Viral Infections of the Lung
Lourdes R. Laraya-Cuasay, Walter T. Hughes in Interstitial Lung Diseases in Children, 2019
The third most important cause of interstitial viral lung infection in children is the parainfluenzae viruses. Parainfluenza viruses 1, 2, and 3 are responsible for the majority of human parainfluenza lower respiratory tract disease. Parainfluenza types 1 and 2 tend to be etiologically associated with croup and type 3 with pneumonitis. The pneumonitis caused by parainfluenza virus 3 is indistinguishable from that caused by respiratory syncytial virus and is second only to RSV as a cause of bronchiolitis in infants and children. Studies performed by investigators from the University of North Carolina at Chapel Hill, accumulated over an 11-year period in a pediatric practice, encompassed approximately 7000 lower respiratory tract infections including croup, tracheal bronchitis, bronchiolitis, and pneumonia. RSV and parainfluenza viruses types 1, 2, and 3 accounted for 48% of the isolates from patients with pneumonia. The risk of hospitalization for illness associated with para-influenza type 3 was considerably less than that for RSV despite the fact that infection rates were similar. The risk for infection with parainfluenza virus type 3 during the first 4 months of life was inversely related to the level of neutralizing antibody measurable in cord serum at the time of birth. This suggests a protective role for passively acquired maternal antibody.34 Lower respiratory tract disease associated with primary parainfluenza virus infection is seven times that associated with reinfection.
The Transfer of Passive and Active Immunity
Gérard Chaouat in The Immunology of the Fetus, 2020
Cramer et al.40 suggest that in the future, “immunologic engineering” might be employed to enhance the fetal response against infectious agents (or tolerance to selected tissue antigens). In practice this might be difficult to achieve,3 since a compromise must be made in order to administer the antigen early enough so that interference by maternal antibody will not block the response and late enough so that the fetal immune system is developed sufficiently to mount a response. Furthermore, it is well established that in many diseases the host immune response may well contribute towards the inflammatory component of the pathological process, thus augmentation of the fetal immune response at this stage might not be desirable and might adversely modify certain congenital infections.71 Finally, there is the question of induction of tolerance, which, though rare, does occur to some extent naturally, as explained earlier.
Therapeutic Apheresis in Children
James L. MacPherson, Duke O. Kasprisin in Therapeutic Hemapheresis, 2019
Immunologic factors play an important role in the growth and metastasis of neuroblastoma. Frequently, the tumor is infiltrated with lymphocytes and plasma cells. The patient’s lymphocytes may also react against neuroblastoma cells in tissue culture.31 In some cases the lymphocytes of the patient’s mother will also react with neuroblastoma cells. In spite of these facts, the tumor may not be rejected. Several hypotheses have been proposed to explain these findings. One explanation suggests that a blocking factor that coats the tumor antigens develops in these individuals. With the tumor coated with these blocking factors, the patient’s lymphocytes cannot recognize the foreign tumor antigens. The blocking factor may be an antibody. The antibody may be produced by the patient or in some cases the antibody may have been produced by the patient’s mother and crossed the placenta during the pregnancy. Since the amount of maternal antibody is limited, this may explain why the prognosis for this disease is significantly better if the patient is less than one year of age. The incidence of spontaneous remission is also higher in the very young patient.
Neonatal hemochromatosis in a newborn with Down syndrome
Published in Fetal and Pediatric Pathology, 2020
Rasheeda M, Suvendu Purkait, Amit Kumar Satapathy, Joseph John, Susama Patra, Suvradeep Mitra
The pathogenesis of GALD-NH is not well elucidated. The mother appears to be exposed to a hitherto unknown fetal antigen that invokes the formation of a maternal antibody. This antibody damages the hepatocytes after transplacental spread. Consequently, the hepatocytes bear the major brunt of the disease incurring a loss of hepatocyte mass with subsequent replacement fibrosis. The antigen–antibody complex formation on the surface of hepatocytes initiate a complement cascade that augurs into the formation of C5b-9 membrane attack complex (MAC) and the latter can be detected by immunohistochemical technique [2]. Importantly, the massive hepatocellular loss reduces the production of hepcidin leading to an absence of the negative ferroportin feedback. This leads onto the excess iron transport to the fetal liver. Remarkably, ferroportin expressing tissues (reticuloendothelial system) exhibit a lack of siderosis whereas tissues expressing ZIP14 without any ferroportin expression show siderotic deposits [2].
The role of the placenta in drug transport and fetal drug exposure
Published in Expert Review of Clinical Pharmacology, 2018
Placental transfer of immunoglobulins is of great clinical and research interest from several aspects: A variety of maternal antibodies are critical in providing the fetus and newborn passive immunity against serious human pathogens. Maternal immunoglobulin G (IgG), transferred across the placenta to the fetus during intrauterine life, is an important component of the neonatal immunological defense mechanisms against infection.The introduction of biologic therapy with therapeutic monoclonal antibodies to the treatment strategies of many maternal immunological conditions has raised concerns around fetal exposure to agents that may affect the development of its own immunity and response to pathogens.Maternal autoimmune IgG antibodies such as those found in maternal lupus erythematosus, antiphospholipid syndrome, Hashimoto disease ext, may cross the placenta and adversely affect the developing fetus. Among the possible injuries are congenital lupus, fetal cardiac block, or fetal thyroid dysfunction. Often, they may also significantly diminish placental function and cause fetal death or stillbirth.
Influenza vaccine programs for children in low- and middle-income countries: current status and way forward
Published in Expert Review of Vaccines, 2019
Justin R Ortiz, Kathleen M Neuzil
One option to improve the feasibility of vaccine delivery to the youngest children would be to incorporate influenza vaccines into the early EPI schedule. Influenza vaccination has been studied in an open-label safety and immunogenicity trial among infants aged as young as 6 weeks, and was shown to be safe with only mild local and systemic reactions [95,96]. Postvaccination seroprotection rates were assessed each year of the two-year study for H1N1 (32–46%), H3N2 (47–59%), and B (0–21%). Children with maternal antibodies at baseline (HA inhibition titers ≥1:8) were significantly less likely to have a fourfold rise in antibody titer after vaccination, indicating significant maternal antibody interference. Children of mothers who had not been immunized against influenza during pregnancy have seroresponses similar to those of 6-month-old children [96]. WHO has advocated for age de-escalation studies of the Russian LAIV, which may be a more programmatically feasible alternative to IIV when given during a routine EPI visit [97].