Maternal and child health after injuries: a two-year follow-up of a nationally representative sample.

OBJECTIVE: The objective of this study was to examine the association between childhood injury and health outcomes among survivors and their mothers using a national survey in the United States (US). STUDY DESIGN: This was a longitudinal analysis of a nationally representative sample. METHODS: Secondary analysis of the 1997-2013 Medical Expenditure Panel Survey (MEPS) was performed. Children (aged 2-18 years) with or without injuries were followed up for two years. Injuries captured in the study were those associated with at least one hospitalization, emergency department visit, or office-based visit. Outcome measures were child and maternal general and mental health status. Multiple mixed-logistic regressions were used with suboptimal health defined as the response of poor or fair health versus good, very good, or excellent health. RESULTS: Of the 63,422 children analyzed, 3251 (4.9%) were injured, representing 3.6 million US children. Injured children were more likely to be male, white, and older than those without injuries (P < 0.01). About a fifth of injured children suffered head injuries. Injuries were strongly associated with suboptimal general and mental health status in children (adjusted odds ratios [AORs], 1.35 and 1.36, respectively, P < 0.05). Mothers of children with injuries were also more likely to report suboptimal mental health (AOR, 1.30, P < 0.05). CONCLUSION: Injuries among children are associated with lasting adverse effects in general and mental health. To improve health outcomes of pediatric injuries, further follow-up care may be needed to ensure that they return to pre-injury health levels. These results highlight the importance of primary prevention and the long-term impact of injuries on the health of children and their mothers.

C-Peptide replacement therapy in type 1 diabetes: are we in the trough of disillusionment?

Type 1 diabetes is associated with such complications as blindness, kidney failure, and nerve damage. Replacing C-peptide, a hormone normally co-secreted with insulin, has been shown to reduce diabetes-related complications. Interestingly, after nearly 30 years of positive research results, C-peptide is still not being co-administered with insulin to diabetic patients. The following review discusses the potential of C-peptide as an auxilliary replacement therapy and why it's not currently being used as a therapeutic.

Temporal Progression of Lesions in Guinea Pigs Infected With Lassa Virus.

Lassa virus (LASV) infection causes an acute, multisystemic viral hemorrhagic fever that annually infects an estimated 100 000 to 300 000 persons in West Africa. This pathogenesis study evaluated the temporal progression of disease in guinea pigs following aerosol and subcutaneous inoculation of the Josiah strain of LASV as well as the usefulness of Strain 13 guinea pigs as an animal model for Lassa fever. After experimental infection, guinea pigs ( Cavia porcellus; n = 67) were serially sampled to evaluate the temporal progression of infection, gross and histologic lesions, and serum chemistry and hematologic changes. Guinea pigs developed viremia on day 5 to 6 postexposure (PE), with clinical signs appearing by day 7 to 8 PE. Complete blood counts revealed lymphopenia and thrombocytopenia. Gross pathologic findings included skin lesions and congested lungs. Histologic lesions consisted of cortical lymphoid depletion by day 6 to 7 PE with lymphohistiocytic interstitial pneumonia at 7 to 8 days PE. Scattered hepatocellular degeneration and cell death were also noted in the liver and, to a lesser extent, in other tissues including the haired skin, lung, heart, adrenal gland, lymph nodes, thymus, and spleen. The first cell types to demonstrate staining for viral antigen were fibroblastic reticular cells and macrophages/dendritic cells in the lymph nodes on day 5 to 6 PE. This study demonstrates similarities between Lassa viral disease in human infections and experimental guinea pig infection. These shared pathologic characteristics support the utility of guinea pigs as an additional animal model for vaccine and therapeutic development under the Food and Drug Administration's Animal Rule.

Pathogenesis of Bolivian Hemorrhagic Fever in Guinea Pigs.

Machupo virus, the cause of Bolivian hemorrhagic fever, is a highly lethal viral hemorrhagic fever with no Food and Drug Administration-approved vaccines or therapeutics. This study evaluated the guinea pig as a model using the Machupo virus-Chicava strain administered via aerosol challenge. Guinea pigs (Cavia porcellus) were serially sampled to evaluate the temporal progression of infection, gross and histologic lesions, and sequential changes in serum chemistry and hematology. The incubation period was 5 to 12 days, and complete blood counts revealed leukopenia with lymphopenia and thrombocytopenia. Gross pathologic findings included congestion and hemorrhage of the gastrointestinal mucosa and serosa, noncollapsing lungs with fluid exudation, enlarged lymph nodes, and progressive pallor and friability of the liver. Histologic lesions consisted of foci of degeneration and cell death in the haired skin, liver, pancreas, adrenal glands, lymph nodes, tongue, esophagus, salivary glands, renal pelvis, small intestine, and large intestine. Lymphohistiocytic interstitial pneumonia was also present. Inflammation within the central nervous system, interpreted as nonsuppurative encephalitis, was histologically apparent approximately 16 days postexposure and was generally progressive. Macrophages in the tracheobronchial lymph node, on day 5 postexposure, were the first cells to demonstrate visible viral antigen. Viral antigen was detected throughout the lymphoid system by day 9 postexposure, followed by prominent spread within epithelial tissues and then brain. This study provides insight into the course of Machupo virus infection and supports the utility of guinea pigs as an additional animal model for vaccine and therapeutic development.

Pathology of experimental Machupo virus infection, Chicava strain, in cynomolgus macaques (Macaca fascicularis) by intramuscular and aerosol exposure.

Machupo virus, the causative agent of Bolivian hemorrhagic fever (BHF), is a highly lethal viral hemorrhagic fever of which little is known and for which no Food and Drug Administration-approved vaccines or therapeutics are available. This study evaluated the cynomolgus macaque as an animal model using the Machupo virus, Chicava strain, via intramuscular and aerosol challenge. The incubation period was 6 to 10 days with initial signs of depression, anorexia, diarrhea, mild fever, and a petechial skin rash. These were often followed by neurologic signs and death within an average of 18 days. Complete blood counts revealed leukopenia as well as marked thrombocytopenia. Serum chemistry values identified a decrease in total protein, marked increases in alanine aminotransferase and aspartate aminotransferase, and moderate increases in alkaline phosphatase. Gross pathology findings included a macular rash extending across the axillary and inguinal regions beginning at approximately 10 days postexposure as well as enlarged lymph nodes and spleen, enlarged and friable liver, and sporadic hemorrhages along the gastrointestinal mucosa and serosa. Histologic lesions consisted of foci of degeneration and necrosis/apoptosis in the haired skin, liver, pancreas, adrenal glands, lymph nodes, tongue, esophagus, salivary glands, stomach, small intestine, and large intestine. Lymphohistiocytic interstitial pneumonia was also present. Inflammation within the central nervous system (nonsuppurative encephalitis) was histologically apparent approximately 16 days postexposure and was generally progressive. This study provides insight into the course of Machupo virus infection in cynomolgus macaques and supports the usefulness of cynomolgus macaques as a viable model of human Machupo virus infection.

Low-titre auto-antibodies predict autoimmune disease during interferon-alpha treatment of chronic hepatitis C.

BACKGROUND: In this study, we determined whether low-titre auto-antibodies are a risk factor for the development of autoimmune disease during interferon-alpha (IFNalpha) therapy for chronic hepatitis C (CHC) infection. METHODS: Eighty-three patients with circulating hepatitis C virus RNA and chronic viral hepatitis on liver biopsy, who had not received IFNalpha, were assessed for serum auto-antibodies (anti-nuclear antibodies (ANA), anti-smooth muscle antibodies, thyroid microsomal antibodies, thyroglobulin antibodies) and thyroid function tests. RESULTS: Thirty-five patients had one or more pre-existing auto-antibody. The majority were low titre ANA. Seven of the 35 patients had clinical autoimmune disease or immune-mediated disorders, predominantly thyroid disease. Twenty patients with low titre auto-antibodies received treatment with IFNalpha and of these 20 patients, six patients developed adverse effects with a possible auto-immune basis. In comparison, only five of the 48 patients without auto-antibodies had immune-mediated disorders and no patient developed autoimmune complications during therapy with IFNalpha. CONCLUSIONS: These results suggest that the presence of low-titre auto-antibodies may be a risk factor for the development of autoimmune dysfunction during IFNalpha therapy for chronic hepatitis C. Patients with no detectable auto-antibodies have a low risk for developing autoimmune complications during treatment with IFNalpha.

Assessment of two 'low-tech' genetic health care procedures performed by prenatal care providers in Washington state: implications for future policy development activities.

Equity in health care demands that patients be treated fairly, impartially and with justice. Health care professionals and others have long been aware of the concept of equity, and the many inequities that exist in our health care system. As part of our analysis of postpartum data collected between 1993 and 1996 by the Washington Pregnancy Risk Assessment Monitoring System (PRAMS) from self-administered patient surveys, we explored equity as it pertains to two 'low-tech' prenatal genetic health care procedures: (1) whether or not prenatal care providers asked their patients about a family history of birth defects/genetic disorders, and (2) whether or not prenatal care providers talked to their patients about prenatal testing for birth defects/genetic disorders. Overall, about 80% of pregnant women reported that they had been asked about their family history of birth defects/genetic disorders, and about 85% said that their prenatal care provider(s) had talked to them about prenatal testing. Maternal characteristics associated with a lower likelihood of receiving these two low-tech genetic health care procedures appeared to be young maternal age, and low education and income levels, regardless of where women with these attributes received their prenatal care (e.g. community, migrant, health department or military health care clinics, private physicians, or health maintenance organizations).

Viral etiology and epidemiology of acute respiratory infections in children in Nairobi, Kenya.

Acute respiratory infection (ARI) is the most common cause of illness and death in young children worldwide. Because of inadequate laboratory facilities and financial resources the etiological agents responsible for most cases in developing countries remain unknown, thus obviating appropriate management. Therefore, an ARI program was commenced at the Kenyatta National Hospital, Nairobi, Kenya in 1981 with the objectives of establishing the microbial causes, clinical presentations, and diagnoses of ARI in children under 5 years of age and of developing simple, rapid, and inexpensive diagnostic techniques. Viruses were demonstrated in 54% of the 822 children studied, but over half of the viruses identified were types not commonly associated elsewhere with the causation of severe ARI. Respiratory syncytial, parainfluenza, and adenoviruses occurred in the same age groups and during similar weather conditions as elsewhere. Measles virus occurred most frequently in those 7 to 9 months old. Herpes simplex, rhino-, and enteroviruses play causative roles in some cases of severe ARI in Kenyan children. A combination of immunofluorescent and cell culture techniques were shown to be essential for the detection of viruses.

Investigation of the effectiveness of measles vaccination in children in Kenya.

Laboratory studies were performed on 128 children clinically diagnosed as measles when seen at the Infectious Diseases Hospital, Kenyatta National Hospital (IDH), Nairobi (86 cases) and the Rural Health Training Centre, Maragua, Central Province (42 cases) between 9 July and 31 August 1984. A concurrent measles infection was confirmed in 95% of the children seen at IDH and in 85% of those seen at Maragua, with similar proportions of confirmations in children who had, and who had not, received measles vaccine. No differences in the number of sero-conversions nor in the absolute levels of acute or convalescent HI antibody titres could be detected between vaccinated and unvaccinated children. Analysis of the cases seen at Maragua indicates that about two thirds of the children who had received vaccine were protected. A pilot study of vaccinating children at 8 months and again at 12-13 months is suggested in an attempt to eradicate measles.

Detection of rotavirus by a latex agglutination test, Rotalex: comparison with electron microscopy, immunofluorescence, polyacrylamide gel electrophoresis, and enzyme linked immunosorbent assay.

A commercially available latex agglutination test, Rotalex (Orion Diagnostics, Finland), for detecting rotaviruses was evaluated in comparison with four other tests (electron microscopy, immunofluorescence, polyacrylamide gel electrophoresis, and enzyme linked immunosorbent assay) routinely used in our laboratories. Although Rotalex was the least complex method, it showed lack of specificity and sensitivity when carried out according to the manufacturer's instructions. Four basic modifications of Rotalex are described. These include the use of Hank's balanced salt solution, increasing the incubation time to 20 min, reading the agglutination result by an experienced observer, and the use of 50 mm square glass plates. The modified procedure gave results which were comparable with those obtained by electron microscopy, immunofluorescence, polyacrylamide gel electrophoresis, and enzyme linked immunosorbent assay. The latter techniques, when used to detect rotavirus, all gave similar results.

The association of extrahepatic bile duct atresia and neonatal Epstein-Barr virus infection.

An infant with uncorrectable extrahepatic bile duct atresia was found to have evidence of Epstein-Barr virus infection during the neonatal period. It is probable that the infection was acquired in utero. In view of the association of hepatitis with the Epstein-Barr virus in later life, it is possible that this infection was responsible for the development of bile duct obstruction.

Application of immunofluorescence to a study of measles.

A new and rapid method for the laboratory diagnosis of measles, using the fluorescent antibody technique applied to nasopharyngeal secretions is described. The reliability of the method was best shown by correlation with clinical diagnosis, which gave an overall agreement of 95% in 53 cases of typical clinical measles and 72 control children. Correlation with results of tissue culture and serology was also good, though these methods are in practice too infrequently successful to be used as the main standards of reliability. The antiserum used for immunoflorescence showed no cross-reactivity with other viruses. Viruses could be identified by the fluorescent antibody technique from 4 days before to 10 days after the onset of the rash in a high proportion of cases. The wider applications of this method include rapid diagnosis of measles before the rash has appeared; in cases where clinical diagnosis is in doubt, especially in dark-skinned children, or when the illness has been modified by previous vaccination; prevention of cross-infection by early detection of measles; and investigation of the immune response and its relationship to nutritional status.

The relationship between measles virus infection and subacute sclerosing panencephalitis (SSPE).

On theoretical grounds we propose that the essential step in the development of subacute sclerosing panencephalitis (SSPE) after measles virus infection involves a reverse transcriptase-mediated change to a DNA form, probably brought about by co-infection with a leukovirus at a critical point in time. We further suggest that this new DNA then replicates either as the core of a new slow virus or as a membrane-attached viroid exhibiting a form of non-structural integration with host cell DNA resembling that found with the herpes viruses.