MATERNAL INFECTION DURING PREGNANCY

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

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