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Biomedical subjects

C Halpin

Publications and source records attributed to C Halpin.

30 records · Page 2Linked to original sources
PubMed1991

Hearing loss and pneumococcal meningitis: an animal model.

Clinical studies of predisposing factors in the development of hearing loss secondary to bacterial meningitis have produced conflicting results. An animal model of meningogenic labyrinthitis was developed for more precise study of these parameters. Rabbits were inoculated intrathecally with 10(5) pneumococci to induce meningitis. Hearing thresholds were measured using auditory-evoked responses to 1 kHz, 10 kHz, and click stimuli before infection and every 12 hours thereafter. Profound deafness occurred in all subjects at an average of 48 hours following infection. The incidence and severity of hearing loss was strongly correlated with the duration of meningitis. Temporal bone histology revealed acute inflammation of all perilymphatic spaces including the cochlear aqueduct. This model demonstrated that the risk and severity of hearing loss increase with the duration of meningitis and suggested that the cochlear aqueduct is an anatomic pathway for the extension of infection from the cerebrospinal fluid to the cochlea. The implications for therapy in humans is discussed.

Acoustic Stimulation↗
PubMed1989

The reaction specificities of the thylakoidal processing peptidase and Escherichia coli leader peptidase are identical.

Proteins which are transported across the bacterial plasma membrane, endoplasmic reticulum and thylakoid membrane are usually synthesized as larger precursors containing amino-terminal targeting signals. Removal of the signals is carried out by specific, membrane-bound processing peptidases. In this report we show that the reaction specificities of these three peptidases are essentially identical. Precursors of two higher plant thylakoid lumen proteins are efficiently processed by purified Escherichia coli leader peptidase. Processing of one precursor, that of the 23 kd photosystem II protein, by both the thylakoidal and E. coli enzymes generates the correct mature amino terminus. Similarly, leader (signal) peptides of both eukaryotic and prokaryotic origin are cleaved by partially purified thylakoidal processing peptidase. No evidence of incorrect processing was obtained. Both leader peptidase and thylakoidal peptidase are inhibited by a synthetic leader peptide.

Amino Acid Sequence↗
PubMed1983

Experimental cryptosporidiosis in calves: clinical manifestations and pathological findings.

Twenty-two calves between one and 20 days old were infected orally or by contact with cryptosporidia. Calves were maintained as either specific pathogen free, colostrum fed or sucking and were inoculated with either a bacteria free or a contaminated cryptosporidium preparation. Enteritis was characterised by depression, anorexia and diarrhoea and cryptosporidium oocysts were excreted during the clinical course of the illness. In the initial stages of the disease, cryptosporidium infestation was found throughout the small intestine; in the later stage the large intestine was also affected. Villous atrophy and fusion was present at small intestinal sites infected with cryptosporidia and lactase levels were depressed. No lesions were seen in infected large intestinal mucosa. Although the incubation period was longest (five to seven days) in calves infected by contact, there were few differences in the clinical course of disease or the pathological findings between any of the infected calves.

Animals↗
PubMed1983

Intestinal changes associated with rotavirus and enterotoxigenic Escherichia coli infection in calves.

Newborn calves inoculated with rotavirus, enterotoxigenic Escherichia coli (ETEC) serotype 020:K' x 106':K99:HNM, either alone or in combination, became depressed, anorectic, diarrhoeic and dehydrated. ETEC did not adhere to the intestine although there was extensive proliferation in the lumen. Only slight mucosal changes were induced by ETEC and the activity of membrane bound lactase remained normal. More severe mucosal damage and a decrease in lactase activity were found in newborn calves inoculated with either rotavirus or rotavirus and ETEC in combination. The most severe clinical illness was found in calves inoculated with both rotavirus and ETEC. Calves inoculated at 1 week of age with either rotavirus or ETEC remained clinically normal. Rotavirus infection produced slight mucosal changes and a reduction of lactase activity. In contrast, colostrum-fed or suckling calves up to 2 weeks old inoculated with both rotavirus and ETEC became clinically affected, showed severe mucosal damage and decreased lactase activity. There was no bacterial adhesion to the intestinal mucosa as observed by immunofluorescent labelling and light microscopy.

Animals↗
PubMed1982

Enterocolitis in piglets caused by Cryptosporidium sp. purified from calf faeces.

Twelve gnotobiotic piglets were dosed with a bacteria-free calf faecal homogenate which contained Cryptosporidium oocysts. The infection induced severe enterocolitis in piglets when inoculated at 1 day of age, moderate diarrhoea at 7 days of age and a subclinical infection at 15 days of age. In piglets aged 3 days or less, the entire intestine was extensively infected with Cryptosporidium and the mucosa was severely damaged. In piglets 7 days of age or older, the upper small intestine was sparsely infected with the organisms, but the ileum and the large bowel were heavily infected with associated mucosal damage.

Aging↗
PubMed1982

Experimental colibacillosis in gnotobiotic piglets exposed to 3 enterotoxigenic serotypes.

Three strains of enterotoxigenic Escherichia coli (ETEC) (064:KSNT, K88ac; 020:KSNT, K88ac and 08:K85ab, K99) originally cultured from outbreaks of diarrhoea in piglets a few hours old, were administered orally to gnotobiotic piglets. There was a marked age-related difference in the clinical response to infection between the 3 strains although they all produced heat-stable toxin. All 3 strains produced severe clinical signs of depression, anorexia, vomiting, diarrhoea, followed by dehydration and death in one-day-old piglets. In piglets infected at 3 days of age the two K88+ ETEC caused diarrhoea and death but the K99+ ETEC induced moderate diarrhoea only. In piglets infected at 7 days of age, the 064 strain produced severe diarrhoea and death, and 020 strain caused mild diarrhoea in 3 of 6 piglets with one death while the 08 strain caused no illness. Pathological changes in the intestinal tract associated with these infections were minimal, or absent. Immunofluorescent staining with homologous hyperimmune sera demonstrated adherence of the 3 ETEC strains to the brush border of small intestinal epithelial cells. Fluorescing organisms were observed in all infected piglets irrespective of the severity of clinical signs but the degree and extent of colonisation varied with the age of the piglets and the infecting strain. This may explain the difference in clinical response between the 3 strains.

Animals↗