Letters to the Editor
P
Potential Transmission of
Herpes Simplex Virus Via
Vaginal Seeding
To the Editors:
W e report a case of neonatal herpes
simplex infection following vaginal
seeding after elective cesarean section.
A 2-week-old female infant was
referred to a tertiary pediatric hospital with
confirmed herpes simplex virus (HSV)
infection, initially presenting with vesicles
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in a symmetrical distribution over both eye-
lids at 10 days of life. She was delivered
by elective cesarean section, with intact
amniotic membranes at 38 weeks’ gesta-
tion and had received “vaginal seeding” at
birth whereby her eyelids, mouth and skin
were rubbed with a swab, incubated in
her mother’s vagina, before delivery. Her
mother reported a history of occasional oral
“cold sores” but no history of genital her-
pes. She reported no oral HSV lesions since
the infant’s birth.
Vesicular lesions were clustered
over the infant’s eyelids only, with no
lesions in other areas. HSV-1 was detected
from vesicular fluid by polymerase chain
reaction. The infant appeared systemically
well with normal complete blood count
and liver function tests. Cerebrospinal fluid
examination demonstrated 7 white cells/μL
(0 polymorphonuclear cells and 7 mono-
nuclear cells) and 1845 red cells, with a
negative HSV polymerase chain reaction.
An ophthalmologic examination confirmed
no corneal lesions. The infant was admitted
for management of neonatal HSV disease
(skin, eye, mucous membrane type - SEM)
and received standard treatment with intra-
venous aciclovir 20 mg/kg thrice daily for
14 days.
Neonatal HSV is an important infec-
tion with high morbidity and mortality.
The proportion of genital HSV-1 to HSV-2
infection is increasing,1 and genital HSV
may be asymptomatic. Approximately
60%–80% of women who deliver a HSV-
infected infant have no evidence of genital
HSV infection at the time of delivery nor
have a history or a partner reporting a his-
tory of genital herpes.2 The neonate in our
The authors have no funding or conflicts of interest
to disclose.
Address for correspondence: Julie Huynh, MB BS,
FRACP, Department of Infectious Diseases and
Microbiology, Children’s Hospital Westmead,
170 Hawkesbury Rd, Westmead, NSW, Australia.
E-mail: Julie.Huynh@health.nsw.gov.au.
Copyright © 2018 Wolters Kluwer Health, Inc. All
rights reserved.
ISSN: 0891-3668/18/3711-e278
DOI: 10.1097/INF.0000000000001965
e278 | www.pidj.com The Pediatric Infectious Disease Journal  •  Volume 37, Number 11, November 2018
Copyright © 2018 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
case acquired HSV infection after vaginal
seeding, and her mother was not counse-
led about HSV. It is fortunate that the HSV
infection was limited to SEM type disease
in our case; however, neonatal herpes infec-
tion should always be considered a serious,
sometimes fatal infection, with potential
for disseminated or central nervous sys-
tem disease and associated neurodevelop-
mental sequelae. While we cannot prove
the vaginal seeding led to infection, there
are a number of considerations that raise
this important possibility. These include
the prominent symmetrical localization of
vesicles over both eyelids where she was
swabbed, and the timing of infection within
the first 2 weeks of life (suggesting peripar-
tum acquisition).
Vaginal seeding is a practice that aims
to transfer a mother’s vaginal microbiome
to newborns delivered by cesarean section.3
This technique involves incubating sterile
gauze in the mother’s vagina, removing it
before delivery and rubbing it against the
skin, eyelids and mouth of the newborn soon
after birth. This practice is occurring against
a background of increasing rates of cesarean
section (up to 30% of live births)4 and increas-
ing research attention on the development of
the infant microbiome.5 The long-term health
outcomes and harms of vaginal seeding have
not yet been reported. It is important that this
lack of safety data is emphasized as part of
antenatal care for pregnant women consider-
ing vaginal seeding.
To our knowledge, this is the first
case of neonatal herpes simplex infection,
documented following vaginal seeding. We
believe that further study on benefits and
harms of vaginal seeding should be con-
ducted before introducing this practice out-
side a carefully monitored research setting.
ACKNOWLEDGMENTS
The authors thank the family of their
patient who provided consent for this pub-
lication.
Julie Huynh, MB BS, FRACP
Department of Immunology and Infectious
Diseases
Sydney Children’s Hospital
Randwick, New South Wales, Australia
Department of Infectious Diseases and
Microbiology
Children’s Hospital at Westmead
Westmead, New South Wales, Australia
Pamela Palasanthiran, MB BS, MD,
FRACP
Brendan McMullan, MB BS,
FRACP, FRCPA
Department of Immunology and Infectious
Diseases
Sydney Children’s Hospital
School of Women's and Children's Health,
University of New South Wales
Randwick, New South Wales, Australia
REFERENCES S
1. Haddow LJ, Dave B, Mindel A, et al. Increase in
rates of herpes simplex virus type 1 as a cause of
anogenital herpes in Western Sydney, Australia,
between 1979 and 2003. Sex Transm Infect.
2006;82:255–259.
P
2. Whitley RJ, Corey L, Arvin A, et al. Changing
presentation of herpes simplex virus infection in
neonates. J Infect Dis. 1988;158:109–116.
3. Cunnington AJ, Sim K, Deierl A, et al. “Vaginal P
seeding” of infants born by caesarean section.
BMJ. 2016;352:i227.
4. Centers for Disease Control and Prevention.
L
National vital statistics system—birth data.
2016. Available at: http://www.cdc.gov/nchs/
births.htm. Accessed October 22, 2016.
H
5. Dominguez-Bello MG, De Jesus-Laboy KM,
Shen N, et al. Partial restoration of the micro- 2
biota of cesarean-born infants via vaginal micro-
bial transfer. Nat Med. 2016;22:250–253.
Shanghai Fever in a
Healthy Infant
First Report in South America
To the Editors: 0
W
e read with great interest the study pub-
lished by Chuang et al1 that described
4 different presentations of gastrointestinal
Pseudomonas aeruginosa infections in chil-
dren. One of these presentations is known as
T
Shanghai fever, rare community-acquired P.
aeruginosa enteritis associated with sepsis
that affects previously healthy infants. To
this date, most case reports were restricted
to East Asian countries.2 To our knowledge,
we describe the first case of Shanghai Fever
in South America.
N
A previously healthy 7-month-old
boy was admitted to our hospital in São
Paulo, Brazil, after 3 days of fever, vomiting 2
and bloody stools. He started on ceftriax-
one because of suspected bacterial enteritis
and was transferred to the pediatric inten-
sive care unit because of septic shock with
disseminated intravascular coagulation. He
was fully immunized against rotavirus.
On the next day of admission, 2
necrotic skin lesions suggestive of ecthyma
gangrenosum were observed on his right leg
The authors have no funding or conflicts of interest
to disclose.
Address for correspondence: Giuliana Stravinskas
Durigon, MD, PhD; E-mail: giuliana.durigon@
gmail.com.
Copyright © 2018 Wolters Kluwer Health, Inc. All
rights reserved.
ISSN: 0891-3668/18/3711-e278
DOI: 10.1097/INF.0000000000002005
The Pediatric Infectious Disease Journal  •  Volume 37, Number 11, November 2018 Letters to the Editor
and perineum, measuring 2 and 1 cm, respec-
tively. Surgical debridement was performed,
and material was sent for culture analysis.
Ceftriaxone was changed to piperacillin-
tazobactam for empirical P. aeruginosa cov-
erage. The child continued to worsen with
need of mechanical ventilation, continuous
hemodialysis and was put on broad-spec-
trum antibiotics (Vancomycin and Merope-
nem). On the eleventh day of the disease, he
presented peritonism and severe abdominal
distension. Laparotomy revealed 3 bowel
perforations in sigmoid colon and proximal
rectum, and a colostomy was performed. He
showed clinical improvement and was dis-
charged after 28 days of admission.
Cultures from ecthyma gangrenosum
biopsy and peritoneal fluid yield P. aeruginosa.
Blood cultures were negative. Primary and
acquired immunodeficiencies were ruled out
after an extensive investigation. He remained
well after 8 months of follow-up, with com-
plete recovery and intestinal reconstruction.
Chuang et al2 described the biggest
case series of Shanghai fever in 27 patients
in Taiwan. He defined the disease with the
following criteria: (1) community-onset diar-
rhea with fever, (2) sepsis and (3) growth of
P. aeruginosa from blood or another sterile
body site. The median age was 7 months, and
clinical features were fever (100%), diarrhea
(96%), necrotizing enteritis (85%), septic
shock (81%), ecthyma gangrenosum (63%),
dyspnea (47%), vomiting (44%), bowel per-
foration (33%) and seizures (26%).2
The presence of P. aeruginosa in
stool cultures from healthy children is rare
and its significance is controversial.1,3 A
Brazilian study found that P. aeruginosa is
a common cause (28%) of nosocomial diar-
rhea in adults in intensive care unit, but none
of the patients had systemic symptoms.4 As
shown by Chuang et al,2 Shanghai fever is
not associated to hospital-acquired coloni-
zation, but is caused by more virulent com-
munity strains of P. aeruginosa, demonstrat-
ing a higher cytotoxic and invasive profiles.
Unfortunately, we were unable to per-
form molecular analysis or virulence assays
in our isolate. On the other hand, the case
we described is compatible with Shanghai
fever syndrome. The patient had no history
of traveling outside Brazil during his life.
Therefore, it is possible that more virulent
strains of P. aeruginosa are not restricted to
Asian countries and may cause Shanghai
fever in Brazil.
Fernando Domingues Penteado, MD
Vera Bain, MD
Giuliana Stravinskas Durigon, MD,
PhD
Nadia Litvinov, MD
Maria Fernanda Badue Pereira, MD,
MSc
© 2018 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2018 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Heloisa Helena de Sousa Marques,
MD, PhD
Pediatric Infectious Diseases Unit
Instituto da Criança, Hospital das Clínicas
Universidade de São Paulo (HC-FMUSP)
São Paulo, SP, Brazil
REFERENCES
1. Chuang CH, Janapatla RP, Wang YH, et al.
Pseudomonas aeruginosa-associated diar-
rheal diseases in children. Pediatr Infect Dis J.
2017;36:1119–1123.
2. Chuang CH, Wang YH, Chang HJ, et al.
Shanghai fever: a distinct Pseudomonas aerugi-
nosa enteric disease. Gut. 2014;63:736–743.
3. Cheng YL, Lee HC, Yeung CY, et al. Clinical
significance in previously healthy children of
Pseudomonas aeruginosa in the stool. Pediatr
Neonatol. 2009;50:13–17.
4. Marcon AP, Gamba MA, Vianna LA.
Nosocomial diarrhea in the intensive care unit.
Braz J Infect Dis. 2006;10:384–389.
Predictors of Intravenous
Immunoglobulin
Nonresponse and Racial
Disparities in Kawasaki
Disease
To the Editors:
W
e read with great interest the study
by Clark et al1 which for the first
time suggested that the Black race may be
at risk factor for inravenous immunoglobu-
lin (IVIG) resistance in a racially diverse
Kawasaki disease (KD) population. In
their study, response to IVIG was observed
in 75% of Black patients versus 86% of
Non-Black (P = 0.02). Black ethnicity
was also associated with higher erythro-
cyte sedimentation rate, lower hemoglobin
and lower albumin, but not with echocar-
diographic abnormalities upon diagnosis
or cardiac sequelae. Early identification of
risk factors for IVIG nonresponse is crucial
in KD patients, as adjunctive therapies can
be offered to nonresponders to prevent car-
diac sequelae.2
Therefore, we retrospectively ana-
lyzed data from 157 patients hospitalized
between 2006 and 2016 in a French pediatric
tertiary hospital in Paris, France. Our hospi-
tal predominantly receives patients from the
North-Western region of Paris and suburbs.
Similar to the study by Clark et al, hemo-
globin was lower in Black patients (mean
10.2 vs. 10.8 g/dL, P = 0.01; Table 1). In
Copyright © 2018 Wolters Kluwer Health, Inc. All
rights reserved.
ISSN: 0891-3668/18/3711-e279
DOI: 10.1097/INF.0000000000002083
our cohort, response to IVIG was observed
in 39/55 (71%) Black children and 74/102
(73%) non-Black children (P = 0.83). Addi-
tionally, rates of initial cardiac abnormali-
ties and coronary artery aneurysms were
similar in both groups (18/55 and 4/55 in
Black children vs. 30/102 and 3/102 in non-
Blacks, P = 0.72 and P = 0.24). Thus, in our
population, black race was not a risk factor
for severe KD.
It is to note that in our cohort, Black
patients originated predominantly from
Sub-Saharan African countries (49/55) and
the Caribbean (6/55). These proportions
were likely to be different in the study by
Clark et al and might explain the observed
differences. Different environmental factors
in North America and Europe may further
contribute to the observed divergences.
Our data suggest that Black race may
not be a predictive factor for IVIG resist-
ance in all KD cohorts, and therefore cau-
tion should be displayed when considering
this parameter for treatment intensifications.
Additional studies will be necessary to fur-
ther elucidate the relative importance of eth-
nical backgrounds in the response to IVIG
in KD.
Jean Gaschignard, MD, PhD
Service de pédiatrie générale, maladies
infectieuses et médicine interne
Centre de référence des rhumatismes
inflammatoires et maladies auto-immunes
systémiques rares de l’enfant (RAISE)
Hôpital Robert Debré, Assistance Publique
Hôpitaux de Paris
Paris, France
Université Paris Diderot-Sorbonne
Paris-Cité, Centre de recherche sur
l’inflammation
Institut National de la Santé et de la
Recherche Médicale
Paris, France
Ulrich Meinzer, MD, PhD
Service de pédiatrie générale, maladies
infectieuses et médicine interne
Centre de référence des rhumatismes
inflammatoires et maladies auto-immunes
systémiques rares de l’enfant (RAISE)
Hôpital Robert Debré, Assistance Publique
Hôpitaux de Paris
Paris, France
Université Paris Diderot-Sorbonne
Paris-Cité, Centre de recherche sur
l’inflammation
Institut National de la Santé et de la
Recherche Médicale
Paris, France
Institut Pasteur
Unité biologie et génétique de la paroi
bactérienne
Paris, France
www.pidj.com | e279