Effect of Eimeria maxima infection upon the invasion of Salmonella serovar typhimurium through the intestine of chicken.
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Biomedical subjects
Publications and source records attributed to E Baba.
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Twenty-one of 56 germ-free chickens died after receiving an oral inoculation of a broth culture of Clostridium perfringens. At necropsy there was detachment and disruption of the epithelial layer at the tips of villi and sloughed epithelial cells in the duodenum. These are characteristic lesions of necrotic enteritis. Germ-free chickens receiving either purified alpha-toxin or the supernatant of broth cultures of C perfringens died, but no bird died after receiving supernatant of broth cultures neutralised by anti-alpha-toxin serum. It was concluded that alpha-toxin of C perfringens was the cause of death in young germ-free chickens.
The effect of Eimeria tenella infection on the caecal population of lincomycin-resistant Clostridium perfringens (KGW 851) newly introduced into chickens was studied. Four groups of chickens consisted of: (1) Uninoculated controls; (2) inoculated with C perfringens (KGW 851); (3) inoculated with E tenella; and (4) inoculated with C perfringens (KGW 851) followed by E tenella. Five chickens in each group were necropsied on each of days 0, 3, 5, 7, 10 and 14 after the E tenella inoculation. The mean total C perfringens counts in the caecal contents increased at five days after E tenella inoculation and reached maximum counts at seven days after the inoculation. Also lincomycin-resistant C perfringens readily established itself at approximately one 10th of the total C perfringens population in the presence or absence of E tenella infection.
White Leghorn cockerels, 11 to 22 days old, were inoculated each with a single oral dose of 4-5 X 10(4) sporulated oocysts of Eimeria tenella. Radiographic study of urinary backflow in infected chickens injected with sodium iothalamate subcutaneously indicated that retrograde movement of ceca was impaired particularly 7, 10, and 14 days after infection. No inflow was noted 7 days after infection when barium sulfate was inoculated into cloaca. Weight of cecal contents examined 7 days after infection was significantly smaller than uninfected control. Number of cecal feces was counted every 24 h beginning 4 through 14 days after infection. The counts in infected birds were significantly fewer than uninfected control 8, 9, and 10 days after infection. Outflow of cecal contents was studied in chickens surgically injected with barium sulfate into cecum 7 days after infection. Radiographic study indicated that most of uninfected control ceca excreted or evacuated the medium between 10 and 24 h after injection, while a few infected birds cleared ceca during the same period.
Monoflora chickens were established at the age of 2 days by an oral inoculation of one of six species of bacteria (Lactobacillus acidophilus, Bifidobacterium thermophilum, Bacteroides vulgatus, Clostridium perfringens, Escherichia coli, or Streptococcus faecalis). Two days later the chickens were infected with Eimeria tenella (5 X 10(4) oocytes per bird). There were four groups: uninfected birds as controls, the birds infected with either bacteria or E. tenella alone, and the birds infected with bacteria and E. tenella. As observed under the scanning electron microscope (SEM) seven days after E. tenella infection, damage of the cecal mucosa in all groups infected with bacteria + E. tenella was more severe than in that infected with E. tenella alone. Most severe damage to the cecal mucosa was found in the birds infected with either C. perfringens or B. thermophilum combined with E. tenella.
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Salmonella typhimurium was recovered from cecal contents and the cecal wall of gnotobiotic chickens infected with S. typhimurium (10(4) cfu/bird) 2, 4, 6, or 8 days after Eimeria tenella infection (5 X 10(4) oocysts/bird) and killed 1 day after S. typhimurium infection. Bacterial counts in the cecal contents of chickens killed 5, 7, and 9 days after S. typhimurium and E. tenella infection were significantly greater than those in chickens infected with S. typhimurium alone. Number of S. typhimurium in the cecal wall of birds killed 5 or 7 days after coccidial infection were significantly greater than those of birds infected with S. typhimurium alone. It appears that S. typhimurium easily invaded the cecal wall, which had been damaged by coccidial infection.
Monoflora chickens were established at 2 days of age by an oral inoculation with one of six species of bacteria (Lactobacillus acidophilus, Bifidobacterium thermophilum, Bacteroides vulgatus, Clostridium perfringens, Escherichia coli, or Streptococcus faecalis) and were infected with Eimeria tenella (5 X 10(4) oocysts per bird) 2 days later. There were two experimental groups for each bacterium: birds infected with bacteria alone and birds infected with a combination of bacteria and E. tenella. Seven days after E. tenella infection, counts of B. thermophilum in the cecal contents were significantly lower for E. tenella-infected birds than for those infected by B. thermophilum alone, whereas 10 days after E. tenella infection, counts were higher for E. tennella-infected birds. The population of L. acidophilus in the cecal contents of the E. tenella-infected chickens 10 days after inoculation was significantly greater than that in uninfected chickens. No significant differences were observed between the numbers of B. vulgatus, C. perfringens, and S. faecalis in cecal contents of groups with and without E. tenella infections.
Establishment of a specific pathogen-free (SPF) rabbit colony was attempted by transferring a total of 127 hysterectomy-derived rabbits directly into a barrier room where SPF rats had been reared. All rabbits except four died of mucoid enteritis-like diarrhea during 2 and 6 weeks of age. A second experiment consisted of four groups of hysterectomy-derived rabbits including: (1) noninoculated controls; (2) rabbits inoculated with suspension of feces from the survivors; (3) rabbits inoculated with a bacterial inoculum (Bacteroides spp. and Eubacterium sp. isolated from conventional rabbits); and (4) rabbits inoculated with Streptococcus faecalis in addition to the inoculum used for group 3. All rabbits in group 1 died of diarrhea by 3 weeks of age. Survival rates of groups 2, 3 and 4 are 53%, 38% and 40%, respectively. On 7 days after the inoculation, Bacteroides was not recovered from fecal samples of group 1, but was recovered from many samples of the inoculated groups. Populations of Enterobacteriaceae and Clostridium in the samples in group 1 were larger than each of those in the inoculated groups. The present results suggest that the lethal diarrhea, after transferring hysterectomy-derived animals directly into a barrier room, can be controlled by inoculation with non-pathogenic anaerobes, especially Bacteroides.
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Piglets were each orally inoculated daily for 4 consecutive days, with 10(4)-10(5) nalidixic acid-resistant Salmonella typhimurium and, starting 1 day after inoculation, with 50 000 Isospora suis sporulated oocysts. Control pigs were given S. typhimurium alone following the same inoculation schedule. Fecal samples were taken 5, 7 and 10 days after the coccidial inoculation, and all the pigs were necropsied 13 days after inoculation. S. typhimurium counts in the feces and in the cecal contents and the numbers of pigs positive for presence of S. typhimurium in the mesenteric lymph nodes of the dual-infected pigs were significantly (P less than 0.05) smaller than in those infected with S. typhimurium alone.
The gnotobiotic chicks infected with Eimeria tenella received an oral inoculation of Salmonella typhimurium 4 or 8 days after E. tenella infection. Chicks were necropsied one day after the salmonella infection. In the experiments 1 and 2, there were two groups; birds infected with S. typhimurium alone and birds infected with a combination of E. tenella and S. typhimurium. The number of S. typhimurium in the cecal contents was significantly greater in the concurrent infections than S. typhimurium infection alone. The S. typhimurium counts in the cecal wall of gnotobiotic chickens killed 5 days after E. tenella infection were significantly greater than those of chickens infected with S. typhimurium alone. In the experiment 3, the scanning electron microscopic study was made on damage of cecal mucosa. There were four groups; uninfected birds as control, birds infected with E. tenella, birds infected with S. typhimurium and birds infected with a combination of E. tenella and S. typhimurium. No damage was observed on the cecal mucosa of both the control and the S. typhimurium infection alone. The concurrent infections caused greater damage on the cecal mucosa than did the E. tenella infection alone.
Experimental infections of Salmonella typhimurium, S. agona, S. enteritidis or S. infantis were studied in chicks infected with Eimeria tenella. In all experiments, 4-d old birds were given 5 daily oral doses of approximately 10(4) salmonella organisms per bird. One day before this inoculation one group of birds received a single dose, in the range 1 X 10(4) to 4 X 10(4) sporulated oocysts of E. tenella per os whilst the other group was not inoculated and served as the control. Chicks were examined post morten 7, 10 or 14 d after receiving coccidia. With S. typhimurium infection, the number of salmonellas in the caeca of the E. tenella-infected birds was greater than in those infected only with salmonella. With S. agona and S. enteritidis, the counts of salmonella in the caeca and the numbers of birds positive for salmonella in the caeca and liver were greater in the E. tenella-infected birds. The rate of infection of S. infantis was not increased by caecal coccidiosis.
With more than 3 years' follow-up, dramatic clinical transfiguration of granuloma annulare was observed in a 59-year-old man with perforating granuloma annulare. The eruption was at first localized, then became generalized, developed perforations, and subsided in parallel with the improvement of associated diabetes mellitus. After reviewing 23 cases of perforating granuloma annulare from the literature, the authors divided the eruptions into two types according to their clinical features, naming one type papular perforating type (P-type) and the other ulcerative perforating type (U-type). U-type is strongly correlated with diabetes; patients with this type require detailed laboratory examination for the presence of diabetes mellitus.
To investigate a possible mechanism involved in the enhancement of Salmonella typhimurium infection in chickens concurrently infected with Eimeria tenella, S typhimurium was given orally to chickens 7 days after E tenella inoculation. The number of viable S typhimurium decreased in the ceca of chickens not inoculated with E tenella, whereas the number gradually increased in the ceca of chickens inoculated with E tenella. Cecal contents were analyzed for pH value, oxidation-reduction potential, and amounts of short-chain fatty acids and bile acids. In the ceca of E tenella-inoculated chickens, the oxidation-reduction potential significantly (P less than 0.05) shifted to the oxidative phase, and the concentration of volatile fatty acids (acetic acid, propionic acid, and butyric acid) significantly (P less than 0.05) decreased. In both aerobic and anaerobic incubations, the number of viable S typhimurium in vitro decreased as the molar concentration of fatty acids increased. Experimental evidence indicated that multiplication of S typhimurium in the ceca of E tenella-inoculated chickens was associated with decreased concentrations of volatile fatty acids.
Three experiments were conducted to examine whether Salmonella typhimurium infection is enhanced by concurrent infection with Eimeria tenella, E. acervulina, or E. maxima. There were two groups in each experiment: birds infected with a daily oral dose of approximately 1 X 10(4) cfu of S. typhimurium for 5 days after coccidial infection and birds infected with S. typhimurium alone with the similar exposure schedule. Chickens were necropsied 7, 10, and 14 days after coccidial infection. The numbers of S. typhimurium in the contents of ceca and small intestine were counted, and numbers of chickens positive for S. typhimurium in the liver and bile were examined. In E. tenella infection, the S. typhimurium counts in the ceca and small intestine of concurrently infected chickens were significantly greater than those of birds infected with S. typhimurium alone. In E. acervulina infection, the S. typhimurium counts in the ceca of chickens killed 14 days after E. acervulina infection and the numbers of birds positive for S. typhimurium in the ceca of chickens killed 10 and 14 days after E. acervulina infection were significantly greater than those of chickens infected with S. typhimurium alone. In E. maxima infection, the numbers of birds positive for S. typhimurium in the ceca and liver of chickens killed 7 days after E. maxima infection were significantly greater than those of birds infected with S. typhimurium alone. Results of this study indicate that infection with E. acervulina or E. maxima is able to enhance S. typhimurium infection in chickens.
Effect of Eimeria tenella infection on Salmonella typhimurium infection of chickens was tested using feed experimentally contaminated with S. typhimurium. Four experiments were conducted. In Experiments 1 and 2, chickens received feed contaminated with 10(3) or 10(2) cfu of S. typhimurium per g for 5 days after E. tenella infection. In Experiments 3 and 4, chickens were fed feed contaminated with 10(2) or 10 cfu of S. typhimurium per g for 3 days before E. tenella infection. In all experiments, chickens were necropsied 3 to 14 days after E. tenella infection. The number of S. typhimurium in the cecal contents was counted and the presence of the organism in the liver and bile was examined. In Experiments 1 and 2, there was no significant difference in S. typhimurium infection between the group infected with S. typhimurium alone and the group infected with both E. tenella and S. typhimurium. In Experiments 3 and 4, S. typhimurium counts in the cecal contents of chickens in the concurrently infected group were significantly greater than those of chickens in the S. typhimurium alone-infected group.
Gnotobiotic chickens infected with Eimeria tenella (5 X 10(4) oocysts per bird) received an oral inoculation of 100 Salmonella typhimurium two, four, six or eight days after coccidial infection at four days old. When S typhimurium was given two or four days after E tenella infection, S typhimurium counts in the caecal contents were similar to the counts in birds infected with S typhimurium alone. When S typhimurium was given six or eight days after E tenella infection, counts of the organism were significantly greater than with S typhimurium infection alone. There were no differences in the number of chickens positive for S typhimurium in the caecal contents, bile, liver and spleen between the two groups.