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Four cases of fatal echovirus 11 disease occurred in premature infants during a community outbreak of enteroviral disease in Massachusetts in 1979. Each infant developed nonspecific symptoms and jaundice at 4 to 6 days of age, and subsequent progressive hepatic failure and generalized bleeding. Only one infant survived longer than six days. Virus was recovered from multiple sites premortem, and from virtually all tissue cultured at autopsy. Myocarditis was not present clinically or pathologically. Clinical and laboratory evidence implicated perinatal transmission of virus from mother to infant. Three mothers experienced a febrile illness with abdominal pain within the last five days of pregnancy. In two, the illness led to a false diagnosis of abruptio placenta and interruption of pregnancy by cesarian section. Review of case reports of this syndrome caused by other echovirus serotypes revealed that many had similar perinatal events. Each mother ultimately developed neutralizing antibody to echovirus 11. However, all four infants were born without passively acquired antibody, probably because they were delivered prior to the appearance of specific maternal IgG. Although laboratory studies by others have shown other factors may be responsible for the ability of enterovirus to cause overwhelming disease in neonates, uncontrolled data from these four infants and their mothers suggest that timing of maternal illness in relation to delivery of the infant may also be important.

Melioidosis, caused by Pseudomonas pseudomallei, occurs in tropical areas and is diagnosed mostly in adults. In Khon Kaen, a province of northeast Thailand, five cases of infantile melioidosis were managed at Srinagarind Hospital. The patient's specimens were submitted to microbiologic and serologic examination for P. pseudomallei demonstrated by indirect hemagglutination. Possible modes of transmission such as environment, perinatal exposure and venereal transmission were investigated.

Repeated bacterial infections are frequent in children with AIDS owing to the B cell abnormalities produced by HIV infection. We report on two infants who presented with hypogammaglobulinaemia and with no HIV antibodies, but with epidemiological, immunological, and clinical features of AIDS.

Seven premature infants contracted asymptomatic hepatitis A while hospitalized in an intensive care nursery (nursery A) from May through August 1981. Fifteen secondary cases occurred between Aug 13 and Oct 14 and included six family members of nursery A infants, five nursery A nurses, and three nurses and a physician at two other nurseries--B and C. Nurseries B and C had each received an infected infant transferred from nursery A in July. An epidemiologic investigation was conducted to determine the mode of transmission of hepatitis A in infants. A common vehicle was not identified. Review of dates of onset of illness in adults suggested that hepatitis A was transmitted in at least two generations of illness in infants at nursery A. Evaluation of infant handling in nursery A, using a case-control study, suggested that hepatitis A was transmitted among infants by nurses. Asymptomatic infected premature infants can be a source of hepatitis A in nursery infants and personnel and in the community.

Five patients in a newborn intensive care unit (NICU) developed primary bacteremia due to Klebsiella during a 12-day period, May 2 through June 2, 1979, after feeding for 24-96 hr with contaminated breast milk. All patients had been fed via nasoduodenal tube with milk obtained from a single donor. The donor milk collected via electric suction pump was positive by gram stain for gram-negative rods and by culture for Klebsiella pneumoniae. A culture of hand-expressed milk was negative for gram-negative rods. The breast-pump tubing and safety trap were grossly contaminated with K. pneumoniae. Institution of proper sterilization to the pump equipment controlled the outbreak. This outbreak is the first documentation of nosocomial bacteremia as a major infectious complication of feedings of premature infants with contaminated breast milk.

A case of neonatal septicemia resulting from group B Streptococcus, type Ic is reported. The infection occurred in a premature infant delivered by cesarean section, which followed fetal distress. The same organism was isolated from a high vaginal swab taken from the mother who had had premature rupture of the membranes 48 hours before admission to the hospital. Both infant and mother made satisfactory recoveries. This is the first case of neonatal group B streptococcal infection reported from Nigeria.

Premature identical twins are described who according to molecular fingerprinting of their viral isolates, demonstrate a nonmaternal nursery source for their acquired cytomegalovirus (CMV) infections. The babies were born via cesarean section at 29 weeks gestation. Weekly urine screening of the infants indicated that at birth both were CMV-negative. Twin B developed CMV at 6 weeks of age, while Twin A developed his infection when he was 9 weeks old. Three months following delivery cervical and urine cultures of the infants' mother were negative and she had no detectable CMV antibody. At 6 months postpartum (2 months following both infants' discharge home) a repeat urine culture of their mother was positive for CMV, and here CMV-CF titer had risen to 1:128. DNA fingerprinting by restriction endonuclease digestion analyses of the viruses isolated from the two infants indicate that they were infected with different strains of CMV. In addition the DNA fingerprinting pattern of the mother's isolate is identical to that of Twin A. These cases give further evidence that hospitalized infants may acquire CMV from hospital sources and document by molecular fingerprinting for the first time to our knowledge that these babies may transmit the virus to CMV-seronegative individuals. This study also demonstrates how restriction endonuclease digestion analyses can be used as a powerful tool to study the epidemiology of CMV infections.

Two babies in a neonatal unit presented on the same day with meningitis due to echovirus 11, which was thought to have been introduced by staff. At this time echovirus 11 was also isolated from the stools of eight other babies; five of them did not have signs of infection. No intervention was made except to emphasise the importance of handwashing. There was evidence of secondary spread to two babies who were both clinically well. The attack rate was twelve (29%) of forty-one babies exposed. Seven of the twelve infected babies were born before 30 weeks' gestation and would have had little or no maternal antibody, yet only two of the seven babies had signs of infection. Despite lack of special measures, all babies recovered. Most cases of horizontally acquired neonatal echovirus infection are mild: extreme measures in the management of outbreaks are unnecessary.

Relapsing fever is caused by the Borrelia species of spirochetes. Louse-born epidemics of the disease may occur but the endemic disease is usually transmitted to humans by the bite of an infected tick (Ornithodorus). Transplacental infection was suggested more than 75 years ago (1) but has been rarely documented (2). We describe a case of neonatal relapsing fever where maternal infection was the probable cause of the premature delivery and infection in the infant.

Of the babies admitted to the Special Care Baby Unit of the Royal Free Hospital over 20 months, 10.2% were infected or colonised by klebsiella. The fluorescent antibody technique was used to identify epidemics caused by three strains: capsular type 8 K. aerogenes, type 68 K. oxytoca, or type 13 K. aerogenes, each of which was predominant at a different time, exhibited a difference in virulence, and showed a predilection for different sites of infection. Intestinal colonisation was frequently followed by the presence of sepsis in other sites by the same capsular type. Antibiotic administration led to a higher incidence of klebsiella infection, while the widespread use of compounds containing hexachlorophane could have contributed to skin colonisation and infection by klebsiella. An environmental survey indicated that 1% Hycolin failed to disinfect the incubators, that the babies were the reservoirs of the organisms, and that transmission was due to inadequate hand-washing of nurses and mothers. The mothers were found to have been uninformed of hygienic techniques. They were observed in various practices which could have contributed to the spread of the organism, including contaminating communal areas and handling babies other than their own. It has been recommended that the mothers of premature infants be instructed in the hygienic measures required in dealing with this susceptible population and that the nursing and medical staff be more strict in their own observance of these procedures.

A multicentre, controlled trial was carried out to determine whether removal of leucocytes from blood by means of 'Imugard IG500' (Terumo) filters would prevent transfusion-acquired cytomegalovirus (CMV) infection in newborn infants. 72 infants whose mothers were seronegative and who received some seropositive blood were followed for 6 months for evidence of CMV infection. There were no significant differences between the groups who received filtered and unfiltered blood in median gestation, birthweight, or amount of seropositive blood received (median volume 32.5 ml and 34.5 ml, respectively). 9 (21%) of the 42 infants who received unfiltered blood and none of the 30 who received filtered blood were infected with CMV. All infected infants weighed less than 1500 g at birth; they represented 31% of very low birthweight (VLBW) infants at risk of CMV infection. None of 24 VLBW infants who received filtered seropositive blood was infected. 1 infected infant died and 5 had clinical features consistent with CMV infection. The results show that transfusion-acquired CMV infection is preventable by filtration of blood through a leucocyte filter. This method has advantages over other methods of removing leucocytes or the use of only seronegative blood for newborn infants.

To eradicate Candida from a neonatal unit the authors used increasingly strigent protocols of prophylaxis and treatment. Finally all carriers were identified and treated with nystatin. A strict routine for washing hands was introduced. As a result of these measures the cross infection rate within the hospital was very low (3%). The eradication was maintained by constant surveillance (weekly oral and rectal swabs) because of regular reintroduction of Candida by babies who had been infected before transfer to the unit. The other conclusions were that post natal infection is usually due to cross infection and rarely from mother. The gut and perianal skin are important reservoirs of infection. Erythema of the buttocks almost disappeared after the eradication of Candida. Guteal erythema commonly preceded of manifestations of Leiner's disease.