Obstetric and Perinatal Infections

p.313-321

Introduction:

p     placental barrier

n    Protects fetus from circulating microbes

p     susceptible tissues (maternal and fetal)

n    Placenta

n    Fetus

n    Lactating mammary glands

p     infections occur during pregnancy, at birth and postnatally

n    both mother and fetus/newborn are susceptible

p   During and after delivery

Infections during pregnancy:

•             maternal immune status changes during pregnancy

–          baby is a “foreigner” but must not be rejected by mother

–       Absence or low density of MHC antigens on placental cells

–       Covering antigens with blocking antibodies

–       alternations in maternal immune response

–          effect of malnutrition – impairs host defenses

•             fetal immune status – susceptible to infections

–          no IgG is produced

–          no IgA or IgM produced until late in pregnancy

–          little or no cell mediated response

n           This is good – no host-vs-graft reaction.

•             infections more severe during pregnancy or latent infections can reactivate (fig. 23.1, fig. 23.2)

•              most infections lead to stillbirth

n           pathogens that infect fetus leading to abortions or stillbirth

p         HSV, CMV, rubella, syphilis

n           others infect and interfere with fetal development à damaged baby

•              congenital infections (fig. 23.3)

–           occur in utero

–           usually mild infections for mother

–           fetus unable to mount cell-mediated response

–          if not stillborn à small, failure to thrive babies

–          fetal malformations (viruses act as teratogens)

–       Routine screening for rubella, HIV

–           maternal antibody protection

–          Strong response - May help control infection

–          Poor – increases infection in fetus

•             congenital rubella

–           susceptibility of fetus highest during first trimester

–          fetal death occurs

–       viruses attack blood vessels in developing organs

–        interferes with development of heart, brain, eyes and ears à abnormalities (fig.23.5)

p         Clinical manifestations

•             congenital rubella

–           25% develop diabetes mellitus later in life

–           fetus produces IgM against rubella

–           After birth, infant sheds virus and is contagious for several months (throat and urine)

–           completely preventable by vaccine (MMR)

•              congenital cytomegalovirus infection

–           mothers pass CMV to fetus due to diminished T-cell response

–           40% of fetuses infected in mothers with primary CMV infections à 5% have congenital abnormalities

–          Reactivations of CMV infections à fetal damage uncommon

–           1-2% of all babies in USA born infected à 10% symptomatic

–           effects include:

–          mental retardation, spasticity, eye abnormalities, deafness, hepatosplenomegaly, thrombocytopenic purpura and anemia

–           Condition is diagnosed by:

p         Detection of CMV-specific IgM in newborn

p         Isolation of virus from urine

p         Molecular detection of viral genome

•             congenital syphilis

–           rare in US due to screening and treatment

–          treatment of mother before fourth month prevents fetal infection

–           effects include

–          snuffles (rhinitis), skin and mucosal lesions, hepatosplenomegaly, lymphadenopathy and abnormalities of skin, teeth and cartilage

–           fetus produces IgM

•              congenital toxoplasmosis

–           caused by Toxoplamsa gondii

–           incidence of infection and severity of sequelae increases with fetal age

–          14% in first trimester

–          59% in third trimester

–          Effects (may not be apparent at birth):

§        Convulsions, microcephaly, chorioretinitis, hepatosplenomegaly, jaundice, hydrocephaly, mental retardation and defective vision

–           fetus can produce IgM

–           antibiotic treatment is spiramycin

–           no vaccine, prevention by avoidance of primary infection

•             congenital HIV infection

–           infection can occur:

–          in utero – avoid infection by chemotherapy

–          at birth – avoid infection by delivery by C-section

–          after birth – avoiding breastfeeding

–           sequelae usually appear after birth

–          Poor weight gain, susceptibility to sepsis, developmental delays, lymphocytic pneumonitis, oral thrush, enlarged lymph nodes, hepatosplenomegaly, diarrhea and pneumonia, encephalopathy and AIDS

–           laboratory diagnosis based on detection of:

–          virus DNA and RNA by molecular methods

–          HIV antibodies

•             congenital and neonatal listeriosis

–           caused by Listeria monocytogenes

–          Gram positive rod, psychrophile

–           Human exposure via animals or infected foods

–          Mild flu-like illness in mother

–          When infect placenta à infect fetus

–           fetal effects

–          abortion, premature delivery, neonatal septicemia or pneumonia

–          Diagnosis: isolation from blood, CSF or lesions of newborn

–           antibiotic treatment

–          penicillin or ampicillin

–           no vaccine, prevention is by avoidance of exposure

Infections occurring at birth

p    Effects on the fetus and newborn

n     Routes of infection (fig. 23.8)

Viral infections:

•      Rubella and CMV

p    Less damage to fetus if maternal infection occurs late in pregnancy

•      varicella-zoster virus

p    Primary infection during first 20 weeks à limb deformities and other lesions

•      HSV

p    Primary infection during first 20 weeks à neonatal morbidity or mortality

Bacterial group – more important late in pregnancy

•       Group B streptococcus

p     10-30% pregnant woman are infected

•       Escherichia coli

•       Klebsiella

•       Proteus

•       Bacteriodes

•       Staphylococci

•       Mycoplasma hominis

p     neonatal sepsis often leads to meningitis

n      Fatal unless treated à blind antibiotic treatment

p     labor and/or breast feeding can contribute to fetal infection

n      Direct infection as fetus passes through birth canal (Fig. 23.9)

n      Herpes simplex virus:

p     cutaneous lesions, severe CNS involvement

n      Gonococci, chlamydia or staphylococci:

p     infect eye and cause ophthalmia neonatorum

p      Many neonatal infections occur due to non-hygienic behavior of caregivers

n      Group B strep, G – bacilli-  Cross-infection in the nursery

n      HSV – from cold sores of attending adults

n      Staphylococci – noses and fingers of adult carriers

p     Colonize infant, enter nipple during feeding and cause breast abscess

p     Fetus à sticky eye, skin sepsis, and staphylococcal scalded skin syndrome

n      C. tetani – infection of umbilical stump with spores

Infections of the mother

•             infection of the uterine tissue

•             puerpural sepsis

•           infection of genital tract after childbirth

•            major cause of maternal death in 1800’s

•          Undiagnosed or untreated, still a major cause of maternal death.

•           bacteria responsible

•          staphylococci (S.aureus)

•          Streptococci (group A streptococcus, S.pyogenes) 

•          From nose, throat or skin of hospital attendants