Specificity of monoclonal antibodies to strains of Dickeya sp. that cause bacterial heart rot of pineapple.

During a severe outbreak of bacterial heart rot that occurred in pineapple plantations on Oahu, Hawaii, in 2003 and years following, 43 bacterial strains were isolated from diseased plants or irrigation water and identified as Erwinia chrysanthemi (now Dickeya sp.) by phenotypic, molecular, and pathogenicity assays. Rep-PCR fingerprint patterns grouped strains from pineapple plants and irrigation water into five genotypes (A-E) that differed from representatives of other Dickeya species, Pectobacterium carotovorum and other enteric saprophytes isolated from pineapple.

Characterization of Erwinia chrysanthemi from a Bacterial Heart Rot of Pineapple Outbreak in Hawaii.

The first reported outbreak of bacterial heart rot of pineapple (Ananas comosus var. comosus) in Hawaii occurred in December 2003. Of immediate concern was the differentiation of heart rot caused by Erwinia chrysanthemi from a soft rot caused by E.

Lectin-like factor and co-factor in serum from cystic fibrosis heterozygotes.

Previous attempts to use an assay for a serum lectin-like factor as a carrier test for the cystic fibrosis gene have not been successful because food intake and effects of serum storage have interfered. A revised method for detecting the lectin-like factor employs the serum IgM fraction, rather than whole serum, separated on an S-300 Sephacryl gel filtration column. Elevated lectin titers were found in 95 percent of 43 obligate heterozygotes, 89 percent of patients with cystic fibrosis, 64 percent of siblings of patients with cystic fibrosis, and 5 percent of 60 control subjects.

Presence of a serum hemagglutinin (lectinlike factor) in cystic fibrosis homozygotes and heterozygotes.

A lectinlike activity was discovered in serum from 25 patients with CF, 70 obligate heterozygotes (parents), and 18 of 27 siblings (67%) of 675 controls, 4.2% were found to have a positive test for the CF-lectin, approximating the 5% estimated prevalence of CF heterozygotes. The CF-lectin can be detected by dextran-enhanced agglutination of mouse RBCs and confirmed by agglutination inhibition with D-fructose.

Abnormal response of cultured lymphocytes to phytohemagglutinin and autologous serum in cystic fibrosis.

Lymphocytes from adults homozygous or heterozygous for cystic fibrosis show biochemical abnormalities when cultured for 48 hours in the presence of phytohemagglutinin and autologous serum. In contrast to the 45 per cent increase in total protein and beta-glucuronidase concentrations seen in healthy control subjects when measured per 10(10) cells, both concentrations decreased by 1 per cent in adults heterozygous for cystic fibrosis and by 18 per cent in adults homozygous for cystic fibrosis. The abnormal response of the lymphocytes from persons with cystic fibrosis was due to a serum factor and not to any intrinsic abnormality of the lymphocytes.

Interference with alpha-antitrypsin studues in stored serum by presumed bacterial proteases.

Contamination of werum by certain gram-negative bacteria has been shown to spoil the serum for measurement of trypsin inhibitory capacity (STIC) or for antitrypsin phenotyping. Such sera develop intense fibrinolytic activity when the STIC has dropped to itsminimal level, but antitrypsin concentration as measured by radial immunodiffusion remainsconstant. Cultures of ENTEROBACTER, Klebsiella, Bacillus subtilis, and Pseudomonas species were shown to have this capability, but production of the fibrinolytic enzyme by the bacteria was most proficient in the presence of human serum.