The microbial content of unexpired pasteurized milk from selected supermarkets in a developing country

Objective

To determine the presence and levels of microbes in unexpired pasteurized milk from randomly selected supermarkets in Kingston, Jamaica.

Methods

The quantitative study used a stratified random sampling technique in the selection of the 20 representative milk samples from six (6) supermarkets. Microbiological tests such as methylene blue reduction, standard plate count (SPC), coliform plate count (CPC), purity plate culture, gram staining and biochemical tests were performed to examine the microbes in purchased unexpired pasteurized milk.

Results

One sample (BCr016) had a pH of 4.0, a rancid odour and curdled appearance. It decolourized within one hour during the methylene blue reduction test and was classified as class 4 milk. Seven of the samples were sterile with no microbe growth on the plate count agar and violet red bile salt agar (VRBA). The milk samples that appeared to be safe for consumption were all 10, 11, 12 and 13 days before expiration. The VRBA sample BCr016, had a colony count of 13 400 CFU/ mL. There was the presence of Escherichia coli in sample LCr021 which had a standard plate count of 1 580 SPC/mL and a coliform count of 500 CFU/mL. Enterobacter sp. was present in colonies from BCr016 and all the other milk samples.

Conclusions

Unacceptable levels of Enterobacter spp. and Escherichia coli were found in most of the samples. Effective measures to ensure safe milk for human consumption such as the phosphatase test and methylene blue reduction test should be routinely performed on each batch of milk processed by dairy plants.     

A probable new Helicobacter species isolated from a patient with bacteremia

A probable new Helicobacter species was isolated from the blood of a 14-month-old aboriginal child who presented with vomiting, diarrhea, fever, and dry cough. The most similar 16S rRNA gene sequence was that of Helicobacter fennelliae CCUG 18820(T) but the new sequence differed from it by at least 32 base substitutions and by the presence of a large (353-nucleotide) intervening sequence.     

Whole genome comparison of Campylobacter jejuni human isolates using a low-cost microarray reveals extensive genetic diversity

Campylobacter jejuni is the leading cause of bacterial food-borne diarrhoeal disease throughout the world, and yet is still a poorly understood pathogen. Whole genome microarray comparisons of 11 C. jejuni strains of diverse origin identified genes in up to 30 NCTC 11168 loci ranging from 0.7 to 18.7 kb that are either absent or highly divergent in these isolates. Many of these regions are associated with the biosynthesis of surface structures including flagella, lipo-oligosaccharide, and the newly identified capsule. Other strain-variable genes of known function include those responsible for iron acquisition, DNA restriction/modification, and sialylation. In fact, at least 21% of genes in the sequenced strain appear dispensable as they are absent or highly divergent in one or more of the isolates tested, thus defining 1300 C. jejuni core genes. Such core genes contribute mainly to metabolic, biosynthetic, cellular, and regulatory processes, but many virulence determinants are also conserved. Comparison of the capsule biosynthesis locus revealed conservation of all the genes in this region in strains with the same Penner serotype as strain NCTC 11168. By contrast, between 5 and 17 NCTC 11168 genes in this region are either absent or highly divergent in strains of a different serotype from the sequenced strain, providing further evidence that the capsule accounts for Penner serotype specificity. These studies reveal extensive genetic diversity among C. jejuni strains and pave the way toward identifying correlates of pathogenicity and developing improved epidemiological tools for this problematic pathogen.     

Stability of synaptic density and spine volume in dentate gyrus of aged rats

The number of synapses per unit volume and per granule cell and the size of dendritic spines were studied in the dentate gyrus of Sprague-Dawley rats 6, 24, and 30 months of age. Neither synaptic density nor mean spine volume showed any age-related trends. An increase in granule cell packing density at 24 months and concomitant stability of the height of the granule cell layer is consistent with the idea that postnatal generation of granule cells may continue late into life. Possible explanations for the discrepancies in the literature regarding synaptic loss in this area include differences in morphometric techniques, age of animals used, regional differences within dentate gyrus, and sampling variability. Generalized synapse loss in the senescent rodent brain remains to be established.     

Neutral lipid from proteinuric rat urine is a novel inhibitor of the red blood cell calcium pump.

Proteinuria may be associated with hypertension and progression of renal insufficiency, which in turn may accompany abnormalities in cell calcium homeostasis. Therefore, urine from rats made proteinuric by puromycin aminoglycoside administration was analyzed, in a search for factors affecting cellular calcium transport. Proteinuric urine was fractionated by thin-layer chromatography and HPLC, and the effects of the fractions on the plasma membrane calcium pump in human red blood cells were assessed. Proteinuric urine contained a powerful specific inhibitor of the calcium pump that had little or no effect on the Na+/K+- or Mg2+-ATPases. The inhibitor was characterized as a neutral lipid, migrating as a single band, that inhibited 45Ca2+ efflux. To confirm the presence of an inhibitor in other proteinuric states, the urine from two patients with proteinuria was examined and subjected to chromatography as in the rat studies. These thin-layer chromatographic fractions contained a very strong inhibitor of the red blood cell calcium pump, suggesting that this substance may have relevance for the pathogenesis of proteinuric renal disease in human patients. Rat proximal tubule cells in tissue culture, when challenged with lipid-replete albumin, secreted an inhibitor of the calcium pump that migrated in the same chromatographic band as the urine factor. Therefore, the processing of fatty acids borne by albumin into endocytosing proximal tubular epithelium results in the synthesis and release of a previously unknown lipid modulator of the calcium pump, an effect that may predispose kidney tissue toward elevations in cytosolic calcium levels in target cells.     

Absence of linkage and linkage disequilibrium to chromosome 15q11-q13 markers in 139 multiplex families with autism.

Chromosomal region 15q11-q13 has been implicated to harbor a susceptibility gene or genes underlying autism. Evidence has been derived from the existence of cytogenetic anomalies in this region associated with autism, and the report of linkage in a modest collection of multiplex families. Most recently, linkage disequilibrium with the marker GABRB3-155CA2 in the candidate locus GABRB3, located in this region, has been reported. We searched for linkage using eight microsatellite markers located in this region of chromosome 15 in 147 affected sib-pairs from 139 multiplex autism families. We also tested for linkage disequilibrium in the same set of families with the same markers. We found no evidence for excess allele sharing (linkage) for the markers in this region. Also, we found no evidence of linkage disequilibrium, including for the locus GABRB3-155CA2. Thus, it appears that the role of this region of chromosome 15 is minor, at best, in the majority of individuals with autism.     

Exclusion of Linkage to the HLA Region in Ninety Multiplex Sibships with Autism

Several studies have suggested a role for the histocompatibility complex of loci (HLA) in the genetic susceptibility to autism. We have tested this hypothesis by linkage analysis using genetic marker loci in the HLA region on chromosome 6p in multiplex families with autism. We have examined sharing of alleles identical by descent in 97 affected sib pairs from 90 families. Results demonstrate no deviation from the null expectation of 50% sharing of alleles in this region; in fact, for most marker loci, the observed sharing was less than 50%. Thus, it is unlikely that loci in this region contribute to the genetic etiology of autism to any significant extent in our families.