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Preventing Foodborne Infection in Pregnant Women and Infants
... On the other hand, Alonso et al. (1984) stated that patients with AIDS developed up to 50% cerebral toxoplasmosis. Bazaco et al. (2008) stated that to avoid nosocomial toxoplasmosis one of the duties the nurse is to offer well cooked meat and well washed green salad to the pregnant women to prevent them from acquiring toxoplasmosis and to delivery infants with congenital infection. Besides, T. gondii antibodies were reported in the Egyptian blood donors associated the risk factors for the blood transmission . ...
... Foodborne disease is defined as any illness related to food ingestion or caused by an infectious agent carried by food. In some cases of foodborne infection, a pregnant woman may not feel sick but may still pass the illness to the fetus [15]. For instance, untreated infections may cause stillbirth, preterm labor or miscarriage by mechanisms including direct fetal infection, placental damage, and severe maternal illness. ...
Gastrointestinal infection with Shiga toxin-producing Escherichia coli (STEC) causes diarrhea, hemorrhagic colitis, and hemolytic uremic syndrome (HUS), characterized by hemolytic anemia, thrombocytopenia and acute renal failure. The main virulence factor of STEC is Shiga toxin (Stx), which is responsible for HUS development. STEC can produce Stx type 1 and/or 2 (Stx1, Stx2) and their variants, Stx2 being more frequently associated with severe cases of HUS. This pathology occurs in 5–15% of cases with STEC infection when Stx gain access to the bloodstream and causes damage in the target organs such as the kidney and brain. STEC infections affect mainly young children, although the large HUS outbreak with a new Stx2-producing STEC O104:H4 in Europe in 2011 involved more adults than children, and women were over-represented. Maternal infections during pregnancy are associated with adverse pregnancy outcomes. Studies in rats showed that Stx2 binds to the utero-placental unit and causes adverse pregnancy outcomes. In this article, we provide a brief overview of Stx2 action on placental tissues and discuss whether they might cause pregnancy loss or preterm birth.
Since 1973, CDC has maintained a collaborative surveillance program for collection and periodic reporting of data on the occurrence and causes of foodborne-disease outbreaks (FBDOs) in the United States.
1998-2002.
The Foodborne Disease Outbreak Surveillance System reviews data on FBDOs, defined as the occurrence of two or more cases of a similar illness resulting from the ingestion of a common food. State and local public health departments have primary responsibility for identifying and investigating FBDOs. State, local, and territorial health departments use a standard form to report these outbreaks to CDC. In 1998, CDC implemented enhanced surveillance for FBDOs by increasing communication with state, local, and territorial health departments and revising the outbreak report form. Since 2001, reports of FBDOs are submitted through a web application on the Internet called the electronic Foodborne Outbreak Reporting System (eFORS).
During 1998-2002, a total of 6,647 outbreaks of foodborne disease were reported (1,314 in 1998, 1,343 in 1999, 1,417 in 2000, 1,243 in 2001, and 1,330 in 2002). These outbreaks caused a reported 128,370 persons to become ill. Among 2,167 (33%) outbreaks for which the etiology was determined, bacterial pathogens caused the largest percentage of outbreaks (55%) and the largest percentage of cases (55%). Among bacterial pathogens, Salmonella serotype Enteritidis accounted for the largest number of outbreaks and outbreak-related cases; Listeria monocytogenes accounted for the majority of deaths of any pathogen. Viral pathogens, predominantly norovirus, caused 33% of outbreaks and 41% of cases; the proportion of outbreaks attributed to viral agents increased from 16% in 1998 to 42% in 2002. Chemical agents caused 10% of outbreaks and 2% of cases, and parasites caused 1% of outbreaks and 1% of cases.
Following implementation of measures to enhance outbreak surveillance, the annual number of FBDOs reported to CDC increased during this period compared with previous years. Viral pathogens accounted for an increased proportion of outbreaks each year during this reporting period and a higher proportion of outbreaks of known etiology during this reporting period than preceding reporting periods, probably reflecting the increased availability of improved viral diagnostic tests. S. Enteritidis continued to be a major cause of illness and L. monocytogenes was a major cause of death. In addition, multistate outbreaks caused by contaminated produce and outbreaks caused by Escherichia coli O157:H7 remained prominent.
Methods to detect FBDOs are improving, and several changes to improve the ease and timeliness of reporting FBDO data have been implemented (e.g., a revised form to simplify FBDO reporting by state health departments and improved electronic reporting methods). State and local health departments continue to investigate and report FBDOs as part of efforts to better understand and define the epidemiology of foodborne disease in the United States. At the regional and national levels, surveillance data provide an indication of the etiologic agents, vehicles of transmission, and contributing factors associated with FBDOs and help direct public health actions to reduce illness and death caused by FBDOs.
Seven serologically related, but antigenically different, botulinum toxins (BoNTs) have been identified including types A, B, C, D, E, F, and G. The bacterium Clostridium botulinum along with some strains of Clostridium baratti and Clostridium butyricum are known to produce botulinum toxins responsible for 4 forms of botulism poisoning including food-borne botulism, inhalation botulism, wound botulism, and infant botulism. Botulism toxins consist of a heavy chain (100 kDa), responsible for binding to target cells, and a light chain (50 kDa) responsible for catalytic protein cleaving activity. Light chain has been identified as a zinc endopeptidase that cleaves proteins forming the synaptic vesicle docking and fusion complex (Simpson 1996; Lacy and Stevens 1997). The standard for detection of BoNT toxins is the mouse bioassay, which is able to detect as little as 0.02 ng of toxin. Strengths of the mouse bioassay include conceptual simplicity and sensitivity. While the non-selectivity of the mouse bioassay enables it to detect any BoNT serotype, additional neutralization assays are necessary to determine serotype. Other limitations of the mouse bioassay include expense, expertise related to maintaining mouse-rearing facilities, and time, because as much as 4 d may be required to obtain results (Hallis and others 1996; Witcome and others 1999). Several attempts to replace the mouse bioassay have been made. Methods that have been developed and hold promise for future replacement of the mouse bioassay include mass spectroscopy, immunoassays, polymerase chain reaction (PCR) assays, and assays based upon protease activities of BoNTs. Currently, no single assay appears to be capable of replacing the broadly applicable mouse bioassay.
Although the worldwide incidence of infant botulism is rare, the majority of cases are diagnosed in the United States. An infant can acquire botulism by ingesting Clostridium botulinum spores, which are found in soil or honey products. The spores germinate into bacteria that colonize the bowel and synthesize toxin. As the toxin is absorbed, it irreversibly binds to acetylcholine receptors on motor nerve terminals at neuromuscular junctions. The infant with botulism becomes progressively weak, hypotonic and hyporeflexic, showing bulbar and spinal nerve abnormalities. Presenting symptoms include constipation, lethargy, a weak cry, poor feeding and dehydration. A high index of suspicion is important for the diagnosis and prompt treatment of infant botulism, because this disease can quickly progress to respiratory failure. Diagnosis is confirmed by isolating the organism or toxin in the stool and finding a classic electromyogram pattern. Treatment consists of nutritional and respiratory support until new motor endplates are regenerated, which results in spontaneous recovery. Neurologic sequelae are seldom seen. Some children require outpatient tube feeding and may have persistent hypotonia.
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