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55 Cards in this Set
- Front
- Back
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What are the 4 scenarios that can happen in perinatal infection |
1- feal demise or preterm birth 2- congenital abnormalities 3- serious neonatal consequences (when infection acquired around time of birth and transmitted through vaginal canal) 4- long term consequences\ disease (deafness at 6 yo) |
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How rubella transmitted and is there any preventive measures for transmission |
By droplets so mafi preventive measure |
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What is the aim of rubella susceptibility screening IF done?? |
We screen Ab (IgG) to check if there is immunity against rubella
If no, in current pregnancy there is nothing we can do as preventive —> it helps to vaccine AFTER delivery to prevent future pregnancies
MMR is live attenuated vax that is contraindic during pregnancy |
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Clinical symptoms ofmother with rubella |
Febrile rash Can be asymptomatic in up to 50% of cases |
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Congenital rubella defects |
Sensorineural deafness, blindness, cataracts, heart defect, encephalitis and microcephaly and endocrine problems |
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Transmission inc with ______ gestational age because ____but severity of infection _______ because ________ |
Increase because maturity of placent and more permeable Decrease severity with advanced gestational age (cz organogenesis already happened) |
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Risk of teratogenicity if infection before conception and if after 20 weeks |
Very lowwwww |
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Infection <16 weeks of rubella what should i consider |
Termination |
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Rublla encountered : indicate risk 0-16w 16-20w >20 w |
1- congenital rubella 2- minimal risk of deafness 3- no risk |
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How toxoplasmosis parasite transmitted and could it be prevented ?? |
Thro cat feces, soil or uncooked meat or unwashed vegetables Yes can be prevented tho hand washing and avoiding cats and uncooked meat (Cat feces can be encountered by cows and could contaminate plants and vegetablees) |
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Clinical presentation |
- Usually asymptomatic cervical lymphadenopathy - after IP of around 10 days non specific symptoms can occur as diffuse lymphadenopathy, low grade fever, malaise, myalgia, HSM - self limited and benign infec in immunocompetant adult |
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Should we treat toxoplasmosis even if it is asymptomatic in newborn ?? And what meds and how long if yes? |
Offcourse cz risk of hearing loss in first 6 years of life I need to treat for one year pyrimethamine and sulfadiazine and leucovorin |
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Toxoplasmosis triad in newborn |
1- chorioretinitis 2- hydrocephalus or microcephaly 3- periventricular calcifications |
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Clinical signs of toxoplasmosis at birth and later sequale |
Most are asymptomatic byt 90% develop later sequale as haring loss and blindness and neurodevelopmental delay |
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How to dx maternal infection ?? And what could complicate interpretation of results?? |
- Thro serological testing of antibodies IgG yaane chronic immunity IgM yaane acute infection - High titers of Both Igm AND IGG may persist for years complicating the diagnosis - high rate of false +ve and -ve can result and special lab should do the test |
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Negative IgM , +VE igG What i can interpret? Is she immunized? Does this reslt concern me? |
Previous infection occured No guaranteed immunity No concerns oftransmision cz not primary infec akid |
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Does negative igm and igg exclude acute infec? |
No cz can be window period were seroconversion didnt happen yet |
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Both igg and igm +ve what possibilities exist? Do i have alot of concerns?? What further tests is needed? |
1- recent infec, but ma ktir mnkhaf laeno it is no primary infec (+ve igg) —> repeat test in 2-3w to check if igg inc (showing recent infec) 2- false +ve (persist for years) - if infection confirmed: igg avidity testing needed (avidity inc with time) so i can estimate the time of infection and evaluate the risk |
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When my most concerns are? |
When acute infec during organogenesis |
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Do i care if infec occured before pregnancy |
Little to no risk |
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What is the principle of avidity |
Avidity is strength of ag-ab interaction Maturing b lymphocytes inc avidity of lymphocytes So binding of Ag to the igg still exist even if i add urea. |
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Do i have iu transmission in every maternal infection ?? |
Not nacessarily |
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How to dx fetal toxoplasmosis ?? Initial test? |
Initially we do US: we monitor any IC calcification, HSM, ascitis, microcephaly , IUGR —> IF THEY EXIST , i suspect infection 2- i should confirm dx by amniocentesis (after 18w o gestation) —> do pcr - before 18 w risk of false -ve |
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Le m hkina aan US in rubella |
Cz functional signs not seen on US And because im sure that there are defects if too early rubella infection is present |
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Fi routine screening for toxoplasmosis?? |
No , only in immunosuppressed px M ktir elon feyde |
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Primary syphilis clincal manifestions, |
Painless genital ulcers after 3-8 weeks after infection
Can be on cervix and go unnoticed |
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Prognosis of primary syphilis ? |
Either 1- self limited Or if untx can develop to 2- secondary syphilis |
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Describe secodary syphilis and when does it happen |
6 w to 6 m after infect Development of rash + \ or lesions of mucous membrane (condylomata lata) |
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Prognosis of secondary syphilis |
1- 20% develop tertiary cardiovascular syphilis 2- 10 % develop neurosyphilis |
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Early untreated syphilis in pregnant what happens to baby |
75% - 100% are infected 25% stillbirth |
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Penicllin g safe in preg? |
Yes |
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Fetal complications if vertical transmisiion of syphilis occur |
1- FGR and fetal hydrops, 2- congenital syphilis (which may cause long-term disability), 3- stillbirth, preterm birth and neonatal death |
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Routine screening for syphilis? |
Yes we screen ALL pregnant women cz tx is very effective |
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How do we screen? |
2 steps: test non treponemal abs and if +ve —> we go to treponemal ab testing to confirm dx |
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Non trepon tests are: Can they be false? |
VDRL and RPR Yes false negative or false positive in lupus px so further confirmation is essential |
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Treponemal test |
TPHA FTA |
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serological tests CAN detect syphilis in its incubation stage (25 DAYS) ?? |
None of these serological tests will detect syphilis in its incubation stage |
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Syphilis management |
1- search for other sti 2- test partners 3- test older children (screen for congenital infection) 4- penicillin g |
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Why do i prefer inhospiTal tx of syphilis ?? What symptoms can occur ? |
Because of jarish -herxheimer rxn which is release of proinflammatory cytokines from dying MO —> it is manageble but need close monitoring - rash and fever and worsening symptoms - uterine contractions and fetal distress |
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Should i treat baby if i treat the mom during pregnancy ?? |
Laa |
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What clinic presentation in neoborn with syphilis and doe he need tx? |
Asymptomatc aktr l waet He need immediate tx or he will HAVE DEVELOPMENTAL DELAY, SEIZURES or death |
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Bl syphilis baby has malformations? |
A2al ktir Predominant symptms are edema, IUGR, hydrops pretermbirth still birth w hek khbarrr |
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CMN transmission |
Thro sex, blood or body fluid contct |
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Adults symptoms with primary CMV |
Usually asypmpt, but can develop mononucleosis- like syndrome including fever, chills etc |
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Adults symptoms with primary CMV |
Usually asypmpt, but can develop mononucleosis- like syndrome including fever, chills etc |
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Cmv remainsin the body ?? |
Yes it repains latent , recurrence by rectivation otr reinfection (secondary infections) can occur |
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How vertical transmission of cmv?? And which route represent most sign risk for clinical sequalae |
1- transplacental (this one carries most sign risk) 2- during delivery (genital tract ecretions) 3- breastfeeding (if active infection)
CMV from 2&3 clinically are asymptomatic and not associated with severe neonatal sequelae |
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CMV babies a the adult are _____ |
Asymptomatic |
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Cmv is the _______ congenital infect (least or most common) |
Mossst |
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Symptomatic congeital CMV infection: |
Jaundice, HSM, petechiae , hydrops, GR , thrombocytopenia, myocarditis |
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• The incidence of severe fetal infection is much__________ after recurrent maternal infection than after ________ Infection In cmv and toxoplasmosos |
Lower
Primary |
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_____________ is typically the most severe sequela of secondary infection of CMV |
Congenital hearing loss |
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What MO can cause the fetus to have an aplastic anemia. And how clinically presented |
Parvovirus Presented as hydrops seen on US |
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What MO can cause pregnancy loss and preterm birth |
Listeria (moe still birth) Malaria (more low birth weight) Parvovirs (hydrops and aplastic anemia) |
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4 Infections if acquired around the time of delivery with serious neonatal consequences (check slide 47) |
Herpes GBS Chlamydia Gonorrhea |
