?38.5°C (at all GA); and (3) maternal chorioamnionitis (at all GA).
Hence, mothers with MIF ?38.5°C do not always receive IAP. Indeed,
Centers for Disease Control and Prevention guidelines define MIF as
temperature ?38°C.7Neonatologists do not have clear guidelines of
how to manage a subgroup of term healthy neonates born after MIF,
ROM ?18 hours, unknown maternal GBS status, and no IAP.
Several potential predictors of EOS have been previously
tested. Abnormal CBC (WBC ?30,000/mm3or WBC ?5000/mm3,
absolute neutrophil count ?1500/mm3, or I/T ratio ?0.2) did not
prove to be a reliable predictor of EOS.9In our study, normal CBC
had a high negative predictive value for unfavorable outcome. CRP
values 24 hours after birth were shown to be elevated in association
with several intrapartum risk factors, and hence this test might be
useful only in excluding EOS.10In the present study, all neonates
had normal CRP ?1.0 mg/dL and none had proven EOS.
Molecular techniques serve as useful adjunct to standard culture-
have received IAP. Jordan and Durso11reported an overall agreement
between results of blood culture and real-time PCR of 94.1%. Contrary
to this, 16S rRNA PCR showed high specificity and negative predictive
value but low sensitivity in detecting EOS.12In our study, all 36
neonates born after MIF had both negative blood cultures and negative
PCR. Hence, PCR appears as a promising tool for excluding bacterial
EOS in neonates born after MIF. Nonetheless, we are aware of our
small sample size and that in the era of IAP, proven EOS has become
very rare, and that a very large sample size will be needed to reliably
confirm our findings.
The role of epidural analgesia in causing MIF is controversial.
Some studies showed a significantly increased risk for MIF in
mothers receiving epidural analgesia,13–16with significantly in-
creased neonatal sepsis evaluations.14,16On the other hand, Dashe
et al17found that MIF in the absence of proven placental inflam-
mation was not increased after epidural analgesia. In our study,
58.3% had epidural analgesia, a fact that can reduce concerns of
neonatologists regarding MIF, but might not lessen the need for
sepsis evaluations in neonates born after MIF.
Based on our results, we herein suggest the following ap-
proach to term healthy neonates born after MIF, ROM ?18 hours,
and unknown maternal GBS status. If maternal IAP for GBS was
administered ?4 hours before delivery, we recommend clinical
follow-up for 48-72 hours only. If IAP was not administered or
given ?4 hours before delivery, then laboratory evaluation (CBC ?
differential, blood culture, CRP, and PCR) and clinical follow-up for
48-72 hours are indicated. Empiric antibacterial therapy should be
started only in those neonates with one or more of the following:
amnionitis, suspected clinical sepsis, CRP ?1.0mg/dL, or positive
16S rRNA gene PCR amplification.
The authors thank Dr. Raia Shalginov for molecular PCR
tests, and pediatric residents and nurses for their help in collecting
1. Schrag SJ, Hadler JL, Arnold KE, Martell-Cleary P, Reingold A,
Schuchat A. Risk factors for invasive, early-onset Escherichia coli
infections in the era of widespread intrapartum antibiotic use. Pediatrics.
2. Oddie S, Embleton ND. Risk factors for early onset neonatal group B
streptococcal sepsis: case-control study. BMJ. 2002;325:308.
3. Adair CE, Kowalsky L, Quon H, et al. Risk factors for early-onset group
B streptococcal disease in neonates: a population-based case-control
study. CMAJ. 2003;169:198–203.
4. Chen KT, Ringer S, Cohen AP, Lieberman E. The role of intrapartum
fever in identifying asymptomatic term neonates with early-onset neo-
natal sepsis. J Perinatol. 2002;22:653–657.
5. Petrova A, Demissie K, Rhoads GG, Smulian JC, Marcella S, Ananth
CV. Association of maternal fever during labor with neonatal and infant
morbidity and mortality. Obstet Gynecol. 2001;98:20–27.
6. Lin FY, Brenner RA, Johnson YR, et al. The effectiveness of risk-based
intrapartum chemoprophylaxis for the prevention of early-onset neonatal
group B streptococcal disease. Am J Obstet Gynecol. 2001;184:1204–1210.
7. Center for Disease Control and Prevention. Prevention of perinatal group
B streptococcal disease. Revised guidelines from CDC. MMWR Recomm
8. Deleted in Proof.
9. Ottolini MC, Lundgren K, Mirkinson LJ, Cason S, Ottolini MG. Utility
of complete blood count and blood culture screening to diagnose
neonatal sepsis in the asymptomatic at risk newborn. Pediatr Infect Dis
10. Mathai E, Christopher U, Mathai M, Jana AK, Rose D, Bergstrom S. Is
C-reactive protein level useful in differentiating infected from unin-
fected neonates among those at risk of infection? Indian Pediatr.
11. Jordan JA, Durso MB. Real-time polymerase chain reaction for detect-
ing bacterial DNA directly from blood of neonates being evaluated for
sepsis. J Mol Diagn. 2005;7:575–581.
12. Jordan JA, Durso MB, Butchko AR, Jones JG, Brozanski BS. Evaluating
the near-term infant for early onset sepsis: progress and challenges to
consider with 16S rDNA polymerase chain reaction testing. J Mol
13. Goetzl L, Rivers J, Zighelboim I, Wali A, Badell M, Suresh MS.
Intrapartum epidural analgesia and maternal temperature regulation.
Obstet Gynecol. 2007;109:687–690.
14. Yancey MK, Zhang J, Schwarz J, Dietrich CS III, Klebanoff M. Labor
epidural analgesia and intrapartum maternal hyperthermia. Obstet Gy-
analgesia and intrapartum fever. Am J Perinatol. 2000;17:127–130.
16. Lieberman E, Lang J, Richardson DK, Frigoletto FD, Heffner LJ, Cohen A.
Intrapartum maternal fever and neonatal outcome. Pediatrics. 2000;105:8–13.
17. Dashe JS, Rogers BB, McIntire DD, Leveno KJ. Epidural analgesia and
intrapartum fever: placental findings. Obstet Gynecol. 1999;93:341–344.
NASAL CARRIAGE OF METHICILLIN-RESISTANT
STAPHYLOCOCCUS AUREUS IN HOUSEHOLD
CONTACTS OF CHILDREN WITH
COMMUNITY-ACQUIRED DISEASES IN TAIWAN
Yhu-Chering Huang, MD, PhD,*† Chen-Fang Ho, MD,*
Chih-Jung Chen, MD,* Lin-Hui Su, MS,†‡ and Tzou-Yien Lin, MD*†
Abstract: Nasal carriage of methicillin-resistant Staphylococcus
aureus was detected in 18 (32%) of 57 children with community-
acquired methicillin-resistant S. aureus infection and 30 (25%) of
121 household contacts. By genotyping comparison, 94% and 64%
of the colonization isolates from the patients and the contacts,
respectively, were indistinguishable from the clinical isolates.
Key Words: community-acquired, methicillin-resistant
Staphylococcus aureus, household, Taiwan
Accepted for publication June 5, 2007.
From the *Division of Pediatric Infectious Diseases, Chang Gung Children’s
Hospital; †College of Medicine, Chang Gung University; and ‡Depart-
ment of Clinical Pathology, Chang Gung Memorial Hospital, Kweishan,
Supported by a grant from National Science Council of Executive Yuan,
Taiwan (NSC 93-2314-B-182A-042).
Address for correspondence: Yhu-Chering Huang, MD, PhD, Department
of Pediatrics, Chang Gung Children’s Hospital, No. 5, Fu-Shin Street,
Kweishan, Taoyuan, Taiwan. E-mail: firstname.lastname@example.org.
Huang et al
The Pediatric Infectious Disease Journal • Volume 26, Number 11, November 2007
© 2007 Lippincott Williams & Wilkins
ing and may now involve persons without risk factors predisposing
for acquisition.1–3In the United States, CA-MRSA strains have been
recognized as a novel pathogen that is genetically different from the
nosocomial MRSA.2They are characterized by limited antibiotic
resistance, share 2 common pulsed field gel electrophoresis (PFGE)
patterns (USA 300 and USA 400), and contain type IV staphylo-
coccal cassette chromosome (SCCmec).1–3SCCmec is the genetic
element that carries the methicillin-resistant gene, mecA, and there
are at least 5 SCCmec types identified at present.
In Taiwan, epidemiologic data4–7showed that between 1997
and 2003, MRSA accounted for 9.8-36% of community-acquired S.
aureus infections in children without risk factors and MRSA colo-
nization rate in the general population ranged from 1.9% in school
children, 5.3% in healthy children presented for healthcare visits, to
10.8% in health care workers and 13.6% in contacts of CA-MRSA
infection. To understand the transmission of CA-MRSA isolates in
the households, we conducted an epidemiologic investigation to
survey the nasal carriage of MRSA among the household contacts of
children with CA-MRSA infection.
ecent reports indicate that community-acquired methicillin-resis-
tant Staphylococcus aureus (CA-MRSA) infections are increas-
MATERIALS AND METHODS
Between August 2004 and May 2005, once a hospitalized
patient with CA-MRSA infection, which was defined as an MRSA
infection documented within 72 hours of admission, was identified
at Chang Gung Children’s Hospital, an investigator (C.-F.H.) would
interview the care provider of the patients to complete a question-
naire about hospitalization, surgery, dialysis, a permanent indwell-
ing catheter or percutaneous medical device, a known positive
culture for MRSA before this infection, and history of residence in
a long-term care facility within the previous 12 months. Patients
with any of these conditions were defined as having an identifiable
risk factor.2Those ?1 year of age were defined as without identi-
fiable risk factor if they do not have any condition after birth, except
birth in the hospital. After a written consent was obtained from the
guardians and/or the case patients, a survey culture of the anterior
nares was obtained from the case patients and their household
contacts within 1 week of when the MRSA was identified.
Identification of MRSA was confirmed according to Clinical
and Laboratory Standards Institute guidelines, 2005. PFGE with
SmaI digestion was performed as described previously.5,8Two
isolates were considered to be indistinguishable, highly related, or
distinct if the bands were identical, fewer than 4-band differences, or
4 or more bands differences.
SCCmec typing was determined by a multiplex polymerase
chain reaction strategy described previously.9SCCmec typing for
type VTwas modified from Boyle-Vavra et al.7The presence of
Panton-Valentine leukocidin (PVL) genes was determined by a
polymerase chain reaction strategy described previously.10All clin-
ical isolates underwent multilocus sequence typing as described
During the study period, 109 children ?18 years of age with
CA-MRSA infections were identified. The household members of
57 children were available and willing to come to the hospital for
sampling and included in this study. Of the 57 case patients, 49
patients (86%) presented with simple skin and/or soft tissue infec-
tion. Identifiable risk factor for MRSA acquisition was identified in
12 (21%) children.
Of the 57 families included, a total of 121 household contacts
were sampled. There was 1 member sampled in 17 households, 2
members in 27 households, and 3 or more members in 13 house-
holds. MRSA was detected in 30 contacts (25%) from 23 families
(40%). Six households had 2 or more contacts positive for MRSA.
Grandparents (35%) and mothers (33%) had the highest frequency
of MRSA carriage (Table 1). Among the 57 case patients, nasal
carriage of MRSA was detected in 18 case patients (32%). Two
other case patients had MSSA colonization.
Seven PFGE patterns were identified. PFGE patterns D
(accounting for 71% and 49% of the clinical and colonized
isolates, respectively) and C (accounting for 15% and 32% of the
clinical and colonized isolates, respectively) were the 2 most
common patterns. SCCmec VTwas the predominant type (67% of
the clinical isolates and 47% of the colonized isolates), followed
by type IV (27% of the clinical isolates and 45% of the colonized
isolates). PVL genes were detected in 77% of the clinical isolates
and in 55% of the colonization isolates. From the 48 clinical
isolates, 7 sequence types (STs) were identified by multilocus
sequence typing and ST59 was the most common ST, accounting
for 79%. Altogether, ST59/PFGE type D/SCCmec VT/presence of
PVL genes identified in 30 (67%) clinical isolates and ST59/
PFGE type C/SCCmec IV/absence of PVL genes in 7 (15%)
clinical isolates were the 2 most common clones.
Among the 16 paired clinical-colonization isolates available
for clonal comparison from the case patients, 15 pairs (94%) were
considered to be indistinguishable (also the same SCCmec types,
STs, and PVL genes). Whereas, among the 28 paired isolates from
the households, 18 pairs (64%), 5 pairs (18%), and 5 pairs were
considered to be indistinguishable, highly related and distinct,
Results from this study indicate that nasal carriage of MRSA
was detected in about one-third of the case patients and more than
90% of the colonization isolates were indistinguishable from the
clinical isolates, suggesting that colonization of MRSA may be
associated with subsequent infection.
Nasal carriage of MRSA was also detected in one-fourth of
the household contacts surveyed. This rate was significantly higher
than that in children without designated risk factors for the acqui-
sition of MRSA in Taiwan (1.9–5.3%).4,7Approximately two-thirds
of the colonization isolates from household contacts were indistin-
guishable from the clinical isolates, indicating that MRSA can
indeed spread in the household once MRSA emerges in a household
Nasal Carriage of Methicillin-Resistant Staphylococcus aureus (MRSA)
Distribution of 121 Household Members From 57 Families Sampled for
FatherMother GrandparentsSiblings Others
No. positive for MRSA (%)
23 (40)5 (14) 16 (33)7 (35)1 (11) 1 (14)
The Pediatric Infectious Disease Journal • Volume 26, Number 11, November 2007 CA-MRSA in Households
© 2007 Lippincott Williams & Wilkins
member. However, distinct clones were identified in one-third of the Download full-text
isolates from household contacts, suggesting that not all MRSA
isolates from the contacts were related to the case patient.
In this prospective study, we also found that there was a pre-
dominant clone of MRSA characterized by ST59, PFGE pattern D
(similar to PFT USA 100012), SCCmec VT, and presence of PVL gene
among the CA-MRSA isolates in Taiwanese children and this clone
accounted for two-thirds of the clinical isolates. These findings are
consistent with those reported previously from Taiwan,7,12suggesting
that this clone has been circulating in the Taiwan community.
1. Deresinski S. Methicillin-resistant Staphylococcus aureus: an evolution-
ary, epidemiologic, and therapeutic odyssey. Clin Infect Dis. 2005;40:
2. Naimi TS, LeDell KH, Como-Sabetti K, et al. Comparison of commu-
nity- and health care-associated methicillin-resistant Staphylococcus
aureus infection. JAMA. 2003;290:2976–2984.
3. Kaplan SL, Hulten KG, Gonzalez BE, et al. Three-year surveillance of
community-acquired Staphylococcus aureus infections in children. Clin
Infect Dis. 2005;40:1785–1791.
4. Chen CJ, Huang YC. Community-acquired methicillin-resistant Staphylo-
coccus aureus in Taiwan. J Microbiol Immunol Infect. 2005;38:376–382.
5. Chen CJ, Huang YC, Chiu CH, Su LH, Lin TY. Clinical features and
genotyping analysis of community-acquired methicillin-resistant Staph-
ylococcus aureus infections in Taiwanese children. Pediatr Infect Dis J.
6. Huang YC, Su LH, Lin TY. Nasal carriage of methicillin-resistant
Staphylococcus aureus in contacts of an adolescent with community-
acquired disseminated disease. Pediatr Infect Dis J. 2004;23:919–
7. Boyle-Vavra S, Ereshefsky B, Wang CC, Daum RS. Successful
multiresistant community-associated methicillin-resistant Staphylo-
coccus aureus lineage from Taipei, Taiwan, that carries either the
novel staphylococcal chromosome cassette mec (SCCmec) type VTor
SCCmec type IV. J Clin Microbiol. 2005;43:4719–4730.
8. Huang YC, Chou YH, Su LH, Lien RI, Lin TY. Methicillin-resistant
Staphylococcus aureus colonization and its association with infection
among infants hospitalized in neonatal intensive care units. Pediatrics.
9. Oliveira DC, de Lencastre H. Multiplex PCR strategy for rapid identi-
fication of structural types and variants of the mec element in methicil-
lin-resistant Staphylococcus aureus. Antimicrob Agents Chemother.
10. Lina G, Piemont Y, Godail-Gamot F, et al. Involvement of Panton-
Valentine leukocidin-producing Staphylococcus aureus in primary skin
infections and pneumonia. Clin Infect Dis. 1999;29:1128–1132.
11. Enright MC, Day NP, Davies CE, Peacock SJ, Spratt BG. Multilocus
sequence typing for characterization of methicillin-resistant and methi-
cillin-susceptible clones of Staphylococcus aureus. J Clin Microbiol.
12. Wang CC, Lo WT, Chu ML, Siu LK. Epidemiological typing of
community-acquired methicillin-resistant Staphylococcus aureus iso-
lates from children in Taiwan. Clin Infect Dis. 2004;39:481–487.
IMMUNE RECONSTITUTION INFLAMMATORY
SYNDROME ASSOCIATED WITH PROGRESSIVE
MULTIFOCAL LEUKOENCEPHALOPATHY IN A
PERINATALLY ACQUIRED HUMAN
Tong Wei Ch’ng, MD, and Arry Dieudonne, MD
Abstract: Perinatally infected children represent a large proportion
of the youth living with human immunodeficiency virusinfection/
acquired immunodeficiency syndrome (HIV/AIDS). Because of
nonadherence to treatment, an increasing number of perinatally
acquired HIV-infected adolescents and young adults are showing
virologic failure and immune suppression. We report a case of
progressive multifocal leukoencephalopathy secondary to immune
reconstitution inflammatory syndrome in a perinatally HIV-infected
young adult, occurred shortly after the revision of an antiretroviral
regimen. The patient showed marked improvement with the combi-
nation of corticosteroid and antiretroviral treatment.
Key Words: perinatally acquired HIV infection, immune
reconstitution inflammatory syndrome, multifocal
Accepted for publication May 30, 2007.
From the Division of Pediatric Pulmonary, Allergy, Immunology and Infec-
tious Diseases, Department of Pediatrics, University of Medicine and
Dentistry of New Jersey (UMDNJ), Newark, NJ.
Address for correspondence: Tong Wei Ch’ng, MD, 185 South Orange
Avenue, Medical Science Building, No. F570 (A), Newark, New Jersey
07103. E-mail: email@example.com.
She was doing relatively well with optimal antiretroviral therapy
under the care of her grandmother, but treatment adherence became
increasingly sporadic as she reached adolescence. She eventually
developed severe immune suppression at 17 years of age. Her
lymphocytes subset counts (CD4?) ranged from 17 ? 103to 110 ?
103cells/mL (1–6%), and viral loads 30,000–420,000 copies/mL.
Despite being severely immunocompromised, she remained clini-
cally stable. She gave birth to a healthy non-HIV-infected son at the
age of 19.
In October 2006, her antiretroviral regimen was revised based
on her HIV genotyping results, which showed resistance to her most
recent antiretroviral regimen (didanosine, emtricitabine/tenofovir).
Because she had failed to withstand and tolerate different regimens
in the past, a new regimen of abacavir, tenofovir, and ritonavir-
boosted atazanavir was chosen. Her HIV viral loads and CD4?at
the time of new antiretroviral initiation were 98,032 copies/mL and
10 ? 103cells/mL (1%), respectively. After repeated lengthy dis-
cussions with her and her grandmother regarding the severity of her
underlying immunodeficiency and the importance of medication
adherence, she finally promised to adhere strictly to her new anti-
retroviral regimen. Her grandmother also vowed to supervise her
future medication administration.
Three weeks later, she drove herself to the emergency depart-
ment complained of a 2-day history of speech difficulty, right facial
drooping, and right-sided weakness. General physical examination
showed no lymphadenopathy, normal chest and cardiovascular find-
ings, and no organomegaly. On neurologic examination, she was
alert and orientated, able to follow multistep commands, and had no
visual abnormality. Despite her complaint of difficulty with word
finding, her speech was normal for fluency, naming, comprehension,
articulation, and repetition. Cranial nerve examination showed sig-
nificant right lower facial paralysis. Motor examination revealed
right-sided weakness; she had active movement of her right arms
and legs against gravity but not against resistance. Deep tendon
reflexes were brisk on the right side.
Her initial laboratory data in the emergency department
showed: white blood cell count of 4.1 ? 103/mm3(neutrophils 42%,
lymphocytes 40%, monocytes 11%, eosinophils 6%, basophils 1%);
hemoglobin 13.9%; platelet 172 ? 103/mL; HIV viral loads 11,800
copies/mL. Toxoplasma serology was negative. Cerebrospinal fluid
(CSF) analysis was normal. Cryptococcal antigen and India ink tests
were negative. CSF polymerase chain reaction for JC virus (JCV)
and herpes simplex virus were sent. Brain computer tomography
22-year-old Hispanic female perinatally infected with human
immunodeficiency virus (HIV) was diagnosed at 2 years of age.
Ch’ng and Dieudonne
The Pediatric Infectious Disease Journal • Volume 26, Number 11, November 2007
© 2007 Lippincott Williams & Wilkins