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 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Describing the course of illness of six newborn infants suffering from connatal respectively postnatal acquired cytomegalovirus infection most important problems of this disease during neonatal period are discussed. There are reviewed: questions according diagnostic specificity of CMV-infection in the newborn; neurologic and sensorineural sequelae; the influence of prematurity and immune deficiency on the severity of the disease; possibility of chemotherapy against CMV and; the morbidity of preterm infants following postnatal, especially transfusion-associated CMV-infection.
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PMID:[Clinical aspects and problems of cytomegalovirus infections in newborn and premature infants]. 166 63

We treated eight children, aged 7 weeks to 17 years, for lung abscess. Each abscess followed an episode of aspiration or a bacterial pneumonia. Associated conditions were leukemia, congenital immune deficiency, endocarditis, cerebral palsy, and prematurity. Seven of the 8 children had polymicrobial infections, usually containing both aerobic and anaerobic bacteria. The success of medical treatment by antibiotics and chest physiotherapy was age related; 3 of the 8 children, aged 10 to 17 years, recovered on this regimen, whereas five children, aged 7 weeks to 7 years, required catheter drainage or resection for cure. Drainage by catheter pneumonostomy was performed for solitary peripheral bacterial abscesses. A large intercostal catheter was inserted into the cavity, either operatively or percutaneously. Wedge resection was performed for multiple, central, or fungal abscesses. Pneumonostomy was curative in 3 of 4 children. One chronic abscess recurred after pneumonostomy and required resection. Wedge resection was curative in the two children who came to thoracotomy; lobectomy was not necessary. Although all eight children recovered from their lung abscesses, three of them died within a year of sepsis. Lung abscess today occurs in immunocompromised children who are vulnerable to fatal infections. Chest physiotherapy is unlikely to achieve good drainage in children under 7 years of age. Medical failures can be identified within the first week of treatment. Early and aggressive surgical treatment is indicated in such children, and may be lifesaving.
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PMID:Drainage of pediatric lung abscess by cough, catheter, or complete resection. 373 40

Fungal infections of the heart are infrequent postoperative complications in children, yet, when present are often fatal. Children autopsied at The Johns Hopkins Hospital from 1889 to the present were studied for cardiac fungal infection. Among the 14 children so identified, 8 developed cardiac fungal infection after surgery. All postoperative cardiac infections were caused by Candida species. All were autopsied since 1959. Gastrointestinal surgery was performed in 6 patients and cardiac surgery in 2. Candida infection was not confined to the endocardium; endocarditis developed in 2 patients, pericarditis in 1, and myocarditis in 5. None received cytotoxic agents or corticosteroids. Two patients died from direct cardiac involvement. Other deaths were related to Candida sepsis or bronchopneumonia. A clinical diagnosis of cardiac fungal infection was never made. Prolonged administration of multiple antibiotics, central venous catheterization, prematurity and immune deficiency predisposed to cardiac and systemic candidiasis. Clinical features facilitating early diagnosis are discussed. Removal of central venous catheters infected with Candida did not eliminate the source of continued sepsis, since Candida-laden vegetations related to the catheter adhered to the superior vena cava and endocardial surface. Postoperative cardiac candidiasis is a relatively new and persistent problem of early diagnosis and therapy. The post-surgical pediatric patient has major predisposing factors for cardiac candidiasis, which, if unrecognized, may be a source for continued dissemination or may in itself be the cause of death.
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PMID:Postoperative Candida infections of the heart in children: clinicopathologic study of a continuing problem of diagnosis and therapy. 738 69

Human immunodeficiency virus type-1 (HIV-1)-associated neurologic disease, known as "HIV-1-associated progressive encephalopathy" (PE), is a common concomitant in the progression towards AIDS. PE, characterized by a triad of symptoms including impaired brain growth, progressive motor dysfunction, and loss or plateau of developmental milestones, is believed to result from both direct and indirect effects of HIV-1 infection on the central nervous system (CNS). Consequent to the hallmark systemic immune deficiency of HIV infection, the CNS becomes susceptible to opportunistic infections which add further morbidity and mortality, and may contribute either directly or indirectly to neurologic symptoms which can often mimic PE. Static encephalopathies (SE) represent fixed, nonprogressive neurologic or neurodevelopmental deficits in HIV-infected children. SE may or may not be caused by HIV infection but are often associated with such identifiable insults as prematurity, in utero exposure to toxins or infectious agents, or head trauma. Additional neurological manifestations of HIV infection are seizures, cerebrovascular complications (i.e., stroke), myelopathies, neuromuscular syndromes, and CNS complications of opportunistic infections. Neurobehavioral aberrations have also been observed in pediatric HIV infection. In addition to the neuropathogenesis, theories regarding the timing and detection of the neurological problems associated with pediatric HIV infection are discussed along with a presentation of current treatment paradigms and their rationales. The importance of identifying the numerous environmental factors, including nutritional status, that may confound the ability to discriminate between a primary or secondary role of HIV infection in the various neurological problems of HIV infection is discussed.
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PMID:Neurological and developmental problems in pediatric HIV infection. 886 30

A medical officer for the Expanded Program on Immunization (EPI) of the World Health Organization (WHO) calls for staff at all health facilities to screen and, if appropriate, immunize every infant, child, and woman of reproductive age attending health facilities. Routine immunization services tend to miss many women and children who should be immunized. Three important components comprise the health team approach needed to avoid missed opportunities: awareness to screen, a well-organized referral system within each health facility, and regular availability of vaccines. In the health facility, the nonimmunized child is at risk of contracting measles, so all such children should be immunized before they leave the health facility. The WHO/EPI medical officer presents five ways to avoid missed opportunities: screen and immunize at every opportunity, administer all required vaccines, stress real and avoid false contraindications, train staff, and open new vials of vaccine when needed. Contraindications to immunization include severe adverse reactions after a dose of vaccine (collapse or shock, convulsions without fever, anaphylaxis, or encephalitis/encephalopathy), neurological disease (for vaccines containing whole cell pertussis), immune deficiency diseases or immunosuppression due to drugs (generally for live vaccines), and symptomatic HIV infections (for BCG or yellow fever vaccines). The following conditions do not preclude immunization: minor illnesses (e.g., upper respiratory infections); allergy, asthma, hay fever, or "snuffles"; prematurity, small-for-date infants; malnutrition; breast feeding; family history of convulsions; treatment with antibiotics, low-dose corticosteroids, or locally acting steroids; eczema or localized skin infection; chronic diseases of the heart, lung, kidney, or liver; stable neurological conditions (e.g., Down syndrome), and history of jaundice after birth. WHO/EPI has an exit survey for use at district-level clinics or hospitals available so program managers can learn if they are missing chances to immunize children.
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PMID:Opportunities to immunise. 1229 31

Neonatal diabetes mellitus is a rare (1/400 000 newborns) but potentially devastating condition, which may be transient or permanent; typical symptoms occur within the first 4 wk of life. The transient form is a developmental insulin production disorder that resolves postnatally. Fifty to 60% of cases can be seen as transient form. Cases that require lifelong insulin therapy can be described as permanent condition. This fraction of cases is less common than the transient form. There are no clinical features that can predict whether a neonate with diabetes mellitus but no other dysmorphology will eventually have permanent neonatal diabetes mellitus (PNDM) or transient neonatal diabetes mellitus. Some metabolic or genetic defects such as complete deficiency of glucokinase or heterozygous activating mutations of KCNJ11, encoding Kir6.2, were found in patients with PNDM. A preterm female infant with a gestational age of 36 wk was admitted to the neonatal intensive care unit in the first hours of life due to prematurity and intra-uterine growth retardation. She was diagnosed as having arthrogryposis multiplex congenita on the first day. Hyperglycemia was detected on the third day of life, and she required insulin treatment. The patient is now 6 yr old with PNDM, arthrogryposis multiplex, neurogenic bladder, immune deficiency, constipation, and ichthyosis. Is this a new form of neonatal diabetes mellitus?
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PMID:Permanent neonatal diabetes with arthrogryposis multiplex congenita and neurogenic bladder - a new syndrome? 1705 50

In this report, we describe a brother and sister who presented at birth with short-limb skeletal dysplasia, polyhydramnios, prematurity, and generalized edema. Dysmorphic features included broad nose, thick ears, thin lips, micrognathia, inverted nipples, ulnar deviation at the wrists, spatulate fingers, fifth finger camptodactyly, nail hypoplasia, and talipes equinovarus. Other features included short stature, microcephaly, psychomotor retardation, B-cell lymphopenic hypogammaglobulinemia, sensorineural deafness, retinal detachment and blindness, intestinal malrotation with poor gastrointestinal motility, persistent hyponatremia, intermittent hypoglycemia, and thrombocytopenia. Cardiac anomalies included PDA, VSD, hypertrophic cardiomyopathy, and arrhythmias. The brother had a small penis with hypospadias, hypoplastic scrotum, and non-palpable testes. Skeletal findings included absent ossification of cervical vertebral bodies, pubic bones, knee epiphyses, and tali. Both sibs died before age 2 years, one of overwhelming sepsis and the other of cardiorespiratory failure associated with her cardiomyopathy. Metabolic studies showed a type 1 pattern of abnormal serum transferrin glycosylation. Fibroblasts synthesized truncated LLOs, primarily Man(7)GlcNAc(2), suggestive of CDG-Ig. Both sibs were compound heterozygotes for a novel 301 G > A (G101R) mutation and a previously described 437 G > A (R146Q) mutation in ALG12. Congenital disorders of glycosylation should be considered for children with undiagnosed multi-system disease including neurodevelopmental delay, skeletal dysplasia, immune deficiency, male genital hypoplasia, and cardiomyopathy.
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PMID:Expanding spectrum of congenital disorder of glycosylation Ig (CDG-Ig): sibs with a unique skeletal dysplasia, hypogammaglobulinemia, cardiomyopathy, genital malformations, and early lethality. 1750 7

Aspergillosis is an uncommon infection in neonates. However, it has been an emerging problem for preterm infants in recent years because of long-term parenteral nutrition, multiple-antibiotic therapy and immune deficiency due to prematurity. We report a preterm neonate with disseminated cutaneous lesions due to primary cutaneous aspergillosis. She died despite an early treatment with liposomal amphotericin B. Fungal infections should be remembered in preterms whose clinical conditions and laboratory tests for infection deteriorate, despite an appropriate antibiotic and supportive therapy.
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PMID:Primary cutaneous aspergillosis in an extremely low birth weight preterm. 2019 1

Respiratory syncytial virus (RSV) causes respiratory tract infections, especially among young infants. Practically, all infants are infected during epidemics and the clinical presentation ranges from subclinical to fatal infection. Known risk factors for severe RSV infection include prematurity, age of <2 months, underlying chronic lung or heart diseases, serious neurological or metabolic disorders, immune deficiency (especially a disorder of cellular immunity), crowded living conditions, and indoor smoke pollution. Twin studies indicate that host genetic factors affect susceptibility to severe RSV infection. Pattern recognition receptors (PRRs) are the key mediators of the innate immune response to RSV. In the distal respiratory tract, RSV is recognized by the transmembrane Toll-like receptor 4 (TLR4) and adapter proteins, which lead to production of proinflammatory cytokines and subsequent activation of the adaptive immune response. Surfactant proteins A and D are able to bind both RSV and TLR4, modulating the inflammatory response. Genetic variations in TLR4, SP-A, and SP-D have been associated with the risk of severe RSV bronchiolitis, but the results have varied between studies. Both the homozygous hyporesponsive 299Gly genotype of TLR4 and the non-synonymous SP-A and SP-D polymorphism influence the presentation of RSV infection. The reported relative risks associated with these markers are not robust enough to justify clinical use. However, current evidence indicates that innate immune responses including pattern recognition receptors (PRRs) and other components in the distal airways and airspaces profoundly influence the innate immune responses, playing a key role in host resistance to RSV in young infants. This information is useful in guiding efforts to develop better means to identify the high-risk infants and to treat this potentially fatal infection effectively.
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PMID:Pattern recognition receptors and genetic risk for rsv infection: value for clinical decision-making? 2096 41

The administration of the adequate amount of nutrients helps to improve a correct short-term linear growth and long-term neurocognitive development. To reduce the extra-uterine growth delay in very low birth weight infants (VLBW) the best strategy of nutrition (parenteral or enteral) should be established rapidly, since the first day of life. In preterm infants, nutrition can be administered parenterally and enterally. Prematurity is the most frequent indication for parenteral nutritional support due to intestinal functional immune deficiency, deficiency of digestive enzymatic systems and reduced nutritional reserve of these infants. In terms of enteral nutrition, breast milk is the first choice. In case of preterm and VLBW infants, fortifiers are used to overcome breast milk's protein and mineral deficiencies. When breast milk is not available, specific infant formula is the alternative.
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PMID:Feeding of preterm infants and fortification of breast milk. 2867 79


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