Selective neonatal BCG vaccination—a re-audit

Acta Pædiatrica ISSN 0803–5253

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Selective neonatal BCG vaccination—a re-auditP Venkatesan (vp [email protected]), S Jayakumar, N ShariefBasildon University Hospital NHS Trust, Essex, UK

CorrespondenceDr. P Venkatesan, 22 Upper Abbey Road, BrightonBN2 0AD, UK.Tel: 07886399103 | E-mail:vp [email protected]

Received5 April 2006; revised 5 April 2006; accepted 29May 2006

DOI:10.1111/j.1651-2227.2006.00010.x

Tuberculosis is re-emerging as a global problem. Nearly overa million new cases of Paediatric TB are reported world-wide every year (1). A recent survey shows resurgence andincrease in notification of TB in England and Wales (2). Se-lective neonatal BCG rather than universal immunisationis practised in UK since the 1960s for babies born to par-ents from high-risk ethnic groups (originating from countrieswith TB rate > 40/100 0003) and family history of TB. An au-dit conducted at Basildon & Thurrock area in 2001 revealeda selective neonatal BCG uptake of 85% and recommendedimmunisation before discharge from hospital and commu-nity follow up of missed infants (4).

We conducted a retrospective audit for the year 2003 tomonitor the progress of uptake. The antenatal computer gen-erated a list of infants recommended for BCG and the com-munity child health computer generated a list of immunisedinfants in the year 2003. A total of 364 infants were rec-ommended for selective neonatal BCG during the antenatalvisits comprising 9% of the total births in 2003. The compar-ison of data and telephonic interview with parents showedthat 275 (80%) were immunised, of which 269 (98%) wereimmunised in hospital before discharge whereas 6 (2%) wereimmunised in the community in the post-neonatal period.

Our audit showed an 80% uptake in 2003 (Fig. 1) indi-cating lack of progress of uptake (identified reasons behindnonvaccination are outlined in the figure). There were 47eligible infants who were not offered the vaccine during theantenatal visit but were later identified as eligible and im-munised in hospital, emphasising the usefulness of hospitalcoverage.

Neonatal BCG vaccine has shown a protective efficacy of64% (5) and a much higher protection against miliary andmeningeal tuberculosis (6). Studies show inconsistencies inidentifying ‘at risk’ infants due to complex selection criteriaresulting in low coverage (7), which was evident in our au-dit, especially interracial parentage. Only 40% with familyhistory of tuberculosis were vaccinated on the basis of theirethnic origin and the remaining 60% of white Caucasian ori-gin were missed. Telephonic interview with parents showed

the lack of awareness and knowledge of the vaccine. Re-ports of increased risk of TB in Indian Subcontinent andblack African children even born in UK (8) emphasis theneed for increased vigilance among these groups.

It is clear from two audits performed in the same settingsthat surveillance needs to be improved. Awareness amongparents should be increased by simple measures like offer-ing the BCG leaflet during the initial antenatal visit and ed-ucation of health professionals in identifying ‘at risk’ groups,probably by simplifying the eligibility criteria. Family history

Figure 1 Analysis of vaccination status for year 2003.

C©2006 The Author(s)/Journal Compilation C©2006 Foundation Acta Pædiatrica/Acta Pædiatrica 2007 96, pp. 145–149 145

Selective neonatal BCG vaccination Venkatesan et al.

of TB needs to be prioritised irrespective of the ethnic back-ground. Immunisation in hospital before discharge needs tobe actively encouraged as it becomes quite difficult to trackthe infants in the community due to various reasons likenonattendance to clinics, moving to different areas and lackof updated contact details.

References

1. Raviglione MC, Snider DE Jr, Kochi A. Global epidemiology oftuberculosis. Morbidity and mortality of a worldwide epidemic.JAMA 1995; 273: 220–6.

2. Atkinson P, Taylor H, Sharland M, Maguire H. Resurgence ofpaediatric tuberculosis in London. Arch Dis Child2002;86:264–5.

3. Joint Tuberculosis Committee of the British Thoracic Society.Control and prevention of tuberculosis in the UK: code ofpractice 1994. Thorax 1994;49:1193–200.

4. Bakshi D, Sharief N. Selective neonatal BCG vaccination.Acta Paediatr 2004;93:1–3.

5. Packe GE, Innes JA. Protective effect of BCG vaccination ininfant Asians: a case-control study. Arch Dis Child1988;63:277–81.

6. Rodrigues LC, Diwan VK, Wheeler JG. Protective effect ofBCG against tuberculosis meningitis and miliary tuberculosis:a meta-analysis. Int J Epidemiol 1993;22:1154–8.

7. Deshpande SA. Ethnic differences in the rates of BCGvaccination. Arch Dis Child 2004;89:48–9.

8. Balasegaram S, Watson JM, Rose AMC, et al. A decade ofchange: tuberculosis in England and Wales 1988–98. Arch DisChild 2003;88:772–77.

Cervical mycobacterial lymphadenitis in Swedish children during the post-BCG vaccination eraBjorn Petrini ([email protected])1, Rutger Bennet2

1. Department of Clinical Microbiology Karolinska University Hospital Solna and MTC, Karolinska Institutet, Stockholm, Sweden

2. Department of Pediatrics Astrid Lindgren Chilndrens’ Hospital Karolinska University Hospital Solna, and Karolinska Institutet, Stockholm, Sweden

CorrespondenceB Petrini, Karolinska University Hospital, SolnaSE-17176, Stockholm, Sweden.Tel:+468 51772877 | Fax: +468 308099 |Email: [email protected]

Received19 June 2006; revised 19 June 2006; accepted 26June 2006

DOI:10.1111/j.1651-2227.2007.00043.x

Sir,General BCG vaccination of newborns was practiced in

Sweden from the 1920s, and offered an important protec-tion against disseminated tuberculosis (TB) and meningitisin children. It became established as a children’s vaccina-tion in many European countries during the 1940s. From1975 onwards it was, however, in Sweden replaced by selec-tive vaccination of those whose parents originate from TBhigh-endemic countries, encompassing approximately 15%of all Swedish children. Incidence of cervical lymphadeni-tis caused mainly by Mycobacterium avium-intracellulare-complex (MAC) now became several-fold elevated in thenon BCG-vaccinated children. It rose from 0.06/ 100 000during 1969–1974 to 5.7/100 000 during 1981–1985 (ratio5.9) (1). In line with this, a prospective study in the Nether-lands 2001 through 2003 showed an annual incidence of77 NTM infections per 100 000 children (2). However, in-creasing frequency has been reported also from countrieswhere general BCG vaccination was never practiced, such asCanada, where the incidence of NTM infections in children

almost doubled from 1990–1999 to 2000–2004 (3). Duringthe 1990s, improved species diagnosis of NTM became feasi-ble, for example by 16S rDNA sequencing. Several less com-mon or new species causing lymphadenopathy in childrenwere described (4).

We have compared culture positive cervical lymphadeni-tis caused by mycobacteria in children attending the AstridLindgren Children’s Hospital, Karolinska University Hos-pital, Solna, during 1989–1993 and 2000 through 2004. Inthe catchment area of approximately 1.7 million inhabitants,MAC was by far the most common mycobacterial finding incervical lymph node infection. M. malmoense, not uncom-mon in Scandinavia, accounted for fewer isolates, and M.tuberculosis was rare, observed only in two non-Europeanchildren and BCG in one.

Specific culture on fine-needle biopsy aspirate from sus-pected mycobacterial lymphadenitis is a valuable tool foretiological diagnosis of such infection. Contrasting to M. tu-berculosis infections that are rare in Swedish children, NTMinfection of cervical lymph nodes is a benign condition that

146 C©2006 The Author(s)/Journal Compilation C©2006 Foundation Acta Pædiatrica/Acta Pædiatrica 2007 96, pp. 145–149

Venkatesan et al. Selective neonatal BCG vaccination

Table 1 Mycobacterial species cultured from punctates of cervical lymph nodesof children in the Stockholm area (number of patients)

Time period MAC M. malmoense M. tuberculosis BCG

1989–1993 19 5 1 02000–2004 25 9 2 1

usually heals spontaneously in 3–6 months. Surgery may of-fer an accelerated recovery in selected cases, but carries arisk of nerve damage and disfiguring scar formation. Drugtreatment has not proved to be efficacious in this condi-tion, and side effects may not be worth the possible benefit(5). BCG may offer a limited protection against NTM lym-phadenitis, which, however, does not justify general vacci-nation, taking into account the benign character of the infec-tion and potential risks of vaccination side effects (6). More-over, alternative explanations to the increasing frequency ofNTM infection have been suggested.

References

1. Romanus V, Hallander HO, Wahlen P, Olinder-Nielsen AM,Magnusson PH, Juhlin I. Atypical mycobacteria inextrapulmonary disease among children. Incidence in Swedenfrom 1969 to 1990, relating to changing BCG-vaccinationcoverage. Tuber Lung Dis 1995; 76: 300–10.

2. Haverkamp MH, Arend SM, Lindeboom JA, Hartwig NG, vanDissel JT. Nontuberculous mycobacterial incidence in children:a 2-year prospective surveillance study in the Netherlands. ClinInfect Dis 2004; 39: 450–6.

3. Vu TT, Daniel SJ Quach C. Nontuberculous mycobacteria inchildren: a changing pattern. J Otolaryngol 2005; 34: S40–4.

4. Petrini B. Non-tuberculous mycobacterial infections. Scand JInfect Dis. 2006; 38: 246–55.

5. Lundberg B, Eriksson M, Petrini B. Complicated course of localmycobacterial infection in an immunocompetent girl. Scand JInfect Dis 1996; 28: 99–100.

6. Jeppson O, Petrini B, Andersson J, Heurlin N, Malm G. Defecthandling of BCG. Lancet 1988; 2: 570.

A case of epicanthus, telecanthus, high palate, transitional vertebra associatedwith vesicoureteral refluxOzgur Cogulu ([email protected])1, Burak Durmaz1,2, Cihangir Ozkinay2 and Ferda Ozkinay1

1. Department of Pediatrics and

2. Department of Medical Genetics, Ege University, Faculty of Medicine, Izmir, Turkey

KeywordsEpicanthus, Telecanthus, Transitional vertebrae, Vesicoureteral reflux

CorrespondenceO. Cogulu, MD, Ege University Faculty of Medicine,Department of Pediatrics, 35100,Bornova-Izmir,Turkey.Tel: +90 232 3398198 | Fax +90 232 3398781 |Email: [email protected]

Received3 July 2006; accepted 21 July 2006

DOI:10.1111/j.1651-2227.2007.00050.x

The anomalies in the orbital region can be isolated or part ofa syndrome (1). Genetic counselling to families who worryabout their children with minor anomalies should providesufficient information; therefore, we aimed to report our caseto contribute to our knowledge of cases having both telecan-thus and epicanthus.

Our patient is the first child of non-consanguineous par-ents. He was born at 38 weeks of gestation by caesareansection with no history of complications. His birth weightwas 3450 g (50–75th percentile). He was hospitalized at6 months of age because of urinary infection. Despite ofthe antibiotic treatments, urinary infection reoccurred fourtimes within a year. At most recent review, aged 18 monthsold, his weight was 9800 g (25–50th percentile), his heightwas 79 cm (90th percentile) and occipitofrontal circum-ference was 48 cm (75–90th percentile). His hair with awidow’s peak was yellow unlike his family. The ears were an-

teverted and he had depressed nasal bridge. He was noted tobe dysmorphic in the orbital region, namely, epicanthus andtelecanthus (Fig. 1). His eyes were almond-shaped and hehad down-slanting palpebral fissures. The control abdominalUSG and dimercapto-succinic acid scintigraphy (DMSA)were normal, but micturating cystouretherography (MCU)showed a second-degree vesico-uretheral reflux (VUR) inthe left urethra. His lumbosacral X-ray showed a transitionalvertebra in the level of L5 and his karyotype was noted as46,XY.

Minor anomalies are discriminated from common vari-ants by appearing less common than 4% in the population(2,3). Telecanthus, epicanthus, high palate and transitionalvertebra are minor anomalies in the presented case (4,5).Although minor anomalies in themselves do not seriouslyaffect the child, they may be associated with major anoma-lies or be features of certain syndromes (6). In conclusion,simple orbital findings, as well as other organ systems should


Selective neonatal BCG vaccination Venkatesan et al.

Figure 1 Proband aged 18 months old showing epicanthus and telecanthus.

be taken into account in detail during the evaluation of apatient that will be helpful for establishing an accurate diag-nosis and subsequently for appropriate genetic counselling,prognosis and disease management.

References

1. Helene D. Dysmorphology and the orbital region: a practicalclinical approach. Survey Ophthalmol 2004; 49: 547–61.

2. Aase JM. Principles of normal and abnormal embryogenesis. In:Diagnostic embryogenesis. New York: Plenum Medical BookCompany, 1990: 5–13.

3. Merks JH, van Karnebeek CD, Caron HN, Hennekam RC.Phenotypic abnormalities: terminology and classification. Am JMed Genet A 2003; 123: 211–30.

4. Usher CH. Pedigrees of hereditary epicanthus. Biometrika1935; 27: 5–25.

5. Juberg RC, Hirsch R. Expressivity of heritable telecanthus infive generations of a kindred. Am J Hum Genet 1971; 23:547–54.

6. Hunter AG. Medical genetics: 2. The diagnostic approach to thechild with dysmorphic signs. CMAJ 2002; 167: 367–72.

Olfactory function in children with cystic fibrosisChristian A Mueller ([email protected])1, Christian Quint1, Talin Gulesserian2, Andreas F P Temmel1, Thomas Hummel31. Department of Otorhinolaryngology, MedicalUniversity of Vienna, AKH Wien, Vienna, Austria

2. Department of Pediatric and Adolescent Medicine, Division of Pediatric Cardiology, Medical University of Vienna, AKH Wien, Vienna, Austria

3. Smell & Taste Clinic, Department of Otorhinolaryngology, University of Dresden Medical School, Dresden, Germany

CorrespondenceChristian A. Mueller, M.D., Department ofOtorhinolaryngology,Medical University of Vienna, AKH Wien,Waehringer Guertel 18-20,1090 Wien, Austria.Tel/Fax: +43-1-8651097 |Email: [email protected]

Received13 April 2006; accepted 2 June 2006

DOI:10.1111/j.1651-2227.2007.00034.x

Main causes of olfactory dysfunction, as seen in specialisedclinics, include sinonasal disease, upper respiratory tract in-fection, and head trauma (1). However, many other diseasesare associated with smell loss, e.g. neurodegenerative dis-eases like Alzheimer’s or Parkinson’s disease, internal dis-eases like hepatic or renal disorders, and endocrine disorderslike diabetes mellitus (2).

Cystic fibrosis (CF) has also been discussed to alter thesense of smell (3–5). However, results from previous inves-

tigations are contradictory. In an early study by Henkin andPowell, 11 CF patients from 6 to 20 years of age and 8healthy volunteers were studied (3). Using a test procedurebased on the method of ascending limits olfactory sensitivitywas reported to be approximately 10.000 times higher in CFpatients than in controls. However, Hertz and co-workerswere unable to confirm these findings (4). Olfactory thresh-olds for 1-butanol were significantly higher (meaningthat olfactory sensitivity was lower) in the patient group

148 C©2006 The Author(s)/Journal Compilation C©2006 Foundation Acta Pædiatrica/Acta Pædiatrica 2007 96, pp. 145–149

Venkatesan et al. Selective neonatal BCG vaccination

Table 1 Characteristics of subjects with cystic fibrosis (CF; n = 21) and healthycontrols (n = 21) (means (SD)) [m/f: male/female subjects; T = odor thresh-olds, D = odor discrimination, I = odor identification, TDI = TDI score]

CF Controls

Age 14.8 (2.3) 14.8 (2.1)Sex 14m/7f 12m/9fT 6.2 (1.6) 7.1 (0.9)D 11.8 (1.9) 13.1 (1.8)I 12.5 (1.9) 12.0 (1.5)TDI 30.5 (3.2) 32.1 (3.1)

consisting of 19 children with CF compared to 19 healthycontrols matched for age and sex. In addition, in a detectiontask with the same odorant at a concentration slightly abovethreshold levels no significant differences could be foundbetween the two groups. Similar findings were reported byWeiffenbach and McCarthy who observed elevated olfactorythresholds in 20 CF patients aged 13–53 years compared to15 control subjects (5).

The aim of the present study was to re-investigate olfactoryfunction in young patients with CF using an extensive andvalidated olfactory test (6).

The investigation included 42 children (26 boys, 16 girls;mean age 14.8 years, range 12–18 years); 21 children werepatients with CF, another 21 children served as healthycontrols.

Anterior rhinoscopy was performed to ascertain that noneof the subjects exhibited an obstruction of the nasal cavityor signs of inflammation of the nasal mucosa.

Olfactory testing: Smell function was measured usingthe ’Sniffin’ Sticks’ (Burghart medical technology, Wedel,Germany) which is based on pen-like odor dispensing de-vices (6). Tests were performed for butanol odor thresholds,odor discrimination and odor identification. The combinedresults of the three subtests allowed to categorize the pa-tients’ overall olfactory sensitivity.

Results (Table 1): Overall olfactory function did not differsignificantly between groups [factor’ group’: F′(1,40) = 2.87,

p = 0.098]. However, the interaction between factors ’group’and ’olfactory test’ (F[2,80] = 4.25 p = 0.019) suggested thatthe two groups behaved differently with regard to the threeolfactory tests. Post hoc testing showed that the CF groupexhibited lower scores for odor thresholds (p = 0.03) andodor discrimination (p = 0.03), but that there was no groupdifference for odor identification (p = 0.28).

Taken together, the present study produced the followingfindings: (a) CF patients exhibit lower olfactory sensitivity interms of olfactory thresholds and odor discrimination com-pared to healthy controls, (b) odor identification scores, aswell as overall olfactory sensitivity do not differ significantlybetween children with CF and healthy controls.

In conclusion, certain aspects of olfactory function seemto be impaired in children with CF. However, it seems thatas long as nasal polyposis is not present, smell impairmentis not present for all dimensions of olfactory function whichmay not translate into a clinically significant deficit.

References

1. Temmel AFP, Quint C, Schickinger-Fischer B, Klimek L, StollerE, Hummel T. Characteristics of olfactory disorders in relationto major causes of olfactory loss. Arch Otolaryngol Head NeckSurg 2002; 128: 635–41.

2. Schiffman SS. Taste and smell in disease (first of two parts).NEJM 1983; 308: 1275–9.

3. Henkin RI, Powell GF. Increased sensitivity of taste and smellin cystic fibrosis. Science 1962; 138: 1107–8.

4. Hertz J, Cain WS, Bartoshuk LM, Dolan TF Jr. Olfactory andtaste sensitivity in children with cystic fibrosis. Physiol Behav1975; 14: 89–94.

5. Weiffenbach JM, McCarthy VP. Olfactory deficits in cysticfibrosis: distribution and severity. Chem Senses 1984; 9:193–9.

6. Hummel T, Sekinger B, Wolf SR, Pauli E, Kobal G. ‘Sniffin’sticks’: olfactory performance assessed by the combined testingof odor identification, odor discrimination and olfactorythreshold. Chem Senses 1997; 22: 39–52.


Selective neonatal BCG vaccination—a re-audit

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