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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute respiratory infections cause four and a half million deaths among children every year, the overwhelming majority occurring in developing countries. Pneumonia unassociated with measles causes 70% of these deaths; post-measles pneumonia, 15%; pertussis, 10%; and bronchiolitis and croup syndromes, 5%. Both bacterial and viral pathogens are responsible for these deaths. The most important bacterial agents are Streptococcus pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. The data on bacterial etiology of pneumonia during the first 3 months of life are limited, and almost no information on the role of chlamydia and pertussis in this age period is available. The distribution of viral pathogens in developing countries can be summarized as follows: respiratory syncytial virus, 15%-20%; parainfluenza viruses, 7%-10%; and influenza A and B viruses and adenovirus, 2%-4%. Mixed viral and bacterial infections occur frequently. Risk factors that increase the incidence and severity of lower respiratory infection in developing countries include large family size, lateness in the birth order, crowding, low birth weight, malnutrition, vitamin A deficiency, lack of breast feeding, pollution, and young age. Effective interventions for prevention and medical case management are urgently needed to save the lives of many children predisposed to severe disease.
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PMID:Epidemiology of acute respiratory infections in children of developing countries. 186 76

The isolation of measles virus in primary Rhesus monkey kidney cells (PRMK) in patients with documented giant-cell pneumonia who have presented without a rash is limited. The diagnosis usually is made by cytologic examination of nasal or bronchial secretions in which characteristic multinucleated giant cells with intranuclear and intracytoplasmic inclusion bodies are observed. The diagnosis of giant-cell pneumonia has been associated with measles virus but not exclusively. Canine distemper, herpes group viruses, and parainfluenza infections have been associated with these cells. In addition, vitamin A deficiency also has been cytologically associated with multinucleated giant cells. The authors describe the isolation of measles virus from bronchial washing and sputum in PRMK cells at 4 days from an 11-year-old child with acute interstitial pneumonia who was in remission for acute lymphocytic leukemia. Classic cytopathologic effect (CPE) consisting of syncytial and hole formation on the PRMK monolayer was apparent. In addition, a foamy appearance of the monolayer was noted in an otherwise clean lot of monkey cells. Confirmatory testing with measles antibody of the infected areas of the monolayer by indirect immunofluorescence (IFA) was positive for measles antigen and negative for mumps, parainfluenza (types I, II, and III) and influenza A and B virus. Serologic studies for measles antibody revealed an IFA IgG titer of greater than 1:10,240, and an IgM titer of 1:128. Cytologic examination of the same bronchial fluid revealed the typical giant cells with characteristic inclusions associated with measles virus. Because this disease usually is severe, and often fatal, prompt recognition of this virus is essential, not only to the patient, who can be treated with immunoglobulin and/or antiviral therapy, but also to prevent the spread of the virus to other patients and medical personnel. These findings also support direct evidence for the etiologic role of measles virus in giant-cell pneumonia that has been detected either histologically or cytologically and in tissue culture at autopsy.
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PMID:Isolation of measles virus in primary rhesus monkey cells from a child with acute interstitial pneumonia who cytologically had giant-cell pneumonia without a rash. 222 Jun 74

Treatment with high dose vitamin A has recently been recommended for children with measles in communities where vitamin A deficiency is a recognized problem. However, the relationship between vitamin A and measles mortality has not been clearly established. We studied serum vitamin A levels in 283 children less than or equal to 5 years of age admitted to Mama Yemo and Kalembe Lembe Hospitals in Kinshasa, Zaire, between January and March, 1987. Vitamin A levels were determined by high performance liquid chromatography. Vitamin A levels ranged from less than 5 to 63 micrograms/dl (median, 8). The overall case-fatality rate was 26 per cent. On univariate analysis, age less than 24 months, pneumonia on admission, lymphopenia (less than 2000/mm3), and lower vitamin A levels were associated with death during hospitalization. In a multivariate logistic regression model, a vitamin A level less than 5 micrograms/dl was associated with fatal outcome for children younger than 24 months old (relative risk = 2.9, 95 per cent CI 1.3, 6.8), but not for older children. Further studies are needed to determine whether low vitamin A levels predispose children to severe measles and the role of vitamin A supplements in the prevention of measles mortality.
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PMID:Vitamin A levels and mortality among hospitalized measles patients, Kinshasa, Zaire. 275 67

The vitamin A concentration in liver samples taken at autopsy from the central portion of the right lobe of 57 infants 0-1 year old was determined by a dual spectrophotometric and colorimetric assay. Death was due to respiratory disease (30%), complications of premature birth (16%), infections (14%), hemorrhage (14%), pneumonia (10%), cerebral edema (7%), and miscellaneous causes (9%). Gross malnutrition was noted in only 2 of these children. The median vitamin A concentration was 61 micrograms of retinol/g liver, with a range of 6-293 micrograms/g. The percent distribution of liver vitamin A levels in micrograms/g was: less than 5 (0%); 5-10 (7%); 10-20 (5%); 20-40 (16%); 40-80 (42%); 80-120 (14%); greater than 120 (16%). The mean liver level in 9 stillborn full-term infants (60 micrograms/g) was markedly lower than in 7 stillborn premature infants (125 micrograms/g). The median value for 22 infants from indigent families (54 micrograms/g) was lower than that of 35 infants from non-indigent families (65 micrograms/g). By applying the criteria that liver reserves of vitamin A less than or equal to 5 micrograms retinol/g of liver indicate a high risk of vitamin A deficiency and those less than 20 micrograms retinol/g of liver denote an inadequate reserve, no infant was at high risk but 12% had insufficient reserves.
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PMID:Concentration of vitamin A in the liver of foetuses and infants dying of various causes in Brasilia, Brazil. 650 Aug 35

Measles, a highly contagious viral disease, kills several hundred thousand infants and young children yearly. Essentially all children will become infected; at least 1% of those living in developing countries will die unless protected by immunization. In urban areas, peak incidence occurs in those younger than three years. The youngest and most undernourished children suffer the most severe complications and the highest risk of death. Diarrhea, malnutrition, pneumonia, and blindness associated with vitamin A deficiency are the worst complications. The infection is preventable by the timely administration of a potent vaccine. This endeavor requires a well-managed technical and administrative network that remains difficult to organize in many areas of the world. The vaccine is efficacious and has few adverse effects but must be provided to children during the short interval between loss of transplacentally acquired antibodies and the acquisition of natural infection. The improvements in heat stability of the vaccine increase the likelihood of providing potent vaccine, but a well-managed cold chain remains a prerequisite for any successful immunization program. Health education, improved management skills, publicity, and community support are all important factors for ultimately preventing the morbidity and mortality from this disease.
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PMID:Selective primary health care: strategies for control of disease in the developing world. IV. Measles. 684 6

A prospective study was undertaken from April 1988 to April 1989, to assess the diarrheal and respiratory complications of measles. Standard definitions were used for the cases, Measles Associated Diarrhea (MAD) and Measles Related Pneumonia (MRP). Children with diarrhea not related to measles were recruited for comparison for MAD. There was a total of 454 cases, measles 53 (11.7%), measles associated diarrhea (MAD) 113 (24.9%), measles related pneumonia (MRP) 186 (41.0%) and MAD with MRP 102 (22.5%). Children under 10 months and 24 months were 11% and 51.5%, respectively. Altogether 215/401 (53.6%) and 288/401 (71.8%) had diarrhea and pneumonia. Children who had been measles vaccinated were 8.4%. The overall case fatality was 4.2%. Case fatality in pneumonia was 1.1%. There was no statistically significant difference between the MAD and diarrhea in relation to religion, water supply, the method of excreta disposal, nutritional status and immunization status other than measles vaccination. There was significant difference in the nature of stools between the two groups, the stools of MAD were more of dysenteric in nature (p < 0.005). Vitamin A deficiency as evidenced by eye signs, was significantly more in MAD than in diarrhea (p < 0.001). It is recommended that Vitamin-A be given to all children with measles, complication due to diarrhea be promptly and adequately treated and to consider measles vaccination earlier than 9 months.
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PMID:Measles associated diarrhea and pneumonia in south India. 788 16

A prospective study of 90 children admitted to Ethio-Swedish Children's Hospital in Addis Ababa, Ethiopia, in 1992 with severe protein-energy malnutrition assessed the clinical profile and patterns of infection. The children, who ranged in age from 4 to 60 months, suffered from marasmus (49%), marasmic-kwashiorkor (42%), and kwashiorkor (19%). Septicemia, the most alarming complication of severe protein-energy malnutrition, was present in 32 children (36%); gram-negative enteric bacilli were the most common bacterial pathogen. 57 children (63%) had pneumonia and 23 (26%) had tuberculosis. Another 33 (37%) had a urinary tract infection. 17 children (19%) presented with diarrhea, 33 (37%) had clinical and radiologic evidence of rickets, and 15 (17%) had clinical evidence of vitamin A deficiency. There were 29 deaths in this series (from septicemia, gastroenteritis, pneumonia, and disseminated tuberculosis), for a case fatality rate of 32%. Mortality was significantly greater among children with a total serum protein of 5 gm% or less and those with systemic infection. This profile differs from those recorded in other developing countries, suggesting that severe protein-energy malnutrition has clinical and geographic heterogeneity.
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PMID:Clinical profile and pattern of infection in Ethiopian children with severe protein-energy malnutrition. 806 77

Vitamin A deficiency is a major public health problem in the countries of the Sahel. It causes xerophthalmia and high rates of child mortality and it occurs mostly in underdeveloped regions. People of all ages may suffer from vitamin A deficiency but it is a particular problem in pre-school-age children. Each year, about 250,000 children throughout the world become blind due to vitamin A deficiency. Measles, pneumonia and diarrhea reduce the child's reserves of retinol and increase the dietary requirement for vitamin A. Improvement of social conditions is a radical approach to preventing vitamin A deficiency. Three strategies are currently in use: horticultural activities and health education; fortification of food products; distribution of high-dose vitamin A capsules.
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PMID:[Strategies to control vitamin A deficiency]. 964 44

Vitamin A deficiency and acute lower respiratory tract infections coexist as important public health problems in many developing countries. We carried out a randomized, double-blind, placebo-controlled trial to examine whether large doses of vitamin A given to Tanzanian children who are admitted to the hospital with nonmeasles pneumonia would reduce the severity of respiratory disease. Six hundred eighty-seven children were randomly assigned to receive either placebo or vitamin A [200 000 IU (60 mg retinol equivalents) for children > 1 y of age and 100000 IU (30 mg retinol equivalents) for infants] on the day of admission and another dose on the following day. Of the 346 children in the vitamin A group, 13 died in the hospital, compared with 8 of 341 children in the placebo group; the relative mortality was 1.63 (95% CI: 0.67, 3.97; P = 0.28). The mean number of days of hospitalization was the same in both groups (4.2 d). There were no differences between the vitamin A and placebo groups in the duration of hospital stay when examined within categories of children stratified by age, sex, breast-feeding status, nutritional status at baseline, or quartile of dietary vitamin A intake in the 4 mo before admission to the hospital. There were also no differences in the mean number of days of fever, rapid respiratory rate, or hypoxia, whether these endpoints were examined in the total number of subjects or in a subset with more severe clinical conditions at baseline. Large doses of vitamin A had no protective effect on the course of pneumonia in hospitalized Tanzanian children.
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PMID:Vitamin A supplementation and severity of pneumonia in children admitted to the hospital in Dar es Salaam, Tanzania. 966 91

In Japan, chronic lung disease (CLD) is defined as an oxygen requirement greater than that obtainable in room air at 28 days of age, with symptoms of persistent respirator distress and a hazy or emphysematous and fibrous appearance upon chest x-ray. A total of 4964 infants weighing less than 1500 g at birth and born in 1990 were admitted to and cared for at level II and III neonatal care centers in Japan. A total of 4293 infants (86.3%) survived at 28 days after birth. Analyses of infants who developed CLD through their preceding illnesses and chest x-ray findings resulted in the classification of CLD into six types. Types I and II are defined as CLD following the acute stage respiratory distress syndrome (RDS). Type I is the typical case of bronchopulmonary dysplasia (BPD) as described previously, whereas Type II shows atypical radiological findings, namely only diffuse haziness without typical emphysema and fibrosis. Type III has a history of intrauterine inflammation. Chest x-ray shows the typical bubbling and cystic appearance described in the original report of Wilson-Mikity syndrome or neonatal pulmonary emphysema in the very low birth weight infant. Type III also has atypical radiological findings in cases with intrauterine infection. Type IV does not have a history of either intrauterine inflammation or RDS but shows typical emphysematous and fibrous appearance upon chest x-ray. Type V includes those with atypical chest x-ray appearance similar to Type II but without history of RDS and intrauterine inflammation. CLD is a heterogeneous condition which shows different spectra. However, the cardinal event is common to all types--the excessive inflammatory response caused by various insults to the immature airways and alveoli, such as oxygen, barotrauma, infection and so on. The excessive inflammatory response leads to lung tissue damage and the abnormal healing process due to immaturity, (such as vitamin A deficiency and insufficient oxygen radical scavenging system) and results in dysplasia and metaplasia of the respiratory system. The treatment of respiratory distress due to CLD also acts as an insult to the lungs and thus forms a vicious cycle. The different spectra of the disease are most possibly attributed to the difference in the timing and the kind of insults to the lungs. In Type I and II CLD, the insults are given in the first hours of life when the infants with surfactant deficiency receive high concentrations of oxygen for stabilization before the surfactant replacement. In Type III and III' CLD the insults are most likely given before birth. Excessive and sustained inflammatory response in the lungs with different onset times may result in the development of Type IV and V CLD. The strategy for the prevention of CLD should be different according to the origins and causes. The prevention of Type I and II CLD, or CLD following RDS, should be accomplished by successful prophylactic surfactant replacement therapy. Another procedure may be the application of high frequency oscillatory ventilation (HFOV) in the acute stage of RDS or at the time of stabilization right after birth. Types III and III' CLD present the most difficult challenge for prevention strategy because the disease process already started before birth. At the moment there are no effective measures for prevention. The strategy for the prevention of Type IV and V CLD may reside in the early detection and treatment of patent ductus arteriosus, sepsis and airway infection including pneumonia.
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PMID:Chronic lung disease of the very low birth weight infant--is it preventable? 967 27


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