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.

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 0 or A erythrocytes. In 1972 we reported on an infectious abacterial enteritis resembling transmissible gastroenteritis (TGE) of swine (

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.

The sheath surface of Brugia pahangi microfilariae (mf) and the cuticle surface of Dirofilaria immitis mf were compared with regard to the ultrastructural arrangement of neutral and charged polysaccharides and binding of immunoglobulins from dog sera. Brugia pahangi: mf demonstrated large amounts of neutral sugar and negatively charged sugars just above the sheath surface, projecting some distance from the surface, in addition to a dense layer of sulphated material on the sheath surface. Microfilariae from high microfilaremic dogs showed no innately bound IgG or IgM when examined fresh from serum nor did they bind IgG or IgM from normal (NDS) or infected (IDS) dog sera after 48 h maintenance in RPMI 1640. Many of these mf did bind IgG and IgM from hyperimmune dog serum (ImDS) and these immunoglobulins were found binding at a distance from the sheath similar to that of the sugars. Dirofilaria immitis mf demonstrated much less neutral sugar at the cuticle surface, no negatively charged sugars and a diffuse, rather than dense, distribution of sulfated material extending from the cuticle. The majority of these mf showed innately bound IgG and IgM. After 48 h maintenance in RPMI 1640 D. immitis mf bound and shed IgG and IgM from NDS, high microfilaremia D. immitis IDS and D. immitis mf ImDS at distinctly different rates.

Piglets weaned abruptly and precociously at 3 weeks of age and placed in a crowded nursery commenced diarrhea 3 to 5 days later. Death losses were low (approximately 6%), but weight gain ceased for 2 weeks. Large numbers of rotavirus (reo-like) particles were seen by electron microscopy in diarrhetic fluids. Sections of intestines showed a loss of adsorptive surface in that villi were shortened and fused with adjacent villi. Immunofluorescence revealed rotaviral antigens within damaged enterocytes. Rotavirus-containing gut fluid was harvested from sick, weaned piglets. This fluid, filtered free of bacteria, was used to inoculate per os colostrum-deprived piglets. These infected piglets developed diarrhea and dehydration, and large numbers of rotaviral particles were seen in their diarrhetic fluid. Also, rotaviral antigens were present in aberrant enterocytes, and the intestinal villi were shortened. Since the weaned piglets (3 weeks old) came from sows that were providing their piglet's intestine with passive antibody protection via milk, we concluded that the abrupt removal of the piglet from the gut-bathing antibody combined with the stress of weaning produced a neonate vulnerable to the ubiquitous rotavirus. Similar circumstances may prevail and operate in exacerbating rotaviral diarrhea in neonates of other species of mammals.