PATHO OB: Infectious Diseases in Pregnancy

Dr. Fulgado – October 1, 2018

MATERNAL AND FETAL IMMUNOLOGY  Does not appear to be more frequent or severe in pregnant
 Pregnancy-Induced Immunological Changes women.
 It is known that pregnancy is associated with an increase in the
CD4+ T cells that secrete Th2-type cytokines VARICELLA ZOSTER HERPES ZOSTER/SHINGLES
(PRIMARY INFECTION) (SECONDARY INFECTION)
 Th2-type increases, while Th1-type cytokines are somehow
Lesions are generalized Lesions predominate only in one
suppressed
Pruritic dermatomal area
 The predominance of the Th2-type cytokines is the reason why
With greater effects in the fetus Painful
the maternal body does not reject the foreign pregnancy inside Less infections unless you get
 Fetal and Newborn Immunology contaminated with the vesicle
 Fetal cell-mediated and humoral immunity begin to develop by
9 to 15 weeks’ gestation  VZV pneumonia: most common cause of mortality
 Primary fetal response to infection is immunoglobulin M  Most dreaded complication
(IgM)
 Evident with a positive chest x-ray
 Passive immunity is provided by IgG transferred across the
 Risk factors for VZV pneumonia include: smoking and having
placenta.
more than 100 cutaneous lesions.
 By 16 weeks, this transfer begins to rise rapidly
 Symptoms of VZV pneumonia usually appear 3 to 5 days into
 By 26 weeks, fetal concentrations are equivalent to those
the course of illness.
of the mother.
 Fever, tachypnea, dry cough, dyspnea, and pleuritic pain are
 After birth, breastfeeding is protective against some infections,
characteristic.
although this protection begins to decline at 2 months of age.
 Nodular infiltrates are similar to other viral pneumonias
 Vertical transmission in pregnancy
 Admit the mother is she develops pneumonia
 Passage of infection occurs via 3 pathways:
 Supportive management
 Passage from the mother to her fetus of an infectious
 Counsel the mother properly
agent through the placenta (transplacental)
 It is important to ask the mother the week or month of
 During labor or delivery as the baby will pass through the
pregnancy when she got infected
vaginal wall
 Breastfeeding
FETAL AND NEONATAL INFECTIONS
NEONATAL TRANSMISSION
VIRAL INFECTIONS
<13 weeks 0.4%
VARICELLA-ZOSTER VIRUS 13-20 weeks Highest
 Varicella–zoster virus (VZV) >20 weeks Rare/No evidence
 Double-stranded DNA herpesvirus acquired predominately  If the primary infection is acquired before or during labor, the
during childhood, and 90 percent of adults have serological incidence of disseminated visceral or CNS disease in the neonate is
evidence of immunity increased.
 One of the most dreaded infection during pregnancy
Congenital varicella syndrome
MATERNAL INFECTION  Does not manifest as the typical maculopapular rash
 Primary infection  Possible outcome if the varicella virus is acquired at around 13 to 20
 Varicella or chickenpox weeks.
 Transmitted by direct contact with an infected individual,  Some features include:
although respiratory transmission has been reported.  Chorioretinitis
 Incubation period is 10 to 21 days  Microphthalmia
 Initially presents as a maculopapular rash starting at the trunk  Cerebral cortical atrophy
that eventually produce a vesicular/blister type lesion at the  Growth restriction
center  Hydronephrosis
 Presents with a 1- to 2-day flulike prodrome, which is  Limb hypoplasia
followed by pruritic vesicular lesions that crust after 3 to 7 days  Cicatricial skin lesions
 Affected patients are then contagious from 1 day before the .
onset of the rash until the lesions become crusted. DIAGNOSIS
 More risky for the fetus  Usually diagnosed clinically
 Secondary infection  Tzanck’s smear
 Herpes zoster or Shingles  Tissue culture
 Reactivation of the primary varicella infection years later  Direct fluorescent antibody testing
 Presents as a unilateral dermatomal vesicular eruption  NAAT (nucleic acid amplification test) of vesicular and amniotic fluid
associated with severe pain.

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018

 Detailed anatomical sonographic evaluation performed at least 5  Intracranial calcifications

weeks after maternal infection may disclose abnormalities  Chorioretinitis
(sensitivity is low)  Mental and motor retardation
 Sensorineural deficits
MANAGEMENT  Hepatosplenomegaly
 Maternal Infection  Jaundice
 Any patient diagnosed with primary varicella infection or  Hemolytic anemia
herpes zoster should be isolated from pregnant women.  Thrombocytopenic purpura
 Supportive care
 Hospitalization especially if with VZV pneumonia DIAGNOSIS
 Give IV acyclovir therapy 500 mg/m2 or 10 to 15 mg/kg  Routine prenatal CMV serological screening is currently not
every 8 hours. recommended
 Maternal Viral Exposure  Done only if you CMV on your ultrasound
 Varicella-zoster immune globulin (VariZIG) within 96 hours  Maternal diagnosis
of exposure up to 10 days  CMV IgG and IgM
 Indications:  Both should be positive
 Exposed gravidas with a negative history for  Enzyme immunoassay (CMV IgG avidity)
chickenpox should undergo VZV serological testing.  Confirming primary viral infection
 Exposed pregnant women who are susceptible  High anti-CMV IgG avidity indicates primary maternal
(seronegative) should be given infection >6 months before testing
 If acquired before or during delivery  Viral culture
 Vaccination  Minimum of 21 days is required before findings are considered
 The vaccine is not recommended for pregnant women or for negative
those who may become pregnant within a month following  Prenatal diagnosis
each vaccine dose.  Ultrasound
 If woman is exposed postpartum, vaccine can be given  MRI
 Attenuated vaccine virus is not secreted in breast milk.  PCR detection of viral DNA in amniotic fluid and blood (CMV
NAAT) of amniotic fluid
CYTOMEGALOVIRUS  Gold standard for fetal infection
MATERNAL INFECTION
 Most infections are asymptomatic
 10 to 15 percent of infected adults have a mononucleosis-like
syndrome characterized by:
 Fever, pharyngitis, lymphadenopathy, and polyarthritis
 Immunocompromised women may develop myocarditis,
pneumonitis, hepatitis, retinitis, gastroenteritis, or
meningoencephalitis.
 Women who are seronegative before pregnancy, but who develop
primary CMV infection during pregnancy, are at greatest risk to have
an infected fetus
 Pregnancy does not increase the risk or severity of maternal CMV
infection.

RATES OF TRANSMISSION
1st trimester 30-36%
2nd trimester 34-40%
3rd trimester 40-72%

FETAL INFECTION
 Newborns with apparent sequelae of in-utero-acquired CMV
infection are described as having symptomatic CMV infection.
 Congenital infection is a syndrome that may include (blueberry
muffin-like):
 Growth restriction
 Microcephaly

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018

MANAGEMENT AND PREVENTION  Other symptoms may include arthralgias or arthritis, head and
neck lymphadenopathy, and conjunctivitis
 No proven treatment available for CMV infection
 Incubation period is 12 to 23 days
 Limited to symptomatic treatment only
 Congenital rubella syndrome
 If recent primary CMV infection is confirmed, amniotic fluid analysis
 Cataracts, microphthalmia, congenital glaucoma, and
should be offered.
pigmentary retinopathy
 Counseling regarding fetal and neonatal outcome depends on the
 Cardiac septal defects and pulmonary artery stenosis
gestational age during which primary infection is documented.
 Sensorineural deafness – the most common congenital defect
 No CMV vaccine available
 CNS defects (microcephaly, mental retardation)
 Avoid primary infection during pregnancy
 Purpura
 Basic measures such as good hygiene and hand washing have
 Hepatosplenomegaly/jaundice
been promoted, particularly for women with toddlers in day-
 Radiolucent bone densities
care settings
 Reports of delayed morbidities associated with congenital
rubella syndrome may include a rare, progressive
RUBEOLA (MEASLES) AND RUBELLA (GERMAN MEASLES)
panencephalitis, insulin-dependent diabetes mellitus, and
MEASLES (RUBEOLA) thyroid disorders
 Clinical symptoms:  Diagnosis
 High fever  May be isolated from the urine, blood, nasopharynx, and
 Cough, coryza, and conjunctivitis (3 C’s) cerebrospinal fluid for up to 2 weeks after rash onset
 Erythematous maculopapular rash: on the face and neck and  Diagnosis is usually made with serological analysis.
then spreads to the back, trunk, and extremities  Specific IgM antibody can be detected using enzyme-linked
 Koplik spot: small white lesions with surrounding erythema immunoassay for 4 to 5 days after onset of clinical disease, but
found within the oral cavity. antibody can persist for up to 6 weeks after appearance of the
 Complications: rash.
 Diarrhea (most common)
 Pneumonia (most common cause of mortality) MANAGEMENT AND PREVENTION
 Acute disseminated encephalomyelitis (ADEM) DURING PREGNANCY
 Subacute sclerosing panencephalitis (SSPE) RUBEOLA RUBELLA
 Complications during pregnancy:
Treatment No specific treatment No specific treatment
 Abortion Supportive therapy Supportive therapy
 Preterm delivery
 Low birth weight Exposure during
 Risk of serious infection if measles develop shortly before birth pregnancy:
 Diagnosis of acute infection is most commonly performed by immunoglobulin
serological evidence of IgM antibodies, although RTPCR tests are maybe given within 5
available. days
 The virus does not appear to be teratogenic. However, rates of Prevention MMR Vaccine: not recommended during
spontaneous abortion, preterm delivery, and low-birthweight pregnancy; pregnancy avoided 1 month after
neonates are increased with maternal measles vaccination; safe for breastfeeding

GERMAN MEASLES (RUBELLA) INFLUENZA VIRUS

 A complete teratogen  RNA virus (Orthomyxoviridae)

 Causes abortion and severe congenital malformations (in the first  Influenza A and B form one genus of these RNA viruses, and both
trimester) cause epidemic human

RATE OF FETAL INFECTION MATERNAL AND FETAL INFECTION

<12 weeks 90%  Pregnant women appear to be more susceptible to serious
13-14 weeks 50% complications, particularly pulmonary involvement
>14 weeks 25%  Viremia is infrequent, and transplacental passage is rare
 Possible outcomes in pregnancy:
 Maternal rubella  Neural tube defects
 Mild febrile illness with a generalized maculopapular rash  Stillbirth
beginning on the face and spreading to the trunk and  Preterm delivery
extremities.  1st trimester abortion
 25 to 50 percent of infections are asymptomatic

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018

DIAGNOSIS PREVENTION
 Usually symptomatic PROPHYLAXIS FOR PERINATAL INFECTIONS
 May be detected in nasopharyngeal swabs using viral antigen rapid  ACOG and CDC Recommendation:
detection assays  All women at 35-37 weeks AOG be screened form Group B
 Reverse transcriptase–polymerase chain reaction (RT-PCR) Streptococcus disease by getting a vaginal or rectal culture
 Gold standard for diagnosis  2 cases that do not require screening:
 More sensitive and specific test, although not widely available  Identified infection (if the patient has already been
positive for GBS during the current pregnancy)
MANAGEMENT  Previous infant had invasive GBS disease

Two classes of antiviral medications are currently available (All are

FDA Category C drugs):
 Neuraminidase inhibitors: highly effective for the treatment of
early influenza A and B.
 Oseltamivir (Tamiflu): taken orally for treatment and for
chemoprophylaxis
 75 mg BID x 5 days within 48 hours of symptoms
 75 mg OD x 7 days (chemoprophylaxis)
 Zanamivir (Relenza): inhaled for treatment
 Peramivir (Rapivab): administered intravenously.
 Adamantanes: resistance reported
 Amantadine
 Rimantadine, which were used for

PREVENTION
 Flu Vaccination
 All pregnant women must be vaccinated including those who
will be pregnant during influenza season and those with
chronic medical disorders (DM, heart disease, asthma, HIV)

BACTERIAL INFECTIONS
GROUP B STREPTOCOCCUS
 Streptococcus agalactiae is a group B organism that can be found
to colonize the gastrointestinal and genitourinary tract in 10 to 25
percent of pregnant women
 Note: for planned CS of a positive for GBS mother, no need to
give the prophylaxis. However, if there is no rupture of
MATERNAL AND PERINATAL INFECTION
membranes, give the prophylaxis
 Ranges from asymptomatic colonization to septicemia.
 Implicated in adverse pregnancy outcomes: Intrapartum Anti-microbial Prophylaxis
 Preterm labor  Preventive antimicrobials administered 4 or more hours before
 Prematurely ruptured membranes delivery are highly effective
 Clinical and subclinical chorioamnionitis  Regardless of screening method, penicillin remains the first-line
 Fetal infections agent for prophylaxis, and ampicillin is an acceptable alternative
 Maternal bacteriuria  Women with a penicillin allergy and no history of anaphylaxis are
 Pyelonephritis given cefazolin
 Osteomyelitis  Those at high risk for anaphylaxis should have antimicrobial
 Postpartum mastitis susceptibility testing performed to exclude clindamycin resistance.
 Puerperal infections
 Postpartum endometritis
 It remains the leading infectious cause of morbidity and mortality
among infants in the United

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018

FETAL EFFECTS
 Intracranial calcifications
 Hydro-/microcephaly
 Low birth weight
 Hepatosplenomegaly
 Jaundice
 Anemia  hydrops

DIAGNOSIS
 Ultrasound
 Congenital toxoplasmosis is suspected when:
 Hydrocephaly
 Placental thickening
 Intracranial calcifications
 Ascites
 Hyperechoic bowels
REGIMEN TREATMENT  Growth restricted form
Recommended Penicillin G, 5 million units IV initial dose,  Prenatal diagnosis of congenital toxoplasmosis is performed using
then 2.5 to 3.0 million units IV every 4 hours PCR amplification of toxoplasma DNA in amniotic fluid
until delivery  Sensitivity of PCR varies with gestational age and is lowest
Alternative Ampicillin, 2g IV initial dose, then 1g IV before 18 weeks
every 4 hours or 2g every 6 hours until
delivery
MANAGEMENT
Penicillin allergic
Patients not at high risk Cefazolin, 2g IV initial dose, then 1g IV  Spiramycin
for anaphylaxis: every 8 hours until delivery  Used in women with acute infection early in pregnancy to
Patients at high risk for Clindamycin, 900mg IV every 8 hours until reduce vertical transmission.
anaphylaxis and with delivery  Because it does not cross the placenta, spiramycin may not be
GBS susceptible to used to treat fetal infection
clindamycin:  Pyrimethamine-Sulfadiazine + Folinic acid
Patients at high risk for Vancomycin, 1g IV every 12 hours until  Selected for maternal infection after 18 weeks’ gestation or if
anaphylaxis and with delivery fetal infection is suspected.
GBS resistant to
clindamycin or
susceptibility unknown PREVENTION
 There is no vaccine for toxoplasmosis, so avoidance of infection is
PROTOZOAL INFECTIONS necessary if congenital infection is to be prevented.
 Efforts include:
TOXOPLASMOSIS
 Cooking meat to safe temperatures
 Obligate intracellular parasite Toxoplasma gondii
 Peeling or thoroughly washing fruits and vegetables
 Risk of transmission is higher in advancing age, however, severity of
 Cleaning all food preparation surfaces and utensils that have
fetal infection is much greater in early pregnancy
contacted raw meat, poultry, seafood, or unwashed fruits and
 Human infection is acquired by eating raw or undercooked meat
vegetables
infected with tissue cysts or by contact with oocysts from cat feces
 Wearing gloves when changing cat litter, or else delegating this
in contaminated litter, soil, or water.
duty
 Avoiding feeding cats raw or undercooked meat and keeping
MATERNAL EFFETCS cats indoors.
 Most acute maternal infections are subclinical and are detected only
by prenatal or newborn serological screening. MALARIA
 In some cases, maternal symptoms may include fatigue, fever,
 Transmitted by infected Anopheles mosquitoes, six species of
headache, muscle pain, and sometimes a maculopapular rash and
Plasmodium cause human disease—falciparum, vivax, two species
posterior cervical lymphadenopathy.
of ovale, malariae, and knowlesi
 In immunocompetent adults, initial infection confers immunity, and
 Pregnant women have increased susceptibility to malarial infections
prepregnancy infection nearly eliminates any risk of vertical
 Antibodies to the parasite surface antigen VAR2CSA mediate
transmission.
placental accumulation of infected erythrocytes and lead to the
harmful effects of malaria

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018

MATERNAL AND FETAL INFECTION

 Clinical findings are fever, chills, and flulike symptoms including
headaches, myalgia, and malaise, which may occur at intervals.
 Symptoms are less severe with recurrences.
 Malaria may be associated with anemia and jaundice, and falciparum
infections may cause kidney failure, coma, and death.
 Associated with:
 Still births
 Preterm births
 Low birth weight infants
 Maternal anemia

DIAGNOSIS
 Identification of parasites by microscopical evaluation of a thick and
thin blood smear remains the gold standard for diagnosis.
 Malaria-specific antigens are now being used for rapid diagnostic
testing.

TREATMENT
 Pregnant women diagnosed with uncomplicated malaria caused by
P. vivax, malariae, ovale, and chloroquine-sensitive P. falciparum
 Chloroquine
 Hydrochloroquine

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018

VIRAL INFECTIONS  No treatment or vaccination is available

 Tramission:
MUMPS VIRUS
 May be transmitted by maternal secretions to the fetus at
 Primarily infects the salivary glands but also may involve the gonads,
delivery
meninges, pancreas, and other organs.
 Transplacental passage has also been reported
 It is transmitted by direct contact with respiratory secretions, saliva,
 Congenital malformation rates may be slightly increased in
or through fomites.
fetuses of pregnant women who had serological evidence of
 Most transmission occurs before and within 5 days of parotitis onset,
coxsackievirus
and droplet isolation is recommended during this time
 Viremia can cause fetal hepatitis, skin lesions, myocarditis, and
 Treatment
encephalomyelitis
 Symptomatic, and mumps during pregnancy is no more severe
 Higher rates of cardiac anomalies and of low-birthweight,
than in nonpregnant adults.
preterm, and small-for-gestational-age newborns
 Women who develop mumps in the first trimester may have a
 Polioviruses
greater risk of spontaneous abortion.
 Cause highly contagious infections that are subclinical or mild.
 Infection in pregnancy is not associated with congenital
 The virus is trophic for the CNS, and it can cause paralytic
malformations, and fetal infection is rare
poliomyelitis
 MMR Vaccine
 Perinatal transmission has been observed, especially when
 Contraindicated in pregnancy according to the CDC
maternal infection developed in the third trimester
 No malformations attributable to MMR vaccination in
 Inactivated subcutaneous polio vaccine is recommended for
pregnancy have been reported, but pregnancy should be
susceptible pregnant women who must travel to endemic areas
avoided for 30 days after mumps vaccination.
or are placed in other high-risk situations.
 Vaccine may be given to susceptible women postpartum, and
 Live oral polio vaccine has been used for mass vaccination
breastfeeding is not a contraindication.
during pregnancy without harmful fetal effects

RESPIRATORY VIRUSES
 Cause the common cold, pharyngitis, laryngitis, bronchitis, and
pneumonia.
 Rhinovirus, coronavirus, and adenovirus are major causes of the
common cold.
 The potential teratogenic effects of respiratory viruses are
controversial
 There was an association with fetal-growth restriction, nonimmune
hydrops, foot/hand abnormalities, and neural-tube defects.
 Adenoviral infection is a known cause of childhood myocarditis.
HANTAVIRUSES
 Members of the family Bunyaviridae.
 Associated with a rodent reservoir, and transmission involves
inhalation of virus excreted in rodent urine and feces.
 Hantavirus pulmonary syndrome: cause maternal death, fetal
demise, and preterm birth.
ENTEROVIRUSES
 Include coxsackie virus, poliovirus, and echovirus.
 They are trophic for intestinal epithelium but can also cause
widespread maternal, fetal, and neonatal infections that may include
the CNS, skin, heart, and lungs.
 Most maternal infections are subclinical yet can be fatal to the fetus–
neonate
 Coxsackie virus infections with group A and B are usually
asymptomatic.
 Symptomatic infections (usually group B) include aseptic
meningitis, poliolike illness, hand foot and mouth disease,
rashes, respiratory disease, pleuritis, pericarditis, and
myocarditis.
PARVOVIRUS
 This B19 virus causes erythema infectiosum, or fifth disease
 Replicates in rapidly proliferating cells such as erythroblast
precursors  lead to anemia, which is its primary fetal effect.
 Only individuals with the erythrocyte globoside membrane P
antigen are susceptible.
 Main mode of parvovirus transmission is respiratory or hand-to-
mouth contact
 Infection is common in spring months
 Maternal infection rate is highest in women with school-aged
children and in day-care workers
 Develops viremia 4 to 14 days after exposure, and an otherwise
immunocompetent individual is no longer infectious at the onset of
the rash.
MATERNAL INFECTION
 In 20 to 30 percent of adults, infection is asymptomatic.
 Fever, headache, and flulike symptoms may begin in the last few
days of the viremic phase.
 Several days later, a bright red rash with erythroderma affects the
face and gives a slappedcheek appearance.
 Rash becomes lacelike and spreads to the trunk and extremities.
 With recovery, IgM antibody is generated 7 to 10 days postinfection,
and production persists for 3 to 4 months
FETAL INFECTION
 There is vertical transmission to the fetus in up to a third of maternal
parvovirus infections
 Fetal infection has been associated with abortion, nonimmune
hydrops, and stillbirth
 It is the most frequent infectious agent of nonimmune hydrops

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PATHO OB | Infections Diseases in Pregnancy
Dr. Fulgado – October 1, 2018
 Critical period for maternal infection leading to fetal hydrops was
estimated to be between 13 and 16 weeks’ gestation, which
coincided with the period in which fetal hepatic hemopoiesis is
greatest.
DIAGNOSIS AND MANAGEMENT
 Diagnosis is generally made by maternal serological testing for
specific IgG and IgM antibodies
 Viral DNA may be detectable by PCR in maternal serum during the
prodrome and persist for months to years after infection.
 Fetal infection is diagnosed by detection of B19 viral DNA in
amnionic fluid or IgM antibodies in fetal serum obtained by
cordocentesis
 Serial sonography every 2 weeks should be performed in women
with recent infection
 Middle cerebral artery (MCA) Doppler interrogation can also be
used to predict fetal anemia
 Fetal blood sampling is warranted with hydrops to assess the degree
of fetal anemia.
 With transfusion, 94 percent of hydrops cases resolve within 6 to 12
weeks, and the overall mortality rate is <10 percent.
 Most fetuses require only one transfusion because hemopoiesis
resumes as infection resolves.
 Concurrent fetal thrombocytopenia worsens the prognosis
PREVENTION
 No parvovirus vaccine is available
 No evidence suggests that antiviral treatment prevents maternal or
fetal infection.
 Infected children do not require isolation.
WEST NILE VIRUS
 Most common cause of arthropod-borne viral encephalitis in the
United States
 Typically acquired through mosquito bites in late summer or
perhaps through blood transfusion
 Incubation period is 2 to 14 days
 Most persons have mild or no symptoms.
 Presenting symptoms may include:
 Fever, mental status changes, muscle weakness, and coma
 Adverse effects of West Nile viremia on pregnancy are unclear.
DIAGNOSIS
 Based on clinical symptoms and the detection of viral IgG and IgM
in serum and IgM in cerebrospinal fluid.
MANAGEMENT
 No known effective antiviral treatment
 Management is supportive.
PREVENTION
 Primary strategy for preventing exposure in pregnancy is the use of
insect repellant containing N,N-diethyl-m-toluamide (DEET).
 This is considered safe for use among pregnant
 Avoiding outdoor activity and stagnant water and wearing
protective clothing are also recommended.
CORONAVIRUS INFECTIONS
 Although experience with MERS-CoV is sparse in pregnancy,
infection has been reported to cause maternal and perinatal deaths
EBOLA VIRUS
 Transmitted by direct person-to-person contact
 Produces a severe hemorrhagic fever with pronounced
immunosuppression and disseminated intravascular coagulopathy.
 Treatment is supportive
 Mortality rate approaches 50 percent.
 CDC concludes that pregnant women are at increased risk for severe
illness and death
ZIKA VIRUS
 First major mosquito-borne teratogen
 Transmission:
 Primarily transmitted by mosquito bite
 Sexual transmission is also possible
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Dr. Fulgado – October 1, 2018
MATERNAL–FETAL INFECTION
 Zika infection may be asymptomatic or cause mild symptoms of
rash, fever, headache, arthralgia, and conjunctivitis lasting a few
days.
 Virus is typically detectable in blood around the time of symptom
onset and may persist days to months in pregnant women
 Serum IgM antibodies typically become detectable within the first
two weeks after symptom onset and remain a median of four
months
 Guillain-Barré syndrome may develop following infection
 Fetus can be severely infected whether or not the mother is
symptomatic
 In the most severely affected fetuses, a congenital Zika syndrome
has been described that includes:
 Microcephaly, lissencephaly, ventriculomegaly, intracranial
calcifications, ocular abnormalities, and congenital
contractures
DIAGNOSIS
 Diagnosis of this infection in pregnant women is made with
detection of Zika virus RNA in blood or urine or by serological
testing.
 Serological assays for Zika IgM antibodies may cross react with
other flaviviruses. Thus, a positive assay result is followed by
another assay containing virus-specific neutralizing antibodies
 Detection of Zika virus RNA by PCR confirms infection
 Testing recommendations and interpretation have evolved for
pregnant women who are symptomatic and those who are
asymptomatic but have ongoing exposure risk.
 This risk includes living in or traveling to an area with active
local transmission.
MANAGEMENT
 Currently, no specific treatment or vaccine is available for Zika
infection, although several vaccine candidates are in development
 Prophylaxis includes protective netting and insect spray to control
the vector mosquito and avoidance of sexual contact with partners
recently exposed.
BACTERIAL INFECTIONS
GROUP A STREPTOCOCCUS
 Infections caused by Streptococcus pyogenes are important in
pregnant women.
 This organism is the most frequent bacterial cause of acute
pharyngitis and is associated with several systemic and cutaneous
infections.
 Produces numerous toxins and enzymes responsible for its local and
systemic toxicity.
 Remains the most common cause of severe maternal postpartum
infection and death worldwide, and the incidence of these infections
is rising
 The early 1990s saw the emergence of streptococcal toxic shock
syndrome, manifested by hypotension, fever, and evidence of
multiorgan failure with associated bacteremia.
 Treatment includes clindamycin plus penicillin therapy and often
surgical debridement
 No vaccine for group A streptococcus is commercially available.
METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS
 Considered the most virulent of the staphylococcal species
 Community-acquired MRSA (CA-MRSA) is diagnosed when
identified in an outpatient setting or within 48 hours of
hospitalization in a person without traditional risk factors.
 Such risk factors include prior MRSA infection, hospitalization,
dialysis or surgery within the past year, and indwelling
catheters or devices
 Hospital-associated MRSA (HA-MRSA) infections are nosocomial.
 Most cases of MRSA in pregnant women are CA-MRSA
MRSA AND PREGNANCY
 Anovaginal colonization with S aureus is identified in 10 to 25
percent of obstetrical patients
 Skin and soft tissue infections are the most common presentation
of MRSA in pregnant women
 Mastitis and breast abscesses
 Perineal abscesses, wound infections at sites such as
abdominal and episiotomy incisions, and chorioamnionitis
 Osteomyelitis
 Vertical transmission is rare (Jimenez-Truque, 2012; Pinter, 2009).
MANAGEMENT
 Uncomplicated superficial infections are primarily managed by
drainage and local wound care.
 Recent evidence suggests benefit from antibiotic therapy in
addition to incision and drainage of smaller abscesses
 Severe superficial infections, especially those that fail to respond to
local care or those in patients with medical comorbidities, are
treated with MRSA-appropriate antibiotics.
 Purulent cellulitis should be treated empirically for CA-MRSA until
culture results are available.
 Most CA-MRSA strains are sensitive to trimethoprim-
sulfamethoxazole and clindamycin
 Vancomycin remains the first-line therapy for inpatient serious
MRSA infections.
PREVENTION
 Control and prevention of HA-MRSA and CA-MRSA rely on
appropriate hand hygiene and prevention of skin-to-skin contact or
contact with wound dressings.
 Decolonization should be considered only in cases in which a patient
develops recurrent superficial infections despite optimal hygiene
measures or if ongoing transmission occurs among household or
close contacts
 Decolonization measures include nasal treatment with
mupirocin, chlorhexidine gluconate baths, and oral rifampin
therapy if previous measures have failed.
 Routine decolonization is not effective in the general
obstetrical population.
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 Women with culture-proven CA-MRSA infection during pregnancy,
we add singledose vancomycin to routine beta-lactam perioperative
prophylaxis for cesarean deliveries and higher-order perineal
lacerations.
LISTERIOSIS
 Uncommon but probably underdiagnosed cause of neonatal sepsis
 Outbreaks have been caused by raw vegetables, coleslaw, apple
cider, melons, milk, fresh Mexican-style cheese, smoked fish, and
processed foods such as pâté, hummus, wieners, and sliced deli
meats
 More common in pregnant women, immunocompromised patients,
and the very old or young
MATERNAL AND FETAL INFECTION
 Listeriosis during pregnancy may be asymptomatic or may cause a
febrile illness that is confused with influenza, pyelonephritis, or
meningitis
 Diagnosis usually is not apparent until blood cultures are reported
as positive.
 Occult or clinical infection also may stimulate labor.
 Discolored, brownish, or meconium-stained amnionic fluid is
common with fetal infection, even in preterm gestations.
 Maternal listeriosis causes fetal infection that characteristically
produces disseminated granulomatous lesions with microabscesses
 Chorioamnionitis is common, and placental lesions include multiple,
well-demarcated macroabscesses.
MANAGEMENT AND PREVENTION
 Treatment with ampicillin plus gentamicin is usually recommended
because of synergism against Listeria species
 Trimethoprim-sulfamethoxazole can be given to penicillin-allergic
women
 No vaccine is available.
 Prevention is by washing raw vegetables, cooking all raw food, and
avoiding the implicated foods listed previously
SALMONELLOSIS
 Salmonella gastroenteritis
 Contracted through contaminated food.
 Symptoms that nclude nonbloody diarrhea, abdominal pain,
fever, chills, nausea, and vomiting begin 6 to 48 hours after
exposure.
 Diagnosis is made by stool studies
 Intravenous crystalloid solutions are given for rehydration.
 Antimicrobials are not given in uncomplicated infections
because they do not commonly shorten illness and may
prolong the convalescent carrier state.
 Rare case reports have linked Salmonella bacteremia with abortion
 Typhoid fever caused by Salmonella typhi
 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
 Antepartum typhoid fever resulted in abortion, preterm labor,
and maternal or fetal death
 Fluoroquinolones and third-generation cephalosporins are the
preferred treatment.
 Typhoid vaccines appear to exert no harmful effects when
administered to pregnant women and are given in an epidemic
or before travel to endemic areas.
SHIGELLOSIS
 Clinical manifestations range from mild diarrhea to severe
dysentery, bloody stools, abdominal cramping, tenesmus, fever, and
systemic toxicity.
 Although shigellosis may be self-limited, careful attention to
treatment of dehydration is essential in severe cases.
 Antimicrobial therapy is imperative, and effective treatment during
pregnancy includes fluoroquinolones, ceftriaxone, or azithromycin.
 Shigellosis can stimulate uterine contractions and cause preterm
birth
HANSEN DISEASE
 Also known as leprosy
 Caused by Mycobacterium leprae
 Diagnosis is confirmed by PCR
 Multidrug therapy with dapsone, rifampin, and clofazimine is
recommended for treatment and is generally safe during pregnancy
 Excessive incidence of low-birthweight newborns among infected
women.
 Neonatal infection apparently is acquired from skin-to-skin or
droplet transmission
 Vertical transmission is common in untreated mothers
LYME DISEASE
 Caused by the spirochete Borrelia burgdorferi
 Most commonly reported vector-borne illness in the United States
 Follows tick bites of the genus Ixodes
 There are three stages
 Early infection—stage 1
 Causes a distinctive local skin lesion, erythema migrans,
which may be accompanied by a flulike syndrome and
regional adenopathy.
 If untreated, disseminated infection—stage 2
 Follows in days to weeks
 Multisystem involvement is frequent
 Skin lesions, arthralgia, myalgia, carditis, and meningitis
predominate.
 If still untreated after several weeks to months, late or
persistent infection—stage 3—manifests in perhaps half of
patients.
 Native immunity is acquired, and the disease enters a
chronic phase in about 10 percent.
 Some patients remain asymptomatic, but others in the
chronic phase develop various skin, joint, or neurological
manifestations
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Dr. Fulgado – October 1, 2018

 Transplacental transmission has been confirmed, but no

congenital effects of maternal borreliosis have been
conclusively identified

DIAGNOSIS
 Clinical diagnosis is important because serological and PCR testing
has many pitfalls
 IgM and IgG serological testing is recommended in early infection
and is followed by Western blotting for confirmation

MANAGEMENT
 For early infection, treatment with doxycycline, amoxicillin, or
cefuroxime is recommended for 14 days, although doxycycline is
usually avoided in pregnancy.
 A 14- to 28-day course of IV ceftriaxone, cefotaxime, or penicillin G
is given for complicated early infections that include meningitis,
carditis, or disseminated infections.
 Chronic arthritis and post-Lyme disease syndrome are treated with
prolonged oral or IV regimens, however, symptoms respond poorly
to treatment

PREVENTION
 No vaccine is commercially available.
 Avoiding areas with endemic Lyme disease and improving tick
control in those areas is the most effective prevention.
 Self-examination with removal of unengorged ticks within 36 hours
of attachment reduces infection risk
 For tick bites recognized within 72 hours, a single 200-mg oral dose
of doxycycline may reduce infection development.
 Prompt treatment of maternal early infection should prevent most
adverse pregnancy outcomes

PROTOZOAL INFECTIONS
AMEBIASIS
 Approximately 10 percent of the world population is infected with
Entamoeba histolytica, and most are asymptomatic (Andrade, 2015).
 Amebic dysentery, however, may take a fulminant course during
pregnancy, with fever, abdominal pain, and bloody stools.
 Prognosis is worse if complicated by a hepatic abscess.
 Diagnosis is made by identifying E histolytica cysts or trophozoites
within a stool sample.
 Management
 Therapy is similar to that for the nonpregnant woman, and
metronidazole or tinidazole are the preferred drugs for amebic
colitis and invasive disease.
 Noninvasive infections may be treated with iodoquinol or
paromomycin.

USE AT YOUR OWN RISK!! NO PROOF READING DONE!!

Source: some parts of the PPT (hindi ko napicture-an lahat), recordings,

majority from William’s 25th edition

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