Search PubMed⌕ Search

Biomedical subjects

C A Mebus

Publications and source records attributed to C A Mebus.

At least 73 records · Page 4Linked to original sources

Comparison of results using electron microscope, immunodiffusion and fluorescent antibody analyses to detect rotavirus in diarrheic fecal samples of calves.

Seventy-nine diarrheic calf fecal samples were examined by electron microscopy, immunodiffusion and the fluorescent antibody technique for the presence of rotavirus (reovirus-like agent). Thirty-eight (48%) of the samples were positive by electron microscopy, 59% by immunodiffusion and 20% positive by fluorescent antibody technique analyses. Another 9% were suspect-positive by fluorescent antibody technique. Chymotrypsin treatment of the fecal samples increased the ease of observing the viral particles by electron microscopy and also intensified the immunodiffusion arcs obtained. Immunodiffusion analyses using specific antisera to the virus would appear to be a practical method of detecting rotavirus in diarrheic fecal samples.

Animals↗

Ulcerative diseases of animals with an infectious etiology.

The oral lesions of five viral diseases of cattle are compared. Two of the diseases, foot-and-mouth disease and vesicular stomatitis, cause vesicles, and rinderpest, bovine virus diarrhea and malignant catarrhal fever produce sharply demarcated erosive lesions. Gross lesions of different diseases appear similar: however, histologically, there are subtle differences in the development of the lesions.

Animals↗

Neonatal calf diarrhea caused by a virus that induces villous epithelial cell syncytia.

Intestinal lesions caused by a virus serologically unrelated to the calf diarrheal rotavirus or coronavirus were studied in gnotobiotic calves. The virion purified from feces from infected calves was a fringed particle with a diameter of about 100 nm. The incubation period from time of inoculation per orum to onset of diarrhea in calves was as short as 8 hours. The viral infection in bacteria-free calves or calves not contaminated with pathogenic bacteria caused severe illness for only 24 hours. When bacteria such as the K99 antigen Escherichia coli were present, the combined infection caused mortality. Lesions occurred only in the small intestinal villous epithelium. Calves euthanatized shortly before or after the onset of diarrhea had developed villous epithelial cell syncytia that contained numberous virions in the cytoplasm. Within 2 to 3 hours after onset of diarrhea, the infected cells were shed and the villi had denuded tips or had cuboidal to squamous epithelial cells.

Animals↗

Intestinal lesions induced in gnotobiotic calves by the virus of human infantile gastroenteritis.

Four gnotobiotic calves with intestinal lesions induced by third and fourth calf passages of virus of human infantile gastroenteritis were studied by light microscopy, scanning and transmission electron microscopy, and by immunofluorescence. Calves, 25--72 hours old, were examined 0.5 hours, 3 hours, 7 hours, and 48 hours after the onset of diarrhea. Intestinal histology of infected calves was compared to that of two noninoculated gnotobiotic calves 48 and 72 hours old. The sequence of events in the small intestine was infection of the absorptive villous epithelial cells, replacement of the tall columnar villous epithelial cells with cuboidal and squamous cells, shortening of the villi, enlargement of reticular cells, lymphocytic infiltration of the villous lamina propria and repair.

Animals↗

Scanning electron, light, and immunofluorescent microscopy of intestine of gnotobiotic calf infected with reovirus-like agent.

Intestinal lesions caused by a calf diarrheal reovirus-like agent were studied by scanning electron microscopy, light microscopy, and immunofluorescent microscopy in 2 gnotobiotic calves inoculated per orum. The calves were euthanatized 6 hours after the onset of diarrhea. Villi in the cranial and middle parts of the small intestine appeared shortened. In these areas, the epithelium was composed of low columnar and cuboidal cells. Villi in the caudal part of the small intestine were short. By scanning electron microscopy, the villous epithelium in the caudal part of the small intestine of both calves and the ridge epithelium in the ansa spiralis coli of 1 calf were composed of various sized cells which gave the surfaces an irregular appearance. The amount of mucopolysaccharide in the colonic epithelial cells of both calves was greatly reduced. The combined use of scanning electron and light microscopic techniques enabled obtaining a more accurate description of the intestinal lesions than either technique alone.

Animals↗

Scanning electron microscopy of trachea and bronchi from gnotobiotic pigs inoculated with Mycoplasma hyopneumoniae.

Areas of trachea and right apical and right dorsal diaphragmatic bronchi from gnotobiotic neonatal pigs were examined by scanning electron and transmission electron microscopy at 7, 13, and 21 days after pigs were given intranasal inoculation of Mycoplasma hyopneumoniae. Similar areas were examined by scanning electron microscopy from 2 noninoculated neonatal pigs. Tracheal and bronchial lesions were observed in all inoculated pigs. Severe bronchial lesions were in grossly affected lobes. Early infection consisted of mycoplasmas on ciliated epithelial cells. As the interval between inoculation and euthanasia increased, mycoplasmas and leukocytes on the tracheal and bronchial surfaces became more numerous and fewer cilia remained.

Animals↗

Diarrhea caused in gnotobiotic piglets by the reovirus-like agent of human infantile gastroenteritis.

One- to four-day-old gnotobiotic piglets were inoculated orally with a reovirus-like agent obtained from human infants with acute gastroenteritis. Diarrhea developed in the piglets two to seven days after inoculation and was reproduced for five serial passages in one sequence and for three passages in another. Nineteen of 21 inoculated piglets developed diarrhea; reovirus-like particles were observed in intestinal contents and/or fecal samples from 17 animals with illness and from two inoculated piglets that did not develop diarrhea. One piglet, for which daily fecal samples were examined by electron microscopy, shed the largest number of virus particles at the onset of diarrhea. Immunofluorescent antibody responses to the reovirus-like agent were detected in sera from the seven inoculated animals that were tested.

Animals↗

Diarrhea in gnotobiotic calves caused by the reovirus-like agent of human infantile gastroenteritis.

Gnotobiotic newborn calves were found to be susceptible to infection with the reovirus-like agent of human infantile gastroenteritis (HRVL). Infection was based on (i) seroresponse using immunofluorescence and (ii) fecal shedding of virus particles using electron microscopy. Virus was detected in fecal samples for at least 2 to as long as 7 days after inoculation, although peak virus concentrations were observed on days 1 to 4. Diarrheal illness was observed in seven calves on second to fourth serial passage of HRVL in calves but in none of four animals studied on first passage. Diarrhea began 15 to 30.5 h (mean = 22.3 h) post-inoculation and lasted less than 24 h; three of the seven animals that developed diarrhea were also depressed or anorectic.

Animals↗

Patterns of shedding of human reovirus-like agent in gnotobiotic newborn piglets with experimentally-induced diarrhea.

Virus shedding patterns of neonatal gnotobiotic piglets infected with the reovirus-like agent of human infantile gastroenteritis were studied. Fecal viral counts were highest before or at the onset of diarrhea. In diarrheic piglets, viral particles were usually observed for only 1-2 days after the onset of diarrhea, and total duration of shedding was 2-6 days. One infected piglet shed virus for 4 days but did not develop diarrhea. The presence of virus at or about the time of illness is consistent with the induction of diarrhea in piglets inoculated with the human reovirus-like agent.

Animals↗