i) CMV is an RNA virus

ii) It is the most common intra-uterine infection

iii) Congenital CMV can be caused by maternal primary infection or reactivation and both are of the same severity

iv) The incidence of primary CMV infection acquired during pregnancy is 5–10%

v) Primary CMV infection is associated with a 40% risk of congenital CMV infection

vi) At least 50% of infected infants will show clinical signs at birth

vii) There is a 20% mortality associated with symptomatic congenital CMV

viii) Infants can become infected by breast feeding if the mother is seropositive.

vii) What treatment options are available?

i) It is a large double stranded DNA virus

ii) It is a small single stranded DNA virus

iii) It replicates in rapidly dividing cells

iv) Approximately 25% of adults show evidence of a previous infection

v) A rash and arthralgia occur in the second phase of the illness. At this point, the child is still infectious

vi) The more severe the infection in a pregnant woman, the more severe the fetal infection

vii) If parvovirus B19 infection occurs during pregnancy, the majority of fetuses will be affected

viii) The outcome of the fetus depends on the point at which the infection occurred in pregnancy.

i) Congenital CMV

ii) Congenital toxoplasmosis

iii) Congenital Epstein–Barr virus

iv) Congenital varicella

v) Congenital rubella

vi) Congenital herpes

vii) Congenital TB.

i) The risk of congenital infection remains constant throughout pregnancy

ii) The risk of congenital infection is up to 90% in the third trimester

iii) Congenital infection is more severe if maternal infection is acquired in the third trimester

iv) In the UK, about 60% of women are sero-positive

v) Congenital infection occurs in 1 in 100 exposed babies

vi) Increasing gestational age at seroconversion is associated with an increased risk of mother-to-child transmission

vii) CSF will show a lymphocytosis

viii) Toxoplasmosis cannot be treated

ix) If diagnosed antenatally in the first trimester the mother can be treated with pyrimethamine and sulfadiazine to decrease the risk of fetal infection

x) If there are no eye signs within the first year of birth, the infant is unlikely to develop ocular problems.

vi) What do you do now?

vii) What does this result mean?

viii) Which of the following treatments would you consider?

i) Admit the baby to the NICU for observation

ii) Admit the baby to the NICU for observation and routine surface swabs

iii) Admit the baby to the NICU for a septic screen (blood cultures, FBC and CRP) and await results before considering antibiotics

iv) Admit the baby to NICU, perform septic screen and start antibiotics

v) Reassure and discharge home

vi) Allow to go home with instructions if the baby becomes unwell to seek medical advice

vii) Discuss with the mother and say that she must stay in and the baby must be observed for a further 24 hours

viii) Observe the baby for another 12 hours; allow to go home with instructions if the baby becomes unwell to seek medical advice.

i) Reassure the mother that no treatment is needed

ii) Reassure mother but isolate baby in side room

iii) Check the mother and baby’s immune status and then give VZIG to both

iv) Check the mother’s immune status and if negative give her VZIG

v) Check the baby’s immune status and if negative give the baby VZIG

vi) Give the baby and mother VZIG

vii) Give the baby VZIG and aciclovir.

i) Bacillus fragilis

ii) Bacillus cereus

iii) Bacteroides fragilis

iv) Campylobacter jejuni

v) Haemophilus influenzae

vi) Proteus mirabilis

vii) Salmonella typhi

viii) Group B streptococcus (GBS)

ix) Staphylococcus aureus

x) Klebsiella

xi) Serratia marcescens.

i) Mother is HBsAg negative and HBeAg negative

ii) Mother is HBsAg negative and HBeAg positive

iii) Mother is HBsAg positive and HBeAg negative

iv) Mother is HBsAg positive and HBeAg positive

v) Mother had acute hepatitis during pregnancy

vi) Mother where eAg and eAb status are unknown.

i) Describe the skin.

ii) What is the diagnosis?

Figure 10.1.

iii) What is the likely organism responsible?

iv) What is the treatment?

v) What is the prognosis?

i) It is a notifiable disease

ii) Causes hydrocephalus

iii) Causes thymic hypoplasia

iv) Causes corneal opacity

v) Causes bony abnormalities

vi) Causes IUGR

vii) Causes microphthalmia

viii) Causes conductive deafness

ix) Causes PDA

x) Causes aortic stenosis

xi) Infection during the first 12 weeks of pregnancy results in congenital infection and/or miscarriage in all cases

xii) Congenital infection can occur if mum is infected during the 2nd trimester

xiii) The infant is extremely infectious in the immediate postnatal period but this is no longer a risk after the first 4 weeks of life

xiv) Rubella is increasing in the immigrant population.

i) What do these test show?

ii) What test do you carry out to confirm this?

iii) What do you do now? Name two things.

iv) Which one test would confirm a diagnosis of congenital syphilis?

v) If the test is negative, what does this show?

vi) What information do you need from the mother?

vii) What other test might be helpful in assessing the risk to the baby?

viii) What do you do?

i) Infected infants should remain in the cots they currently occupy; all staff involved in the care of the baby should adopt barrier nursing procedures

ii) Wearing of sterile gloves avoids the need for repeated hand washing

iii) Infected babies may be nursed by the same member of staff as uninfected infants

iv) Regular skin disinfection is of established benefit in most cases

v) Topical antibiotic ointment should always be used

vi) Use of separate gowns for each baby is an extremely important element of infection control

vii) Screening of all babies and all staff may be implicated

viii) Staffing levels are closely related to the incidence of nosocomial infection, as is the availability of hand washing facilities

ix) Units should be closed to all admissions as soon as the possibility of an outbreak is considered

x) Environmental screening is of no value

xi) Meticulous attention to hand hygiene is by far the most important element in reducing the spread of infection

xii) There is good evidence that standards of hand hygiene are normally very high in neonatal intensive care units

xiii) Soap and water hand wash is more effective than the use of alcohol-based hand rub

xiv) Topical cord care at birth has a major role in reducing the incidence of infection.

i) False – CMV is a DNA virus of the herpes virus group.

ii) True – it affects up to 2.5% of live born infants a year worldwide. In the UK the incidence is approximately 0.2%.

iii) False – fetal infection is more likely to occur and is more severe after primary maternal infection than after reactivation of latent infection. The earlier the infection occurs in pregnancy the worse the outcome. ¹

iv) False – the incidence is thought to be 1–4%.

v) True.²

vi) False – overall, only 10–15% of infected infants show clinical signs at birth but up to 90% of these will develop long-term sequelae. ³

vii) True – reports state mortality ranges between 10% and 30% although much higher in premature infants.

viii) True – in the postpartum period, mother to infant transmission can occur as up to 88% of seropositive mothers shed the virus into their milk. Approximately 50% of these infants will become infected. CMV excretion is usually the result of reactivation in a seropositive mother; most infants will not develop clinical signs due to the presence of maternally derived transplacental antibodies. This is usually a benign and asymptomatic infection.

i) Echogenic bowel, intracranial calcification, cortical dysplasia.

ii) Answers a, b, c, e, g and h are correct. Hepatosplenomegaly and petechiae secondary to thrombocytopenia are relatively common manifestations of congenital CMV in the neonatal period. Jaundice is also common but this is usually a conjugated hyperbilirubinaemia as CMV hepatitis can cause both intrahepatic and extrahepatic bile duct destruction. ⁴ Intracranial manifestations of congenital CMV are microcephaly and periventricular calcification where the infection has caused brain necrosis. Lissencephaly and polymicrogyria can be present depending on the timing of the infection, lissencephaly occurring with an earlier infection. Defective enamelisation occurs in 40% of symptomatic infants at birth and 5% of asymptomatic infants. Inguinal hernias can occur with congenital CMV in male infants although the reason for this is unclear.

iii) Up to 80% of symptomatic newborns will develop sequelae such as mental retardation, cerebral palsy, visual defects and sensorineural hearing loss. Symptoms at birth are associated with a worse prognosis. ⁵

iv) Up to 15% of infants who are asymptomatic at birth will have neurodevelopmental problems and sensorineural (SN) deafness. SN deafness is the most common abnormality seen in congenital CMV infection, occurring in 30–65% of symptomatic infants and up to 15% of asymptomatic infants. It usually develops after the newborn period and tends to be progressive. Cochlear implants have been used successfully.

v) Answer c is correct.

vi) PCR testing on a urine sample needs to be done within the first 3 weeks after birth. If the test is carried out after 3 weeks it is difficult to distinguish between a congenital, perinatal or postnatal infection. Infants infected at birth after exposure to infected secretions during delivery may start shedding virus by 3 weeks of age.

vii) There are currently a few antiviral chemotherapeutic agents, such as ganciclovir and foscarnet, that are available for treatment of serious, life-threatening or sight-threatening CMV in the immunocompromised patients. Cidofovir is also licensed for CMV retinitis. A randomised, controlled multicentre clinical trial investigated the use of ganciclovir for the treatment of infants with congenital CMV infection with evidence of CNS involvement. ⁷ Ganciclovir (or placebo) was given intravenously as an infusion every 12 hours for 6 weeks. The ganciclovir group were significantly more likely to have improved or normal hearing at 6 months of age compared to the placebo group. They also showed improvement in their liver function tests and head circumference. No change in mortality was demonstrated and currently there are no published data on long-term outcome. Ganciclovir is not thought to be beneficial for infants who show severe intracranial pathology antenatally. Several centres in the UK are using a six-week course of intravenous ganciclovir and then switching over to oral valganciclovir, with close monitoring of levels and viral load to assess response. The main side effects of ganciclovir are secondary to bone marrow suppression. Nigro⁸ described a study using CMV specific hyperimmune globulin and found that pregnant women whose amniotic fluid was CMV positive, and who were given passive immunisation, had a lower rate of congenital CMV when compared to a control group. There are currently no randomised trials looking at this preventative treatment.

i) False.

ii) True – it was discovered in 1975 and is a small, singled stranded DNA virus consisting of about 5600 base pairs.

iii) True – it has a predilection for rapidly dividing cells, hence the affinity for erythrocyte precursor cells. A characteristic haemolytic anaemia can occur in the fetus.

iv) False – about 50% of adults show serological evidence of a previous infection with p antigen and are therefore immune.

v) False – there is an incubation period of about 10 days when flu-like symptoms and viraemia occur; 7–10 days after this, the second phase occurs with joint pain and the characteristic rash, but no viraemia. 30% of infections may be asymptomatic.

vi) False – there is no correlation between the severity of maternal infection and fetal infection.

vii) False – the incidence of parvovirus infection in pregnancy is 0.3–3.7%. ⁹ The overall risk of fetal infection is 30–50%. Most fetal infections are self-limited and do not result in adverse outcome. In 1–2% of fetuses with serological evidence of infection, parvovirus will cause abortion, stillbirth or hydrops. Between 10% and 25% of cases of non-immune hydrops are related to parvovirus.

viii) True – around 1 in 10 women infected before 20 weeks of gestation will suffer a fetal loss due to B19. The risk of an adverse outcome of pregnancy after this stage is remote. Infected women can be reassured that the maximum possible risk of a congenital abnormality due to B19 is under 1% and that long-term development will be normal. ¹⁰

i) False.

ii) True – the risk of congenital disease is lowest (10–25%) when maternal infection occurs during the first trimester and highest (60–90%) when maternal infection occurs during the third trimester. The overall risk of congenital infection from acute T. gondii infection during pregnancy is approximately 20–50%. ^{11. and 12.}

iii) False – congenital disease is more severe when infection is acquired in the first trimester.

iv) False – about 30% of women are sero-positive in the UK.

v) False – congenital infection occurs in less than 1 in 1000 infants. ¹³

vi) True – increasing gestational age at seroconversion is strongly associated with increased risk of mother-to-child transmission (OR 1.15, 95% CI 1.12–1.17) and decreased risk of intracranial lesions (0.91, 0.87–0.95), but not with eye lesions (0.97, 0.93–1.00). ¹⁴

vii) True – the CSF will show raised protein, lymphocytosis and tachizoites (cysts of T. gondii). PCR on the CSF will confirm the diagnosis.

viii) False – infants with congenital toxoplasmosis should be treated for a year to avoid adverse outcomes. They should be given spiramycin for 4–6 weeks, alternating with 3 weeks of pyrimethamine and sulfadiazine, beginning shortly after birth and continuing for 12 months. The medications are synergistic against toxoplasma. A recent study¹⁵ showed that in infants with moderate or severe neurological disease at birth, more than 72% had normal neurological and/or cognitive outcomes, if treated, and none had sensorineural hearing loss. 91% of children without substantial neurological disease and 64% of those with moderate or severe neurological disease at birth did not develop new eye lesions. All children without substantial neurological disease at birth who received treatment had normal cognitive, neurological and auditory outcomes.

ix) False – the mother can be treated antenatally if infection is diagnosed by PCR of the amniotic fluid. The treatment is with spiramycin as pyrimethamine and sulfadiazine are contraindicated in the first trimester as pyrimethamine is a folate antagonist. Spiramycin is a macrolide antibiotic.

x) False – in a recent study 24% of children developed retinal lesions over a six-year follow-up period. In only 11% was a diagnosis of retinochoroiditis made during the first month of life and half of the lesions were diagnosed after 1 year of age. The delay in onset of lesions is an important consideration when counselling families. ¹⁶

i) The baby should be resuscitated using an ABC approach and taken to the neonatal unit for ongoing care and management.

ii) Ask about possible events that may make infection more likely. Was there prolonged rupture of membranes? Did the mother have any episodes of raised temperature? If there have been any previous pregnancies were any infants treated for infection? Ask about UTIs (these are important risk factors for neonatal sepsis) as well as increasing the risk of premature birth, pre-eclampsia and low birth weight infants. ¹⁷

iii) Blood culture, urine culture, FBC, CRP and CXR. Blood culture is the definitive test. The majority of blood cultures taken will grow in 48 hours if they are going to be positive. The majority of neonatal infections are associated with a bacteraemia and thus a positive blood culture. Urine culture is an important investigation if sepsis is suspected. The drawback with urine analysis and culture is obtaining the specimen. If a baby is unwell and presumed septic, the easiest way to obtain a sample is by suprapubic aspiration of urine. This avoids the contamination which happens in the majority of bag urine specimens. If a bag urine specimen is thought to be positive, it must have at least 150 white cells/mm ³ and a pure growth of more than 10 ⁵ organisms/mL urine. Be wary of any organisms other than E. coli or a mixed growth. If this is the case, an SPA will have to be obtained to confirm the infection.

A full blood count itself is not very useful. However a differential white count is of help. A low neutrophil count, <2.0–2.5×10 ⁹/L in the first 2 days of life, suggests that there is a bacterial infection. After this time, either neutropenia or neutrophilia (>7.5–8.0×10 ⁹/L) may occur. Other helpful markers of infection may be the ratio of immature to total number of neutrophils. The maximum acceptable ratio for excluding sepsis during the first 24 hours is 0.16. In most newborns, the ratio falls to 0.12 within 60 hours of life. An I/T ratio of >0.2 has been shown to be a good marker for infection. As well as being used in early onset sepsis, an I/T ratio >0.16 differentiated between Gram-positive, Gram-negative and fungal infections ( p=0.007) in late-onset infections. The sensitivity of the I/T ratio is in the range 60–90%, and elevations may be observed with other physiological events, limiting the positive predictive value of these ratios. An elevated I/T ratio should be used in combination with other signs when diagnosing sepsis. ¹⁸

C-reactive protein is a good indicator of infection if serial measurements are made and the trend analysed. It is better than white blood cell indices as an infection marker. It takes a few hours to rise and therefore should not be used to decide when to start antibiotics. Culture-proven sepsis is unlikely if the CRP does not rise within 48 hours of the onset of the illness, and thus it is generally safe to stop antibiotics if the cultures are negative and the CRP is normal at 48 hours. ¹⁹

All infants with suspected sepsis should have a chest X-ray.

iv) There has been much research and interest into procalcitonin. Procalcitonin (PCT) and C-reactive protein (CRP) concentrations in umbilical cord blood of 197 neonates were measured to evaluate their value as markers of infection. Sixteen of the neonates were infected. The sensitivity and specificity were 87.5% and 98.7% for PCT, and 50% and 97%, for CRP. It seems therefore that serum PCT in cord blood could be a useful and early marker of antenatal infection. ²⁰ Other groups have made similar observations and suggest that a procalcitonin level >2.3 ng/mL or a CRP >30 mg/L indicates a high likelihood for neonatal sepsis, and antibiotic therapy should be continued even in the presence of sterile cultures. ²¹ Research has also shown that a raised interleukin-6 and TNF-alpha are good indicators of early sepsis. ²²

v) After resuscitation, stabilisation and investigations, antibiotics should be given immediately. Most units have policies for which antibiotic to use, but in general for early onset sepsis (which is most likely in this infant’s case) the antibiotics need to cover group B Streptococcus, Listeria and Gram-negative organisms such as E. coli. A combination of a penicillin and gentamicin would be a good choice as there is synergistic action between the two against GBS. Cephalosporins alone will have no coverage for E. coli or Listeria.

vi) Most people in this situation with such a high CRP would carry out a lumbar puncture. If the platelet count was below 50, then a platelet transfusion should be given before the lumbar puncture.

vii) It is unlikely that this baby has meningitis. Generally in meningitis a polymorphonuclear count is >30/mm ³. When blood-stained CSF is obtained, the ratio of red to white cells should be calculated and if there is no infection, the ratio of red to white cells should be more than 500 to 1 (this can be most accurately calculated from the peripheral white cell to red cell ratio). The protein is difficult to interpret as the CSF is heavily blood stained. Without a blood glucose level, it is difficult to interpret the glucose of 1.4 mmol/L in the CSF. The CSF glucose should be at least 50% of the blood glucose level and a level <1.0 mmol/L suggests bacterial meningitis. Ideally a lumbar puncture should be performed prior to starting antibiotics. The one dose of antibiotics that has been given pre lumbar puncture may mean that cultures are less likely to be positive, but a lumbar puncture should still be performed in any baby who is sick with presumed sepsis as the cell count may be highly informative.

viii)

ix)

i) Yes – Bacillus fragilis is a Gram-positive bacillus that does cause osteomyelitis.

ii) No – Bacillus cereus is another Gram-positive bacilli that causes meningitis and pneumonia.

iii) No – Bacteroides fragilis is a Gram-negative bacillus that causes meningitis.

iv) No – Campylobacter jejuni is another Gram-negative bacillus that characteristically causes meningitis and gastroenteritis. It is, like other Gram-negative rods, part of the normal gut flora, but all can cause disease when they reach tissues outside the lumen of the gut.

v) Yes – Haemophilus influenzae is a Gram-negative rod that can cause not only osteomyelitis but pneumonia and meningitis.

vi) No – Proteus mirabilis is a Gram-negative bacillus that causes meningitis and abscesses.

vii) No – Salmonella typhi classically causes gastroenteritis and typhoid fever. This organism is much more common in the developing world.

viii) Yes – group B streptococcus is otherwise known as Streptococcus agalactiae. It is a Gram-positive coccus that can cause infection in most tissues – osteomyelitis, empyema, brain abscess, endocarditis, cellulitis and UTI. It is a commensal of the gut and the vagina and colonises up to a third of pregnant women in the UK. There are nine serotypes, but types I, II and III are responsible for most neonatal infections. The osteomyelitis seen with GBS can be a subtle presentation with only one site being affected. Commonly hip, knee, pelvis and humerus.

ix) Yes – Staphylococcus aureus, a Gram-positive coccus, is associated with a high mortality and morbidity. Some strains are more virulent than others, due to extracellular factors and toxins. It is the primary cause of infection in bones, joints and skin. Pustular skin lesions are classic and there is rapid seeding to bones, joints and lungs. It is a relatively rare cause of meningitis and very rarely a UTI. A clear association has been shown between the severity of bacteraemia and mortality. ⁴⁰ The systemic infection leads to marked neutropenia and thrombocytopenia with a rapidly increasing CRP.

x) No – Klebsiella is a Gram-negative bacillus that causes urinary tract infections and meningitis. Gram-negative bacilli are thought to account for about 20% of cases of late-onset neonatal sepsis and even higher numbers in the developing world. The mortality from systemic infections is extremely high, especially in preterm infants. There is a link between Gram-negative bacilli and the severity of bronchopulmonary dysplasia. ⁴¹

xi) No – Serratia marcescens is an opportunistic Gram-negative bacillus which is often seen in the developed world and typically infects compromised hosts. It commonly causes a septicaemia with associated meningitis, with a high mortality. It has been reported as a causative organism in infected ventriculo-peritoneal shunts. It occurs sporadically in the NICU, primarily in premature infants requiring support, and appears late in their hospital course. There are very occasional cases of neonatal osteomyelitis being caused by Serratia marcescens but affected infants had underlying immunodeficiency disorders. ^{42. and 43.}

i) The baby’s skin shows desquamation which has been provoked by rubbing the skin’s surface. This is called Nikolsky’s sign. This occurs after an initial scarlatiniform rash, which is usually present on the face and in the flexures. If denudation occurs, this is followed by drying of the skin and a further desquamation phase that lasts for a few days. The mucosal surfaces are unaffected.

ii) The diagnosis is staphylococcal scalded skin syndrome, previously known as Ritter’s disease.

iii) The responsible organism is Staphylococcus aureus. The commonest source of infection is an infected umbilical stump.

iv) The infant should be treated with intravenous flucloxacillin.

v) Infants respond extremely well to intravenous antibiotics and the skin heals with no sequelae.

i) Yes – rubella was made a notifiable disease in 1988, and is monitored through clinical and laboratory reports. ⁴⁴

ii) No – toxoplasmosis causes hydrocephalus. Rubella does not. It does cause microcephaly and delayed developmental milestones.

iii) Yes – although this is not present at birth, infants may develop this along with reduced cellular immunity and thyroid autoantibodies. Some infants with congenital rubella do not present in the neonatal period with the well described rubella syndrome including jaundice, thrombocytopenia and hepatosplenomegaly. They present in later life with neurological problems, heart disease, eye defects and deafness.

iv) Yes – corneal opacities are present in congenital rubella.

v) Yes – irregular lucencies in the bone and abnormal trabecular pattern in the long bones. The X-ray appearance is said to resemble a stick of celery.

vi) Yes – one-third of affected babies are growth restricted.

vii) Yes – micro-ophthalmia does occur as well as glaucoma. One study reported that up to 78% of affected infants developed ocular abnormalities and no significant association was found between gestational age at time of maternal infection and the incidence of individual ocular conditions. ⁴⁵

viii) No – conductive deafness does not occur in congenital rubella, it is usually sensorineural deafness and commonly bilateral. These deficits occur in up to 66% of affected infants. ⁴⁶

ix) Yes – cardiac abnormalities, especially PDA, occur in up to 58% of infants.

x) No – aortic stenosis does not occur. Peripheral pulmonary stenosis is a frequent finding and due to viral damage to endothelium of large blood vessels.

xi) No – although the risk of congenital infection is highest in the first trimester, not all infants are affected; approximately 10–20% are not.

xii) Yes – although the incidence decreases with increasing gestation. Congenital rubella is rare after 20 weeks’ gestation.

xiii) No – the infants can continue to shed the virus up to months after delivery and therefore appropriate precautions should be taken with female nursing and medical personnel.

xiv) Yes – despite the incidence of congenital rubella dramatically falling with the introduction of the MMR immunisation programme, there are still cases occurring. The majority of the mothers are from the immigrant population and there is a drive by the World Health Organization to improve the global control of rubella and CRS. ^{45. and 47.}

i) RPR (rapid plasma reagin test) is a non-treponemal serological test and TPHA ( Treponema pallidum haemagglutination assay) is a treponemal test. Both being reactive show that the mother may have syphilis.

ii) You must confirm with a treponemal test that is different from that used in screening such as the treponemal ELISA for IgG and IgM.

iii) You must:

iv) A positive anti-treponemal EIA IgM is consistent with a diagnosis of congenital infection. It should be repeated to confirm.

v) Serology can be negative in babies infected late in pregnancy. A negative IgM should be repeated at 1, 2 and 3 months of age as the IgM response may be suppressed.

vi) It is vitally important to see if the mother has been treated adequately for syphilis to assess the risk to the baby. The baby is at low risk if the mother has been treated fully in this pregnancy starting at least 30 days before the baby was born.

vii) Quantitative non-treponemal serological titres (VDRL/RPR) are useful to assess risk to the baby. If the titres are four-fold higher than the mother’s titres, the infant is at high risk and needs treating. If the titres are the same or less than four-fold the maternal titre, treatment of the infant depends on the adequacy of maternal treatment.

viii) Due to inadequate maternal treatment, the infant needs treating with benzyl penicillin 30 mg/kg IV (50,000 units/kg) 12-hourly for 7 days and then 8-hourly for 10 days treatment in total. Follow-up at three and sixth months and one year with VDRL/RPR is required.

i) False – if several infants are affected by the same organisms, it is more sensible to cohort infants, separating them from uninfected infants. Although this is dependent on available space and staffing, it should always be attempted where highly resistant or highly infective organisms are spreading. Once cohorted, all staff involved in the care of the baby should adopt barrier nursing procedures.

ii) False – the use of gloves may have a role in the reduction of infection, but there is good evidence that scrupulous attention to hand hygiene is of paramount importance.

iii) False – nursing staff should care for segregated cohorts in this situation.

iv) False – there was a vogue for regular skin disinfection in the early years of neonatal care. This policy led to widespread damage of babies, including significant brain damage with the use of hexachlorophene. ⁵⁰

v) False – topical antibiotic therapy may be indicated but should always be targeted toward a specific organism (e.g. Staphylococcal aureus cord infection) and should never be routine and generalised.

vi) False – although the wearing of gowns may contribute to reducing the spread of infection, there is some evidence to suggest that the impact is minimal and other infection control measures are more important. ⁵¹

vii) True – the source of infection often remains unclear but it is advisable to screen other babies to identify asymptomatic carriers. If the means of spread is uncertain, staff screening may sometimes be of value, but must be managed tactfully and diplomatically.

viii) True – staff numbers and the thoroughness of their hand washing have been shown to be very important elements in reducing infection rate. ⁵²

ix) False – although this may be indicated on rare occasions, such a decision should only be taken following advice from microbiology and infection control specialists. Proper barrier nursing and meticulous attention to hygiene should allow a unit to function without having to resort to closure.

x) False – there are documented cases where the source of the infection has been environmental and thus full screening including settle plates may be useful if all other actions fail to identify a source or means of spread.

xi) True.

xii) False – there are published data which suggest that effective hand washing of an appropriately high standard may be performed in little more than 20% of patient contacts. Even more worryingly, there are incidents where hands are not cleansed adequately (or at all) between patients – even when there has been contact with body fluids or excreta. ⁵³

xiii) False – there is now good evidence that the proper use of alcohol-based hand rub between patients is more effective in infection control than the use of soap and water.

xiv) False – there is no evidence that application of sprays, creams or powders is any better than keeping the baby’s cord clean and dry at birth. ⁵⁴