Lecture_07. TORCH infections and HIV-AIDS iewborn.
Congenital Infections so-called TORCH infections (toxoplasmosis, other, rubella, Cytomegalovirus infection, and herpes simplex infection). The newborn infant is more vulnerable than the older child to certain infections. The preterm baby is even less able to withstand infection and more liable to suffer serious complications. Infection of the fetus can result in embryonic death, stillbirth, prematurity, intrauterine growth retardation, developmental abnormalities or congenital disease.
Clinical findings are rarely disease specific but include
· Low birthweight for gestational age.
· Prematurity.
· Seizures
· Chorio-retinitis
· Purpura
· Chronic rash
· Cerebral calcification
· Micro-ophthalmia
· Jaundice
· Anaemia
· Hepatosplenomegaly
· Pneumonitis
CLINICAL Congenital CMV infection may be present as Cytomegalic inclusion disease:
· Approximately 10% of congenitally infected infants have clinical evidence of disease at birth. The most severe form of congenital CMV infection is referred to as cytomegalic inclusion disease (CID).
· CID almost always occurs in women who have primary CMV infection during pregnancy, although rare cases are described in women with preexisting immunity who presumably have reactivation of infection during pregnancy.
· CID is characterized by intrauterine growth retardation, hepatosplenomegaly, hematological abnormalities (particularly thrombocytopenia), and a variety of cutaneous manifestations, including petechiae and purpura (ie, blueberry muffin baby). However, the most significant manifestations of CID are those involving the central nervous system. Microcephaly, ventriculomegaly, cerebral atrophy, chorioretinitis, and sensorineural hearing loss are the most common neurological consequences of CID.
· Intracerebral calcifications typically demonstrate a periventricular distribution and commonly are encountered by CT scan. The finding of intracranial calcifications is predictive of cognitive and audiologic deficits in later life and predicts a poor neurodevelopmental prognosis.
· Overall, 90% of infants who survive symptomatic CID have significant long-term neurological and neurodevelopmental sequelae. Indeed, it has been estimated that congenital CMV may be second only to Down syndrome as an identifiable cause of mental retardation in children.
Asymptomatic congenital CMV
· Most infants with congenital CMV infection are born to women who have preexisting immunity to CMV. These infants appear clinically normal at birth; however, even though infants with congenital CMV infection appear well, they may have subtle growth retardation compared to uninfected infants. Although asymptomatic at birth, these infants, nevertheless, are at risk for neurodevelopmental sequelae.
· The major consequence of inapparent congenital CMV infection is sensorineural hearing loss. Approximately 15-20% of these infants will have unilateral or bilateral deafness. Routine newborn audiologic screening may not detect cases of CMV-associated hearing loss because this deficit may develop months or even years after delivery.
Acquired CMV infection:
· Perinatal acquisition of CMV usually occurs secondary to exposure to infected secretions in the birth canal or via breastfeeding. Most infections are asymptomatic. Indeed, in some reviews, CMV acquired through breast milk has been referred to as a form of natural immunization.
· Some infants who acquire CMV infection perinatally may have signs and symptoms of disease, including lymphadenopathy, hepatitis, and pneumonitis, which may be severe on occasion. Interestingly, these infections do not appear to carry any risk of neurological or neurodevelopmental sequelae.
Investigations
· Urine culture for CMV (must be in first two weeks of life to confirm congenital infection). Urine must be chilled and transported immediately to the lab on melting ice.
· Cord or infant blood for CMV PCR .
· Head ultrasound.
· Long term: serial audiology and developmental assessment, head circumference, ophthalmology.
TREATMENT
Medical care consists of good nutritional support, vigorous supportive care for end-organ syndromes (particularly pneumonia in immunocompromised patients), and specific antiviral therapy.
Currently, 3 antiviral therapies are approved for prophylaxis and/or therapy of CMV infection. Experience with these agents is limited in children.
Ganciclovir (Cytovene) Pediatric Dose <3 months: Not established; >3 months: Administer as in adults. Adult Dos:
· Induction: 5 mg/kg IV bid for 2-3 wk, followed by maintenance dose;
· IV maintenance: 5 mg/kg IV qd for the duration of therapy; 2.5 mg/kg/dose IV q8h has been used in some patients with CMV pneumonitis
· PO maintenance: 1 g PO q8h limited to HIV-positive individuals ieed of long-term anti-CMV therapy for CMV retinitis
Relatively little information exists concerning the use of GCV in the setting of congenital CMV infection. Because some of the neurological sequelae of congenital CMV, particularly sensorineural hearing loss, progress postnatally, the presentation of results from a recently terminated nationwide collaborative trial are of interest. Intravenous GCV led to improvement or stabilization of hearing in a significant number of 6-month-old infants. Case reports have suggested the efficacy of GCV for acutely ill neonates with life-threatening CMV disease (eg, pneumonia).
Cidofovir (Vistide) — Nucleotide analog that selectively inhibits viral DNA production in CMV and other herpes viruses. Pediatric Dose not established.
Foscarnet (Foscavir) — Organic analog of inorganic pyrophosphate that inhibits replication of known herpesviruses, including CMV, HSV-1, and HSV-2. Pediatric Dose <12 years: Not established; >12 years: Administer as in adults. Adult Dose 90 mg/kg IV q12h infused over a minimum of 1 h for 14-21 d.
Immunoglobulins — Used as passive immunization for the prevention of symptomatic CMV disease. Have been useful in the control of CMV disease.
Immune globulin intravenous (Gamimune, Gammagard, Sandoglobulin, Gammar-P) Adult Dose 500 mg/kg IV qod for 10 doses in combination with GCV, followed by 500 mg/kg IV 2 times per wk for 8 additional doses. Pediatric Dose Not established.
CMV-Ig (CytoGam) — A CMV hyperimmunoglobulin has been shown to decrease incidence of CMV disease when administered posttransplant to high-risk transplant recipients.
Prevention:Until the goal of a CMV vaccine is realized, educating women of childbearing age about the risks of CMV and about how to avoid disease transmission are the only control strategies available.
Rubella
CLINICAL
Congenital rubella history focuses on the following:
· The number of weeks of pregnancy when maternal exposure to rubella occurred (The risk of congenital rubella syndrome is higher if maternal exposure occurs during the first trimester.)
· Maternal history of immunization or medical history of rubella
· Evidence of intrauterine growth retardation during pregnancy
· Manifestations suggestive of congenital rubella syndrome in a child
Physical: The classic triad presentation of congenital rubella syndrome consists of the following:
· Sensorineural hearing loss is the most common manifestation of congenital rubella syndrome. It occurs in approximately 58% of patients. Studies have demonstrated that approximately 40% of patients with congenital rubella syndrome may present with deafness as the only abnormality without other manifestations. Hearing impairment may be bilateral or unilateral and may not be apparent until the second year of life.
· Ocular abnormalities including cataract, infantile glaucoma, and pigmentary retinopathy occur in approximately 43% of children with congenital rubella syndrome. Both eyes are affected in 80% of patients, and the most frequent findings are cataract and rubella retinopathy. Rubella retinopathy consists of a salt-and-pepper pigmentary change or a mottled, blotchy, irregular pigmentation, usually with the greatest density in the macula. The retinopathy is benign and nonprogressive and does not interfere with vision (in contrast to the cataracts) unless choroid neovascularization develops in the macula.
· Congenital heart disease including patent ductus arteriosus (PDA) and pulmonary artery stenosis is present in 50% of infants infected in the first 2 months of gestation. Cardiac defects and deafness occur in all infants infected during the first 10 weeks of pregnancy and deafness alone is noted in one third of those infected at 13-16 weeks of gestation.
Other findings in congenital rubella syndrome include the following:
· Intrauterine growth retardation, prematurity, stillbirth, and abortion
· Central nervous system abnormalities, including mental retardation, behavioral disorders, encephalographic abnormalities, hypotonia, meningoencephalitis, and microcephaly
· Hepatosplenomegaly
· Jaundice
· Hepatitis
· Skin manifestations, including blueberry muffin spots that represent dermal erythropoiesis and dermatoglyphic abnormalities
· Bone lesions, such as radiographic lucencies
· Endocrine disorders, including late manifestations in congenital rubella syndrome usually occurring in the second or third decade of life (eg, thyroid abnormalities, diabetes mellitus)
· Hematologic disorders, such as anemia and thrombocytopenic purpura
Investigations Mother: Check antenatal serology and perform if result not available (mother may have IgG from infection very early in pregnancy, so documented seropositivity from a previous pregnancy is more reliable). Baby: Infection of the fetus is CHRONIC, so congenitally infected infants will shed virus at high titre for many months.
· Urine and CSF for rubella virus PCR.
· White blood cells (cord blood or infant blood) for rubella PCR.
· Serum (cord or infant blood) for rubella IgM.
TREATMENT
Medical Care: Treatment is supportive. Provide vision screening and hearing screening for asymptomatic newborns.
Treatment of symptomatic newborns is as follows:
· Provide careful evaluation of the eyes and ophthalmology referral for babies with corneal clouding, cataract, and retinopathy. Corneal clouding may indicate infantile glaucoma.
· Babies with congenital rubella syndrome who develop respiratory distress may require supportive treatment in the intensive care unit.
· Hepatosplenomegaly is monitored clinically. No intervention is required.
· Patients with hyperbilirubinemia may require phototherapy or exchange transfusions if jaundice is severe to prevent kernicterus.
· True hemorrhagic difficulties have not been a major problem; however, IVIG may be considered in infants who develop severe thrombocytopenia. Corticosteroids are not indicated.
· Infants who have a rubella-related heart abnormality should be carefully observed for signs of congestive heart failure. Echocardiography may be essential for diagnosis of heart defects.
Contact isolation is required for patients with congenital rubella during hospitalizations because babies are infected at birth and usually are contagious until older than 1 year unless viral cultures have produced negative results.
Drug therapy is currently not a component of the standard of care for rubella.
CLINICAL History: Pediatric toxoplasmosis can be acute or chronic, asymptomatic or symptomatic, and congenital or postnatally acquired.
Congenital toxoplasmosis is the consequence of transplacental hematogenous fetal infection by T gondii during primary infection in pregnant women. Primary infection in an otherwise healthy pregnant woman is asymptomatic in 60% of cases. Symptoms during pregnancy are frequently mild. The most common manifestations are fatigue, malaise, a low-grade fever, lymphadenopathy, and myalgias. Latent Toxoplasma infection with reactivation during pregnancy may lead to congenital infection only in immunocompromised women (most commonly, those with AIDS).
The classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications cannot be used as a strict diagnostic criterion for congenital toxoplasmosis because a large number of cases would be missed. Congenital toxoplasmosis may occur in the following forms:
· Neonatal disease
· Disease occurring in the first months of life
· Sequelae or relapse of previously undiagnosed infection
· Subclinical infection
When clinically recognized in the neonate, congenital toxoplasmosis is very severe. Signs of generalized infection are usually present, such as intrauterine growth retardation, jaundice, hepatomegaly, splenomegaly, lymphadenopathy, and a rash. Neurologic signs are severe and always present. They include microcephaly or macrocephaly, bulging fontanelle, nystagmus, abnormal muscle tone, seizures, and delay of developmental milestone acquisition.
· Most cases of chorioretinitis result from congenital infection, although patients are often asymptomatic until later in life. Symptoms include blurred vision, scotoma, pain, photophobia, and epiphora. Impairment of central vision occurs when the macula is involved, but vision may improve as inflammation resolves. Relapses of chorioretinitis are frequent but rarely accompanied by systemic signs or symptoms.
· Latent toxoplasmosis may reactivate in women with human immunodeficiency virus (HIV) and result in congenital transmission. Congenital toxoplasmosis in the infant with HIV appears to run a more rapid course than in infants without HIV.
Physical:
· Lymphadenopathy is the most common form of symptomatic acute toxoplasmosis in immunocompetent individuals.
· Patients typically present with painless firm lymphadenopathy that is confined to one chain of nodes, which are most commonly cervical. The suboccipital, supraclavicular, axillary, and inguinal groups may also be involved.
· Ophthalmologic examination reveals multiple yellow-white cottonlike patches with indistinct margins located in small clusters in the posterior pole.
· Characteristically, a focal necrotizing retinitis develops that may atrophy and generate black pigment, or it may be associated with panuveitis. Papillitis is usually indicative of CNS disease. Flare-up of congenitally acquired chorioretinitis is often associated with scarred lesions in proximity to the fresh lesions.
· Because of multifocal involvement of the CNS, clinical findings vary widely. They include alterations in mental status, seizures, motor weakness, cranial nerve disorders, sensory abnormalities, cerebellar signs, meningismus, movement disorders, and neuropsychiatric manifestations in patients with immunocompromise.
Investigation of babies born to toxoplasma IgM positive mothers
The following samples will enable search for toxoplasma DNA (by PCR) in baby’s blood, placenta and amniotic fluid.
If suspected after delivery:
· Maternal serum for toxoplasma IgG and IgM
· Infant serum (red top) for toxoplasma IgG, IgM and infant blood (CPD or EDTA tube) for PCR
Treatment
· prenatal treatment of the mother in preventing adverse fetal outcomes with spiramycin. If documented fetal infection is noted in the prenatal period (via amniotic PCR), consider treatment with pyrimethamine and sulfadiazine.
· Treat infant for clinically, serologically, or maternally apparent disease with pyrimethamine and sulfadiazine for 1 year. Folinic acid should be given to prevent bone marrow suppression. A year of treatment allows the infant to become immunocompetent and will reduce neurologic sequelae compared to a shorter course of treatment. A pediatric infectious disease (ID) consultation should be obtained.
· Corticosteroid for ocular disease and CNS infection (high level of CSF protein), add prednisone 1mg/kg/d divided q 12 hours until CSF protein is normal and/or ocular inflammation resolves.
MEDICATION
· Sulfadiazine (Microsulfon) Pediatric Dose: Acquired toxoplasmosis: >1 year: 75 mg/kg/d PO once, followed by 50 mg/kg/d for 2-4 wk; Congenital toxoplasmosis: 100 mg/kg/d PO once, followed by 100 mg/kg/d divided q12h for 2-6 mo.
· Dapsone (Avlosulfon) Pediatric Dose: >1 month: 1 mg/kg/d PO; not to exceed 25 mg/d.
· Clindamycin (Cleocin) Pediatric Dose: 8-20 mg/kg/d PO as hydrochloride (cap) or 8-25 mg/kg/d PO as palmitate (susp) divided tid/qid; not to exceed 1.8 g/d. 20-40 mg/kg/d IV/IM divided tid/qid; not to exceed 4.8 g/d/
· Pyrimethamine (Daraprim) Pediatric Dose: 2 mg/kg/d PO divided q12h for 2-4 d initially, then 1 mg/kg/d PO qd or divided q12h for 1 mo; not to exceed 25 mg/d.
· Azithromycin (Zithromax) Pediatric Dose: 10 mg/kg as single dose on day 1, not to exceed 500 mg/d; followed by 5 mg/kg on days 2-5, not to exceed 250 mg/d.
· Spiramycin (Rovamycine) Pediatric Dose: 50-100 mg/kg/d PO divided bid/qid for 3-4 wk.
· Leucovorin (Wellcovorin) — Also called folinic acid. Derivative of folic acid used with folic acid antagonists, such as sulfonamides and pyrimethamine. Pediatric Dose: 5-10 mg PO 3 times/wk
Prevention:
Preventing the infection is particularly important for women who are pregnant and for patients who are seronegative and immunocompromised.
· Avoid consuming raw or undercooked meat, unpasteurized milk, and uncooked eggs.
· Wash hands after touching raw meat and after gardening or having other contact with soil.
· Wash fruits and vegetables.
· Avoid contact with cat feces.
· To attempt to prevent congenital toxoplasmosis, routine serologic screening of pregnant women has been performed in order to identify fetuses at risk of becoming infected.
Herpes Simplex infection
Clinical findings
· Average incubation 6 days; can be up to 20.
· Disseminated disease may mimic fulminate sepsis with seizures, jaundice, hepatitis, encephalitis, DIC, or pneumonia. If untreated, up to 90% mortality.
· Local mucocutaneous disease may be mild. Conjunctivitis, keratitis, or chorioretinitis can result in vision loss and blindness.
Investigations
· Skin vesicles: swab for viral culture and HSV PCR
· Swabs from eyes, mouth/nasopharynx for HSV culture.
· WBCs (CPD or EDTA tube) for HSV PCR
· CSF – cells, protein, glucose, culture, viral culture and HSV PCR.
· Head CT/EEG may localise disease but not essential.
· Subtype specific (HSV1 and 2) serology may be useful on mother and baby.
· Ophthalmic consultation.
Prevention and treatment.
· Any active lesions during pregnancy should be cultured to confirm disease. Active disease at delivery mandates C-section. Routine use of PCR to identify asymptomatic shedders is not yet standard of care.
· If vaginal delivery occurs over active lesions or >4 hours, begin acyclovir 30 mg/kg/d IV Q8h for 14-21 days. doses as high as 45-60 mg/kg/d divided q8h have been used in full-term infants. Premature infants: 20 mg/kg/d PO/IV divided q12h for 14-21 d.
· Infected mother and infant should be kept in contact isolation.
Chlamydial Infections Chlamydia can cause diseases of many systems. The most frequent disease, caused by Chlamydia trachomatis, is a sexually transmitted.
Pathophysiology: C trachomatis is an obligate intracellular bacterium that infects the urethra and cervix. The bacterium usually is spread through sexual activity and can be spread vertically, causing conjunctivitis and pneumonia iewborns. The transmission rate from infected mother to newborn is 50%, causing conjunctivitis (most cases) or pneumonia (10-20%). The incubation period is 1-5 weeks.
CLINICAL History:
· Symptoms for pneumonia begin in children aged 1-3 months and for conjunctivitis in children aged 1-2 weeks.
· Cough, fever in pneumonia (classic description is afebrile)
· Eye discharge, swelling in conjunctivitis
· Mother with diagnosed or suspected chlamydial infection during pregnancy
Physical:
· Fever, cough, wheezing, and pulmonary crackles in pneumonia
· Conjunctival erythema, mucoid discharge, and/or periorbital swelling in conjunctivitis
Lab Studies:
Nonculture tests that detect antigens or deoxyribonucleic acid (DNA) of chlamydia using molecular techniques
· Direct immunofluorescent antibody (DFA, MicroTrak), enzyme immunoassay (EIA, Chlamydiazyme), and DNA probes (PACE Gen-Probe) all are approximately 80% sensitive and 95% specific.
· Polymerase chain reaction (PCR) and ligase chain reaction (LCR) have sensitivity and specificity approaching 100% but still are very expensive to perform on a routine basis.
Infants with suspected pneumonitis
· Perform a nasopharyngeal (NP) swab for chlamydia culture. Currently available rapid tests are not approved for use on NP-derived specimens.
· In severe or complicated cases, bronchoalveolar lavage fluid can be sent for chlamydia culture as well. A CBC that demonstrates peripheral eosinophilia in the right clinical situation offers additional supportive evidence for C trachomatous pneumonia.
Infants with suspected chlamydia conjunctivitis
· Perform an antigen/DNA detection test and/or chlamydia culture by scraping of palpebral conjunctiva.
· If the mother has had documented chlamydial infection during pregnancy that went untreated, treat the infant presumptively, even without confirmation of infection.
TREATMENT
· Erythromycin (E.E.S., Eryc, E-Mycin) – Newborns with chlamydia conjunctivitis or pneumonia: Erythromycin (base) 50 mg/kg/d PO divided qid for 14 d.
· Amoxicillin (Trimox, Amoxil) – 30-40 mg/kg/d PO divided tid for 7-10 d.
· Sulfisoxazole — Less effective than most other regimens. Pediatric Dose: 120-150 mg/kg/d PO divided qid.
Syphilis Syphilis is a communicable disease caused by Treponema pallidum, which belongs to the Spirochaetaceae family.
Pathophysiology: Congenital syphilis is caused by transplacental transmission of spirochetes; the transmission rate approaches 100%. Perinatal death may result from congenital infection in more than 40% of affected, untreated pregnancies. Among survivors, manifestations traditionally have been divided into early and late stages. Manifestations are defined as early if they appear in the first 2 years of life and late if they develop after age 2 years.
Because inflammatory changes do not occur in the fetus until after the first trimester of pregnancy, organogenesis is unaffected. Nevertheless, all organ systems may be involved. With early-onset disease, manifestations result from transplacental spirochetemia and are analogous to the secondary stage of acquired syphilis. Congenital syphilis does not have a primary stage. Late-onset disease is seen in patients older than 2 years and is not considered contagious.
CLINICAL History: Most recognized syphilitic disease in children is congenital. A pregnant woman with syphilis who has not received therapy or who has received inadequate therapy may transmit the infection to the fetus at any clinical stage of the disease.
Early-onset congenital syphilis
· Most affected infants are asymptomatic at birth and are identified only by routine prenatal screening. If untreated, symptoms develop within weeks or months. The typical stillborn or highly symptomatic newborn is born prematurely with an enlarged liver and spleen, skeletal involvement, and often pneumonia and bullous skin lesions.
· The earliest signs of congenital syphilis may be poor feeding and snuffles (ie, syphilitic rhinitis).
Physical: Early-onset congenital syphilis
· Early manifestations of congenital infection are varied and involve multiple organ systems. The most striking lesions affect the mucocutaneous tissues and bones. Mucous patches, rhinitis, and condylomatous lesions are highly characteristic features of mucous membrane involvement in congenital syphilis.
· Nasal fluid is highly infectious. Snuffles are followed quickly by a diffuse maculopapular desquamative rash that involves extensive sloughing of the epithelium, particularly on the palms and soles and about the mouth and anus. In contrast to acquired syphilis, a vesicular rash and bullae may develop. These lesions are highly infectious.
· Hepatomegaly is reported in almost 100% of cases, and biochemical evidence of liver dysfunction usually is observed.
Late-onset congenital syphilis
· Scarring from the early systemic disease causes late manifestations of congenital syphilis.
· Manifestations include neurosyphilis and involvement of the teeth, bones, eyes, and the eighth cranial nerve.
Investigations
· Peripheral blood counting, liver function tests and syphilis serology on infant blood
· Maternal syphilis serology.
· CSF for VDRL, cells protein and glucose.
· Long bone xrays.
· Darkfield microscopy of skin lesions, nasal discharge, placental tissue or amniotic fluid may show spirochaetes (but majority of cases have none of these).
TREATMENT
· Congenital syphilis iewborns: Aqueous crystalline penicillin G is recommended if congenital syphilis is proved or highly suspected. The recommended dosage is 100,000-150,000 U/kg/d IV q8-12h to complete a 10- to 14-day course.
· Congenital syphilis in older infants and children: Treat diagnosed infants older than 4 weeks with aqueous crystalline penicillin (200,000-300,000 U/kg/d IV q6h for 10-14 d).
· Neurosyphilis: The recommended treatment is aqueous crystalline penicillin G, 200,000-300,000 U/kg/d IM (50,000 U/kg q4-6h) for 10-14 days, followed by a single dose of benzathine penicillin 50,000 U/kg/dose in 3 weekly doses.
Further Outpatient Care:
· Follow up congenital syphilis with evaluation at ages 1, 2, 4, 6, and 12 months. Obtaiontreponemal titers at ages 3, 6, and 12 months after conclusion of treatment. Nontreponemal antibody titers should decline by age 3 months and should be nonreactive by age 6 months. Consider retreatment for patients with persistently stable titers, including low titers.
· Infants who are treated for congenital neurosyphilis should undergo repeat clinical evaluation and CSF examination at 6-month intervals until their CSF examination result is normal. A positive CSF VDRL result at age 6 months is an indication for retreatment.
Prevention: Indications for syphilis screening include the following:
· All women at first prenatal visit and high-risk women again at 28 weeks’ gestation
· All women delivering a stillborn infant
· All newborns older than 22 weeks’ gestation whose mothers were not screened
Listeria Infection Listeriosis is an infection caused by a gram-positive motile bacterium, Listeria monocytogenes. Listeriosis is relatively rare and occurs primarily iewborn infants, elderly patients, and patients who are immunocompromised.
Pathophysiology: Ingestion of Listeria by pregnant women can result in a flulike illness. Many pregnant women can carry Listeria asymptomatically in their GI tract or vagina. Maternal infection with Listeria can result in chorioamnionitis, premature labor, spontaneous abortion, or stillbirth. Fetal infection can occur via transplacental transmission. Vertical transmission also can occur from mother to infant via passage through an infected birth canal or ascending infection through ruptured amniotic membranes.
Two clinical presentations of neonatal infections occur, early onset (<5 d) and late onset (>5 d). Early-onset neonatal listeriosis usually is associated with sepsis or meningitis. Late-onset neonatal listeriosis frequently presents with purulent meningitis. Listeriosis often involves many organs with microabscesses or granulomas.
Mortality/Morbidity: Early-onset neonatal listeriosis has a 20-30% mortality rate. Late-onset neonatal listeriosis has a 0-20% mortality rate. Hydrocephalus, mental retardation, and other CNS sequelae have been reported in survivors of Listeria meningitis.
CLINICAL
· Early-onset neonatal infections (<5 d) begin at the mean age of 1.5 days.
· Late-onset neonatal infections (>5 d) begin at the mean age of 14 days.
Physical: Listeriosis presents in the same manner as other more commoeonatal pathogens, such as group B streptococci and Escherichia coli.
· Respiratory distress – Tachypnea, grunting, apnea, and retractions
· Temperature instability
· Poor feeding
· Lethargy/irritability
· Seizures
· Granulomatous rash – Disseminated small pale nodules
Lab Studies:
1. Blood culture
2. Cerebrospinal fluid culture
3. Respiratory tract culture
4. Histopathology and culture of rush
5. Culture of other infected tissues: (Joint, Pericardial fluid, Pleural fluid, Amniotic fluid, Placenta, Gastric aspirate).
Imaging Studies: CT scan or MRI may be useful to detect abscesses in brain or liver.
References:
1. Avery‘s neonatology: pathophysiology and management of the newborn / G. B. Avery, M. G. MacDonald, M. M. K. Seshia [et al.]. – 6th ed. – Philadelphia : Lippincott Williams and Wilkins, 2005. – 354 p.
2. Nelson Textbook of Pediatrics, 19th Edition. – Expert Consult Premium Edition – Enhanced Online Features and Print / by Robert M. Kliegman, MD, Bonita M.D. Stanton, MD, Joseph St. Geme, Nina Schor, MD, PhD and Richard E. Behrman, MD. – 2011. – 2680 p.
3. Pediatrics / Edited by O.V. Tiazhka, T.V. Pochinok, A.M. Antoshkina/ – Vinnytsa: Nova Knyha Publishers, 2011. – 584 p.
4. Baschat AA, Galan HL, Ross MG, Gabbe SG. Intrauterine growth restriction. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: Normal and Problem Pregnancies. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012:chap 31.
5. Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection, June 2003.
6. Public Health Service Task Force Recommendations for Use of Antiretroviral Drugs in Pregnant HIV-1-Infected Women for Maternal Health and Interventions to Reduce Perinatal HIV-1 Transmission in the United States, June 2003.
