Intestinal colonization of neonatal animals by Campylobacter fetus subsp. jejuni

Field, L H; Underwood, J L; Pope, Leodocia; Berry, L. Joe

doi:10.1128/iai.33.3.884-892.1981

Cited by 42 publications

(18 citation statements)

References 38 publications

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“…Several investigators have attempted to colonize conven-tional mice with C. jejuni (3,13,14,20,25). Field and her associates (13,14) could not colonize adult mice with C. jejuni unless antibiotics were given to the mice before an intragastric inoculation. Merrell et al (25) found it necessary to perform laparotomies and directly inject C. jejuni into the ilea and colons of NMR1 mice to establish a transient colonization.…”

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Colonization and infection of athymic and euthymic germfree mice by Campylobacter jejuni and Campylobacter fetus subsp. fetus

Yrios¹,

Balish²

1986

Infect Immun

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Human clinical strains of Campylobacter jejuni and Campylobacter fetus subsp. fetus colonized the gastrointestinal tracts of both athymic (nulnu) and euthymic (+Inu) germfree mice (BALB/c). Viable Campylobacter spp. (109 to 1010 CFU/g [dry weight] of cecum and colon contents) were isolated on day 3 after oral challenge, and similar large numbers of viable cells were evident at several intervals during a 10-month experiment. The stomachs and upper small intestines of nulnu and +/nu mice that were monoassociated for 224 days with C. jejuni 45100 contained 3 to 4 logs fewer viable bacteria than did their ceca or colons. Athymic mice that were monoassociated for 224 days with C. fetus subsp. fetus had 2 to 3 logs more viable Campylobacter spp. in their upper gastrointestinal tracts than did their +/nu littermates. Large viable populations (-109/g of contents) of C. fetus subsp. fetus were in the ceca and colons of both nulnu and +Inu mice. All C. jejuni strains used in this study chronically infected the mesenteric lymph nodes of both nulnu and +Inu mice. C. jejuni strains 24 and INN 73-83, which were cytotoxic for Chinese hamster ovary cells in vitro, were also more frequently isolated from the livers, spleens, and kidneys of nulnu mice than was the weak cytotoxin-producing strain 45100. Additionally, heat-labile-enterotoxin-producing C. jejuni INN 73-83 was recovered more frequently from the internal organs of monoassociated +Inu mice than were any other Campylobacter spp. tested. Natural gastrointestinal colonization of neonatal nulnu and +Inu mice (born to Campylobacter-colonized mothers) with Campylobacter spp. appeared to be delayed until approximately 1 to 2 weeks after birth. Conventionalization of C. jejuni 45100-monoassociated BALB/c mice with a complex mouse fecal microflora eliminated viable C. jejuni from the mesenteric lymph nodes by day 14 and from the cecum by day 78. These findings show that the gnotobiotic BALB/c mouse is a new model for studying acute and chronic host-Campylobacter sp. interactions.

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“…Microbiol. 1983, B110, p. 41), gnotobiotic chickens (24) and dogs (29), hamsters (19), guinea pigs (5,37,38), rabbits (7,14), rats (14), mice (3,11,13,14,20,22,23,25), and dogs and cats (30).…”

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Colonization and infection of athymic and euthymic germfree mice by Campylobacter jejuni and Campylobacter fetus subsp. fetus

Yrios¹,

Balish²

1986

Infect Immun

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“…The young mice had decreased D-glucose and D-galactose absorption in the distal four-fifths of their small intestines, whereas absorption in the older mice was unimpaired. When Field and colleagues fed C. jejuni to neonatal mice, transient intestinal colonization was noted (10). Mortality after infection varied from 0 to 13%.…”

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Experimental Campylobacter jejuni Infection of Adult Mice

1983

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HA-ICR adult mice were studied to develop an animal model for Campylobacter jejuni enteritis in humans. Fecal and ileal cultures made by selective and nonselective methods showed that C. jejuni and related organisms are not bowel commensals. Intragastric feeding of 108 CFU of three different strains of C. jejuni produced infection in 100% of the animals, and infection rates were dose dependent. Pretreatment with antibiotics or opiates was not necessary to induce infection. Fresh isolates and strains passed on artificial media yielded similar infection rates. Infected mice did not show signs of illness, but transient bacteremia within 10 min of oral infection was observed in nearly 100%. The small intestine was the principal target organ, with epithelial inflammation seen 48 h after infection. Control mice offour species had undetectable serum immunoglobulin G antibody specific for the infecting strain, but infected mice showed peak titers at 1 week with rapid decline. Immunoglobulin M titers rose minimally, and immunoglobulin A titers did not rise. Infected mice uniformly became chronic asymptomatic excretors, shedding 104 to 106 CFU/g of feces; a minority were biliary carriers. Intestine carriage was most pronounced in the stomach and proximal small intestine. Because this experimental infection led to bacteremia, transient pathological changes, and immunoglobulin G titer rises, this model may be useful for evaluating the effects of prophylactic and therapeutic interventions.

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“…Alternatively, the strain of hamsters used in this study might be refractory to symptomatic infection. An early study by Field et al (5) found that hamsters were resistant to colonization; however, a lower inoculum (6.5 x 108 CFU) was used. Additional studies are needed with hamsters from different sources to assess this possibility.…”

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Infection of adult Syrian hamsters with flagellar variants of Campylobacter jejuni

1990

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Two variants of Campylobacterjejuni IN1 differing in the expression of flagella, IN1 (Fla' Mot', wild type) and IN1-NM (Fla-Mot-), were tested for their ability to establish infection in adult hamsters. Animals were challenged intracecally with 2 x 109 to 5 x 1010 CFU and monitored for evidence of infection. None of the challenged animals developed illness. There was a significant difference, however, in the ability of IN1 to infect hamsters (35 of 43) compared with that of IN1-NM (1 of 42) (P < 0.01). Additionally, eight animals challenged with IN1-NM excreted only the campylobacters of Fla' phenotype, which were shown to be identical with the parental Fla' Mot' type. Both groups of animals developed serum immunoglobulin G antibodies to outer membrane proteins of IN1 as measured by an enzyme-linked immunosorbent assay; however, only animals that excreted Fla' organisms developed antiflagellin antibodies. In vitro reversibility from Fla' to Flaoccurred with a frequency of 9.2 x 10-6 per cell per generation; however, reversion from Flato Fla' could not be detected in vitro. Further characterization of IN1-NM showed that it produced a cytoplasmic 62K flagellin subunit protein, but this protein lacked six epitopes detected in IN1 and also differed in its two-dimensional gel electrophoresis pattern. The results of these studies support the concept that an intact flagellum is necessary for intestinal infection with C. jejuni and that this model may be useful for studying the immune response to C. jejuni.Studies during the past few years have shown that the flagella of Campylobacterjejuni, a common cause of human gastrointestinal infection, may be important pathogenic determinants in helping the organism establish infection in the gastrointestinal tract. In vitro studies suggest a role for flagella in pathogenesis by means of motility (15) or attachment (14, 21), but the mechanism is not known. Few studies have been performed in animals (1,4,20,21,28) or humans (2) addressing the role of campylobacter flagella in causing infection. A few previous studies have used aflagellate variants in vivo; however, these variants have had relatively high frequencies of reversion (4) to the motile phenotype.In 1985, Humphrey et al. (9, 10) reported on a hamster model of C. jejuni infection. We developed this model in our laboratory to study the biologic function of campylobacter flagella in vivo. Contrary to the reports by Humphrey and colleagues, with identical protocols we were unable to induce diarrhea or colitis in hamsters. During the course of these experiments, however, we found significant differences in the ability of the flagellate and nonflagellate variants of C. jejuni to establish asymptomatic infection. Importantly, we used a Fla-variant with high in vitro stability to assess the importance of campylobacter flagella in infection. Additionally, infected hamsters mounted a systemic immune response to local infection with C. jejuni and, in preliminary experiments, were protected from homologous challenge. MATERIALS AND...

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Intestinal colonization of neonatal animals by Campylobacter fetus subsp. jejuni

Cited by 42 publications

References 38 publications

Colonization and infection of athymic and euthymic germfree mice by Campylobacter jejuni and Campylobacter fetus subsp. fetus

Colonization and infection of athymic and euthymic germfree mice by Campylobacter jejuni and Campylobacter fetus subsp. fetus

Experimental Campylobacter jejuni Infection of Adult Mice

Infection of adult Syrian hamsters with flagellar variants of Campylobacter jejuni

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