MATERNAL INFECTION DURING PREGNANCY

1. WELCOME

2. INFECTIONS
DURING PREGNANCY
BY:
MR.DINABANDHU BARAD
MSC TUTOR,
SUM NURSING COLLEGE,
SIKSHA O ANUSANDHAN
DEEMED TO BE UNIVERSITY

3. BACTERIAL INFECTIONS
• Pregnant women are susceptible to infections during pregnancy and her immune
system works in focus by up regulation to fight infections and down regulation to
prevent foetal rejection.
• These two processes coexist; however, they do not counteract each other.

4. BACTERIAL INFECTIONS
The bacterial infections most often associated with pregnancy are
• Urinary tract infections
• Genital tract infections
• Pulmonary
• Dermatological
• Central nervous system

5. COMMON INFECTIONS DURING
PREGNANCY

6. • One of the risks associated with bacterial infections is preterm labour.
• The event that may cause premature labour consists of bacteria-releasing
endotoxins (lipopolysaccharides) or exotoxins that initiate cytokine and
interleukin responses.
BACTERIAL INFECTIONS

7. • These responses in turn affect the decidua, membranes, or prostaglandin
production that leads to uterine contractions.
• With these contractions come cervical dilation and a potential opening for more
microbes into the uterus.
• Other risks associated with bacterial infection include maternal or neonatal
sepsis, foetal distress, and foetal demise
BACTERIAL INFECTIONS

8. The bacteria may enter the amniotic cavity by the following pathways:
• Ascending from either the cervix or vagina.
• Haematogenous spread with trans placental passage, usually associated
with maternal bacteraemia.
• Entry through the fallopian tubes or peritoneal cavity.
• Nosocomial through amniocentesis or chorionic villus sampling.
BACTERIAL INFECTIONS

9. • The most common of these pathways is ascending infection.
• The most prevalent bacteria associated with maternal or foetal risks during
gestation include many exogenous and endogenous organisms
BACTERIAL INFECTIONS

10. • Chlamydia trachomatis
• Bordetella pertussis
• Calmymmatobacterium granulomatis
• Hemophilus ducreyi (Chancroid)
• Hemophilus influenza
• Listeria monocytogenes
• Neissiera gonorrhoeae
• Salmonella typhi
• Group Aβ -hemolytic streptococci (Streptococcuspyogenes)
EXOGENOUS PATHOGENS

11. • Bacteroidacea
• Clostridia
• Escherichia coli
• Gardnerella vaginallis (Hemophilus vaginallis)
• Proteus
• Staphylococcus aureus
• Staphylococcus epidermidis
• Group B hemolytic streptococci.
ENDOGENOUS PATHOGENS

12. GROUP B BETA-HEMOLYTIC
STREPTOCOCCI (GBS)
• Group B beta-hemolytic streptococci (GBS) are gram-positive cocci that grow in
chains.
• They lack a protein, which exists on the Group A streptococci, and
hence demonstrates a different degree of virulence.
• GBS is a normal constituent of the vaginal flora and the gastrointestinal tract.

13. GROUP B BETA-HEMOLYTIC
STREPTOCOCCI (GBS)
• Faecal colonization exceeds any other colonization rates.
• Between 14 and 25% of pregnant women may be continually, intermittently, or
transiently colonized.
• GBS is rarely a cause of maternal morbidity. It is, however, the most common
cause of neonatal sepsis, meningitis, and pneumonia.

14. GROUP A BETA-HEMOLYTIC
STREPTOCOCCUS
(STREPTOCOCCUS PYOGENES)
• Streptococcus pyogenes is a gram-
positive cocci.
• Its capsule contains hyaluronic acid,
which lyses endothelium cells, and it has
the M protein to interfere with
phagocytic cells.

15. GROUP A BETA-HEMOLYTIC
STREPTOCOCCUS
• Infections are associated with puerperal sepsis, prepubertal vulvovaginitis,
endometritis–salpingitis–peritonitis, and necrotizing fascitis.
• In gravid women Streptococcus pyogenes can be present as part of the normal
vaginal flora; however, infections can occur if there is a break in the mucosal
epithelial barrier.
• Clinically, it presents as a high maternal fever and uterine tenderness.

16. GROUP A BETA-HEMOLYTIC
STREPTOCOCCUS
(STREPTOCOCCUS PYOGENES)
• Other evidence of infection of the uterus and pelvis can include leukocytosis,
tachycardia, edematous soft uterus, and a serosanguinous vaginal discharge.
• Maternal septicemia will occur before foetal involvement occurs, but with
ruptured membranes, it can ascend to infect the foetus, amniotic fluid, and
chorion.
• Treatment includes penicillin, ampicillin, or vancomycin.

17. LISTERIA MONOCYTOGENES
• Listeria monocytogenes is a gram-positive,
catalase-positive bacillus in the
corynebacteriaceae family.

18. LISTERIA MONOCYTOGENES
• The gastrointestinal tract is the most likely
usual reservoir for Listeria
monocytogenes.
• The depressed cell-mediated immunity
during pregnancy may be responsible for
the unusual high incidence in pregnant
women.

19. LISTERIA MONOCYTOGENES
• If Listeria chorioamnionitis is diagnosed preterm, in utero therapy with high-dose
penicillin or trimethoprim-sulfamethoxazole should be attempted in order to
avoid the high risk of preterm delivery.

20. LISTERIA MONOCYTOGENES
• Preterm labour occurs in 50% of cases. Treatment may include ampicillin with
clavulanic acid, erythromycin, or trimethoprim-sulfamethoxazole.
• The most effective strategy to prevent this disease is to eliminate the most likely
source; contaminated food

21. HAEMOPHILUS INFLUENZAE
• Haemophilus influenzae is a
gram-negative capsulated
coccus that forms short chains.
• Its prevalence is low, but it has
a high infectious rate.

22. HAEMOPHILUS INFLUENZAE
• Infections associated with this organism include meningitis, epiglotitis,
pneumonia, otitis, and bronchitis.
• There is a higher correlation with postpartum maternal infections than neonatal
disease.
• Treatment includes cefotaxime, ceftriaxone, or trimethoprim-sulfamethoxazole.

23. ESCHERICHIA COLI
• E.coli is a motile gram-
negative bacillus, which is
part of the normal flora
of the intestine and
vagina.

24. ESCHERICHIA COLI
• It is by far, the most common cause of urinary tract infections (UTI) and neonatal
sepsis with an incidence is 0.5–1.5 cases per 1000 live births.
• It is also associated with chorioamnionitis, postpartum endometritis, and septic
abortions, often a part of a polymicrobial infection.
• UTIs in pregnancy are associated with pyelonephritis and preterm labor.

25. ESCHERICHIA COLI
• They have also been known to increase IgM lymphoblastic responses in neonates.
• Treatment is with cephalosporins, trimethoprim-sulfamethaxazole, ampicillin
with clavulanic acid, or gentamicin, depending on the site.

26. VIRAL INFECTIONS
• The impact of a maternal viral infection on the foetus ranges from abortion,
stillbirth, preterm labour and delivery, physical defects, intrauterine growth
disturbances, and the postnatal persistence of infection.
• Many viral agents have been reported to affect the developing foetus in utero,
transmission occurring by the transplacental passage of the virus during the
period of maternal viremia.

27. VIRAL INFECTIONS
The mechanisms by which viral agents may produce adverse effects on the foetus
include
• placental dysfunction secondary to maternal infection (fever, toxins, altered
placental circulation, thrombosis, or placentitis producing hypoxia with altered
cell growth and subsequent foetal damage),
• chromosomal damage,
• cellular necrosis
• antigen–antibody formation

28. RUBELLA
• The rubella virus
produces an acute,
contagious exanthem
that usually occurs in
epidemics.

29. EXANTHEM
• An exanthem is a widespread rash occurring
on the outside of the body and usually
occurring in children.
• An exanthem can be caused by toxins,
drugs, or microorganisms, or can result from
autoimmune disease.

30. RUBELLA
• The rubella virus, is spread by nasopharyngeal droplets from which the virus
implants and multiplies in the respiratory epithelium, with an incubation period
of 14–21 days.
• The typical maculopapular rash and generalized lymphadenopathy of rubella
infection is preceded by a short period of prodromal symptomatology with
malaise, fever, headache, conjunctivitis, and pharyngitis.

31. CERVICAL LYMPHADENOPATHY

32. RUBELLA
• The duration of the rash is usually 3 days, commencing on the face and migrating
caudally.
• It is the potential teratogenic effect of the rubella virus in pregnancy that
produces most concern.
• Intrauterine transmission of the virus occurs after primary infection of the
mother.

33. RUBELLA
• The gestational age of the foetus at the time of maternal infection is the principal
factor determining pregnancy outcome.
• Infections beyond 16–20 weeks of gestation do not appear to result in congenital
anomalies, probably because of foetal structural development and developing
immunologic competence.

34. CYTOMEGALOVIRUS
• Cytomegalovirus (CMV) is a
double-stranded DNA
herpes virus and is highly
species specific.

35. CYTOMEGALOVIRUS
• The Herpesvirus family is characterized by latency and reactivation phenomena.
• CMV is not highly contagious; it spreads by close contact with infected
secretions.

36. CYTOMEGALOVIRUS
• CMV may be excreted in the urine and bodily secretions of those infected, and
viral transmission to an uninfected host occurs by close body contact.
• Human blood, marrow, or organs may be a source of infection if received from a
seropositive donor.
• The newborn may be congenitally infected by the transplacental passage,contact
with maternal genital tract secretions or breast milk.

37. CYTOMEGALOVIRUS
• The severity of congenital infection appears to be related to the gestational age
at the time of exposure to the virus.
• Infection occurs with similar frequency in all trimesters although in the first half
of pregnancy the risk of significant foetal anomalies is greater.
• The overall rate of vertical transmission for CMV is in the order of 35–40%.

38. HERPES SIMPLEX VIRUS
Herpes simplex virus
(HSV), a double-stranded
DNA virus, produces a
range of infections.

39. HERPES SIMPLEX VIRUS
• HSV type 2 is most often associated with genital herpes infection.
• HSV damages the neonate mainly through intrapartum infections, but can also
cause congenital disease.

40. HERPES SIMPLEX VIRUS
• Primary HSV infection in early pregnancy has been associated with as high as a
10% incidence of central nervous system and musculoskeletal defects in the
foetus.
• The transplacental transmission of HSV and secondary foetal infection may
produce a severe in utero infection leading to foetal death.

41. HERPES SIMPLEX VIRUS
The foetal effects that have been reported include
• Cutaneous defects (scars, calcifications, vesicles),
• Microcephaly
• Hydranencephaly
• Cerebral and cerebellar necrosis
• Intracranial calcification
• Microphthalmia
• Hepatosplenomegaly
• Chorioretinitis
• Bone anomalies

42. THANK YOU