Cronobacter Support
02-19-2009, 07:09 PM
Clinical Symptoms of E. sakazakii Infections
Onset of E. sakazakii infections is characterized by signs and symptoms typical of infections caused by other gram-negative organisms. These symptoms include poor feeding response, irritability, jaundice, grunting respirations, and instability of body temperature. In a la rge number of the neonatal cases, infection progressed to meningitis (an acute inflammation of the membranes of the brain and spinal cord), with survivors suffering from severe neurological impairment. Ventriculitis (inflammation in the ventricles of the brain), brain cysts and abscesses, cerebral infarction, and late development of hydrocephalus (abnormal increase in the amount of cerebrospinal fluid within the cranial cavity) are characteristic of central nervous system infections. Other medical conditions have also been associated with E. sakazakii infections, including bacteremia (bacteria in the blood) as well as necrotizing enterocolitis (localized death of small and large intestine tissues). After the first signs of sepsis appear, death may occur within a few hours to several days. In survivors, continued colonization by E. sakazakii varies from 2 to 8 weeks.
Treatment and Mortality Rates of E. sakazakii Infections
E. sakazakii infections before 1985 were frequently treated with ampicillin, gentamicin, and/or chloramphenicol. After 1985, the third-generation cephalosporins were commonly used in conjunction with ampicillin and gentamycin.
Higher case-fatality rates have been reported for premature or low birth weight infants than full-term or infants with birth weights ³ 2.5 kg (50% versus 30%). Improvements in treatment, however, have affected the casefatality rate, with 62% of meningitis patients dying before the use of third-generation cephalosporins and only 14% dying after the introduction of third-generation cephalosporins. Only one death has been reported in the absence of meningitis, a neonate exhibiting bacteremia.
Source of E. sakazakii Infections
In early cases of E. sakazakii infections, an environmental source of the organism could not be identified. Vertical transmission from the mother’s birth canal to newborns was ruled out as cases occurred after caesarean section, and colonization of newborns at birth was not demonstrated. In more recent cases, environmental sampling has yielded evidence of contaminated blenders used to prepare infant formula and recovery of E. sakazakii isolates from a dish brush and a stirring spoon. To date, no subtyping has been reported for the isolates recovered from the blenders, whereas the plasmid profiles of the brush and spoon isolates did not match those of the patients. Dried infant formula, on the other hand, has been identified epidemiologically as the source of E. sakazakii in three outbreaks of neonatal meningitis and linked to one outbreak of necrotizing enterocolitis. In these outbreaks, E. sakazakii isolates from implicated milk powders either had the same plasmid profile, multilocus enzyme profiles, or pulsed-field gel electrophoresis profiles as those isolates from the patients. Presently, approved technology is not available to render powdered milk formulas commercially sterile. Hence, E. sakazakii could be present in formulas at substantially lower levels than those considered acceptable by the Codex Alimentarius for levels of coliforms in milk-based powdered infant formula. Prolonged periods of unrefrigerated storage after hydration of the powdered infant formula before feeding may subsequently enable substantial growth of the organism.
Onset of E. sakazakii infections is characterized by signs and symptoms typical of infections caused by other gram-negative organisms. These symptoms include poor feeding response, irritability, jaundice, grunting respirations, and instability of body temperature. In a la rge number of the neonatal cases, infection progressed to meningitis (an acute inflammation of the membranes of the brain and spinal cord), with survivors suffering from severe neurological impairment. Ventriculitis (inflammation in the ventricles of the brain), brain cysts and abscesses, cerebral infarction, and late development of hydrocephalus (abnormal increase in the amount of cerebrospinal fluid within the cranial cavity) are characteristic of central nervous system infections. Other medical conditions have also been associated with E. sakazakii infections, including bacteremia (bacteria in the blood) as well as necrotizing enterocolitis (localized death of small and large intestine tissues). After the first signs of sepsis appear, death may occur within a few hours to several days. In survivors, continued colonization by E. sakazakii varies from 2 to 8 weeks.
Treatment and Mortality Rates of E. sakazakii Infections
E. sakazakii infections before 1985 were frequently treated with ampicillin, gentamicin, and/or chloramphenicol. After 1985, the third-generation cephalosporins were commonly used in conjunction with ampicillin and gentamycin.
Higher case-fatality rates have been reported for premature or low birth weight infants than full-term or infants with birth weights ³ 2.5 kg (50% versus 30%). Improvements in treatment, however, have affected the casefatality rate, with 62% of meningitis patients dying before the use of third-generation cephalosporins and only 14% dying after the introduction of third-generation cephalosporins. Only one death has been reported in the absence of meningitis, a neonate exhibiting bacteremia.
Source of E. sakazakii Infections
In early cases of E. sakazakii infections, an environmental source of the organism could not be identified. Vertical transmission from the mother’s birth canal to newborns was ruled out as cases occurred after caesarean section, and colonization of newborns at birth was not demonstrated. In more recent cases, environmental sampling has yielded evidence of contaminated blenders used to prepare infant formula and recovery of E. sakazakii isolates from a dish brush and a stirring spoon. To date, no subtyping has been reported for the isolates recovered from the blenders, whereas the plasmid profiles of the brush and spoon isolates did not match those of the patients. Dried infant formula, on the other hand, has been identified epidemiologically as the source of E. sakazakii in three outbreaks of neonatal meningitis and linked to one outbreak of necrotizing enterocolitis. In these outbreaks, E. sakazakii isolates from implicated milk powders either had the same plasmid profile, multilocus enzyme profiles, or pulsed-field gel electrophoresis profiles as those isolates from the patients. Presently, approved technology is not available to render powdered milk formulas commercially sterile. Hence, E. sakazakii could be present in formulas at substantially lower levels than those considered acceptable by the Codex Alimentarius for levels of coliforms in milk-based powdered infant formula. Prolonged periods of unrefrigerated storage after hydration of the powdered infant formula before feeding may subsequently enable substantial growth of the organism.