The incidence of infection in the fetus and
newborn infant is high. As many as 2% of fetuses are infected in utero and up
to 10% of infants are infected during delivery or in the first few months of
life. The predominant microorganisms known to cause these infections are
cytomegalovirus, herpes simplex virus, rubella virus, Toxoplasma gondii, Treponema pallidum, chlamydia, group B Streptococcus, Enterococcus
spp., Escherichia coli, and anaerobic
bacteria. All of these agents can colonize or infect the mother and infect the
fetus or newborn either intrauterinely or during the passage through the birth
canal. Although anaerobic bacteria cause a small number of these infections,
the conditions predisposing to anaerobic infections in newborns are similar to
those associated with aerobic micro-organisms. Furthermore, the true incidence
of anaerobic infections may be underestimated because techniques for the
recovery and isolation of anaerobic bacteria are rarely used, or are
inadequate. Several factors have been associated with acquisition of local or
systemic infection in the newborn. Most of these factors are vague and
difficult to define; however, most studies have described the presence of one
or more risk factors in the pregnancy and delivery of these infants: premature
and prolonged rupture of membranes (longer than 24 hours), maternal peripartum
infection, premature delivery, low birth weight, depressed respiratory function
of the infant at birth or fetal anoxia, and septic or traumatic delivery.1–3
Maternal infection at the time of delivery, can
be associated with the development of infection in the newborn. Transplacental
hematogenous infection that can spread before or during delivery is another way
in which the infant can be infected.4 The acquisition of infection
while the newborn passes through the birth canal is, however, the most frequent
mode of transfer.
During pregnancy the fetus is shielded from the
flora of the mother’s genital tract. Potentially pathogenic bacteria are found
in the amniotic fluid (AF) even when the membranes are intact. Prevedourakis et
al5 documented bacterial invasion of the intact amnion in nearly 8%
of the pregnant women in their sample, but this was of no consequence to the
mother or the newborn infant. It was suspected that the AF may have
antibacterial properties, probably owing to lack of nutritional factors.5,6
The AF actively inhibited the growth of aerobic bacteria, through a
phosphate-sensitive cationic protein that is regulated by zinc. 7
Its activity was independent of the muramidase and peroxidases and spermine.
The pH of the amniotic fluid is the only variable predictive of bacterial
growth in amniotic fluid in a laboratory model.8
The antimicrobial properties of the AF also
vary with the period of gestation; it is the least inhibitory against E. coli and Bacteroides fragilis during the first trimester and most inhibitory
during the third trimester.8,9 The relative scarcity of the B. fragilis population in the cervix at
term labor and the added inhibitory effect of the AF at term may together
explain the relatively low incidence of B.
fragilis infections at full term as compared to postabortal sepsis.10–12
Following the rupture of the membranes, the
colonization of the newborn is initiated4 by further exposure to the
flora during the infant’s passage through the birth canal. When premature
rupture of the membranes occurs, the ascending flora can cause infection of the
amniotic fluid with involvement of the fetal membranes, placenta, and umbilical
cord.13 Aspiration of the infected amniotic fluid can cause
aspiration pneumonia. Since anaerobic bacteria are the predominant organisms in
the mother’s genital flora,14 they become major pathogens in
infections that follow early exposure of the newborn to that flora.
Genetic factors may be responsible for the
predominance of sepsis in the newborn male.15 The immaturity of the
immunologic system, which is manifested by decreased function of the phagocytes
and decreased inflammatory reactions, may also contribute to the susceptibility
of infants to microbial infection.16,17 The presence of anoxia and
acidosis in the newborn may interfere also with the defense mechanisms.
The
support systems and procedures used in regular nurseries and intensive care
units can facilitate the acquisition of infections. Offending instruments
include umbilical catheters, arterial lines, and intubation devices.
Contamination of equipment such as humidifiers and supplies such as intravenous
solutions and infant formulas and poor isolation techniques can result in
outbreaks of bacterial or viral infections in nurseries. Such spread is thought
to contribute to clustering of cases of necrotizing enterocolitis in newborns.
Conjunctivitis and Dacryocystitis
Conjunctivitis: Conjunctivitis in the newborn
infant usually is due to chemical and mechanical irritation caused by the
instillation of silver nitrate drops or ointment into the eye in order to
prevent gonorrheal ophthalmia. Chemical conjunctivitis differs from infective
forms in that it becomes apparent almost immediately after the instillation.
The most common causes of infectious conjunctivitis in descending order of
frequency are Chlamydia trachomatis, Neisseria gonorrhoeae, Staphylococcus, inclusion conjunctivitis
caused by groups A and B Streptococcus,
Enterococcus, Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas
aeruginosa, Escherichia coli, Moraxella catarrhalis, Neisseria meningitidis, Corynebacterium
diphtheriae, herpes simplex virus, echoviruses, and Mycoplasma hominis.. Clostridia and peptostreptococci
were implicated as probable causes of neonatal conjunctivitis.18
The
classical ophthalmia neonatorum caused by N.
gonorrhoeae is an acute purulent conjunctivitis that appears from two to five
days after birth. If untreated, the infection progresses rapidly until the eye
becomes puffy and the conjunctiva is intensely red and swollen. The subsequent
outcome would be corneal ulceration. Ophthalmia caused by organisms other than
gonococcus, including Clostridium
spp., occurs usually from 5 to 14 days following delivery, is indistinguishable
clinically, and the conjunctival inflammatory reaction usually is milder than
in ophthalmia caused by gonococci.
The conjunctiva of newborns
acquires facultative and anaerobic bacteria during birth primarily from the
mother’s cervical flora during passage through the birth canal. The role of
anaerobes in neonatal conjunctivitis was investigated by obtaining conjunctival
cultures from 35 babies prior to silver nitrate application and 48 hours later.
19 On initial culture, 46
facultative bacteria and 27 anaerobes were recovered. The organisms isolated in
almost all of these cases were present also in the mother’s cervical cultures
and in the baby’s gastric aspirates, taken concomitantly.
Isenberg et al20
who studied 106 infants, 50 delivered by cesarian section, and 56 delivered
vaginally illustrated that those delivered by cesarean section had
significantly fewer bacterial species and total number of organisms per subject
than the infants delivered vaginally. The conjunctivae of infants delivered
vaginally had significantly more bacteria characteristic of vaginal flora.
Clostridium spp.
were recovered from two infants who developed conjunctivitis.14,18 Clostridium perfringens was recovered
from one newborn, and Clostridium
bifermentans with Peptostreptococcus
spp. were recovered from the other infant with neonatal conjunctivitis. Similar
organisms were recovered from the mother’s cervix immediately after delivery.
These infections were noted on the second and third day postdelivery. The
conjunctivitis was characterized by a profuse yellow-green discharge and the
eyelids were edematous in both newborns, and there were no other abnormal
findings. Local therapy was initiated with 2% penicillin eye drops (two drops
every two hours). The conjunctivitis subsided within three days, and repeat
cultures of the eyes after 10 days were sterile. The babies were followed for
three months with no residual of infection noted.
Of interest is that the silver
nitrate solution of 1% currently used in newborns was efficacious in preventing
in vitro growth of clostridia. However, in a concentration of 0.1% or lower, it
was only bacteriostatic or ineffective. The common practice of rinsing the eyes
with distilled water after the addition of silver nitrate to prevent chemical
conjunctivitis may alter the ability of this solution to effectively inhibit
certain strains of Clostridium spp.
Because anaerobic bacteria
have been recovered from children22 and adults23,24
suffering from bacterial conjunctivitis, their presence in neonatal
conjunctivitis is not surprising. These organisms, however, are not the most
prevalent cause of inflammation of the eye in these age groups. Their presence
should be suspected in children whose aerobic and chlamydial cultures are
negative, in those who do not respond to conventional antimicrobial therapy,
and in those at high risk of developing anaerobic infection (i.e., the presence
of maternal amnionitis or premature rupture of membranes).
The experience acquired from
the documented cases of anaerobic conjunctivitis indicates that local therapy
with appropriate antimicrobial agents is generally adequate.
Conjuctivitis newborn
Dacryocystitis:
The
predominant bacteria causing acute dacryocystitis in neonates are aerobic
organisms such as Streptococcus
pneumoniae and Staphylococcus aureus,25,26 Anaerobic
bacteria have been rarely recovered in these patients.27 We recently
reported two newborns who developed acute dacryocystitis caused by anaerobic
bacteria.28
Peptostreptococcus
micros and Prevotella intermedia were recovered in one
newborn, and Peptostreptococcus magnus and
Fusobacterium nucleatum in the other.
Parenteral therapy was given to both newborns and the first patient had
surgical drainage. The anaerobes isolated are likely of endogenous origin
because they are members of the normal oral and skin flora29 and
normal conjunctival flora.30,31
The
actual prevalence of these organisms in dacryocystitis in infants has yet to be
investigated by prospective studies. This is of particular importance because
these organisms are often resistant to the antimicrobials used for therapy of
dacryocystitis. We elected to treat the patients for at least 21 days to
achieve complete eradication of the infection. It is recommended that specimens
of dacryocystitis be cultured for both aerobic and anaerobic bacteria so that
proper antimicrobial therapy can be directed against the pathogens.
Dacryocystitis newborn
Suppurative parotitis and sialadenitis
Staphylococci
are the usual bacterial etiology of suppurative parotitis and sialadenitis in
newborns. Anaerobic bacteria from aspirates of the infected gland in two
infants with suppurative parotitis. Peptostreptococcus
intermedius and Prevotella
melaninogenica were isolated from one child and Prevotella intermedia from the other patient. 31a Complete recovery occurred after 4
weeks of antimicrobial therapy.
Anaerobes
were recovered from aspirates of an infected salivary gland in 2 newborns with
suppurative sialadenitis. Peptostreptococcus magnus, Prevotella
intermedia and Streptococcus pyogenes
were isolated from one newborn and Prevotella
melaninogenica and Fusobacterium
nucleatum from the other patient.
31b
Complete recovery occurred following surgical
drainage and antimicrobial therapy.
These reports illustrates the potential
importance of anaerobes in acute suppurative sialadenitis in newborns. The
isolation of anaerobes is not surprising since these bacteria are the
predominant organisms in the oropharynx where they outnumber aerobes in the
ratio of 10 to 1 to 100 to one in the neonate as well , and are important
pathogens in other suppurative infection in and around the oropharynx. Prevotella spp. are the most common
anaerobic Gram-negative bacilli found in oral flora and like Fusobactrium and Peptostreptococcus
spp., are frequently isolated from odontogenic orofacial infections.
Suppurative parotitis newborn
Suppurative sialadenitis newborn
Cephalohematoma
Cephalohematomas
are rare complications that occur in less than 3% of all deliveries and are
associated with instrumented delivery and prolonged labor. Six newborns with
cephalohematoma infected by anaerobes were reported. 31c Polymicrobial
infection was present in all instances, where the number of isolates varied
from two to four. Two patients had anaerobes only and the other four had mixed
flora of strict anaerobes and facultatives. There were 16 bacterial isolates
(12 anaerobic, 4 aerobic). The anaerobic isolates were Peptostreptococcus spp. (5 isolates), Prevotella spp. (4), B.
fragilis group (2), and Propionibacterium
acnes (1). The aerobic isolates were E.
coli (2), S. aureus (1) and group
B streptococci (1). Blood cultures were positive for three patients.
The
most common predisposing conditions were vacuum extraction and amnionitis (4
instances of each), instrumental delivery (3), electronic fetal monitoring (2),
prolonged delivery (1), and premature rupture of membranes (1). All patients
underwent drainage, and four also had surgical incision and drainage.
Osteomyelitis developed in one instance and scalp abscess developed in two
patients, both of whom had electronic fetal monitoring. All patients eventually
recovered from infection after receiving parenteral and subsequent oral
antibiotic therapy for a total of 14-38 days. This report highlights the
polymicrobial nature and potential importance of anaerobic bacteria in infected
cephalohematoma in newborns.
Cephalohematoma in a newborn
Pneumonia
Pneumonia in the newborn can
be classified according to the mode of acquiring the infection and the time
when the infection takes place. The infection can be acquired in utero by
transplacental route or following intrauterine infection. The pneumonia could
be acquired during delivery by aspiration of bacteria that colonize the birth
canal. The type of infection contracted after birth is acquired by contact with
environmental objects (e.g., a tracheostomy tube) or by human contact.
Aspiration can occur in up to 80% of intubated premature infants 32
and is common newborns with gastroesophageal reflux 33 or those who
require general anesthesia 34 and have swallowing dysfunction.
35
Congenital and intrauterine
pneumonia usually is caused by viruses such as herpes simplex, cytomegalovirus,
or rubella, and can be caused also by intrauterine exposure to Treponema pallidum, Mycobacterium
tuberculosis, or Listeria
monocytogenes. Aspiration during delivery or after intubation can be caused
by the mother’s vaginal flora, and the patient’s oral flora once that had
developed. Early neonatal pneumonia is mainly caused by bacteria, group B
streptococcus, Escherichia coli and
listeria being the most frequently involved; 36 Herpes simplex is
the main viral agent. These agents may also be responsible for late forms, as
do Chlamydia trachomatis and the
pathogen agents of community acquired pneumonia.
.
During vaginal delivery, the
neonate is exposed to the cervical birth canal flora, which includes both
aerobic and anaerobic bacteria. Almost every normal baby born by
vaginal delivery swallows potentially pathogenic aerobic and anaerobic
bacteria.19 These bacteria can be cultured in the infant's gastric
contents. In a few instances, especially in high-risk infants, aspiration of,
or exposure to, these organisms can lead to the development of infections. The
diagnosis of bacterial pneumonia can be achieved by cultures of tracheal
aspirate, pleural fluids, needle aspirates of the lungs, and blood cultures.
The major bacterial causes
perinatal pneumonia are Enterobacteriacae, Staphylococcus
aureus, group B beta-hemolytic streptococci, group D streptococci, and alpha-hemolytic
streptococci 36 In approximately 40% of the cases previously
reported, no organisms were recovered at necropsy. Although the role of
anaerobes as a cause of pulmonary infection in adults is well established
37 only two reports 38,39 described the isolation of Bacteroides fragilis from children with
perinatal pneumonia.
Harrod and Stevens 38
described two newborns who presented with neonatal aspiration pneumonia that developed
following maternal amnionitis. B.
fragilis was recovered from the blood of these children.
Brook, et al.39
reported three newborns with neonatal pneumonia caused by B. fragilis group. The mothers of all three infants had premature
rupture of their membranes and subsequent amnionitis. The maternal membranes
ruptured more than 24 hours before delivery, and the amniotic fluid was foul
smelling. Organisms identical to those recovered from the newborns were
recovered from the amniotic fluid of two of the mothers. In all three
instances, the organisms were recovered from tracheal aspirates and in two from
blood cultures as well. Two of the newborns were treated with ampicillin and
gentamicin but succumbed to their infections; one of these infants also had meningitis.
The third baby, treated with clindamycin, recovered.
Anaerobic Gram negative
bacilli (e.g. Prevotella, Porphyromonas and Bacteroides
sp.) are part of the normal flora of the female genital tract.19
These organisms are involved frequently in ascending infections of the uterus
and have been recognized as pathogens in septic complications of pregnancy,
such as amnionitis, endometritis, and septic abortion, and from infection in
other clinical settings.40 Amnionitis may develop prior to delivery
resulting in an early exposure of the infant to the offending organism(s).
Furthermore, the relative immaturity of the cellular and humoral immune systems
of the newborn may permit localized infections to invade the blood stream.
Tracheal aspirates of infants
who have recently had an endotracheal tube placed may be useful for diagnosing
pneumonia and for identifying the causative agent.41 Repeated
aspirates can reveal the presence of newly acquired organisms that may cause
the pneumonia. 42
Pulmonary anaerobic infections
tend to occur in association with aspiration, tissue anoxia, and trauma. Such
circumstances usually are present in high-risk newborns, which make them more
vulnerable to anaerobic pneumonia, especially in the presence of maternal
amnionitis.
In most instances, a beta
lactam antibiotic and one of the aminoglycosides are administered for treatment
of infection or pneumonia in newborns. While most anaerobic organisms are
susceptible to penicillins, members of the B.
fragilis group and growing numbers of other anaerobic gram negative bacilli
(e.g. pigmented Prevotella and Porphyromonas 43 can be resistant to
these agents. The first two described newborns,29 who died of their
infections, received the conventional antimicrobial therapy of a combination of
ampicillin and gentamicin that was inappropriate for their infection. The third
newborn, however, received a broader coverage that included therapy with
clindamycin, a drug shown to be effective in the treatment of anaerobic
infections in adults44 and children.45 Because
clindamycin does not penetrate the blood-brain barrier in sufficient
quantities, it is not recommended for treatment of meningitis. Other
antimicrobial agents with better penetration to the central nervous system,
such as chloramphenicol, a carbapenem (i.e. imipenem), a combination of a
penicillin plus a beta lactamase inhibitor or metronidazole, should be
administered in the presence of meningitis.
Ascending cholangitis following porto-enterostomy
Extrahepatic biliary atresia is an obliterative
cholangiopathy that involves all or part of the extrahepatic biliary tree and,
in many instances, the intrahepatic bile ducts. In the United States , from 400 to 600 new
cases of biliary atresia are encountered annually.46 The diagnosis
is usually suggested by the persistence of jaundice for 6 weeks or more after
birth. Several factors have been considered for the pathogenesis of
extrahepatic biliary atresia, including viral infection (e.g. cytomegalovirus),
47 metabolic insults, and abnormalities in bile duct morphogenesis.
Although selected patients benefit from prompt diagnosis and Kasai
portoenterostomy surgical intervention48,49 within the first 60 days
of life, many ultimately require liver transplantation because of portal
hypertension, recurrent cholangitis, and cirrhosis. 50
Infection of the biliary tract and rarely liver
abscess are a known complication following Kasai ’s
procedure. About half of the patients who undergo the Kasai
procedure develope post surgical cholangitis .51 Most episodes
occurred within 3 months of the operation. Factors associated with cholangitis
included good or partial restoration of bile flow, abnormal intrahepatic bile
ducts or cavities at the porta hepatis, and routine postoperative use of
antibiotics. External jejunostomy is not effective in preventing cholangitis.
Fever decreased bile flow, increased erythrocyte sedimentation rate and signs
of shock are frequently observed.
Early bacterial studies of cholangitis
following Kasai’s procedure revealed coliform bacilli, Proteus species, and enterococci to be the predominant isolates
recovered from these patients.52,53 However, adequate culture
methods for anaerobic bacteria were not performed in most of these studies. The
largest study reporting the bacterial growth within the biliary tract following
the Kasai operation was done by Hitch and
Lilly,52 who studied 19 patients over 23 months, obtaining 283
cultures. These investigators used methods for recovery of aerobic as well as
anaerobic bacteria and reported the colonization of all the biloenteric
conduits with colonic flora within the first postoperative month. Escherichia coli, and Klebsiella, Enterococcus , Pseudomonas,
Proteus, and Enterobacter spp. were the predominant aerobic isolates. Bacteroides spp., including B. fragilis, were recovered in 11% of
the cultures. These authors report the recovery of similar organisms during
episodes of cholangitis.
Studies in adults demonstrated that E. coli,
klebsiellae, Enterobacter organisms,
enterococci, and anaerobes (B. fragilis group and Clostridium spp. ) are the main isolates recovered from patients
with biliary tract infection. 53-57
Brook and Altman studied the aerobic and
anaerobic microbiology of the bile duct system in six children with cholangitis
following Kasai ’s procedure.58
Fourteen aerobic bacteria were recovered from all six specimens, and 3
anaerobic organisms were recovered from three. The predominant aerobes were Klebsiella pneumoniae (4 isolates), Enterococcus spp. (3), and E. coli
(2). The anaerobes recovered were B.
fragilis (2) and C. perfringens (one).
Since that report, we have isolated anaerobes in three more patients, which
were two strains of C. perfringens and one B. fragilis. These
findings demonstrate the role of anaerobic organisms in cholangitis following
hepatic porto-enterostomy.
The mechanism by which both aerobic and
anaerobic bacteria reach the bile ducts in patients who had undergone Kasai ’s procedure is probably by an ascending mode from
the gastrointestinal tract. This mode of spread is favored by the surgical
procedure that approximates a part of the jejunum to the bile system, by the
lack of the normal choledochal sphincter action, and by the stasis that can
develop after the surgery. Other mechanisms of development of cholangitis are
transhepatic filtration of bacteria from the portal venous blood into the
cholangiole and periportal lymphatic infection.
The anaerobes recovered in children with
ascending cholangitis5,58 are part of the normal gastrointestinal
flora in infants. The initial sterile meconium becomes colonized within 24
hours with aerobic and anaerobic bacteria, predominantly E. coli, Clostridium species, B. fragilis,
and streptococci.59 The isolation rate of B. fragilis and other
anaerobic bacteria in the gastrointestinal tract of term babies approaches that
of adults within one week.59
Although the number of infants studied so far
is small, the data suggest that anaerobes play a major role in cholangitis
following Kasai ’s procedure, and that
specimens obtained from these patients should be cultured routinely for
anaerobic as well as aerobic bacteria. It is conceivable that some of the
reported failures of conventional antimicrobial therapy to cure patients with
postsurgical cholangitis60 could be due to failure to use antimicrobial
agents effective against anaerobic bacteria, especially those belonging to the B. fragilis
group.
While most anaerobic organisms are susceptible
to penicillins, members of the B. fragilis group are known to be resistant
to these agents.42 In administering therapy to infected patients,
consideration should be given to the possible presence of anaerobic organisms.
It is reasonable, therefore, to treat children with this infection with
antimicrobial agents effective also against B.
fragilis and Clostridium sp., at least until results of cultures are known.
Extrahepatic biliary atresia
Anaerobic
bacteremia in newborns
The
awareness of the role of anaerobic bacteria in neonatal bacteremia and sepsis
has increased in recent years. The incidence of recovery of anaerobes in
neonatal bacteremia varies between 1.8% and 12.5% [61]. Of the 179 cases
reported in the literature and reviewed by Brook [61], 73 were due to Bacteroides spp. (69 were the B. fragilis group), 57 Clostridium spp.
(mostly C. perfringens), 35 Peptostreptococcus spp., 5 P. acnes, 3 Veillonella spp., 3 Fusobacterium
spp, and 2 Eubacterium spp.
Multiple
organisms, aerobic and anaerobic, were isolated from eight patients reported in
one study [62], anaerobic co isolates from 6 (5 Peptostreptococcus spp., one Veillonella
parvula) and aerobic co isolates from only two (Escherichia coli and
alpha-hemolytic streptococcus). In one patient, reported by Noel et al. [63], Bacteroides vulgatus was isolated from a
single blood culture along with 4 aerobic bacteria (Streptococcus faecalis, E. coli, Streptococcus faecium and Klebsiella
pneumoniae).
Simultaneous
isolation of the anaerobes from other sites was reported by several authors [62-69].
This was especially common with B.
fragilis and Clostridium spp.
Chow
and co-workers [62] reported the simultaneous isolation of Bacteroides spp. from gastric aspirate in four instances, from the
amniotic fluid or uterus at cesarean section in two cases, and from the
maternal and fetal placental surfaces and the external auditory canal in one
instance each.
Brook
et al. [70] reported the concomitant recovery of B. fragilis group from lung aspirates of two patients with pneumonitis;
Harrod and Sevens [71] recovered B.
fragilis from the inflamed placenta; Dysant and associates [67] and Brook
et al. [65], Kasik et al. [66] and Webber and Tuohy [72] recovered B. fragilis from the cerebrospinal fluid
of a total of four patients with meningitis. Brook [65] isolated B. fragilis from an occipital abscess
that developed following neonatal monitoring with scalp electrodes. Ahonkhai et
al. [73] described the concomitant isolation of C. perfringens in the placenta of a newborn.
Kosloske
et al. [74] recovered Clostridium spp.,
B. fragilis, and Eubacterium spp. from the peritoneal cavity of four patients with
necrotizing enterocolitis. Brook et al. [68] isolated Clostridium difficile from the peritoneal cavity and the blood of a
newborn with necrotizing enterocolitis. Other cases of concomitant isolation
include Spark and Wike [75] who reported four cases of isolation of Clostridium spp. from omphalitis, Heidemann
et al. [69] who recovered a gas forming C.
perfringens in the cerebrospinal fluid of a newborn with meningitis, and Freedman and Hollander who isolated C. perfringens in the blood of a newborn
after abdominal surgery [76].
Newborn in intensive care unite
REFERENCES
1. Oray-Schrom P, Phoenix C, St Martin D,
Amoateng-Adjepong Y. Sepsis workup in febrile infants 0-90 days of age with
respiratory syncytial virus infection. Pediatr Emerg Care. 2003;19:314-9.
2. Waheed M, Laeeq A, Maqbool S. The etiology
of neonatal sepsis and patterns of antibiotic resistance. J Coll
Physicians Surg Pak. 2003 ;13:449-52.
3. Lott JW. Neonatal bacterial sepsis. Crit
Care Nurs Clin North Am. 2003;15:35-46.
4. Benson KD, Luchansky JB, Elliott JA, Degnan
AJ, Willenberg HJ, Thornbery JM, Kay HH. Pulsed-field fingerprinting of vaginal
group B streptococcus in pregnancy. Obstet Gynecol. 2002;100:545-51.
5. Prevedourakis, C., Papadimitriou, G.,
Ioannidou, A.: Isolation of pathogenic bacteria in the amniotic fluid during
pregnancy and labor. Am. J. Obstet. Gynecol. 106:400-2, 1970.
6. Yoshio H, Tollin M, Gudmundsson GH,
Lagercrantz H, Jornvall H, Marchini G, Agerberth B. Antimicrobial polypeptides
of human vernix caseosa and amniotic fluid: implications for newborn innate
defense. Pediatr Res. 2003 ;53:211-6.
7. Larson, B., Snyder, I.S., Galask, R.P.:
Bacterial growth inhibition by amniotic fluid. Am. J. Obstet. Gynecol.
119:492-7, 1974.
8. Silver, H.M., Siler-Khodr T, Prihoda TJ,
Gibbs RS.: The effects of pH and osmolality on bacterial growth in amniotic
fluid in a laboratory model. Am. J. Perinatol. 9:69-74, 1992.
9. Talmi YP, Sigler L, Inge E, Finkelstein Y,
Zohar Y. Antibacterial properties of human amniotic membranes. Placenta.
1991;12:285-8..
10. Ledger,
W.J., Sucet, R.L., Headington, J.T.: Bacteroides species as a cause of severe
infections in obstetrics and gynaecologic patients. Surg. Gynecol. Obstet.
133:837-42, 1971.
11. Pearson,
H.E., Anderson, G.V.: Perinatal deaths associated with Bacteroides infections.
Obstet. Gynecol. 30:486-92, 1967.
12. Ismail,
M.A., Salti GI, Moawad AH.: Effect of amniotic fluid on bacterial recovery and
growth: clinical implications. Obstet. Gynecol. Surv. 44:571-7, 1989.
13. Benirschke,
K.: Routes and types of infection in the fetus and newborn. Am. J. Dis. Child.
99:714-21, 1960.
14. Brook, I.,
Barrett CT, Brinkman CR 3rd, Martin WJ, Finegold SM.: Aerobic and anaerobic
flora of maternal cervix and newborn gastric fluid and conjunctiva: a
prospective study. Pediatrics 63:451-5, 1979.
15. Washburn,
T.C., Medearis, D.N., Jr., Childs, B.: Sex differences in susceptibility to
infection. Pediatrics 35:57-64, 1965.
16. Miller,
EM., Stiehm, E.R.: Phagocytic opsonic and immunoglobulin studies in the
newborns. Calif. Med. 119:43-63, 1972.
17. Fleer A,
Gerards LJ, Verhoef J. Host defence to bacterial infection in the neonate.
J Hosp Infect.
Suppl A:320-7. 1988.
18. Teoh DL,
Reynolds S.: Diagnosis and management of pediatric conjunctivitis. Pediatr
Emerg Care. 2003 ;19:48-55.
19. Brook, I.,
Martin, W.J., Finegold, S.M.: Effect of
silver nitrate application on the conjunctival flora of the newborn, and the occurrence of clostridial
conjunctivitis. J. Pediatr. Ophthalmol. Strabismus 15:179, 1978.
20. Isenberg,
S.J., Apt L, Yoshimori R, McCarty JW, Alvarez SR..: Source of the conjunctival
bacterial flora at birth and implications for ophthalmia neonatorum
prophylaxis. Am J Ophthalmol 15;106:458-62, 1988.
21. Krohn,
M.A., Hillier SL, Bell TA, Kronmal RA, Grayston JT..: The bacterial etiology of
conjunctivitis in early infancy. Am J Epidemiology 138: 326, 1993.
22. Brook, I.:
Anaerobic and aerobic bacterial flora of acute conjunctivitis in children.
Arch. Ophthalmol. 98:833, 1980.
23. Perkins,
R.E., Kundsin RB, Pratt MV, Abrahamsen I, Leibowitz HM.: Bacteriology of normal
and infected conjunctiva. J. Clin. Microbiol. 1:147-9, 1975.
24. Brook, I.,
Pettit TH, Martin WJ, Finegold SM.: Anaerobic and aerobic bacteriology of acute
conjunctivitis. Ann. Ophthalmol. 11:389-93, 1979.
25. Pollard,
Z.F.: Treatment of acute dacryocystitis in neonates. J Pediatr Ophthal
Stabismis 28:351-3, 1991.
26.
Huber-Spitzy, V., E., Steinkogler FJ, Huber E, Arocker-Mettinger E,
Schiffbanker M.: Acquired dacryocystitis: microbiology and conservative
therapy. Acta Ophthalmol (Copenh) 70:745-9, 1992.
27. Evans,
A.R., Strong JD, Buck AC..: Combined anaerobic and coliform infection in acute
dacryocystitis. J Pediatr Ophthal Strabismis 28:292-4, 1991.
28. Brook, I.:
Dacryocystitis Caused by Anaerobic Bacteria in the Newborn. Ped Inf. Dis J. 17:
172-3, 1998.
29. Rosebury,
T.: Microorganisms indigenous to man. New York: McGraw-Hill, 1996.
30. Matsura,
H.: Anaerobes in the bacterial flora of the conjunctival sac. Jpn J Ophthalmol
116-24, 1971.
31. Perkins,
R.E., Abrahamson, I., Leibowitz, H.M.: Bacteriology of normal and infected
conjunctiva. J Clin Microbiol 1:147-9, 1975.
31a.Brook I.
Suppurative parotitis caused by anaerobic bacteria in newborns. Pediatr Infect
Dis J.;21:81-2. 2002.
31b. Brook I.
Suppurative sialadenitis associated with anaerobic bacteria in newborns.
Pediatr Infect Dis J. 2006;25: 280.
31c. Brook I.
Infected neonatal cephalohematomas caused by anaerobic bacteria. J Perinat Med.
2005;33:255-8.
32. Goodwin,
S.R., Graves SA, Haberkern CM..: Aspiration in intubated premature infants.
Pediatrics 75:85-8, 1985.
33.
Mukhopadhyay, K., Narang A, Kumar P, Chakraborty S, Mittal BR..:
Gastroesophageal reflux and pulmonary complication in a neonate. Indian Pediatr
35:665-8, 1998.
34. Borland,
L.M., Sereika SM, Woelfel SK, Saitz EW, Carrillo PA, Lupin JL, Motoyama EK.:
Pulmonary aspiration in pediatric patients during general anesthesia: incidence
and outcome. J Clin Anesth 10:95-102, 1998.
35. Kohda, E.,
Hisazumi H, Hiramatsu K..: Swallowing dysfunction and aspiration in neonates
and infants. Acta Otolaryngol Suppl (Stockh) 517:11-6, 1994.
36. Albertini,
M.: Neonatal pneumonia. Arch Pediatr 5 Suppl 1:57s-61s, 1998.
37. Bartlett,
J.C., Finegold, S.M.: Anaerobic infections of the lung and pleural space. Am.
Rev. Respir. Dis. 110:56-77, 1974.
38. Harrod,
J.R., Stevens, D.A.: Anaerobic infections in the newborn infant. J. Pediatr.
85:399-402, 1974.
39. Brook, I.,
Martin, W.J., Finegold, S.M.: Neonatal pneumonia caused by members of the
Bacteroides fragilis group. Clin. Pediatr. 19:541-5, 1980.
40. Price B,
Martens M. Outpatient management of pelvic inflammatory disease. Curr Womens
Health Rep. 1:36-40. 2001.
41. Ruderman,
J.W., Srugo I, Morgan MA, Vinstein AL, Brunell PA.: Pneumonia in the neonatal
intensive care unit. Diagnosis by quantitative bacterial tracheal aspirate
cultures. J Perinatol 14:182-6, 1994.
42. Akhtar, N.,
Stromberg D, Rosenthal GL, Bowles NE, Towbin JA..: Tracheal aspirate as a
substrate for polymerase chain reaction detection of viral genome in childhood
pneumonia and myocarditis. Circulation 99:2011-8, 1999.
43. Rasmussen,
B.A., Bush K, Tally FP..: Antimicrobial resistance in anaerobes. Clin Infect
Dis 24 Suppl 1:S110-20, 1997.
44. Gorbach,
S.L., Thadepalli, H.: Clindamycin in the treatment of pure and mixed anaerobic
infections. Arch. Intern. Med. 134:87-92, 1974.
45. Brook, I.:
Clindamycin in the treatment of aspiration pneumonia in children. Antimicrob.
Agents Chemother. 15:342-5, 1979.
46. Lefkowitch,
J.H.: Biliary atresia. Lefkowitch JH: Mayo Clin Proc 73:90-5, 1998.
47. Tarr, P.I.,
Haas, J.E., Christie, D.L.: Biliary atresia, cytomegalovirus, and age at
referral. Pediatrics 97:828-31, 1996.
48. Kasai M,
Mochizuki I, Ohkohchi N, Chiba T, Ohi R. Surgical limitation for biliary
atresia: indication for liver transplantation. J Pediatr Surg. 1989;24:851-4..
49. Bezerra JA.
Potential etiologies of biliary atresia. Pediatr Transplant. 2005;9:646-51.
50. Kobayashi
H, Stringer MD. Biliary atresia. Semin Neonatol. 2003 ;8:383-91.
51. Krishna M,
Keaveny AP, Genco PV, Rosser BG, Dickson RC, Nguyen JH, Steers JL, Nakhleh RE.
linicopathological review of 18 cases of liver allografts lost due to bile duct
necrosis.
Transplant
Proc. 2005 ;37:2221-3.
52. Hitch,
D.C., Lilly, J.R.: Identification, quantification and significance of bacterial
growth within the biliary tract after Kasai’s operation. J. Pediatr. Surg.
13:563-9, 1978.
53. Brook, I.:
Aerobic and anaerobic microbiology of biliary tract disease. J Clin Microbiol.
27:2373-5, 1989.
54. Finegold,
S.M.: Anaerobic bacteria in human disease. New York: Academic Press, 1977.
55. England,
D.M., Rosenblatt, J.E.: Anaerobes in human biliary tracts. J. Clin. Microbiol.
6:494-8, 1977.
56. Shimada,
K., Inamatsu, T., and Yamashiro, M.: Anaerobic bacteria in biliary disease in
elderly patients. J. Infect. Dis. 135:850-4, 1977.
57.
Lykkegaard-Nielsen, M., Asnaes, S., Justesen, T.: Susceptibility of the liver
and biliary tract to anaerobic infection in extrahepatic biliary tract
obstruction: III. Possible synergistic effect between anaerobic and aerobic
bacteria: An experimental study in rabbits. Scand. J. Gastroenterol. 11:263-72,
1976.
58. Brook, I.,
Altman, P.: The significance of anaerobic bacteria in biliary tract infection
after hepatic portoenterostomy for biliary. Surgery 95:281-3, 1984.
59. Long, S.S.,
Swenson, R.M.: Development of anaerobic fecal flora in healthy newborn infants.
J. Pediatr. 91:298-301, 1977.
60. Chaudhary,
S., Turner, R.B.: Trimethoprim-sulfamethoxazole for cholangitis following
hepatic portoenterostomy for biliary atresia. J. Pediatr 99:656-8, 1981.
6I. Brook. Bacteremia due to anaerobic bacteria
in newborns. J Perinatol, 10 (1990). 351–356.
62. A.W. Chow,
R.D. Leake, T. Yamauchi, B.F. Anthony, L.B. Guze. The significance of anaerobes
in neonatal bacteremia: analysis of 23 cases and review of the literature.
Pediatrics, 54 (1974),736–745.
63. Noel, D.A. Laufer, P.J. Edelson. Anaerobic
bacteremia in a neonatal intensive care unit: an eighteen-year experience.
Pediatr Infect Dis J, 7 (1988), 858–862.
64. S. Ohta, S. Shimizu, S. Fujisawa, M.
Tsurusawa. Neonatal adrenal abscess due to Bacteroides. J Pediatr, 93
(1978),1063–1064.
65. I. Brook. Osteomyelitis
and bacteremia caused by Bacteroides
fragilis. Clin Pediatr, 19 (1980), 639–640.
66. J.W. Kasik,
D.L. Bolam, R.M. Nelson. Sepsis and meningitis associated with anal dilation
in newborn infant. Clin Pediatr, 9
(1984), 509–510.
67. N.K.
Dysart, W.R. Griswold, J.E. Schanberger, P.J. Goscienki, A.W. Chow. Meningitis
due to Bacteroides fragilis in a
newborn. J Pediatr, 89 (1976), 509–10.
68. I. Brook,
G. Avery, A. Glasgow. Clostridium difficile in pediatric infections. J Infect,
4 (1982), 253–257.
69. S.M.
Heidemann, K.L. Meest, E. Perrin, A.P. Sarnaik. Primary meningitis in infancy.
Pediatr Infect Dis J, 8 (1989), 126–128.
70. I. Brook,
W.J. Martin, S.M. Finegold. Neonatal pneumonia caused by members of the
Bacteroides fragilis group. Clin Pediatr, 19 (1980), 541–543.
71. J.R.
Harrod, D.A. Stevens. Anaerobic
infections in the newborn infant. J Pediatr, 85 (1974), 399–402.
72. S.A.
Webber, P. Tuohy. Bacteroides fragilis
meningitis in a premature infant successfully treated with metronidazole.
Pediatr Infect Dis J, 7 (1988), 886–887.
73. V.I.
Ahonkhai, M.H. Kim, K. Raziuddin, E.J. Goldstein. Perinatal Clostridium
perfringens infection Clin Pediatr, 20 (1981), 532–533.
74. A.M.
Kosloske, J.A. Ulrich. A bacteriologic basis for clinical presentation of
necrotizing enterocolitis. J Pediatric Surg, 15 (1980), 558–564.
75. R.P. Spark,
D.A. Wike. Nontetanus clostridial neonatal fatality after home delivery. Ariz
Med, 10 (1983), 697–700.
76. S.
Freedman, M. Hollander. Clostridium
perfringens septicemia as a postoperative complication of the newborn
infant. J Pediatr, 71 (1967),576–578.
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