Monday, December 25, 2006
A field study of the microbiological quality of fresh produce of domestic and Mexican origin.
Int J Food Microbiol. 2006 Nov
Department of Food Science, College of Life Science and Agriculture, North Carolina State University, Raleigh, NC 27695-7624, USA. email@example.com
Produce is responsible for an increasingly larger proportion of foodborne disease outbreaks. In particular, the globalization of the food supply may introduce new food safety risks and allow widespread distribution of contaminated food, particularly produce. The objectives of this study were to: (i) compare the overall quality of domestic and Mexican produce throughout the packing process; (ii) examine changes in microbiological quality of both domestic and Mexican produce at each stage of production and processing; and (iii) evaluate the prevalence of select pathogens on fresh produce, including leafy green, herbs, melons, and vegetables. Furthermore, we also sought to characterize the antibiotic resistance profiles of Enterococcus faecium and Enterococcus faecalis strains isolated from fresh produce.
A total of 466 produce and matching environmental swab samples was collected from various locations in packing sheds in the southern US from November 2002 through December 2003. These samples were assayed by enumerative tests for total aerobic bacteria (APC), total coliforms, total Enterococcus, and E. coli. Produce samples were also analyzed for the presence of Salmonella, Listeria monocytogenes, Shigella, and E. coli O157:H7. A total of 112 E. faecium and E. faecalis isolates were further screened for antibiotic resistance using a panel of seventeen antibiotics.
Overall, the microbiological quality of fresh produce ranged from 4.0 to 7.9 log(10) CFU/g (APC); less than 1.0 log(10) to 4.5 log(10) CFU/g (coliforms); less than 1.0 log(10) to 4.0 log(10) CFU/g (E. coli); and less than 1.0 log(10) to 5.4 log(10) CFU/g (Enterococcus). No Salmonella, Shigella, or E. coli O157:H7 were detected from the 466 25-g produce samples tested.
However, three domestic cabbage samples were found to be positive for L. monocytogenes. Of the Enterococcus isolates, E. faecium had a higher degree of resistance to antibiotics in general, while Enterococcus spp. isolated from Mexican produce had a higher degree of antibiotic resistance when compared to strains isolated from produce samples of domestic origin. Despite increased attention to the role of imported produce in foodborne disease, this study does not support the assumption that domestic produce is of higher microbial quality than Mexican produce.
PMID: 17045687 [PubMed - indexed for MEDLINE]* * * * * *
A field study of the microbiological quality of fresh produce.
J Food Prot. 2005 Sep
Department of Food Science, College of Life Science and Agriculture, North Carolina State University, Raleigh, North Carolina 27695-7624, USA.
The Centers for Disease Control and Prevention has reported that foodborne disease outbreaks associated with fruits and vegetables increased during the past decade. This study was conducted to characterize the routes of microbial contamination in produce and to identify areas of potential contamination from production through postharvest handling. We report here the levels of bacterial indicator organisms and the prevalence of selected pathogens in produce samples collected from the southern United States. A total of 398 produce samples (leafy greens, herbs, and cantaloupe) were collected through production and the packing shed and assayed by enumerative tests for total aerobic bacteria, total coliforms, total Enterococcus, and Escherichia coli. These samples also were analyzed for Salmonella, Listeria monocytogenes, and E. coli O157:H7. Microbiological methods were based on methods recommended by the U.S. Food and Drug Administration.
For all leafy greens and herbs, geometric mean indicator levels ranged from 4.5 to 6.2 log CFU/g (aerobic plate count); less than 1 to 4.3 log CFU/g (coliforms and Enterococcus); and less than 1 to 1.5 log CFU/g (E. coli). In many cases, indicator levels remained relatively constant throughout the packing shed, particularly for mustard greens. However, for cilantro and parsley, total coliform levels increased during the packing process. For cantaloupe, microbial levels significantly increased from field through packing, with ranges of 6.4 to 7.0 log CFU/g (aerobic plate count); 2.1 to 4.3 log CFU/g (coliforms); 3.5 to 5.2 log CFU/g (Enterococcus); and less than 1 to 2.5 log CFU/g (E. coli).
The prevalence of pathogens for all samples was 0, 0, and 0.7% (3 of 398) for L. monocytogenes, E. coli O157:H7, and Salmonella, respectively. This study demonstrates that each step from production to consumption may affect the microbial load of produce and reinforces government recommendations for ensuring a high-quality product.
PMID: 16161682 [PubMed - indexed for MEDLINE]
Sunday, December 10, 2006
The Link Between AIDS and Malaria
BEIJING, Dec. 8 (Xinhuanet) -- A new study conducted in Africa suggests malaria makes people more likely to contract AIDS and vice versa.
Reseachers studied disease patterns in 200,000 adults in Kenya and reported HIV makes people more vulnerable to malaria by weakening their immune system and malaria may worsen a patient's pre-existing HIV infection, possibly making it more communicable.
The scientists discovered within this group that about 5 percent of all HIV infections could be attributed to malaria, and 10 percent of all adult malaria episodes could be attributed to HIV. The study suggests that malaria may be a contributing factor to the HIV/AIDS epidemic in sub-Saharan Africa.
"These are two elephants affecting public health in Africa," said the study's lead author Leith Abu-Raddad of the Fred Hutchinson Cancer Research Center in Seattle. "Any interaction between them is consequential. We can't yet say how many cases of HIV malaria has caused over all of Africa."
Dual infection has created an estimated 8,500 new HIV cases and nearly a million malaria episodes since 1980, the researchers said.
AIDS, the disease caused by HIV, and malaria are two of biggest causes of death in sub-Saharan Africa, killing an estimated four million people a year combined.
Scientists have known for some time that the immune system suppression caused by HIV can increase both the risk and severity of malaria infection.
But the idea that malaria might fuel the transmission of HIV is more recent.
"Malaria cannot be the only reason why HIV has so predominantly affected sub-Saharan Africa," said James Whitworth, a scientist not involved in the study, of the medical research nonprofit Wellcome Trust in London. "But it is certainly plausible that is has been an important cofactor in driving transmission."
Malaria sufferers often experience repeated, nonlethal outbreaks of the disease's flulike symptoms, with episodes varying in severity.
Studies have shown that in people infected with both diseases, the amount of HIV virus in their bodies goes up significantly during these malaria episodes.
Other research has shown that as the amount of HIV virus goes up, so does the likelihood of HIV transmission through sexual intercourse.
These two factors together can make HIV spread more rapidly in populations where malaria is present.
The discovery of a significant HIV-malaria link suggests the need for a coordinated approach in fighting both diseases, scientists say.
"It highlights the need to integrate health programs," said Jonathan Mermin, a physician with the U.S. Centers for Disease Control and Prevention working in Kenya. "People with HIV should be provided with insecticide-treated bed nets and [anti-malaria medications]."
"Efforts to prevent and eliminate malaria should be increased, alongside efforts to prevent and treat HIV infection," he added.
Monday, December 04, 2006
Bacterial and opportunistic infections during anti-TNF therapy.
German Rheumatism Research Centre, Epidemiology Unit, Chariteplatz 1, D-10117 Berlin, Germany.
Tumour necrosis factor alpha (TNF-alpha) plays a crucial role in host defence against bacterial infections. Summarizing the results, the findings of immunological and clinical research suggest a higher infection risk in rheumatoid arthritis and ankylosing spondylitis patients receiving anti-TNF treatment. This is especially true for granulomatous infections in patients treated with the monoclonal TNF-alpha antibodies infliximab or adalimumab. Furthermore, patients treated with TNF inhibitors have a higher susceptibility to infections because of their higher active and more severe disease. Therefore, patients receiving anti-TNF treatment should be closely monitored for serious infections. A rapid and sufficient treatment of infections that are not mild and transient is recommended. There are atypical signs and symptoms as well as atypical pathogen that should be considered. Patients should be educated about how to avoid infectious complications.
PMID: 17127203 [PubMed - in process]
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Anti-TNF antibody therapy in rheumatoid arthritis and the risk of serious infections and malignancies: systematic review and meta-analysis of rare harmful effects in randomized controlled trials.
Division of Rheumatology and Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA. firstname.lastname@example.org
CONTEXT: Tumor necrosis factor (TNF) plays an important role in host defense and tumor growth control. Therefore, anti-TNF antibody therapies may increase the risk of serious infections and malignancies.
OBJECTIVE: To assess the extent to which anti-TNF antibody therapies may increase the risk of serious infections and malignancies in patients with rheumatoid arthritis by performing a meta-analysis to derive estimates of sparse harmful events occurring in randomized trials of anti-TNF therapy.
DATA SOURCES: A systematic literature search of EMBASE, MEDLINE, Cochrane Library, and electronic abstract databases of the annual scientific meetings of both the European League Against Rheumatism and the American College of Rheumatology was conducted through December 2005. This search was complemented with interviews of the manufacturers of the 2 licensed anti-TNF antibodies.
STUDY SELECTION: We included randomized, placebo-controlled trials of the 2 licensed anti-TNF antibodies (infliximab and adalimumab) used for 12 weeks or more in patients with rheumatoid arthritis. Nine trials met our inclusion criteria, including 3493 patients who received anti-TNF antibody treatment and 1512 patients who received placebo.
DATA EXTRACTION: Data on study characteristics to assess study quality and intention-to-treat data for serious infections and malignancies were abstracted. Published information from the trials was supplemented by direct contact between principal investigators and industry sponsors.
DATA SYNTHESIS: We calculated a pooled odds ratio (Mantel-Haenszel methods with a continuity correction designed for sparse data) for malignancies and serious infections (infection that requires antimicrobial therapy and/or hospitalization) in anti-TNF-treated patients vs placebo patients. We estimated effects for high and low doses separately. The pooled odds ratio for malignancy was 3.3 (95% confidence interval [CI], 1.2-9.1) and for serious infection was 2.0 (95% CI, 1.3-3.1). Malignancies were significantly more common in patients treated with higher doses compared with patients who received lower doses of anti-TNF antibodies. For patients treated with anti-TNF antibodies in the included trials, the number needed to harm was 154 (95% CI, 91-500) for 1 additional malignancy within a treatment period of 6 to 12 months. For serious infections, the number needed to harm was 59 (95% CI, 39-125) within a treatment period of 3 to 12 months.
CONCLUSIONS: There is evidence of an increased risk of serious infections and a dose-dependent increased risk of malignancies in patients with rheumatoid arthritis treated with anti-TNF antibody therapy. The formal meta-analysis with pooled sparse adverse events data from randomized controlled trials serves as a tool to assess harmful drug effects.
PMID: 16705109 [PubMed - indexed for MEDLINE]
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Rates of serious infection, including site-specific and bacterial intracellular infection, in rheumatoid arthritis patients receiving anti-tumor necrosis factor therapy: results from the British Society for Rheumatology Biologics Register.
British Society for Rheumatology Biologics Register.
British Society for Rheumatology Biologics Register Control Centre Consortium, Manchester, UK.
OBJECTIVE: To determine whether the rate of serious infection is higher in anti-tumor necrosis factor (anti-TNF)-treated rheumatoid arthritis (RA) patients compared with RA patients treated with traditional disease-modifying antirheumatic drugs (DMARDs).
METHODS: This was a national prospective observational study of 7,664 anti-TNF-treated and 1,354 DMARD-treated patients with severe RA from the British Society for Rheumatology Biologics Register. All serious infections, stratified by site and organism, were included in the analysis.
RESULTS: Between December 2001 and September 2005, there were 525 serious infections in the anti-TNF-treated cohort and 56 in the comparison cohort (9,868 and 1,352 person-years of followup, respectively). The incidence rate ratio (IRR), adjusted for baseline risk, for the anti-TNF-treated cohort compared with the comparison cohort was 1.03 (95% confidence interval 0.68-1.57). However, the frequency of serious skin and soft tissue infections was increased in anti-TNF-treated patients, with an adjusted IRR of 4.28 (95% confidence interval 1.06-17.17). There was no difference in infection risk between the 3 main anti-TNF drugs. Nineteen serious bacterial intracellular infections occurred, exclusively in patients in the anti-TNF-treated cohort.
CONCLUSION: In patients with active RA, anti-TNF therapy was not associated with increased risk of overall serious infection compared with DMARD treatment, after adjustment for baseline risk. In contrast, the rate of serious skin and soft tissue infections was increased, suggesting an important physiologic role of TNF in host defense in the skin and soft tissues beyond that in other tissues.
PMID: 16868999 [PubMed - indexed for MEDLINE]