Effects of nursing on growth and development of small bowel mucosa in newborn piglets.

Trophic factors in natural milk are potential mediators of the rapid growth of intestine in neonates. To determine whether nursing stimulates growth and development of small bowel mucosa, litters of piglets were divided into suckled and artificially reared groups at birth. The latter animals were raised in an automated feeding device (Autosow) with an artificial diet simulating the nutritional composition of sow milk. At 2, 8, and 15 d of age, animals were killed and 10-cm segments of jejunum, mid-bowel, and ileum were removed. Mucosal homogenates were prepared for enzyme assay and measurement of mucosal mass. Mean body weight, total length of bowel, and circumference of bowel segments did not differ between the two feeding groups at any age studied. As anticipated, mean mucosal ornithine decarboxylase activity decreased (p less than 0.001) and measurements of mucosal mass increased (p less than 0.001) with age; however, mean values for each of these measures were never greater in the nursed animals in comparison to the artificially reared group in any segment at any age. In addition, levels of disaccharidase activity did not correlate with the feeding regimen. To investigate the possibility that unanticipated growth factors in the artificial diet might have accounted for the apparent lack of trophic effect of nursing compared to artificial rearing, we evaluated the effects of this diet and of sow colostrum on 3H-thymidine incorporation in Swiss 3T3 cells in vitro. Colostrum, but not artificial diet, stimulated greater incorporation of 3H-thymidine than culture medium alone (p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Protection of agammaglobulinemic piglets from porcine rotavirus infection by antibody against simian rotavirus SA-11.

Rotavirus, a double-stranded RNA virus, has been implicated as a diarrhea-provoking agent in a variety of animal species. Several previous reports have shown that immunization with a single serotype may result in increased in vitro neutralization titers against serotypes not represented in the immunogen. This study was undertaken to determine whether antibody from cows immunized against simian rotavirus strain SA-11 (which is alien to pigs) could protect neonatal piglets from infection with a North Carolina isolate of porcine rotavirus. Accordingly, cows were immunized with SA-11 and an immunoglobulin G (IgG)-rich fraction was isolated from their colostrum. An IgG-rich fraction was similarly isolated from colostrum of nonimmunized cows. At equal concentrations, IgG from SA-11-immunized cows had two- to fourfold higher neutralization titers to seven of eight test strains of rotavirus, including SA-11 (serotype 3); human rotavirus serotypes 1, 3, and 4; North Carolina porcine rotavirus (serotype undetermined); Ohio State porcine rotavirus (serotype 5); and bovine rotavirus (serotype 6). The IgG-rich fractions were fed as dietary supplements to agammaglobulinemic piglets infected with the North Carolina porcine rotavirus. IgG from the SA-11-immunized cows was about eightfold more effective in protecting piglets than was IgG from nonimmunized cows.

Diarrhea: the nemesis of the artificially reared, early weaned piglet and a strategy for defense.

Rearing early weaned piglets artificially for the purpose of increasing the efficiency of the sow is an attractive management concept. However, high death losses resulting from diarrhea in artificially reared piglets have dampered enthusiasm for early weaning. Enterotoxigenic Escherichia coli, transmissible gastroenteritis virus and rotavirus are the three main enteropathogens responsible for causing the diarrhea. The enteropathogens infect the small intestine, which produces a secretory or malabsorptive diarrhea. In nature, the nursing piglet is protected from the enteropathogens by antibody bathing his gut. The source of the antibody is the dam's colostrum and milk. It should be possible to protect artificially reared, early weaned piglets from enteropathogens by feeding them diets that contain antibodies to putative enteropathogens.

Rotaviral antibodies in cow's milk.

In the past, it has been reported that neonatal diets made from unheated cow's milk were superior to those made from heated cow's milk. It was observed that piglets were equally protected from rotaviral diarrhea when they were fed diets made from either unheated milk that came from a cow immunized against porcine rotavirus or from a cow that was not immunized. Because of this observation, we examined four pools of "normal" cows' colostrum and 58 samples of "normal" cow's milk for the presence of antibody to rotavirus. All pools of colostrum, collected in four different years, had immunofluorescent antibody titers of 1:100 to rotavirus. Seventy-two percent of the samples of milk were also positive--titer no higher than 1:10. Antibodies to rotavirus were found in cow's milk at a creamery prior to but not after pasteurization. Rotaviral antibodies were detected in one out of eight brands of milk bought at the market--perhaps indicating inadequate pasteurization for this brand. These results support the proposition that, at least in part, unheated milk is superior to heated milk because unheated milk contains antibody to an ubiquitous enteropathogen like rotavirus.

Rotavirus and hemolytic enteropathogenic Escherichia coli in weanling diarrhea of pigs.

Since the turn of the century, Escherichia coli has been implicated in the etiology of weanling diarrhea (colibacillosis). However, rotavirus--a virus that destroys enterocytes--has been shown recently to be causally associated with weanling diarrhea of pigs. The role of both rotavirus and hemolytic enteropathogenic E. coli in weanling diarrhea was assessed in this study. Pigs from a closed herd were farrowed and weaned by two markedly different systems: an "intensive care sanitary" system and a "conventional unsanitary" system. Pigs weaned at 3 weeks of age in the sanitary system usually experienced a rotaviral diarrhea about 16 days postweaning. No hemolytic E. coli were detected in feces from these pigs. Peers weaned at the same time by the unsanitary system commenced diarrhea 3 days postweaning. Rotavirus and nonhemolytic E. coli were detected in the feces at the onset of diarrhea and for a few days thereafter. Then, the aerobic fecal flora shifted to nearly pure hemolytic enteropathogenic E. coli. About 10 days later, the diarrhea waned, and the fecal flora shifted back to nonhemolytic E. coli. This hemolytic E. coli shedding pattern could not be duplicated in artificially inoculated sanitary pigs unless they were inoculated with the hemolytic E. coli during a rotaviral-associated diarrhea. Otherwise, the shedding of hemolytic E. coli was fleeting, and the diarrhea, if present, was mild. Pigs developed humoral antibodies to the rotavirus but not to the hemolytic E. coli. We conclude that rotavirus damages the epithelium of the small intestines, which changes the luminal environment to one that favors colonization by enteropathogenic E. coli.

Rearing regimen producing piglet diarrhea (rotavirus) and its relevance to acute infantile diarrhea.

Piglets were weaned when 1 day old and thus were denied further access to the antibodies supplied by their dam's milk. They were placed in a nursery in which contamination by the ubiquitous rotavirus steadily increased with continuous use causing a progressive increase in the incidence of vomiting, diarrhea, and death among the piglets. A similar syndrome involving an antigenically related rotavirus and analogous management practices occurs in human infants.

Reovirus-like agent associated with fatal diarrhea in neonatal pigs.

Large numbers of a reovirus-like agent were visualized with electron microscopy in bacteria-free gut homogenates obtained from piglets with a fatal diarrhea resembling transmissible gastroenteritis. The syndrome, of vomiting, diarrhea, dehydration, and death, was reproduced in piglets artificially infected with these bacteria-free gut homogenates. Reovirus-like particles persisted in serial piglet passage and none was seen in uninfected, asymptomatic controls. Hyperimmune sera (made in recovered piglets) aggregated the reovirus-like particles, as judged by immunoelectron microscopy, and neutralized the infectious agent. The cytoplasm in enterocytes on infected intestinal epithelium fluoresced when this hyperimmune sera was used in an indirect fluorescent antibody test. Feeding cow colostrum or diets containing porcine gamma globulin protected infected piglets. No cytopathogenic effect was noted in infected tissue cultures, nor did this agent affect neonatal guinea pigs, hamsters, mice, and rats. The agent did not agglutinate human O or A erythrocytes.