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Biomedical subjects

R B Hornick

Publications and source records attributed to R B Hornick.

At least 19 recordsLinked to original sources
PubMed1995

Infecting dose and severity of typhoid: analysis of volunteer data and examination of the influence of the definition of illness used.

Data from volunteers challenged with Salmonella typhi were reanalysed to explore the relationship between challenge dose and severity of disease. Among 120 ill volunteers who received between 10(5) and 10(9) organisms, dose was weakly correlated with peak temperature (r = 0.22, 95% CI 0.04-0.39), duration of temperature above 103 degrees F (39.4 degrees C: r = 0.13, 95% CI - 0.03 to 0.55) and symptom score (r = 0.27, 95% CI 0.09-0.43). The association with symptom score was lost after adjusting for year, and the findings depended on the definition of illness used: with stricter definitions the associations with temperature were also lost. The study shows the need for caution in interpreting the relationship between dose and severity of disease.

Administration, Oral↗
PubMed1982

Anatomical and immunological responses of rabbit gallbladders to bacterial infections.

To study the sequential morphological and immunological response of the rabbit gallbladder to bacterial infection and to compare the inflammatory responses with different pathogens, gallbladders were infected with Streptococcus faecalis and two strains of Escherichia coli, one of which produced enterotoxin. Gallbladder infection was produced either by intravenously injecting bacteria into rabbits with a small liver infarct or by injecting bacteria directly into the gallbladder of normal rabbits. The percentage of gallbladders infected intravenously with a nonenterotoxigenic E. coli strain was 86% at 1 week, 70% at 3 weeks, and 15% at 6 weeks. Epithelial necrosis and leukocyte infiltration were prominent 1 week after infection. At 3 and 6 weeks after infection, there was crypt distortion and increased mucus secretion in the epithelium as shown by periodic acid-Schiff staining. The lamina propria was infiltrated with mononuclear cells, many of which were plasma cells. Myofibroblasts (contractile fibroblasts) were also identified on transmission microscopy, In addition to these changes, toxigenic E. coli produced subepithelial capillary dilation in the villus core. Morphological changes (excluding toxin-associated changes) were related to the duration of infection rather than to the specific species of infecting bacteria. Infected gallbladders studied by immunofluorescence had a greater than 50-fold increase in plasma cells compared with control cells. In addition, the number increased with the duration of infection. Immunoglobulin A cells were the major cell type in gallbladders infected by intravesical injection, whereas immunoglobulin G cells predominated in gallbladders infected intravenously. The gallbladder appears to mount a local immune response to bacterial infection.

Animals↗
PubMed1981

Model of intraabdominal abscess in mice.

Intraperitoneal inoculation of sterile mouse feces into mice produced intraabdominal abscesses. The addition of Bacteroides fragilis increased the incidence and the number of abscesses.

Abdomen↗
PubMed1981

Biohydrogenation of cholesterol as an index of bacterial 7 alpha-dehydroxylase activity.

Fecal steroid compositions of 82 human subjects of various ages and diets and gastrointestinal status were examined by gas liquid chromatography. Progressive increases in bacterial activities on both bile acids and neutral sterols were observed with the advance of age in infants and children. The patterns in the 4-year-olds approached those observed in adults. Bacterial activities on fecal steroids were found to be decreased in adult subjects with acute shigellosis and in those challenged by castor oil. In contrast, no significant changes in fecal steroid profiles were observed in the subjects with traveller's diarrhea associated with toxigenic Escherichia coli. The effects of diarrhea on fecal steroids of infants under 1 1/2 years were less consistent than those of adults. However, a close relationship was observed between the degree of 7 alpha-dehydroxylation of cholic acid (expressed as the ratio of deoxycholic to the sum of deoxycholic and cholic acids) and the percentage of cholesterol in the feces (r = -0.921, p less than 0.001). The correlation between the production of lithocholic acid and the percentage cholesterol was also good (r = -0.739, p less than 0.001). Analysis of neutral steroids may be a good index of intraluminal bile acid metabolism.

Adolescent↗
PubMed1979

Immunity of cholera in man: relative role of antibacterial versus antitoxic immunity.

Purified cholera toxoid is antigenic when given enterally and orally. Purified toxoid fails to provide protection against experimental challenge. Clinical cholera confers formidable protection against homologous or heterologous rechallenge. Failure to culture vibrios from intestinal fluid or stool of re-challenge volunteers suggests that the predominant immune mechanism is antibacterial rather than antitoxic.

Antibodies, Bacterial↗
PubMed1979

The problem of emesis during oral glucose-electrolytes therapy given from the onset of severe cholera.

In an attempt to obviate the need for intravenous fluids by preventing dehydration, 57 adult volunteers who experienced induced clinical cholera during a vaccine development programme were treated from the onset of diarrhoea with oral glucose-electrolytes therapy. 44 individuals with mild to moderately profuse diarrhoea (less than 8 L. total volume) were maintained in normal water and electrolyte balance with oral therapy alone. 13 individuals with severe diarrhoea (greater than 8 L. total volume) could not be maintained in balance with oral therapy alone, due chiefly to emesis during the first day of illness. Emesis occurred in the absence of significant dehydration or acidosis. Since emesis precludes effective early oral therapy in severe cases, domiciliary oral therapy is unlikely to eliminate cholera mortality. Rural diarrhoea treatment centres using oral therapy with limited amounts of intravenous fluids when needed, could reduce case fatality from cholera and related diarrhoeas virtually to zero with least expense.

Adolescent↗
PubMed1979

Immunity to enterotoxigenic Escherichia coli.

Enterotoxigenic Escherichia coli strains represent the most frequent etiological agent of travelers diarrhea. Challenge studies with several of these strains were undertaken in volunteers to evaluate the mechanisms of disease-induced immunity. Seventeen students and other community volunteers were given 10(6) or 10(8) organisms of E. coli B7A (O148:H28), which produces heat-labile and heat-stable enterotoxins. Ten individuals developed diarrheal illness closely resembling natural travelers diarrhea; of these ten, rises in titer of serum antitoxin and anti-O antibody occurred in eight (80%). Eight of the volunteers who developed diarrhea in the first test agreed to undergo rechallenge 9 weeks later with 10(8) B7A organisms. Only one of these eight "veterans" developed diarrhea versus seven of twelve controls given the same challenge (P = 0.05). Despite clinical protection, all "veterans" excreted B7A after rechallenge. Four controls who developed diarrhea during the homologous B7A rechallenge test were rechallenged 9 weeks later with 10(9) organisms of E. coli strain E2528-C1 (O25:H-), which produces only heat-labile enterotoxin and possesses a different O, H, and pili antigen composition than B7A. Three of four "veterans" and two of six controls developed comparable diarrhea. These studies demonstrate that prior disease due to enterotoxigenic E. coli confers homologous immunity against subsequent challenge, and the operative mechanism apparently is not bactericidal and is not mediated by serum anti-O antibodies. Heterologous protection was not conferred where the only common antigen was heat-labile enterotoxin, indicating that serum infection-derived antitoxin to heat-labile enterotoxin also is not protective.

Antibodies, Bacterial↗
PubMed1978

Cholera, non-vibrio cholera, and stomach acid.

Fasting and postprandial stomach acid production were low in 16 of 37 Bangalees convalescing from cholera or non-vibrio cholera. Gastric juice of hypochlorhydric patients did not kill cholera vibrios in vitro, whereas that from normochlorhydric patients rapidly killed vibrios in concentrations up to 10(10)/ml. To determine whether hypoacidity resulted from cholera or was a common predisposing factor, basal and betazole-hydrochloride-stimulated acid production were measured before and after cholera in a second group of patients consisting of American volunteers participating in a vaccine development programme. Cholera did not alter the stomach acid secretion of American volunteers, but low precholera basal acid production predispose to severe cholera. The results indicate that hypochlorhydria observed in convalescent Bangalee cholera patients is not caused by cholera, and must therefore have preceded it. Idiopathic tropical hypochlorhydria may be a major factor accounting for the high incidence of diarrhoea due to acid-sensitive pathogens in developing countries.

Achlorhydria↗
PubMed1978

Cannabis, hypochlorhydria, and cholera.

In 90 volunteers participating in a vaccine-development programme consumption of beer more than 3 days a week was linked with high stomach acid output, and smoking of cannabis greater than 2 days a week was linked with low acid output. In 92 volunteers challenged with Vibrio cholerae or enterotoxigenic Escherichia coli, heavy use of cannabis was associated with more voluminous diarrhoea. Cannabis use may be an important factor predisposing to severe diarrhoea.

Achlorhydria↗
PubMed1978

Rocky mountain spotted fever caused by blood transfusion.

Transfusion of 500 ml of blood, contributed by a donor three days before the onset of Rocky Mountain spotted fever and refrigerated for nine days, caused this disease in the recipient. The blood donor died of Rocky Mountain spotted fever after six days; rickettsia were identified in various tissues by immunofluorescence techniques. The recipient of the blood became mildly ill and recovered fully; specific antibiotic treatment was initiated on the fourth day of illness. Diagnosis of Rocky Mountain spotted fever was confirmed in the recipient by positive serologic reactions and isolation of Rickettsia rickettsii from blood after inoculation in animals and tissue culture.

Aged↗
PubMed1978

Escherichia coli strains that cause diarrhoea but do not produce heat-labile or heat-stable enterotoxins and are non-invasive.

Three enteropathogenic Escherichia coli (E.P.E.C.) strains (O127:K63:H6, O128:K67:H2, and O142:K86:H6) isolated from outbreaks of infantile diarrhoea and one strain from the "normal" colonic flora (E. coli HS) of a healthy adult were fed in doses of 10(6), 10(8), and 10(10) organisms in NaHCO3 to adult volunteers. The strains, which had been stored for 7--9 years, gave negative results in sensitive tests for heat-labile (L.T.) enterotoxin (Y-1 adrenal-cell test), heat-stable (S.T.) enterotoxin (infant mouse assay), invasiveness (guineapig eye test), and gross fluid accumulation (infant rabbit assay). Two strains (O142 and O127) caused diarrhoea. L.T. or S.T. enterotoxins were not found in E. coli stool isolates from individuals with diarrhoea and no one had a rise in L.T. antitoxin titre; the findings suggest that L.T. and S.T. enterotoxins were not involved in pathogenesis of the diarrhoea. Non-invasive E.P.E.C. strains probably induce diarrhoea by a mechanism (presumably an enterotoxin) distinct from L.T. or S.T. enterotoxins.

Adult↗
PubMed1978

Invasive Escherichia coli.

The present evidence indicates that Shigella-like pathogenicity is determined by a multiplacity of genes. Although deliberate attempts have been made to confer invasive virulence on E. coli strain K12 by employing classical procedures of recombination with virulent S. flexneri donor strains, they have not yet been successful. While we should, theoretically, be able to achieve this, the practical problem of testing for pathogenicity precludes screening larger numbers of hybrid clones for the acquisition of virulence. This increases the difficulty of successfully realizing that end. Nevertheless, since invasive-type pathogenicity is determined by multiple genetic loci, we consider it unlikely that random insertion of foreign DNA into the E. coli K12 genome could supply all of the genetic information necessary to convert this organism into an invasive enteric pathogen.

Colon↗