Neonatal Sepsis

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Transcript Neonatal Sepsis

Neonatal Sepsis
APPROPRIATE USE
OF ANTIBIOTICS

Newborns are extremely
susceptible to infection, and sepsis
is a significant cause of morbidity
and mortality in this population

Neonatal sepsis is a systemic
inflammatory response syndrome (SIRS)
that is secondary to infection.

Systemic inflammatory response
syndrome is defined by the presence of
two or more of the following variables:
fever or hypothermia, tachycardia,
tachypnea or hyperventilation, and an
abnormally high or low white blood cell
count.

Neonatal sepsis is categorized
according to the infant’s postnatal
age at onset of disease.

early-onset sepsis occurring at or
before 72 hours of life, and late
onset occurring at greater than 72
hours to 7 days.

In early-onset sepsis,

vertical transmission through ascending amniotic
fluid infection

acquisition of bacterial flora from the mother’s
anogenital tract during vaginal delivery.

Some bacteria cross the placenta : Treponema
pallidum and Listeria monocytogenes.

maternal anogenital colonization , most
commonly responsible for early-onset sepsis:
group B streptococci (GBS) and Gram-negative
enteric bacilli.

The overall incidence of early-onset sepsis 0.98 per 1000 live
births

the highest rates occur among preterm and low birth weight
infants, 10.96 per 1000 live births

Mortality rates are also inversely proportional to gestational
age.

The most common causative bacteria are GBS and
Escherichia coli, accounting for 38% to 43% and 24% to 29% of
early-onset cases, respectively.
Staphylococcus aureus, viridans group Streptococci,
Enterococci, group A Streptococci, Listeria
monocytogenes, Haemophili, and other Gramnegatives, including Klebsiella, Enterobacter,
Citrobacter, Acinetobacter, and Pseudomonas, are
also known pathogens associated with early-onset
neonatal sepsis.

In late-onset sepsis, acquisition of
infection is through the infant’s
environment. including part of the
flora of their caregivers.

Extreme prematurity is one of the greatest
risk factors for late-onset sepsis


long hospital stays and indwelling
vascular catheters
improved surgical care and survival for
neonates with congenital heart

Common causes of late-onset infection in
very low birth weight and premature
infants include coagulase-negative
staphylococci and S. aureus, as well as
invasive candidiasis, pseudomonas and
other gram negative enterobacteriacea.
Group B streptococcus and E. coli are
also commonly implicated in late-onset
sepsis.

Escherichia coli is frequently a cause of
urosepsis in young infants.
 Appropriate
diagnosis is
important for appropriate
antibiotics usage.

The clinical signs of sepsis in a neonate are
often nonspecific. Detection requires that
clinicians maintain a high index of
suspicion.

Common presenting signs include respiratory
distress, hemodynamic instability with poor
perfusion or shock, and temperature instability.

Lethargy or poor feeding may be the only
symptoms initially.

Metabolic changes may include hyperglycemia
or hypoglycemia, acidosis, and jaundice.

Meningismus is uncommon in neonates

Full fontanelle, irritability, lethargy, and seizures
may occur.

Because signs and symptoms are
nonspecific, the clinical diagnosis of
neonatal sepsis is extremely challenging.

A definitive diagnosis requires the
isolation of a pathogen from a normally
sterile body site, including blood,
cerebrospinal fluid (CSF), and urine.

A blood culture (with a collection volume of 1 mL)
should be drawn in any infant with suspected
sepsis.

A lumbar puncture should also be considered in
any infant with suspected sepsis.

There’s poor correlation between results of blood
and CSF cultures

failure to perform a lumbar puncture may result in
missed diagnoses.

Cerebrospinal fluid : based on the infant’s
gestational age, postnatal age, and birth weight .

CSF WBC count of greater than 20 to 30 cells/μL is
consistent with meningeal inflammation.

neonatal meningitis can occur with normal CSF
parameters

some overlap in CSF values between neonates
with and without meningitis

In suspected infants with NL CSF findings, repeat LP 24 to 48
hours later will show pleocytosis if true meningeal inflammation
is present.

CSF Gram stain may be helpful,

a negative Gram stain does not exclude the diagnosis.

In traumatic LP, do not adjust the CSF WBC based on the red
blood cell counts. treat presumptively for meningitis
pending CSF culture results.

For early-onset sepsis, a urine culture is not required.

Suprapubic aspiration or sterile catheterization for urine
cultures.

indirect markers of infection

none are definite

they can be used to help identify infected
infants and guide decisions on duration of
antimicrobial therapy.

WBC with differential

6 to 12 hours after birth are more likely to reflect
an inflammatory response

both high and low WBC, low or high absolute
neutrophil count, and high percentage of
immature to total white blood cells.

flow cytometery for the future

C-reactive protein levels increase within 6 to 8
hours after infection and peak after 24 hours.

The sensitivity of CRP for neonatal sepsis is lowest
early in infection, and sensitivity generally
increases with serial values obtained 24 to 48
hours after onset of symptoms.
Serial determinations may be useful for R/O sepsis
or in monitoring response to treatment.

Procalcitonin peak 12 hours following
infection. Increased levels also with
noninfectious causes, such as respiratory
distress syndrome.

Procalcitonin appears to have better
sensitivity but less specificity than cRP

Specific cytokines
the most important information
guiding clinical decisions continues
to be the patient’s overall clinical
status and culture data.

MANAGEMENT
APPROPRIATE USE OF
ANTIBIOTICS

Ampicillin and an aminoglycoside are recommended as
empiric therapy for early-onset sepsis.

coverage against GBS and E. coli, the most common
causative pathogens, as well as Listeria monocytogenes.

Empiric use of third-generation cephalosporins is not
recommended.

(because of concerns for development of resistance and the
increased risk for invasive candidiasis)

if Gram negative meningitis is suspected,
then it is recommended to add
cefotaxime to the empiric regimen, given
its excellent CNS penetration.

Cefotaxime is preferred over ceftriaxone
(because risk for kernicterus and its association with
biliary sludging.)

Empiric therapy for late-onset sepsis usually
consists of vancomycin and an aminoglycoside.

providing coverage for coagulase-negative
Staphylococci, S. aureus, and Gram-negative
organisms.
In a stable neonate & where MRSA is not prevalent
start with cloxacillin and aminoglycoside ?!


consider empiric antifungal coverage for invasive
candidiasis. (GA<28 wk, CV line, ET, PLT<100000, carbapenems)
if Gram-negative meningitis is suspected, consider
adding a third-generation cephalosporin.
A fourth generation cephalosporin (cefepime) or
Carbapenems may be considered, depending on
local resistance patterns or if the patient had
previously received therapy with a third-generation
cephalosporin.
Recommended meningitic doses of meropenem may
be toxic at lower gestational ages and may produce
seizures.
Consider Acyclovir if signs of encephalitis

Once a pathogen is identified, therapy should be
tailored to the species and antimicrobial
susceptibilities.

Duration determined by : the site of infection
and
the patient’s clinical response.

Bacteremia without a focus of infection is usually treated for 7
to 10 days.

Early preterm infants (<32 weeks’ gestational age) may
require slightly longer treatment courses of 10 to 14 days.

Gram-negative bacteremia tends to be treated with longer
courses of 10 to 14 days.

uncomplicated GBS meningitis is treated for 14 to 21
days.

Longer courses are needed for other focal
complications of GBS infection.

Aminoglycoside continues until CSF sterilization. (not
more than 2 weeks)

Gram-negative bacterial meningitis, treatment is for
21 days, or 2 weeks beyond
the first negative CSF culture, whichever is longer.
A lumbar puncture before discontinuation of
antibiotics to confirm response to treatment.

Neonatal pneumonia is also categorized
into two patterns of disease according to
timing and route of acquisition.

Empiric antibiotic treatment for earlyonset pneumonia includes ampicillin and
an aminoglycoside.
for late onset pneumonia it depend on local
bacterial resistanc patterns in both the hospital and
the community.
 Vancomycin and an aminoglycoside are commonly
used as empiric therapy to provide coverage
against coagulase negative Staphylococci and
methicillin-resistant S.aureus (MRSA).

If Pseudomonas is suspected, an aminoglycoside
plus an anti-pseudomonal beta-lactam, such as
ceftazidime or piperacillin-tazobactam, should be
given.
Duration of therapy for uncomplicated pneumonia is 7
to10 days.
Urinary tract infection

Sterile urine culture

Any growth of a urinary pathogen from bladder
aspirate is considered significant. Catheterization
cultures with greater than 1000 colony-forming
units per milliliter are considered meaningful.

Urinalysis lacks specificity and sensitivity for
diagnosis of UTI in neonates.
Blood cultures one third will have bacteremia with
the same organism.
very low threshold for performing a lumbar
puncture the risk for concomitant meningitis is 1%
tact infectiono 2%.

Empiric antibiotic includes ampicillin and an aminoglycoside.

In hospitalized infants with late-onset infections vancomycin
and an aminoglycoside to provide coverage for hospital
associated infections with coagulase-negative Staphylococci
and MRSA.

a urine culture may need to be repeated 2 to 3 days after
start of treatment to confirm sterilization of the urine. If cultures
remain positive further evaluated for a potential reservoir of
infection.

The duration of therapy is generally 10 to 14 days for
uncomplicated bacterial UTI. Neonates are usually given
intravenous antibiotics for the entire course,

Although in older infants oral antibiotics after clinical
improvement.
OSTEOMYELITIS AND SEPTIC ARTHRITIS

In neonates, the most common route for infection
to the bone or joint is by hematogenous spread.

The most common causative organisms are S.
aureus,E. coli, and GBS.

Less common pathogens include group A
Streptococcus, N. gonorrhoeae, and other
enteric Gram-negative bacilli.

Fluid collections in soft tissue or bone should be aspirated and
sent for Gram stain and culture. Patients with joint involvement
should have synovial fluid sent for Gram stain and culture.

Blood cultures should be obtained in all patients positive in
50% of cases.

Lumbar puncture should be performed on ill-appearing
infants or those with positive blood cultures.

Recommended empiric antibiotic treatment includes
vancomycin and an aminoglycoside

Therapy can be narrowed once the causative organism is
isolated.

Joint infections and bony abscesses require surgical drainage.

The total duration of therapy is 4 to 6 weeks for uncomplicated
cases.

Parenteral therapy at least until clinical improvement and
normalization of the inflammatory markers .

when cultures are negative, It is often difficult to
determine an appropriate duration of antibiotic
therapy for suspected sepsis.

In well-appearing infants without clinical or
hematologic evidence for infection, standard
practice is to discontinue antibiotics if cultures
have been negative after 48 hours.
More Challenging

Management decisions are much more challenging for those
infants in whom sepsis is highly suspected but cultures are
negative, which is often the case for preterm infants.

Infants whose mothers received antibiotics during labor may
have false-negative blood cultures because of antibiotic
suppression.

Cerebrospinal fluid culture data may be lacking in infants who
are not clinically stable enough to tolerate a lumbar puncture.

Noninfectious conditions mimicking sepsis can also
complicate the clinical picture.

in such cases, consider each patient’s clinical course.

Retrospective cohort studies : potential harm associated with
longer duration of empiric antibiotics when cultures are
negative, including increased risk for necrotizing enterocolitis
and death among premature infants.
Thank you
Bacterial Infections
by Organ System
MENINGITIS

Bacterial meningitis is more common in the first
month of life than at any other age.

Incidence of neonatal bacterial meningitis is
estimated to be 0.25 per 1000 live births.

As with neonatal sepsis, neonatal meningitis can
be categorized into two patterns of disease: early
onset and late onset.

The causative pathogens for neonatal meningitis are similar to
those for neonatal sepsis.

Group B streptococcus is the most common cause of neonatal
meningitis.

Gram-negative enteric bacilli cause 30% to 40% of cases of
neonatal meningitis, and E. coli accounts for approximately
50% of the Gram-negative isolates

important Gram-negative organisms include Klebsiella,
Enterobacter, Citrobacter, and Serratia species.

A known complication of Citrobacter meningitis is brain
abscesses,
obtain brain imaging

Listeria monocytogenes ,relatively uncommon, association
with thromboencephalitis.

Nosocomial pathogens include coagulase-negative
Staphylococci, Candida, and resistant Gram-negative
organisms, particularly Pseudomonas.

Cerebrospinal fluid : based on the infant’s
gestational age, postnatal age, and birth weight .

CSF WBC count of greater than 20 to 30 cells/μL is
consistent with meningeal inflammation.

neonatal meningitis can occur with normal CSF
parameters

some overlap in CSF values between neonates
with and without meningitis

In suspected infants with NL CSF findings, a repeat lumbar
puncture obtained 24 to 48 hours later will show pleocytosis if
true meningeal inflammation is present.

CSF Gram stain may be helpful,

a negative Gram stain does not exclude the diagnosis.

In traumatic LP, do not adjust the CSF WBC based on the red
blood cell counts. treat presumptively for meningitis
pending CSF culture results.

Empiric therapy for early-onset meningitis includes ampicillin
and an aminoglycoside. If infection with a Gram-negative
organism is suspected, the regimen should be expanded to
include cefotaxime in addition to ampicillin and an
aminoglycoside.

Aminoglycosides are not used as monotherapy because of
their poor CNS penetration.

Once a pathogen is identified, therapy should be tailored
according to the causative organism.
Gram-negative meningitis is treated with a thirdgeneration
cephalosporin (cefotaxime) for at least 21 days, or for 14 days
after the first negative CSF culture.
 An aminoglycoside is added until CSF sterilization.

A fourthgeneration cephalosporin (cefepime) or a carbapenem
(meropenem) in combination with an aminoglycoside should be
considered for infection with members of the Enterobacteriaceae
family with inducible beta-lactamase resistance (e.g.,
Citrobacter, Enterobacter, Serratia) and for Pseudomonas.
recommended meningitic doses of meropenem may be toxic at
lower gestational ages and may produce seizures.
A lumbar puncture should be considered before discontinuation of
antibiotics to confirm response to treatment.

Listeria monocytogenes is not susceptible to cephalosporins and should
be treated with ampicillin and an aminoglycoside until CSF sterilization,
followed by ampicillin monotherapy for 14 days after first negative
culture.

The same therapy is recommended for infection with Enterococcus.
Meningitis with coagulase-negative Staphylococci is seen in
preterm infants and is often associated with the presence of a
foreign body in the CNS. Most of these organisms are resistant to
penicillin, and treatment with vancomycin is often required.
Duration is generally 14 to 21 days after CSF sterilization, with
removal of any foreign body if possible.
There is no evidence that corticosteroids improve the outcome for
neonatal bacterial meningitis other than tuberculosis meningitis.
PNEUMONIA

Neonatal pneumonia is also categorized into two
patterns of disease according to timing and route
of acquisition.

Early-onset pneumonia is usually acquired within
the first 3 days of life via vertical transmission,
including aspiration of infected amniotic fluid and
transplacental transmission.

Late-onset pneumonia occurs after the first week
of life,

and infection arises from pathogenic organisms
in the infant’s environment. The risk for late-onset
pneumonia is highest among infants who require
mechanical ventilation. Other risk factors include
extreme prematurity, prolonged hospitalization,
and previous bloodstream infection.

The most common causes of early-onset pneumonia are GBS,
S. pneumoniae, nontypable H. influenzae, S. aureus, E. coli,
Klebsiella, and atypical organisms. Ureaplasma urealyticum
(development of chronic lung disease ).

Chlamydia trachomatis pneumonia can occur in the first
week of life, typically between 2 and 4 weeks of age.

Syphilis, Listeria monocytogenes, and Mycobacterium
tuberculosis (TB) are much less common

In late-onset pneumonia ,

Streptococcus pneumoniae a predominant causative
pathogen

Other important pathogens include S. aureus, S. pyogenes,
non-typable H. influenza, Gram-negative enteric organisms.
Staphylococcus aureus, Streptococci, Klebsiella pneumoniae,
Citrobacter, Enterobacter, Serratia, and Pseudomonas have
the potential to cause extensive lung injury, abscess formation,
empyema, pneumatoceles.
Bordetella pertussis infection in young infants can lead to
respiratory failure and death.

Empiric antibiotic treatment for early-onset pneumonia

includes ampicillin and an aminoglycoside.

Empiric antibiotic therapy for late onset pneumonia depend
on local bacterial resistanc patterns in both the hospital and
the community.

Vancomycin and an aminoglycoside are commonly used
as empiric therapy to provide coverage against
coagulase negative Staphylococci and methicillin-resistant S.
aureus (MRSA).

If Pseudomonas is suspected, an aminoglycoside
plus an anti-pseudomonal beta-lactam, such as ceftazidime
or piperacillin-tazobactam, should be given.

Recommended duration of therapy for uncomplicated
pneumonia is 7 to 10 days.
URINARY TRACT
INFECTIONS

The incidence of bacteriuria in term newborns is
estimated to be 0.1% to 1%.1,9 The incidence is
higher in preterm infants and is thought to be
around 2%.

Infection of the urinary tract in neonates is
thought to be acquired either through
hematogenous spread or by ascending infection,
which is often associated with anatomic
abnormalities

Urinary tract abnormalities are seen

in approximately 20% to 50% of infants with UTI

The most common causative pathogen for neonatal UTI is E.
coli, which has been isolated in approximately 80% of cases in
some large series.

Other common causative organisms : Enterobacteriaceae,
Klebsiella, Enterobacter, Proteus, Citrobacter, Salmonella, and
Serratia.

Gram-positive organisms are isolated much less frequently
than Gram-negative organisms, although Enterococci, S.
aureus, and coagulase negative Staphylococci are also
known to cause UTI in newborns.

Definitive diagnosis must be made by urine culture with
specimens obtained by catheterization or suprapubic bladder
aspiration.

Any growth of a urinary pathogen from bladder aspirate is
considered significant. Catheterization cultures with greater than
1000 colony-forming units per milliliter are considered
meaningful.
Urinalysis lacks specificity and sensitivity for diagnosis of UTI in
neonates.
Blood cultures should be obtaine for all infants with suspected
UTI, as one third with UTI will have bacteremia with the same
organism.
Clinicians should have a very low threshold for performing a
lumbar puncture in neonates with UTI because the risk
for concomitant meningitis is 1% to 2%.

Empiric antibiotic treatment for neonatal UTI includes
ampicillin and an aminoglycoside. Hospitalized infants with
late-onset infections should be given vancomycin and an
aminoglycoside to provide coverage for hospital associated
infections with coagulase-negative Staphylococci and MRSA.
If the infection is caused by a highly resistant pathogen, or if
there is a known anatomical abnormality,

a urine culture may need to be repeated 2 to 3 days after
start of treatment to confirm sterilization of the urine.

If cultures remain positive despite adequate therapy, the
infant should be further evaluated for a potential reservoir of
infection.

The duration of therapy is generally 10 to 14 days for
uncomplicated bacterial UTI. Neonates are usually given
intravenous antibiotics for the entire course, although older
infants are often switched to oral antibiotics after
demonstration of clinical improvement.

All neonates with UTI should undergo radiographic evaluation
because of the high prevalence of urinary tract abnormalities.
If prenatal ultrasound data are not available, a renal
ultrasound should be performed after the infant has clinically
stabilized. Ultrasound can detect structural abnormalities,
although it cannot detect vesicoureteral reflux or renal
scarring. Voiding cystourethrogram is performed to detect
vesicoureteral reflux, and this is usually done 3 to 6 weeks after
completion of antibiotic treatment.

If renal damage is suggested by ultrasound,

renal cortical scintigraphy can be performed .
OSTEOMYELITIS AND
SEPTIC ARTHRITIS

In neonates, the most common route for infection
to the bone or joint is by hematogenous spread.

The most common causative organisms are S.
aureus,E. coli, and GBS.

Less common pathogens include group A
Streptococcus, N. gonorrhoeae, and other
enteric Gram-negative bacilli.

Imaging studies should be obtained for any patient with
suspected osteomyelitis or septic arthritis. The radiologic
investigation usually starts with plain radiographs.

Soft tissue swelling is the earliest finding 48 hours after onset of
infection.

Bony changes, 7 to 10 days after onset of infection. further
imaging is often required for patients in whom there is a high
index of suspicion.

Ultrasound can detect subperiosteal collections and joint
effusions, so it is very useful in cases of suspected septic
arthritis.

Ultrasound can also detect findings of acute osteomyelitis,
although this is highly dependent on the duration of infection
as well as operator experience.

Bone scintigraphy is more sensitive than plain films for
detecting osteomyelitis early on, and it is useful for detecting
multiple foci of infection.

Magnetic resonance imaging (MRI) is extremely
useful in the evaluation for osteomyelitis. Bony
changes can be detected within 24 to 48 hours
after onset of symptoms.

it provides excellent anatomic detail. It also
provides better information on growth plate
involvement than does bone scintigraphy.

Fluid collections in soft tissue or bone should be aspirated and
sent for Gram stain and culture. Patients with joint involvement
should have synovial fluid sent for Gram stain and culture.
Blood cultures should be obtained in all patients positive in
50% of cases.

Lumbar puncture should be performed on ill-appearing
infants or those with positive blood cultures.

Recommended empiric antibiotic treatment includes
vancomycin for broad Gram-positive coverage and an
aminoglycoside or third-generation cephalosporin for Gramnegative coverage.

Therapy can be narrowed once the causative organism is
isolated.

Joint infections and bony abscesses require surgical drainage.

The total duration of therapy is 4 to 6 weeks for uncomplicated
cases.

Parenteral therapy should be continued at least until the
patient demonstrates clinical improvement and the
inflammatory markers have normalized.
OPHTHALMIA NEONATORUM

Ophthalmia neonatorum is conjunctivitis that
occurs in the first month of life.

Bacterial causes include S. aureus, nontypable H.
influenzae, S. pneumoniae, enteric Gramnegative
bacilli, GBS, N gonorrhoeae, and Chlamydia
trachomatis.

The differential also includes viral causes,
particularly herpes simplex virus, and noninfectious causes such as chemical conjunctivitis.

Conjunctivitis in neonates is managed aggressively because
of the high risk for associated systemic illness and
complications.

Prophylactic administration of ophthalmic antibiotic agents
shortly after birth greatly reduces the risk of gonococcal
conjunctivitis, but not chlamydial disease.

Regimens with equal efficacy include 0.5% erythromycin
ointment, 1% tetracycline ointment, and silver nitrate solution.

If gonococcal infection is suspected, CSF and blood cultures

should be obtained

Purulent ocular discharge should be sent for Gram stain and
culture. Culture on selective media (e.g., Thayer-Martin) is
needed to evaluate for gonococcal infection.

Additionally, conjunctival specimens obtained from an everted
eyelid should be sent for C. trachomatis testing. Specimens must
contain conjunctival epithelial cells; ocular exudates are not
adequate specimens for testing.

Culture of the organism is the gold standard for diagnosis of C.
trachomatis infection in infants. Nucleic acid amplification tests
may also be considered because they have been found to have
high specificity and sensitivity

In infants with signs of pneumonia, testing for C. trachomatis can
be sent from nasopharyngeal specimens.

Any infant with signs of systemic illness should have blood and
CSF cultures obtained.

Systemic antibiotics are required to treat conjunctivitis

resulting from N. gonorrhoeae and C. trachomatis. For

other causes of bacterial conjunctivitis, topical antibiotic

ointment or solution given for 7 to 10 days provides

adequate therapy. Infants with gonococcal eye disease

should be hospitalized and monitored for response

to treatment as well as for signs of disseminated

disease. Recommended treatment for conjunctivitis is a

single dose of intramuscular or intravenous ceftriaxone

(25–50 mg/kg). The eyes should also be irrigated frequently

with sterile saline until the discharge has resolved.

Recommended treatment for either chlamydial conjunctivitis

or pneumonia is oral erythromycin (50 mg/kg per

day in four divided doses) for 14 days.
OMPHALITIS

Bacteria can reach the bloodstream through patent vessels of
the newly cut cord and lead to systemic infection and severe
complications.

Common pathogens include S. aureus, group A Streptococci,
GBS, and Gramnegative bacilli, including E. coli, Klebsiella,
and Pseudomonas.

Polymicrobial infections may occur.

Anaerobic bacteria can contribute to infection, especially in
infants born to mothers with chorioamnionitis.

The clinical presentation is characterized by purulent

drainage from the umbilical stump, with surrounding
erythema, induration, and tenderness.

Foul smelling drainage is suggestive of infection with
anaerobic bacteria.

Infants with more severe infection will display systemic signs of
illness.

Involvement of the abdominal wall or extensive edema should
prompt consideration for necrotizing fasciitis as a
complication. Other complications include peritonitis, intraabdominal abscess, suppurative thrombophlebitis of portal or
umbilical veins.

Purulent discharge for Gram stain and culture.

Blood and CSF cultures should be obtained from infants with
signs of systemic illness.

Treatment an anti-staphylococcal penicillin and an
aminoglycoside.

If the prevalence of methicillin-resistant S. aureus is high,
vancomycin should be used.

The addition of clindamycin or metronidazole for anaerobic
involvement, especially for foul smelling discharge or history of
maternal chorioamnionitis.

For uncomplicated cases, duration of treatment is typically 10
days. A switch to oral therapy for completion of the course of
treatment may be considered.