INFECTION DURING PREGNANCY (CYTOMEGALY (CMV) (DIAGNOSIS (LABORATORY TESTS,…
INFECTION DURING PREGNANCY
Other – (HIV, HPV, B19 virus)
an antropozoonosis caused by Toxoplasma Gondii
food contaminated by cat’s excrements (vegetables, fruits),
meat of animals with toxoplasmosis,
transmission of oocytes on dirty hands,
accidental contact with trophozoites,
transplacental transmission of toxoplasma to the fetus: congenital toxoplasmosis
Primary infection with Toxoplasma gondii during pregnancy – risk of congenital toxoplasmosis
Prophylaxis of toxoplasmosis infection in pregnancy
Gloves to activities requiring contact with materials potentially contaminated with cat’s excrements (gardening, sandpit), careful washing hands and nail cleaning.
House cats: keeping them at home, feeding only with heat treated, canned or dry food, regular (every 24 hours) removing garbage and cat’s excrements (gloves), disinfection of cat’s trays with hot water for 5 min before refilling
Eating only well cooked meat (>67°C), freezing meat to at least –20°C, (in this temperature T. gondii cysts die, cleaning of surfaces and kitchen tools.
Avoiding eating raw eggs and milk.
Washing vegetables and fruits before eating.
Avoiding drinking water potentially contaminated with cat’s excrements
It is important to remeber, that:
– pickling, smoking or drying meat not always eliminates oocysts of toxoplasmosis,
– keeping food in refrigerator does not kill toxoplasmosis (able to survive after 68 days in temperature +4°C),
– Warming up foos in microvawe does not kill toxoplasmosis
Risk of vertical transmission of toxoplasma to the fetus depends on the gestational age
primary infection in 1st trimester – 17% of congenital infections,
primary infection in 3rd trimester – 65% of congenital infections
The risk of severe congenital infection in the fetus is the highest if the infection in the mother occurs in I trimester of pregnancy
Most maternal infections are asymptomatic, toxoplasmosis may mimic flu or mononucleosis:
painfull enlargement of lyph nodes (especially on the neck), tiredness, discomfort, headaches
The infection has a tendency to selflimitation and doesn’t need treatment.
Active infection during pregnancy is confirmed by:
presense of specific antibodies IgM in serum of the mother, high level of IgG
considerable increase (4-fold) of IgG and/or IgM antibodies titer in the mother’s serum, analyzed twice in 3-4 weeks time gap
presense of specific antibodies IgA and/or IgE
Previous infection of Toxoplasma gondii:
presence of stable titers of IgG antibodies
IgG antibodies appear in the serum later than IgM; they are detectable about 1-2 weeks after infestation, the highers titers are observed about 12 weeks to 6 months from fresh infection. They are detectable for years and usually all the life.
IgM antibodies become detectable in the serum about 10 days after infestation and remain elevated for 6 months; ELISA test detects them up to 7-12 years after the infection, their presence does not confirm recent infection;
IgA and IgE in IFA-test (immunofluorescence test) confirm recent infection
IgG antibodies appear 2 weeks after infection and are present for all the life
Determining time of infection in pregnancy
risk of trasmission to the fetus
proper prenatal counseling
Avidity of IgG antibodies – the strength of antibodies binding with toxpolasma
low – up to 5 months
high – after 5 months
In a suspicion of recent infection
repeated lab tests after 2 -3 weeks,
imminent spiramycin therapy should be considered before obtaining repeated results.
DIFFERENTATION OF IgG ANTIBODIES
low avidity (<0.200) --> acute invasion (last 5 months)
high avidity (> 0.300) --> chronic invasion (more than 5 months) --> independently of IgG level and IgM presence
HIGH AVIDITY IN THE FIRST TRIMESTER
infection before conception --> no risk of congenital infection
HIGH AVIDITY IN THE SECOND TRIMESTER
infection after conception --> risk of fetal infection
1) diagnosis of primary infection,
2) no possibility of exclusion of primary infection
3) detection of typical fetal abnormalities in ultrasound (II–2B).
Cordocentesis – antibodies or antigens assessment
Amniocentesis – presence of toxoplasma DNA
Claasic congenital toxoplasmosis:
chorionitis and retinitisi,
High probability of intrauterine infection:
proved maternal infection
ultrasound markers of infection: intracranial calcifications, microcephaly, hydrocephaly, ascites, spleno- and hepatomegaly, severe IUGR
Does not decrease risk of vertical transmission
May decrease symptoms in a fetus/neonate
confirmed maternal infection
no fetal infection
Spiramycin – macrolid, concentrates in the placenta, poorly penetrates to the fetus, cannot be used in fetal infection treatment
Doses: 1g (3 mln j.) per os every 8 hours till the end of pregnancy if PCR in amniotic fluid was negative
Confirmed or strongly suspected fetal infection
Pyrimethamine – antagonist of folic acid, synergistic with sulfonamides. Should not be used in the 1st trimester (teratogenic potential). Cause transient, dose-dependent bone marrow suppresion – used together with folic acid.
Combined treatment with pyrimethamine and sulfadiazine – significan decrease of disease severity.
presence of specific IgM or IgA antibodies in neonatal serum
detection of patogen cysts in the placenta
rash, fever, hydrocephalus, hepato- and splenomegaly, jaundice, ascites, retinitis and choroinitis, seizures,, psychomotoric developement delay
most infections asymptomatic,
frequent cause of marbidity and mortalisty of people with immunodeficiency
the most frequent cause of congenital infections
0.2 – 2.4% of all neonates
belongs to the family of Herpesviridae (DNA)
most common cause of congenital infection and non-hereditary deafness.
PATHS OF CMV INFECTION
In early childchood, puberty and reproductive period by:
sexual contacts, droplets path, blood and it’s products, placenta
During delivery: vaginal discharge, cervical discharge
Fetal symptoms: ventriculomegaly and intracellular inclusions
primary, recurrent, infection reactivation, superinfection with another strain
PRIMARY CMV INFECTION
In first half of pregnancy:
malformations, low birth weight, intracranial calcifications , microcephaly
In second half of pregnancy:
acute infection with involvement of internal organs: hepatitis, pneumonia, purpura, thrombocytopenia
less dangerous for the fetus because antibodies have proctective effect, at the presence of IgG antibodies infection may be asymptomatic
INTRA- AND POSTPARTUM INFECTIONS (55%)
asymptomatic or mild infection
pneumonia, liver function deterioration
fever, fatigue, headache, muscle ache, cough, enlargement of lymph nodes, rarely hepatomegaly
90% asymptomatic infections
IgM (+) - acute infection - IgG (+)
IgG (+) - acute or previous infection
Increase of IgG from low to high titers during 2-3 weeks ⇒ reinfection
increased lymphocytes, thrombocytopenia
liver enzymes, virus culture, DNA of the virus (PCR)
ultrasound of the fetus: oligo- or polyhydramnios, ascites, intestinal paralysis, hydrops, IUGR, hepato- and splenomegaly, microcephaly, intracranial calcifications, ventriculomegaly
FETAL BLOOD TESTS
virus culture from amniotic fluid (confirms transmission of the virus, not infection)
There is no treatment of infection in the fetus
Symptomatic treatment of the pregnant women and prophylaxis
90% of children infected during pregnancy and delivery die before 10th year of life
HIV is non-teratogenic.
Vertical transmission – the most frequent cause of children HIV infections in the world.
Transmission during pregnancy, labor and breastfeeding (90%).
Antiviral polytherapy during pregnancy and labor and in the child for 46 weeks after delivery, elective cesarean section and avoiding breastfeeding may decrease incidence to 1%.
Infections from the mother:
65% - during labor,
10-20% - during breastfeeding
FACTORS INCREASING RISK OF VERTICAL TRANSMISSION
low number of CD4+ leukocytes,
high level of viremia
preterm delivery (all invasive procedures, premature amniotic fluid leakage for more than 4 hours)
infection in birth canal
The risk of pregnancy complications in HIV (+) women is low.
Vitamin A deficiency
REDUCING THE RISK OF VERTICAL TRANSMISSION OF HIV
zydovudine treatment (monitoring of maternal viremia)
elective cesarean section at 37 weeks,
preventing preterm delivery,
limiting exposition of the fetus to maternal blood – avoiding invasive diagnosis and therapy
infection treated before pregnancy, high risk of transmission → continuation in 1st trimester
not treated before pregnancy → treatment from 14th weeks
pregnant women in early stage of the disease, low risk of transmission → treatment from 14th week
MANAGEMENT OF HIV POSITIVE WOMEN
Papp smear every 6 months (dysplasia, CIN)
vaginal discharge culture (bacterias, fungus, chlamydia, gonorrhoea) → treatment is necessary !
tests for HCV, HBV
at 35 weeks – drugs for labor
cd4, viremia – every 12 weeeks
90% pass chickenpox in childhood, risk of disease during pregnancy – 5%
Up to 19 weeks – 1-2% of congenital malformations
After 20 weeks – 1.7% of shingles in childhood
Perinatal period – 20% symptomatic chickenpox in neonate, 30% mortality!!!
Symptoms in pregnanct woman from 5 days before to 3 days after delivery – VZIG for neonate!!!!!
Varicella (chickenpox) and herpes zoster (shingles)
defects of eyeballs
VZIG – up to 3-4 days after exposition, after confirming serologic status.
Treatment – Acyclowir
Not dangerous, fetus is protected by IgG
URINARY TRACT INFECTIONS
The most frequent infections during pregnancy.
The most frequent causes: E.Coli (90%), Proteus, Streptococcus Foecalis, Ureaplasma
Factors favoring infections:
anatomy (short urethra, proximity of vagina and anus
distention of ureters, renal pelvises and calyces (progesterone),
distention and displacement of urinary bladder
The most frequent form is urinary bladder infection (cystitis), frequently preceeded with asymptomatic bacteriuria.
Not treated leads to acute pyelonehritis with typical symptoms: Goldflam symptom, fever, pain, Dysuric symptoms.
All pregnant patients with pyelonephritis should be hospitalized
Asymptomatic bacteriuria – Amoxicillin 3g, Cefalexin 2g, Ampicillin 250-500mg for 14-21 days; Nitrofurantoin 50-100mg 4 x daily with vit. C for 14-21 days (hemolysis in cases of glucose-6-phosphate dehydrogenase)
Acute cystitis – Ampicillin, Nitrofurantoin for 14-21 days
Acute pyelonephritis – Ampicillin 1-2g 4 x daily for 6 weeks
Recurrent infections – Ampicillin 2x250mg daily, Nitrofurantoin 1x100 mg – till the end of pregnancy
Disorder of vaginal bacterial flora (lack of Lactobacillus), with growth of bacterias, mainly anaerobic (Gardnerella, Prevotella, Mycoplasma, Mobiluncus)
Amsel criteria: vaginal discharge pH >4.5, fish smell, clue cells, increased amount of white or gray vaginal discharge
PPROM, preterm delivery, low birth weight, chorioamnionitis
Group B streptococci (GBS)
preterm delivery, PPROM
puerperium infections: wound infections, endometritis, adnexitis, sepsis
pneumonia, upper respiratory tract infections
meningitis, encephalitis, sepsis
Screening for colonization with GBS in anus and vagina between 34 and 37 weeks of gestation.
Primary symptomatic genital herpes infection
Acyclovir 400mg orally 3 x daily for 7-10 days, or 200mg 5 x daily for 7-10 days
Acyclovir 400mg orally 3 x daily for 5 days or 200mg 4 x daily for 5 days.
Oral or intravenous treatment with standard doses of Acyclovir in 1st and 2nd trimester.
Continuation of treatment till delivery prevents recurrence and enables vaginal delivery.
HSV-1 – the orofacial infections and encephalitis
HSV-2 – the genital manifestation
causes spontanous abortion, stillbirth, IUGR, preterm labour, neonatal HSV sepsis syndrome and encephalitis
risk of vertical transmission of HSV (types 1 and 2) is greatest during primary maternal infection
Caesarean section is recommended for all women presenting with first-episode genital herpes at the time of delivery.
If a patient has frequent symptomatic recurrences during pregnancy, the use of acyclovir from 36 weeks is recommended, and vaginal delivery is not contraindicated.
Route of transmission
Intrauterine: via the transplacental (haematogenous) route any time during pregnancy.
Perinatal: shortly before onset of labour or during delivery via the haematogenous or genital route.
Postnatal transmission: Breastfeeding is the only vertical route.
foodborne illness caused by Listeria monocytogenes.
can result in fetal death or chronic intrauterine and congenital or perinatal infection.
1) early type – preterm labour, septic shock, pneumonitis
2) late type (7 days after labour)- meningitis, hydrocephalus
an acute child-age disease and is caused by Rubella virus –RNA virus
Spread is via respiratory droplets or in-utero transmission
If infection occurs in the first trimester of pregnancy, the risk of fetal infection and damage is high (about 90% in the first two months of pregnancy, and 50% in the third), and termination of pregnancy is usually recommended.
Congenital rubella syndrome
Eye defects including cataracts and congenital glaucoma.
Heart disease, including patent ductus arteriosus and peripheral pulmonary artery stenosis
Sensorineural deafness-the most common single defect
Central nervous system defects, Pigmentary retinopathy
Purpura, Hepatosplenomegaly and jaundice
Before pregnancy If immunity to rubella is not confirmed, the vaccine should be offered. It is recommended, that pregnancy should be avoided for 1 month after the vaccine is administered.
caused by Treponema pallidum
Untreated maternal syphilis results in fetal infection 75-90%
Early infection most often results in spontaneous abortion.
late infections often present in children over 2 years of age.
Veneral Disease Research Laboratory (VDRL) slide test or rapid plasma reagin (RPR) test should be performed at the first prenatal visit.
trepomnema test is used to confirm a positive result. These include : FTA – ABS, MHA – TP, TP – PA.
Penicillin is the treatment of choice
Erythromycin can be curative for the mother, but it does not prevent all congenital syphilis. Infants born to mothers treated with erythromycin or a non-penicillin regimen for syphilis during pregnancy should be retreated as though they have congenital syphilis.