PERINATAL INFECTION AND COMPLICATION
Mechanism of perinatal infections:
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Infants can be infected by direct contact with:
1. Infected maternal secretions and mucous membranes, such as bacterial, herpes
and papilloma viruses or Mother - vaginitis, amnionitis, or UTI.
2. Infected blood and cellular elements, such as Hepatitis B and C viruses, HIV.
Risks factors for maternal and child infections:
1. Absence of pre-natal care: Malnutrition, untreated infections – STIs.
2. Difficult pregnancy, toxemia, prematurity.
3. Prolonged rupture of membranes.
4. Traumatic birth.
5. Post-partum infections related to poor hygiene.
Infections:
•
Acronym TORCH is used to describe infections that can be devastating to the fetus
or newborn:
1. Toxoplasmosis.
2. Other infections.
3. Rubella.
4. Cytomegalovirus.
5. Herpes
•
Many other infections may adversely affect fetus so resummarized as STORCH5.
STORCH5:
•
TORCH is a group of infectious diseases that can cause illness in pregnant women
and may cause birth defects in their newborns.
•
The test is a screen for the presence of any of the antibodies to these infections.
Confirmation of an active infection may require more specific tests.
•
Syphilis Toxoplasma, Rubella, CMV, HSV, HIV, Hepatitis, Human parvovirus, HPV
Toxoplasma & Toxoplasmosis:
•
Toxoplasma gondii
•
Parasitic protozoa
•
Host = cat
•
Risk factors: consumption raw / undercooked meat, contact cat faeces,
contaminated water.
•
Ingest cysts -> rupture in stomach -> releasing tachyzoites.
Toxoplasmosis:
•
Parasitic infection cause by Toxoplasma gondii.
•
One of the common infections worldwide.
•
Infection leads to lifelong immunity (10-40% +ve).
•
Risk of fetal infection depends on trimester.
•
Consequences:
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Classic triad hydrocephalus.
-
Intracranial calcifications.
-
Chorioretinitis.
•
25% of infected fetuses are symptomatic (mental retardation, seizure, CNS, &
hepatosplenomegaly).
Tachyozoite:
•
Invade all mammalian cell (except RBCs).
•
Multiplies intracellularly.
•
Destroys host.
•
Spreads throughout body via bloodstream.
Toxoplasmosis:-
•
A parasite acquired by contact with cat feces or raw meat.
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Transmitted through the placenta.
Congenital toxoplasmosis includes the following possible signs:-
1. Low birth weight.
2. Enlarged liver and spleen.
3. Jaundice.
4. Anemia.
5. Inflammation of eye structures.
6. Neurological damage.
Seronegative Pregnant Women:-
•
Likelihood / severity intrauterine infection depends on timing.
•
10-25 % of infection transmitted in 1st trimester&75-90% in 3rd.
Maternal Symptoms of Infection:-
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Slight fever.
•
Aches.
•
Fatigue.
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Rash (rare).
•
Lymphadenopathy (commonest).
Congenital toxoplasmosis
•
Possible signs:
1. Low birth weight.
2. Enlarged liver and spleen.
3. Jaundice.
4. Anemia.
5. Inflammation of eye structures.
6. Neurological damage.
•
Infection early in pregnancy:-
1. Chorioretinitis.
2. Cerebral calcification.
3. Hydro/microcephalus.
•
Infection late in pregnancy:-
1. Subclinical.
2. Chorioretinitis.
3. Hepatosplenomegaly.
4. Jaundice, rash.
Diagnosis:-
A. Pregnant mother:-
1. Serology; IgM, IgG, compared to booking blood. Antibody avidity.
2. Confirm by demonstration of parasite in LN, CSF.
B. Fetus:-
1. Repeat serology.
2. IgM production may be delayed 2-3 months.
3. Maternal IgG may be passively acquired.
4. Clearance of IgG in first year of life excludes infection UNLESS child is being
treated.
Preventive measures:-
1. Cook all meat thoroughly
2. Wash hands and all kitchen surfaces after handling raw meat
3. Avoid uncooked eggs and unpasteurized milk
4. Wash fresh fruits and vegetables well
5. Avoid materials contaminated with cat feces
Treatment:-
1. Treatment in pregnancy -> 60-70% prevention congenital infection.
2. Spiramycin or pyrimethamine/sulfadiazine/leucovorin.
3. Termination.
Rubella (German Measles):-
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Togavirus, ss RNA enveloped.
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Manifests as German measles.
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Respiratory transmission.
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Viraemia 5-7 days post exposure.
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The period of infectivity is 7 days before the rash to 5 days after the rash appears.
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Vaccine available, given in childhood.
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Mild viral disease.
•
Low fever and rash.
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Destructive to developing fetus:-
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If it occurs early in pregnancy, it can disrupt formation of major body systems.
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If it occurs later in pregnancy, it can cause damage to organs already formed.
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If woman receives a rubella vaccine prior to pregnancy, then she should not get
pregnant for at least 3 months.
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Not given during pregnancy because vaccine is from a live virus.
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Risk of fetal infection affected by GA.
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Consequences:-
1. Spontaneous abortion
2. IUGR
3. Congenital heart disease
4. CNS (deafness, cataracts, retinopathy, microcephaly, calcifications, mental
retardation)
5. Hepatosplenomegally
6. Thrombocytopenic purpura
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Seronegative Pregnant Women.
Maternal Symptoms of Infection:-
1. About 50% asymptomatic.
2. Maculopapular rash.
3. Fever.
4. Lymphadenopathy.
5. Fatigue.
6. Sore throat.
Effects on embryo or fetus:-
1. Microcephaly (small head size).
2. Mental retardation.
3. Congenital cataracts.
4. Deafness.
5. Cardiac effects.
6. Intrauterine growth restriction (IUGR).
Congenital Rubella Syndrome:-
•
Consist of a triad of abnormalities affecting eyes, ears & heart
1. Micro-ophthalmia, glaucoma, pigmentary retinopathy.
2. Sensorineural deafness.
3. Ventricular septal defect, pulmonary artery / valvular stenosis, patent ductus
arteriosus.
Diagnosis:-
•
Maternal testing (IgM & IgG) and fetal testing (IgM in umbilical blood or IgG in
infant’s blood after 5 months).
Treatment:-
•
None; mother can deliver vaginally.
Prevention:-
1. Screen all pregnant women in 1st visit.
2. Avoid exposure during pregnancy.
3. Vaccination of seronegative women in postpartum period and contraception for 3
months.
Treatment / Prevention:-
1. Live-attenuated virus vaccine as part of MMR given in childhood.
2. Screening of pregnant women to determine immune status and advise
accordingly.
3. Vaccination post-partum for non-immune women.
4. Only fetal intervention=termination.
Cytomegalovirus (CMV):-
•
DNA virus of Herpesvirus family.
•
Establishes in latent form in host, allowing periodic reactivation.
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Transmission via body fluids ie. Saliva.
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>90% adults immune.
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Caused by DNA herpes virus.
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One of the most common congenital viral syndrome.
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Transmitted via exposure to infected blood, other body fluid, or organ
transplantation.
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50% of pregnant women are seropositive.
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Infection in Pregnant Woman.
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Reactivation of latent infection or primary infection
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Foetal infection by reactivation less likely.
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Maternal Symptoms Infection:-
1. Normally asymptomatic
2. Fever
3. Headache
4. Fatigue
5. Myalgia
6. Sore throat
Cytomegalic Inclusion Disease
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90-95% develop normally.
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Mild illness:-
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Interstitial pneumonitis.
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Hepatosplenomegaly & jaundice.
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Thromobocytopenia.
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Purpura.
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Classical, severe disease:-
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IUGR.
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Chorioretinitis.
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Sensorineural deafness.
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Microcephaly.
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CNS abnormalities.
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Infected infant may have:-
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Mental retardation
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Seizures
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Blindness
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Deafness
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Dental abnormalities
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Petechiae
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Treatment:-
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No effective treatment is known.
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Therapeutic abortion may be offered if CMV infection is discovered early in
pregnancy.
Risk of fetal infection:-
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50% in all trimesters with 1ry infection and < 1% with recurrent one
Diagnosis:-
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Symptomatic infection appears as a mononucleosis-like syndrome with hepatitis
(rarely seen).
•
Asymptomatic infection is more common.
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Viral culture of amniotic fluid, urine, or other body fluid.
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Maternal and fetal Ab’s testing.
Treatment:-
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If active: Acyclovir
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Route of delivery: Vaginal.
Herpes Simplex Virus (HSV):-
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HSV type 1 & 2.
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DNA virus of herpes virus family.
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Spread by sexual contact or oral transmission.
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HSV-II causes 90%, HSV-I causes 10%.
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Most contagious STD and most common cause genital ulcer.
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HSV-II accounts for 70% & HSV-I for 30%.
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50% of pregnant women are seropositive.
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Types of genital herpes infections.
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Primary.
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Recurrent.
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Dx: culture from ulcer or smear or ELISA.
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1ry infection:-
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Spontaneous abortion,
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IUGR,
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IUFD,
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Preterm labour.
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No malformation syndrome. Neonatal attack rate 50%, mortality 50%.
Congenital infection:-
1. Maternal viraemia may occur rarely leading to congenital infection.
2. If occurs <20w gestation.
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20-25% risk miscarriage.
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Still birth.
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Microcephaly, hydrocephalus, chorioretinitis, hepatosplenomegaly.
3. Neonatal infection during passage through birth canal more common.
Treatment:-
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antiviral agents, symptomatic relief, and abstinence from sexual contact
Route of delivery:-
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Caesarean section if active genital lesions are present at time of delivery and no
documented fetal infection otherwise vaginally.
Neonatal management:-
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No need for isolating the fetus from the mother or stop breastfeeding unless a
lesion is present.
Varicella Zoster virus (VZV):-
•
DNA virus of Herpesvirus family.
•
Spread by direct contact or airborne.
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Becomes latent and can be reactivated.
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Infectious before symptoms apparent.
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Pregnant women:-
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> 85 % immune due to exposure in childhood.
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Infects placenta causing focal necrosis.
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CVS 2 % risk if first 20w pregnancy.
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Miscarriage 3 % if first 16 weeks pregnancy.
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Premature labour.
Congenital Varicella syndrome:-
1. Microcephaly.
2. Cerebral cortical atrophy.
3. Cerebellar hypoplasia.
4. Mental retardation.
5. Convulsions.
6. Limb hypoplasia, malformed digits.
7. Skin scarring.
8. Cataracts, chorioretinitis, microphthalmia.
Diagnosis:-
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Pregnant mother:-
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Characteristic chickenpox.
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Culture/ of virus from vesicles.
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Fetal:-
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Specific IgM often undetectable at birth.
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Persistent specific IgG.
Human Parvovirus B19:-
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DNA virus
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Causes erythema infectiosum, fifth disease or slapped cheek syndrome.
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Transmitted by droplets (respiratory).
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Congenital infection:-
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More pronounced during 2nd rather than 1st trimester.
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Severe and often fatal in fetus.
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~9% fetal loss 4-6 weeks after development of rash in mother.
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Hydrops foetalis most common manifestation.
Diagnosis:-
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Pregnant mother:-
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Specific IgM.
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IgG seroconversion.
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Elevated serum a-feto-protein.
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Fetus:-
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Ultrasound for symptoms associated with hydrops (abnormal accumulation of
serous fluid in skin (edema) and body cavities (pericardial, pleural, or ascitic
effusions). (cordocentesis/amniocentesis).
Hepatitis B Virus (HBV) Infection:-
•
Infection caused by DNA hepadenavirus type I.
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Transmitted via body fluids. Mother-infant transmission causes 40% of all chronic
infections.
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Types of infection:-
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Asymptomatic: 75% of all infected patients
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Acute hepatitis: Jaundice and liver enzymes
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Chronic hepatitis: In 10% of infected adults and 80% of infected infants.
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Sequelae of Chronic Hepatitis:-
1. Immunological markers: HBsAg for screening. Others HBcAg & HBeAg
2. Maternal: cirrhosis and hepatocellular carcinoma.
3. Fetal: uncommon infection, occurs in third trimester, can cause premature birth,
low birth weight or neonatal death.
4. Carrier mothers may transmit infection in 10% if only HBsAg or 80% if both
HBsAg & HBeAg.
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Dx: all pregnant women should be screened for HBsAg at 1st visit (repeat at 28
wks if high risk).
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Route of delivery: vaginal.
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Prevention:-
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Neonates of HBsAg +ve women should receive HBIg and active vaccine.
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Avoid scalp electrode, scalp needles after delivery, and avoid breastfeeding
Hepatitis C Virus (HCV) Infection:-
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Non-A non-B hepatitis or post-transfusion hepatitis.
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Named HCV in 1989.
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Often asymptomatic.
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Long incubation period to clinical endpoint.
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1/3 acute infections recover.
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6 genotypes.
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HCV vertical transmission:-
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Some evidence intrauterine / perinatal acquisition.
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Maternal HCV RNA levels important predictive factor.
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Co-infection with HIV predisposes to transmission.
Human Immunodeficiency Virus (HIV):-
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More than 30 million worldwide HIV positive.
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Three strains recognised HIV-1, HIV-2 and HIV-O.
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More than 50% infected children present with lymphadenopathy/
hepatosplenomegaly in first year life.
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About 30-50% diagnosed opportunistic infections, 48% expected to die before 3rd
birthday.
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Single-stranded RNA virus causes AIDS
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Virus transmitted via sexual contact with infected partner, blood Tx, transplacental,
& needle stick
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1 in 3 neonates delivered to HIV +ve mothers
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HIV screening is recommended for all high-risk mothers:
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Anaemia in pregnancy .
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Intrauterine growth restriction.
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Preterm labour.
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Birth weight less than 2,500 g.
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Apgar score less than 7.
Diagnosis congenital HIV:
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Maternal anti-HIV crosses placenta, persists up to 18m.
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Gold standard HIV DNA on peripheral blood lymphocytes.
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+ve 72h birth = intrauterine transmission.
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By 3mo 95% of those infected detected.
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Maternal blood should be tested in parallel to check primers work.
Management of HIV +ve Mother:-
1. Maternal counseling.
2. Antiviral prophylaxis (start at 14wks).
3. Multidrug antiviral therapy if viral load is high.
4. Treatment for infectious diseases.
5. Maternal vaccination against HBV.
6. Maternal prophylaxis for P. carinii pneumonia.
7. Avoid scalp electrode or instrumental delivery.
8. Mode of delivery (caesarean section is protective).
Management of Genital Warts in Pregnancy:-
1. Genital warts can proliferate and become more friable during pregnancy.
2. Caused by HPV,STD
3. Cytotoxic agents (podophyllin, podofilox,) should not be used.
4. Cryotherapy, TCA, BCA, and surgical removal may be used.
5. Prevention value of cesarean delivery is unknown, thus C-section should not be
performed to prevent transmission to neonate,only in severe aggressive lesion.
Syphilis:-
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Caused by Treponema pallidum.
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Treponemes appear able to cross the placenta at any time during pregnancy,
thereby infecting the fetus.
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WHO estimates responsible for:
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460 000 stillbirths/miscarriages.
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270 000 congenital syphilis.
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270 000 low birth weight/premature babies.
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Syphilis vertical transmission:
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Occurs after 16th wk gestation.
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Greatest risk when in early stages of infection, but can be at any stage for
transmission to occur.
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Silver and immunofluorescence staining of the fetal tissue, or polymerase chain
reaction and rabbit infectivity testing of amniotic fluid showed that T pallidum
gains access to the fetal compartment as early as 9–10 weeks.
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Screening:
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EIA on booking bloods.
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Rapid plasma reagin (RPR) or venereal disease research laboratory (VDRL) test
combined with confirmation of reactive individuals with treponemal tests such as
the fluorescent treponemal antibody absorption (FTA-ABS) assay.
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High risk – repeat serologic testing – 3rd trimester and at delivery.
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Clinical manifestations:-
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Cervical changes, such hyperaemia and friability, during pregnancy may facilitate
the entry and lead to spirochaetaemia.
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Histological changes of congenital and acquired syphilis are vasculitis and its
consequences, necrosis and fibrosis.
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After incubation period of 3–90 days, a solitary papule with central ulceration,
teeming with spirochaetes found on the genitalia, and on the rectal and the oral
mucosa.
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In about 2–6 weeks after the chancre resolves, systemic manifestations of the
disease appear including headache, fever, lymphadenopathy, symmetrically
distributed maculopapular rash found on the palms and the soles.
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The mother can transmit the infection transplacentally to the fetus or during
passage through the birth canal by contact of the newborn with a genital lesion.
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Complications and treatment:-
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Syphilis can seriously complicate pregnancy and result in spontaneous abortion,
stillbirth, non-immune hydrops, intrauterine growth restriction, and perinatal
death.
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Early syphilis - Benzathine penicillin IM in a single dose.
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Late syphilis - Benzathine penicillin G 7.2 million units total, administered as 3
doses of 2.4 million units IM each at 1-week intervals.
Listeria:-
•
Listeriosis is an infection caused by the Gram-positive motile bacterium Listeria
monocytogenes.
•
Principal route of acquisition of Listeria is through the ingestion of contaminated
food products.
•
Pathophysiology:-
-
Ingestion of Listeria by pregnant women can result in nausea, vomiting, diarrhea,
fever, malaise, back pain, and headache.
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Many pregnant women can carry Listeria asymptomatically in their GI tract or
vagina.
-
Maternal infection with Listeria can result in chorioamnionitis, premature labor,
spontaneous abortion, or stillbirth.
-
Fetal infection can occur via transplacental transmission.
•
Vertical transmission:-
-
Occur from mother to infant via passage through an infected birth canal or
ascending infection through ruptured amniotic membranes.
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Two clinical presentations of neonatal infections occur:
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early onset (<5 d) – associated with sepsis or meningitis via transplacental
transmission.
-
late onset (>5 d) - presents with purulent meningitis through vaginal
transmission.
•
Clinical manifestations:-
-
Listeria may proliferate in the placenta and cause infection due to impaired cell-
mediated immunity during pregnancy.
-
Fever, myalgias, arthralgias, back pain, and headache are classic symptoms of
bacteremia.
-
Listeriosis during pregnancy usually occurs during the third trimester, when cell-
mediated immunity is at its lowest.
-
Preterm labor and/or delivery is common. Abortion, stillbirth, and intrauterine
infection are possible.
•
Treatment:-
-
Antibiotics – Ampicillin and aminoglycosides.
-
Careful monitoring of the patient's temperature, respiratory system, fluid and
electrolyte balance and nutrition.
Group B Streptococcus:-
•
Is the causative agent of postpartum infection and as the most common cause of
neonatal sepsis.
•
Group B streptococci colonize the vaginal and gastrointestinal tracts in healthy
women, with carriage rates 15%-45%.
•
Neonates can acquire the organism vertically in utero or during delivery from the
maternal genital tract.
•
Only 1-2% of colonized neonates develop invasive disease.
•
Group B streptococcal - prematurity and prolonged rupture of the membranes.
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Pathogenesis:-
-
Neonatal group B streptococcal disease is divided into early and late disease.
-
Early sepsis often presents within 24 hours of delivery but can become apparent
up to 7 days postpartum. Pneumonia with bacteremia is common, while
meningitis is less likely.
-
Late sepsis between one week postpartum and age 3 months. Involves group B
Streptococcus serotype III, typically characterized by bacteremia and meningitis.
•
Prevention and treatment:-
-
Intrapartum antimicrobial prophylaxis.
-
Women without a known group B streptococci status delivering before 37 weeks'
gestation with premature rupture of the membranes or intrapartum fever are also
candidates for intrapartum antimicrobial prophylaxis.
-
Penicillin or ampicillin is the initial approach. Clindamycin and erythromycin are
standard in individuals with penicillin allergy.
Chlamydia:-
•
Chlamydia trachomatis - obligate, intracellular bacterium with 15 immunotypes:
•
A-C - trachoma
•
D-K - genital tract infections
•
L1-L3 - lymphogranuloma venereum
•
One of the leading causes of infertility in women.
•
Screening:-
-
To prevent consequences of untreated chlamydial infection such as pelvic
inflammatory disease, infertility and ectopic pregnancy.
-
Screening for chlamydial infection in all pregnant women aged 24 years or
younger and in older pregnant women who are at increased risk.
•
Pathophysiology:-
-
Infection of the genital tract is the most common clinical presentation. The
incubation period is 1-3 weeks.
-
Co infection with................
-
Chlamydia is transmitted via the birth canal of an infected mother, and neonates
exposed to chlamydia at birth may develop conjunctivitis 5-13 days later.
-
C trachomatis - pneumonia in the newborn.
-
Chlamydial infection develops in 60% of neonates born vaginally to infected
mothers.
•
Diagnosis:-
-
Cell culture.
-
Direct fluorescent antibody.
-
Nucleic acid amplification techniques.
-
Enzyme immunoassay.
-
Collect specimens from urethra, endocervix, rectum, or conjunctivae.
•
Treatment:-
-
First-line drugs - Azithromycin and doxycycline.
-
Second-line drugs – erythromycin.
Diagnosis and Treatment of perinatal infections:-
1. Identify risk factors.
2. Evaluate clinical features and laboratory support.
3. Empirical or specific antimicrobial agents.
4. Share information between obstetrical and pediatric/ family medicine providers.
5. Post-partum follow-up.