Search

Background Pseudomonas aeruginosa, a non-fermentative, gram-negative rod, is responsible for a wide variety of clinical syndromes in NICU patients, including sepsis, pneumonia, meningitis, diarrhea, conjunctivitis and skin infections. An increased number of infections and colonisations by P. aeruginosa has been observed in the neonatal intensive care unit (NICU) of our university hospital between 2005 and 2007. Methods Hand disinfection compliance before and after an educational programme on hand hygiene was evaluated. Identification of microrganisms was performed using conventional methods. Antibiotic susceptibility was evaluated by MIC microdilution. Genotyping was performed by PFGE analysis. Results The molecular epidemiology of Pseudomonas aeruginosa in the NICU of the Federico II University hospital (Naples, Italy) and the infection control measures adopted to stop the spreading of P. aeruginosa in the ward were described. From July 2005 to June 2007, P. aeruginosa was isolated from 135 neonates and caused severe infections in 11 of them. Macrorestriction analysis of clinical isolates from 90 neonates identified 20 distinct genotypes, one major PFGE type (A) being isolated from 48 patients and responsible for 4 infections in 4 of them, four other distinct recurrent genotypes being isolated in 6 to 4 patients. Seven environmental strains were isolated from the hand of a nurse and from three sinks on two occasions, two of these showing PFGE profiles A and G identical to two clinical isolates responsible for infection. The successful control of the outbreak was achieved through implementation of active surveillance of healthcare-associated infections in the ward together with environmental microbiological sampling and an intense educational programme on hand disinfection among the staff members. Conclusion P. aeruginosa infections in the NICU were caused by the cross-transmission of an epidemic clone in 4 neonates, and by the selection of sporadic clones in 7 others. An infection control programme that included active surveillance and strict adherence to hand disinfection policies was effective in controlling NICU-acquired infections and colonisations caused by P. aeruginosa.

OBJECTIVES: To investigate the molecular epidemiology of extended-spectrum beta-lactamase (ESBL)-producing Klebsiella pneumoniae in the neonatal intensive care unit of a university hospital in Italy. METHODS: Antibiotic susceptibility was evaluated by disc diffusion and Etest. ESBLs were identified by isoelectric focusing, PCR and DNA sequencing analysis. Genotyping was performed by PFGE analysis. Conjugation was performed by broth mating. RESULTS: Molecular typing of K. pneumoniae isolates identified three distinct PFGE patterns. Isolates of PFGE profile A were isolated during an epidemic in 1996, while isolates of PFGE profiles B and C were sequentially isolated from September 2002 to December 2004, when 233 colonizations and 19 infections by K. pneumoniae occurred. All K. pneumoniae strains of different PFGE types were identified as ESBL producers. DNA sequencing of amplified beta-lactamase genes identified a novel bla(TEM) ESBL (bla(TEM-136)) along with bla(SHV-1) in chromosomal and plasmid DNA from K. pneumoniae of PFGE type A, respectively, and bla(TEM-1) and bla(SHV-12) in plasmid DNA from K. pneumoniae of PFGE types B and C. Conjugation experiments demonstrated that resistance to third-generation cephalosporins, along with an approximately 80 kb plasmid containing bla(SHV-12) and bla(TEM-1), was transferred from K. pneumoniae epidemic strains of PFGE types B and C to a susceptible Escherichia coli host at a frequency of 4 x 10(-6) and 1 x 10(-6) cfu/recipient cell, respectively. CONCLUSIONS: The selection of ESBL-producing clones and the transfer of the bla(SHV-12) ESBL gene between different clones were responsible for the spread of K. pneumoniae in the neonatal intensive care unit.

Gestational maturation of gastrointestinal motility is a key factor in readiness of the preterm neonates for enteral nutrition. Since gastric motility mainly depends on the electrical activity of the smooth muscle cells, it was of interest to investigate the developmental aspects of electrical activity of the stomach. The latter was recorded weekly through cutaneous electrogastrography in 27 preterm infants (aged 29-34 weeks of gestation). Recordings were done for 1 hr before and 1 hr after meal. The electrogastrographic variables measured were: percentage of normal gastric rhythm, ie, 2-4 cpm; percentage of tachygastria (4 cpm); the fed-to-fasting ratio of the dominant electrogastrographic power; and the instability coefficient of the dominant frequency. Data were compared with those measured in 10 full-term infants. Peaks of normal electrical activity (2-4 cpm) were present in most of the recordings at all the gestational ages; however, percentages of both normal electrical rhythm and tachygastria in preterm infants were similar to those measured in full-term infants (mean +/- SD) (normal rhythm; fasting: 70.2 +/- 3.8, fed: 72.2 +/- 5.0; tachygastria: fasting: 24.6 +/- 4.0, fed: 19.1 +/- 3.5) by 35 weeks of gestation (normal rhythm; fasting: 67.5 +/- 2.0, fed: 69.6 +/- 4.4; tachygastria: fasting: 27.1 +/- 4.0, fed: 25.6 +/- 4.1). The coefficient of instability of the dominant frequency in preterm infants was also similar to the value measured in full-term infants by 35 weeks of gestation, whereas the EGG power showed a significant increase in the postprandial state at all the gestational ages. We conclude that a maturation pattern of the electrical activity of the stomach can be detected by means of a noninvasive tool such as cutaneous electrogastrography: a normal electrical rhythm can be detected at very early gestational ages; however, this activity becomes dominant at around the 35 weeks of gestational age. In preterm infants developmental changes of gastric electrical activity are a function of advancing postnatal age.

During a five years period 8 newborns on 2035 admissions developed septic arthritis representing a very low incidence of 4%. Umbilical catheters were used in 3 patients. Staphylococcus aureus was the most frequent etiologic agent and in 6/8 cases blood cultures were positive for the same pathogen agent. Because of the paucity of clinical signs in the first period in the sick neonate, detection of the disorder by the radiologist assumes great importance in the neonatal intensive care unit, as early recognition and therapy may prevent residual deformity.

SUMMARYAn epidemic caused bySerratia marcescensthat involved 26 infants admitted to the Neonatal Intensive Care Unit (NICU) and 82 infants admitted to the Nursery of the 2nd Medical School of Naples is reported. Two different biotypes ofS. marcescenswith two completely different epidemiological patterns were identified. The prevalent biotype (A8b trigonelline –) was isolated in the delivery room, in the operating room, in the Nursery and in the NICU from items, healthy infant excreters and affected infants; the second biotype (A3a) was isolated only in the NICU from staff, two healthy infant excreters and two affected infants. Colonization of the throat and the gastrointestinal tract was frequent. Infected and colonized infants were the most important reservoir for serratia in the Nursery and in the NICU particularly for the type strain A3a. A mucus aspiration apparatus contaminated in the delivery room and the contamination of several instruments and items probably had a major role in the initiation and maintenance of the spread of the A8b strain. Mass contamination of the nursery has been related to overcrowding and a lack of the control measures; the transfer of high-risk colonized infants caused spread in the NICU.In the NICU the attack rate was 26%; 69% of infants became ill; the case fatality ratio was 19%. Epidemiological investigation of the infants at risk showed some factors predisposing to infection with serratia. The hygienic measures failed to control the spread of serratia and it was necessary to refuse new admissions to pregnant women in order to decontaminate and re-organize the wards.

Cow's milk proteins and ovalbumin have been recently identified in human breast milk(1). The aim of this investigation was to determine whether wheat gliadin is also present in human milk. Following the ingestion of a test meal of 20 g gluten, samples of breast milk were collected from 53 women at various stage of lactation. Gliadin was assessed by a double-antibody sandwich ELISA and 5 ng/ml or more could be measured in this way. Despite the presence of specific antibodies, prechallenge milk did not inhibit significantly the ELISA. After ingestion, gliadin was detected in breast milk from 41/53 women at 1 week after delivery, 8/17 at 6 weeks, 3/6 at 3 months and 2/4 at 5 months. The gliadin concentration ranged from 5 to 95ng/ml. Maximum levels in breast milk were found 2-4 hours after ingestion; however, gliadin could not be detected simultaneously in serum. The transfer of gliadin from mother to child early in his life might be critical for the development in later life of an appropriate specific immune response. 1)Kilshaw P.J.:Int.Archs Allergy appl.Immun. 75, 8-15,1984.