PubMed Health⌕ Search

Biomedical subjects

B Currie

Publications and source records attributed to B Currie.

90 records · Page 5Linked to original sources
PubMed1988

A focus of Rocky Mountain spotted fever within New York City.

In the spring and summer of 1987, four persons acquired Rocky Mountain spotted fever within New York City, an area in which the disease had not previously been known to be endemic. Three of the four patients were residents of the Soundview area of the Bronx. All diagnoses were confirmed by indirect fluorescent-antibody tests. Environmental investigation revealed that the tick vector for Rickettsia rickettsii, Dermacentor variabilis, was present in a local park. Of the 66 specimens of D. variabilis collected, 5 (8 percent) were positive for rickettsiae from the spotted fever group. Of an additional 96 specimens of D. variabilis, 5 (5 percent) were found positive for rickettsiae by a more specific monoclonal antibody assay. Eight additional New York City parks in all five boroughs were searched for ticks. D. variabilis was found in only one other park; of the 147 ticks collected there, none were positive for rickettsiae. These findings emphasize the focal nature of Rocky Mountain spotted fever and the need to consider that disease in the differential diagnosis of any obscure acute febrile illness, even in the absence of a history of travel to known endemic areas.

Adult↗
PubMed1988

Resolution of neurotoxicity with anticholinesterase therapy in death-adder envenomation.

A case of the reversal of death-adder (Acanthophis antarcticus) neurotoxicity by treatment with neostigmine methylsulphate in a Papua New Guinean villager is described. While antivenom remains the mainstay in the treatment of snake-bite envenomation, the possible role of anticholinesterase therapy for death-adder bites in Papua New Guinea is discussed. In addition, some problems with first-aid management are outlined.

Adult↗
PubMed1984

Seasonal patterns of asthma: a clue to etiology.

An extensive data set of daily hospital emergency room visits for asthma for two geographic areas (1953-77 in New Orleans and 1969-77 in New York City) was examined for seasonality. Previous studies using smaller data bases have reported an autumn increase (principally during October and November) in the number of emergency room visits for asthma in many locations in this country (including New Orleans and New York City). The results of this study indicated that for every hospital and every year of observation in New York City the number of asthma emergency room visits increased in September, reached a peak in October and November and declined in December. In contrast, in New Orleans an autumn increase in the number of asthma emergency room visits was not consistently observed, being absent or reduced during many years. The distribution of asthma epidemic days (days on which the number of asthma emergency room visits was greatly elevated) by month was also examined. In New York City, there was a tendency for these days to occur during September, October, and November while in New Orleans there was an equal likelihood of epidemic days occurring in April, May, and June as well as during September, October, and November. The observations tend to suggest different etiologies for asthma attacks in the two geographic areas.

Adolescent↗
PubMedDate not supplied

Disruption of erythrocyte rosettes and agglutination of erythrocytes infected with Plasmodium falciparum by the sera of Papua New Guineans.

People living in areas endemic for Plasmodium falciparum develop humoral responses which may contribute to protection against clinical disease but the specificity of such protective antibody responses remains to be defined. Antibodies disrupting erythrocyte rosettes have been associated with protection against cerebral malaria, and antibodies agglutinating infected erythrocytes with reduced episodes of clinical disease. We have studied the capacity of serum from Papua New Guinean adults and children with a spectrum of malaria exposure, including children and adults at the time of clinical disease, to disrupt erythrocyte rosettes and cause agglutination of infected erythrocytes. Using a single parasite isolate, almost all sera from adults from highly endemic areas agglutinated infected erythrocytes, and the majority disrupted rosettes, in some cases at greater titres than hitherto described. There was a correlation between rosette disruption and agglutination in highly exposed adults. Rosette disrupting antibodies were equally frequent in children with cerebral and uncomplicated malaria. Antibodies causing rosette disruption were frequent only in adults with a long history of malarial exposure. Rosette disrupting antibodies do not appear to protect Papua New Guinean children or adults against cerebral malaria.

Adult↗
PubMedDate not supplied

New Orientia tsutsugamushi strain from scrub typhus in Australia.

In a recent case of scrub typhus in Australia, Orientia tsutsugamushi isolated from the patient's blood was tested by sequence analysis of the 16S rDNA gene. The sequence showed a strain of O. tsutsugamushi that was quite different from the classic Karp, Kato, and Gilliam strains. The new strain has been designated Litchfield.

Adult↗
PubMedDate not supplied

Urban envenomation.

Explore the source record for details and available documents.

Humans↗
PubMedDate not supplied

Mapping a conserved conformational epitope from the M protein of group A streptococci.

The carboxyl terminus of the M protein of group A streptococci (GAS) is highly conserved and contains epitopes that have been shown to induce opsonic antibodies and protection against GAS infection. This region of the protein can also stimulate T cells, which can react in vitro with heart antigens. Since different segments of the carboxyl terminus may be involved in immunity to GAS and in the pathogenesis of autoimmune disease (rheumatic heart disease), it is important to precisely define critical epitopes. However, the M protein is known to be a coiled coil, and a critical immunodominant antibody-binding epitope within this region (peptide 145, a 20-mer with the sequence LRRDLDASREAKK-QVEKALE) is shown here to be conformational. Thus, small synthetic overlapping peptides of 8-12 amino acids in length that span peptide 145 (p145) were unable to capture antibodies present in p145-immune mouse sera or in endemic human sera, even though antibodies raised to these small peptides coupled to diphtheria toxoid could bind the smaller peptides and, in some cases, p145. A series of mutated peptides in which every residue of p145 was sequentially altered also failed to identify critical residues for antibody binding. We thus devised a strategy to produce chimeric peptides in which small peptides copying the M protein sequence were displayed within a larger 28-mer peptide derived from the sequence of the GCN4 leucine zipper DNA binding protein of yeast. A 12-amino-acid window of the p145 sequence was inserted into the GCN4 peptide in such a way as to preserve any potential helical structure. The window was moved along one residue at a time to give a series of peptides representing p145. Circular dichroism demonstrated that these larger chimeric peptides and p145, but not a shorter 12-mer peptide, displayed alpha-helical potential in 50% trifluoroethanol. Certain chimeric peptides efficiently captured antibodies specific for p145 and thus enabled us to map the minimal antibody-binding sequence. RRDLDASREAKK, referred to as J(1)2. The chimeric peptide containing this sequence, referred to as J2, was able to inhibit opsonization of GAS by human antisera containing anti-peptide 145 antibodies. The T-cell response from p145-immunized responder B10.BR mice to J2 and J(I)2 was much lower than the response to p145 and mapped to a different peptide.

Animals↗