SEMINAR

ON

INTRAUTERINE INFECTION (CONGENITAL INFECTION)

GUIDE: CO-GUIDE:

DR. INDRA BHATI DR. HANSLATA GEHLOT

PRAMOTED BY :

DR. C.P. KACHHAWAHA

PRESENTED BY :

DR. DHARA

DR. S.N. MEDICAL COLLEGE,

UMAID HOSPITAL, JODHPUR (RAJ.)

INTRAUTERINE INFECTIONINTRAUTERINE INFECTIONOrOr

(CONGENITAL INFECTION(CONGENITAL INFECTION ))

DefinitionDefinition: - intrauterine infections are the : - intrauterine infections are the infections that occur in fetus during pregnancy infections that occur in fetus during pregnancy & child birth.& child birth.IntroductionIntroduction:: Fetal infections are an important Fetal infections are an important cause of mortality & morbidity. Mother may or cause of mortality & morbidity. Mother may or may not experience active symptoms of may not experience active symptoms of infection during pregnancy. Infection may occur infection during pregnancy. Infection may occur at any time during gestation and their at any time during gestation and their severity severity depending ondepending on 1.1. Virulence of the agent Virulence of the agent 2. Susceptibility & gestational age of fetus, and 2. Susceptibility & gestational age of fetus, and 3. Route of infection.3. Route of infection.

Most common and important fetal infections may beMost common and important fetal infections may be

Bacterial, Viral and ProtozoanBacterial, Viral and Protozoan Bacterial agents areBacterial agents are Group B streptococcal (strep. Group B streptococcal (strep.

agalactiae )agalactiae ) SyphilisSyphilis Escherichia coliEscherichia coli Staphylococcus aureusStaphylococcus aureus KlebsiellaKlebsiella ProteusProteus Pseudomonas auraginousPseudomonas auraginous ListeriaListeria TuberculosisTuberculosis

Viral agents areViral agents are CytomegalovirusCytomegalovirus Rubella Rubella HIVHIV Genital herpesGenital herpes VaricellaVaricella Viral hepatitisViral hepatitis Parvovirus B19 infectionParvovirus B19 infection

Protozoan agents Protozoan agents Toxoplasmosis Toxoplasmosis Malarial (Plasmodium)Malarial (Plasmodium)

The most serious and most common intrauterine The most serious and most common intrauterine infections, and the impact of these infections on the infections, and the impact of these infections on the mother and infant, are shortly discussed below.mother and infant, are shortly discussed below.

TORCH INFECTION: TORCHTORCH INFECTION: TORCH is acronym of is acronym of

T- T- ToxoplasmaToxoplasma

O-O- Other infections areOther infections areSyphilisSyphilisHepatitis viral infectionHepatitis viral infectionVericella zosterVericella zosterParvovirus B19Parvovirus B19Listeria Listeria E.coliE.coliGBS infectionGBS infection

R-R- RubellaRubella

C-C- Cytomegalovirus infectionCytomegalovirus infection

H-H- Herpes simplex virus Herpes simplex virus

ToxoplasmosisToxoplasmosisThis is a parasitic infection caused by Toxoplasma This is a parasitic infection caused by Toxoplasma gondii. gondii. Most infants are asymptomatic during the neonatal Most infants are asymptomatic during the neonatal period but manifestation occurs in 2nd & 3rd decade period but manifestation occurs in 2nd & 3rd decade of life.of life.

Parasite toxoplasma gondii exists in three formsParasite toxoplasma gondii exists in three forms:: The trophozoite (tachyzoite): The trophozoite (tachyzoite): Infect all nucleated cells in the host, replicate, and Infect all nucleated cells in the host, replicate, and cause cause

tissue damagetissue damage. . The tissue cyst (bradyzoite): The tissue cyst (bradyzoite): The second form of parasite is formed within host cell as The second form of parasite is formed within host cell as early early as the 8th day of an acute infection and probably as the 8th day of an acute infection and probably persists through- out the life of the host.persists through- out the life of the host.The skeleton, heart muscles, and brain are the most The skeleton, heart muscles, and brain are the most commoncommon sites for latent infection. sites for latent infection. The oocyst (sporozoite):The oocyst (sporozoite): are produced in the small intestine of cats. are produced in the small intestine of cats. Once shed, the oocyst sporulates in 1-5 days and Once shed, the oocyst sporulates in 1-5 days and becomes infectious, remain infectious for more than 1 becomes infectious, remain infectious for more than 1 yearyear

Route of infection:Route of infection: Infection occur through mouth by Ingestion of Infection occur through mouth by Ingestion of contaminated raw food, raw or uncooked meat contaminated raw food, raw or uncooked meat etc.etc.Tissue cyst and oocyst are resistant to stomach Tissue cyst and oocyst are resistant to stomach and small intestine but all forms of the parasite and small intestine but all forms of the parasite are destroyed by adequate freezing and are destroyed by adequate freezing and heating.heating.

Life cycleLife cycle:: cat is definitive host in which sexual phase of cat is definitive host in which sexual phase of

the cycle is completed.the cycle is completed. Oocyst excreted in cat Oocyst excreted in cat

fecesfeces..Contaminated soil ingested by birds, Contaminated soil ingested by birds, mammals, and man (intermediate host) mammals, and man (intermediate host)

Maternal infectionMaternal infectionMaternal infection with toxoplasma is mild or Maternal infection with toxoplasma is mild or asymptomatic. Most common clinical signs are asymptomatic. Most common clinical signs are adenopathy and fatigue without fever.adenopathy and fatigue without fever.Congenital infectionCongenital infection::Congenital transplacental transmission occurs Congenital transplacental transmission occurs only during only during acute maternal infectionacute maternal infection..Vertical transmission is low (15-20%) in first Vertical transmission is low (15-20%) in first trimester because placenta act as barrier but trimester because placenta act as barrier but foetal damage is high foetal damage is high While in third trimester infectivity is high While in third trimester infectivity is high (60%) but foetal damage is less as compare (60%) but foetal damage is less as compare fetal damage occur in early trimester. i.e. fetal damage occur in early trimester. i.e. increasing gestational age increases the fetal increasing gestational age increases the fetal infection rate but diminishes severity. infection rate but diminishes severity.

Rate of infectionRate of infection

1st trimester: 10-15 % but fetal damage is 1st trimester: 10-15 % but fetal damage is highesthighest2nd trimester: 25 % but fetal damage is less as compare2nd trimester: 25 % but fetal damage is less as compare3rd trimester: 60 % but fetal damage is 3rd trimester: 60 % but fetal damage is lowestlowest

Symptom:Symptom: Infected infant born with normal Infected infant born with normal appearance but manifestations occur after appearance but manifestations occur after several year of life.several year of life.

Chorioretinis – leads to blindness Chorioretinis – leads to blindness Hydrocephalus Hydrocephalus Intracranial calcification shows area of brain Intracranial calcification shows area of brain

damage by parasitedamage by parasite Hearing loss (deaf)Hearing loss (deaf) Mental retardationMental retardation SeizureSeizure Microcephaly Microcephaly Hepatoslenomegaly Hepatoslenomegaly Erythroblastosis Erythroblastosis

The classic triad of congenital toxoplasmosisThe classic triad of congenital toxoplasmosis HydrocephalusHydrocephalus ChorioretinitisChorioretinitis Intracranial calcificationIntracranial calcification

Diagnosis:Diagnosis: Most commonly used method is antibody Most commonly used method is antibody detectiondetection

Interpretation:Interpretation: IgG(-) IgG(-) IgM(-)IgM(-) no infection not immune no infection not immune

IgG(+)IgG(+)IgM(-)IgM(-) infection previous to prenancyinfection previous to prenancy

IgG(-)IgG(-)IgM(+)IgM(+) recent infection. Fetus at recent infection. Fetus at

riskrisk

IgG(+)IgG(+) acute or chronic infection. acute or chronic infection.IgM(+)IgM(+) repeat in 2 month repeat in 2 month

IgM stable---------old infection with persistently raised IgMIgM stable---------old infection with persistently raised IgMIgM to increasing-- infection acquired in the last 2 month IgM to increasing-- infection acquired in the last 2 month fetus at risk fetus at risk

Treatment:Treatment:

Aim is to decrease the incidence & severity of congenital Aim is to decrease the incidence & severity of congenital infection.infection.

If IgM positive i.e. acute infection start spiramycin therapy If IgM positive i.e. acute infection start spiramycin therapy Spiramycin 1gm for 3 weeks. Stop for 1 wk than restart. 3 Spiramycin 1gm for 3 weeks. Stop for 1 wk than restart. 3 cycle.cycle.

Spiramycin delays vertical transmission to fetus Spiramycin delays vertical transmission to fetus If intrauterine infection is establishaed pyrimethamine, If intrauterine infection is establishaed pyrimethamine,

sulfonamide, and folinic acid are added. sulfonamide, and folinic acid are added. Tab pyrimethamine 25mg +sulfadiszine 3 gm for 3weeks. Tab pyrimethamine 25mg +sulfadiszine 3 gm for 3weeks. Fetal infection diagnosed before 17 wks should be treated Fetal infection diagnosed before 17 wks should be treated

with sulfadiazine alone b/c in first trimester with sulfadiazine alone b/c in first trimester pyrimethamine may affect organogenesis.pyrimethamine may affect organogenesis.

Prevention:Prevention:

••There is no vaccine for toxoplasma but following measure There is no vaccine for toxoplasma but following measure reduces congenital infection reduces congenital infection

• • Cook meat to safe temperaturesCook meat to safe temperatures• • Peel or thoroughly wash fruits and vegetablesPeel or thoroughly wash fruits and vegetables• • Clean cooking surface and utensils that contain raw Clean cooking surface and utensils that contain raw

materialsmaterials• • Avoid feeding cat's raw or undercooked meat and keep Avoid feeding cat's raw or undercooked meat and keep

cats indoors cats indoors

Rubella-:Rubella-:

(German measles) (Rubella is a Grk word that means little (German measles) (Rubella is a Grk word that means little red). red). This virus typically causes infection of minor import in the This virus typically causes infection of minor import in the absence of pregnancy. absence of pregnancy. During pregnancy, however, it has been directly During pregnancy, however, it has been directly responsible for abortion and severe congenital responsible for abortion and severe congenital malformation.malformation.

CausativeCausative Agent is Rubella virus (Toga virus)Agent is Rubella virus (Toga virus)Wild rubella virus is highly contagious, with only minimal contact Wild rubella virus is highly contagious, with only minimal contact necessary for transmission. necessary for transmission. Rubella occurs predominantly in young children, adolescent and most Rubella occurs predominantly in young children, adolescent and most commonly in springtime.commonly in springtime.

Maternal manifestations:Maternal manifestations: Rubella cause fever, malaise, lymphadenopathy, facial rash, Rubella cause fever, malaise, lymphadenopathy, facial rash, postaurical adenopathy, flu-like symptom, arthralgia and arthritis are postaurical adenopathy, flu-like symptom, arthralgia and arthritis are characteristic of the condition.characteristic of the condition.

Immunity:Immunity: acquired immunity is life longacquired immunity is life long. . Second infections occurring during pregnancy are not Second infections occurring during pregnancy are not associated with congenital infections associated with congenital infections

Congenital infection:Congenital infection:

Rubella is one of the most teratogenic agent.Rubella is one of the most teratogenic agent.If infection occurs before 20 wks of gestation i.e. during organogenesis, If infection occurs before 20 wks of gestation i.e. during organogenesis, child born with severe congenital malformation known as congenital child born with severe congenital malformation known as congenital rubella syndrome.rubella syndrome.The possibilities of fetal infection are 61 % when maternal transmissions The possibilities of fetal infection are 61 % when maternal transmissions occur during the first 4 wks of gestation (post conception weeks). occur during the first 4 wks of gestation (post conception weeks). Possibilities are Possibilities are

61 %61 % at 4 wks at 4 wks26 %26 % at 5-8 wks at 5-8 wks08 %08 % at 9-12 wks at 9-12 wks<1 %, <1 %, after 12 wks after 12 wks

Infection in first week of gestation leads to spontaneous abortion.Infection in first week of gestation leads to spontaneous abortion.Congenital rubella syndrome:Congenital rubella syndrome: it comprisesit comprisesAuditory manifestation Auditory manifestation 60-75 %60-75 % (deafness) (deafness)Ophthalmic Ophthalmic 50-90 %50-90 % (blindness) (blindness)Cardiac manifestation Cardiac manifestation 40-85 %40-85 % (PDA) (PDA)Cerebral manifestation Cerebral manifestation 25-45 %25-45 %Prematuritly Prematuritly LBWLBWNeonatal thrombocytopenia Neonatal thrombocytopenia AnemiaAnemiaHepatitisHepatitisSkin lesion -blueberry manifestation Skin lesion -blueberry manifestation

Blueberry muffinBlueberry muffin

The extended congenital rubella syndrome:The extended congenital rubella syndrome: With progressive pan-encephalitis and type 1 diabetes, may not With progressive pan-encephalitis and type 1 diabetes, may not develop clinically until the 2nd or 3rd decade of life.develop clinically until the 2nd or 3rd decade of life.Transmission:Transmission: infection can be communicated 7 days before and 4 days after infection can be communicated 7 days before and 4 days after appearance of rash. Rash occurs 2-3 wks following exposure.appearance of rash. Rash occurs 2-3 wks following exposure.Rash usually last 3 days Rash usually last 3 days "3 day measles“"3 day measles“DiagnosisDiagnosis based on IgG & IgM antibodies detection. based on IgG & IgM antibodies detection.Sample may be chorionic villi sampling (CVS), amniotic fluid and fetal Sample may be chorionic villi sampling (CVS), amniotic fluid and fetal blood.blood.Most common used test is Most common used test is Haemagglutination inhibition test &Haemagglutination inhibition test & others are ELISA, RIA & IFA RT-PCRothers are ELISA, RIA & IFA RT-PCRTreatment:Treatment:There is no specific therapy for either maternal or congenital rubella There is no specific therapy for either maternal or congenital rubella infection.infection.Maternal disease is almost always mild and self-limiting.Maternal disease is almost always mild and self-limiting.If primary maternal infection occurs during the first 5 month of If primary maternal infection occurs during the first 5 month of pregnancy, termination option should be discussed with mother. pregnancy, termination option should be discussed with mother. Treatment of newly born babies is focused on management of the Treatment of newly born babies is focused on management of the complications.complications.Prevention:Prevention: Rubella is preventable infection. Rubella is preventable infection. Rubella vaccine as a part of MMR vaccine must be given to all Rubella vaccine as a part of MMR vaccine must be given to all female children during childhood.female children during childhood. Conception also should be avoided for 3 month following Conception also should be avoided for 3 month following vaccination.vaccination.

CYTOMEGALO VIRUS:CYTOMEGALO VIRUS:

Human herpes virus 5.CMV seed in Human herpes virus 5.CMV seed in body fluid of infected person such as body fluid of infected person such as Urine, Saliva, Blood, Tears, Semen, Urine, Saliva, Blood, Tears, Semen, Breast milk.Breast milk.

IncidenceIncidence 0.7-4 % of all pregnancies 0.7-4 % of all pregnancies complicated by primary infection. Upto 13.5 complicated by primary infection. Upto 13.5 % are complicated by recurrent infection.% are complicated by recurrent infection.

Maternal manifestations:Maternal manifestations: Maternal Maternal manifestations aremanifestations are mostly asymptomatic, mostly asymptomatic, about 15% develop mononucleosis like about 15% develop mononucleosis like syndrome characterized by fever, syndrome characterized by fever, pharyngitis, lymphadenopathy and pharyngitis, lymphadenopathy and polyarthritispolyarthritis. .

CMV infection in pregnancy leads to CMV infection in pregnancy leads to

congenital manifestations arecongenital manifestations are PneumoniaPneumonia Gastrointestinal manifestationGastrointestinal manifestation Retinal manifestation -blindness Retinal manifestation -blindness Neurological diseaseNeurological disease LBWLBW MicrocephalyMicrocephaly Hearing lossHearing loss Vision impairment Vision impairment Mental retardation Mental retardation ThrombocytopeniaThrombocytopenia HepatosplenomegalyHepatosplenomegaly IUGRIUGR Non immune hydrops Non immune hydrops

Ventriculomegaly & calcification in congenital Ventriculomegaly & calcification in congenital CMVCMV

CMV tetrad:CMV tetrad: Mental retardation,Microcephaly,ChorioretinitisMental retardation,Microcephaly,Chorioretinitis

& Cerebral calcification.& Cerebral calcification.

Primary CMV:Primary CMV: 30-40 % risk of fetal transmission, 10 % babies born with 30-40 % risk of fetal transmission, 10 % babies born with

clinical signs of infection, 30% with severe infection dies, 80% of clinical signs of infection, 30% with severe infection dies, 80% of

survivors have severe neurological morbidity.survivors have severe neurological morbidity.

Recurrent CMVRecurrent CMV 0.15-2% risk of fetal transmission. Infant are usually 0.15-2% risk of fetal transmission. Infant are usually

symptomatic. Most common sequelae is isolated hearing loss.symptomatic. Most common sequelae is isolated hearing loss.

Diagnosis:Diagnosis: detection of IgG & IgM antibodies detection of IgG & IgM antibodies

Treatment:Treatment: No specific treatment or vaccine is available for CMV No specific treatment or vaccine is available for CMV

infection.infection.

ImmunoglobinImmunoglobin:: Igs should be used as prophylaxis for susceptible Igs should be used as prophylaxis for susceptible

women against primary CMV infection in pregnancy.women against primary CMV infection in pregnancy.

Gancyclovir & Fascornet :Gancyclovir & Fascornet : These antiviral agents are effective in the These antiviral agents are effective in the

treatment and prophylaxis of the dissemination of CMV in adult treatment and prophylaxis of the dissemination of CMV in adult

immunocomprimised patient.immunocomprimised patient.

Herpes simplexHerpes simplex:: two types of virus HSV-1 & HSV-2. two types of virus HSV-1 & HSV-2.

HSV-1 responsible for the non genital herpes. Genital herpes usually HSV-1 responsible for the non genital herpes. Genital herpes usually

caused by HSV-2, is sexually transmitted disease that causes painful sore caused by HSV-2, is sexually transmitted disease that causes painful sore

on genitals. Women who have their first outbreak of genital herpes during on genitals. Women who have their first outbreak of genital herpes during

pregnancy are at high risk miscarriage or delivering a low birth weight pregnancy are at high risk miscarriage or delivering a low birth weight

baby.baby.

According to American college of Obstetricians and Gynecologists, HSV-2 According to American college of Obstetricians and Gynecologists, HSV-2

infections clinically may be divided into three groups:infections clinically may be divided into three groups:

1. 1. Primary infection Primary infection is indicated by no prior antibodies to HSV-1 or HSV-2.is indicated by no prior antibodies to HSV-1 or HSV-2.

2. 2. NonprimaryNonprimary first episode defines newly acquired HSV-2 infection with first episode defines newly acquired HSV-2 infection with

preexisting HSV-1 cross reacting antibodies.preexisting HSV-1 cross reacting antibodies.

3. 3. Recurrent infection Recurrent infection is reactivation of prior HSV-1 or HSV- 2 infection in is reactivation of prior HSV-1 or HSV- 2 infection in

the presence of antibodies to the same type of HSV.the presence of antibodies to the same type of HSV.

Congenital infection:Congenital infection: Majority infections 85% occur during birth . Majority infections 85% occur during birth .

5% infection occur in intra uterine life. 10% acquired postnataly 5% infection occur in intra uterine life. 10% acquired postnataly

Risk of vertical transmission from mother to fetusRisk of vertical transmission from mother to fetus

a. 30-60 % if primary genital HSV infection at the time a. 30-60 % if primary genital HSV infection at the time of of

delivery.delivery.

b. 3 % if recurrent genital lesion at deliveryb. 3 % if recurrent genital lesion at delivery

Symptoms: manifests in 3 form Symptoms: manifests in 3 form

1. Skin eye mouth herpes (best prognosis) external lesion but no 1. Skin eye mouth herpes (best prognosis) external lesion but no

internal organ involvement. Disease is localized to the skin, eye, or internal organ involvement. Disease is localized to the skin, eye, or

mucocutaneous membranes. Vesicles typically appear on the 6th mucocutaneous membranes. Vesicles typically appear on the 6th

to 9th day of neonatal life. Infants with three or more recurrence of to 9th day of neonatal life. Infants with three or more recurrence of

vesicles have an increased risk of neurological complications.vesicles have an increased risk of neurological complications.

2. CNS infection . Herpes infection of brain 2. CNS infection . Herpes infection of brain & CNS (high morbidity & mortality) & CNS (high morbidity & mortality) presents as Encephalitis, seizure, presents as Encephalitis, seizure, lethargy, tremors, irritibilty, feed poorly, lethargy, tremors, irritibilty, feed poorly, unstable temp. bulged frontanaele. unstable temp. bulged frontanaele. Symptom develop 10th to 14th day of life.Symptom develop 10th to 14th day of life.3. Disseminated herpes (DIS) infection. 3. Disseminated herpes (DIS) infection. Most severe form of infection with highest Most severe form of infection with highest mortality. Affects internal organs as liver mortality. Affects internal organs as liver lungs lungs

Other Other 4. Prematurity 4. Prematurity 5. Sepsis 5. Sepsis

ACOG Recommendation for the HSV infections in the ACOG Recommendation for the HSV infections in the pregnancypregnancy

Women with active recurrent genital herpes should be offered Women with active recurrent genital herpes should be offered suppressive viral therapy at or beyond 36 wks of gestation.suppressive viral therapy at or beyond 36 wks of gestation.

LSCS delivery is indicated in women with active genital herpes LSCS delivery is indicated in women with active genital herpes or prodromal symptoms or prodromal symptoms

LSCS is not recommended for women with a h/o HSV infection LSCS is not recommended for women with a h/o HSV infection but no active lesions during labor.but no active lesions during labor.

Routine antepartum genital HSV cultures in asymptomatic Routine antepartum genital HSV cultures in asymptomatic patient not recommended patient not recommended

Routine HSV screening of pregnant women is not Routine HSV screening of pregnant women is not recommended.recommended.

Management:Management: active herpes with a term pregnancy—cesarean active herpes with a term pregnancy—cesarean sectionsection

Antiviral agents such as vidarabin & acyclovir should be start Antiviral agents such as vidarabin & acyclovir should be start at 38 wks of gestation.at 38 wks of gestation.

Mother and infant with HSV should be in contact isolation.Mother and infant with HSV should be in contact isolation. Antiviral agents should be given to infant as per clinical Antiviral agents should be given to infant as per clinical

manifestation. manifestation.

Other Infection:Other Infection:

Syphilis:Syphilis: causative agent is Treponema pallidum, a spirochete which is readily causative agent is Treponema pallidum, a spirochete which is readily

identified by dark field microscopyidentified by dark field microscopy. Worldwide approximate 1 million . Worldwide approximate 1 million

pregnancies are affected by syphilis and pregnancies are affected by syphilis and 46% of them end up in abortion or 46% of them end up in abortion or

perinatal death,perinatal death, 27% premature 27% premature and 27%are born with congital syphilis. and 27%are born with congital syphilis.

Route of infectionRoute of infection:: in women syphilis is acquired by sexual contact through in women syphilis is acquired by sexual contact through

small abrasion on skin and genital mucosa.small abrasion on skin and genital mucosa.

Maternal infection:Maternal infection:.. There are 30% chance of acquire the disease following There are 30% chance of acquire the disease following

exposure to an infected sexual partner.exposure to an infected sexual partner.

Incubation period is about 3 wks but range is 9-90days.Incubation period is about 3 wks but range is 9-90days. Any stage of infectious Any stage of infectious

maternal syphilis may result in fetal infectionmaternal syphilis may result in fetal infection

Pathological changes in placenta:Pathological changes in placenta:

With syphilitic infection placenta becomes With syphilitic infection placenta becomes

large and pale. Microscopically villi large and pale. Microscopically villi

appear to have lost their characteristic appear to have lost their characteristic

arborescent appearance and to have arborescent appearance and to have

become thicker and club shaped. Vessels become thicker and club shaped. Vessels

markedly diminish in number and in markedly diminish in number and in

advanced case almost entirely disappear.advanced case almost entirely disappear.

IncidenceIncidence

Lesions:Lesions: Primary chancrePrimary chancre are are painlesspainless, red, round , red, round

ulceration with an indurate base and well formed ulceration with an indurate base and well formed border and local painless lymphadenopathy. border and local painless lymphadenopathy. Frequency of perinatal transmission is 40-50 %.Frequency of perinatal transmission is 40-50 %.

Secondary lesionSecondary lesion target like lesions on palmar target like lesions on palmar and plantar surface are characteristic lesion. and plantar surface are characteristic lesion. Other lesions are cutaneous rash, mucous patch, Other lesions are cutaneous rash, mucous patch, codyloma latum of genitalia, and generalized codyloma latum of genitalia, and generalized lymphadenopathy. Frequency of perinatal lymphadenopathy. Frequency of perinatal transmission is 40-50 %.transmission is 40-50 %.

Tertiary lesionsTertiary lesions involved CNS(neurosyphilis) involved CNS(neurosyphilis) cardiovascular system and bones. Frequency of cardiovascular system and bones. Frequency of perinatal transmission is < 10 %perinatal transmission is < 10 %

Diagnosis:Diagnosis: syphilis cause serological reactions that are syphilis cause serological reactions that are used for confirmation of disease used for confirmation of disease

Non specific Non specific RPR (rapid plasma reagin)RPR (rapid plasma reagin)VDRL (venereal disease research laboratory)VDRL (venereal disease research laboratory)

Specific reactionsSpecific reactionsFTA ABS (Fluorescent treponemal antibody FTA ABS (Fluorescent treponemal antibody

absorption absorption test) test) MHATP (micro agglutinationassay for antibodies MHATP (micro agglutinationassay for antibodies

against T.pallidum)against T.pallidum)Congenital syphilis:Congenital syphilis: T. pallidum can cross placenta and T. pallidum can cross placenta and

cause congenital fetal infection at any time during cause congenital fetal infection at any time during pregnancy. Mostly occur in 4th month of pregnancy. pregnancy. Mostly occur in 4th month of pregnancy. Congenital syphilis is a multisystem disease. Organism may Congenital syphilis is a multisystem disease. Organism may cause: cause: StillbirthStillbirth

PretermPreterm Growth retardationGrowth retardation Fetal hydropsFetal hydrops Neonatal infectionNeonatal infection

Manifestations of Congenital syphilisManifestations of Congenital syphilis Most of infant look healthy at birth few, has vesicular bullous Most of infant look healthy at birth few, has vesicular bullous

eruption usually on palm & sole. From 4 days to 3 wks of life, eruption usually on palm & sole. From 4 days to 3 wks of life, symptom may begin and may be grouped as follows:symptom may begin and may be grouped as follows:1. Flu like syndrome 1. Flu like syndrome Meningeal signMeningeal sign Lacrimation (iritis)Lacrimation (iritis) Nasal discharge mucous membrane red swollen eroded loaded Nasal discharge mucous membrane red swollen eroded loaded

with T pallidum with T pallidum Sore throat pharynx with mucous patch.Sore throat pharynx with mucous patch. Generalized arthralgia splinting of arms and legs, Generalized arthralgia splinting of arms and legs,

osteochondritis on x-ray film, periostitis particularly tibia osteochondritis on x-ray film, periostitis particularly tibia (saber sign)(saber sign)

2. Generalized lymphadenopathy 2. Generalized lymphadenopathy Cervical, epitrochlear, inguinal, axillary, poplitealCervical, epitrochlear, inguinal, axillary, popliteal Hepatoslenomegaly- if severe, probability of aneamia, purpura, Hepatoslenomegaly- if severe, probability of aneamia, purpura,

jaundice, edema, hypoalbuminemiajaundice, edema, hypoalbuminemia3. Rash 3. Rash Maculopapular, postular, and bullous eruptions may all appear Maculopapular, postular, and bullous eruptions may all appear

together together Occasionally postular lesions may coalesce to form condyloma latumOccasionally postular lesions may coalesce to form condyloma latum

Hutchinson teeth in congenital syphilis Periostitis of long bone in infant

IncidenceIncidence of preterm delivery is 50% in mother of preterm delivery is 50% in mother with primary & secondary syphilis, 20% in latent with primary & secondary syphilis, 20% in latent syphilis and 9% in late syphilis.syphilis and 9% in late syphilis.

DiagnosisDiagnosis based on type of lesions based on type of lesions By dark field microscopic examinationBy dark field microscopic examination VDRL & RPR for screeningVDRL & RPR for screening FTA ABS & MHA TP for confirmation FTA ABS & MHA TP for confirmation Causes of false positive RPR & VDRL tests Causes of false positive RPR & VDRL tests

are are Autoimmune diseaseAutoimmune disease Febrile illnessFebrile illness Intravenous drug abuseIntravenous drug abuse Immunization Immunization Lab. ErrorLab. Error

Treatment Treatment Early latent syphilis:Early latent syphilis: (<1 year) benzathine (<1 year) benzathine

penicillin G 2.4 million units IM in single dose penicillin G 2.4 million units IM in single dose Late Latent syphilisLate Latent syphilis (>1 year) benzathine (>1 year) benzathine

penicilline G 7.2 million units total dose, 2.4 penicilline G 7.2 million units total dose, 2.4 million units IM each week interval million units IM each week interval

Neurosyphilis :Neurosyphilis : procaine penicillion G 7.2 procaine penicillion G 7.2 million units im once daily plus million units im once daily plus probenecid,500 mg qid both for 10-14 days.probenecid,500 mg qid both for 10-14 days.

Rx of syphilis in penicilline sensitive PtRx of syphilis in penicilline sensitive PtDesensitization Desensitization Erythromycin 500 mg qid for 15 days Erythromycin 500 mg qid for 15 days Tetracycline 500 mg qid for 15 days Tetracycline 500 mg qid for 15 days

Listeria Monocytogenes:Listeria Monocytogenes: gram positive rod gram positive rod shaped bacteria. Listeria monocytogenes generally shaped bacteria. Listeria monocytogenes generally occurs in pregnancy with immunocompromised. Most occurs in pregnancy with immunocompromised. Most common serotype is 1/2a, 1/2b,4b. Listeria common serotype is 1/2a, 1/2b,4b. Listeria monocytogenes is a intracellular pathogens that monocytogenes is a intracellular pathogens that commonly occurs in deficit cell mediated immunity. commonly occurs in deficit cell mediated immunity. Because of intracellular it is not eliminated by Because of intracellular it is not eliminated by antibodies. It cause invasive syndrome such as antibodies. It cause invasive syndrome such as Meningitis Meningitis SepsisSepsisChorioamnionitisChorioamnionitisStillbirth Stillbirth IUD IUD Recurrent abortion Recurrent abortion

Rx Rx iv ampicillin, penicillin with amino glycoside.iv ampicillin, penicillin with amino glycoside.

Viral Hepatitis:Viral Hepatitis: viral hepatitis is an infection that viral hepatitis is an infection that may have serious implication during pregnancy. may have serious implication during pregnancy. There are atleast five types of viral hepatitis A,B,D, There are atleast five types of viral hepatitis A,B,D, C, & EC, & E

A, C, D, & E –RNA Virus A, C, D, & E –RNA Virus B- DNA VirusB- DNA Virus Hepatitis B & C may transmit through placenta to Hepatitis B & C may transmit through placenta to

fetus and cause congenital infection. Hepatitis E is fetus and cause congenital infection. Hepatitis E is not transmitting through placenta but cause not transmitting through placenta but cause fulminanatfulminanat hepatitishepatitis in pregnancy. in pregnancy.

Hepatitis A:Hepatitis A: is uncommonly diagnosed during is uncommonly diagnosed during pregnancy because signs & symptoms are pregnancy because signs & symptoms are unspecific and the majority of infected individual are unspecific and the majority of infected individual are asympomatic. The virus is nonteratogenic and there asympomatic. The virus is nonteratogenic and there is no evidence of vertical transmission. The infection is no evidence of vertical transmission. The infection may cause an increased frequency of preterm birth. may cause an increased frequency of preterm birth. The diagnosis is made by determination of specific The diagnosis is made by determination of specific antihepatitis a virus IgM.antihepatitis a virus IgM.

RxRx Bed rest & supportive therapy.Bed rest & supportive therapy.Adequate nutrition.Adequate nutrition.

Hepatits BHepatits B is the cause of 40-45 % of all case of is the cause of 40-45 % of all case of hepatitishepatitis

IncidenceIncidence 1-2/1000 de novo1-2/1000 de novo 5-15/1000 chronic infection5-15/1000 chronic infection Hepatitis B partially double stranded DNA virus. HBsAg is Hepatitis B partially double stranded DNA virus. HBsAg is

marker of ongoing HBV infection, its persistency marker of ongoing HBV infection, its persistency indicates chronic infection.indicates chronic infection.

HBeAg is marker of infectivity and viral replication.HBeAg is marker of infectivity and viral replication. Transmission:Transmission: highly infectious agent. highly infectious agent. Maternal infectionsMaternal infections:: pregnant women may be affected pregnant women may be affected

by acute HBV infection or chronic infection. Acute by acute HBV infection or chronic infection. Acute infection is manifestes by Flu like symptoms in 25 % pt., infection is manifestes by Flu like symptoms in 25 % pt., rest are asymptomatic. 90% of individuals have rest are asymptomatic. 90% of individuals have spontaneous complete resolution of acute infection, spontaneous complete resolution of acute infection, fewer then 1% will die due to fulminant hepatis and 5-fewer then 1% will die due to fulminant hepatis and 5-10% become chronic carrier manifested by continous 10% become chronic carrier manifested by continous presence of HbsAg in their serum.presence of HbsAg in their serum.

Chronic carrier hepatitis Chronic carrier hepatitis -70% having chronic persistent hepatitis -70% having chronic persistent hepatitis (disease does not progress and liver enzyme are (disease does not progress and liver enzyme are normal)normal)-30% having chronic active hepatitis follow a -30% having chronic active hepatitis follow a different course and frequently develop different course and frequently develop cirrhosis, hepatic failure and primary HCC.cirrhosis, hepatic failure and primary HCC.

Diagnosis Diagnosis based on antigens antibody HBsAg Anti based on antigens antibody HBsAg Anti HBcAg, antiHBsAg liver enzyme will elevated.HBcAg, antiHBsAg liver enzyme will elevated.Persistency of HBsAg indicate chronic infection.Persistency of HBsAg indicate chronic infection.Presence of HbeAg indicated highly infectious Presence of HbeAg indicated highly infectious carriercarrier

ScreeningScreening all pregnant women should be all pregnant women should be screened for HBV infectionscreened for HBV infectionScreening is usually performed during the first Screening is usually performed during the first prenatal checkup timeprenatal checkup time

Neonatal transmission:Neonatal transmission: most newborns are results most newborns are results of vertical transmission from chronic carrier or follow of vertical transmission from chronic carrier or follow acute infection in last trimester of pregnancy.acute infection in last trimester of pregnancy.

Incidence in 1st & 2nd trimester is 10 %Incidence in 1st & 2nd trimester is 10 % when the acute infection occurs in the 3rd trimester, when the acute infection occurs in the 3rd trimester,

80-90% of the new born will be infected. The higher 80-90% of the new born will be infected. The higher risk of vertical transmission is from chronic carrier risk of vertical transmission is from chronic carrier with positive HBeAg.with positive HBeAg.

Transplacental infection of the fetus is rare and viral Transplacental infection of the fetus is rare and viral DNA rarely found in the Amniotic fluid and cord blood.DNA rarely found in the Amniotic fluid and cord blood.

Most neonatal infection are the result of contact with Most neonatal infection are the result of contact with infected maternal blood and vaginal secretions during infected maternal blood and vaginal secretions during parturition or acquired during breast feeding.parturition or acquired during breast feeding.

Infected new born are usually asymptomatic but if Infected new born are usually asymptomatic but if they are untreated, approximately 85% will they are untreated, approximately 85% will developed chronic infection.developed chronic infection.

Breast feeding should be discourage in infant born Breast feeding should be discourage in infant born from HBsAg positive mother.from HBsAg positive mother.

Prevention of Neonatal infection :Prevention of Neonatal infection : Can be Can be prevented by generalized screening of the overall prevented by generalized screening of the overall obstetrical population and administration of hepatitis B obstetrical population and administration of hepatitis B Ig and hepatitis B recombinant vaccine to the new Ig and hepatitis B recombinant vaccine to the new born of women positive for HBsAg.born of women positive for HBsAg.

In case of HBsAg positive mother, HBeAg should be In case of HBsAg positive mother, HBeAg should be done ,if positive than active and passive immunization done ,if positive than active and passive immunization to baby should be provided to baby should be provided

Current recommendation is to administer HBV immuno Current recommendation is to administer HBV immuno globulin 0.5 ml im to new born within 12 hrs of Birth globulin 0.5 ml im to new born within 12 hrs of Birth followed by the first dose of hepatitis B vaccine 0.5 ml followed by the first dose of hepatitis B vaccine 0.5 ml im at birth then 1month and 6 month.im at birth then 1month and 6 month.

Efficacy of active and passive immunization is 85%-Efficacy of active and passive immunization is 85%-95%.95%.

Vaccination for HBV infection can be performed during Vaccination for HBV infection can be performed during pregnancy and is Advisable in Sero-negative women at pregnancy and is Advisable in Sero-negative women at high risk for infection.high risk for infection.

Hepatitis CHepatitis C it affects 1-5% of all pregnancy and is it affects 1-5% of all pregnancy and is more frequent in women with HIV infection.more frequent in women with HIV infection.

Transmission Transmission infection acquired through infection acquired through infected blood & blood productsinfected blood & blood products by sexual intercourseby sexual intercourse vertical transmission during pregnancyvertical transmission during pregnancy (3-6%). (3-6%). Chronicity is more with hepatitis C infection as Chronicity is more with hepatitis C infection as

compare to HBV.compare to HBV. Majority of hepatitis C virus infection are Majority of hepatitis C virus infection are

asymptomatic.asymptomatic. Liver enzymes are elevated and chronicity develop Liver enzymes are elevated and chronicity develop

cirrhosis cirrhosis TreatmentTreatment

symptomatic supportsymptomatic supportin symptomatic patient alpha-interferon in symptomatic patient alpha-interferon

and and antiviral ribavirin is benefialantiviral ribavirin is benefial

Malaria: Malaria: malaria is protozoal parasitic infestation. malaria is protozoal parasitic infestation. causative agentcausative agent is Plasmodiumis Plasmodium has four species P. has four species P. vivex, P.falciparum, P.malarae, P.ovalevivex, P.falciparum, P.malarae, P.ovale

Route of infection mosquito bite,infected blood Route of infection mosquito bite,infected blood transfusion,transplacental transfer from mother to transfusion,transplacental transfer from mother to fetus during pregnancy.fetus during pregnancy.

P.falciparum is responsible for most of deathsP.falciparum is responsible for most of deaths Placental parasitization occurs in 15-60%of affected Placental parasitization occurs in 15-60%of affected

person. Passive transfer of antibodie to the fetus person. Passive transfer of antibodie to the fetus occur, hence congenital malaria is rare.occur, hence congenital malaria is rare.

Maternal manifestation:Maternal manifestation:Fever -three phage cold, hot, sweating. Fever -three phage cold, hot, sweating. VomitingVomitingMalaiseMalaiseHeadacheHeadacheCerebral malariaCerebral malaria

Effects on pregnancyEffects on pregnancy:: increased risk of increased risk of Abortion, Preterm, IUGR, IUD, HyperpyrexiaAbortion, Preterm, IUGR, IUD, Hyperpyrexia Anaemai, Convulsion, Hypoglycemia & Jaundice.Anaemai, Convulsion, Hypoglycemia & Jaundice.

Complication:Complication: HypoglycemiaHypoglycemia DehydrationDehydration AcidosisAcidosis AnaemiaAnaemia Renal failureRenal failure Acute pulmonary oedemaAcute pulmonary oedema CoagulopathyCoagulopathy ConvulsionConvulsion Circulatory collapseCirculatory collapse Fluid & electrolyte imbalanceFluid & electrolyte imbalance Jaundice Jaundice & Death.& Death.

M/MM/M:: investigation PBF, MP-QBC, PCR investigation PBF, MP-QBC, PCR Rx:- Rx:- Antimalarial medicationAntimalarial medication

Supportive medicationSupportive medication Nursery care.Nursery care.

HIVHIV The human immunodeficiency virus is the cause The human immunodeficiency virus is the cause of the acquired immune deficiency syndrome of the acquired immune deficiency syndrome (AIDS).HIV is infecting a growing number of women in (AIDS).HIV is infecting a growing number of women in the reproductive age and as a consequence the the reproductive age and as a consequence the number of infant born to HIV infected mother is also number of infant born to HIV infected mother is also rapidly increasing.rapidly increasing.

There is a significant difference in the incidence, There is a significant difference in the incidence, progression of HIV infection, and use of therapeutic progression of HIV infection, and use of therapeutic agents between industrialized and underdeveloped agents between industrialized and underdeveloped countries.countries.

There are five type of retroviruses HIV-1, HIV-2, HIV-I, There are five type of retroviruses HIV-1, HIV-2, HIV-I, HIV-II, and HIV-IV, three of them are associated with HIV-II, and HIV-IV, three of them are associated with human disease. HIV-1, HIV-2 cause of AIDS and HIV-I human disease. HIV-1, HIV-2 cause of AIDS and HIV-I is also causal agent of T cell leukemia/lymphoma. is also causal agent of T cell leukemia/lymphoma. Attachment of the virus to the host cell is a critically Attachment of the virus to the host cell is a critically important step in the mechanism of infection. important step in the mechanism of infection.

Individuals at high risk for HIV Individuals at high risk for HIV infectioninfection

Prostitutes (sex worker)Prostitutes (sex worker) IV drug abusersIV drug abusers Women whose partners areWomen whose partners are

Know HIV positive Know HIV positive

IV drug abusersIV drug abusers

HemophiliacsHemophiliacs

Homosexual experiencesHomosexual experiences Blood transfusion before 1985 Blood transfusion before 1985

Maternal infectionMaternal infection Maternal HIV is acquired primarily by sexual contact Maternal HIV is acquired primarily by sexual contact

or by parenteral exposure to infected blood or blood or by parenteral exposure to infected blood or blood products. Most sexual transmission is result of products. Most sexual transmission is result of receptive vaginal or anal intercourse with infected receptive vaginal or anal intercourse with infected partners.partners.

Most of pregnant women with infection are Most of pregnant women with infection are asymptomatic in carrier phase. asymptomatic in carrier phase.

Characteristics sign & symptomCharacteristics sign & symptom: generalized lymph : generalized lymph node enlargement, fever, night sweats, weight loss node enlargement, fever, night sweats, weight loss and unusual recurrent infection such as herpes or and unusual recurrent infection such as herpes or candidias.candidias.

Final stage of disease is severe dysfunction of Final stage of disease is severe dysfunction of immune system that is characterized by local immune system that is characterized by local infections or opportunistic infections such as infections or opportunistic infections such as candidias, CMV, herpes, histoplama, Cryptococcus, candidias, CMV, herpes, histoplama, Cryptococcus, pneumocystis carinii develop Kaposi's sarcoma, pneumocystis carinii develop Kaposi's sarcoma, lymphoma of the brain or multiple recurrent bacterial lymphoma of the brain or multiple recurrent bacterial infection.infection.

Fetal transmissionFetal transmission:: Approximately 24% of infants born to HIV infected Approximately 24% of infants born to HIV infected

mother will demonstrate the presence of the disease mother will demonstrate the presence of the disease by 1 year of age. The virus is excreted in breast milk by 1 year of age. The virus is excreted in breast milk and breast feeding is contraindicated in HIV infected and breast feeding is contraindicated in HIV infected women. In non breast feeding mother 60-80% of women. In non breast feeding mother 60-80% of transmission occurs during labor & delivery & rest transmission occurs during labor & delivery & rest during antepartum. during antepartum. Frequency of vertical Frequency of vertical transmission increases in relation to the duration of transmission increases in relation to the duration of rupture of membranesrupture of membranes and caesarian section is and caesarian section is protective. protective.

The majority of babies born to HIV-positive mothers The majority of babies born to HIV-positive mothers have no physical signs of infection. Few of them may have no physical signs of infection. Few of them may exhibit the HIV embryopathy characterized by exhibit the HIV embryopathy characterized by Growth retardation, Microcephaly, and craniofacial Growth retardation, Microcephaly, and craniofacial abnormalities. abnormalities.

Preventive measure Preventive measure 1.Detection of HIV infection during pregnancy1.Detection of HIV infection during pregnancy – –

screening test for HIV should be done in 1st ANC screening test for HIV should be done in 1st ANC visit.visit.

2.Antepartum care2.Antepartum care a. evaluation for other STDa. evaluation for other STD b. serial USG to follow fetal growthb. serial USG to follow fetal growth c.c. weekly nonstrees test after 32 wks weekly nonstrees test after 32 wks d. measurement of CD4 cells every trimesterd. measurement of CD4 cells every trimester

I.I. If CD 4 cell count is greater than 500 regular If CD 4 cell count is greater than 500 regular obstetric careobstetric care

II.II. If CD4 cell count is less than 500, start If CD4 cell count is less than 500, start azidothymidine(AZT),100 mg five times daily.azidothymidine(AZT),100 mg five times daily.

III.III.If CD4 cell less than 200, start prophylaxis for If CD4 cell less than 200, start prophylaxis for opportunistic infections.opportunistic infections.

3.Intrapartum management3.Intrapartum management A.A. If patient not taking any ART agent start ZDV it reduce If patient not taking any ART agent start ZDV it reduce

frequency of infection to 5-8%.frequency of infection to 5-8%.B.B. If baby is delivered by LSCS with ZDV neonatal If baby is delivered by LSCS with ZDV neonatal

incidence is 2%incidence is 2%C.C. In the absence of treatment or LSCS incidence of In the absence of treatment or LSCS incidence of

neonatal infection is about 25%neonatal infection is about 25%D.D. LSCS indicated in case, if >1000 copies/ml viral copy.LSCS indicated in case, if >1000 copies/ml viral copy.E.E. ZDV-2 mg/kg IV in 1 hrs than 1mg/kg IV infusion till ZDV-2 mg/kg IV in 1 hrs than 1mg/kg IV infusion till

delivery & to newborn 2 mg/kg oral stat than 1mg/kg 6 delivery & to newborn 2 mg/kg oral stat than 1mg/kg 6 hrsly for 6 wks hrsly for 6 wks

4.4. Postpartum care-Postpartum care- universal precaution should be universal precaution should be continue in postpartum period. The mother should be continue in postpartum period. The mother should be instructed to avoid breast feeding.instructed to avoid breast feeding.

5. HAART-5. HAART- highly active antiretroviral therapy. highly active antiretroviral therapy.

Group B streptococcal infection (GBS):Group B streptococcal infection (GBS):

This is a cause of severe congenital infection. A This is a cause of severe congenital infection. A leading cause of life-threatening perinatal leading cause of life-threatening perinatal infection.infection.

15-30% of women are asymptomatic carriers.15-30% of women are asymptomatic carriers.

Risk factors for infection areRisk factors for infection areRupture of membrane for more than18hr.Rupture of membrane for more than18hr.Preterm deliveryPreterm deliveryPROMPROMMultifetal pregnancyMultifetal pregnancyIntrapartum feverIntrapartum feverMultiple digital P/V examination during labor Multiple digital P/V examination during labor ChorioamnonitisChorioamnonitis

GBS infection manifestsGBS infection manifests (Clinical manifestation (Clinical manifestation…)…) Stillbirth particularly before 28 wks of gestation Stillbirth particularly before 28 wks of gestation Infants born with infection manifest as Infants born with infection manifest as

1 early onset1 early onset Symptoms develop within few hrs (80 % within 6 hrs of Symptoms develop within few hrs (80 % within 6 hrs of

delivery) to first weeks of life, such as delivery) to first weeks of life, such as Respiratory distressRespiratory distressLethargyLethargyHypotension Hypotension SepsisSepsis

4 % neonatal mortality of term infants and 25 %mortality in 4 % neonatal mortality of term infants and 25 %mortality in preterm infants. preterm infants.

2 late onset2 late onset symptoms occurs between first weeks to third Week such as symptoms occurs between first weeks to third Week such as

Meningitis is most commonMeningitis is most commonPneumonia Pneumonia Sepsis Sepsis

Maternal manifestation isMaternal manifestation is

15%-30% women are asymptomatic carriers.15%-30% women are asymptomatic carriers. Asymptomatic bacteriuriaAsymptomatic bacteriuria ChorioamnionitisChorioamnionitis Postpartum endometritisPostpartum endometritis Wound infectionWound infection Sepsis Sepsis

Diagnosis based on Diagnosis based on

Culture of sample obtained from lower 1/3 vagina & Culture of sample obtained from lower 1/3 vagina & anorectal region anorectal region

Gram staining Gram staining Other methods are immunofluorescent antibodies, latex Other methods are immunofluorescent antibodies, latex

agglutination, colorimetric assays, and enzyme agglutination, colorimetric assays, and enzyme immunoassays PCR.immunoassays PCR.

Preventive measuresPreventive measures:: Indications are Indications are1. Positive GBS screening during the present 1. Positive GBS screening during the present

pregnancy pregnancy 2. GBS bactiriuria during the present pregnancy 2. GBS bactiriuria during the present pregnancy 3. Previous infant with invasive GBS disease 3. Previous infant with invasive GBS disease 4. Deliveries at < 37 wks4. Deliveries at < 37 wks5. Rupture of membrane >18 hrs 5. Rupture of membrane >18 hrs 6. Intrapartum fever > 38.0c6. Intrapartum fever > 38.0c

Universal screening algorithmUniversal screening algorithm

Vaginal and rectal GBS screening cultures at 35-37 Vaginal and rectal GBS screening cultures at 35-37 wks of gestation of ALL pregnant women (unless wks of gestation of ALL pregnant women (unless patient had GBS bacteriuria during the current patient had GBS bacteriuria during the current pregnancy or a previous infant with invasive GBS pregnancy or a previous infant with invasive GBS disease)disease)

Intrapartum prophylaxis indicatedIntrapartum prophylaxis indicated

•• Previous infant with invasive GBS diseasePrevious infant with invasive GBS disease

• • GBS bacteriuria during current pregnancyGBS bacteriuria during current pregnancy

•• Positive GBS screening culture during current Positive GBS screening culture during current pregnancy (unless a planned LSCS, in the pregnancy (unless a planned LSCS, in the absence of labor or amniotic membrane absence of labor or amniotic membrane rupture, is performed)rupture, is performed)

•• Unknown GBS status and of following Unknown GBS status and of following - delivery at<37 wks of gestation- delivery at<37 wks of gestation

- amniotic membrane rupture >18 hrs- amniotic membrane rupture >18 hrs

- Intrapartum temp. >38.c- Intrapartum temp. >38.c

Intrapartum prophylaxis not indicatedIntrapartum prophylaxis not indicated

• • Previous pregnancy with a positive GBS Previous pregnancy with a positive GBS screening culture, unless a culture was also screening culture, unless a culture was also positive during current pregnancy.positive during current pregnancy.

• • Planned LSCS, in the absence of labor or Planned LSCS, in the absence of labor or amniotic membrane rupture, is performed amniotic membrane rupture, is performed regardless of maternal GBS culture status.regardless of maternal GBS culture status.

• • Negative vaginal and rectal GBS screening Negative vaginal and rectal GBS screening culture in late gestation during the current culture in late gestation during the current pregnancy, regardless of intrapartum risk pregnancy, regardless of intrapartum risk factors .factors .

Comments on prenatal screening alogrithmComments on prenatal screening alogrithm New recommendation in centers for disease New recommendation in centers for disease

control and prevention (CDC) guideline:control and prevention (CDC) guideline:

• • Universal prenatal culture based screening for Universal prenatal culture based screening for vaginal and rectal GBS colonization of all pregnant vaginal and rectal GBS colonization of all pregnant women at 35-37 wks of gestation.women at 35-37 wks of gestation.

• • Updated prophylaxis regimens for women with Updated prophylaxis regimens for women with penicillin allergy.penicillin allergy.

•• Detailed instruction on prenatal specimen Detailed instruction on prenatal specimen collection And expanded methods of GBS culture collection And expanded methods of GBS culture processing, including instruction on susceptibility processing, including instruction on susceptibility testing .testing .

•• Recommendation against routine Recommendation against routine intrapartum antibiotic prophylaxis for intrapartum antibiotic prophylaxis for GBS colonized women under going GBS colonized women under going planned LSCS deliveries who have not planned LSCS deliveries who have not begun labor or rupture of membranes.begun labor or rupture of membranes.

• • A suggested algorithm for management of A suggested algorithm for management of patient with threatened preterm delivery.patient with threatened preterm delivery.

• • An updated algorithm for management of An updated algorithm for management of newborn exposed to intrapartum newborn exposed to intrapartum antibiotic prophylaxis.antibiotic prophylaxis.

Recommendation that remain the same Recommendation that remain the same

• • Penicillin is first line of agent for intrapartum Penicillin is first line of agent for intrapartum prophylaxis, with ampicillin an acceptable alternative.prophylaxis, with ampicillin an acceptable alternative.

• • Women whose culture is are unknown at the time of Women whose culture is are unknown at the time of delivery should be managed according to the risk delivery should be managed according to the risk approach; the obstetrics risk factors remain unchanged.approach; the obstetrics risk factors remain unchanged.

• • Women with negative vaginal and rectal GBS screening Women with negative vaginal and rectal GBS screening culture with in 5 weeks of delivery do not require intra-culture with in 5 weeks of delivery do not require intra-partum antimicrobial prophylaxis for the GBS.partum antimicrobial prophylaxis for the GBS.

• • Women with GBS bacteriuria of any concentration Women with GBS bacteriuria of any concentration during their current pregnancy or who previously gave during their current pregnancy or who previously gave birth to an infant with GBS disease should receive birth to an infant with GBS disease should receive intrapartum anti-microbial prophylaxes.intrapartum anti-microbial prophylaxes.

• • In absence of GBS urinary tract infection antimicrobial In absence of GBS urinary tract infection antimicrobial agents should not be used.agents should not be used.

Recommend regimens for intrapartum Recommend regimens for intrapartum antimicrobial prophylaxis for GBS infection.antimicrobial prophylaxis for GBS infection.

RecommendedRecommended Penicillin G 5 millions U IV initial dose, Penicillin G 5 millions U IV initial dose, then 2.5 millions U every 4 hrs until then 2.5 millions U every 4 hrs until delivery.delivery.

AlternativeAlternative Ampicillin 2 gm IV initial dose then 1 Ampicillin 2 gm IV initial dose then 1 gm IV every 8 hrs.gm IV every 8 hrs.

If penicillin If penicillin allergicallergic

Cefozolin 2gm IV then 1 gm IV 8 hrs Cefozolin 2gm IV then 1 gm IV 8 hrs until deliveryuntil delivery

Or Clindamycin, 900mg IV 8hourslyOr Clindamycin, 900mg IV 8hoursly

Or Erythromycin 500mg every 6hrsOr Erythromycin 500mg every 6hrs

Or Vancomycin 1gm IV BDOr Vancomycin 1gm IV BD

For Prophylaxis given IV penicillin 5 mU every 4 hrs until delivery. Ampicillin 2 gm IV state than 1 gm every 4 hrs until delivery.

Onset of labor or rupture of membrane at <37 wks of gestation with significant risk for imminent preterm delivery.

No GBS culture GBS culture + GBS culture -

Obtain vaginal & rectal GBS culture & initiate IV penicillin

Penicillin IV for 48 hrs (during tocolysis)

No GBS prophylaxis

No growth at 48 hrs IAP AT DELIVERY

Stop penicillin

GBS+