Monday, September 21, 2020

INFECTIONS IN PREGNANCY – CYTOMEGALOVIRUS

 

CAUSATIVE ORGANISM:

Cytomegalovirus (CMV) or herpesvirus type 5(HHV-5). Family: Herpesviridae

TRANSMISSION:

CMV is transmitted through exposure to bodily fluids. Such as Urine, Feces, Blood, Semen, Urogenital secretions, Breast milk, urine. Vertical (Transplacental), Blood Transfusion, Organ Transplant.

RISK FACTORS:  

Higher socioeconomic class (less likely to have immunity through childhood infection), immunosuppression (e.g. HIV).

EPIDEMIOLOGY:

CMV is ubiquitous, 50% adults develop immunity in pregnant women. 1% of seronegative pregnant women will contract CMV antenatally.

CLINICAL FINDINGS and COMPLICATIONS: 

o   Congenital- 90% infected infants appear normal, later 20% develop sensory nerve hearing loss, psychomotor mental retardation, or both. The infants with symptomatic illness (about 0.1% of all births) show congenital defects or disorders (jaundice, anemia, hepatosplenomegaly, thrombocytopenia, low birth weight, microcephaly, and chorioretinitis).

o   Perinatal- Almost all of these perinatally infected infants have no discernible illness unless the baby is premature or immunocompromised. CMV can also be efficiently transmitted from mother to child by breast milk, but these postpartum infections are also usually benign.

o   Post neonatal- CMV infections during childhood and adulthood are totally asymptomatic. CMV may cause a mononucleosis-like syndrome.

o   Adults: Persons having AIDS, latent CMV may be reactivated and cause very serious disease. interstitial pneumonia (90% mortality), chorioretinitis, gastroenteritis, neurologic and other organs involvements.

SIGNS:

Often no clinical signs, may find lymphadenopathy.

PATHOLOGY/PATHOGENESIS:

Incubation period 1–2 months.

Cytomegalovirus infects epithelial cells and leukocytes. In vitro, CMV DNA can be demonstrated in monocytes showing no cytopathology, indicating a restricted growth potential in these cells. In addition to nuclear inclusions (“owl eye cells”), CMV produces perinuclear cytoplasmic inclusions and enlargement of the cell (cytomegaly), a property which gives the virus its name. Following primary infection can remain dormant and then reactivate (e.g. in immunosuppression).

 

INVESTIGATIONS

Bloods: CMV IgM (current infection)/IgG (immunity).

USS: Fetal anomaly scan.

Other: Amniocentesis for CMV PCR (6–9 weeks after primary infection).

MANAGEMENT:

No treatment to prevent transmission to fetus. May offer termination of pregnancy if evidence of CNS damage. Ganciclovir, a nucleoside analog of acyclovir (INN: Aciclovir), inhibits CMV replication and reduces the severity of CMV syndromes, such as retinitis and gastrointestinal disease. When given with hyper immune globulin, ganciclovir is thought to reduce the mortality. Neonatal gancyclovir can attenuate audiological complications.

PROGNOSIS:

Rate of transmission to the fetus is 40%. Of these, only 10% will develop the congenital Syndrome. Ninety percent of babies who are symptomatic at birth will have later neuro-developmental problems.

Friday, September 18, 2020

INFECTIONS IN PREGNANCY – HERPES SIMPLEX

CAUSATIVE ORGANISM:  Herpes Simplex Virus (HSV).

TRANSMISSION:   

    By physical contact, sexual contact, vertical.

RISK FACTORS: 

    Unprotected sex, immunosuppression (e.g. HIV), other STIs.

EPIDEMIOLOGY: 

    Herpes simplex infects 2% of pregnant women.

SYMPTOMS: 

    Burning sensation, pain, pruritis, dysuria (note: may be asymptomatic).

SIGNS: 

    Clusters of vesicles with surrounding erythema, can progress to ulcerated lesions which crust over, may be associated with local lymphadenopathy.

PATHOLOGY/PATHOGENESIS

DNA virus (herpes family), two types – HSV-1 is transmitted by oral-to-oral contact to cause oral herpes (which can include symptoms known as “cold sores”), but can also cause genital herpes.HSV-2 is a sexually transmitted infection that causes genital herpes. Both HSV-1 and HSV-2 infections are lifelong. Dormant period: Following primary infection, HSV remains dormant in nerve ganglia and can be reactivated to form recurrent lesions. Spread to neonate: Mainly direct contact with infected maternal secretions (but transplacental transmission possible), risk of neonatal transmission at vaginal delivery – 41% with primary lesions, 2% with recurrent lesions.

INVESTIGATIONS:

Usually diagnosed clinically. Microbiology: Swabs for viral culture/PCR, STI screen. Bloods: HSV antibody (primary infection in third trimester).

MANAGEMENT

Antenatal: Aciclovir (200 mg 5 times daily for 5 days) in primary infection. Treatment with acyclovir and valacyclovir by 36 weeks of pregnancy to term reduces the frequency of clinical manifestations, vertical transmission, elimination of the virus during birth by reducing the percentage of caesarean

Delivery with primary HSV: If within 6 weeks of likely delivery, advise Caesarean section. If opts for vaginal delivery, give IV aciclovir intrapartum, avoid prolonged ruptured membranes/FSE/FBS.

Delivery with recurrent HSV: Does not necessitate Caesarean section. Women may opt for Caesarean if lesions detected at onset of labour – can offer daily aciclovir from 36/40 to reduce likelihood of lesions.

COMPLICATIONS

Maternal: Disseminated herpes (encephalitis, hepatitis, disseminated skin lesions) rare but not uncommon in pregnancy.

Neonatal: It affects skin/eyes/mouth, CNS or multiple organs. The risk of neonatal infection varies from 30% to 50% for late onset HSV infections (last trimester), whereas early pregnancy infection carries a risk of about 1%. When primary HSV infection occurs during late pregnancy

PROGNOSIS:

  •  HSV disease localized to the skin, eye, and/or mouth (SEM); this syndrome is associated with a low mortality but it has a significant morbidity, and it may progress to encephalitis or disseminated disease if left untreated;
  • HSV encephalitis with or without skin, eye, and/or mouth involvement which causes neurologic morbidity among the majority of survivors; 
  • Disseminated HSV which manifests as severe multiorgan dysfunction (including central nervous system, liver, lung, brain, adrenals, skin, eye, and/or mouth) and has a mortality risk that exceeds 80% in absence of therapy