Journal of Antimicrobial Chemotherapy (1979) 5 (Suppl. A), 1-12
Neonatal and perinatal infection: routes of transmission and prevention
Public Health Laboratory and Department of Microbiology, Central Middlesex Hospital, Acton Lane, London NWIO, England
The changing pattern of infection
No one concerned with the problems of neonatal infection can fail to be impressed by the remarkable sequential changes in its principal aetiology which have taken place during the last four decades (Figure 1). The ~-haemolytic streptococcus, once the scourge of maternity hospitals, has now virtually ceased to be a problem (Williams, Blowers, Garrod & Shooter, 1966). Its place was taken by the staphylococcus (Schaffer, 1958) which monopolized nursery infections, as it did all hospital infections, for nearly two decades to be itself replaced by the Gram-negative bacilli (Williams, 1971). Escherichia coli has now been joined by the Group B streptococcus as the principal cause of major neonatal sepsis (Jeffery, Mitchison, Wigglesworth & Davies, 1977) and there is already some indication that anaerobic organisms may be about to play an increasing role in this condition (Leading Articles, 1978a, b and c). It is easier, however, to record these changes than to explain why they have occurred. Yet nothing could be more fundamental to the question of prevention and control. Has the infectivity pattern changed because of the numerous preventive measures (often costly and time consuming) imposed in many hospitals, or does it reflect biological changes, as yet poorly understood, in the organisms themselves? Before considering this question, it is necessary to ask an even more fundamental question: why does infection occur at all? For the first half of this century the quest for the answer to this question would have been directed almost entirely at the organism. However, we are now more aware that whether or not infection occurs-as distinct from colonization-depends on the outcome of an interaction between the organism and its host, and that there are a number of important determinants on either side of this equation which affect this outcome (Table I). The newborn infant fulfils only too well the main qualifications for increased susceptibility to infection. All neonates are at the extreme of age-sometimes exceptionally so; they are deficient at birth in IgM and IgG, with reduced serum opsonic activity and ability to activate complement. Newborn infants-partIcularly preterm males-are indeed highly susceptible hosts (Quie, Davis & Dosset, 1971; Davies, 1971; Krugman, Ward & Katz, 1977a; Marshall, 1978). Physiological prematurity, resulting in periods of apnoea and oxygen depletion, may itself add to the infection risk; furthermore, it will almost certainly lead to admission 1
0305-7453/79/0A0001 + 12 $01.00/0
© 1979 The British Society for Antimicrobial Chemotherapy
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
D. A. McSwiggan
2
D. A. McSwiggan Figure 1. The changing pattern of neonatal infection.
Group A streptococci ........................................................................................................ . S. aureus ........................... _ _ _ _ _ _ _ .................................................. .
Enterobacteriaciae
Pseudomonas spp. .. .................................................. - - - - - - - - - - - - - -
Group B streptococci ........................................................................... _ _ _ _ _ __ Anaerobes ....................................................................................... _ _ __ ?
1950
1960
1970
1980
_ _ _ Predominant cause of neonatal infection ............ Infrequent cause of neonatal infection
Table I. Some determinants of the hospital infection equation
Host susceptibility factors Immunologically compromised Breached integrity Extremes of age
Microbial infectivity factors Virulence Drug resistance Spreadability Detectability
to a special care or intensive care unit and the employment of invasive life support systems which will jeopardize further the premature infant's vulnerable defences. Although until recently the organism has been considered to play the major role in determining infection, remarkably little is known about what characteristics make a specific organism become, for a particular time, 'leader of the pack' (Williams, 1978). Some types of organisms are inherently more virulent than others; but do they acquire or lose virulence with the passage of time? Do other microbial characteristics matter? The answer to the first question is apparently yes, an organism can lose virulence. This would seem to be the reason for the dramatic decline in the severity of ~-haemolytic streptococcal infections during the late 1930's. Even while he was conducting the Medical Research Council trial of Prontosil at Queen Charlotte's Hospital, Leonard Colebrook commented on the decreasing severity of these infections. He was clearly concerned that this loss of virulence might appear to be responsible for the success due to Prontosil (Colebrook & Kenny, 1936). The answer to the second question is somewhat more speculative but also seems to be in the affirmative. Because it alarms us, we sometimes think of virulence as being an asset to an organism. Of course, the opposite is really the case. For a parasite, such as a staphylococcus, living reasonably harmoniously with its host, the sudden acquisition of virulence is a disaster. Its presence will usually be declared by the sepsis it causes and its potential hosts will try to dissociate themselves from it by the use of antibiotics, disinfectants and segregation. Such an organism would very rapidly face biological eclipse, unless it also possessed two other characteristics-antibiotic resistance and an enhanced ability to spread among hosts. By means of these two additional characteristics it might survive for a sufficient period to lose its virulence and resume its former less remarkable career. Should it have acquired a particularly bad
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
1940
Routes of transmission and prevention
3
Incidence of neonatal infection
Neonatal sepsis is not notifiable and in the absence of a national source of data, opinion on the overall situation is somewhat speculative. Perhaps the nearest thing we do have to national data are the reports to the PHLS Communicable Disease Surveillance Centre (Galbraith, 1977). This unit has recently reported an analysis of neonatal meningitis and bacteraemia and some of the data from this analysis are shown in Table II. The number of cases reported is remarkably small, representing less than one major neonatal infection per reporting laboratory per year. It is clear nevertheless that E. coli and the other Gram-negative bacilli account for more than half these infections. The group-B streptococci however account for a substantial proportion of infections and an even higher proportion of fatal cases, having an overall mortality of 43 %as against 31 %
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
reputation, then a change of name, that is, a shift of phage pattern, would help the organism to become less detectable while rehabilitating itself. This course of events could be put forward to explain the pattern of behaviour of Staphylococcus aureus phage type 80later 80/81. This organism, which began its career in the nursery during the early 50's, soon became widely involved in hospital sepsis generally (Williams, 1976). It eventually subsided into semi-retirement in the 1960's, with a considerable modification to its phage type (Asheshov & Winkler, 1966). Some part of the now predominant role of Gram-negative bacilli in neonatal infections may also be attributable to increased virulence; E. coli possessing the KI antigen accounts for about 80 % of neonatal meningitis (Davies, 1977). There are, however, reasons for believing that a great part of the increase in Gram-negative infection resulted more from changes relating to the population at risk rather than to enhanced virulence of these organisms (Hoffman & Finberg, 1955; Williams, 1971). At the 1970 International Conference on Nosocomial Infection, the section devoted to 'Emerging Pathogens' (1971) made no reference to group-B streptococci, yet within a decade these organisms have become the major cause of neonatal infection, surpassed only by E. coli. What event has taken place to promote this change? The organism itself has long been recognized as an occasional cause of maternal and neonatal infection (Parker, 1977). Has it now acquired a new virulence and an enhanced ability to colonize the maternal bowel and genital tract? The answers to these questions are at present far from clear. As already stated, a predominant role for a 'new' cause of neonatal infection may now be emerging. There has been a considerable number of reports, mainly within the last two years, of nursery infections with anaerobic organisms. A common feature in virtually all cases has been the difficulty in identifying the infecting agent or its toxin (Chin, Leake, Yamanchi, Antony & Guze, 1974; Rom, Flynn & Noone, 1977; Arnon, Midura, Damus, Wood & Chin, 1978; Larson, Price, Honour & Borriello, 1978; Morbidity & Mortality Weekly Report, 1978). It is to be expected that the number of infections (or toxaemias) associated with these organisms will appear to increase with our ability to detect these difficult agents. It thus seems probable that the changes observed in the pattern of neonatal infection over the last four decades have been due in part to the variation in the population at risk, in part due to variation in biological characteristics of the organisms and perhaps in some measure, more recently, to an improvement in our ability to detect previously unrecognized causes for infection and disease in the newborn.
D. A. McSwiggan
4
Table II. Neonatal meningitis: septicaemia
(July 1976-June 1977)
E. coli
Gp. B streptococci S. aureus
Pseudomonas Other GNB Other GPB Other organisms
CSF
Blood
(%)
(%)
40 14 4 8
36 18 16 3 8 12 7
13
2 19
Adapted from P.H.L.S. unpublished data (CDR 77/49).
for E. coli infections. In the United States, the information on neonatal infections on a national basis is somewhat better-if one accepts the inherent limitations of deriving reliable data on hospital infection rates from numerous disparate sources. The National Nosocomial Infection Study (NNIS) has been collecting, analysing and reporting uniformly collected data from about eighty hospitals for nearly a decade. It has the advantage of deriving rates and these have shown remarkably little variation over the period of the study. Some data relating to nursery infections have been extracted (Tables III and IV) from the report for 1976, the last full year for which information is available (Center for Disease Control: National Nosocomial Infections Study Report, 1978). It would seem inadvisable to extrapolate too freely from the American position to the situation in our own hospitals. Indeed, it is clear that the relationship between neonatal bacteraemia and meningitis in the NNIS report differs considerably from that shown in CDSC analysis. Nevertheless, a considerable degree of comparability probably exists. For example, the experience in my own hospital (Table V) does not differ substantially from the American pattern; the similarity in the large proportion of cutaneous and mucocutaneous infections is apparent and the overall infection rate is the same as that recorded for the community-teaching group of hospitals which is the type most closely relating to my own in function. The considerable variation in the infection rate among the Table III. Infection rates per 10,000
discharges 1976 Newborn Cutaneous Bacteraemia Respiratory Surgical wounds Urinary tract Gastrointestinal C.N.S. All sites
%
Adapted from NNIS Report (1978).
61·1 26·3 19·0 8·7 8·0 4·6 4·3 1·5
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
100 100 CSF = 52 isolates Blood = 184 isolates
Routes of transmission and prevention
5
Table IV. Newborn nursery infections Community hospital Community-teaching Federal Municipal or county University
0·9 1·1 0'3 3·1 3'0
All hospitals
1'6
Adapted from NNIS Report (1978).
S. aureus
14 Cutaneous Wound infection Nasal discharge Eye discharge
9
Mucocutaneous
2
2 2 1
C. albieans
2
Strep. pyogenes E. eoli
1 Catheter tip (clinical meningitis)
4
K. pneumoniae N. gonorrhoeae
Meningitis Septicaemia Urinary infection 1 Eye discharge 1 Eye discharge
2 1 1
Total 23/2,006 unit discharges (1·1 %) various categories of American hospitals is thought to be related to the proportion of infants receiving intensive care, a feature which is likely to cause similar variation in rates among hospitals in this country and which underscores the problem of extrapolation from data from a small number of specialized units. One feature from our own results which merits comment is the absence of group-B streptococci from the table. Despite the fact that this organism is isolated regularly from routine specimens from infants admitted to the Special Care Baby Unit we have not during an eighteen month period been able to incriminate it in a specific infection. The NNIS has not yet published an analysis of the various organisms involved in its nursery infections. Such information would be of great interest as it would chart quantitatively the changes in the pattern of neonatal infection over the last decade. Routes of infection
In the prenatal period infecting organisms may reach the fetus via the maternal blood supply. This route of infection is particularly important in view of the increasing concern over the part played by viruses in fetal abnormalities (Hanshaw & Dudgeon, 1978). Instrumentation of the uterine cavity is an uncommon but documented route of introducing infection to the fetus (National Registry for Amniocentesis Study Group, 1976). However, ascending infection, caused by organisms normally present in the maternal genital tract, probably constitutes the commonest hazard of infection in the perinatal
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Table V. Infections in the nursery and special care baby unit (Central Middlesex Hospital-IS month Survey)
6
D. A. McSwiggan
Prevention and control Many of the preventive measures in use today have not been put to the test of controlled trials. It would seem that the fall in infection which coincided with the introduction of
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
period. Although infection may occur through intact membranes (Gamsu, 1973) it is following rupture that the risk of infection is greatest. Lanier, Scarbrough, Fillingam & Baker (1965) have shown that the risk increases directly with the time to delivery and is probably at a maximum by 24 h. At birth and thereafter the importance of the human carrier as a major source of pathogenic organisms cannot be overemphasized. Birth canal, skin, nose and bowel of mother, nursery personnel and other infants are commonly colonized-and indeed sometimes infected-with organisms which have given rise to nursery epidemics and sporadic neonatal infections (Szanton, 1957; Williams, Blowers, Garrod & Shooter, 1966c; Eisenach, Reber, Eitzman & Baer, 1972; Parker, 1977). On the other hand it is clear that the majority of neonates become colonized, sometimes with apparently pathogenic organisms (Krugman, Ward & Katz, 1977b) without becoming clinically infected. Whatever the source, the hands of the attendants appear to be by far the most important means of transmitting infection to the newborn. This is hardly surprising if we remember that 'the hands which move soiled napkins and bedding are the hands that feed and minister' (Davies, 1971). Indeed transmission of infection to the newborn by nurses' hands (and prevention by handwashing) is one of the few instances where the epidemiological process concerned has been properly demonstrated by a controlled trial (Mortimer, Wolinsky, Gonzaga & Rammelkamp, 1966). Although airborne transmission in the general nursery is relatively unimportant as a cause of infection (Mortimer et al., 1966) the microenvironment of the incubator presents a very different situation almost entirely due to the production of infected aerosols arising from contaminated nebulisers and humidifiers. Only resuscitators, among labour ward and nursery equipment present a hazard of such proportions (for references see Center for Disease Control: National Nosocomial Infections Study Quarterly Report, 1973). Infected disinfectants are perhaps 'runners-up' to humidifying and resuscitating equipment as sources of Gram-negative infections in hospitals generally. These substances have been shown to harbour a large variety of Gram-negative bacilli often multiplying in the fluid itself or in the cork or bottle liners (Center for Disease Control: National Nosocomial Infections Study Quarterly Report, 1974 lists thirty references.) Constant vigilance is therefore advizable wherever disinfectants are in use (see below-surveillance). Milk is a particularly good medium for bacterial multiplication and contaminated milk or milk products have resulted in outbreaks in the population often involving predominantly babies and infants (Weekly Epidemiological Record 1974, 1977). When such infection is introduced into the nursery a disastrous situation may arise (Ensign & Hunter, 1946). It must be recognized however that in this type of situation, spread within the nursery may be via the hands of infected or colonized staff. Although the nursery milk kitchen itself is rightly considered a potentially dangerous area (Lowbury, Ayliffe, Geddes & Williams, 1975) the lack of documentary evidence for nursery infections arising directly from infected feeds would seem to suggest that this type of occurrence is extremely rare. It is perhaps somewhat paradoxical that several recent nursery outbreaks associated with feeds have been related to contaminated expressed breast milk and not formula feeds (Center for Disease Control: National Nosocomial Infection Study Report 1978; Stiver, Albritton, Clark, Friesen & White, 1977.)
Routes of transmission and prevention
7
Surveillance It seems desirable to have some system for collecting relevant data on the endemic
infection situation in order to determine as soon as possible any significant change in the pattern. There are various views on how surveillance should be organized (see Systems for Control, 1971 for discussion) but little evidence of their effectiveness (Morbidity & Mortality Weekly Report, 1978.) The surveillance scheme in use at Central Middlesex Hospital is based on five activities (Table VI). First and most important, the medical laboratory staff or the Control of Infection (C.L) Nurse visit the wards to investigate any infection which seems to be hospital-acquired immediately it comes to attention. Second, a daily summary oflaboratory reports is passed to the C.L Nurse who scrutinizes them for any sign of 'clustering' of similar isolates which might indicate that something potentially undesirable is going on. Its third function is to ensure that patients or staff identified as particular infection hazards are properly segregated. This may entail isolation for the mother or infant and suspension from patient care for nursing staff, until considered no longer a hazard (see below with reference to salmonella screening). Bacteriological sampling of the environment is of very limited value in the prevention of infection and is generally to be discouraged (Center for Disease Control: National Nosocomial Infections Study Report, 1974). It may be desirable, however, to monitor on a regular basis certain high risk environmental sources such as humidifiers, when in use, to ensure that decontamination is satisfactory; 'in use' tests of disinfectants should be carried out on a regular basis (Maurer, 1974). The fifth function of surveillance is to check that the preventive measures which have been agreed are actually being carried out; to teach and to update and revise them in accordance with the changing pattern of events.
Table VI. A system of surveillance activity 1. Direct clinical enquiries relating to an infection.
2. 3. 4. 5.
Ongoing survey of laboratory reports supplemented by ward enquiries when indicated. Monitoring microbial screens on patients and staff. Minimal environmental sampling of selected areas e.g. humidifiers, disinfectants. Teaching and monitoring control procedures.
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
control measures was taken as sufficient evidence of their effectiveness. There is now more awareness that the preventive measures taken may have had little (and in some cases nothing) to do with the reduction in infection. Conscious of the need for more information on what measures are really effective the Center for Disease Control, Atlanta has organized a study, the SENIC Project, to determine effectiveness of infection control measures (Morbidity & Mortality Weeldy Report, 1978). Unfortunately, it may be some time before this project provides the information on which to base well founded control programmes. For the present therefore, such preventive measures we choose to advocate should be based on sound principles, common sense and be relevant to the local current situation. It has been said that nurses' time is our scarcest commodity (Parker, 1971). We must look most critically, therefore, at those time consuming and restrictive control procedures which are most extravagant in this regard.
8
D. A. McSwiggan
Preventive measures
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Surveillance alone will not stop perinatal and neonatal infections occurring, nor prevent their spread should they occur. More active measures are required. However optimistic we may feel about the effectiveness of such measures, it is probably advisable to assume that they will not be successful on every occasion. As the nursery provides a particularly susceptible population should an epidemiologically inclined organism gain access, it seems reasonable to reduce the number exposed to risk to the minimum. This can be achieved by rooming-in newborns with their mothers, by having several small nurseries rather than one larger or by cohorting infants (Williams, Blowers, Garrod & Shooter, 1966b). Salmonella introduced into the nursery or special care unit via a maternal excretor can result in serious illness among neonates (Rowe, Giles & Brown, 1969). It is our practice to screen, for salmonella excretion, women between the thirty-eighth and thirty-ninth week of pregnancy. Those found to be excreting salmonella are eventually admitted for confinement in isolation and special precautions taken concerning the infant. It is not possible to calculate quantitively the benefits of this programme. However it identifies annually about six or more salmonella excretors (including recently, a very profuse excretor of S. typhi) while the burden on the laboratory is comparatively insignificant in terms of the number of stool specimens examined from other sources. Such a screening programme might well be unsuitable for maternity units with a different type of laboratory facility. The benefits to the fetus and newborn of treating maternal infection are possibly best demonstrated by the virtual eradication of congenital syphilis in this country. By 1968 congenital syphilis had dropped to 4~;'; of its rate at the inception of the national health service, nearly five times greater than the fall in (adult) acquired syphilis during the same period (Annual Report, 1969; Report, 1949.) A major part of this achievement can be attributed to the identification of infected mothers and their effective treatment during routine antenatal care. Obstetric intervention to prevent prolonged labour is now standard practice. In circumstances where membranes have been ruptured for 12 h without onset of labour a decision should be made to terminate labour within the next 12 h (Lanier et at., 1965) unless gross prematurity presents a greater risk than infection. At the present time the most important single measure in the prevention of neonatal infection is handwashing between each infant handling. What should be used to wash hands may still be a matter for debate, but there can be little doubt that handwashing itself is a significant measure in reducing neonatal sepsis (for full discussion and references see Center for Disease Control: National Nosocomial Infections Study Report, 1975). The use of masks and gowns, on the other hand, has been shown to make little or no difference to nursery infection rates (Williams & Oliver, 1969). The danger associated with certain types of equipment, particularly nebulisers, humidifiers and resuscitators has already been mentioned. Nebulizers are probably better not used. Many units, my own included, run incubators without humidification, humidifiers being used only when oxygen is administered. When humidifiers are in use they should be decontaminated daily. If detachable they should be autoclaved, otherwise they should be emptied completely, cleaned with detergent, dried and refilled with sterile water (Center for Disease Control: National Nosocomial Infections Study Report, 1973). Tubing and traps on resuscitators should be changed and autoclaved after every use.
Routes of transmission and prevention
9
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
It is established practice to require surgical instruments and equipment to be sterile. Should we accept a lower standard for certain 'disposable' items (such as fetal monitoring electrodes) in order to allow their re-use? Resterilizing such items without commercial facilities is usually not practical; autoclaving is likely to destroy or distort plastics or interfere with conductivity of electrical equipment. Chemical disinfection cannot be relied upon to sterilize and the degree of decontamination achieved is very difficult to monitor. It is usually cheaper, in the long term to treat disposables-however expensiveas disposable. With the general availability of commercial ready-to-use sterile feeds the hazards, potential or real, of the nursery kitchen should now be virtually eliminated. The product should be supplied to each mother together with a sterile teat and she should assemble the feed herself. As already referred to in a different context, it is somewhat paradoxical that today's problems appear to relate more to human milk feeds than to artificial feeds. Expressed breast milk (EBM), despite some doubts about nutritional adequacy (Davies, 1977; Fomon & Ziegler, 1977) has been advocated for preterm infants because it is believed to provide protection against infection. The protective effect appears to be found in both the cellular element (Pitt, 1976; Goldman, 1977) and in the aqueous phase (Bullen, 1977). It seems possible to collect breast milk from an infant's mother under conditions which permit it to be stored at 4"C and provide it in feeds for her own child without further treatment for up to 24 h. However, donor milk usually requires freezing and at least a proportion of it pasteurizing also (Williamson, Hewitt, Finucane & Gamsu, 1978) before being fed to 'foreign' infants. It is claimed that these two processes seriously reduce the EBM's protective value; the cellular protection being destroyed by freezing (Ford, Law, Marshall & Reiter, 1977) and the humoral protective element considerably reduced by pasteurization (Evans, Ryley, Neale, Dodge & Lewarne, 1978). Information is required to determine the value of frozen and pasteurized milk on the one hand and on the other, the practicality and acceptability of using unfrozen, unpasteurized donor EBM. Until these problems have been investigated more fully, a caution against extending donor EBM services in United States hospitals has come from the Center for Disease Control, Atlanta. A full discussion on this subject can be found in the Center of Disease Control: National Nosocomial Infections Study Report (1978) and in the report of the Second Workshop by Fomon (1977). It has been asked 'Is intensive care becoming too intensive?' ('JFL', 1977). Undoubtedly there are infants whose best hope of survival will depend on such care. There are, however, others where the benefit must be carefully balanced against the risks inherent in the more aggressive forms of special care. Many of these preterm neonates are being virtually committed to infection as a result of the often multiple invasion of their exterior defences by monitoring and life support apparatus. Perhaps one hopeful sign in this field is the recent interest in the development of non-invasive techniques for both prenatal and postnatal monitoring (Rooth, 1975; Cooke, Rolse & Howat, 1977.) Finally it is prudent to remember that infection in the nursery travels both ways. This is perhaps of most particular importance for female doctors and nurses who may be (unknowingly) in close contact with infants with congenital rubella, who may be heavy excretors of virus. It is advisable that all staff in contact with infants have their rubella status determined and those not immune should be vaccinated.
10
D. A. McSwiggan Acknowledgement
I am indebted to the Director of the Communicable Disease Surveillance Centre for permission to use the data in Table II.
References
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Annual Report of the Chief Medical Officer of the Department of Health & Social Security for the Year 1968. H.M.S.O. (1969), p. 258. Arnon, S. S., Midura, T. F., Damus, D., Wood, R. M. & Chin, J. Intestinal infection and toxin production of Clostridium botulinum as one cause of sudden infant death. Lancet i: 1273-6 (1978). Asheshov, E. H. & Winkler, K. C. Staphylococcus aureus strain of the '52, 52A, 80, 81,' Complex. Nature 209: 638-9 (1966). Bullen, J. J. Human milk and gut infection in the newborn. British Journal of Hospital Medicine 18: 220-31 (1977). Center for Disease Control: National Nosocomial Infections Study Quarterly Report, Third Quarter 1972, issued 1973. Recommendations for the Decontamination and Maintenance of Inhalation Therapy Equipment (1973), pp. 12-17. Center for Disease Control: National Nosocomial Infections Study Quarterly Report, First and Second Quarters 1973, issued 1974. Statement on Microbiologic sampling in the Hospital (1974), pp. 18-20. Center for Disease Control: National Nosocomial Infections Study Quarterly Report, Fourth Quarter 1972, issued 1974. Disinfectant or Infectant: The Label Doesn't Always Say (1974), pp.18-23. Center for Disease Control: National Nosocomial Infections Study Quarterly Report, Third and Fourth Quarters 1973, issued 1975. Personal Handwashing Practices for the Prevention of Nosocomial Infections (1975), pp. 19-28. Center for Disease Control: National Nosocomial Infections Study Report Annual Summary 1976, issued 1978. Reported Nosocomial Infections, 1976 (1978), pp. 1-10. Center for Disease Control: National Nosocomial Infections Study Report Annual Summary 1976, issued 1978. Nosocomial Salmonellosis in Infants Associated with Consumption of Contaminated Human Milk: A Report of Two Outbreaks (1978), pp. 14-15. Center for Disease Control: National Nosocomial Infections Study Report Annual Summary 1976, issued 1978. Human Milkfor Feeding Premature Infants: Benefits, Risks and Precautions for a Donor Program (1978), pp. 16-18. Chin, A. W., Leake, R. 0., Yamanchi, T., Antony, B. F. & Guze, L. B. The significance of anaerobes in neonatal bacteraemia. Paediatrics 54: 736-45 (1974). Colebrook, L. & Kenny, M. Treatment with prontosil of puerperal infections due to haemolytic streptococci. Lancet ii: 1319-22 (1936). Cooke, R. W. I., Rolse, P. & Howat, P. A technique for the non-invasive estimation of cerebral blood flow in the newborn infant. Medical Engineering Technology 1: 263-6 (1977). Davies, D. P. Adequacy of expressed breast milk for early growth of preterm infants. Archives of Disease in Childhood 52: 296-301 (1977). Davies, P. A. Bacterial infections in the foetus and newborn. Archives of Disease in Childhood 46: 1-27 (1971). Davies, P. A. Neonatal Bacterial Meningitis. British Journal of Hospital Medicine 18: 425-34 (1977). Eisenach, K. D., Reber, R. M., Eitzman, D. V. & Baer, H. Nosocomial infections due to kanamycin resistant R-factor carrying enteric organisms in an intensive care nursery. Paediatrics 50: 395-402 (1972). Emerging Pathogens. In Proceedings of the International Conference on Nosocomial Infections (Brachman, P. S. & Eickhoff, T. c., Eds). Waverley Press, Baltimore (1971), pp. 103-56. Ensign, P. R. & Hunter, C. A. An epidemic of diarrhoea in the newborn nursery caused by a milkborne epidemic in the community. Journal of Paediatrics 29: 620-8 (1946).
Routes of transmission and prevention
11
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Evans, T. J., Ryley, W. C., Neale, L. M., Dodge, J. A. & Lewarne, V. M. Effect of storage and heat on antimicrobial proteins in human milk. Archives of Disease in Childhood 53: 239-41 (1978). Fomon, S. J. Human milk.in premature infant feeding: report of second workshop. American Journal of Public Health 67: 361 (1977). Fomon, S. J. & Ziegler, E. E. Protein intake of premature infants: interpretation of data. Journal of Paediatrics 90: 504-6 (1977). Ford, J. E., Law, B. A., Marshall, V. M. E. & Reiter, B. Influence of the heat treatment of human milk on some of its protective constituents. Journal of Paediatrics 90: 29-35 (1977). Galbraith, N. S. National centre for surveillance and control of communicable disease. Proceedings of the Royal Society of Medicine 70: 889-93 (1977). Gamsu, H. Intrauterine bacterial infections. In Intrauterine infections. Ciba Foundation Symposium 10. New Series, Amsterdam Associated Medical Publishers (1973), pp. 135-46. Goldman, A. S. Human milk, 1eucocytes and immunity. Journal of Paediatrics 90: 167-8 (1977). Hanshaw, J. B. & Dudgeon, J. A. Viral Diseases of the Foetus and Newborn. WBS Saunders, Philadelphia, London and Toronto (1978). Hoffman, M. A. & Finberg, L. Pseudomonas infections in infants associated with high humidity environments. Journal of Paediatrics 46: 626-30 (1955). Jeffery, M., Mitchison, R., Wigglesworth, J. S. & Davies, P. A. Early neonatal bacteraemia. Archives oj Disease in Childhood 52: 683-6 (1977). 'JFL' Is intensive care becoming too intensive? Paediatrics (Neonatology Supplement) 59: 1064-5 (1977). Krugman, S., Ward, R. & Katz, S. L. Sepsis in the newborn. In Infectious Diseases of Children. Mosby, St. Louis (1977a), pp. 194-205. Krugman, S., Ward, R. & Katz, S. L. Sepsis in the newborn: In Infectious Diseases of Children Mosby, St. Louis (1977b), pp. 199. Lanier, L. R., Scarbrough, R. W., Fillingim, D. W. & Baker, R. E. Incidence of maternal and foetal complications associated with rupture of the membranes before onset of labour. American Journal of Obstetrics and Gynaecology 93: 398-404 (1965). Larson, H. E., Price, A. B., Honour, P. & Borriello, S. P. Clostridium difficile and the Aetiology of Pseudomembranous Colitis. Lancet i: 1063-8 (1978). Leading Article. Necrotising enterocolitis. British Medical Journal i: 132 (1978a). Leading Article. Pseudomembranous colitis. Lancet i: 1080-1 (1978b). Leading Article, A new role for botulism. Lancet i: 1295-6 (1978c). Lowbury, E. J. L., Ayliffe, G. A. J., Geddes, A. M. & Williams, J. D. Control of Hospital Infection. A Practical Handbook. Chapman & Hall, London (1975), pp. 239-41. Marshall, W. C. The (L;-:elopment of immune mechanisms in the foetus and newborn. In Viral Diseases of the Foetus and Newborn. (Hanshaw, J. B. & Dudgeon, J. A., Eds) WBS Saunders, Philadelphia, London & Toronto (1978), pp. 259-77. Maurer, I. M. Hospital Hygiene. Arnold, London (1974), pp. 74-9. Morbidity and Mortality Weekly Report Vol. 27. Infection surveillance and control programs in U.S. hospitals: an assessment (1978), pp. 139-45. Morbidity and Mortality Weekly Report Vol. 27. Follow-up on infant botulism (1978), pp. 17-23. Mortimer, E. A., Wolinsky, E., Gonzaga, A. J. & Rammelkamp, C. H. Role of Airborne Transmission in Staphylococcal Infections. British Medical Journal i: 319-22 (1966). National Registry for Amniocentesis Study Group. Journal of the American Medical Association 236: 1471-6 (1976). Parker, M. T. Current national patterns. Proceedings of the International Conference on Nosocomiaiinfections (1971), pp. 35-41. Parker, M. T. Neonatalstreptococcalinfections.Postgraduate Medical Journal53: 598-605 (1977). Pitt, J. Breast milk leucocytes. Paediatrics 58: 769-70 (1976). Quie, P. G., Davis, A. T. & Dossett, J. H. Host Susceptability in the Foetal Neonatal and Paediatric Age Groups. Proceedings of the International Conference on Nosocomial Infections (1971), pp. 158-63. Report of the Ministry of Health for the Year Ended 31st March 1949. H.M.S.O. (1949), p. 235. Rom, S., Flynn, D. & Noone, P. Anaerobic infection in a neonate. Archives of Disease in Childhood 52: 740-1 (1977).
12
D. A. McSwiggan
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Rooth, G. Transcutaneous oxygen tension measurements in newborn infants. Paediatrics 55: 232-5 (1975). Rowe, B., Giles, C. & Brown, G. L. Outbreak of Salmonella virchow in a maternity hospital. British Medical Journal iii: 561-4 (1969). Schaffer, T. E. Staphylococcal infections in newborn nurseries. Proceedings of the National Conference on Hospital Acquired Staphyloccocal Disease. Washington D.C., U.S. Department of Health Education & Welfare, Publication 60 (1958). Stiver, H. G., Albritton, W. L., Clark, J., Friesen, P. & White, F. M. H. Nosocomial colonisation and infection due to E. coli 0125K70 epidemiologically linked to expressed breast milk feedings. Canadian Journal of Public Health 68: 479-82 (1977). Systems for Control. In Proceedings of the International Conference on Nosocomial Infections (Brachman, P. S. & Eickhoff, T. C., Eds). Waverley Press, Baltimore (1971), pp. 272-317. Szanton, V. L. Epidemic salmonellosis: a thirty month study of eighty cases of Salmonella orianburg infection. Paediatrics 20: 794-808 (1957). Weekly Epidemiological Record. Salmonella Surveillance 49: 258 (1974). Weekly Epidemiological Record. Salmonella Surveillance 52: 285 (1977). Williams, R. E. 0., Blowers, R., Garrod, L. P. & Shooter, R. A. Hospital Infection: Causes and Prevention. Lloyd-Luke, London (1966a), p. 9. Williams, R. E. 0., Blowers, R., Garrod, L. P. & Shooter, R. A. Hospital Infection: Causes and Prevention. Lloyd-Luke, London (1966b), pp. 63-4. Williams, R. E. 0., Blowers, R., Garrod, L. P. & Shooter, R. A. Hospital Infection: Causes and Prevention. Lloyd-Luke, London (1966c), pp. 51-76. Williams, R. E. O. Changing Perspectives in Hospital Infection. Proceedings of the International Conference on Nosocomial Infection (1971), pp. 1-10. Williams, R. E. O. The flux of infection. Proceedings of the Royal Society of Medicine' 69: 797-803 (1976). Williams, R. E. O. Infection and the injured patient: lessons and opportunities. Injury 9: 227-35 (1978). Williams, C. P. S. & Oliver, T. K. Nursery routines and staphylococcal colonisation of the newborn. Paediatrics 44: 640-6 (1969). Williamson, S., Hewitt, J. H., Finucane, E. & Gamsu, H. R. Organisation of bank of raw and pasteurised human milk for neonatal intensive care. British Medical Journal i: 393-5 (1978).
Neonatal and perinatal infection: routes of transmission and prevention
Public Health Laboratory and Department of Microbiology, Central Middlesex Hospital, Acton Lane, London NWIO, England
The changing pattern of infection
No one concerned with the problems of neonatal infection can fail to be impressed by the remarkable sequential changes in its principal aetiology which have taken place during the last four decades (Figure 1). The ~-haemolytic streptococcus, once the scourge of maternity hospitals, has now virtually ceased to be a problem (Williams, Blowers, Garrod & Shooter, 1966). Its place was taken by the staphylococcus (Schaffer, 1958) which monopolized nursery infections, as it did all hospital infections, for nearly two decades to be itself replaced by the Gram-negative bacilli (Williams, 1971). Escherichia coli has now been joined by the Group B streptococcus as the principal cause of major neonatal sepsis (Jeffery, Mitchison, Wigglesworth & Davies, 1977) and there is already some indication that anaerobic organisms may be about to play an increasing role in this condition (Leading Articles, 1978a, b and c). It is easier, however, to record these changes than to explain why they have occurred. Yet nothing could be more fundamental to the question of prevention and control. Has the infectivity pattern changed because of the numerous preventive measures (often costly and time consuming) imposed in many hospitals, or does it reflect biological changes, as yet poorly understood, in the organisms themselves? Before considering this question, it is necessary to ask an even more fundamental question: why does infection occur at all? For the first half of this century the quest for the answer to this question would have been directed almost entirely at the organism. However, we are now more aware that whether or not infection occurs-as distinct from colonization-depends on the outcome of an interaction between the organism and its host, and that there are a number of important determinants on either side of this equation which affect this outcome (Table I). The newborn infant fulfils only too well the main qualifications for increased susceptibility to infection. All neonates are at the extreme of age-sometimes exceptionally so; they are deficient at birth in IgM and IgG, with reduced serum opsonic activity and ability to activate complement. Newborn infants-partIcularly preterm males-are indeed highly susceptible hosts (Quie, Davis & Dosset, 1971; Davies, 1971; Krugman, Ward & Katz, 1977a; Marshall, 1978). Physiological prematurity, resulting in periods of apnoea and oxygen depletion, may itself add to the infection risk; furthermore, it will almost certainly lead to admission 1
0305-7453/79/0A0001 + 12 $01.00/0
© 1979 The British Society for Antimicrobial Chemotherapy
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
D. A. McSwiggan
2
D. A. McSwiggan Figure 1. The changing pattern of neonatal infection.
Group A streptococci ........................................................................................................ . S. aureus ........................... _ _ _ _ _ _ _ .................................................. .
Enterobacteriaciae
Pseudomonas spp. .. .................................................. - - - - - - - - - - - - - -
Group B streptococci ........................................................................... _ _ _ _ _ __ Anaerobes ....................................................................................... _ _ __ ?
1950
1960
1970
1980
_ _ _ Predominant cause of neonatal infection ............ Infrequent cause of neonatal infection
Table I. Some determinants of the hospital infection equation
Host susceptibility factors Immunologically compromised Breached integrity Extremes of age
Microbial infectivity factors Virulence Drug resistance Spreadability Detectability
to a special care or intensive care unit and the employment of invasive life support systems which will jeopardize further the premature infant's vulnerable defences. Although until recently the organism has been considered to play the major role in determining infection, remarkably little is known about what characteristics make a specific organism become, for a particular time, 'leader of the pack' (Williams, 1978). Some types of organisms are inherently more virulent than others; but do they acquire or lose virulence with the passage of time? Do other microbial characteristics matter? The answer to the first question is apparently yes, an organism can lose virulence. This would seem to be the reason for the dramatic decline in the severity of ~-haemolytic streptococcal infections during the late 1930's. Even while he was conducting the Medical Research Council trial of Prontosil at Queen Charlotte's Hospital, Leonard Colebrook commented on the decreasing severity of these infections. He was clearly concerned that this loss of virulence might appear to be responsible for the success due to Prontosil (Colebrook & Kenny, 1936). The answer to the second question is somewhat more speculative but also seems to be in the affirmative. Because it alarms us, we sometimes think of virulence as being an asset to an organism. Of course, the opposite is really the case. For a parasite, such as a staphylococcus, living reasonably harmoniously with its host, the sudden acquisition of virulence is a disaster. Its presence will usually be declared by the sepsis it causes and its potential hosts will try to dissociate themselves from it by the use of antibiotics, disinfectants and segregation. Such an organism would very rapidly face biological eclipse, unless it also possessed two other characteristics-antibiotic resistance and an enhanced ability to spread among hosts. By means of these two additional characteristics it might survive for a sufficient period to lose its virulence and resume its former less remarkable career. Should it have acquired a particularly bad
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
1940
Routes of transmission and prevention
3
Incidence of neonatal infection
Neonatal sepsis is not notifiable and in the absence of a national source of data, opinion on the overall situation is somewhat speculative. Perhaps the nearest thing we do have to national data are the reports to the PHLS Communicable Disease Surveillance Centre (Galbraith, 1977). This unit has recently reported an analysis of neonatal meningitis and bacteraemia and some of the data from this analysis are shown in Table II. The number of cases reported is remarkably small, representing less than one major neonatal infection per reporting laboratory per year. It is clear nevertheless that E. coli and the other Gram-negative bacilli account for more than half these infections. The group-B streptococci however account for a substantial proportion of infections and an even higher proportion of fatal cases, having an overall mortality of 43 %as against 31 %
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
reputation, then a change of name, that is, a shift of phage pattern, would help the organism to become less detectable while rehabilitating itself. This course of events could be put forward to explain the pattern of behaviour of Staphylococcus aureus phage type 80later 80/81. This organism, which began its career in the nursery during the early 50's, soon became widely involved in hospital sepsis generally (Williams, 1976). It eventually subsided into semi-retirement in the 1960's, with a considerable modification to its phage type (Asheshov & Winkler, 1966). Some part of the now predominant role of Gram-negative bacilli in neonatal infections may also be attributable to increased virulence; E. coli possessing the KI antigen accounts for about 80 % of neonatal meningitis (Davies, 1977). There are, however, reasons for believing that a great part of the increase in Gram-negative infection resulted more from changes relating to the population at risk rather than to enhanced virulence of these organisms (Hoffman & Finberg, 1955; Williams, 1971). At the 1970 International Conference on Nosocomial Infection, the section devoted to 'Emerging Pathogens' (1971) made no reference to group-B streptococci, yet within a decade these organisms have become the major cause of neonatal infection, surpassed only by E. coli. What event has taken place to promote this change? The organism itself has long been recognized as an occasional cause of maternal and neonatal infection (Parker, 1977). Has it now acquired a new virulence and an enhanced ability to colonize the maternal bowel and genital tract? The answers to these questions are at present far from clear. As already stated, a predominant role for a 'new' cause of neonatal infection may now be emerging. There has been a considerable number of reports, mainly within the last two years, of nursery infections with anaerobic organisms. A common feature in virtually all cases has been the difficulty in identifying the infecting agent or its toxin (Chin, Leake, Yamanchi, Antony & Guze, 1974; Rom, Flynn & Noone, 1977; Arnon, Midura, Damus, Wood & Chin, 1978; Larson, Price, Honour & Borriello, 1978; Morbidity & Mortality Weekly Report, 1978). It is to be expected that the number of infections (or toxaemias) associated with these organisms will appear to increase with our ability to detect these difficult agents. It thus seems probable that the changes observed in the pattern of neonatal infection over the last four decades have been due in part to the variation in the population at risk, in part due to variation in biological characteristics of the organisms and perhaps in some measure, more recently, to an improvement in our ability to detect previously unrecognized causes for infection and disease in the newborn.
D. A. McSwiggan
4
Table II. Neonatal meningitis: septicaemia
(July 1976-June 1977)
E. coli
Gp. B streptococci S. aureus
Pseudomonas Other GNB Other GPB Other organisms
CSF
Blood
(%)
(%)
40 14 4 8
36 18 16 3 8 12 7
13
2 19
Adapted from P.H.L.S. unpublished data (CDR 77/49).
for E. coli infections. In the United States, the information on neonatal infections on a national basis is somewhat better-if one accepts the inherent limitations of deriving reliable data on hospital infection rates from numerous disparate sources. The National Nosocomial Infection Study (NNIS) has been collecting, analysing and reporting uniformly collected data from about eighty hospitals for nearly a decade. It has the advantage of deriving rates and these have shown remarkably little variation over the period of the study. Some data relating to nursery infections have been extracted (Tables III and IV) from the report for 1976, the last full year for which information is available (Center for Disease Control: National Nosocomial Infections Study Report, 1978). It would seem inadvisable to extrapolate too freely from the American position to the situation in our own hospitals. Indeed, it is clear that the relationship between neonatal bacteraemia and meningitis in the NNIS report differs considerably from that shown in CDSC analysis. Nevertheless, a considerable degree of comparability probably exists. For example, the experience in my own hospital (Table V) does not differ substantially from the American pattern; the similarity in the large proportion of cutaneous and mucocutaneous infections is apparent and the overall infection rate is the same as that recorded for the community-teaching group of hospitals which is the type most closely relating to my own in function. The considerable variation in the infection rate among the Table III. Infection rates per 10,000
discharges 1976 Newborn Cutaneous Bacteraemia Respiratory Surgical wounds Urinary tract Gastrointestinal C.N.S. All sites
%
Adapted from NNIS Report (1978).
61·1 26·3 19·0 8·7 8·0 4·6 4·3 1·5
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
100 100 CSF = 52 isolates Blood = 184 isolates
Routes of transmission and prevention
5
Table IV. Newborn nursery infections Community hospital Community-teaching Federal Municipal or county University
0·9 1·1 0'3 3·1 3'0
All hospitals
1'6
Adapted from NNIS Report (1978).
S. aureus
14 Cutaneous Wound infection Nasal discharge Eye discharge
9
Mucocutaneous
2
2 2 1
C. albieans
2
Strep. pyogenes E. eoli
1 Catheter tip (clinical meningitis)
4
K. pneumoniae N. gonorrhoeae
Meningitis Septicaemia Urinary infection 1 Eye discharge 1 Eye discharge
2 1 1
Total 23/2,006 unit discharges (1·1 %) various categories of American hospitals is thought to be related to the proportion of infants receiving intensive care, a feature which is likely to cause similar variation in rates among hospitals in this country and which underscores the problem of extrapolation from data from a small number of specialized units. One feature from our own results which merits comment is the absence of group-B streptococci from the table. Despite the fact that this organism is isolated regularly from routine specimens from infants admitted to the Special Care Baby Unit we have not during an eighteen month period been able to incriminate it in a specific infection. The NNIS has not yet published an analysis of the various organisms involved in its nursery infections. Such information would be of great interest as it would chart quantitatively the changes in the pattern of neonatal infection over the last decade. Routes of infection
In the prenatal period infecting organisms may reach the fetus via the maternal blood supply. This route of infection is particularly important in view of the increasing concern over the part played by viruses in fetal abnormalities (Hanshaw & Dudgeon, 1978). Instrumentation of the uterine cavity is an uncommon but documented route of introducing infection to the fetus (National Registry for Amniocentesis Study Group, 1976). However, ascending infection, caused by organisms normally present in the maternal genital tract, probably constitutes the commonest hazard of infection in the perinatal
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Table V. Infections in the nursery and special care baby unit (Central Middlesex Hospital-IS month Survey)
6
D. A. McSwiggan
Prevention and control Many of the preventive measures in use today have not been put to the test of controlled trials. It would seem that the fall in infection which coincided with the introduction of
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
period. Although infection may occur through intact membranes (Gamsu, 1973) it is following rupture that the risk of infection is greatest. Lanier, Scarbrough, Fillingam & Baker (1965) have shown that the risk increases directly with the time to delivery and is probably at a maximum by 24 h. At birth and thereafter the importance of the human carrier as a major source of pathogenic organisms cannot be overemphasized. Birth canal, skin, nose and bowel of mother, nursery personnel and other infants are commonly colonized-and indeed sometimes infected-with organisms which have given rise to nursery epidemics and sporadic neonatal infections (Szanton, 1957; Williams, Blowers, Garrod & Shooter, 1966c; Eisenach, Reber, Eitzman & Baer, 1972; Parker, 1977). On the other hand it is clear that the majority of neonates become colonized, sometimes with apparently pathogenic organisms (Krugman, Ward & Katz, 1977b) without becoming clinically infected. Whatever the source, the hands of the attendants appear to be by far the most important means of transmitting infection to the newborn. This is hardly surprising if we remember that 'the hands which move soiled napkins and bedding are the hands that feed and minister' (Davies, 1971). Indeed transmission of infection to the newborn by nurses' hands (and prevention by handwashing) is one of the few instances where the epidemiological process concerned has been properly demonstrated by a controlled trial (Mortimer, Wolinsky, Gonzaga & Rammelkamp, 1966). Although airborne transmission in the general nursery is relatively unimportant as a cause of infection (Mortimer et al., 1966) the microenvironment of the incubator presents a very different situation almost entirely due to the production of infected aerosols arising from contaminated nebulisers and humidifiers. Only resuscitators, among labour ward and nursery equipment present a hazard of such proportions (for references see Center for Disease Control: National Nosocomial Infections Study Quarterly Report, 1973). Infected disinfectants are perhaps 'runners-up' to humidifying and resuscitating equipment as sources of Gram-negative infections in hospitals generally. These substances have been shown to harbour a large variety of Gram-negative bacilli often multiplying in the fluid itself or in the cork or bottle liners (Center for Disease Control: National Nosocomial Infections Study Quarterly Report, 1974 lists thirty references.) Constant vigilance is therefore advizable wherever disinfectants are in use (see below-surveillance). Milk is a particularly good medium for bacterial multiplication and contaminated milk or milk products have resulted in outbreaks in the population often involving predominantly babies and infants (Weekly Epidemiological Record 1974, 1977). When such infection is introduced into the nursery a disastrous situation may arise (Ensign & Hunter, 1946). It must be recognized however that in this type of situation, spread within the nursery may be via the hands of infected or colonized staff. Although the nursery milk kitchen itself is rightly considered a potentially dangerous area (Lowbury, Ayliffe, Geddes & Williams, 1975) the lack of documentary evidence for nursery infections arising directly from infected feeds would seem to suggest that this type of occurrence is extremely rare. It is perhaps somewhat paradoxical that several recent nursery outbreaks associated with feeds have been related to contaminated expressed breast milk and not formula feeds (Center for Disease Control: National Nosocomial Infection Study Report 1978; Stiver, Albritton, Clark, Friesen & White, 1977.)
Routes of transmission and prevention
7
Surveillance It seems desirable to have some system for collecting relevant data on the endemic
infection situation in order to determine as soon as possible any significant change in the pattern. There are various views on how surveillance should be organized (see Systems for Control, 1971 for discussion) but little evidence of their effectiveness (Morbidity & Mortality Weekly Report, 1978.) The surveillance scheme in use at Central Middlesex Hospital is based on five activities (Table VI). First and most important, the medical laboratory staff or the Control of Infection (C.L) Nurse visit the wards to investigate any infection which seems to be hospital-acquired immediately it comes to attention. Second, a daily summary oflaboratory reports is passed to the C.L Nurse who scrutinizes them for any sign of 'clustering' of similar isolates which might indicate that something potentially undesirable is going on. Its third function is to ensure that patients or staff identified as particular infection hazards are properly segregated. This may entail isolation for the mother or infant and suspension from patient care for nursing staff, until considered no longer a hazard (see below with reference to salmonella screening). Bacteriological sampling of the environment is of very limited value in the prevention of infection and is generally to be discouraged (Center for Disease Control: National Nosocomial Infections Study Report, 1974). It may be desirable, however, to monitor on a regular basis certain high risk environmental sources such as humidifiers, when in use, to ensure that decontamination is satisfactory; 'in use' tests of disinfectants should be carried out on a regular basis (Maurer, 1974). The fifth function of surveillance is to check that the preventive measures which have been agreed are actually being carried out; to teach and to update and revise them in accordance with the changing pattern of events.
Table VI. A system of surveillance activity 1. Direct clinical enquiries relating to an infection.
2. 3. 4. 5.
Ongoing survey of laboratory reports supplemented by ward enquiries when indicated. Monitoring microbial screens on patients and staff. Minimal environmental sampling of selected areas e.g. humidifiers, disinfectants. Teaching and monitoring control procedures.
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
control measures was taken as sufficient evidence of their effectiveness. There is now more awareness that the preventive measures taken may have had little (and in some cases nothing) to do with the reduction in infection. Conscious of the need for more information on what measures are really effective the Center for Disease Control, Atlanta has organized a study, the SENIC Project, to determine effectiveness of infection control measures (Morbidity & Mortality Weeldy Report, 1978). Unfortunately, it may be some time before this project provides the information on which to base well founded control programmes. For the present therefore, such preventive measures we choose to advocate should be based on sound principles, common sense and be relevant to the local current situation. It has been said that nurses' time is our scarcest commodity (Parker, 1971). We must look most critically, therefore, at those time consuming and restrictive control procedures which are most extravagant in this regard.
8
D. A. McSwiggan
Preventive measures
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Surveillance alone will not stop perinatal and neonatal infections occurring, nor prevent their spread should they occur. More active measures are required. However optimistic we may feel about the effectiveness of such measures, it is probably advisable to assume that they will not be successful on every occasion. As the nursery provides a particularly susceptible population should an epidemiologically inclined organism gain access, it seems reasonable to reduce the number exposed to risk to the minimum. This can be achieved by rooming-in newborns with their mothers, by having several small nurseries rather than one larger or by cohorting infants (Williams, Blowers, Garrod & Shooter, 1966b). Salmonella introduced into the nursery or special care unit via a maternal excretor can result in serious illness among neonates (Rowe, Giles & Brown, 1969). It is our practice to screen, for salmonella excretion, women between the thirty-eighth and thirty-ninth week of pregnancy. Those found to be excreting salmonella are eventually admitted for confinement in isolation and special precautions taken concerning the infant. It is not possible to calculate quantitively the benefits of this programme. However it identifies annually about six or more salmonella excretors (including recently, a very profuse excretor of S. typhi) while the burden on the laboratory is comparatively insignificant in terms of the number of stool specimens examined from other sources. Such a screening programme might well be unsuitable for maternity units with a different type of laboratory facility. The benefits to the fetus and newborn of treating maternal infection are possibly best demonstrated by the virtual eradication of congenital syphilis in this country. By 1968 congenital syphilis had dropped to 4~;'; of its rate at the inception of the national health service, nearly five times greater than the fall in (adult) acquired syphilis during the same period (Annual Report, 1969; Report, 1949.) A major part of this achievement can be attributed to the identification of infected mothers and their effective treatment during routine antenatal care. Obstetric intervention to prevent prolonged labour is now standard practice. In circumstances where membranes have been ruptured for 12 h without onset of labour a decision should be made to terminate labour within the next 12 h (Lanier et at., 1965) unless gross prematurity presents a greater risk than infection. At the present time the most important single measure in the prevention of neonatal infection is handwashing between each infant handling. What should be used to wash hands may still be a matter for debate, but there can be little doubt that handwashing itself is a significant measure in reducing neonatal sepsis (for full discussion and references see Center for Disease Control: National Nosocomial Infections Study Report, 1975). The use of masks and gowns, on the other hand, has been shown to make little or no difference to nursery infection rates (Williams & Oliver, 1969). The danger associated with certain types of equipment, particularly nebulisers, humidifiers and resuscitators has already been mentioned. Nebulizers are probably better not used. Many units, my own included, run incubators without humidification, humidifiers being used only when oxygen is administered. When humidifiers are in use they should be decontaminated daily. If detachable they should be autoclaved, otherwise they should be emptied completely, cleaned with detergent, dried and refilled with sterile water (Center for Disease Control: National Nosocomial Infections Study Report, 1973). Tubing and traps on resuscitators should be changed and autoclaved after every use.
Routes of transmission and prevention
9
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
It is established practice to require surgical instruments and equipment to be sterile. Should we accept a lower standard for certain 'disposable' items (such as fetal monitoring electrodes) in order to allow their re-use? Resterilizing such items without commercial facilities is usually not practical; autoclaving is likely to destroy or distort plastics or interfere with conductivity of electrical equipment. Chemical disinfection cannot be relied upon to sterilize and the degree of decontamination achieved is very difficult to monitor. It is usually cheaper, in the long term to treat disposables-however expensiveas disposable. With the general availability of commercial ready-to-use sterile feeds the hazards, potential or real, of the nursery kitchen should now be virtually eliminated. The product should be supplied to each mother together with a sterile teat and she should assemble the feed herself. As already referred to in a different context, it is somewhat paradoxical that today's problems appear to relate more to human milk feeds than to artificial feeds. Expressed breast milk (EBM), despite some doubts about nutritional adequacy (Davies, 1977; Fomon & Ziegler, 1977) has been advocated for preterm infants because it is believed to provide protection against infection. The protective effect appears to be found in both the cellular element (Pitt, 1976; Goldman, 1977) and in the aqueous phase (Bullen, 1977). It seems possible to collect breast milk from an infant's mother under conditions which permit it to be stored at 4"C and provide it in feeds for her own child without further treatment for up to 24 h. However, donor milk usually requires freezing and at least a proportion of it pasteurizing also (Williamson, Hewitt, Finucane & Gamsu, 1978) before being fed to 'foreign' infants. It is claimed that these two processes seriously reduce the EBM's protective value; the cellular protection being destroyed by freezing (Ford, Law, Marshall & Reiter, 1977) and the humoral protective element considerably reduced by pasteurization (Evans, Ryley, Neale, Dodge & Lewarne, 1978). Information is required to determine the value of frozen and pasteurized milk on the one hand and on the other, the practicality and acceptability of using unfrozen, unpasteurized donor EBM. Until these problems have been investigated more fully, a caution against extending donor EBM services in United States hospitals has come from the Center for Disease Control, Atlanta. A full discussion on this subject can be found in the Center of Disease Control: National Nosocomial Infections Study Report (1978) and in the report of the Second Workshop by Fomon (1977). It has been asked 'Is intensive care becoming too intensive?' ('JFL', 1977). Undoubtedly there are infants whose best hope of survival will depend on such care. There are, however, others where the benefit must be carefully balanced against the risks inherent in the more aggressive forms of special care. Many of these preterm neonates are being virtually committed to infection as a result of the often multiple invasion of their exterior defences by monitoring and life support apparatus. Perhaps one hopeful sign in this field is the recent interest in the development of non-invasive techniques for both prenatal and postnatal monitoring (Rooth, 1975; Cooke, Rolse & Howat, 1977.) Finally it is prudent to remember that infection in the nursery travels both ways. This is perhaps of most particular importance for female doctors and nurses who may be (unknowingly) in close contact with infants with congenital rubella, who may be heavy excretors of virus. It is advisable that all staff in contact with infants have their rubella status determined and those not immune should be vaccinated.
10
D. A. McSwiggan Acknowledgement
I am indebted to the Director of the Communicable Disease Surveillance Centre for permission to use the data in Table II.
References
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Annual Report of the Chief Medical Officer of the Department of Health & Social Security for the Year 1968. H.M.S.O. (1969), p. 258. Arnon, S. S., Midura, T. F., Damus, D., Wood, R. M. & Chin, J. Intestinal infection and toxin production of Clostridium botulinum as one cause of sudden infant death. Lancet i: 1273-6 (1978). Asheshov, E. H. & Winkler, K. C. Staphylococcus aureus strain of the '52, 52A, 80, 81,' Complex. Nature 209: 638-9 (1966). Bullen, J. J. Human milk and gut infection in the newborn. British Journal of Hospital Medicine 18: 220-31 (1977). Center for Disease Control: National Nosocomial Infections Study Quarterly Report, Third Quarter 1972, issued 1973. Recommendations for the Decontamination and Maintenance of Inhalation Therapy Equipment (1973), pp. 12-17. Center for Disease Control: National Nosocomial Infections Study Quarterly Report, First and Second Quarters 1973, issued 1974. Statement on Microbiologic sampling in the Hospital (1974), pp. 18-20. Center for Disease Control: National Nosocomial Infections Study Quarterly Report, Fourth Quarter 1972, issued 1974. Disinfectant or Infectant: The Label Doesn't Always Say (1974), pp.18-23. Center for Disease Control: National Nosocomial Infections Study Quarterly Report, Third and Fourth Quarters 1973, issued 1975. Personal Handwashing Practices for the Prevention of Nosocomial Infections (1975), pp. 19-28. Center for Disease Control: National Nosocomial Infections Study Report Annual Summary 1976, issued 1978. Reported Nosocomial Infections, 1976 (1978), pp. 1-10. Center for Disease Control: National Nosocomial Infections Study Report Annual Summary 1976, issued 1978. Nosocomial Salmonellosis in Infants Associated with Consumption of Contaminated Human Milk: A Report of Two Outbreaks (1978), pp. 14-15. Center for Disease Control: National Nosocomial Infections Study Report Annual Summary 1976, issued 1978. Human Milkfor Feeding Premature Infants: Benefits, Risks and Precautions for a Donor Program (1978), pp. 16-18. Chin, A. W., Leake, R. 0., Yamanchi, T., Antony, B. F. & Guze, L. B. The significance of anaerobes in neonatal bacteraemia. Paediatrics 54: 736-45 (1974). Colebrook, L. & Kenny, M. Treatment with prontosil of puerperal infections due to haemolytic streptococci. Lancet ii: 1319-22 (1936). Cooke, R. W. I., Rolse, P. & Howat, P. A technique for the non-invasive estimation of cerebral blood flow in the newborn infant. Medical Engineering Technology 1: 263-6 (1977). Davies, D. P. Adequacy of expressed breast milk for early growth of preterm infants. Archives of Disease in Childhood 52: 296-301 (1977). Davies, P. A. Bacterial infections in the foetus and newborn. Archives of Disease in Childhood 46: 1-27 (1971). Davies, P. A. Neonatal Bacterial Meningitis. British Journal of Hospital Medicine 18: 425-34 (1977). Eisenach, K. D., Reber, R. M., Eitzman, D. V. & Baer, H. Nosocomial infections due to kanamycin resistant R-factor carrying enteric organisms in an intensive care nursery. Paediatrics 50: 395-402 (1972). Emerging Pathogens. In Proceedings of the International Conference on Nosocomial Infections (Brachman, P. S. & Eickhoff, T. c., Eds). Waverley Press, Baltimore (1971), pp. 103-56. Ensign, P. R. & Hunter, C. A. An epidemic of diarrhoea in the newborn nursery caused by a milkborne epidemic in the community. Journal of Paediatrics 29: 620-8 (1946).
Routes of transmission and prevention
11
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Evans, T. J., Ryley, W. C., Neale, L. M., Dodge, J. A. & Lewarne, V. M. Effect of storage and heat on antimicrobial proteins in human milk. Archives of Disease in Childhood 53: 239-41 (1978). Fomon, S. J. Human milk.in premature infant feeding: report of second workshop. American Journal of Public Health 67: 361 (1977). Fomon, S. J. & Ziegler, E. E. Protein intake of premature infants: interpretation of data. Journal of Paediatrics 90: 504-6 (1977). Ford, J. E., Law, B. A., Marshall, V. M. E. & Reiter, B. Influence of the heat treatment of human milk on some of its protective constituents. Journal of Paediatrics 90: 29-35 (1977). Galbraith, N. S. National centre for surveillance and control of communicable disease. Proceedings of the Royal Society of Medicine 70: 889-93 (1977). Gamsu, H. Intrauterine bacterial infections. In Intrauterine infections. Ciba Foundation Symposium 10. New Series, Amsterdam Associated Medical Publishers (1973), pp. 135-46. Goldman, A. S. Human milk, 1eucocytes and immunity. Journal of Paediatrics 90: 167-8 (1977). Hanshaw, J. B. & Dudgeon, J. A. Viral Diseases of the Foetus and Newborn. WBS Saunders, Philadelphia, London and Toronto (1978). Hoffman, M. A. & Finberg, L. Pseudomonas infections in infants associated with high humidity environments. Journal of Paediatrics 46: 626-30 (1955). Jeffery, M., Mitchison, R., Wigglesworth, J. S. & Davies, P. A. Early neonatal bacteraemia. Archives oj Disease in Childhood 52: 683-6 (1977). 'JFL' Is intensive care becoming too intensive? Paediatrics (Neonatology Supplement) 59: 1064-5 (1977). Krugman, S., Ward, R. & Katz, S. L. Sepsis in the newborn. In Infectious Diseases of Children. Mosby, St. Louis (1977a), pp. 194-205. Krugman, S., Ward, R. & Katz, S. L. Sepsis in the newborn: In Infectious Diseases of Children Mosby, St. Louis (1977b), pp. 199. Lanier, L. R., Scarbrough, R. W., Fillingim, D. W. & Baker, R. E. Incidence of maternal and foetal complications associated with rupture of the membranes before onset of labour. American Journal of Obstetrics and Gynaecology 93: 398-404 (1965). Larson, H. E., Price, A. B., Honour, P. & Borriello, S. P. Clostridium difficile and the Aetiology of Pseudomembranous Colitis. Lancet i: 1063-8 (1978). Leading Article. Necrotising enterocolitis. British Medical Journal i: 132 (1978a). Leading Article. Pseudomembranous colitis. Lancet i: 1080-1 (1978b). Leading Article, A new role for botulism. Lancet i: 1295-6 (1978c). Lowbury, E. J. L., Ayliffe, G. A. J., Geddes, A. M. & Williams, J. D. Control of Hospital Infection. A Practical Handbook. Chapman & Hall, London (1975), pp. 239-41. Marshall, W. C. The (L;-:elopment of immune mechanisms in the foetus and newborn. In Viral Diseases of the Foetus and Newborn. (Hanshaw, J. B. & Dudgeon, J. A., Eds) WBS Saunders, Philadelphia, London & Toronto (1978), pp. 259-77. Maurer, I. M. Hospital Hygiene. Arnold, London (1974), pp. 74-9. Morbidity and Mortality Weekly Report Vol. 27. Infection surveillance and control programs in U.S. hospitals: an assessment (1978), pp. 139-45. Morbidity and Mortality Weekly Report Vol. 27. Follow-up on infant botulism (1978), pp. 17-23. Mortimer, E. A., Wolinsky, E., Gonzaga, A. J. & Rammelkamp, C. H. Role of Airborne Transmission in Staphylococcal Infections. British Medical Journal i: 319-22 (1966). National Registry for Amniocentesis Study Group. Journal of the American Medical Association 236: 1471-6 (1976). Parker, M. T. Current national patterns. Proceedings of the International Conference on Nosocomiaiinfections (1971), pp. 35-41. Parker, M. T. Neonatalstreptococcalinfections.Postgraduate Medical Journal53: 598-605 (1977). Pitt, J. Breast milk leucocytes. Paediatrics 58: 769-70 (1976). Quie, P. G., Davis, A. T. & Dossett, J. H. Host Susceptability in the Foetal Neonatal and Paediatric Age Groups. Proceedings of the International Conference on Nosocomial Infections (1971), pp. 158-63. Report of the Ministry of Health for the Year Ended 31st March 1949. H.M.S.O. (1949), p. 235. Rom, S., Flynn, D. & Noone, P. Anaerobic infection in a neonate. Archives of Disease in Childhood 52: 740-1 (1977).
12
D. A. McSwiggan
Downloaded from http://jac.oxfordjournals.org/ at RMIT University Library on July 13, 2015
Rooth, G. Transcutaneous oxygen tension measurements in newborn infants. Paediatrics 55: 232-5 (1975). Rowe, B., Giles, C. & Brown, G. L. Outbreak of Salmonella virchow in a maternity hospital. British Medical Journal iii: 561-4 (1969). Schaffer, T. E. Staphylococcal infections in newborn nurseries. Proceedings of the National Conference on Hospital Acquired Staphyloccocal Disease. Washington D.C., U.S. Department of Health Education & Welfare, Publication 60 (1958). Stiver, H. G., Albritton, W. L., Clark, J., Friesen, P. & White, F. M. H. Nosocomial colonisation and infection due to E. coli 0125K70 epidemiologically linked to expressed breast milk feedings. Canadian Journal of Public Health 68: 479-82 (1977). Systems for Control. In Proceedings of the International Conference on Nosocomial Infections (Brachman, P. S. & Eickhoff, T. C., Eds). Waverley Press, Baltimore (1971), pp. 272-317. Szanton, V. L. Epidemic salmonellosis: a thirty month study of eighty cases of Salmonella orianburg infection. Paediatrics 20: 794-808 (1957). Weekly Epidemiological Record. Salmonella Surveillance 49: 258 (1974). Weekly Epidemiological Record. Salmonella Surveillance 52: 285 (1977). Williams, R. E. 0., Blowers, R., Garrod, L. P. & Shooter, R. A. Hospital Infection: Causes and Prevention. Lloyd-Luke, London (1966a), p. 9. Williams, R. E. 0., Blowers, R., Garrod, L. P. & Shooter, R. A. Hospital Infection: Causes and Prevention. Lloyd-Luke, London (1966b), pp. 63-4. Williams, R. E. 0., Blowers, R., Garrod, L. P. & Shooter, R. A. Hospital Infection: Causes and Prevention. Lloyd-Luke, London (1966c), pp. 51-76. Williams, R. E. O. Changing Perspectives in Hospital Infection. Proceedings of the International Conference on Nosocomial Infection (1971), pp. 1-10. Williams, R. E. O. The flux of infection. Proceedings of the Royal Society of Medicine' 69: 797-803 (1976). Williams, R. E. O. Infection and the injured patient: lessons and opportunities. Injury 9: 227-35 (1978). Williams, C. P. S. & Oliver, T. K. Nursery routines and staphylococcal colonisation of the newborn. Paediatrics 44: 640-6 (1969). Williamson, S., Hewitt, J. H., Finucane, E. & Gamsu, H. R. Organisation of bank of raw and pasteurised human milk for neonatal intensive care. British Medical Journal i: 393-5 (1978).
