Risk assessment and impact of foodborne pathogens on the health of different populations was one of the goals identified in the Presidential Food Safety Initiative three‐year plan. This entailed estimation of dose‐response relationship for foodborne pathogens to humans, either by feeding studies or from outbreaks. For certain pathogens, such as Listeria monocytogenes and Escherichia coli O157:H7, there are no feeding studies due to ethical reasons, and the results from outbreaks are normally used to estimate the infectious dose. The focus of this review is to compile dose‐response information in volunteers for several foodborne pathogens including Salmonella, Shigella spp., Campylobacter jejuni, Vibrio spp., Escherichia coli, Cryptosporidium parvum and Entamoeba coli. The infectious dose for different serovars of Salmonella and strains of E. coli was quite large (> 105 organisms), while the infectious dose for some Shigella spp. seemed to be as low as less than 10 organisms. Toxigenic V. cholerae (O1 and O139 serotypes) were infective at a dose of 104 organisms; a non‐O1 strain was infective at a much higher dose (106 organisms). C. jejuni, C. parvum and Entamoeba coli appeared to have infectious doses as low as 500 organisms, 10 oocysts, and 1 cyst, respectively. The infectious dose and the dose response are dependent upon the strains used, and the age and physical condition of the individuals, and can therefore show wide variations. In addition, since many of the volunteer studies are carried out by feeding the organisms in a nonfood matrix after neutralizing the stomach acidity, results obtained may not reflect the true dose response.
Listeria monocytogenes, isolated from outbreaks in either human or nonhuman primate populations, was administered orally at doses ranging from 10 6 to 10 10 CFU. Four of 10 treated animals delivered stillborn infants. L. monocytogenes was isolated from fetal tissue, and the pathology was consistent with L. monocytogenes infection as the cause of pregnancy loss. For all pregnancies resulting in stillbirths, L. monocytogenes was isolated from maternal feces, indicating that L. monocytogenes had survived and had probably colonized the gastrointestinal tract. Antibodies and antigen-specific lymphocyte proliferation against Listeria increased in animals that had stillbirths.Listeriosis resulting from exposure to food containing the bacterium L. monocytogenes causes serious disease, with case fatality rates between 20 and 40% (33). Listeriosis is especially serious in susceptible populations such as immunocompromised persons and pregnant women (11,14,16,20,24,26,29,32,35). For healthy nonpregnant adults, listeriosis has a relatively low incidence, presumably due to its low infectivity in immunocompetent individuals.Pregnancy-related listeriosis primarily affects the fetus or neonate. The maternal reaction to the presence of Listeria infection is generally an influenza-like episode with fever, backache, and perhaps diarrhea (7,11,13,24,29). The effect of fetal Listeria infection is dependent on the point in gestation time when infection occurs. First-trimester infection leads to spontaneous abortion, whereas second-and third-trimester infections lead to preterm birth followed by neonatal illness or fetal death with preterm delivery of a stillborn (7,11,13).The rhesus monkey (Macaca mulatta), with a reproductive cycle and placenta comparable to those of humans (31), is widely used as an experimental model for human reproduction and development. As with humans, exposure to L. monocytogenes in pregnant nonhuman primates may result in abortions, stillbirths, or neonatal deaths (4, 27; J. Paul-Murphy, J. E. Markovits, I. Wesley, and J. A. Roberts, Lab. Anim. Sci. 40:547 [abstr.], 1990). For humans and nonhuman primates, the pathogenesis and morphological findings associated with stillbirths due to L. monocytogenes are essentially the same (1,4,28,37).Despite several epidemiological studies confirming the relationship between L. monocytogenes and specific foods (soft cheeses, undercooked chicken, paté, etc.) (2, 30), an infectious dose has not been established for healthy or susceptible human populations due to the delay between exposure and the onset of symptoms. The severe ramifications of the disease in highrisk human populations such as pregnant women precludes the use of humans in volunteer feeding studies. Recently, a draft risk assessment of L. monocytogenes in ready-to-eat foods (36) reviewed human epidemiological and animal study data. The risk assessment concluded that mouse studies provide the only acceptable data for developing dose-response information at this time and acknowledged the difficulty with the use of...
India is located between 8.4 and 37.6 degrees N latitude with the majority of its population living in regions experiencing ample sunlight throughout the year. Historically, Indians obtained most of their vitamin D through adequate sun exposure; however, darker skin pigmentation and the changes which have accompanied India's modernization, including increased hours spent working indoors and pollution, limit sun exposure for many. Inadequate sun exposure results in reduced vitamin D synthesis and ultimately poor vitamin D status if not compensated by dietary intake. Dietary vitamin D intake is very low in India because of low consumption of vitamin D rich foods, absence of fortification and low use of supplements. All these factors contribute to poor vitamin D status as measured by low circulating levels of 25-hydroxy vitamin D. Our review searches the published literature specific to India for evidence that would confirm the need to fortify food staples with vitamin D or stimulate public health policies for vitamin D supplementation and dietary guidelines tailored to the Indian diet. This review documents findings of widespread vitamin D deficiency in Indian populations in higher and lower socioeconomic strata, in all age groups, in both genders and people in various professions. Moreover, poor vitamin D status in India is accompanied by increased bone disorders including osteoporosis, osteomalacia in adults and rickets and other bone deformities in children. Without a concerted national effort to screen for vitamin D status, to implement policies or guidelines for vitamin D fortification and/or supplementation and to re-assess recommended dietary intake guidelines, dramatic increase in the number of bone disorders and other diseases may lie ahead.
To investigate the effect of dietary copper deficiency on the function of peritoneal macrophages, weaned male Lewis rats were pair-fed diets containing either adequate (7 mg/kg diet; +Cu) or deficient (0.7 mg/kg diet; -Cu) levels of copper for 5 wk. Cellular copper content and the activity of Cu, Zn superoxide dismutase were significantly lower in both resident and thioglycollate-elicited macrophages from -Cu rats than in cells from +Cu controls. Reduced cellular Cu status was associated with impaired respiratory burst as assessed by zymosan-induced chemiluminescent activity and superoxide anion (O2-) generation. Candidacidal activity of macrophages from -Cu rats was also reduced and was highly correlated with chemiluminescent activity and O2- generation. In contrast, phagocytosis of opsonized erythrocytes by peritoneal macrophages from -Cu rats was normal. Elicited peritoneal macrophages from marginally Cu-deficient rats also killed significantly fewer yeast cells than macrophages from +Cu rats. These results demonstrate that macrophage function is impaired by dietary Cu deficiency and that the candidacidal activity of these cells may provide a sensitive indicator of Cu status.
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