Infeksi Dalam Kehamilan - English

8/21/2019 Infeksi Dalam Kehamilan - English

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Dr. Putri Mirani, SpOG

Sriwijaya University Faculty of Medicine


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TORCH

-Toxoplasma gondii

-Rubella virus

-Cytomegalovirus

-Herpes simplex virus


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Toxoplasmosis

Etiology

Toxoplasma gondii

Transmission

Encysted organism by eating raw orundercooked beef or pork

Contact with oocytes in infected cat feces


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Fetus can be infected transplacentally

Maternal infection

Symptom:Fatigue

Muscle pain

FeverChills

Maculopapular rash

Lymphadenophathy


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Most often maternal infection is subclinical

Infection in pregnancy abortion or live-born

infant with evidence of the disease

Fetal Effect

Overall < 4thinfected newborn with congenitaltoxoplasmosis have evidence of clinical illness

Later develop some sequelae of infection


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Clinically infected infant at birth:

LBW

Hepatosplenomegaly

Icterus

Anemia

Neurological disease: convulsion, intracranial

calcification, MR, hydrocephaly or microcephaly Almost all develop chorioretinitis


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Management Routine screening in US not recommended except

pregnant women with HIV infection

Active toxoplasmosis: antimicrobial treatmentrecommended

Spiramycin reduces incidence fetal infection but

not modify its severity

Pyrimethamine + sulfadiazine, esp if fetus infected


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Also known as German measles

Etiology: Rubella virus

Tipically cause minor infection in the absence ofpregnancy

Directly responsible for inestimabe wastage aswell as for severe congenital malforations duringpregnancy


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Maternal infection Viremia clinically evident disease 1 week

Disease manifestation:Lymphadenopathy

FeverMalaise

Arthralgia

Maculopapular rash begins on the face &spreads to the trunk & extremities


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Fetal Effects

Advance pregnancy fetal infection are less

likely to cause congenital malformations

Most sequelae seen before 20 weeks

Infant born with congenital rubella shed thevirus for many months threat to other infant as

well as to susceptible adults who come in contact

with them


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The extend rubella syndrome, with progressive

panencephalitis & type 1 DM ay not develop

clinically until the 2nd or 3rddecade of life

1/3 infant who are asymptomatic at birth

developmental injury later in life

Other late sequelae: thyroid dis., ocular damage,

MR


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CONGENITAL RUBELLA SYNDROME Eye lesion: cataracts, glaucoma, micropthalia and other

Heart disease: PDA, septal defects & pulmonary arterystenosis

Sensorineural deafness

CNS defect: meningoencephalitis

Fetal growth restriction

Throbocytopenia & anemia

Hepatitis, hepatosplenomegaly, jaundice

Chronic diffuse intersitial pneumonitis

Osseus changes

Chromosomal abnoralities


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To eradicated the disease completely it is

recommended to immunizing women in

chilbearing age

Rubella vaccination should be avoided

shortly before or during pregnancy


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DNA herpesvirus that eventuallyi nfects mosthuman

Most comon cause of perinatal infection

Fetal infection found in 0.5-2% of all newborninfant

Virus transmitted horizontally by droplet infectionvia saliva and urine, vertically from mother tofetus-infant, can also STD


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Maternal infection

No evidence that pregnancy risk or clinical

severity of maternal CMV infection

Most infection are asymptomatic

15% adult have mononucleosis-like synd, ex.Fever, pharyngitis, lymphadenopathy,

polyarthritis


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Primary infection transmitted to fetus 40%

severe morbidity

Infection during pregnancy are reccurent

Congenital infection from reccurent infection less

often associated with clinically apparentsequelae than those from primary infections


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Congenital Infection Congenital infection causes cytomegalic

inclusion disease, syndrome that includes:

LBW

Microcephaly

Intracranial calcifications

Chorioretinitis

Mental & motor retardation

Sensorineural deficits

Hepatosplenoegaly, jaundice

Hemolytic anemia & thrombocytopenic purpura


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Diagnosis

Primary infection fourfold-increased IgG titers inpaired acute & convalescent sera simultaneously

OR detecting maternal IgM CMV antibody

Recurrent infection not accompanied by IgMantibody

In some case effect of fetal infection aredetected by sonography


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Management

Currently no effective management for maternalinfection

Serological screening not recommended because

Not possible to predict which fetuses are infected

There is no vaccine

Attempts to identify and isolated infant secretingCMV expensive & impractical


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VZ-V is a member of DNA herpesvirus family

Almost 95% adults are immune

Primary infection causes chickenpox

Typical maculopapular & vesicular rashaccompanied by constitutional symp & fever for3-5 days


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Infection in adult tend to be more severe than inchildren

Varicella pneumonia is the most seriouscomplication

Develops in about 10% adults

Treatment for varicella pneumonia: oxygenation,assisted ventilation acyclovir IV 10mg/kg/8 hours


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Fetal Effects

Maternal chickenpox during first half of

pregnancy may cause congenital malformations

Chorioretinitis, cerebral cortical atrophy,

hydronephrosis, microcephaly, micropthalmia,

dextrocardia, cutaneous and bony leg defects


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No clinical evidence of congenital malformation

with infection after 20 weeks

The highest risk is between 13-20 weeks, withabsolute risk of embryopathy 2%

Fetal exposure just before or during delivery serious threat to newborn infant


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Management and Prevention

Administration of VZIG prevent or attenuate

infection if given within 96 hours

VZIG dose 125U/kg IM, with max dose 625 units

or 5 vials

Vaccine is not recommended for pregnant

women


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Most common serious liver disease encountered inpregnant women

At least 5 types: Hep A, B, C, D, E

A sixth agent; Hep. G virus a.k.a GBV-C

In many cases, infection are subclinical

Symptoms ay precede jaundice by 1-2 weeks

Symptoms: nausea, vomitting,headache, malaise andlow-grade fever


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Most fatalities due to fulminant hepatic necrosis

which later in pregnancy must be distinguished

from acute fatty liver

fulminant hepatitis have Hep. B infection

Hepatic encephalopathy fulminant hepatitis mortality 80%


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Chronic Hepatitis

May lead to cirrhosis and ultimately liver failure

Most cases due to chronic Hep B or C virus

infection

Pregnancy is uncommon when disease issevere because of anovulation


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There are 4 species of Plasmodium: vivax,

ovale, malariae, falcifarum

Transmitted by the bite of femaleAnophelesmosquito

Episodes 3-4-fold during the later twotrimesters of pregnancy and 2 months

postpartum


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Pregnancy enhanced severity of falciparummalaria, esp nonimmune, nulliparuos women

Insidence of abortion & preterm labor

Stillbirth may caused by plasental & fetalinfection

Neonatal infection is uncommon (7%)


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Clinical presentation

Fever & flu-like symptoms

Chills

Headache Myalgia

Malaise

Symptom may occur at intervals

Symptom less severe in immune patients


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May be asociated with anemia and jaundice

Falcifarum infection kidney failure, coma and

death

Diagnosis

Based on clinical features and identificationintracellular malaria organism on a blood smear


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Management

Commonly used antimalarial drugs NOT

contraindicated during pregnancy

Chloroquine is treatment of choice for all forms

of malaria EXCEPT chloroquine resistant

P.falciparum & newly emerging strains ofresistant P.vivax


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Severe malaria chloroquine IV

Woman with chloroquine resistant inf

Mefloquine orally

Severe resistant malaria Quinine or quinidineIV

Chemoprophylaxis pregnant women travelingto endemic area


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Prophylaxis initiated 1-2 weeks befor traveling

Chloroquine 300mg of base, PO once a week,

continue until 4 weeks after return to nonendemic areas

Travel to endemic area for chloroquine resistant

discouraged during early pregnancy

Infeksi Dalam Kehamilan - English

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