Edward H. Bohl

Morphogenesis of Porcine Rotavirus in Porcine Kidney Cell Cultures and Intestinal Epithelial Cells

The morphogenesis of porcine rotavirus was similar in vitro in porcine kidney (PK) cell cultures and in vivo in porcine epithelial cells as examined by electron microscopy. Infected cells contained cytoplasmic, non-membrane-bound viroplasm and accumulations of virus particles within cisternae of the rough endoplasmic reticulum (RER). Three types of virus particles were noted: double-shelled or complete particles which averaged 77 nm in diam.; single-shelled or naked particles which ranged from 50 to 55 nm in diam.; and electron-dense nucleoids, or cores, 31 to 38 nm in diam. Virus particles acquired outer shells by budding through either matrices of granular, electron-dense viroplasm or membranes of distended RER. Accumulation of numerous single-shelled particles was observed only in PK cell cultures containing a high percentage of infected cells. In these cells, virus release occurred through disruption of the plasma membrane. Tubules, similar in diameter to the single-shelled particles, were observed in the nuclei of a few infected PK cells.

PASSIVE IMMUNITY TO TRANSMISSIBLE GASTROENTERITIS VIRUS: INTRAMAMMARY VIRAL INOCULATION OF SOWS*

Sows were injected intramammarily with live-attenuated TGE virus, an enteric coronavirus--one sow during pregnancy and three sows during lactation. All sows were TGE antibody seronegative prior to inoculation except for one naturally infected sow inoculated during lactation. The animal injected during pregnancy had primarily IgG TGE antibodies in milk from all glands. By contrast, sows injected during lactation had IgA and IgM initially, and later IgA and IgG TGE antibodies in milk from injected and noninjected glands. The seropositive sow had elevated IgA TGE antibody titers in milk after IMm injection. Both seronegative sows inoculated intramammarily during lactation shed TGE virus in milk from injected glands, and their nursing piglets developed mild diarrhea and shed virus in their feces at three to nine DPE of the sows. Milk from IMm injected glands generally had higher TGE antibody titers than milk from noninjected glands. These results suggest that TGE virus replicates in lactating mammary gland tissue, thereby stimulating IgA immunocytes, leading to secretion of IgA antibodies in milk. Whether the intramammary route presents a natural route of enteric virus exposure in lactating animals (by way of infected nursing piglets), leading to IgA-antibody secretion in milk, requires further investigation.

Passive Immunity Against Enteric Viral Infections of Piglets

An immunologic system has evolved whereby newborn animals derive an appreciable degree of protection from enteric infections by means of passive immunity. This report explores some of the facets of this system, using infections of swine with transmissible gastroenteritis virus, rotavirus, or enterovirus as examples. In swine, and probably in most mono gastric animals, passive immunity against enteric infections is dependent on the ingestion — at normal intervals for the particular species — of colostrum or milk which contain appropriate levels of specific antibodies, with those of the IgA class being most protective. In swine, and probably in most mono gastric animals, antibodies of the IgA class appear to occur in mammary secretions only, or primarily, as a result of an appropriate antigenic stimulation of the intestinal tract. This type of information, and the variables involved, is of special value when attempting to design an immunisation programme which will provide passive immunity against enteric infections.

Secretory Antibodies in Milk of Swine Against Transmissible Gastroenteritis Virus

Transmissible gastroenteritis (TGE) of swine is a highly contagious, enteric, viral disease characterized by severe diarrhea and high mortality in pigs under 2 weeks of age. TGE virus primarily infects the epithelial cells of the small intestine, resulting in an atrophy of the villi and a mal absorption syndrome (1). We have previously reported that TGE antibodies were primarily of the IgA class in milk from sows which had been exposed orally to virulent virus, but were primarily of the IgG class in those exposed parenterally to live attenuated virus (2, 3,4) Also, passive immunity against intestinal infection was more closely associated with milk antibodies of the IgA than the IgG class. The present paper provides additional information, with emphasis on the contrasting features of the antibody response in animals which were orally versus intramammarily exposed to virulent TGE virus.

CLINICAL AND PATHOLOGICAL DIFFERENCES IN ENTERIC INFECTIONS IN PIGS CAUSED BY ESCHERICHIA COLI AND BY TRANSMISSIBLE GASTROENTERITIS VIRUS

Diarrhea is probably the most common and, at times, the most serious clinical manifestation of disease in neonatal pigs. Its importance in the United States is indicated by the existence of a cooperative research project (NC-62) involving 12 states in the North Central region giving emphasis to “Enteric Diseases of Young Pigs.” The diseases that have received most attention on this research project have been transmissible gastroenteritis (TGE) and colibacillosis. The former is caused by a virus that is probably a member of the Corona group and the latter by certain strains of Escherichia coli. Since both diseases often occur in pigs of the same age with diarrhea and dehydration as the principal clinical signs, differential diagnosis can be a problem and is of importance because the methods of treatment and control of these two diseases differ. In this report, some of the contrasting features of these two diseases will be emphasized that will assist in their differentiation.