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Biomedical subjects

L J Berry

Publications and source records attributed to L J Berry.

At least 19 recordsLinked to original sources
PubMed1993

Characteristics of an avirulent Campylobacter jejuni strain and its virulence-enhanced variants.

The virulence of Campylobacter jejuni for 11-day-old chick embryos is associated with the ability to invade the chorio-allantoic membrane, to resist phagocytosis and to survive and proliferate in vivo. The pathogenicity of a well characterised avirulent C. jejuni strain was enhanced by passaging it intravenously and chorio-allantoically through chick embryos. The resulting isogenic variants had greatly increased ability to survive in vivo. In this study, the morphological and cell-surface characteristics of the avirulent parental strain were compared with those of the more virulent variants to determine whether pathogenicity was associated with one or more cell-surface constituents. Changes associated with the increased virulence of the two variants included alterations in cultural and cellular morphology, loss of flagella, expression of a new outer-membrane protein, alterations in cell-surface carbohydrates and decreases in cell-surface hydrophobicity.

Agglutination Tests↗
PubMed1991

Virulence of Campylobacter jejuni for chicken embryos is associated with decreased bloodstream clearance and resistance to phagocytosis.

The 11-day-old chicken embryo has been shown to be a useful animal model for comparing the virulence of human isolates of Campylobacter jejuni. Virulence in this system is associated with the ability to invade the chorioallantoic membrane and to survive and proliferate in vivo. In this study, the survival and multiplication of C. jejuni in the embryonic host was investigated. It was possible to enhance the virulence of a relatively avirulent C. jejuni strain by passaging it intravenously through the embryos. The resulting isogenic variants demonstrated enhanced abilities to survive in vivo but were still unable to invade when inoculated onto the chorioallantoic membrane. The bloodstream clearance of C. jejuni was studied, and virulent, but not avirulent, strains persisted and multiplied both in the bloodstream and in embryonic liver. Virulent strains also were cleared significantly more slowly from the bloodstream of adult BALB/c mice after intravenous challenge than were avirulent strains. C. jejuni strains which were cleared slowly in vivo were also ingested slowly in vitro by mouse peritoneal macrophages. Clearance studies in mice pretreated with cobra venom factor demonstrated that opsonization by serum complement was not a prerequisite for clearance of campylobacters from the murine bloodstream.

Animals↗
PubMed1986

The chicken embryo as a model for campylobacter invasion: comparative virulence of human isolates of Campylobacter jejuni and Campylobacter coli.

Eleven-day-old chicken embryos were used to compare the relative virulence of minimally passaged human isolates of Campylobacter jejuni and Campylobacter coli. Graded doses of bacteria were inoculated onto the chorioallantoic membrane, and 50% lethal doses were calculated at 72 h postinfection. Strains varied markedly in their ability to invade the chorioallantoic membrane and kill the embryos. The 50% lethal doses varied by about 6 logs for 25 strains of C. jejuni, and by 2 logs for 5 strains of C. coli. Although both outbred and inbred embryos were employed in the study, the latter were found to be more susceptible to infection with most strains. All isolates were screened for plasmid DNA, but there was no apparent relationship between plasmid content and virulence of strains for the embryos. Neither could virulence be associated with the production of siderophores by the strains. The ability of selected strains of C. jejuni to invade the liver of embryos was also studied. The number of campylobacters culturable from the liver was found to be inversely related to the 50% lethal dose of the strain. By inoculating 11-day-old embryos intravenously, it was possible to demonstrate that a strain of C. jejuni which was poorly virulent after chorioallantoic inoculation was relatively noninvasive. Invasiveness alone, however, could not fully account for the lethality of two highly virulent strains of C. jejuni administered by the intravenous route. Finally, there was no correlation between motility and virulence in this model system.

Animals↗
PubMed1986

Influence of iron on growth, morphology, outer membrane protein composition, and synthesis of siderophores in Campylobacter jejuni.

Three human isolates of Campylobacter jejuni were grown in a biphasic culture medium with and without the addition of a synthetic chelator to induce iron limitation. Cells grown in low-iron medium exhibited slower growth rates and altered cellular morphology. Increased numbers of longer, more filamentous forms were seen in Gram-stained smears. Three proteins, with apparent Mrs of 82,000, 76,000, and 74,000, were consistently present in the outer membrane of cells grown in low-iron medium. At least one of these proteins (76,000 to 74,000) was exposed on the cell surface. A bioassay was used to look for the production of siderophores by these and other strains of C. jejuni. Seven of 26 strains tested produced detectable amounts of siderophores. Growing strains at 42 degrees C failed to suppress siderophore synthesis or to alter the outer membrane protein profiles of iron-starved cells. The ability of three strains to utilize exogenously supplied siderophores for growth in low-iron medium was also examined. All three strains were able to utilize enterochelin and ferrichrome, but none utilized aerobactin, rhodotorulic acid, or desferrioxamine B. The effect of iron on the virulence of C. jejuni for 11-day-old chicken embryos inoculated via the chorioallantoic membrane was also determined.

Animals↗
PubMed1986

Endotoxin treatment inhibits glucocorticoid induction of hepatic enzymes at a late induction step.

Bacterial endotoxin inhibits the glucocorticoid induction of several hepatic enzymes including phosphoenolpyruvate carboxykinase (PEPCK). Experiments were performed to elucidate the mechanism of this inhibition by examination of the early events in the glucocorticoid induction process. At a dose of endotoxin 2-to 10-fold greater than that required to inhibit the induction of PEPCK activity, no effect on the entry of glucocorticoids into hepatocytes or their ability to form complexes with glucocorticoid receptors could be measured. Binding data showed no effect of endotoxin treatment on the association or dissociation kinetics of the steroid-receptor binding reaction. Scatchard analysis revealed no effect on the affinity and number of hepatic glucocorticoid receptor binding sites, indicating that down-regulation of receptors is not responsible for inhibition of induction. Finally, activation of receptor complexes was unaffected as well by endotoxin treatment. We conclude from these data that endotoxin does not act at the early events in the glucocorticoid induction process and must therefore intervene at a subsequent step.

Animals↗
PubMed1985

Viral persistence and abnormalities of the central nervous system after congenital infection of sheep with border disease virus.

Lambs congenitally infected with border disease (BD) virus and sheep exposed to BD virus as adults were studied for one year to determine the pathogenesis of congenital exposure compared with adult exposure to the virus. Persistent BD virus was isolated in tissue culture and detected by immunofluorescence of the peripheral white blood cells, urine, and cerebrospinal fluid of lambs with congenital BD up to one year of age. These animals had no detectable serum neutralizing antibody response to the virus for the same interval. BD virus antigen was also detected by immunofluorescence in many central nervous system tissues of these lambs with congenital BD. Dysmyelination and glial proliferation in the central nervous system and microencephaly were noted in the lambs with congenital BD, and these lesions appeared to remain the same over a 12-month period.

Animals↗
PubMed1985

Inhibition of hepatic phosphoenolpyruvate carboxykinase by avian reticuloendotheliosis viruses.

Severe weight loss is associated with many malignant diseases of humans and animals. Avian reticuloendotheliosis viruses (RE viruses) induce runting in experimentally infected chickens. Chickens infected with a replication-competent RE virus, reticuloendotheliosis-associated virus, weighed 30-50% less than control birds at the time of death. Chickens infected with reticuloendotheliosis virus, a replication-defective acute leukemia virus, weighed 30% less than the controls. The runting induced by RE viruses does not occur because of reduced food intake. Activities of phosphoenolpyruvate carboxykinase, a key gluconeogenic enzyme in the liver, were reduced approximately 40 and 50%, respectively, by infection with reticuloendotheliosis-associated virus and reticuloendotheliosis virus. RE virus infection, however, did not affect the hepatic pyruvate carboxylase activity, indicating that inhibition of phosphoenolpyruvate carboxykinase is not due to a general inhibition of all liver enzymes. Birds given injections of UV-inactivated RE viruses or reticuloendotheliosis virus-transformed, non-virus-producing tumor cells also exhibited a reduction in phosphoenolpyruvate carboxykinase activity.

Animals↗
PubMed1984

The role of gut flora and animal passage in the colonisation of adult mice with Campylobacter jejuni.

Adult female mice were given drinking water containing tobramycin 0.05 mg/ml for a week. After a further day without antibiotic they were inoculated intragastrically with one of three strains of Campylobacter jejuni. Colonisation of the gastrointestinal tract was judged by culturing faecal pellets. Tobramycin-treated mice differed from untreated animals in that many more of them discharged infected pellets, and their pellets contained 5- greater than 300 times more campylobacters. Colonisation could be prevented by inoculating the tobramycin-treated animals intragastrically, 24 h before the administration of C. jejuni, with a bacterial suspension prepared from normal faecal pellets. Coliforms, lactobacilli, the two in combination, and anaerobes grown from faecal pellets were not effective in preventing colonisation. Most of the C. jejuni were found in the large intestine of the tobramycin-fed mice. The persistence of colonisation of six dams nursing C. jejuni-infected offspring ranged from 10 to at least 29 weeks.

Animals↗
PubMed1982

Pathogenesis of atoxinogenic strains of gram--negative bacteria--a hypothesis.

Textbooks of medical microbiology attribute to endotoxin a primary pathogenic role in diseases caused by nontoxinogenic gram negative bacteria. There is little experimental data to support this claim while some observations indicate the contrary. The possibility cannot be ignored that our understanding of the biological effects of endotoxin is based on the administration of endotoxin as a bolus rather than as a continuous release in small amounts over a period of hours or days as probably occurs during an infection. Results are described that clearly show how different the response can be under the two conditions. It is suggested, moreover, that mediators formed primarily by macrophages stimulated by endotoxin may contribute significantly to the pathogenesis of these diseases.

Animals↗
PubMed1982

Inactivated bluetongue virus vaccine in lambs: differential serological responses related to breed.

A mixed breed flock of lambs, consisting of Suffolks, Hampshires, Columbias and Finnish breeds, were vaccinated with binary ethylenimine inactivated blue-tongue virus (BTV) serotypes 11, 17 and a mixture of 11 and 17 in aluminum hydroxide. Agar gel precipitin antibodies were used as an indicator of immunity. Sero-conversion of Hampshires and Suffolk lambs was poor at 43% as compared to 84% in the Columbia and Finn lambs. These results indicate a breed difference in immunological response to inactivated BTV vaccine.

Animals↗
PubMed1981

Persistence and spread of Candida albicans after intragastric inoculation of infant mice.

Infant mice have been shown previously to be a useful model for the study of gastrointestinal (GI) and systemic candidosis. In this study, the virulence of four strains of Candida albicans was compared in intragastrically inoculated infants and in adult mice inoculated intravenously. The four strains differed in their ability to kill both infant and adult mice. A smaller inoculum was required to kill adult mice inoculated intravenously. Neonates could not be inoculated intravenously. The ability of the strains to spread systemically from and to persist for long periods of time in the digestive tract was also examined in intragastrically inoculated infants. The yeast cells spread to liver, lungs, kidneys, and spleen within 30 min postinoculation. Yeast were not detectable in the lungs or in blood from the pleural cavity up to 15 min post-inoculation, thus making it unlikely that systemic spread resulted from faulty inoculation or from aspiration. The region where C. albicans crossed the GI tract of infant mice was visualized histologically in the upper third of the small intestine. The four strains varied in their ability to persist for long periods in the GI tract, in the rate at which they appeared systemically, and in ability to kill infant mice. Three of the four strains colonized the gut for up to 10 weeks postinoculation without use of any compromising agents.

Animals↗
PubMed1981

Intestinal colonization of neonatal animals by Campylobacter fetus subsp. jejuni.

Neonatal mice (2.3 to 2.8 g) were inoculated intragastrically with different human isolates of Campylobacter fetus subsp. jejuni. At weekly intervals thereafter, mice were sacrificed and dilution plate counts were performed on segments of the gastrointestinal tract. Mice were uniformly colonized by some strains for 2 weeks, whereas other strains were being cleared at that time. One strain (BO216) persisted in some mice for 3 weeks. The greatest number of organisms (10(7)) was recovered from the cecum and large intestine. The small intestine had from 10(2) to 10(5) colony-forming units. Colonization of the stomach was not found consistently. One strain killed 13% of the infected mice. Deaths occurred between 1 and 5 days postinfection. Two other strains killed a smaller percentage of challenged animals, and two additional strains killed none. Retarded weight gain was noticed in some, but not all, of the infected mice. The intestines of neonatal rats and rabbits were colonized much the same as those of mice, whereas hamsters were resistant to colonization. Preweanling mice, up to about 6.5 to 7.0 g, could be colonized with C. fetus subsp. jejuni after intragastric challenge, but weanling mice of larger weight (9.8 g) and young adult mice (18.3 g) could not. Scanning electron photomicrographs of the lower ileum showed campylobacters in and below the dried mucous gel that lines the intestines. The use of this model for additional studies is discussed.

Animals↗
PubMed1980

Improved protection against cholera in adult rabbits with a combined flagellar-toxoid vaccine.

Ligated ileal loops of adult rabbits were used to evaluate the prophylactic potential against cholera of a combined vaccine consisting of toxin-free crude flagella (CF) and glutaraldehyde-derived cholera toxoid (TV). The resulting fluid accumulation ratios were compared with those in rabbits immunized with saline (controls) and with CF and TV alone. Data for single vaccines confirmed the superior protection effect of CF over TV. In rabbits vaccinated with both CF and TV, maximal fluid accumulation ratios were not obtained with a challenge dose as high as 5 X 10(9) colony-forming units (CFU). Two rabbits similarly immunized failed to produce positive loops with challenges of 6.3 X 10(8) and 5 X 10(9) CFU, respectively. The vibriocidal titer of serum from rabbits immunized with a killed commercial vaccine in addition to those listed above was determined at intervals for a period of 164 days. No vibriocidal activity was detected in serum of control rabbits and of rabbits vaccinated with TV. Serum from animals given CF or commercial vaccine had similar vibriocidal titers even when the test bacteria were nonflagellated. Protection against challenge as evaluated by ileal loops did not, however, correlate with vibriocidal titer.

Animals↗
PubMed1979

Evaluation of a ribosomal vaccine against pertussis.

A crude ribosomal vaccine derived from Bordetella pertussis administered to ICR and N:NIH (SW) strains of mice protected them effectively against a standardized intracranial challenge. The dose of vaccine that protected half the mice was less for N:NIH (SW) than for ICR mice and compared favorably with a killed reference vaccine. Ribosomes prepared from bacteria ground with washed sea sand were more immunogenic than those obtained by rupture with alumina or with a Braun homogenizer. The protective effect of the crude ribosomes was not an innate part of the organelle but was due to a substance or substances that could be removed from them by a 1 M NH4Cl wash. The material in the wash was highly immunogenic and retained both the histamine-sensitizing and leukocytosis-promoting properties. It lost much of the dermonecrotic activity and was poorly pyrogenic in rabbits. The most potent pyrogen was present in the washed ribosomes, which apparently, retained the endotoxic components of the cell wall. The best vaccines permitted acceptable weight gain in the immunized mice.

Animals↗
PubMed1979

Flagella-induced immunity against experimental cholera in adult rabbits.

The adult rabbit ligated ileal loop model was used to evaluate the prophylactic potential of a crude flagellar (CF) vaccine produced from the classical. Inaba strain CA401. A greater than 1,000-fold increase in the challenge inoculum was required to induce an intestinal fluid response in actively immunized adult rabbits equivalent to that produced in unimmunized animals. Similar protection was afforded against challenge with classical and El Tor biotypes of both Inaba and Ogawa serotypes. Highly virulent 35S-labeled vibrios were inhibited in their ability to associated with the intestinal mucosa of CF-immunized rabbits. The protection conferred by CF immunization was found to be superior to that of a commercial bivalent vaccine and also to that of glutaraldehyde-treated cholera toxoid. The critical immunogenic component of CF appears to be a flagella-derived protein. The immunogenicity of CF was destroyed by heat treatment, and absorption of CF-immune serum with aflagellated mutant vibrios did not diminish its ability to confer a high level of passive protection. The intestinal protection of CF-immunized rabbits was completely reversed by the introduction of both goat anti-rabbit immunoglobulins A and G, but by neither alone.

Animals↗
PubMed1979

Systemic and gastrointestinal candidiasis of infant mice after intragastric challenge.

Systemic and gastrointestinal infection can be established in infant mice after intragastric challenge with Candida albicans. Differences in virulence of the six strains tested were noted. As early as 3 h after infection, some but not all livers, spleens, and kidneys contained C. albicans, but the peak number of colony-forming units in these organs was seen at 6 h. The early colonization of the organs could not be attributed to aspiration of the inoculum since about 90% of lungs and livers tested yielded no colony-forming units at 10 to 15 min postinfection. In animals with systemic infections, lungs, livers, kidneys, and spleens showed similar numbers of colony-forming units within the organs during the first 6 h postinfection- and then the number declined progressively up to 72 h. The gastrointestinal tract was colonized throughout a 20-day period of study. Counts made at intervals beyond day 1 yielded between 10(5) and 10(6) colony-forming units in the stomach, ileum, and cecum. Preparatory techniques for scanning electron microscopy preserved the yeast, intestinal mucus layer, and epithelial surface and made it possible to visualize the association between the pathogen and host tissues within the digestive tract.

Administration, Oral↗