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Microbiology: Perinatal and Pediatric Infections (Freji) CYTOMEGALOVIRUS (CMV): General: Structure: enveloped, dsDNA virus Persists after primary infection: in low-grade chronic or latent states with periodic reactivations Transmission: spread of infected oropharyngeal secretions, sexual intercourse, blood transfusions or mother to fetus spread (transplacental) Maternal CMV Infection: Many adults in the population have Abs to CMV, however, pregnant women can have a primary infection Pregnant women can shed CMV from cervix, urinary tract, throat, and in breast milk post-partum Primary CMV Infection in Pregnancy: Most are asymptomatic (~90%) Symptomatic cases present with many symptoms, including: o Infectious mononucleosis o Hepatitis o Thrombocytopenia o Myocarditis Transmission of CMV to fetus occurs ~50% of the time in mothers infected for the first time during pregnancy Diagnosis: o Isolate virus from urine, buffy coat or cervical secretions o Measure anti-CMV IgM antibodies (indicates primary infection) o Rapid diagnosis using PCR (can perform on any tissue- urine, blood, CSF etc.) Congenital CMV: ~1% of live births: however, only a small amount of these are symptomatic at birth Diagnosis: isolation of CMV from urine or saliva within the first 2 weeks of life Symptomatic Congenital CMV: o Mortality Rate: 15-30%; most survivors have long-term sequelae o Common Findings: petechiae, jaundice, hepato- and splenomegaly, thrombocytopenia, conjugated hyperbilirubinemia o Neurologic abnormalities: microcephaly, seizures, hypotonia, intracranial calcifications o Sensorineuronal hearing loss: most common cause of non-genetic congenital hearing loss o Eye abnormalities: chororetinitis most frequently; also optic atrophy, micopthalmia and cloudy cornea o Dental defects o Urinary CMV shedding: continues for months or years o Treatment: Ganciclovir in symptomatic CMV infection Asymptomatic Congenital CMV: o Can follow primary or reactivate CMV infection in the mother o Urinary CMV shedding: continues for months or years o Sensorineural hearing loss: found less often than in symptomatic CMV o Mental or behavioral problems: seen in some cases o Antiviral therapy NOT recommended Perinatal CMV: CMV is acquired during passage through infected birth canal or by ingestions of CMV-positive breast milk Most cases are asymptomatic Most common clinical illness: self-limited infantile pneumonitis (can be severe in premature infants) No long-term hearing or neurologic deficits HERPES SIMPLEX VIRUS: Maternal HSV Infection During Pregnancy: Only 1/3 of women infected with HSV during pregnancy will have symptoms If infection occurs shortly before delivery, ~50% of newborns will get infected (not enough Ab to pass on yet) Asymptomatic shedding: can occur in pregnant women at or near term (most common type of shedding) Neonatal HSV: Transmission: intrapartum is usual route; can also occur via transplacental spread as well Risk of Transmission: much higher for mothers with primary HSV infection than those with recurrent infection Risk Factors: o Cervical HSV infection o Multiple genital lesions o Prematurity o Prolonged rupture of maternal membranes o Intrauterine instrumentation o Low/absent titers of maternal neutralizing Ab (which normally blocks virus action) Intrauterine HSV Infections: baby born already sick; only small percentage of neonatal cases Hallmarks: vesicular rash present at birth/appears shortly after Associated Abnormalities: microcephly, chorioretinitis, microphthalmia, intracranial calcifications, seizures High Mortality Rate: ~50%; survivors have long-term complications Clinical Manifestations of Neonatal HSV: Asymptomatic Infection: very rare Three Presentations: 1. Skin/Eyes/Mucous Membranes (SEM): Cutaneous Lesions: discrete vesicles, large bullae, or denuded skin (10-11 days old) Eye Disease: keratoconjunctivitis and chorioretinitis Mouth: ulcerative lesions Neurological Abnormalities: can develop in some, although CNS involvement was not evident during acute illness 2. Localized CNS Involvement (Encephalitis): Symptoms: focal or generalized seizures, lethargy, or apnea Skin lesions often absent: makes it hard to diagnose CSF: mononuclear pleocystosis and elevated protein Mortality Rate: fairly high; survivors have long-term sequelae (a small number have a CNS relapse within one month of completing therapy) 3. Disseminated Disease: Presentation: similar to sepsis patient (around age 9-11 days) CNS involvement: only in about 2/3s of cases Other severely infected organs: adrenal glands, GI tract, liver, pancreas, heart, and kidneys High mortality rate: over 50% even with therapy; majority of survivors have severe neurologic impairment Treatment: acyclovir (almost always) or vidarabine Prevention: C-section for women with signs and symptoms suggestive of genital HSV at onset of labor (as long as membrane rupture is not greater than 4-6 hours) Oral acyclovir or valcyclovir given late in pregnancy for women with frequent genital recurrences (in practice, many more than just this receive this therapy) Diagnosis: Isolate virus from vesicular lesions or CSF PCR: detects HSV DNA in CSF, blood and skin lesions (very sensitive and test of choice) VARICELLA ZOSTER (CHICKENPOX AND SHINGLES): Varicella: General Comments: o Highly communicable and usually benign disease of childhood o Most women have Abs to VZV Typical Illness: fever, malaise, pruritic rash o Truncal rash characterized by crops of maculopapules that evolve in to vesicles, which eventually crust over (presence of lesion in various stages of evolution) Complications: bacterial superinfection (most common), pneumonia, arthritis, encephalitis, bleeding diathesis o Adults are more likely to have complications Zoster (General): Rash: unilateral, usually follows distribution of one or more sensory nerve roots (shingles) o Follows same evolutionary pattern as varicella o Painful in adults; not so much in kids Diagnosis: usually done clinically with laboratory confirmation rarely being needed Laboratory confirmation possible via: o Recovery of virus from vesicle fluid or detection of VZV Ags from base of fresh vesicles o PCR detecting VZV DNA (most common now) Fetal Varicella Syndrome: Cause: occurs after maternal chicken pox during the first 20 weeks of pregnancy (although risk of transmission is small) Clinical Findings: o Cutaneous scars, denuded skin o Limb hypoplasia: usually unilateral; most commonly leg o Shingles during infancy o CNS abnormalities: microcephaly, seizures, focal brain calcifications o Ocular abnormalities o Autonomic dysfunction: dysphagia, loss of urinary or bowel sphincter control Neonatal Varicella Syndrome: Cause: most often due to maternal chickenpox during the last 3 weeks of pregnancy (no Abs transferred to help) Illness: o Infection within 5 days of delivery: may be mild but can become severe (fever, hemorrhagic rash, generalized visceral involvement) Mortality high for severe infection: ~30%; usually due to pneumonia o Infection 5-21 days before delivery: illness usually mild Treatment: acyclovir Prevention: infants born to mothers who develop varicella 5 days before or 2 days after delivery should receive 125 units of varicella zoster immune globulin ASAP PARVOVIRUS B19 INFECTION: Maternal B19 Infection: Source: infected respiratory secretions or blood transfusions (uncommon) Higher rates of infections in some women: school teachers, healthcare workers, homemakers Clinical Manifestations: o Asymptomatic: ~20% o Symptomatic: Erythema infectiosum (slapped cheek appearance; most common, usually seen in kids) Influenza-like illness and symmetric polyarthropathy (in adults) o Chronic Condition: Anemia Transient aplastic crisis Hemophagocytic syndrome Fetal B19 Infection: Serious infection that can result in death: o Hydrops fetalis, spontaneous abortion, or stillbirth possible after maternal infection during pregnancy o Chronic anemia (B19 suppresses fetal bone marrow RBC production) o Cardiac dysfunction (direct infection of fetal heart muscles possible) Diagnosis: B19 specific IgM (seen by day 3; can persist for up 2 4 months) B19 specific IgG (by the end of the first week; persists for life) B19 DNA detected in serum/tissues using PCR TOXOPLASMOSIS GONDII: General: Obligate intracellular protozoan 3 forms: tachyzoite, tissue cyst or oocyst Hosts: cats and other felines Infect: humans and other warm blood animals Transmission Primary: o Ingestion of oocyst contaminated food or water o Consumption of cyst-containing raw/undercooked meat o Oocysts from cat litter box material, dust or soil Other Methods: eating raw infected eggs, blood transfusion, organ transplants from positive donors Intrauterine Transmission: from mother to fetus Maternal Toxoplasmosis: Acute Infection: most often asymptomatic If Symptomatic: lymphadenopathy (head and neck region) is the most common illness; causes a small number of infectious mononucleosis cases Possible Complications: hepatitis, pneumonia, myocarditis, encephalitis, deafness Transplacental Spread: o Infection Early in Pregnancy: risk of transmission is the lowest, but transmission during this time causes the most severe disease o Infection Late in Pregnancy: risk of transmission is highest, but disease not as severe Treatment: o Spiramycin sometimes give to reduce risk of fetal infection o If fetal infection occurs, mother treated with pyrimethamine and sulfadiazine (folic acid antagonists) Congenital Toxoplasmosis: Most are asymptomatic at birth: but still affected by disease Symptomatic disease at birth: can be mild, moderate or severe o Often born premature o Only a small number are born with severe disease (survivors have major neurologic sequelae) Symptoms: o CNS Symptoms: vasculitis, thrombosis, infarction of brain tissue, hydrocephalus, intracranial caclifications, hypotonia, microcephaly, seizures o Eye Symptoms: chorioretinitis, chorioretinal scars (important), iritis, optic atrophy, cataracts o Sensorineural hearing loss: not as common as in congenital CMV o Other Symptoms: hepatosplenomegaly, jaundice, petechiae, purpura, anemia, thrombocytopenia Diagnosis: o Isolation of parasite from placenta or blood o PCR to detect DNA in urine, CSF or serum o Specific IgM Abs o Specific IgG Abs (transferred from mother to fetus; typically drop by ~50% per month- if levels do not fall, suspect congenital infection) Treatment: o Pyrimethamine, sulfadiazine and leucovorin for one year o Steroids to treat chorioretinitis or high CSF protein levels o Need a lot of monitoring during therapy (platelet count, neutrophil count etc.) Prognosis: o Regardless of treatment, most will develop chorioretinitis or chorioretinal scars by age 10-20; treatment reduces the severity and frequency of these adverse sequelae o Recurrences of ocular toxoplasmosis occur even if treated infants (although less often than untreated) o Neurologic problems (hydrocephalus, seizures) can occur even with treatment SEPSIS NEONATORUM: General: disease of infants who are less than 1 month of age, are clinically ill, and have positive blood cultures Early Onset: first week of life (often caused by Group B Streptococci and E.coli) Late Onset: after first week of life (often caused by Coagulase-negative Staph picked up in the NICU) Risk Factors: Premature labor Prolonged rupture of fetal membranes Chorioamnionitis Maternal fever Use of arterial and venous umbilical catheters, central venous catheters, or endotracheal tubes Clinical Manifestations: Symptoms (Non-Specific): temperature instability (hyper- or hypothermia), lethargy, apnea, poor feeding, tacynpnea, vomiting, diarrhea, abdominal distention Lab Abornomalities: abnormal WBC count, unexplained metabolic acidosis, hyperglycemia Group B Streptococcal Sepsis: Vertical Transmission of GBS: occurs often, but does not always result in infant colonization Prevention of Transmission: intrapartum antibiotic (usually penicillin) as prophylaxis in women who are carriers of GBS - - Early Onset GBS Sepsis: ~around 20 hours old o Most often in premature infants Other risk factors: low birth weight, early membrane rupture, intrapartum fever, maternal GBS rectovaginal colonization, race (African American), young maternal age (<20) , GBS bacteriuria during pregnancy, previous stillbirth/abortion, previous child with GBS infection o Sudden onset and can be fulminant (life-threatening) o Primary focus of inflammation occurs in the lung (meningitis can also occur) Respiratory distress, apnea, hypotension, DIC o Can be treated so mortality rate not very high (but is inversely related to birth weight) Late Onset GBS Sepsis: ~2-4 weeks of age o Symptoms: insidious onset (poor feeding and fever most common signs) o Presentation: bacteremia without specific focus, follow by meningitis Neurologic deficits: may occur ~1/2 the time after GBS meningitis o Relapse/Reingection: possible but uncommon EPSTEIN-BARR VIRUS: General: Transmission: only found in humans and spread by intimate contact Most common clinical outcome: NOTHING (most often asymptomatic) Other clinical manifestations: infectious mononucleosis (most common if symptomatic), Burkitt’s lymphoma, nasopharyngeal lymphoma, B-cell lymphoma in immunodeficient children Infectious Mononucleosis: Classic Disease: fever, exudative pharyngitis, lymphadenopathy, hepatosplenomegaly, atypical lymphocytes Complications: aseptic meningitis, encephalitis, rupture of spleen (avoid sports), hemolytic anemia, myocarditis, thrombocytopenia Diagnosis: o Heterophile Abs (non-specific; can be done quickly) o EBV specific Abs (ie. to viral capsid Ag, early Ag, nuclear Ag; reserved for more severe cases due to increased accuracy) Treatment: bed rest in acute phase and avoid sports until spleen not palpable o Steroids: used to control tonsilar swelling, splenomegaly, hemolytic anemia and hemophagocytic syndrome HUMAN HERPESVIRUS-6 (HHV-6): General: Most cases are asymptomatic Transmission: infected respiratory secretions Symptomatic cases: most commonly show up as roseola infantum (exanthema subitum) o Reactivation of virus infection can also occur in immunosuppressed patients (BM suppression, hepatitis, pneumonia) Roseola (Exanthem Subitum): Basics: acute febrile illness of infants and young children (6 months-3 years) Fever: abrupt and high spiking, lasts 3-7 days Rash: follows fever; erythematous macular/popular rash that lasts for 2 days, beginning on trunk and spreading outward Complications: febrile seizures most common; others include hemiplegia, encephalopathy, thrombocytopenia purpura STAPHYLOCOCCAL SCALDED SKIN SYNDROME: General: Cause: exotoxin of S.aureus Diagnosis: clinical grounds alone (organism can be isolated from skin or nose but often not needed) Therapy: oral or parenteral Abx; no topical Abx or steroids Symptoms: Children often febrile and uncomfortable Severe Form: o Bullous desquamation of large areas of the skin o Tender erythroderma (baby will cry if you hold them in attempt to soothe) o Positive Nikolsky sign (separate epidermis from dermis when you drag your finger over the skin) Mild Form: o Diffuse scarlantiform erythroderma with sandpaper texture (skin is also tender, but not as extreme) o Cracks appear around the eyes and mouth KAWASAKI DISEASE: General: disease resulting from blood vessel inflammation (medium size arteries most severely affected- coronary and renal arteries are examples) Diagnostic Criteria: Fever lasting at least 5 days (high spiking and remittent; will persist for weeks without treatment) o Treatment: immunoglobulin IV + high dose aspirin Plus, 4 of the following 5 signs: o Bilateral conjunctival injection without exudates (begins after fever; resolves easily with therapy) o Changes of the oral mucosa Lips: erythema, dryness, fissuring, peeling, bleeding Oral/Pharyngeal mucosa: erythema Strawberry tongue Note: if oral ulcers, Koplik spots or exudates present it is NOT Kawasaki o Changes of the hands and feet Palms/Soles: erythema Swelling: of hands and feet Periungual desquamation: of fingers and toes Beau’s Lines: transverse grooves across nails (1-2 months after onset of disease) o Rash (often a diffuse maculopapular erythematous rash; vesicles and bullae not seen) o Cervical lympadenopathy (must be >1.5cm) Least common finding of all (ie. if one is missing, it is probably this one) Node must be nonfluctuent and nonpurulent Disease not explained by any other process Clinical Phases: without treatment (therefore, not seen anymore because usually treated) Acute Febrile Phase: 1-2 weeks Subacute Phase: begins when fever, rash and lymphadenopathy resolve (risk of sudden death the highest) o Aneurysms: usually develop at this stage Convalescent Phase: usually 6-8 weeks after onset of fever Laboratory Features: Can have normal or elevated WBC counts Elevation of ESR and other acute phase reactants Normocytic anemia Thrombocytopenia (uncommon; associated with severe coronary disease and MI) Thrombocytosis Sterile pyruia (urine containing pus) Epidemiology: Most cases in children under 4 years of age (rare <3 months), but can occur in older children and adults Occurs around the word but Asians are at highest risk Cardivascular Manifestations: Many untreated patients develop coronary abnormalities (ie. diffuse dilation or aneursyms) o Aneurysms: ~50% resolve, but the rest have persistent aneurysm (can lead I increased risk of MI and stenosis) o Other Abnormalities: myocarditis, vavulitis, pericardial effusion, MI Management: Therapy in Acute Phase: should be started in first 10 days of illness to reduce risk of coronary artery disease o IGIV high dose (often 2 doses needed) + high dose aspirin for the fever Management: follow up echocardiograms, aspirin for life with those with aneurysms -