Perinatal infections Notes

NOTES NOTES PERINATAL INFECTIONS GENERALLY, WHAT ARE THEY? PATHOLOGY & CAUSES ▪ Infections during pregnancy, birth ▫ Teratogenic/other adverse effects on fetus, neonate ▫ Congenital infections cross placenta, infect fetus in utero ▫ Neonatal infections shortly before, during, after delivery RISK FACTORS ▪ Maternal infection COMPLICATIONS ▪ Premature birth; intrauterine growth restriction; tissue damage, related sequelae SIGNS & SYMPTOMS ▪ Self-limiting to life-threatening conditions 814 OSMOSIS.ORG DIAGNOSIS ▪ Maternal prenatal, delivery history; neonatal physical examination ▪ Imaging LAB RESULTS ▪ Culture, serology testing TREATMENT ▪ Address complications MEDICATIONS ▪ Antimicrobials

Chapter 131 Perinatal Infections CONGENITAL CYTOMEGALOVIRUS INFECTION osms.it/congenital-CMV-infection PATHOLOGY & CAUSES ▪ Clinical syndrome affects developing fetus, neonate ▫ Caused by Cytomegalovirus (CMV) perinatal infection ▫ Herpesvirus family ▪ Enveloped, double-stranded linear DNA, icosahedral viral capsid ▫ Toxoplasmosis, other (syphilis, Varicella zoster, parvovirus B19), rubella, CMV, herpes (TORCH) infection ▫ Tends to become latent, reactivate ▪ Highly-prevalent virus; not very contagious ▫ Infects all ages ▫ Approx. one-third of children are infected with CMV by age five ▫ > half of adults are infected by age 40 ▪ Virus spreads to fetus transplacentally/may be acquired via maternal genital contact during delivery/through breastmilk Maternal infection ▪ Direct infectious body-fluid contact (e.g. saliva, urine, sexually transmitted); blood transfusions; transplanted organs; household contact, close contact with young infected children (e.g. daycare centers) ▫ Usually asymptomatic in adults RISK FACTORS ▪ Maternal infection COMPLICATIONS ▪ Fetal/neonatal ▫ Sensorineural hearing loss (SNHL), chorioretinitis, microcephaly, neurodevelopmental disability, seizure, anemia (hemolytic), pneumonitis, dental irregularity Figure 131.1 Histological sections of chorionic villi demonstrating nuclear inclusions seen in congenital cytomegalovirus infection. SIGNS & SYMPTOMS ▪ Birth ▫ May be asymptomatic ▪ Small for gestational age, petechial rash, “Blueberry muffin” rash, hypotonia, weak suck, hepatosplenomegaly, jaundice DIAGNOSIS DIAGNOSTIC IMAGING CT scan/MRI ▪ Neuroimaging ▫ Intracranial calcification, ventriculomegaly, white matter disease, periventricular leukomalacia, corpus callosum dysgenesis, cerebellar hypoplasia Auditory brainstem response (ABR) ▪ Hearing deficit OSMOSIS.ORG 815

Ultrasound ▪ Suggestive prenatal fetal diagnostic findings ▫ Growth restriction, ventriculomegaly, microcephaly, periventricular calcification, hepatic calcification, hydrops/ascites, echogenic bowel LAB RESULTS TREATMENT ▪ Address complications MEDICATIONS ▪ Antiviral therapy ▫ Intravenous (IV) ganciclovir/oral (PO) valganciclovir ▪ Maternal prenatal, delivery history; positive maternal CMV immunoglobulin G (IgG), CMV immunoglobulin M (IgM) antibody; neonatal examination Microbe identification ▪ Positive culture (urine, saliva) ▪ Polymerase chain reaction (PCR) (blood, urine, saliva) ▪ CMV antigens (pp65) in peripheral leukocytes Blood studies ▪ ↑ liver transaminases ▪ ↑ direct, indirect serum bilirubin ▪ ↓ white blood cells (WBCs), ↓ platelets, ↓ red blood cells (RBCs) Figure 131.2 Retinal photograph demonstrating the necrotizing retinitis of CMV infection. The retinitis will typically spread in a “brush fire” pattern. CONGENITAL RUBELLA SYNDROME osms.it/congenital-rubella-syndrome PATHOLOGY & CAUSES ▪ Syndrome caused by fetal rubella virus infection ▫ Enveloped, positive-sense, singlestranded RNA virus ▫ Rubivirus in Togaviridae family ▫ Humans are only natural hosts Maternal infection ▪ Occurs through droplet inhalation/ direct infectious nasopharyngeal secretion contact → maternal viremia → hematogenous transplacental spread to fetus → persistent fetal infection 816 OSMOSIS.ORG throughout gestation → virus-induced impaired cellular division, direct cytopathic effects ▪ Maternal–fetal transmission, congenital defect risk varies in accordance with maternal infection timing ▫ ↑ ↑ risk: inoculation occurs during first ten gestational weeks ▫ ↑ risk: cardiac, eye defects if inoculation occurs before eight gestational weeks ▫ ↑ risk: hearing deficits if inoculation occurs up to 18 gestational weeks ▫ ↓ risk: inoculation occurs after 18–20 gestational weeks

Chapter 131 Perinatal Infections RISK FACTORS ▪ Maternal non-immunized status, infection COMPLICATIONS ▪ Fetal growth restriction ▪ Hemolytic anemia, thrombocytopenia Neurological, sensory defects ▪ Sensorineural hearing loss ▪ Cataracts, congenital glaucoma, pigmentary retinopathy, microphthalmia ▪ Microcephaly, meningoencephalitis, intellectual disability Congenital heart defects ▪ Patent ductus arteriosus ▪ Pulmonary artery stenosis ▪ Coarctation of aorta Vascular defects ▪ Intimal fibromuscular proliferation, arterial sclerosis, systemi345c hypertension (related to renal disease) ▪ May result in adult coronary, cerebral, peripheral vascular disease Late complications ▪ Diabetes, thyroid disease, growth hormone deficiency, progressive rubella panencephalitis SIGNS & SYMPTOMS ▪ “Blueberry muffin” rash ▫ Purpuric rash indicates cutaneous hematopoiesis ▪ Small for gestational age; low birth weight ▪ Hepatosplenomegaly ▪ Jaundice ▪ Complications present (e.g. cataracts, heart defects) DIAGNOSIS DIAGNOSTIC IMAGING MRI ▪ Head ▫ Periventricular calcifications; demyelination ▪ Long bones ▫ Radiolucent bone lesions; irregular, alternating longitudinal light, dark bands of density (“celery stalk” appearance) LAB RESULTS Viral identification ▪ Nasopharyngeal swabs, blood/cord blood, placenta, urine, cerebrospinal fluid (CSF) ▫ PCR/culture: rubella-specific IgM (usually present at birth); persistent IgG Prenatal diagnosis ▪ Viral isolation from amniotic fluid OTHER DIAGNOSTICS Maternal prenatal history ▪ Rubella exposure ▪ Neonatal exam Figure 131.3 Bilateral cataracts in a newborn baby as a consequence of congenital rubella infection. TREATMENT ▪ No specific treatment ▪ Address complications Prevention ▪ Maternal MMR vaccination before conception OSMOSIS.ORG 817

CONGENITAL SYPHILIS osms.it/congenital-syphilis PATHOLOGY & CAUSES ▪ Congenital infection caused by Treponema pallidum (spirochete bacterium causes syphilis) Maternal infection ▪ Sexually ▫ Direct infectious lesion contact → enters via microscopic abrasions → crosses placenta easily → fetal spirochetemia → widespread dissemination (almost all fetal organs) → congenital syphilis RISK FACTORS ▪ Maternal infection → vertical (transplacental) → fetal transmission COMPLICATIONS ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ Stillbirth Premature birth Nonimmune hydrops Neurological ▫ Sensorineural hearing loss, intellectual disability, seizures Hematologic ▫ Hemolytic anemia, thrombocytopenia Renal ▫ Nephrotic syndrome (immune complex mediated) Ophthalmologic ▫ Chorioretinitis, uveitis, cataract, glaucoma, optic atrophy Gastrointestinal ▫ Necrotizing enterocolitis, ileus, malabsorption Skeletal ▫ Long-bone abnormalities, pathologic fractures Treatment-related complications ▪ Benzathine penicillin G ▫ Jarisch–Herxheimer reaction: release 818 OSMOSIS.ORG of endotoxin-like compounds during penicillin-mediated lysis of T. pallidum → fever/chills, hypotension SIGNS & SYMPTOMS Early congenital syphilis ▪ General ▫ Low birthweight, fever, hepatomegaly, jaundice, lymphadenopathy, painrelated ↓ extremity movement (pseudoparalysis) ▪ Mucocutaneous ▫ Vesicular (pemphigus syphiliticus)/ maculopapular rash ▫ Contagious, wart-like lesions (condylomata lata) ▫ Syphilitic rhinitis (“snuffles”) ▪ Umbilical cord ▫ Necrotizing funisitis (“barber-pole” appearance) Late congenital syphilis ▪ Onset after two years old ▪ Facial features ▫ Frontal bossing, saddle nose, short maxilla, protuberant mandible ▪ Sensory ▫ Impaired vision/hearing ▪ Oropharynx ▫ Hutchinson teeth (widely-spaced; notched incisors); mulberry molars (small, defective molars; cusps covered with globular enamel growths) ▪ Cutaneous ▫ Gummas ▪ Skeletal ▫ Anterior tibia bowing (saber shins), Higouménakis’ sign (sternoclavicular portion of clavicle enlargement), painless arthritis (Clutton’s joints), scaphoid scapula

Chapter 131 Perinatal Infections LAB RESULTS ▪ T. pallidum identification ▫ Dark field microscopy ▫ Direct fluorescent antibody (DFA) staining (nasal secretions, placenta, umbilical cord, autopsy tissue) ▫ Reactive venereal disease research laboratory (VDRL), rapid plasma reagin (RPR) ▪ Blood studies ▫ ↓ platelets, ↑ ↓ WBCs ▪ CSF analysis ▫ Reactive VDRL, pleocytosis, ↑ protein, T. pallidum DNA presence (identified by PCR) TREATMENT Figure 131.4 A newborn baby with a saddle nose malformation and snuffles, both of which are signs of congenital syphilis infection. DIAGNOSIS DIAGNOSTIC IMAGING Long-bone radiographs ▪ Multiple anomalies ▫ E.g. metaphyseal lucent bands, metaphyseal “sawtooth” serration (Wegener sign), “moth-eaten” appearance MEDICATIONS ▪ Intramuscular (IM) benzathine penicillin G Prevention ▪ Screening at first prenatal visit ▫ IM benzathine penicillin G OTHER INTERVENTIONS Prevention ▪ Characteristic fetal congenital infection features detectable via ultrasound ▫ 18–22 weeks of gestation Chest X-ray ▫ Diffuse infiltrate/opacification of both lung fields (“pneumonia alba”) OSMOSIS.ORG 819

GROUP B STREPTOCOCCUS (GBS) INFECTION osms.it/group-b-strep-infection PATHOLOGY & CAUSES ▪ Serious neonatal infection caused by Streptococcus agalactiae ▫ Gram-positive, encapsulated diplococcus ▫ Commonly colonizes maternal gastrointestinal, genital tracts ▫ Produces complete (beta hemolysis) on blood agar plates ▪ Acquired via intra-amniotic infection, ascending infection after amniotic membrane rupture/during birth canal passage Classification ▪ GBS onset timing ▫ Early-onset GBS: presents between 24 hours to six days post-delivery (most common) ▫ Late-onset GBS: 4–5 weeks postdelivery ▫ Late, late-onset GBS: presents in infants > three months (most common in infants with immunodeficiency history/born < 28 gestational weeks) RISK FACTORS ▪ Biologically-female individuals of African descent COMPLICATIONS Bacteremia Sepsis; septic shock Pulmonary hypertension (PPHN) Focal infections ▫ Meningitis, pneumonia, endocarditis septic arthritis, osteomyelitis, cellulitis, adenitis ▪ ↑ preterm infant mortality ▪ ▪ ▪ ▪ SIGNS & SYMPTOMS ▪ Lethargy/irritability; poor feeding ▪ Temperature instability ▪ Respiratory symptoms ▫ E.g. tachypnea, grunting, retractions, apnea, hypoxemia/↓ oxygen saturation ▪ Hypotension ▪ Bulging fontanel, nuchal rigidity (GBS meningitis) ▪ ↓ extremity movement/pain with manipulation GBS bone/joint infection DIAGNOSIS ▪ GBS-positive intrapartum nucleic acid amplification test (NAAT) ▪ Chorioamnionitis ▪ Preterm labor ▪ Premature membrane rupture ≥ 18 hours DIAGNOSTIC IMAGING Maternal presentation ▪ Delivery time ▫ Intrapartum fever ≥ 38°C/100.4°F ▫ Delivery < 37+0 gestational weeks ▫ GBS bacteriuria in current pregnancy LAB RESULTS Demographic risk factors ▪ Young maternal age 820 OSMOSIS.ORG Chest X-ray ▪ Diffuse alveolar infiltrates, pleural effusion indicate GBS pneumonia Neonatal blood studies ▪ ↑ ↓ absolute neutrophil count ▪ ↓ platelet count ▪ Positive blood culture

Chapter 131 Perinatal Infections ▪ ↑ C-reactive protein (CRP) Neonatal CSF analysis ▪ ↑ protein level, WBC count ▪ ↓ glucose level ▪ Positive Gram stain, culture results Urinalysis ▪ Gram stain, culture ▫ Presence of nitrates, leukocyte esterase, bacteria TREATMENT MEDICATIONS ▪ Antibiotics ▫ Penicillin G, ampicillin, nafcillin Prevention ▪ Vaginal-rectal culture: 35–37 gestational weeks ▫ If positive culture →intrapartum antibiotic prophylaxis ▫ Penicillin, ampicillin, cefazolin Figure 131.5 Algorithm for GBS screening and prophylaxis. OSMOSIS.ORG 821

Figure 131.6 Group B streptococcus colonies cultured on blood agar. NEONATAL CONJUNCTIVITIS osms.it/neonatal-conjunctivitis PATHOLOGY & CAUSES ▪ Clinical infection manifestation occurs within first four weeks of life, AKA ophthalmia neonatorum ▫ Most commonly caused by Neisseria gonorrhoeae/Chlamydia trachomatis (coinfection with both microbes common) ▫ Rarely, herpetic conjunctivitis caused by herpes simplex virus (HSV) ▫ Staphylococcus, Streptococcus may also be implicated in some conjunctival infections COMPLICATIONS ▪ ▪ ▪ ▪ Corneal ulceration, scarring Vision impairment, blindness Systemic sequelae of infection HSV: keratitis, keratouveitis SIGNS & SYMPTOMS ▪ Eyelid swelling, watery/mucopurulent discharge, chemosis, micropannus (granulation tissue membrane) Transmission ▪ Primarily via exposure to mother’s infected genital flora during vaginal birth ▪ Ascending infection in case of premature membrane rupture RISK FACTORS ▪ Maternal infection Figure 131.7 The clinical appearance of severe neonatal conjunctivitis. 822 OSMOSIS.ORG

Chapter 131 Perinatal Infections DIAGNOSIS LAB RESUTS Microbe identification ▪ Conjunctival, nasopharyngeal specimens ▫ Culture ▫ Gram stain ▫ Nucleic acid amplification test (NAAT) ▫ Polymerase chain reaction (PCR) ▫ Direct fluorescent antibody (DFA), enzyme immunoassay (EIA) tests ▫ HSV: Giemsa stain, PCR CBC ▪ ↑ eosinophil count TREATMENT ▪ Antibiotics ▫ Gonococcal disease: IV/IM ceftriaxone ▫ Chlamydial disease: oral erythromycin, azithromycin ▫ HSV: acyclovir Prevention ▪ Gonococcal conjunctivitis ▫ Routine neonatal prophylaxis with erythromycin 0.5% ointment OTHER INTERVENTIONS ▪ Treat neonate’s mother, sexual partner ▪ Maternal prenatal screening OTHER DIAGNOSTICS ▪ Maternal history ▪ No prenatal care; untreated C. trachomatis/N. gonorrhoeae infection; neonatal examination NEONATAL HERPES SIMPLEX osms.it/neonatal-herpes-simplex PATHOLOGY & CAUSES ▪ Uncommon, serious neonatal infection caused by herpes simplex virus (HSV-1, HSV-2) ▪ Enveloped, double-stranded DNA virus ▫ HSV-2: most neonatal cases ▫ TORCH infection Transmission ▪ Intrauterine/transplacentally is rare ▪ Intrapartum: ascending infection from maternal genitals during delivery/mother’s infected genital flora exposure ▫ Most maternal HSV infections are clinically inapparent ▪ Postnatal via close contact Inoculation ▪ 2–21 day incubation ▪ Skin, eyes, mouth (SEM) disease ▪ Central nervous system (CNS) disease ▪ Disseminated disease ▫ Multiple organs (e.g. lungs, liver, adrenal, CNS, skin, eye, mouth) RISK FACTORS Maternal infection ▪ ↑ transmission risk with vaginal delivery, prolonged membrane rupture, delivery instruments that disrupt fetal skin barrier COMPLICATIONS ▪ Recurring skin lesions throughout childhood OSMOSIS.ORG 823

▪ CNS HSV ▫ Meningoencephalitis ▪ Disseminated HSV ▫ Hepatitis, disseminated intravascular coagulation (DIC), hemorrhagic pneumonitis ▫ High mortality SIGNS & SYMPTOMS ▪ May be asymptomatic initially ▪ SEM ▫ Mucosal vesiculopustular eruption ▪ CNS HSV ▫ Temperature instability, irritability/ lethargy, bulging fontanelle, seizure ▪ Disseminated HSV ▫ Temperature instability, lethargy, poor feeding, jaundice, hepatosplenomegaly, respiratory distress DIAGNOSIS LAB RESULTS ▪ Microbe identification ▫ Culture (blood, CSF, urine, mucous membrane fluid) ▫ PCR ▪ CNS analysis ▫ CSF ↑ protein, ↑mononuclear pleocytosis ▪ Lesion analysis ▫ Multinucleated giant cells visualized with Giemsa/Wright stain TREATMENT MEDICATIONS ▪ IV acyclovir OTHER INTERVENTIONS ▪ Also treat mother, mother’s partner Figure 131.8 A neonate with herpes simplex vesicles on the scalp. 824 OSMOSIS.ORG

Chapter 131 Perinatal Infections NEONATAL MENINGITIS osms.it/neonatal-meningitis PATHOLOGY & CAUSES ▪ Severe neurological infection complication ▫ High morbidity, mortality rate ▫ Most often occurs during first week of life ▫ Bacterial, viral, fungal infections ▪ Usually caused by variety of bacteria (e.g. GBS, E. coli, S. pneumoniae, Enterococcus, coagulase-negative staphylococci, S. aureus, L. monocytogenes, H. influenzae) RISK FACTORS ▪ Premature birth, low birthweight, maternal infection, sepsis COMPLICATIONS ▪ Cerebral edema/abscess, hydrocephalus, intraventricular hemorrhage, encephalomalacia, cerebral palsy, seizure disorder, auditory/visual sensory deficits ventriculitis, extracerebral fluid collections MRI/CT scan ▪ Detects cerebral edema, infarction/abscess area, CSF obstruction, encephalomalacia, atrophic tissue (cortical, white matter) LAB RESULTS ▪ Microbe identification ▫ CSF ▫ Gram stain, culture, PCR, NAAT ▫ Blood culture (may be negative) ▫ Urine culture ▪ Blood studies ▫ ↑↓ WBC count, left shift, ↓ platelets ▪ CSF ▫ ↑ WBCs, ↑ protein, ↓ glucose SIGNS & SYMPTOMS General ▪ Temperature instability, lethargy, poor feeding, vomiting, diarrhea Neurological ▪ Irritability, hypotonia, tremors, seizures, full/ bulging fontanelle; may have nuchal rigidity Respiratory ▪ Tachypnea, retractions nasal flaring, grunting, apnea DIAGNOSIS Figure 131.9 A sample of cerebrospinal fluid from a neonate with meningitis. There are neutrophils present, denoting an acute inflammatory process as well as cocci arranged in groups and pairs. Culture grew Staphylococcus capitis. DIAGNOSTIC IMAGING Cranial sonography ▪ Assess ventricular size ▫ Detect ventricular hemorrhage, OSMOSIS.ORG 825

TREATMENT MEDICATIONS ▪ Antimicrobials ▫ usually ampicillin + gentamicin + thirdgeneration cephalosporin ▪ Anticonvulsants ▪ IV fluids, vasopressors NEONATAL SEPSIS osms.it/neonatal-sepsis PATHOLOGY & CAUSES ▪ Serious infection; presents within neonate’s first 30 days; characterized by bacteremia/ meningitis ▪ Characterized by onset ▫ Early-onset sepsis: occurs with first 3–7 days ▫ Late-onset sepsis: occurs between 7–30 days ▪ May be bacterial (most common), viral, fungal (more common in preterm infants) → vertical transmission before/during labor/ delivery RISK FACTORS Low birthweight Preterm birth Low Apgar score at five minutes Prolonged membrane rupture Chorioamnionitis Maternal GBS colonization (inadequate intrapartum treatment) ▪ Inborn metabolism errors ▪ Maternal age ≤ 20 ▪ ▪ ▪ ▪ ▪ ▪ COMPLICATIONS ▪ Meningitis, pneumonia, multi-organ failure, necrotizing enterocolitis (NEC), high mortality rate 826 OSMOSIS.ORG SIGNS & SYMPTOMS ▪ May be initially nonspecific ▪ Fever, temperature instability General signs ▪ Lethargy, irritability, poor suck, hypotonia Respiratory distress signs ▪ Tachypnea, grunting, nasal flaring, retractions, apneic periods, cyanosis Hemodynamic instability ▪ Tachycardia/bradycardia, prolonged capillary refill time, hypotension, pallor DIAGNOSIS ▪ Maternal, intrapartum, neonatal history ▪ Compatible clinical presentation LAB RESULTS ▪ Blood, CSF culture ▫ Identify causative microbe ▪ CBC ▫ Neutropenia (due to small neutrophil storage pool) ▪ CSF analysis ▫ ↑ WBCs; protein, glucose may also be ↑

Chapter 131 Perinatal Infections TREATMENT MEDICATIONS ▪ Antibiotics ▪ Vasopressors OTHER INTERVENTIONS ▪ Supplemental oxygen, mechanical ventilation ▪ IV fluids TOXOPLASMOSIS osms.it/toxoplasmosis PATHOLOGY & CAUSES ▪ Congenital infection ▫ Caused by protozoa Toxoplasma gondii ▫ TORCH infection ▪ Obligate intracellular parasite ▪ Transplacental transmission to fetus Biphasic life cycle ▪ Sexual cycle ▫ Occurs exclusively in felines (definitive host) ▪ Asexual cycle ▫ Occurs in other animals, including humans Maternal infection routes ▪ Cats consume infective form (cysts) from prey (e.g. intermediate hosts—rodents, birds) → replication within intestines → oocyst formation → fecal excretion → maternal infection via cat fecal exposure (soil, litter box) ▪ Wild game/animals bred for human consumption (e.g. cattle) may ingest environmental oocytes → infection → maternal consumption of raw/undercooked meat, contaminated water/vegetables → maternal infection RISK FACTORS ▪ Maternal infection ▫ Primary infection during pregnancy/ reactivation in immunocompromised host COMPLICATIONS ▪ ↑ congenital effect severity when infection occurs early in gestation ▫ Classic triad: chorioretinitis, hydrocephalus, intracranial calcification ▫ Sensorineural hearing loss, microcephaly, intellectual disability, motor/cerebellar dysfunction, growth delay, seizure, pneumonitis, anemia, thrombocytopenia SIGNS & SYMPTOMS Subclinical infection ▪ Routine assessment reveals no anomalies ▪ Focused examination may reveal infection signs (e.g. ophthalmologic, CNS imaging) Clinically apparent disease ▪ During neonatal period/first few months of life ▫ May be mild/severe, CNS/ocular complications, purpuric rash (“blueberry muffin” rash), fever, jaundice, hepatosplenomegaly, lymphadenopathy, microphthalmia, hypotonia Late infancy, childhood, adolescence ▪ Undiagnosed/untreated infection emergence/relapse ▫ Complication developments (e.g. chorioretinitis, neurosensory hearing loss) ▫ Growth delay, endocrine abnormalities secondary to hypothalamic, pituitary dysfunction OSMOSIS.ORG 827

DIAGNOSIS DIAGNOSTIC IMAGING ABR ▪ Sensorineural hearing loss CT scan ▪ Neuroimaging ▫ Intracranial calcifications, hydrocephalus (ventriculomegaly), cortical atrophy LAB RESULTS Confirmatory diagnostics ▪ With any of following ▫ Positive IgG with positive IgM (after five days of life), IgA (after ten days of life) + confirmed maternal serology ▫ Positive CSF PCR + confirmed maternal T. gondii infection during pregnancy, characteristic neonatal clinical findings ▫ Positive IgG beyond 12 months of age demonstrates anti-Toxoplasma IgG persistence Ophthalmic examination ▪ Chorioretinitis Neurologic examination ▪ Lumbar puncture ▫ ↑ protein, mononuclear pleocytosis Blood studies ▪ CBC ▫ ↓ RBCs ↓ platelets, ↑ eosinophils ▪ Liver function tests ▫ Possible ↑ aspartate aminotransferase; alanine aminotransferase; total, direct bilirubin Cytologic placental examination ▪ T. gondii cyst/tachyzoite presence 828 OSMOSIS.ORG Figure 131.10 Retinal photograph demonstrating the characteristic “headlight in the fog” appearance of toxoplasma retinitis. TREATMENT MEDICATIONS Neonatal treatment ▪ Antiparasitic therapy ▫ Pyrimethamine + sulfadiazine + folinic acid ▪ Prednisone if ↑ CSF protein Prevention ▪ Maternal antiparasitic therapy ▫ Positive amniotic fluid PCR before 18 gestational weeks ▪ Pyrimethamine + sulfadiazine plus folinic acid until delivery