氨基糖苷类药物耐药率达50%以上,对其他种类的抗菌药耐药率均达20%以上;本试验分离鉴定的致病性大肠埃希氏菌共检出12种耐药相关基因,沙门氏菌共检出10种耐药相关基因,两种细菌耐药基因型与耐药表型符合率均达60%以上,且均为多重耐药。本研究为仔猪腹泻的综合防控提供了理论依据。     

仔猪黄痢病原分离株药敏试验和不同给药方法疗效比较研究

为科学评价河南省仔猪黄痢大肠杆菌地方分离株的耐药性和不同给药方法对仔猪黄痢疗效的影响,本研究首先自河南省25个临床发病猪场病猪体内分离鉴定仔猪黄痢大肠杆菌;通过小白鼠致病力试验以检测大肠杆菌分离株的毒力;采用20种抗菌药物对分离株进行药敏试验以筛选对仔猪黄痢大肠杆菌最敏感的药物;选取敏感药物分别采用口腔灌服、肌肉注射和腹腔注射3种给药方法对临床上仔猪黄痢发病猪进行治疗效果比较试验以确定最佳给药方法。结果自河南省25个发生仔猪黄痢的猪场的病猪体内共分离鉴定出25株大肠杆菌。25株大肠杆菌分离株对小白鼠的致病率为100%;对临床上常用的20种抗菌药物都有耐药现象,但耐药率高低不同(4%～100%);20种抗菌药物中诺氟沙星、氧氟沙星、新霉素和利福平等4种药物的敏感率较高,高敏率分别为92%、88%、88%和80%。3种不同的给药方法对仔猪黄痢病例的治疗效果不同,其中通过口腔灌服和腹腔注射的给药方法对仔猪黄痢的治愈率(分别为92.3%、95.0%)显著高于肌肉注射给药方法(58.8%);腹腔注射组治愈率稍高于口腔灌服组,但二者差异不显著。本研究为临床上仔猪黄痢的防制提供了科学依据。     

Additional dietary zinc for weaning piglets is associated with elevated concentrations of serum IGF-I

Two experiments were performed in order to study how weaning and post-weaning dietary zinc level affect serum IGF-I. Further, whether the growth-enhancing effect of 2500 ppm of dietary zinc (Zn2500) and/or 175 ppm of dietary copper (Cu175) in post-weaning diets is associated with elevated serum IGF-I levels in piglets was studied. Experiment 1 included 54 piglets (six litters of nine piglets). One piglet from every litter was assigned to a control group (blood sampled 1 day before weaning). At weaning the remaining eight piglets from every litter were allocated randomly to four dietary treatments with increasing zinc inclusions (Zn100, Zn250, Zn1000, Zn2500). In exp. 2, 48 piglets (six litters of eight piglets) were allocated to four dietary treatments (Zn100, Zn100Cu175, Zn2500, Zn2500Cu175). All piglets in exp. 1 were blood sampled at -1, 1-2, 5-6 or 14-15 days after weaning and in exp. 2 blood samples were taken from all pigs 5-7 days after weaning. Feed intake was recorded per pen (two piglets) and weight gain was recorded for every piglet. Just after weaning feed intake was very low, piglets lost weight and serum IGF-I decreased in exp. 1. However, the piglets fed 2500 ppm of zinc reached pre-weaning levels of serum IGF-I at 14-15 days post-weaning, whereas piglets receiving lower zinc levels showed no changes in serum IGF-I. In exp. 2, additional dietary zinc in weaning diets for piglets was found to be associated with increased feed intake, improved growth rate and increased serum IGF-I. High levels of dietary copper did not affect any of these measurements. Zinc-induced rise in serum IGF-I was partly due to increased feed intake. After correcting for differences in feed intake, zinc significantly increased serum IGF-I. However, to completely separate effects of feed intake from effects of zinc status, pair-feeding should be considered in future studies.     

Requirement for capsular antigen KX105 and fimbrial antigen CS1541 in the pathogenicity of porcine enterotoxigenic Escherichia coli O8:KX105 strains.

The requirement for capsular antigen KX105 and fimbrial antigen CS1541 in the pathogenicity of porcine enterotoxigenic Escherichia coli O8:KX105 strains lacking the colonization factor antigens K88, K99, 987P and F41 was investigated using two encapsulated strains and their acapsular variants, one of which produced the fimbrial antigen CS1541 in vitro. None of the strains adhered in vitro to enterocytes isolated from newborn colostrum-deprived piglets. All of the strains caused diarrhea in orally infected, hysterotomy-derived, colostrum-deprived piglets although a great variability in the clinical response of the piglets was observed. Colonization of the small intestine of infected piglets by these strains was only moderate and no differences in the ability to colonize the small intestine was noted between the strains. All of the strains reacted in the indirect fluorescent antibody test with both CS1541 and 987P antisera when applied to organisms in the intestines of infected piglets. A control strain expressing the 987P fimbrial adhesin also reacted with the CS1541 antiserum applied to organisms in the intestines of an infected piglet. It was concluded that capsular antigen KX105 was not essential for intestinal colonization and production of diarrhea in hysterotomy-derived colostrum-deprived pigs, and that fimbrial antigen CS1541 does not promote in vitro adherence to enterocyte brush borders but could be important in bacterial colonization in vivo.