Perinatal infections Notes

Contents

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Perinatal infections essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Perinatal infections by visiting the associated Learn Page.
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

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Perinatal infections essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Perinatal infections by visiting the associated Learn Page.