YL6: 04.

31 Infectious Diseases in Pregnancy

10/17/2019 Basic Pathologies 2
09:30-11:30 Christopher Joseph L. Soriano, MD, MHPEd, DPGS
CLINICAL MEDICINE

TABLE OF CONTENTS o Protective but declines after 2 months

o Next months, breastmilk will be solely as nutrients
I. LEARNING OBJECTIVES....................................................................... 1 for baby (source of CHO, water, etc)
II. MATERNAL AND FETAL FACTORS ..................................................... 1 ▪ Doc discussed the importance of Skin-Skin contact
II. VIRAL INFECTIONS .............................................................................. 1 (Unang Yakap) in order to stimulate or warm the
A. RUBELLA ..................................................................................... 1 immune system (pag cold, hindi “aandar”)
B. VARICELLA ZOSTER VIRUS........................................................ 2 → Infected neonate:
C. CYTOMEGALOVIRUS (CMV) ....................................................... 3 ▪ Depression, acidosis, poor sucking, vomiting,
III. BACTERIAL INFECTIONS .................................................................... 3 abdominal distention, respiratory insufficiency,
A. GROUP B STREPTOCOCCUS (GBS) .......................................... 3 lethargic, jittery, hypothermia, low WBC/neutrophils
B. CLOSTRIDIUM INFECTIONS ....................................................... 4
• Infectious diseases
C. LISTERIOSIS ................................................................................ 5
D. SALMONELLOSIS ........................................................................ 6 → Viral
E. SHIGELLOSIS .............................................................................. 6 ▪ Influenza, Respiratory virus, Enterovirus, Measles,
F. LYME DISEASE ............................................................................ 6 Mumps, Rubella, Varicella zoster, Cytomegalovirus
IV. PROTOZOAL INFECTIONS ................................................................. 6 → Bacterial
A. TOXOPLASMOSIS ....................................................................... 6 ▪ Clostridium, Group-B streptococcus, Listeria, MRSA
B. MALARIA ...................................................................................... 7 → Protozoal
C. AMEBIASIS .................................................................................. 7 ▪ Toxoplasmosis, Malaria, Amoeba
V. EMERGING INFECTION ....................................................................... 7
A. ZIKA VIRUS .................................................................................. 7 Table 1. Causes of Fetal and Neonatal Infections
QUICK REVIEW ........................................................................................ 7 Cause of Neonatal Infection
SUMMARY OF TERMS ..................................................................... 7
Transplacental
REVIEW QUESTIONS ...................................................................... 8
REFERENCES .......................................................................................... 9
Viruses: Varicella-zoster, Coxsackie, human
REQUIRED ....................................................................................... 9 parvovirus B19, rubella, CMV, HIV, Zika
APPENDIX ................................................................................................ 9 Intrauterine Bacteria: Listeria, Syphilis, Borrelia
Protozoa: toxoplasmosis, malaria
Ascending Infections
I. LEARNING OBJECTIVES Bacteria: Group B streptococcus, coliforms
Viruses: HIV
• Diagnose a pregnant patient with an infectious disease
Maternal Exposure
• Explain the effects of infectious diseases on the pregnant woman
Bacteria: gonorrhea, chlamydia, group B
and fetus
streptococcus, tuberculosis, mycoplasmas
• Discuss the management plan for a pregnant patient with a given
Intrapartum Virus: HSV, HPV, HIV, hepatitis B, hepatitis C,
infectious disease using evidence-based recommendations and
Zika
ethical standards
External Contamination
Bacteria: staphylococcus, coliforms
Quick Recall on OB Terms Viruses: HSV, Varicella zoster
• AOG: Age of Gestation Human transmission: staphylococcus, HSV
→ How far along the pregnancy Neonatal Respirators and catheters: staphylococcus,
→ Measured in weeks coliforms
→ Current Week - Week of First day of last menstrual cycle
• Normal Gestation: 38-42 weeks II. VIRAL INFECTIONS
→ <37 weeks: premature baby • See appendix for table of the summary of common viral infections
• Gravida: Number of pregnancies • Common vaccines used
• Para: Number of births of viable offspring (including live and → Influenza vaccine
stillbirths) ▪ Given between February – June
→ Reached viable gestational age ▪ Can be administered to pregnant women
• APGAR Score: Assessment of newborn vital signs ▪ Safe to use anytime, however, it is usually given >20
→ Increased risk of neurologic damage as score goes down weeks AOG
→ Measles, Mumps, and Rubella (MMR) Vaccine
▪ Given pre-conceptional or postpartum
II. MATERNAL AND FETAL FACTORS ▪ Mother can still breastfeed
• Maternal and Fetal Vascular Network (placenta) ▪ If a non-gravid woman receives MMR vaccine → can
→ Protect Fetus from infectious agents only try to get pregnant 1 month after administration
of vaccine
→ Conduit for transmission of infection
• Factors that affect disease outcome A. RUBELLA
→ Maternal serological status
→ Gestational age during infection
CASE
→ Mode of acquisition
• 21 y/o, G1P0; 12 weeks AOG
▪ Airborne, aerosol, foodborne, waterborne
• Fever for 3 days
→ Immunological status of mother & fetus
• Maculopapular rash
▪ Consider a congenital anomaly scan
→ Face, then spreads to the trunk and extremities
• Fetal & Neonatal Immunity → Enlarged lymph nodes on the neck
→ 9 – 15 weeks → No visible lesions in the oral cavity
▪ Cell-mediated humoral immunity begin to develop
▪ IgM: primary fetal response to infection What is the most common single fetal defect associated with this
→ 26 weeks infection?
▪ IgG: PASSIVE immunity transferred across placenta Answer: Sensorineural deafness
o Fetal - maternal concentrations
o According to Doc, goal is to “tawid” the immune
system for 26 weeks due to this
Pathology
→ Neonate
▪ Breastfeeding • Also known as German Measles
 RNA Togavirus

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 Transmission is nasopharyngeal secretion B. VARICELLA ZOSTER VIRUS
→ Usually passed to children
 Incubation: 12-23 days
CASE
 Viremia precedes clinical signs by about a week
 Adults are infectious during viremia and through 5-7 days of the • 30 y/o, G2P1 (1001), 30 weeks AOG
rash • Exposed to her 4 y/o child with chicken pox for 2 days

Diagnosis What should be the next step for her?

• History and physical examination A. Give varicella vaccine now
B. Give varicella Ig, if seropositive
• Serological tests for confirmation
C. Give varicella Ig, if seronegative
→ Serum IgM
D. Deliver baby to reduce fetal infection
▪ 4-5 days after onset of clinical disease up to 6 weeks
after the appearance of rash
Answer: C, give varicella Ig if seronegative.
→ Serum IgG
▪ Peaks 1-2 weeks after appearance of rash
 Sonography may identify some abnormalities in the fetus Pathology (2022 Trans)
 Rubella RNA can be found in chorionic villi, amniotic fluid or fetal • NOTE: This was not included in the PPT and was only briefly
blood described by Doc, but might help give context for reviewing
• Causes chicken pox or bulutong
Clinical Manifestations • Double-stranded DNA virus
• Mild febrile illness • Transmission: Direct contact
• Generalized maculopapular rash → Often via respiratory transmission
→ From face to trunk and extremities • Contagious from day 1 of exposure, prior to onset of the rash
• Arthralgias or arthritis • Acquired predominantly during childhood
• Head and neck lymphadenopathy • Immunity and vaccination
• Conjunctivitis → 95% of adults have serologic evidence of immunity
• Up to half of maternal infections are subclinical despite viremia → There is a 60-90% risk of non-immune women to become
infected by Varicella Zoster Virus
Maternal Effects
 First trimester infection is directly responsible for abortion and Clinical Manifestations
severe congenital malformations (2022 Trans) • Flu-like prodrome
• Pruritic vesicular lesions that crust over in 3 to 7 days
Fetal – Neonatal Effects
• One of the most teratogenic agents known for being the worst
during organogenesis
• Congenital Rubella Syndrome
→ Incidence
▪ First 12 weeks – 90%
o Presents with flu-like symptoms in the mother
▪ 13-14 weeks – 54%
▪ End of 2nd trimester – 25%
▪ > 20 weeks – rare
→ Syndrome
▪ Sensorineural deafness Figure 1. Herpes zoster (shingles) clinical manifestation from Varicella
o Most common single defect zoster infection
▪ Eye abnormalities: cataracts and congenital glaucoma
▪ Congenital heart disease: patent ductus arteriosus and Maternal Effects
pulmonary artery stenosis • Varicella pneumonia
▪ Central nervous system defects → Risk factors:
 Other manifestations of congenital rubella syndrome ▪ Smoking
▪ Extended Rubella Syndrome ▪ > 100 cutaneous lesions
o Progressive panencephalitis and type 1 diabetes → Symptoms appear for 3 to 5 days
may not develop until 2nd or 3rd decade of life ▪ Fever
▪ Tachypnea
Management ▪ Dry cough
• No specific treatment for rubella ▪ Dyspnea
• Prenatal serologic screening for rubella ▪ Pleuritic pain
• Vaccination of adult population → Pneumonitis resolves with skin lesions
→ Rubella vaccine (MMR) • Herpes zoster (Shingles)
▪ Pre-conceptional: avoid pregnancy for a month → Reactivation of primary varicella infection
▪ Postpartum vaccination → Unilateral dermatomal vesicular eruption with severe pain
 Tremendous teratogenic damage → Little evidence of congenital malformations
▪ Led to preventive measures with the development of → Broken blisters are contagious, but less so than primary
widespread immunization infection
▪ For complete eradication of the disease
 Women of child-bearing age
▪ Must be informed and educated about the dangers of
rubella infection

Figure 2. Congenital varicella in neonates

Fetal-Neonatal Effects
• Congenital varicella (1st half of pregnancy)

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 → Highest risk: 13 to 20 weeks
→ Features:
▪ Chorioretinitis
▪ Microphthalmia
▪ Cerebral cortical atrophy
▪ Growth restriction
▪ Hydronephrosis
▪ Limb hypoplasia
▪ Cicatricial skin lesions
• Disseminated visceral and CNS disease
→ Exposure just before or during delivery
→ Often fatal Figure 3. CMV Clinical Manifestations. (Left) Patient with CMV
→ Administer varicella-zoster Ig to neonates infection presenting with oral lesions and enlarged lymph nodes.
▪ If mothers present with clinical evidence of varicella 5 (Right) Hepatosplenomegaly in a newborn with Congenital CMV
days before and up to 2 days after delivery (Soriano, 2019)

Diagnosis Clinical Manifestations: Fetal-Neonatal Effects

• Clinical diagnosis: history and physical examination • Symptomatic CMV Infection (5-10%)
• NOTE: The next diagnostic tools were described by Doc as → Growth restriction
expensive and are used only if signs and symptoms from history → Microcephaly, intracranial calcifications
and PE are unclear and need more evidence for confirmation → Chorioretinitis
• Scrap the vesicle base for: → Mental and motor retardation
→ Tzanck smear → Sensorineural deficits
→ Tissue culture → Hepatosplenomegaly, jaundice
→ Direct fluorescent antibody testing → Hemolytic anemia, thrombocytopenic purpura
• Nucleic acid amplification test (NAATs) • Asymptomatic; late-onset (Majority of cases)
→ Tissue sample → Hearing loss
→ Amniotic fluid → Neurologic deficits
→ Chorioretinitis
Management → Psychomotor retardation
• Prenatal/Intrapartum → Learning disabilities
→ Isolate patient
→ Supportive care Management
→ Hospitalize if patient also has pneumonia • No vaccine available
▪ Give Acyclovir IV • Symptomatic treatment
• Pre-conception/Postpartum: Varicella vaccine • Passive immunization with CMV Ig (under study)
→ 2 doses, 4 to 8 weeks apart • Good hygiene and handwashing
→ Contraindicated in pregnancy • Avoid sexual transmission
→ Avoid pregnancy for a month after vaccination
• Varicella Zoster Virus serologic testing: for pregnant women III. BACTERIAL INFECTIONS
with significant exposure to a person with varicella and without a A. GROUP B STREPTOCOCCUS (GBS)
history of chicken pox infection
→ If seropositive: immune
CASE
→ If seronegative: give Varicella zoster Ig, within 96 hours to 10
days of exposure • 35 y/o, G2P1 (1001)
 35 weeks AOG with uterine contractions
 Previous pregnancy with baby developed sepsis
C. CYTOMEGALOVIRUS (CMV)  Poor prenatal follow-up
 Vaginal GBS screening culture (+)
CASE  Dx: GBS infection
• 26 y/o, G1P0, 26 weeks AOG
• CC: sore throat • What is the recommended management for this infection?
• Pertinent PE: Fever, palpable cervical lymph nodes A. Give Ampicillin IV and induce labor
B. Give Ampicillin IV and perform emergency CS
Serologic tests revealed primary CMV infection. What are the known C. Control preterm labor and give steroids for lung maturity
fetal complications? D. Control preterm labor and give Piperacillin IV
A. Hydrocephalus
B. Microcephaly • Answer: C. Control preterm labor and give steroids for lung
C. Congenital cataract maturity
D. Ventricular septal defect • Note: Concern is intrapartum (because patient is not yet going to
give birth). Ampicillin is only indicated during labor and Piperacillin
Answer: B, microcephaly. is not the drug of choice.

Pathology (2022 Trans)

• NOTE: This was not included in the PPT and was only briefly
described by Doc, but might help give context for reviewing
• Most common perinatal infection in the developed world
• Day care centers are the common source
→ Children may transmit the virus to their parents
• Transmission: person-to-person contact
→ Virus is secreted into all body fluids
→ Viral-laden saliva, semen, urine, blood, and other secretions

Figurer 4. Group B Streptococcus (Soriano, 2018)

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 Pathology → NAAT is expensive (Universal vaginal and
• According to Doc Group B Streptococcus is one of the more GBS screening is preferred)
popular bacterial infections → Regimens
→ Part of the body’s normal flora ▪ Penicillin G (IV): Recommended, first line (Textbook)
• S. agalactiae ▪ Ampicillin (IV): Alternative (Clinical practice guidelines,
• Can be found to colonize the gastrointestinal and genitourinary Phil. Ob-Gyne Society)
tract in 20-30% pregnant women (Cunningham et. al., 2014) ▪ If allergic to penicillin:
• Spectrum of maternal and fetal GBS ranges from asymptomatic o Cefazolin
colonization to septicemia (Cunningham et. al., 2014) o Clindamycin
o Vancomycin
Clinical Manifestations ▪ From Doc, make sure to read the labels well. Be
Maternal Effects particular of the IV and IM label to avoid medical
• S. agalactiae has been implicated in adverse pregnancy malpractice.
outcomes:
→ Preterm labor NEED TO KNOW: LEUKORRHEA (2022 Trans)
→ Premature rupture of membranes (PROM) • Pregnant women commonly develop increased vaginal
▪ “Ruptured bag of water” discharge that in many instances is not pathological. Increased
→ Chorioamnionitis (fever) mucus secretion by cervical glands in response to
→ Maternal bacteriuria hyperestrogenemia is a contributing factor. Occasionally,
→ Pyelonephritis troublesome leukorrhea is the result of vulvovaginal infection.
→ Osteomyelitis In the adult woman, most of these are bacterial vaginosis,
→ Postpartum mastitis candidiasis or trichomoniasis. (Cunningham et. al., 2014)
→ Puerperal infection
B. CLOSTRIDIUM INFECTIONS
Fetal-Neonatal Effects Pathology
• Early onset infection • Causative agents:
→ According to Doc, this is what you call “GBS Pneumonia”, → Clostridium perfringens
(“when baby gets sepsis”) → Clostridium tetani
→ Usually seen in government hospitals because, most of the • Transmission:
time, patients just go there in time for labor (no prior check- → Saprophytic inhabitants of the soil, bowel, and female
ups) genital tract
▪ GBS acquired from mother → High incidence in the Philippines due to poor aseptic
→ <7 days of birth technique
→ Septicemia involves signs of serious illness that usually ▪ Aseptic technique refers to the practices performed just
develops within 6-12 hours of birth (Cunningham et. al., before or during a clinical or surgical procedure to
2014) reduce the client's risk of infection by reducing the
▪ Respiratory distress, apnea, hypotension likelihood that microorganisms will enter areas of the
→ Stillbirth body where they can cause infection (AMDD, 2003).
→ Neurologic problems ▪ Pregnant patients are at risk of developing Clostridium
• Late onset infection infections during home births and abortion
→ Manifests as meningitis
▪ 1 week to 3 months after birth NICE TO KNOW (FROM 2022)
▪ Due to serotype III  Aspirin is a cyclooxygenase inhibitor with anti-inflammatory
→ Neurologic problems and antiplatelet properties. It has most commonly been used
▪ It is not uncommon for surviving infants of both early during pregnancy to prevent or delay the onset of
and late onset disease to exhibit devastating preeclampsia. It can be used to prevent stillbirth, fetal growth
neurological sequelae (Cunningham et. al., 2014) restriction, preterm birth and early or recurrent pregnancy loss
→ Pediatricians will check the respiratory rate of the neonate (ACOG, 2018).
after delivery to check if there are any grunting or chest
retractions that are indicative of difficulty breathing (Soriano,
2018)
QUIZ!
Management • Women who underwent unsafe abortion procedures are at risk
• Universal vaginal and GBS screening culture at 35-37 weeks of developing which severe complications?
A. Liver cirrhosis
→ The CDCP recommends universal rectovaginal culture
B. Meningitis
screening for GBS at 35-37 weeks gestation followed by
C. Generalized paralysis and stroke
intrapartum antibiotic prophylaxis for identified carriers.
D. Disseminated Intravascular Coagulopathy (DIC)
(Kasper et. al., 2015)
→ According to Doc, before pregnant patients get admitted in
• Answer: D. (DIC)
The Medical City and once they reach 35-37 weeks, they
need to get this screening (swab in the rectovaginal area) • DIC is a condition in which there is a consumption of
▪ Results will come out in 2-3 hours procoagulant factors leading to intravascular activation of
▪ if (+) and already in labor, patient will be given a drug clotting. Placental abruption is the most common cause of
(not mentioned which) clinically significant consumptive coagulopathy. There is a
▪ if (-) no drug to be given significant amount of procoagulants in retroplacental clots, but
these cannot account for all missing fibrinogen. (Cunningham
→ Important since GBS has a lot of effects (like mentioned
et. al., 2014)
previously)

• Intrapartum antimicrobial prophylaxis

→ Given during labor to prevent transmission (Soriano, 2018) Clinical Manifestations
Clostridium perfringens
→ Indications:
▪ Previous infant with GBS disease • Causes septic abortion
▪ Positive GBS bacteriuria during current pregnancy • Fever, tachycardia out of proportion of the fever
▪ Positive GBS screening culture • Uterine discharge and marked leukocytosis
▪ Unknown GBS status (culture was not done, incomplete • Intravascular hemolysis, jaundice, hemoglobinuria, hypotension,
or results unknown): and renal shutdown (septic shock)
o Delivery <37 weeks • Hepatorenal syndrome
o Amniotic membrane rupture ≥18 hours • Disseminated Intravascular Coagulopathy (DIC)
o Intrapartum temperature ≥ 38°C • Maternal mortality of 21-85% usually results
o Intrapartum NAAT positive for GBS

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 o More expensive as compared to tetanus toxoid
because of additional diphtheria and pertussis
coverage
→ Tetanus Immunoglobulin (Tetanus Ig)
▪ Passive immunity
▪ Post exposure prophylaxis
▪ Used in conjunction with tetanus toxoid (Cunningham,
24th ed., 2014)

Table 2. Tetanus toxoid immunization schedule for women of

childbearing age and pregnant women without previous exposure to
TT, Td or Tdap. (WHO, 2006)
Dose of TT or Td When to Give Expected duration
(according to card of protection
or history)
1 0 (at first contact or None
as early as possible
in pregnancy)

2 >1 month after TT1 1 – 3 yr

>6 months after TT2 > 5 yr

Figure 5. Septic Abortion caused by Clostridium perfringens (Soriano, 3 or during
2018) subsequent
pregnancy
Clostridium tetani >1 year after TT3 or > 10 yr
4 during subsequent
• Causes tetanus neonatorum
pregnancy
→ Infant tetanus: symptoms may or may not be apparent
>1 year after TT4 or For all childbearing
immediately after birth
5 during subsequent age years and
→ Incubation period can be as short as 24 h and as long as pregnancy possibly longer*
16 – 30 d.
*Lifetime Immunity
• Trismus or lockjaw
• Respiratory failure and convulsive seizures
C. LISTERIOSIS
Pathology
• Causative agent:
→ Listeria Monocytogenes
• Common infection, present everywhere
• Cannot be diagnosed, need to do blood culture if you have high
index of suspicion of presence of agent
• “Diagnosis after the fact”
→ Will only know presence of listeriosis after the baby has
already been infected and once placenta has been checked
▪ Most of the time baby is already dead
• Flu-like symptoms
→ Which makes it harder to diagnose because you don’t
normally do a blood culture to a baby with cough and colds

Clinical Manifestations
• 30 y/o, G2P1 (0110) delivered a stillborn preterm baby at 30
weeks AOG
• Amniotic fluid noted to be brownish in color during delivery
Figure 6, A neonate displaying bodily rigidity produced by Clostridium • Disseminated granulomatous lesions with micro abscesses
tetani exotoxin, called “neonatal tetanus” (CDC, 2000) • Chorioamnionitis
• Placental lesions
Management → Pale placenta
• Antibiotic treatment: → Multiple, well-demarcated micro abscesses
→ Aqueous Penicillin IV → Miscarriage or stillbirth
• Vaccination:
→ Tetanus Immunization
▪ Tetanus toxoid (TT)
o Schedule: 0 months, 1 month, 6 months, 1 year,
and another 1 year (DOH)
o Fifth dose confers lifetime immunity (WHO)
o Public Health implications:
→ Freely given by the DOH since it is cheaper
than Tdap
→ One of the six vaccines included in the Figure 7. Pale Placenta (A) and stillborn infant with multiple, well-
Expanded Program on Immunization (EPI) of demarcated micro abscesses (B) resulted from maternal
listeriosis (Cunningham et. al., 2014)
DOH
→ Goal: To eliminate maternal and neonatal
Management
tetanus
• Blood culture if with high index of suspicion of Listeria
→ Downside: Low compliance of the patient as
well as physicians because it requires 5 • Antibiotic treatment
doses to develop life time immunity → Ampicillin + Gentamicin
▪ Adult Tetanus, Diphtheria, Pertussis (Td/Tdap) • Prevention of food-borne transmission
o Schedule: 0 months, 1 month, 6-12 months, then → Washing raw vegetables and fruits
every 10years (POGS, CDC) → Cook all raw food
→ Food sources implicated:
▪ Coleslaw, apple cider, melons

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 ▪ Milk, fresh Mexican-style cheese
▪ Smoked fish, processed foods (e.g. pâté, hummus,
wieners, sliced deli meats)
• Advice pregnant women to prevent eating raw fish and vegetables

D. SALMONELLOSIS
Pathology
• Gastrointestinal Bacterial Infection
• Causative Agent
→ Salmonella enteritidis
→ Salmonella typhimurium
• Maternal transmission
→ Food-borne (e.g. contaminated food, water or milk)
Figure 8. Erythema migrans
Diagnosis
• Stool studies • Erythema migrans
→ Distinctive local skin lesion
Clinical Manifestations (Maternal) • Flu-like syndrome:
• Non-Typhoid Salmonella Gastroenteritis → Arthralgia, myalgia, carditis, meningitis, regional adenopathy
→ Caused by Salmonella enteritidis
→ Non-bloody diarrhea Management
▪ Can lead to death to electrolyte imbalance and • Tick control; removal of unengorged ticks within 36 hours of
dehydration attachment
→ Abdominal pain, nausea, vomiting • Early infection: Amoxicillin or cefuroxime
→ Fever and chills • Complicated early infection: cerfriaxone (IV), cefotaxime or
• Typhoid Fever penicillin G
→ Caused by Salmonella typhi • No vaccine
→ Abortion, preterm labor, maternal or fetal death
IV. PROTOZOAL INFECTIONS
Management A. TOXOPLASMOSIS
• Rehydration Pathology
• Antibiotic treatment • Caused by Toxoplasma gondii
→ Fluoroquinolones • Transmitted to mothers when they eat raw/undercooked meat
→ Cephalosporins (3rd generation) infected with tissue cysts (contaminated cat litter, soil, or water)
• Typhoid vaccine (epidemic or before travel to endemic areas) • Can be passed to offspring through vertical transmission

Diagnosis
E. SHIGELLOSIS
• Anti-toxoplasma IgG and IgM
Pathology
• Polymerase chain reaction (PCR) of amniotic fluid or fetal blood,
• Gastrointestinal Bacterial Infection
NAAT
• Causative agent
• Sonographic findings:
→ Shigella sonnei
→ Intracranial and liver calcifications
• Shigella flexneri
→ Hydrocephaly
→ Shigella boydii
→ Ascites, hyperechoic bowel
→ Shigella dysenteriae
→ Placental thickening
• Maternal transmission
→ Growth restriction
→ Fecal-oral route
Clinical Manifestations
Diagnosis
• Maternal infection (subclinical)
• Stool studies → Initial infection confers immunity
→ Fatigue, fever, headache, muscle pain
Clinical Manifestations (Maternal)
→ Maculopapular rash
• Mild diarrhea to severe dysentery, bloody stools, abdominal
→ Posterior cervical lymphadenopathy
cramping, tenesmus, fever and systemic toxicity
→ Preterm delivery (<37 weeks)
• Fetal infection
Management
→ Most are without obvious stigmata
• Antibiotic treatment:
→ Classic triad: intracranial classifications, chorioretinitis, and
→ Fluoroquinolones hydrocephalus (accompanied by convulsions)
→ Ceftriaxone → Others: low birth weight, hepatosplenomegaly, jaundice,
→ Azithromycin anemia, learning disabilities
• Typhoid vaccine (epidemic or before travel to endemic areas)
Management
F. LYME DISEASE • Routine screening NOT recommended
Pathology → Disease is not that common
• Vector-borne Bacteria • Spiramycin: acute infection in early pregnancy
• Causative agent Pyrimethamine-sulfadiazine with folinic acid: >18 weeks AOG
→ Borrelia burgdorferi or if fetal infection is suspected
• Maternal transmission
→ Tick bites of the genus ixodes Prevention
• MTCT • No vaccine available
→ Transplacental route, but no congenital effects • Preventive measures:
→ Cooking meat to safe temperatures
Diagnosis → Peeling or washing fruits and vegetables
• Clinical diagnosis → Cleaning food preparation surfaces and utensils
• IgG and IgM for early infection; Western blot for confirmation → Wearing gloves when changing cat litter or delegating this
duty
→ Avoiding feeding cats raw or undercooked meat and keeping
Clinical Manifestations (Maternal)
cats indoors

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 • Fetal complication
B. MALARIA → The fetus inside the womb of a pregnant mother may
• Caused by Plasmodium spp. develop abnormality in the size of its head due to incomplete
brain development called microcephaly
Diagnosis
• Blood smear (thick and thin Management
→ This is the gold standard in diagnosing Malaria • Patients infected with Zika virus should:
→ Get plenty of bed rest
Clinical Manifestations → Drink plenty of fluids
• Maternal infection → Take medicine to relieve fever and pain
→ Fever, chills → Use mosquito nets when napping
→ Flu-like symptoms → Wear clothing that covers arms and legs
▪ Headache, myalgia, and malaise → If symptoms worsen or complications develop, see a
→ Anemia, jaundice doctor immediately
→ Falciparum infection
▪ Kidney failure, coma, and death Prevention
• Fetal complication • No vaccine
→ Stillbirth • Avoid infection by preventing mosquito bites
→ Preterm birth, low birth weight → Use insect repellents
→ Falciparum infection: abortion → Use window and door screens
→ Wear long-sleeved shirts and long pants or permethrin-
Management treated clothing
• Chloroquine or hydroxychloroquine → Once a week, empty and scrub, turn over, cover, or throw
→ Uncomplicated Plasmodium (vivax, malariae, ovale) and out items that hold water such as tires, buckets, planters,
chloroquine-sensitive P. falciparum toys, or trash containers
• Mefloquine or quinine sulfate with clindamycin • Women planning to conceive or with exposure
→ Chloroquine-resistant P. falciparum → Delay conception at least 8 weeks after symptom onset or
• Primaquine last possible Zika exposure
→ Given postpartum • Men with possible Zika exposure
• Sulfadoxine-pyrimethamine → Delay coitus at least 6 months from symptom onset or last
→ 2nd & 3rd trimester: to clear placental asymptomatic infections possible exposure
→ Provide up to 6 weeks of post-treatment prophylaxis • Zika virus testing
→ Decrease rate of low birth weight newborns in endemic → Persons with Zika exposure WITH symptoms
areas → Not recommended for:
▪ Zika exposure with no symptoms
Prevention/Prophylaxis ▪ Planning for conception
• Vector control: insecticide-treated netting, pyrethroid ▪ Assessing risk of Zika sexual transmission
insecticides, and DEET-based insect repellent
• Chloroquine & hydroxychloroquine QUICK REVIEW
→ Areas without chloroquine resistance SUMMARY OF TERMS
→ Decreases placental infection • Maternal and Fetal Factors
• Mefloquine → Maternal and fetal vascular network
→ Travelling to chloroquine-resistant P. falciparum areas ▪ Protects fetus from infection
• Primaquine and doxycycline are contraindicated ▪ Conduit for infection
→ Factors that affect disease outcome
C. AMEBIASIS ▪ Maternal serological status
• Caused by Entamoeba histolytica ▪ Gestational age during infection
▪ Mode of acquisition
Diagnosis → Fetal and neonatal immunity
• Fecalysis ▪ 9-15 weeks: cell-mediated humoral immunity begins to
→ Presence of E. histolytica cysts or trophozoites develop; IgM is the primary response
▪ 26 weeks: IgG; passive immunity transferred across
Clinical Manifestations placenta
• Mostly asymptomatic ▪ Neonate: Breastfeeding
• Amebic dysentery • Viral infections
→ Fever, abdominal pain, bloody stools → Influenza Vaccine: can be administered to pregnant women
▪ safe to use anytime
→ Hepatic abscess (worse prognosis)
→ Measles, Mumps, and Rubella (MMR) Vaccine
Management ▪ Given pre-conceptional or postpartum
▪ Mother can still breastfeed
• Amebic colitis and invasive type: Metronidazole or tinidazole
▪ Can try to get pregnant after 1 month
• Non-invasive: Paromomycin
• Rubella: German Measles
→ Incubation of 12-23 days
V. EMERGING INFECTION
→ Serological tests for confirmation
A. ZIKA VIRUS ▪ Serum IgM: 4-5 days after onset of clinical disease
Transmission ▪ Serum IgG: peaks 1-2 weeks after appearance of rash
• Aedes aegypti mosquitoes (which also cause dengue and → Clinical manifestation: Mild febrile illness
chikungunya) ▪ Generalized maculopapular rash
• Condomless sex o From face to extremities
→ Vaginal, anal, fellatio/oral (possible) ▪ Arthralgia
▪ Head and neck lymphadenopathy
Clinical Manifestations ▪ Conjunctivitis
• Onset of symptoms is usually 2-7 days after the mosquito bite ▪ Fetal – Neonatal effects
→ Fever o Congenital Rubella Syndrome
→ Headache → First 12 weeks – 90% incidence
→ Red eyes → Sensorineural deafness
→ Skin rash ▪ Management: MMR Vaccine
→ Joint pain o Pre-conceptional: avoid pregnancy for a month
• 1 in 4 infected with Zika virus develops symptoms o Postpartum vaccination

YL6: 04.LL Basic Pathologies 2: Lecture Title 7 of 11

• Varicella zoster virus: Chicken Pox, or bulutong o Hepatic abscess (worse prognosis)
→ Clinical manifestations: → Management:
▪ Flu-like prodrome, pruritic vascular lesions ▪ Amebic colitis and invasive type: Metronidazole or
▪ Maternal effects: varicella pneumonia, herpes tinidazole
zoster/shingles ▪ Non-invasive: Paromomycin
▪ Fetal-neonatal effects: congenital varicella, • Zika virus
disseminated visceral and CNS disease (if exposed to → Transmitted through Aedes aegypti mosquitoes and
virus before or during delivery) condomless sex
→ Diagnosed primarily with history and physical examination → Causes flu-like symptoms such as fever, headache, red
▪ If unclear diagnosis, infection with virus can be eyes, skin rash, and joint pain 2-7 days after the mosquito
confirmed with Tzanck smear, tissue culture, direct bite
fluorescent antibody testing, and NAATs ▪ Can cause microcephaly in the fetus
→ Management → No vaccine available
▪ Prepartum/intrapartum: isolate patient, supportive care, → Can be prevented through vector control
chest x-ray, hospitalization (if with pneumonia)
▪ Pre-conception and postpartum: varicella vaccine REVIEW QUESTIONS
▪ Exposure to varicella and without history of chicken pox 1. Ronnie wants to find out if he and his wife, May, could try to
infection: VZV serologic testing conceive a child after both of them received their MMR Vaccine
• Cytomegalovirus (CMV) shot. What will you tell them?
→ Clinical manifestations in fetuses or neonates: a) You can try to conceive a child. No problem with that.
▪ Symptomatic CMV infection: growth restriction, b) You can only try 1 week after the administration of the
microcephaly, hepatosplenomegaly, jaundice, etc. vaccine.
(Check table in appendix for complete list) c) You can try now, but wear a condom for protection.
▪ Asymptomatic, late onset sequelae: hearing loss, d) You can only try 1 month after the administration of the
neurologic deficits, chorioretinitis, psychomotor vaccine.
retardation, learning disabilities
→ Management 2. Josie goes to you for consultation and tells you she is currently
▪ No vaccine available trying to conceive a child. During the history-taking, you ask her
▪ Good hygiene and washing, avoid sexual transmission about her vaccines and she says that she does not have any
▪ Symptomatic treatment records for varicella vaccine. When you asked about her history of
• Toxoplasmosis chicken pox, she said she never had it. Which of the following is
→ Caused by Toxoplasma gondii FALSE about the management of her case in relation to VZV?
→ Transmitted to mothers when they eat raw/undercooked a) Offer to give her the vaccine now
meat infected with tissue cysts (contaminated cat litter, soil, b) 2 doses of the vaccine should be administered, 4 to 8 weeks
or water) apart
→ Can be passed to offspring through vertical transmission c) Inform her that she should avoid getting pregnant for a
→ Diagnosis: month after vaccination
▪ IgG/IgM testing, PCR, ultrasonography d) Tell her that the 2nd dose of the vaccine is administered
→ Clinical Manifestations: during the pregnancy
▪ Maternal infection (subclinical)
o Initial infection confers immunity 3. A teenager has come to your clinic after having undergone an
o Fatigue, fever, headache, muscle pain unsafe abortion procedure. She has developed Disseminated
o Maculopapular rash Intravascular Coagulopathy (DIC). What is the most likely and
o Posterior cervical lymphadenopathy reasonable explanation as to why she is experiencing this?
o Preterm delivery (<37 weeks) a) Placental abruption is the most common cause of clinically
▪ Fetal infection significant consumptive coagulopathy.
o Most are without obvious stigmata b) Malignant hypertension secondary to pregnancy contributes
o Classic triad: intracranial classifications, to increased thrombosis, which has been observed to result
chorioretinitis, and hydrocephalus (accompanied in DIC.
by convulsions) c) Sepsis secondary to use of unhygienic tools has produced a
o Others: low birth weight, hepatosplenomegaly, large bacterial burden
jaundice, anemia, learning disabilities d) It is divine punishment.
→ Management:
▪ Spiramycin: acute infection in early pregnancy 4. Infection by a certain bacterium causes trismus or lockjaw.
▪ Pyrimethamine-sulfadiazine with folinic acid: >18 Which of the following statements is related to infection by the
weeks AOG or if fetal infection is suspected same bacteria?
→ Prevention: a) Uterine discharge and marked leukocytosis
▪ No vaccine available b) Tachycardia out of proportion of the fever
▪ Preventive measures in food preparation c) Symptoms may or may not be apparent immediately after
birth because incubation period can be as short as 24 hours
• Malaria
and as long as 16-30 days
→ Caused by Plasmodium spp.
d) A and B
→ Diagnosis: e) A and C
▪ Blood smear
→ Clinical Manifestations:
5. Which form of tetanus immunization is more inexpensive, and is
▪ Fever, chills, flu-like symptoms
▪ Fetal complication: stillbirth, preterm birth, low birth freely given by the DOH?
weight, abortion a) Td/Tdap
→ Management: b) TT
▪ Quinine drugs and other anti-malarials
→ Prevention: 6. Toxoplasmosis infection in pregnant women can be prevented
▪ Vector control and prophylaxis through the following measures EXCEPT
• Amebiasis a) Cooking meat thoroughly
→ Caused by Entamoeba histolytica b) Peeling and washing fruits and vegetables
→ Diagnosis: c) Vaccination
▪ Fecalysis d) Wearing gloves when changing cat litter
o Presence of E. histolytica cysts or trophozoites
→ Clinical Manifestations:
▪ Mostly asymptomatic
▪ Amebic dysentery
o Fever, abdominal pain, bloody stools

YL6: 04.LL Basic Pathologies 2: Lecture Title 8 of 11

7. Usual complication of Zika infection of a pregnant woman on her REFERENCES
baby REQUIRED
a) Spina bifida (1) Christopher Joseph L. Soriano, MD MHPEd FPOGS. 10/18/2019,
b) Cyclopia Infectious Diseases in Pregnancy. [Lecture slides].
c) Hydrocephalus (2) Cunningham, F. G., Leveno, K., & Bloom, S. (2018). Williams
d) Microcephaly Obstetrics, 25th Edition. New York: McGraw Hill Education.

Answers
1A, 2D, 3A – Although B (malignant hypertension) and C (sepsis) may IMPORTANT LINKS
actually contribute to DIC, A (placental abruption, consumptive
coagulopathy) is the explicitly explained reasoning behind the Trans feedback: https://tinyurl.com/AcadsTransFeedback
occurrences of DIC related specifically to unsafe abortions. 4C – A and Errata submission: https://tinyurl.com/ContentErrataSubmission
B describe infection from C perfringens, whereas C alone describes C. Errata tracker: https://tinyurl.com/ErrataTracker
tetani, which is what’s described in the question. 5B. 6C. 7D.

APPENDIX

Table 1. Overview of Viral Infections in Pregnancy

Fetal Neonatal
Virus Clinical Manifestation Maternal Effects Management
Effects
No malformations Influenza vaccine
Fever, dry cough, systemic Pulmonary involvement
Influenza: A(H1N1) or B NTD (rare) Oseltamivir
symptoms severe in pregnancy
Schizophrenia (rare) Zanamivir
Respiratory Virus Common cold, pharyngitis,
Rhinorrhea, sneezing, Teratogenicity
(Rhinovirus, Coronavirus, laryngitis, bronchitis,
congestion controversial
Adenovirus) pneumonia
Inactivated polio vaccine
Entero-virus (Poliovirus) Paralytic poliomyelitis Death (SC), live oral polio
vaccine
Pneumonia, diarrhea, MMR vaccine
Koplik spots, fever, Coryza, Not teratogenic,
Measles abortion, preterm delivery, Breast-feeding allowed
conjunctivitis, cough neonatal infection
low birthweight Serum Ig (IM)
Infection of salivary gland,
Not teratogenic, fetal MMR vaccine
Mumps gonads, meninges, Spontaneous abortion
infection (rare) Breast-feeding allowed
pancreas

Table 2. Viral diseases

Maternal
Disease Pathology/Causative Agent Diagnosis Fetal-Neonatal Effects Management
Effects
Isolate patient
Congenital Varicella/ Le
Supportive care
Chicken History and PE Varicella Foret and Lynch Syndrome
Varicella zoster virus transmitted Chest x-ray
Pox or Tznack smear Pneumonia – exposure before or during
through direct contact or Hospitalization
“bulutong” Tissue culture delivery
respiratory transmission
NAATS Shingles
Varicella zoster Ig
(for neonate)
History and PE

Serologic Tests: Congenital Rubella

IgM (4-5 days after Syndrome (sensorineural
No specific
onset) deafness)
treatment
Rubella virus IgG (1-2 weeks after
onset) Extended Rubella
German Prenatal screening
Incubation period of 12-23 days Abortion Syndrome (Pancephalitis)
Measles for rubella
Sonography
Rubella vaccine
Viremia precedes clinical signs Teratogenic during
MMR (pre-
Rubella RNA from organogenesis
conceptional)
chorionic villi,
amniotic fluid, or
fetal blood

Symptomatic
Treatment
Cytomegalovirus transmitted Symptomatic CMV infection
CMV through contact of body fluids No vaccine
History and PE
Infection Asymptomatic CMV available
Can infect fetus hrough placenta infection
Avoid sexual
transmission
Fever
Rashes No vaccine
Headache
Zika virus testing:
Zika virus that is transmitted Joint pain No specific
Zika Virus should have Zika Microcephalic
through mosquito bites and Muscle pain medicine
Infection exposure and Neurocognitive disabilites
unprotected sexual intercourse Conjunctivitis
symptoms
Preventive
Sometimes measures
asymptomatic

YL6: 04.LL Basic Pathologies 2: Lecture Title 9 of 11

Table 3. Bacterial disease
Fetal-Neonatal
Disease Pathology/Causative Agent Diagnosis Maternal Effects Management
Effects
Universal Vaginal
Screening and GBS
Preterm labor screening culture
Early onset infection
Premature rupture of
(still birth,
Streptococcus agalactiae membranes Intrapartum antimicrobial
neurological defects,
Group B colonizes the GI and Chorioamnionitis prophylaxis (during
septicemia)
Streptococcus genitourinary tract Maternal bactenuria labor)
(GBS) Pyelonephritis
Late onset infection
Osteomyelitis Penicillin G (IV)
(meningitis,
Postpartum Mastilitis Ampicillin (IV)
neurological defects)
Puerperal infection Cefazolin
Clindamycin
Vancomycin
Clostridium
perfringens:
Clostridium perfringens Septic Abortion
Fever and
Clostridium titanic tachycardia Aqueous Penicillin (IV)
Transmitted through Uterine discharge
Clostridium bowel,soil, and female genital Septic shock Clostridium tetani: Tetanus Toxoid
infections tract Hepatorenal Tetanus neonatorum Td/Tap
syndrome
High incidence due to poor DIC Tetanus Ig
aseptic technique
Clostridium tetani:
Trismus or lockjaw
Respiratory failure
Brown amniotic fluid

Disseminated
granulomatous Ampicillin + Gentamicin
Listeriosis Listeria monocytogenes lesion
Proper preparation of food
Chorioamnionitis

Placental lesions
Fluoroquinolones
Non-typhoid
Salmonella enteritidis Cephalosporins
Salmonella
Salmonella typhimurium
Salmonellosis Fecalysis gastroenteritis
Typhoid Vaccine
Food-borne
Typhoid Fever
Rehydration
Mild diarrhea to
Shigella sonnei
severe dysentery
Shigella flexneri Fluoroquinolones
Shigella boydii Cefriaxone
Bloody stools
Shigellosis Shigella dysenteriae Fecalysis Azithromycin
Fever
Systemic toxicity
Feco-oral transmission No vaccine available
Tenesmus
Cramping
Amoxicillin or Cefuroxime
for early infection
For early
Borrelia burgdorferi infection:
Ceftriaxone (IV),
transmitted through Ixodes Serum IgG
Erythema migrants Cefotriaxone (IV), Penicillin
Lyme Disease tick. Serum IgM
Flu-like syndrome G for complicated infection
Can pass through placenta Western
No vaccine
Blot
Tick control
Table 4. Protozoan Diseases
Fetal-Neonatal
Disease Pathology/Causative Agent Diagnosis Maternal Effects Management
Effects
Spiramycin (acute
infection for early
History and
Initial infection Intracranial pregnancy)
PE
confers immunity calcifications
Toxoplasma gondii transmitted Chorioretinitis Pyrimethamine –
Serum anti-
through cats, raw uncooked meat, Fatigue, fever, Hydrocephalus sulfadiazine with
toxoplasma Ig
soil, and water headache, muscle Low birthweight colonic acid (AOG >
Toxoplasmosis (IgG and IgM)
pain Jaundice 18 weeks)
Vertical (mother to child) Hepatosplenomegaly
PCR
transmission Maculopapular rash Anemia No vaccine
Learning disabilities
NAATS
Lymphadenopathy Proper food
Sonography
preparation and
animal handling
Anti-malarial:
Chloroquine
Hydroxychloroquine
Mefloquine
Quinine sulfate with
Flu-like symptoms clindamycin
Plasmodium spp. transmitted Anemia Sulfadoxine-
Still birth
through mosquito bites Jaundice pyrimethamine
Malaria Blood smear Preterm Birth and low
Kidney Failure
birth weight
Vertical transmission is rare Coma DO NOT GIVE:
Death Primaquine
Doxycycline

Prevention:
Vector Control
Prophylaxis
Metronidazole or
Entamoeba histolytica transmitted
Trophozoite Mostly Tinidazple (Invasive
orally
identification asymptomatic No evidence of type)
Amebiasis
through intrauterine infection
Clinically asymptomatic unless host
fecalysis Amoebic dysentery Paromomycin (non
is malnourished/immunosuppressed
invasive type)