Pediatric Infectious Disease
About: Pediatric Infectious Disease is an academic journal. The journal publishes majorly in the area(s): Meningitis & Pneumonia. It has an ISSN identifier of 2212-8328. Over the lifetime, 1147 publication(s) have been published receiving 19074 citation(s).
Topics: Meningitis, Pneumonia, Ureaplasma urealyticum, Otitis, Bacteremia
Papers published on a yearly basis
01 Mar 1986-Pediatric Infectious Disease
01 Sep 1984-Pediatric Infectious Disease
TL;DR: Pertussis (whooping cough), a two-stage process of disease (respiratory colonization and toxin-mediated disease) is caused by B. pertussis, a pathogenic parasite with habitat only in human beings.
Abstract: Pertussis (whooping cough), a two-stage process of disease (respiratory colonization and toxin-mediated disease) is caused by B pertussis The bacterium is unique It is a pathogenic parasite with habitat only in human beings Growth in the pathogenic form, both in in vitro and in vivo, requires conditions that permit the expression of pertussis toxin (PT) (also known as histamine-sensitizing factor, lymphocyte-leukocyte-promoting factor, islet-activating factor and pertussigen) The expression of growth and PT appear to be genetically interrelated For multiplication in vitro the medium must be free of substances, such as fatty acids, that inhibit the enzymatic action required for elaboration of PT In vivo the bacteria are uniquely localized to the cilia of the respiratory epithelium where they multiply In situ the bacteria inhibit natural defenses of the respiratory tract (cilial, phagocytic and other activities); they tend not to spread and do not invade the underlying tissue The extent of the areas of colonization, directly related to the number of bacteria in the infecting inoculum, influences the amount of toxin elaborated and consequently the intensity of the clinical symptoms Other factors that influence the clinical disease are the inordinate susceptibility of the infant and genetically controlled susceptibility A specific role for PT in the initial establishment of the infection is not clear, but it seems definite that PT-specific immunity influences the clearance of colonization in about 4 to 5 weeks The clinical symptoms become manifest when the bacteria are waning This clearance is influenced by the synthesis of IgA antibodies and pertussis toxin antibodies that may act by inhibiting the "enzyme" required for growth or by another mechanism The pathology of the disease is the result of altered cellular functions of toxin-sensitized cells, not by histologic damage PT is composed of two functional components like other exotoxins that cause infectious disease (eg diphtheria, cholera) Certain sites on one component enable PT to bind to specific receptors on tissue cells and enter the cell The toxin ADP ribosylates a regulatory protein of the cytoplasmic membrane and thereby alters the function of the cell Affected (sensitized) cells are insulin-secretory islets of the pancreas, lymphocytes and leukocytes, heart cells and others that have not been clearly identified, eg those that effect paroxysms and neurologic disturbances The altered function of the cell in vitro is irreversible, and the restoration of the function of a particular tissue in vivo appears to be dependent on the renewal of the cells(ABSTRACT TRUNCATED AT 400 WORDS)
01 Nov 1984-Pediatric Infectious Disease
01 Jan 1984-Pediatric Infectious Disease
TL;DR: The cause of the epidemic was not discovered but shellfish and raw fish consumption may have played a part and Pacific Island Polynesians were rectal carriers of L. monocytogenes and were represented among the epidemic cases more often than expected according to birth data.
Abstract: During the 11 months beginning in January, 1980, 22 cases of perinatal Listeria monocytogenes infection occurred at three obstetric hospitals in Auckland, New Zealand. Most cases were due to type 1b strains. Since the previous epidemic here in 1969, about one perinatal infection has been diagnosed annually in the same area. Women presented in preterm (11 of 22 cases) or term labor with signs of amnionitis (11 of 22 cases) and associated fetal distress and/or meconium-stained liquor (14 of 19 cases). A mild "flu"-like illness or urinary tract symptoms were common (18 of 22 women). Five fetal deaths occurred. Three were before 20 weeks of gestation. Most liveborn affected babies had early respiratory symptoms (12 of 14 cases). Meningitis occurred in 4 of 14 infants. There was one death. Vaginal carriage of L. monocytogenes was found in only 1 of 750 consecutive asymptomatic pregnant women who were tested at the time of the epidemic. Rectal carriage was found in 25 (3.3%). Pacific Island Polynesians were rectal carriers of L. monocytogenes and were represented among the epidemic cases more often than expected according to birth data (P less than 0.05 and P less than 0.001, respectively). The cause of the epidemic was not discovered but shellfish and raw fish consumption may have played a part.
01 Sep 1985-Pediatric Infectious Disease
TL;DR: It is concluded that bacterial infection causes serious morbidity in acquired immunodeficiency syndrome and acquired immunosuppressive syndrome-related complex and may be further evidence for altered humoral immunity in the disorder.
Abstract: We have followed 46 children with acquired immunodeficiency syndrome and acquired immunodeficiency syndrome-related complex. Twenty-six patients had at least one episode of serious bacterial infection. Twenty-seven episodes of sepsis were documented in 21 patients. Soft tissue infection was common in both the presence and the absence of documented bacteremia. Urinary tract infection commonly presented as worsening diarrhea in the absence of sepsis. Organisms commonly isolated included Streptococcus pneumoniae, Haemophilus influenzae and Salmonella sp. Staphylococcal infection accompanied episodes of cellulitis/abscess. Escherichia coli commonly caused urinary tract infection in the absence of sepsis. Enteric and nosocomial sepsis was limited to hospitalized, instrumented patients or to individuals who had received prior antibiotic therapy as outpatients. We conclude that bacterial infection causes serious morbidity in acquired immunodeficiency syndrome and acquired immunodeficiency syndrome-related complex and may be further evidence for altered humoral immunity in the disorder.
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