10/04/2018

Infectious Diseases in Pregnancy

3:00-4:30
Th
Obstetrics
LDT 408 Sharon Faith B. Pagunsan, MD, FPOGS, FPIDSOG, FPAFP

OUTLINE  Vertical transmission: passage from the mother to her fetus

I. Legend
II. Basic Principles of Maternal and Fetal Immunology of an infectious agent through the placenta, during labor or
III. Viral, Bacterial, Protozoal and Mycotic Infections delivery, or by breast feeding.
IV. Prevention Precautions for Travel
V. Bioterrorism
Factors that may enhance risk of Neonatal Infection:
VI. Referrences
 PROM common
LEGEND  Prolonged labor
1. Red with mic bullet is from recordings
2. Blue with open book bullet is from book  Obstetrical manipulations more than 5 internal examinations
increases the risk
INFECTIOUS DISEASES IN PREGNANCY
Factors that Influence Disease Outcome
Secondary attack rate: the probability that infection develops in
1. Maternal serological status. a susceptible individual following known contact with an
2. Gestational age at time of infection. infectious person.
3. Mode of acquisition.
4. Immunological status of both mother & fetus. Maternal and Fetal Immunology

 Fetal cell-mediated and humoral immunity develop by 9 to 15

Objectives:
weeks’ gestation.
1. To determine the basic principles of maternal and fetal
 Immunoglobulin M (IgM) - primary fetal response to
immunology;
infection.
2. To identify viral, bacterial, protozoal and mycotic infections;
 Passive immunity - IgG (transferred across the placenta), rapid
3. To know the prevention precautions for travel; &
increase by 16 weeks AOG.
4. To define bioterrorism.
 By 26 weeks  fetal concentrations = mother’s concentration
 After birth, breast feeding is protective against some
MATERNAL AND FETAL IMMUNOLOGY
Pregnancy-Induced Immunological Changes infections  decline at 2 months of age. where does the
newborn get these protective factors? Through the colostrum,
it can protect the baby upto 6 months if exclusively breastfed
Even after intensive study, many of the maternal
 WHO recommendation: “exclusive breastfeeding for the first 6
immunological adaptations to pregnancy are not well
months of life with partial breastfeeding until 2 years of age”
elucidated. It is known that pregnancy is associated
feeding bottles are not allowed in BF friendly hospitals
with an increase in CD4-positive T cells secreting T2-
type cytokines - for example interleukins 4, 5, 10, and
 Infections < 72 hours after delivery  most often caused by
13. Th1-type cytokine production - for example,
bacteria acquired in utero or during delivery.
interferon gamma and interleukin 2 - appears to be
 Infections after 3 days  believed to be acquired after
somewhat suppressed, leading to a Th2 bias in
delivery.
pregnancy. This bias afects the ability to rapidly
eliminate certain intracellular pathogens during
pregnancy, although the clinical implications of this
suppression are unknown. Importantly, the T2 humoral
immune response remains intact.

 Horizontal transmission: spread of an infectious agent from

one individual to another.

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  Secreted into all body fluids transmitted by person-to-person
contact with viral-laden saliva, semen, urine, blood, &
nasopharyngeal and cervical secretions.

Maternal Infection
 Seronegative women before pregnancy are at greatest risk to
,Zika
have an infected fetus.
 Most CMV infection are clinically silent but can be detected
by seroconversion.
 Diagnosis in non primary infection is a challenge.
 Pregnancy does not increase the risk or severity of maternal
CMV infection.
 Most infections are asymptomatic.
 Mononucleosis-like syndrome: fever, pharyngitis,
lymphadenopathy, and polyarthritis.
 Immunocompromised women: myocarditis, pneumonitis,
hepatitis, retinitis, gastroenteritis, or meningoencephalitis.
 Primary infection: ↑ serum aminotransferases or
lymphocytosis.
 Reactivation is asymptomatic, although viral shedding is
common.

Signs of Neonatal Infection:  Transmission rates:

o 1st trimester – 30-36%
 In Utero: depression & acidosis at birth, poor suck, vomiting, o 2nd trimester – 34-40%
or abdominal distention, respiratory insufficiency, lethargy or o 3rd trimester – 40-72%
jittery.  Recurrent maternal infections infects the fetus in only 0.15 to

 Sepsis: hypothermia &  total leukocyte & neutrophil 1 % of cases.

counts.  Naturally acquired immunity during pregnancy  70% risk

although it can also present hyperthermia and/or increased reduction of congenital CMV infection in future pregnancies

total leukocyte and neutrohil counts  Maternal immunity does not prevent recurrences, and
maternal antibodies do not prevent fetal infection. there is
VIRAL INFECTION no such thing as immunity in CMV because it can recur but it
can reduce the risk
 Cytomegalovirus  Enteroviruses: Coxsackievirus
Fetal Infection
 Varicella-Zoster Virus and Poliovirus
 Symptomatic CMV infection: when a newborns has apparent
 Influenza  Parvovirus
sequelae of in-utero-acquired CMV infection.
 Mumps  West Nile Virus
 Rubeola – Measles  Corona Virus Infections  Congenital infection is a syndrome: growth restriction,

 Rubella – German  Ebola Virus  , intracranial calcifications, chorioretinitis, mental and motor

Measles  Zika Virus retardation, sensorineural deficits, hepatosplenomegaly,

 Respiratory Viruses jaundice, hemolytic anemia, & thrombocytopenic purpura.
 Hantaviruses

CYTOMEGALOVIRUS (CMV)

 A ubiquitous DNA herpes virus.

 Most common perinatal infection in the developed world.

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Sagittal (A) and coronal (B) cranial sonograms from a neonate with congenital
cytomegalovirus infection. The arrows indicate periventricular calcifications.
 Of the estimated 40,000 infected neonates born each year,
only 5 to 10 percent demonstrate the syndrome.
 Most infected infants are asymptomatic at birth, but some
develop late-onset sequelae.
 Complications: hearing loss, neurological deficits,
chorioretinitis, psychomotor retardation, and learning
disabilities.
 In dichorionic twins, infections most likely are nonconcordant.
Prenatal Diagnosis
 Routine prenatal CMV serological screening is currently NOT
recommended.
 Pregnant women should be tested if they present with a
mononucleosis-like illness or if congenital infection is
suspected based on abnormal sonographic findings during
prenatal work ups.
 CMV-specific IgG testing (of paired acute and convalescent
sera) - used to diagnosed primary infection.
 CMV IgM does not accurately reflect timing of seroconversion
because IgM antibody levels may be elevated for more than a
year. just because IgM is still there/elevated it doesn’t mean
that the mother just had the infection
 CMV IgM may be found with reactivation disease or
reinfection with a new strain.
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 High anti-CMV IgG avidity indicates primary maternal
infection >6 months before testing.
 Viral culture may be useful; a minimum 21 days is required
before findings are considered negative. only performed at
Resarch Institute for Tropical Medicine (RITM)
 Modalities: Ultrasound, CT scan, & MRI.
 Findings: microcephaly, ventriculomegaly, and cerebral
calcifications; ascites, hepatomegaly, splenomegaly, and
hyper-echoic bowel; hydrops; and oligohydramnios.
 CMV nucleic acid amplification testing (NAAT) of amnionic
fluid: the gold standard for the diagnosis of fetal infection.
 Sensitivities ranged from 70-99% depending on
amniocentesis timing.
 Sensitivity: highest when performed at least 6 wks after
maternal infection and after 21 weeks’ gestation.
 Negative result from amnionic fluid polymerase chain
reaction (PCR) testing does not exclude fetal infection and
may need to be repeated if suspicion for fetal infection is
high.
Management and Prevention
 With primary or recurrent CMV: management is limited to
symptomatic treatment.
 If recent primary infection is confirmed, amnionic fluid
analysis should be offered.
 Counseling depends on the gestational age primary infection
is documented.
 Currently, no proven treatments are available.
 Valacyclovir, 8 g daily PO, showed adverse outcomes in
eight of eleven affected fetuses treated at 25.9 wks AOG.
 Valganciclovir IV administered for 6 wks to neonates with
symptomatic CNS prevented hearing deterioration at 6
months and possibly later.
 Passive immunization with CMV-specific hyperimmune
globulin may lower the risk of congenital CMV infection.
 There is no CMV vaccine.
 Prevention relies on avoiding maternal primary infection, esp.
in early pregnancy. advise the mothers not to go to crowded
places such as malls
 Basic measures: good hygiene & hand washing.
 CMV may be sexually transmitted among infected partners,
but no data address the efficacy of preventive strategies.
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 VARICELLA ZOSTER VIRUS (VZV) o Congenital varicella syndrome rarely develops
 a double-stranded DNA herpesvirus
in cases of maternal herpes zoster
 acquired during childhood
o Zoster is contagious if blisters are broken,
 90% of adults have serological evidence of immunity
although less so than primary varicella.
 82% decline after the introduction of
varicella vaccination  drop in maternal and fetal
Fetal and Neonatal Infection
varicella rates
 first half of pregnancy  may develop
congenital varicella syndrome
Primary Infection (varicella or chicken pox)
 Features
 transmitted by direct contact with an affected
o Chorioretinitis
individual through respiratory transmission
o Microphthalmia
 incubation period: 10 to 21 days
o cerebral cortical atrophy
 nonimmune woman has a 60 to 95% risk of becoming
o growth restriction
infected after exposure
o hydronephrosis
o limb hypoplasia
Maternal Infection
o cicatrical skin lesions
 1 to 2 day flulike prodrome
 Highest risk: Between 13 & 20 weeks
 followed by pruritic vesicular lesions that crust over in
 After 20 weeks gestation: No clinical evidence of
3 to 7 days
congenital infection
 tends to be more severe in adults
 in chicken pox, highest risk is also in the earliest
 affected patients are more contagious from day 1
weeks (between 13 & 20 weeks)
before the onset of rash until the lesions become
 Sporadic reports: CNS abnormalities & skin lesions
crusted
(21 to 28 weeks of gestation)
 Mortality is due to VZV pneumonia
 If the fetus or neonates is exposed to active
o more severe during adulthood and particulary
infection just before or during delivery (before
in pregnancy
maternal antibody has been formed)  serious
 2 - 5% develop pneumonitis
threat to newborns
 Risk factors: smoking & > 100 cutaneous lesions
 Mortality rates - 30 %
 Symptoms of pneumonia - appear 3 to 5 days into the
 Disseminated visceral and CNS disease which is
course of illness
commonly fatal
o fever, tachypnea, dry cough, dyspnea, &
 Varicella-Zoster Immune globulin
pleuritic pain
o should be administered to neonates born to
o Nodular infiltrates are similar to other viral
mothers who have clinical evidence of varicella
pneumonias
5 days before and up to 2 days after delivery
 Although resolution of pneumonitis parallels that of
 this immune globulin is very difficult to acquire
skin lesions, fever and compromised pulmonary
function may persist for weeks
Diagnosis of VZV
 If reactivated years later  causes Herpes Zoster or
 usually clinical
Shingles
 may be isolated by scraping the vesicle base during
o a unilateral dermatomal vesicular eruption
primary infection
associated with severe pain
 Tests: Tzanck smear, tissue culture, or direct fluorescent
o Zoster is contagious if blisters are broken
antibody testing
 just like varicella
 Confirmation of vesicular fluid by Nucleic Acid
o Zoster does not appear to be more frequent
Amplification Tests (NAATs) which are very sensitive
or severe in pregnant women
 Congenital varicella analyzed through NAAT analysis of
amniotic fluid

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  A positive result does not correlate well with the
development of congenital infection
 Sonographic evaluation: At least 5 weeks after maternal
infection may disclose abnormalities but the sensitivity is
low
Management of VZV
 Maternal Viral Exposure
o Exposed gravid with no history for chicken pox
should Undergo VZV serologic testing
 At least 70 percent of these women will
be seropositive, and thus immune
o If susceptible: Give VariZIG (varicella zoster
immune globulin)
 best within 96 hrs (4 days) of exposure
(approved for up to 10 days) to prevent
or attenuate varicella infection
 Maternal Infection
o Any patient diagnosed with primary varicella
infection or herpes zoster should be isolated from
pregnant women
o a chest radiograph is recommended
o Supportive care is given
o Hospitalization only for those who require IV
fluids and w/ pneumonia
 IV acyclovir - 500 mg/m² or 10 to 15
mg/kg every 8 hours is given to women
requiring hospitalization
 For ORAL, give 800 mg 5x a day during
waking hours (6am, 10am, 2pm, 6pm, 10pm)
 Vaccination
o Varivax
 An attenuated live-virus vaccine
recommended for nonpregnant
adolescents and adults with no history of
varicella
 given at 2 doses 4 to 8 weeks apart
o Recommended for adolescents and adults
with no history of varicella
o Vaccine-induced immunity diminishes over time
& the breakthrough infection rate approximates
5% at 10 years
o The vaccine is not recommended for pregnant
women (only the immunoglobulin) or for those
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who may become pregnant within a month
following each vaccine dose.
o Attenuated vaccine virus is not secreted in breast
milk
o Postpartum vaccination of mothers should not be
delayed because of breast feeding
INFLUENZA
 caused by members of the family Orthomyxoviridae
 Influenza A and B - form one genus of these RNA
viruses  known to cause epidemic human disease
 Influenza A viruses – subclassified by hemagglutinin (H)
& neuraminidase (N) surface antigens
 Influenza outbreaks occur annually
 Most recent epidemic (2016-2017) – Influenza A/H3N2
strain
Maternal and Fetal Infection
 Maternal influenza: fever, dry cough, & systemic
symptoms
o usually is not life-threatening in otherwise
healthy adults
 Pregnant women - more susceptible to serious
complications (i.e. pulmonary involvement)
 widespread influenza A infection affected pregnant
women and caused 12 percent of pregnancy-related
deaths
 No firm evidence that influenza A virus causes
congenital malformations
 Higher rates of neural-tube defects in neonates born to
women with influenza early in pregnancy
o This was possibly associated with hyperthermia
 Viremia is infrequent & transplacental passage is rare
 Stillbirth, preterm delivery, & first-trimester abortion
o correlated to severity of maternal infection or
the flu
 Detected in Nasopharyngeal swabs using viral antigen
rapid detection assays
o Reverse transcriptase-polymerase chain reaction
(RT-PCR) - more sensitive & specific test
o Rapid influenza diagnostic tests (RIDTs) – least
indicative (sensitivities of 40-70%)
 Decisions to administer antiviral medications for
influenza treatment or chemoprophylaxis  based on
clinical symptoms & epidemiological factors
Page 5 of 17
  The start of therapy should not be delayed pending For example: Before the end of 2018, they are starting
testing results to produce the vaccine for 2019 since they have already
predicted the strain, so you can have yourself injected
Outpatient Influenza A and B Virus Testing Methods:  Flu vaccine is available as early as February (sometimes
Method Test Time April or May)
Viral cell culture 3-10 d  Vaccination recommended:
Rapid cell culture 1-3 d o all women who will be pregnant during the

Direct (DFA) or Indirect (IFA) 1-4 hr influenza season (optimal: Oct/Nov)

fluorescent antibody assay  our rainy season starts from June

RT-PCR and other molecular 1-6 hr o those affected by chronic medical disorders (i.e.

assays diabetes, heart disease, asthma, or HIV

Rapid influenza diagnostic tests < 30 min infection)

aNasopharyngeal or throat swab  Inactivated vaccine: prevents clinical illness in 70-90 %

only available in RIPF percent of healthy adults

 No evidence of teratogenicity or other adverse maternal

Management or fetal events

we can already give as early as first trimester
 2 classes of antiviral medications:
 Lower rates of influenza in infants up to 6 months of
1. Neuraminidase inhibitors
age whose mothers were vaccinated during pregnancy
o For early influenza A and B
o Immunogenicity of the trivalent inactivated
 Oseltamivir (Tamiflu) – oral & for
seasonal influenza vaccine in pregnant women
chemoprophylaxis
is similar to that in the nonpregnant individual
usually given
 A live attenuated influenza virus is available for
 Zanamivir (Relenza) – inhaled
intranasal use but not recommended for pregnant
contraindicated
women
 Peramivir (Rapivab) - IV
2. Adamantanes – Amantadine & Rimantadine
MUMPS
o influenza A resistance to adamantine was
reported to exceed 90 percent in the United  Uncommon adult infection - caused by RNA paramyxovirus
States. Thus, its use is not currently
 Primarily infects salivary glands mumps (Latin, “to grimace”)
recommended. It is possible that these drugs
may again be effective for subsequently  May involve: gonads, meninges,pancreas
mutated strains.
 Especially males
 Limited experience with all the antiviral agents in
pregnant women
 Transmitted by direct contact: respiratory secretions, saliva,
 FDA category C drugs (use when the potential benefits
or through fomites.
outweigh the risks)
 Start oseltamivir treatment within 48 hours, 75 mg BID  Treatment is symptomatic
PO x 5 days
 mumps during pregnancy is no more severe than in
 Prophylaxis: 75 mg OD PO x 10 days
nonpregnant adults.
 Antibacterial medications added when secondary
bacterial pneumonia is suspected  Mumps in the first trimester risk of spontaneous abortion

 Not associated with congenital malformations & fetal

Vaccination
infection is rare.
 Effective vaccines - formulated annually
the strain of flu is already predicted for that year

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 Vaccination
 Live attenuated Jeryl-Lynn vaccine strain is part of the MMR
vaccine (measles,mumps, & rubella) – contraindicated in
pregnancy.
 No malformations to MMR in pregnancy but pregnancy
should be avoided for 30 days after mumps vaccination.
 We do not plan to give it if there is a plan to get pregnant for
at least a month.
 Vaccine may be given to susceptible women postpartum
 Breast feeding is not a contraindication.
 We advise giving MMR before mother is discharged after
delivery.
RUBEOLA (MEASLES)
 Caused by RNA virus of the family Paramyxoviridae
 Annual outbreaks - late winter & early spring
Transmission - primarily by respiratory droplets
Characterized by: fever, coryza, conjunctivitis, & cough.
Characteristic
 erythematous maculopapular rash – face & neck, spreads to
back, trunk, & extremities.
 Koplik spots - small white lesions with surrounding
erythema - oral cavity.
Diagnosis
 by serology; RT-PCR tests.
 but we can diagnose clinically
Treatment
Treatment is supportive
Pregnant women - IV immune globulin
(IVIG), 400 mg/kg within 6 days of a
measles exposure.
Vaccination - not performed during pregnancy
 Susceptible women can be vaccinated routinely postpartum
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 Breastfeeding is not contraindicated
 Increased rates of spontaneous abortion, preterm delivery,
& low-birthweight neonate.
 if a woman develops measles shortly before birth risk of
serious infection developing in the neonate.
RUBELLA (GERMAN MEASLES)
RNA togavirus - causes infections of minor importance in the
absence of pregnancy.
Rubella infection in the first trimester -poses significant risk for
abortion & severe congenital malformations
Transmission - via nasopharyngeal secretions.
Peak incidence - late winter & spring
Maternal rubella infection - mild, febrile illness with generalized
maculopapular rash beginning on face & spreading to trunk &
extremities
Other symptoms: arthralgias or arthritis, head & neck
lymphadenopathy, & conjunctivitis
Incubation period – 12-23 days
 Viremia precedes clinical signs by a week
 Adults are infectious during viremia & through 7 days after
the rash appears
 Up to a half of maternal infections are subclinical despite
viremia that may cause devastating fetal infection.
Diagnosis
Isolated from urine, blood, nasopharynx, & CSF up to 2 weeks
after rash onset.
Diagnosis – with serological analysis
 Specific IgM antibody detected using enzyme-linked
immunoassay 4-5 days after onset of clinical disease (persist
up to 6 wks after appearance of rash).
 Rubella virus infection transient low levels of IgM.
 Serum IgG antibody peak 1-2 wks after rash onset.
 IgG avidity testing performed concomitant with the
serological tests.
 High-avidity IgG antibodies indicate infection at least 2 mos
in the past.
Page 7 of 17
Fetal Effects
 One of the most complete teratogens.
 A sequelae of fetal infection are worst during organogenesis
 Usually first trimester
 Pregnant women with rubella infection & a rash during first
12 wks AOG congenital infection in 90 %.
 13-14 wks AOG gestation – 50%
 End of 2nd trimester – 25%
 Defects rare after 20 wks AOG
 Neonates born with congenital rubella may shed the virus
for many months thus a threat to other infants &
susceptible adults.
 If they have possible Rubella, they should be isolated.
Congenital rubella syndrome includes
one or more of the following:
• Eye defects - cataracts & congenital glaucoma
• Heart disease - PDA & pulmonary stenosis
• Sensorineural deafness - most common single
defect
• CNS defects - microcephaly, developmental delay,
mental retardation, & meningoencephalitis
• Pigmentary retinopathy, microphthalmia
• Neonatal purpura
• Hepatosplenomegaly & jaundice
• Radiolucent bone disease
Management and Prevention
 No specific treatment
 Droplet precautions for 7 days after onset of rash are
recommended
 Postexposure passive immunization may be of benefit if
given within 5 days of exposure.
 To eradicate rubella & prevent congenital rubella syndrome
- comprehensive approach is recommended for immunizing
the adult population.
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 MMR vaccine should be offered to nonpregnant women of
childbearing age.
 Vaccination of all susceptible hospital personnel who might
be exposed to patients with rubella or have contact with
pregnant women.
 Rubella vaccination should be avoided 1 month before or
during pregnancy.
 No observed evidence that the vaccine induces
malformations
 Prenatal serological screening for rubella is indicated for all
pregnant women.
 Women found to be nonimmune should be offered MMR
vaccine postpartum.
RESPIRATORY VIRUSES
 > 200 antigenically distinct respiratory viruses cause the
common cold, pharyngitis, laryngitis, bronchitis, &
pneumonia
 Rhinovirus, coronavirus, & adenovirus - major causes of
common cold.
 RNA-containing rhinovirus & coronavirus - self-limited
illness: rhinorrhea, sneezing, & congestion
 DNA-containing adenovirus - produce cough & lower
respiratory tract involvement including pneumonia.
 Amnionic fluid viral PCR studies – sensitive for adenovirus
(virus most frequently identified)
 Association with fetal-growth restriction, nonimmune
hydrops, foot/hand abnormalities, & neural-tube defects
 Adenoviral infection - known cause of childhood myocarditis.
HANTAVIRUS
 RNA viruses - members of the family Bunyaviridae
 Associated with a rodent reservoir.
 Transmission involves inhalation of virus excreted in rodent
urine and feces.
 Outbreaks include Sin Nombre virus and Seoul virus, most
recent in early 2017.
Page 8 of 17
 Hantavirus pulmonary syndrome - cause maternal death,
fetal demise, and preterm birth.
 NO evidence of VERTICAL TRANSMISSION of the causative
Sin Nombre virus.
ENTEROVIRUSES
 A major subhroup of RNA picornaviruses, coxsackievirus,
poliovirus and echovirus.
 Trophic for intestinal epithelium but can cause maternal,
fetal and neonatal infections.
 May include CNS, skin, heart and lungs
 Most maternal infections are subclinical yet be fatal to the
fetus-neonate.
 Hepatitis A is an enterovirus
 Coxsackie infections : group A and B are usually
asymptomatic
 Symptomatic infections - usually with group B include :
o Aseptic meningitis, polio-like illness, hand, foot and
mouth disease, pleuritis, pericarditis, myocarditis
 No treatment or vaccinaiton is available
 May be transmitted by maternal secretions at delivery
 Transplacental passage has been reported
 Congenital malformation rates slightly increased in pregnant
women with serological evidence of coxsackievirus
 Viremia leads to fetal hepatitis, skin lesions, myocarditis and
enchephalomyelitis - ALL FATAL
ENTEROVIRUSES (POLIO VIRUSES)
 Highly contagious but subclinical or mild
 Trophic for the CNS and can cause paralytic poliomyelitis
 Pregnant women - more susceptible and higher death rate
 Perinatal transmission occurs during the 3rd trimester
 Inactivated subcutaneous polio vaccine is recommended for
susceptible pregnant women who must travel to endemic
areas.
 Live oral polio vaccine is used for mass vaccination during
pregnancy without harmful fetal effects
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ENTEROVIRUSES (PARVOVIRUSES)
 The B19 virus can cause Eryhtema infectiosum of fifth
disease
 Small, single-stranded DNA virus that replicates in rapidly
proliferating cells, e.g. erythroblast precursors.
 Anemia is the primary fetal effect
 Only individuals with erthrocyte globoside membrane P
antigen are susceptible
 Without EGMPA, you are least likely to be infected
 Main mode of transmission : respiratory or hand-to-mouth
contact
 Maternal infection is the highest with school-aged children
and day-care workers
 Viremia appears 4-14 days after exposure
 Immunocompetent individuals is no longer infections at the
onset of the rash
 Maternal infection :
o 20-30% if adults - asymptomatic
o Viremic phase : Fever. Headache, flu-like symptoms
o Several days later, a bright red rash with erythroderma
affects the face ( slapped-cheek appearance)
 Emphasized
o Rash becomes lacelike and spreads to the trunk and
extremities
o Adults - milder rashes and symmetrical polyarthralgia
o With recovey, IgM antibody is generated 7-10 days
postinfection
o Several days after IgM is produced, IgG antibody is
detectable and persists for life with natural immunity
 Fetal infection :
o Vertical transmission occurs
o Asscoiated with : abortion, nonimmune hydrops and
stillbirth
o Fetal loss - 8-17% before 20 weeks of gestation and 2-
6% after midpregnancy
o Critical for development of fetal hydrops - between 13-
16 weeks of gestation
Diagnosis and management - Parvovirus
 Fetal and maternal viral loads do not predict fetal morbidity
and mortality
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  Most cases, hydrops develop in the first 10 weeks after
infection -> Serial sonography every 2 weeks in women with
recent infection.
 Depending on gestational age, fetal transfusion for hydrops
may improve outcome
 30% mortality in hydropic fetuses without transfusion
 With transfusion, 94% of hydrops resolve within 6-12 weeks
and decreases overall mortality rate below 10%
 Usually patients with hydrops are associated with
Parvovirus
Parvovirus - Prevention
 No Parvovirus vaccine is available
 No evidence suggests that antiviral treatment prevents
maternal or fetal infections
 Pregnant women should be counseled for risks of infection :
o 5% for casual, infrequent contact
o 20% for intense, prolonged work exposure
o And 50% for close, frequent interaction
WEST NILE VIRUS
 Mosquito-borne RNA flavivirus - a human neuropathogen
 Most common cause of arthropod-borne viral encephalitis
in the United States
 Typically acquired through mosquito bites or through blood
transfusion
 Incubation period - 12-14 days
 Most have mild or no symptoms
 Symptoms :
o Fever
o Mental status change
o Muscle weakness
o Coma
Diagnosis and Management - West Nile Virus
 Clinical symptoms and detection of viral IgG and IgM in
serum and IgM in cerebrospinal fluid
 No effective antiviral treatment
 Management : supportive
 Primary strategy for prevention - use of insect repellant
cotaining N. N-diethyl-m-toluamide ( DEET)
CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4
 DEET - considered safe for use among pregnant women
 Recommendations : avoiding outdoor activity and stagnant
water, wearing PPEs.
 Adverse effects of viremia of pregnancy are unclear
 Transmission through breastfeeding - RARE
CORONA VIRUS INFECTIONS
 Single-stranded RNA viruses prevalent worldwide
 Case fatality rate - 10% in nonpregnant, 25% in pregnant
women
 2002 - a virulent strain of coronavirus - Severe acute
respiratory syndrome or SARS was first noted in China.
 Rapidly spread throughout Asia, Europe, North and South
America.
 Transmission is through droplets or contact with infected
secretions, fluids and wastes
 Incubation period : 2-16 days with triphasic pattern to its
clinical progression
 Symptoms :
o 1st week : Prodromal symptoms of fever, myalgias,
headache and diarrhea
o 2nd week : recurrent fever, watery diarrhea, dry
nonproductive cough with mild dyspnea
o 3rd week : at times, lethal phase - seen in about 20% of
patients which can progress to SARS
 Radiographic lung findings:
o Ground glass opacities and airspace consolidations ( Can
rapidly progress 1-2 days)
 No confirmed cases since 2004, CDC now lists SARS-COV as
a “select agent” - potential to pose a severe threat to public
health and safety
 Another novel coronavirus infecting humans with a high-
case fatality rate was detected in the Middle East in 2012 (
MERS-COV)
EBOLA VIRUS
 Member of the RNA Filoviridae Family
 Transmitted by direct person-to-person contact
 Infection causes severe hemorrhagic fever with pronounced
immunosuppression and DIC
 CDC concludes that pregnant women are more susceptible
Page 10 of 17
 ZIKA VIRUS
 RNA virus of the Filoviridae family
 First major mosquito-borne teratogen
 Primarily transmitted by mosquito bite, also by sexual
transmission
 Detected in body fluids for months following acute infection
 Maternal-Fetal infection:
o Adults - asymptomatic or mild symptoms of rash, fever,
headache, arthralgia and conjunctivitis
 With Zika you can have a combination of your
arthralgia and conjunctivitis - Chikungunya
arthralgia but no conjunctivitis
o Virus is detectable in the blood around the time of
symptoms onset and may persist for days to months in
pregnant women
o Fetus - can be severely infected whether or not the
mother is symptomatic
o Mortality - 7% in Brazil
o With birth defects - 5% with Zika infection and 15% with
laboratory-confirmed infection
o Congenital Zika syndrome :
o Microcephaly - Dreaded syndrome
o Lissencephaly
o Ventriculomegaly
o Intracranial calcifications
o Occular abnormalities
o Congenital Contractures
Diagnosis and Management - Zika Virus
 Zika virus RNA
o blood or urine or serological testing
 PCR
o confirmatory
 NO specific treatment or vaccine available
 Prophylaxis: protective netting and insect spray to control
the vector mosquito and avoidance of sexual contact with
recently exposed partners
BACTERIAL INFECTIONS
 Group A Streptococcus
 Group B Streptococcus (GBS)
 Methicillin- Resistant Staph aureus
 Listeriosis
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 Salmonellosis
 Shigellosis
 Hansen Disease
 Lyme Disease
 Tuberculosis
Group A Streptococcus
 Streptococcus pyogenes
o important in pregnant women
o most frequent cause of acute pharyngitis & is
associated with several systemic & cutaneous
infections
o produces numerous toxins & enzymes
responsible for the local & systemic toxicity
o infrequent cause of puerperal infection but
remains the most common cause of severe
maternal postpartum infection and death and
the incidence is rising
o Early 1990s rise in streptococcal toxic shock
syndrome:
 hypotension, fever, & multiorgan
failure with bacteremia
o Pyrogenic exotoxin-producing strains usually
associated with severe disease
o Streptococcal pharyngitis, scarlet fever, &
erysipelas not life threatening
o Treatment: Penicillin
similar in pregnant and nonpregnant
women
 Case-fatality rate approximates 30%
 Morbidity & Mortality rates are improved with early
recognition
 Treatment: clindamycin plus penicillin therapy &
surgical debridement
 No vaccine is commercially available
Group B Streptococcus (GBS)
 Streptococcus agalactiae
o colonize the gastrointestinal & genitourinary
tract in 10-25% of pregnant women
Streptococcus agalactiae is a group B organism that
can be found to colonize the gastrointestinal and
genitourinary tract in 20 to 30 percent of pregnant
women. (Throughout pregnancy, group B
streptococcus (GBS) is isolated in a transient,
intermittent, or chronic fashion. Although the organism
Page 11 of 17
 is most likely always present in these same women,
their isolation is not always homologous.)
 Maternal and Perinatal Infection
o Infections range from asymptomatic
colonization to septicemia
o Streptococcus agalactiae implicated in adverse
pregnancy outcomes
 Adverse pregnancy outcomes: preterm
labor, PROM, clinical & subclinical
chorioamnionitis, & fetal infections
o GBS cause maternal bacteriuria, pyelonephritis,
osteomyelitis, postpartum mastitis, & puerperal
infections
o remains the leading infectious cause of
morbidity and mortality among infants in the
United States
o Neonatal sepsis
 the most common infection with
devastating consequences
o Early-onset disease
 Infection < 7 days after birth;
0.21/1000 live births
o < 72 hrs of life
 most compatible with intrapartum
acquisition of disease & several
unexpected intrapartum stillbirths
newborns with early-onset GBS
infection often had clinical evidence of
fetal infection during labor or at
delivery.
o Septicemia
 serious illness within 6-12hrs of birth
 Respiratory distress, apnea, & HOPN
At the outset, therefore, neonatal infection must be
differentiated from respiratory distress syndrome
caused by insufficient surfactant production of the
preterm neonate (Chap. 34, p. 653). The mortality rate
with early-onset disease has declined to
approximately 4 percent, and preterm newborns are
disparately affected.
o Late-onset disease
 manifests as meningitis 1 week to 3
months after birth seen in 0.32 per
1000 live births
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 Mortality rate less for late-onset
meningitis than for early-onset sepsis
Unfortunately, it is not uncommon for
surviving infants of both early- and
late-onset disease to exhibit
devastating neurological sequelae.
 Prophylaxis for Perinatal Infections
o Recommendation
 universal rectovaginal culture screening
for GBS at 35-37 wks AOG followed by
intrapartum antibiotic prophylaxis for
identified carriers
o Updated Guidelines (early-onset GBS) in 2010
 intrapartum chemoprophylaxis with
PPROM, preterm labor, or penicillin
allergy & new dosing for penicillin G
chemoprophylaxis
As GBS neonatal infections evolved beginning in the
1970s and before widespread intrapartum
chemoprophylaxis, rates of early-onset sepsis ranged
from 2 to 3 per 1000 live births. In 2002, the Centers
for Disease Control and Prevention, the American
College of Obstetricians and Gynecologists, and the
American Academy of Pediatrics revised guidelines for
perinatal prevention of GBS disease. They
recommended universal rectovaginal culture screening
for GBS at 35 to 37 weeks’ gestation followed by
intrapartum antibiotic prophylaxis for women
identified to be carriers. Subsequent to
implementation of these guidelines, the incidence of
early-onset GBS neonatal sepsis has decreased to 0.24
cases per 1000 live births by 2012 (Centers for
Disease Control and Prevention, 2013a). These
guidelines were updated for early-onset GBS infection
in 2010. They expanded laboratory identification
criteria for GBS; updated algorithms for screening and
intrapartum chemoprophylaxis for women with
preterm prematurely ruptured membranes, preterm
labor, or penicillin allergy; and described new dosing
for penicillin G chemoprophylaxis.
o Culture-Based Approach:
 Screening 35-37 wks gestation
 intrapartum antimicrobials given with
RV GBS-positive cultures
 Prophylaxis for history of previous
sibling with GBS invasive disease
Page 12 of 17
  identification of GBS bacteriuria in the 1000 live births (Wendel, 2002). Non-GBS early-onset
current pregnancy sepsis was identified in 0.24 per 1000 live births, and this
The 2010 Centers for Disease Control and Prevention GBS was stable during the past two decades (Stafford, 2012).
Guidelines recommend a culture-based approach. Such a Thus, this approach has results similar to those reported
protocol was also adopted by the American College of by the Centers for Disease Control and Prevention (2010)
Obstetricians and Gynecologists (2013c). This approach is for culture-based prevention.)
designed to identify women who should be given
intrapartum antimicrobial prophylaxis. Women are
Regimens for Intrapartum Antimicrobial Prophylaxis for
screened for GBS colonization at 35 to 37 weeks’ gestation,
Perinatal GBS Disease:
and intrapartum antimicrobials are given to women with
Regimen Treatment
rectovaginal GBS-positive cultures. Selective enrichment
Recommended Penicillin G, 5 MU IV initial
broth followed by subculture improves detection. In
dose, then 2.5-3.0 MU IV
addition, more rapid techniques such as DNA probes and
Q4H until delivery
nucleic acid amplification tests are being developed (Chan,
Alternative Ampicillin, 2g IV initial dose,
2006; Helali, 2012). A previous sibling with GBS invasive
then 1g IV Q 4H or 2g Q6H
disease and identification of GBS bacteriuria in the current
until delivery
pregnancy are also considered indications for prophylaxis.
Penicillin allergic:
o Risk-Based Approach
Patients not at high risk for Cefazolin, 2g IV initial dose,
 Recommended for women in labor
anaphylaxis then 1g IV Q 8H until deliver
with unknown GBS culture results
Patients at high risk for Clindamycin, 900mg IV Q 8H
 Risk factors: delivery < 37 weeks,
anaphylaxis & with GBS until delivery
ruptured membranes > 18 hours, or
susceptible to clindamycin
intrapartum temperature > 100.4F (>
Patients at high risk for Vancomycin, 1g IV Q 12H
38.0C)
anaphylaxis & GBS resistant until delivery
 Parkland Hospital (1995 - prior to
to clindamycin or
consensus guidelines) all term
susceptibility unknown
neonates were given aqueous penicillin
G, 50,000 to 60,000 units IM
 GBS vaccine
A risk-based approach is recommended for women in
o Antibody-producing vaccines have been tested
labor and whose GBS culture results are not known. This
but NONE are clinically available
approach relies on risk factors associated with
 Intrapartum antimicrobial prophylaxis
intrapartum GBS transmission. Intrapartum
o Preventive antimicrobials administered 4 or
chemoprophylaxis is given to women who have any of
more hours before delivery are highly effective
the following: delivery < 37 weeks, ruptured membranes
Penicillin remains the first-line for prophylaxis
> 18 hours, or intrapartum temperature > 100.4F (>
38.0C). (Women with GBS during the current pregnancy
and women with a prior infant with invasive early-onset Methicillin-Resistant Staphylococcus aureus
GBS disease are also given chemoprophylaxis.)  Staphylococcus aureus
At Parkland Hospital in 1995--and prior to consensus o pyogenic G+ organism; most virulent of the
guidelines—we adopted the risk-based approach for staphylococcal species
intrapartum treatment of women at high risk. In o colonizes
addition, all term neonates who were not given  nares, skin, genital tissues, &
intrapartum prophylaxis were treated in the delivery room oropharynx
with aqueous penicillin G, 50,000 to 60,000 units o 20% persistent carriers
intramuscularly. (Rates of early-onset GBS infection and o 30-60% intermittent carriers
sepsis and of non-GBS sepsis decreased to 0.4-0.66 per

CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4 Page 13 of 17

 o 20-50% noncarriers  first-line therapy for inpatient serious
 Colonization MRSA infections
o greatest risk factor for infection
 Methicillin-resistant S. aureus (MRSA) Listeriosis

o colonizes only 2 percent of adults but a  Listeria monocytogenes

significant contributor to the health-care o facultative, intracellular Gm+ bacillus from feces

burden of 1 to 5% of adults

 MRSA infections associated with  cost & higher  Uncommon but probably underdiagnosed cause of

mortality rates neonatal sepsis

 Community-associated MRSA (CA-MRSA)  Thought to be food-borne

o when identified in an outpatient setting or  Outbreaks

within 48 hours of hospitalization o raw vegetables

 Risk factors: o coleslaw

o prior MRSA infection o apple cider

o hospitalization o melons

o dialysis or surgery within the past year o milk

o indwelling catheters or devices (w/in the past o fresh Mexican-style cheese

year) o smoked fish

 Hospital-associated MRSA (HA-MRSA) o processed foods

o are nosocomial.  During pregnancy may be asymptomatic or may cause a

Community-associated MRSA (CA-MRSA) is diagnosed febrile illness confused with influenza, pyelonephritis, or

when identified in an outpatient setting or within 48 meningitis

hours of hospitalization in a person without traditional  Diagnosis

risk factors. The latter include prior MRSA infection, o blood culture

hospitalization, dialysis or surgery within the past year,  Treatment

and indwelling catheters or devices. Hospital-associated o Ampicillin plus Gentamicin or TMP-SMZ

MRSA (HA-MRSA) infections are nosocomial. Most  NO vaccine available

cases of MRSA in pregnant women are CA-MRSA.  Prevention

 Management o washing raw vegetables and cooking all raw

o Uncomplicated superficial infections food

 drainage & local wound care

o Severe superficial infections Salmonellosis

 should be treated with MRSA-  Infections from Salmonella species

appropriate antibiotics o a major & increasing cause of food-borne

o Purulent cellulitis illness

 empiric treatment for CA-MRSA until  Six serotypes including Salmonella subtypes

culture results are available typhimurium & enteritidis

o CA-MRSA  Non-typhoid Salmonella gastroenteritis

 most are sensitive to TMP-SMZ and o contracted through contaminated food

clindamycin  Symptoms:

o linezolid o nonbloody diarrhea

 expensive o abdominal pain

o fever

o doxycycline, minocycline, & tetracycline o chills

 contraindicated in pregnancy o nausea & vomiting (6-48hrs after exposure)

o vancomycin

CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4 Page 14 of 17

 Infections from Salmonella species continue to be a
major and increasing cause of food-borne illness
(Peques, 2012). Six serotypes account for most cases in
the United States, including Salmonella subtypes
typhimurium and enteritidis. Non-typhoid Salmonella
gastroenteritis is contracted through contaminated food.
Symptoms including nonbloody diarrhea, abdominal
pain, fever, chills, nausea, and vomiting begin 6 to 48
hours after exposure.
 Diagnosis
o stool studies
 IV crystalloid
o for rehydration
 Antimicrobials
o not given in uncomplicated infections
o If complicated by bacteremia antimicrobials are
given
 Typhoid fever
o caused by Salmonella typhi
o Transmission: oral ingestion of contaminated
food, water, or milk
o Antepartum typhoid fever  abortion, preterm
labor, & maternal or fetal death
Typhoid fever caused by Salmonella typhi remains a
global health problem, although it is uncommon in the
United States. Infection is spread by oral ingestion of
contaminated food, water, or milk. In pregnant women,
the disease is more likely to be encountered during
epidemics or in those with HIV infection (Hedriana,
1995). In former years, antepartum typhoid fever
resulted in abortion, preterm labor, and maternal or
fetal death (Dildy, 1990).
o Treatment: Fluoroquinolones & 3rd
generation cephalosporins
o For enteric (typhoid) fever  antimicrobial
susceptibility testing is important
o Typhoid vaccines
 no harmful effects when administered
to pregnant women
 given in epidemic or before travel to
endemic areas
Shigellosis
 Bacillary dysentery
o caused by Shigella
CPU College of Medicine | Medentes Cum Corde| 2020 | Group 4
 Relatively common highly contagious cause of
inflammatory exudative diarrhea in adults
 Shigellosis
o more common in children attending day-care
centers
 Transmission
o fecal-oral route
 Clinical manifestations
o mild diarrhea to severe dysentery
o bloody stools
o abdominal cramping
o tenesmus
o fever
o systemic toxicity
Bacillary dysentery caused by Shigella is a relatively
common, highly contagious cause of inflammatory
exudative diarrhea in adults. Shigellosis is more
common in children attending day-care centers and is
transmitted via the fecal-oral route. Clinical
manifestations range from mild diarrhea to severe
dysentery, bloody stools, abdominal cramping,
tenesmus, fever, and systemic toxicity.
 Self-limited
o treatment of dehydration is essential
 Antimicrobial therapy
o Imperative
o include fluoroquinolones, ceftriaxone, or
azithromycin
 Can stimulate uterine contractions and cause preterm
birth
Although shigellosis may be self-limited, careful
attention to treatment of dehydration is essential in
severe cases. We have cared for pregnant women in
whom secretory diarrhea exceeded 10 L/day!
Antimicrobial therapy is imperative, and effective
treatment during pregnancy includes fluoroquinolones,
ceftriaxone, or azithromycin. Antimicrobial resistance is
rapidly emerging, and antibiotic susceptibility testing can
help guide appropriate therapy (Centers for Disease
Control and Prevention, 2013c).
Page 15 of 17
 Protozoal Infections Management:

Toxoplasmosis Prenatal treatment:

 Humoral and cell-mediated immune defenses eliminate  Spiramycin

most of these, but tissue cysts develop In women with acute infection early in

🔊 pregnancy
Two distinct stages:  Pyrimethamin-sulfonamide + folinic acid
 Feline stage Maternal infection after 18 weeks, or if fetal
o In the cat (definitive host) and its prey infection is suspected
o Unsporulated oocysts are secreted in the feces Prevention:
 Nonfeline stage  No vaccine
Tissue cysts with bradyzoites/oocysts are  Avoidance
ingested by intermediate host (humans) o Cooking meat to safe temperatures;
↓ o Peeling/thoroughly washing fruits & vegetables;
Gastric acid digests cysts to release bradyzoites o Cleaning all food preparation surfaces &
↓
utensils that have contacted raw meat, poultry,
Small intestine epithelium infection
seafood, or unwashed fruits & vegetables;
↓
Transformation to tachyzoites o Wearing gloves when changing cat litter, or
↓ delegating this duty; &
Infect all cells within host mammal o Avoiding feeding cats raw or undercooked
↓ meat & keeping cats indoors
Humoral and cell-mediated immune defenses
eliminate these, but tissue cysts develop Amebiasis
↓  Entamoeba histolytica
Lifelong persistence: chronic form of
 Infected persons asymptomatic
toxoplasmosis
 Amebic dysentery: fulminant course during pregnancy with
 Human infection:
fever, abdominal pain, & bloody stools
o Eating infected raw or undercooked meat
 (+) hepatic abscess: worse prognosis
o Contact with oocysts from cat feces
 Diagnosis: identification of E. histolytica cysts or trophozoites
contaminated litter, soil, water
in a stool sample
 Incidence and severity of congenital infection depend on
fetal age at the time of maternal infection
Therapy:
 Risks for fetal infection increases with duration of
*same for preg and non-pregnant women
pregnancy
 Amebic colitis & invasive disease
o 15% at 13 weeks
o Metronidazole
o 44% at 26 weeks
o Tinidazole
o 71% at 36 weeks
 Noninvasive infections
 If infected before 20 weeks, 11% of NB had congenital
o Iodoquinol
toxoplasmosis; 45% after 20 weeks
o Paromomycin
 Severity of fetal infection is much greater in early
pregnancy; fetuses are much more likely to have clinical Mycotic Infections
findings of infection  Dilated fungal infection (usually pneumonitis) during
pregnancy is uncommon with coccidioidomycosis,
Screening and diagnosis blastomycosis, cryptococcosis, or histoplasmosis
 Prenatal screening not recommended
 With IgG antibody before pregnancy, there is no risk for
congenitally infected fetus

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 Travel Precautions during Pregnancy 🔊 If allergic to ciprofloxacin or
 Obstetrical risks, general medical risk, & potentially amoxicillin
hazardous destination risks
 Anthrax vaccine:
 International Society for Tropical Medicines and Center o Inactivated
for Disease Control and Prevention o cell-free product
o 3 injections over 28 days
Bioterrorism
 Risk from anthrax > fetal risks from doxycycline
1. Smallpox
2. Anthrax
Other Bioterrorism Agents
3. Other bioterrorism agents Category A
 Francisella tularensis – tularemia
 Bioterrorism involves the deliberate release of bacteria,  Clostridium botulinum – botulism
viruses, or other infectious agents to cause illness or  Yersinia pestis – plague
death  Viral hemorrhagic fevers – Ebola, Marburg, Lassa,
 These natural agents are often altered to increase their Machupo
infectivity or their resistance to medical therapy
 Clinicians should be alert for significant increases in the Category B&C: multiple agents
number of persons with febrile illnesses accompanied by
References
respiratory symptoms or with rashes not easily
 Doc’s lecture and powerpoint
associated with common illnesses  William’s Obstetrics 25th Ed. Chapter 64

Smallpox
 Variola virus
 Serious weapon
 Highly transmissible; case fatality rate: 30%
 Last case in US: 1949
Worldwide (Somalia): 1977
 Vaccine is a live vaccine virus – pregnancy should be
delayed for 4 weeks.

Anthrax
 Bacillus anthracis
o Gram-positive, spore-forming, aerobic
bacterium
 3 main types:
o Inhalational
 2001 bioterrorist attacks
o Cutaneous
o Gastrointestinal
 Postexposure prophylaxis (2months)
o Ciprofloxacin 500mg BID for 60 days
o Amoxicillin 500mg TID
 Can be substituted if strain is sensitive
🔊If allergic to ciprofloxacin
o Doxycycline 100mg BID for 60 days

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