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Biomedical subjects

H W Moon

Publications and source records attributed to H W Moon.

At least 37 records · Page 2Linked to original sources
PubMed1997

Comparative histopathology of intestinal infections.

Intestinal infections are characterized by a range of histologic changes. Some examples (moving progressively deeper into the tissue from the intestinal lumen) are: 1) Enterotoxigenic E. coli infections are characterized by layers of E. coli adherent to villous epithelium, usually with little or no apparent structural damage to the mucosa. 2) The term enteropathogenic E. coli infection designates a disease characterized by E. coli attached intimately to the epithelial cell surface membrane with effacement of brush border microvilli. 3) Rotavirus infections are characterized by destruction of villous epithelial cells. Parvovirus infections are characterized by destruction of crypt epithelial cells. 4) Some intracellular infections with Campylobacter-like organisms are characterized by epithelial cell hyperplasia. 5) Hemorrhagic colitis in humans, caused by enterohemorrhagic E. coli strains, is characterized by mucosal hemorrhage and edema indicative of vascular necrosis. 6) Most of these lesions are accompanied by some degree of inflammation. Neurophils and lymphocytes mediate some of the structural and functional changes characteristic of these infections. Some changes are mediated directly by microbial products. Additional examples of the complexity of these diseases are: 1) Edema disease of swine is characterized both by adherent E. coli and vascular necrosis (each process mediated by a different bacterial virulence attribute). 2) Rotavirus infections are characterized both by destruction of villous epithelial cells and compensatory hyperplasia of crypt epithelial cells. 3) There is suggestive evidence that enterohemorrhagic E. coli infections may involve: a) destruction of epithelial brush border by attaching-effacing E. coli, b) neutrophil mediated epithelial cell destruction, c) Shiga-like toxin mediated epithelial cell destruction and d) Shiga-like toxin mediated vascular necrosis which in turn causes ischemic damage to epithelium.

Animals↗
PubMed1997

Pathogenesis of O157:H7 Escherichia coli infection in neonatal calves.

Cattle have been implicated as an important reservoir of Shiga-like toxin-producing Escherichia coli (SLTEC) O157:H7, enterohemorrhagic E. coli (EHEC) that cause hemorrhagic colitis and hemorrhagic uremic syndrome in humans. Naturally- or experimentally-infected cattle can shed low levels of E. coli O157:H7 long-term, but little is known about the pathogenesis of E. coli O157:H7 infection in cattle. E. coli O157:H7 induce characteristic attaching and effacing (A/E) mucosal lesions in ceca and colons of 1-day-old gnotobiotic piglets and this model is used to study the pathogenesis of SLTEC infections. A/E lesions were not detected in histologic sections of the intestines from adult cattle or 3- to 14-week-old calves infected with E. coli O157:H7. Our objective was to determine if E. coli O157:H7 induce A/E lesions in neonatal calves. Colostrum-deprived calves (< 12-h-old) were bottle-fed with antibiotic-free milk replacer containing 10(10) colony forming units (CFU) of O157:H7 (SLT-I+, SLT-II+) or nonpathogenic E. coli, necropsied 18 h postinfection and their intestines examined histologically. Bacterial attachment, effacement of microvillous borders, and destruction of epithelium were observed in the intestines of the neonatal calves inoculated with E. coli O157:H7. No lesions were observed in calves inoculated with nonpathogenic E. coli. The distribution of intestinal lesions in neonatal calves resembled that in gnotobiotic pigs. Neonatal calves are apparently more susceptible to A/E lesions induced by E. coli O157:H7 than are older calves or adult cattle and provide a model for studying the pathogenesis of E. coli O157:H7 infections in cattle.

Animals↗
PubMed1997

Pathogenicity of Escherichia coli O157:H7 in the intestines of neonatal calves.

Cattle are an important reservoir of Shiga toxin-producing enterohemorrhagic Escherichia coli (EHEC) O157:H7 strains, foodborne pathogens that cause hemorrhagic colitis and hemolytic uremic syndrome in humans. EHEC O157:H7 strains are not pathogenic in calves >3 weeks old. Our objective was to determine if EHEC O157:H7 strains are pathogenic in neonatal calves. Calves <36 h old inoculated with EHEC O157:H7 developed diarrhea and enterocolitis with attaching and effacing (A/E) lesions in both the large and small intestines by 18 h postinoculation. The severity of diarrhea and inflammation, and also the frequency and extent of A/E lesions, increased by 3 days postinoculation. We conclude that EHEC O157:H7 strains are pathogenic in neonatal calves. The neonatal calf model is relevant for studying the pathogenesis of EHEC O157:H7 infections in cattle. It should also be useful for identifying ways to reduce EHEC O157:H7 infections in cattle and thus reduce the risk of EHEC O157:H7 disease in humans.

Animals↗
PubMed1996

Virulence attributes of Escherichia coli isolated from dairy heifer feces.

Escherichia coli isolates from 1,305 (of 6,894) fecal samples collected during the 1991-1992 USDA, Animal and Plant Health Inspection Service, National Health Monitoring System, Diary Heifer Evaluation Project were tested for virulence attributes associated with human enterohaemorrhagic E. coli (EHEC) and the enterotoxin commonly associated with diarrhoea in newborn calves. Single, random isolates from each heifer were hybridized to probes derived from the 60 mDa EHEC plasmid (CVD 419), E. coli attaching and effacing gene (eae), Shiga-like toxin (slt) genes I and II, and E. coli heat-stable enterotoxin a (STaP). Seventy-seven of the 1305 isolates (5.9%) were slt-positive. Most (81.8%) slt-positive E. coli were also CVD 419 and eae-positive. Only 2 of the slt-positive E. coli isolates were STaP-positive.

Animals↗
PubMed1996

Vaccination with genetically modified Shiga-like toxin IIe prevents edema disease in swine.

Escherichia coli strains producing Shiga-like toxin II variant (SLT-IIe, formerly called SLT-IIv) cause edema disease in weaned pigs. Vaccination of pigs with a genetically modified form of Shiga-like toxin IIe, SLT-IIe(E167Q), has been previously shown to be nontoxic and to induce antibodies to SLT-IIe (V.M. Gordon. S.C. Whipp, H.W. Moon, A.D. O'Brien, and J.E. Samuel, Infect, Immun. 60:485-502, 1992). Fifty micrograms of SLT-IIe(E167Q) toxin was used to vaccinate suckling pigs at 1 and 2 weeks of age. Both vaccinated and nonvaccinated pigs were orally inoculated with an SLT-IIe-producing strain of E. coli after weaning (3 to 4 weeks of age). Pigs fed a low-protein diet that were not vaccinated with SLT-IIe(E167Q) developed subclinical edema disease, histologically evident as vascular necrosis. Pigs fed a high-protein diet that were not vaccinated with SLT-IIe(E167Q) developed clinical edema disease manifested as vascular necrosis, reduced weight gain, ataxia, palpebral edema, lateral recumbency, and death. Pigs vaccinated with SLT-IIe(E167Q) had a reduction in the incidence of subclinical edema disease and never developed clinical edema disease. These data demonstrate that vaccination with a genetically modified form of SLT-IIe prevents edema disease and are consistent with the notion that diet influences susceptibility to edema disease.

Animals↗
PubMed1996

Linear and whorled nevoid hypermelanosis with delayed psychomotor development.

We report a case of a 25-month-old girl presented to us for the evaluation of a severe delayed psychomotor development who also has pigmentary abnormalities. Linear and whorled hyperpigmentations following Blaschko's lines were noticed on her entire body except on her face, palms, soles, eyes and mucous membranes, which closely resembled those found in hypomelanosis of Ito, but inversely pigmented. Histologic examination revealed basal layer hyperpigmentation without incontinence of pigment or dermal melanophages. Chromosomal analysis of cultured peripheral leukocytes and fibroblasts from the hyperpigmented and the hypopigmented skin revealed normal female karyotype with no evidence of mosaicism or chimerism. This entity represents a kind of neurocutaneous syndrome-referred to by some authors as linear and whorled nevoid hypermelanosis.

Child Development↗
PubMed1996

Psychological characteristics of mothers of children with disabilities.

The purpose of this study was to investigate the psychological characteristics of mothers of children with disabilities. This study was performed under the hypotheses that, at the initial diagnosis of the children's disabilities, (1) the mothers suffered from serious psychological distress; (2) the more severe the child's disability was, the more serious the mother's psychological distress was; and that (3) the mother's psychological distress might be resolved within 8 weeks of rehabilitational interventions. The results were as follows: 1) mothers of children with disabilities showed significant (p < 0.05) somatization, depression, anxiety, hostility, and phobic anxiety more so than the control group; 2) there was no significant difference in T scores of 9 dimensions of the Symptom Checklist-90-Revision (SCL-90-R) of the mothers at the initial diagnosis of children's disabilities according to severity of child's disability; 3) there was no significant difference in T scores of 9 dimensions of SCL-90-R in mothers of children with disabilities between at initial evaluation and after 8 weeks of rehabilitational interventions. In conclusion, : 1) mothers of children with disabilities suffered from serious psychological distress at the initial diagnosis of their child's disability; 2) the severity of the child's disability had little influence on the degree of the mother's initial psychological distress; 3) this distress did not resolve with only 8 weeks of rehabilitational interventions. Therefore, effective rehabilitational programs should provide sufficient opportunities for repeated follow-up interviews which offer not only adequate information on the children's disabilities but also psychological support for the mothers.

Adult↗
PubMed1995

Experimental infection of calves and adult cattle with Escherichia coli O157:H7.

Preweaned calves and adult cattle were inoculated with 10(10) CFU of Escherichia coli O157:H7 strain 3081, a calf isolate which produces Shiga-like toxin, to define the magnitude and duration of fecal shedding of E. coli O157:H7 for each age group. Fecal samples of eight of eight, eight of eight, three of eight, and two of eight calves were positive at 2, 7, 14, and 20 weeks, respectively. In contrast, nine of nine, two of nine, and one of nine steers were positive at 2, 7, and 14 weeks, respectively. The magnitude of shedding (CFU per gram) by individual animals at any one time postinoculation varied widely within each age group but was greater for calves as a group. The differences in shedding patterns between adults and calves were statistically significant. After inoculation, 25 of 29 animals remained healthy and 4 of 17 calves had transient diarrhea. Histologic sections of the brain, kidney, jejunum, ileum, cecum, and colon taken at necropsy from nine calves either 3, 14, or 18 days postinoculation or three adults either 2, 3, or 4 days postinoculation were normal. E. coli O157:H7 was recovered from the alimentary tracts of all of the animals necropsied, and there was no evidence of spread to the liver, spleen, or kidneys. Four calves that had ceased shedding were reinfected when inoculated again with the same strain. E. coli O157:H7 was recovered from none of five and two of five adults inoculated with 10(4) and 10(7) CFU, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1995

Hypertrophic neuropathy with complete conduction block-- hereditary motor and sensory neuropathy type III.

Hypertrophic neuropathy is a non-specific consequence of repeated demyelination and remyelination, encountered in a wide range of inherited and acquired disorders. We report an 11-year-old boy with HMSN III, a kind of hypertrophic neuropathy, with clinical, electrophysiologic and pathologic data. The electrophysiologic studies show complete conduction block in the upper and lower extremities with severe abnormal spontaneous activities. The pathologic findings of sural nerve reveal prominent hypomyelination, onion bulb formation, and severe endoneurial collagenization. Complete conduction block with the preservation of fair to good grade muscle strength is an unusual finding in hypertrophic neuropathy and other peripheral neuropathies, in general.

Child↗
PubMed1993

Vaccines for preventing enterotoxigenic Escherichia coli infections in farm animals.

Fimbrial vaccines are routinely given parenterally to pregnant cattle, sheep and swine to protect suckling newborn calves, lambs and pigs against enterotoxigenic Escherichia coli (ETEC) infections. Such vaccines are practical and effective because (1) most fatal ETEC infections in farm animals occur in the early neonatal period when the antibody titres in colostrum and milk are highest; (2) more than 90% of the ETEC in farm animals belong to a small family of fimbrial antigen types; (3) fimbriae consist of good protein antigens on the bacterial surface where they are readily accessible to antibody; (4) fimbriae are required for a critical step (adhesion-colonization) early in the pathogenesis of the disease. ETEC infections continue to be a significant clinical problem in farm animals in spite of extensive use of fimbriae-based vaccines. Definitive data on the efficacy of the commercial vaccines in field use are not available. The prevailing perception among animal health professionals is that the vaccines are effective, that the problem occurs chiefly among non-vaccinated animals, and that in some herds vaccination moves peak prevalence of disease from the first to the second or third week after birth, when mortality is lower. It has been suggested that extensive use of vaccines will rapidly select for the emergence of novel or previously low prevalence fimbrial antigen types. There is no evidence that this has happened after a decade of routine vaccine use in the United States. However, there is no active direct surveillance for such emergence.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

An enzymatic mutant of Shiga-like toxin II variant is a vaccine candidate for edema disease of swine.

Edema disease (ED) of weanling pigs is caused by an infection with Escherichia coli that produces Shiga-like toxin II variant (SLT-IIv). Pathology identical to that caused by ED can be duplicated in pigs that are injected with less than 10 ng of purified SLT-IIv per kg of body weight. Therefore, SLT-IIv was mutated to create an immunoreactive form of the toxin that was significantly reduced in enzymatic activity. Initially, purified SLT-IIv was treated with formaldehyde which abrogated cytotoxic activity. Pigs were vaccinated with the toxoid (100 micrograms) to determine whether a toxoid was a viable vaccine candidate and whether young pigs were capable of mounting an immune response. Although the pigs developed a neutralizing antibody titer (1:128 to 1:512) 28 days postinjection, they also lost weight and developed ED lesions. The deleterious effect of the toxoid appeared to result from residual enzymatic activity or a reversion to a toxic form. An alternative method, site-directed mutagenesis, was employed to consistently reduce the enzymatic activity of SLT-IIv. Glutamate at position 167 of the mature A subunit was replaced by aspartate (E167D), and arginine at position 170 was replaced by lysine (R170K). These mutations reduced cytotoxic activity 10(4)-fold and 10-fold, respectively, while the enzymatic activities were decreased 400-fold and 5-fold, respectively. The activity of a toxin that contained both mutations (SLT-IIvE167D/R170K) closely resembled that of SLT-IIvE167D. When position 167 was replaced by glutamine (E167Q), the cytotoxic activity decreased 10(6)-fold and the enzymatic activity decreased approximately 1,500-fold. Pigs that were vaccinated with purified, mutant toxin designated SLT-IIvE167Q developed a neutralizing antibody titer of 1:512 21 days postinjection, and their tissues were free of ED lesions. These data suggest that SLT-IIvE167Q may represent an effective vaccine against ED.

Animals↗
PubMed1992

Susceptibility of porcine intestine to pilus-mediated adhesion by some isolates of piliated enterotoxigenic Escherichia coli increases with age.

Two porcine isolates of enterotoxigenic Escherichia coli (ETEC) (serogroup O157 and O141) derived from fatal cases of postweaning diarrhea and lacking K88, K99, F41, and 987P pili (4P- ETEC) were tested for adhesiveness to small-intestinal epithelia of pigs of different ages. Neither strain adhered to isolated intestinal brush borders of newborn (1-day-old) pigs in the presence of mannose. However, mannose-resistant adhesion occurred when brush borders from 10-day- and 3- and 6-week-old pigs were used. Electron microscopy revealed that both strains produced fine (3.5-nm) and type 1 pili at 37 degrees C but only type 1 pili at 18 degrees C. Mannose-resistant in vitro adhesion to brush borders of older pigs correlated with the presence of fine pili. These strains produced predominantly fine pili in ligated intestinal loops of both older and newborn pigs, but adherence was greater in loops in older pigs. Immunoelectron microscopic studies, using antiserum raised against piliated bacteria and absorbed with nonpiliated bacteria, of samples from brush border adherence studies revealed labelled appendages between adherent bacteria and intestinal microvilli. Orogastric inoculation of pigs weaned at 10 and 21 days of age indicated significantly (P less than 0.001) higher levels of adhesion by the ETEC to the ileal epithelia of older pigs than to that of younger ones. We suggest that small-intestinal adhesion and colonization by these ETEC isolates is dependent on receptors that develop progressively with age during the first 3 weeks after birth. Furthermore, our data are consistent with the hypothesis that the fine pili described mediate intestinal adhesion by the 4P- ETEC strains studied.

Age Factors↗
PubMed1992

Colonization of the small intestine of weaned pigs by enterotoxigenic Escherichia coli that lack known colonization factors.

Intestinal colonization of 3-week-old weaned pigs by enterotoxigenic Escherichia coli (ETEC) strains that were originally isolated from weaned pigs with fatal diarrhea and that lacked K88, K99, F41, and 987P adhesins (4P- ETEC) was studied by histologic, immunofluorescent, and electron microscopic techniques. In the first experiment, 16 principal pigs were inoculated orogastrically with ETEC strain 2134 (serogroup O157: H19) or 2171 (serogroup 0141:H4), and eight control pigs were not inoculated. In the second experiment, 24 principals were inoculated with ETEC strain 2134, and 12 controls were inoculated with a nonenterotoxigenic strain of E. coli. Principal and control pigs were necropsied at intervals from 24 to 72 hours after inoculation of principals to provide the tissues used for this report. Results from the two experiments and with both ETEC strains were similar and therefore were combined. Adhesion by 4P- ETEC was demonstrated in ileum but not in cecum or colon in 22/40 principal pigs sampled at 24 to 72 hours after orogastric inoculation. Adherent bacteria were most apparent on the intestinal villi covering Peyer's patches. Only occasional adherent bacteria were detected in ileal sections from a few (4/20) of the control pigs. Adherence by 4P- ETEC was characterized by "patches" of bacteria closely associated with the lateral surfaces and less frequently with the tips and the bases of intact villi. In most cases, the adherent bacteria were separated from epithelial cell microvilli and other bacterial cells by a 50-400-nm space. Filamentous bacterial appendages bridged this space and formed a network among adjacent bacteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Pathogenicity of porcine enterotoxigenic Escherichia coli that do not express K88, K99, F41, or 987P adhesins.

Three-week-old weaned and colostrum-deprived neonatal (less than 1 day old) pigs were inoculated to determine the pathogenicity of 2 enterotoxigenic Escherichia coli isolates that do not express K88, K99, F41, or 987P adhesins (strains 2134 and 2171). Strains 2134 and 2171 were isolated from pigs that had diarrhea after weaning attributable to enterotoxigenic E coli infection. We found that both strains of E coli adhered in the ileum and caused diarrhea in pigs of both age groups. In control experiments, adherent bacteria were not seen in the ileum of pigs less than 1 day old or 3 weeks old that were noninoculated or inoculated with a nonpathogenic strain of E coli. These control pigs did not develop diarrhea. Antisera raised against strains 2134 and 2171 and absorbed with the autologous strain, grown at 18 C, were used for bacterial-agglutination and colony-immunoblot assays. Both absorbed antisera reacted with strains 2134 and 2171, but not with strains that express K99, F41, or 987P adhesins. A cross-reaction was observed with 2 wild-type K88 strains, but not with a K12 strain that expresses K88 pili. Indirect immunofluorescence with these absorbed antisera revealed adherent bacteria in frozen sections of ileum from pigs infected with either strain. We concluded that these strains are pathogenic and express a common surface antigen that may be a novel adhesin in E coli strains that cause diarrhea in weaned pigs.

Adhesins, Escherichia coli↗
PubMed1992

An experimental model for subclinical edema disease (Escherichia coli enterotoxemia) manifest as vascular necrosis in pigs.

An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.

Animals↗
PubMed1991

Susceptibility of mast cell-deficient W/Wv mice to Cryptosporidium parvum.

Mast cell-deficient W/Wv infant mice were similar to normal mice in their susceptibility to and recovery from infection with the intestinal protozoan Cryptosporidium parvum. W/Wv adult mice were significantly more susceptible to primary infection than were normal adult mice, but both groups recovered at a similar rate.

Animals↗
PubMed1990

Characterization of bovine septicemic, bovine diarrheal, and human enteroinvasive Escherichia coli that hybridize with K88 and F41 accessory gene probes but do not express these adhesins.

Certain DNA probes derived from accessory genes of cloned K88 and F41 determinants hybridize with Escherichia coli strains that express K88 or F41 and with certain other E. coli strains that do not express these antigens. We found that these probes hybridized with human enteroinvasive E. coli, and with bovine E. coli isolates which produced a fatal septicemia in experimentally infected piglets. These strains did not hybridize with probes derived from the structural subunit genes encoding the K88 and F41 antigens. E. coli strains isolated from turkeys with septicemia, Shigella and Salmonella strains did not hybridize to the K88 and F41 accessory gene probes. The K88 and F41 accessory genes probes hybridized with a 200 kb plasmid which is required for invasion by human enteroinvasive E. coli. The K88 and F41 accessory gene homology in the bovine isolates was located on a 150 kb transmissible plasmid but was unrelated to plasmids encoding aerobactin, Vir, or colicin V, which are suspected virulence factors in septicemic E. coli. A common plasmid-encoded antigen was associated with bovine isolates that hybridized with the K88 and F41 accessory gene probes. This included strains which express CS31A, a surface antigen associated with bovine septicemic E. coli, which also hybridized with the K88 and F4 accessory gene probes. The results suggest that the K88 and F41 accessory gene probes hybridized with sequences that may be associated with a common mechanism of pilus expression in distinct groups of E. coli pathogens.

Animals↗