Serum trace element of chidren with and without bronchopneumonia / Niveles de oligoelementos en el suero de niños con bronconeumonía y sin ella

Objectives: trace elements like Zinc (Zn), iron (Fe) and copper (Cu) have a significant influence in maintaining the normal metabolic, modulating immune function and influencing the susceptibility of the organism to infection. But the relationship between trace element and bronchopneumonia was unclear. Methods: In this study, 28 children with bronchopneumonia and 46 healthy age-matched children were recruited. Serum (Zn), Cu, Fe, calcium (Ca) and/or magnesium (Mg) levels in children with and without bronchopneumonia were determined by atomic absorption spectrophotometry. Results: The results show that several microelement levels such as Zn, Ca, Mg, and Fe in bronchopneumonia group are lower than in control group. In bronchopneumonia group, serum Ca level is positively associated with zinc (Zn) (p < 0.05) and iron (Fe) (p < 0.05), while there is a pronounced positive correlation between copper (Cu) and calcium (Ca) (p < 0.05), magnesium (Mg) (p < 0.05). Conclusion: Serum trace element level may be associated with risk of bronchopneumonia among children (AU)

Objetivos: oligoelementos como zinc (Zn), hierro (Fe) y cobre (Cu) tienen una influencia significativa en el mantenimiento de la función inmune y del metabolismo normales; modulan la función immune e influyen en la susceptibilidad del organismo ante infecciones. Pero la relación entre trazas de estos elementos y la bronconeumonía resultó incierta. Métodos: en este estudio fueron incluidos 28 niños con bronconeumonía y 46 niños sanos agrupados por edad. Se determinaron los niveles de Zn, Cu, Fe, calcio (Ca) y/o magnesio (Mg) en el suero de los niños con bronconeumonía y sin ella mediante espectrofotometría de absorción atómica. Resultados: los resultados muestran que varios niveles de microelementos como Zn, Ca, Mg y Fe en el grupo con bronconeumonía son menores que en el grupo control. En el grupo de niños con bronconeumonía el nivel de Ca en el suero está asociado positivamente con el zinc (Zn) (p < 0,05), mientras que hay una correlación positiva entre el cobre (Cu) y el calcio (Ca) (p < 0,05), magnesio (mg) (p < 0,05). Conclusión: el nivel de oligoelemento en el suero puede estar asociado con el riesgo de bronconeumonía entre los niños (AU)

[Clinical application of tidal breathing lung function test in 1-4 years old children with wheezing diseases].

OBJECTIVE: To study the clinical significance of tidal breathing lung function test in 1-4 years old children with wheezing diseases. METHODS: A total of 141 1-4 years old children with wheezing diseases were enrolled as the observed groups (41 cases of asthma, 54 cases of asthmatic bronchitis, and 46 cases of bronchopneumonia). Thirty children without respiratory diseases were enrolled as the control group. All the recruits underwent tidal breathing lung function test. The observed groups underwent bronchial dilation test, and tidal breathing flow volume (TBFV) parameters were evaluated before and after bronchial dilation test. RESULTS: The observed groups showed obstructive ventilatory disorder (65%) according to the TBFV loop, and their ratio of time to peak tidal expiratory flow (TPTEF) to total expiratory time (TE) and ratio of volume to peak expiratory flow (VPEF) to total expiratory volume (VE) were significantly lower than in the control group (P<0.05). The asthma subgroup had significantly improved TPTEF/TE and VPEF/VE after bronchial dilation test (P<0.05). Taking an improvement rate of ≥ 15% either for TPTEF/TE or for VPEF/VE as an indicator of positive bronchial dilation test, the bronchial dilation test had a sensitivity of 47% and a specificity of 84% in diagnosing asthma in 1-4 years old children. The positive rate was 28% among the children in the asthma subgroup with an TPTEF/TE ratio of ≥ 23% before bronchial dilation test, versus 65% in those with an TPTEF/TE ratio of <23%. CONCLUSIONS: Obstructive ventilatory disorder is the main impairment of tidal breathing lung function in 1-4 years old children with wheezing diseases. Tidal breathing bronchial dilation test can reflect a reversal of airway obstruction to a certain extent. The sensitivity of bronchial dilation test for the diagnosis of asthma is not satisfactory in 1-4 years old children with wheezing diseases, but this test has a relatively high diagnostic value in children with severe airway obstruction.

Extracellular matrix remodeling genes polymorphisms and risk of chronic bronchitis and recurrent pneumonia in children.

We investigated the association of matrix metalloproteinases, the disintegrin and metalloprotease 33 and the tissue and serum inhibitors of proteinase gene polymorphisms with severe chronic respiratory diseases in Tatar children. We analyzed the case-control data sample from a total of 592 Tatar individuals, consisting of 119 children with chronic bronchitis, 138 with recurrent pneumonia and 335 control children residing in Ufa (Russia). The percentage of heterozygous genotype for the MMP9 (2660A>G) was higher among healthy children (52.54% vs 36.13% in chronic bronchitis patients, P(adj)=0.0033, P(cor)=0.033, odds ratio (OR)=0.51; and 36.96% in recurrent pneumonia group, P(adj)=0.0034, P(cor)=0.034, OR=0.53). The MMP12 (-82A>G) locus was associated with chronic bronchitis in the additive model (P(adj)=0.0091, P(cor)=0.09, OR=0.45, ß=-0.798). The relationship between the 6A6A genotype of MMP3 (-1171 5A>6A) (P(adj)=0.0013, P(cor)=0.013, OR=3.91) and the 6A-A haplotype of MMP3 (-1171 5A>6A) and MMP12 (-82A>G) and recurrent pneumonia were unraveled (Padj=0.001, P(cor)=0.01, OR=2.07). This haplotype was also associated with a higher risk of chronic bronchitis (P(adj)=0.0012, P(cor)=0.012, OR=2.15). The TIMP3 (-1296T>C) was associated with recurrent pneumonia in the dominant model (P(adj)=0.0031, P(cor)=0.031, OR=1.91). The MMP9, MMP3 and TIMP3 (tissue inhibitors of matrix metalloproteinases) polymorphisms and MMP3 and MMP12 haplotypes may play a substantial role in susceptibility to severe airway and lung injury in children with chronic bronchitis and recurrent pneumonia.

Natural history of inhalation melioidosis in rhesus macaques (Macaca mulatta) and African green monkeys (Chlorocebus aethiops).

Burkholderia pseudomallei, the causative agent of melioidosis, is recognized as a serious health threat due to its involvement in septic and pulmonary infections in areas of endemicity and is recognized by the Centers for Disease Control and Prevention as a category B biothreat agent. An animal model is desirable to evaluate the pathogenesis of melioidosis and medical countermeasures. A model system that represents human melioidosis infections is essential in this process. A group of 10 rhesus macaques (RMs) and 10 African green monkeys (AGMs) was exposed to aerosolized B. pseudomallei 1026b. The first clinical signs were fever developing 24 to 40 h postexposure followed by leukocytosis resulting from a high percentage of neutrophils. Dyspnea manifested 2 to 4 days postexposure. In the AGMs, an increase in interleukin 1ß (IL-1ß), IL-6, IL-8, gamma interferon (IFN-γ), and tumor necrosis factor alpha (TNF-α) was observed. In the RMs, IL-1ß, IL-6, and TNF-α increased. All the RMs and AGMs had various degrees of bronchopneumonia, with inflammation consisting of numerous neutrophils and a moderate number of macrophages. Both the RMs and the AGMs appear to develop a melioidosis infection that closely resembles that seen in acute human melioidosis. However, for an evaluation of medical countermeasures, AGMs appear to be a more appropriate model.

Severe course of community-acquired pneumonia in an adult patient who is heterozygous for Q481P in the perforin gene: are carriers of the mutation free of risk?

Most cases of autosomal recessive hemophagocytic lymphohistiocytosis (HLH) are associated with over 50 mutations in the perforin gene. Some of these mutations have no clear functional association. Only homozygous patients display a full-blown syndrome, whereas no severe disease has been described in heterozygous carriers of these mutations despite the presence of functional and phenotypic alterations in cytotoxic cells. We study the family of a child who died from HLH at 6 months of age due to a Q481P mutation in the perforin gene. The study is particularly interesting because the patient's heterozygous father experienced severe community-acquired pneumonia that could be attributed to deficient in vitro NK cell activity despite normal perforin expression. This case report suggests that impaired NK cell activity in a heterozygote can result in poorer initial control of infections with severe clinical expression.

Comparison of nifedipine and captopril in children with pulmonary hypertension due to bronchopneumonia.

This study included 40 children, who were diagnosed with pneumonia and pulmonary hypertension (from the radiographic and clinical features), was performed at Yuzuncu Yil University Faculty of Medicine, Department of Pediatrics, from September 2003 to July 2005. Patients who had pneumonia and congenital heart disease or systemic hypertension or renal and liver disease together were excluded from the study. Blood gas analysis and oxygen concentration, measured with pulse oximetry, were performed in all patients. Besides chest X-ray, electrocardiography and echocardiographic search was also carried out. Echocardiographic examination was performed by using M mode, two-dimensional echocardiography and colored Doppler sonotron Vingmed CFM 725. At echocardiographic examination, pulmonary hypertension is defined as above 35 mmHg of pulmonary artery pressure. For echocardiographic examination, patients with pulmonary hypertension were divided into two groups. Captopril (2 mg/kg/day, three doses a day) and nifedipine (0.5 mg/kg/day, three doses a day) were given to the first and the second group, respectively. Echocardiography was performed daily until normal pulmonary artery pressure was achieved. At the beginning of the treatment, the patients were treated with double antibiotics and antibiotic change was carried out in needed cases at the follow up. Digoxin was administered to the cases of respiratory infection with heart failure.

Laryngeal lesion in leprosy and the risk of aspiration.

Leprosy affects the larynx, damaging its mucosa and sensory nerves and loss of sensation may result in aspiration of food and secretions. The laryngeal lesion may be insidious. Post-mortem studies showed bronchopneumonia that could have originated from aspiration. In patients with laryngeal symptoms, dysphagia or aspiration pneumonia loss of laryngeal sensation should be looked for.

[Physiopathology of cystic fibrosis and of infections associated to this disease]. / Aspecte ale fiziopatologiei mucoviscidozei si a infectiilor bronhopulmonare asociate acesteia.

Cystic fibrosis (CF) is one of the most common lethal inherited diseases in the caucasian population. The hope of understanding the physiopathology of CF appeared after identification of the gene which encodes CF. The alteration in CFTR protein breaks the hydric balance of the mucosal secretions, producing mucus with increased viscosity. Broncho-pulmonary infections are constant encountered because of the stasis of the mucus. The most common bacterial pathogens in the sputum of patients with MV are Haemophilus influenzae, Staphylococcus aureus, Pseudomonas aeruginosa, Burkholderia cepacia. MV remains a severe, incurable disease, but the evolution is getting better because of the improvements of care methods.

Use of treatment records and lung lesion scoring to estimate the effect of respiratory disease on growth during early and late finishing periods in South African feedlot cattle.

Growth, morbidity, and slaughter data from 2,036 calves in 2 South African feedlots were used to estimate the effect of bovine respiratory disease (BRD) and of lung lesion type and extent on growth during the early (processing to d 35) and late (d 35 to slaughter) finishing periods. Calves were weighed at processing (d 5 after arrival), on d 35, and at slaughter after a mean of 137 d on feed. All calves were monitored twice daily and were treated for BRD if rectal temperature was > 40 degrees C or if other specific signs of BRD were present. After slaughter, the occurrence and extent of parenchymal bronchopneumonic lesions and pleural adhesions were recorded. Subclinical BRD (never treated but with lung lesions at slaughter) occurred in 29.7% and clinical BRD in 22.6% of calves. Lung lesions were present in 43% of calves at slaughter; 8.6% had parenchymal lesions and 38.8% had pleural adhesions. Using a combined case definition (treated for BRD and/or lung lesions present at slaughter), the incidence of BRD was 52.5%. During the early finishing period, clinical BRD reduced ADG by 216 g (P < 0.001), subclinical BRD reduced ADG by 91 g (P < 0.001), and the combined effect of BRD was a 143 g reduction in ADG (P < 0.001). After d 35, animals treated for BRD tended to grow faster than those with subclinical BRD (P = 0.11), indicating that treatment was generally successful in reducing economic losses. The extent of bronchopneumonic lesions at slaughter was not associated with reduced growth during the early finishing period (P = 0.27), but extensive lesions reduced ADG by 88 g during the late period (P = 0.02). In contrast, the extent of pleural adhesions was not associated with reduced growth rate during the late finishing period (P = 0.37) but was strongly associated with reduced ADG before d 35; there was a 101 g reduction (P < 0.001) and a 220 g reduction (P = 0.01) for adhesions involving < 50% and > 50% of the pleural surfaces, respectively. Thus, although the presence of bronchopneumonic lesions and pleural adhesions at slaughter were both associated with reductions in overall ADG, they were indicative of production losses having occurred at different times during the finishing period. The overall effect of BRD was a 24 g reduction in ADG (P = 0.02) and a 5.1 d increase in days on feed (P < 0.001). The hidden cost of reduced growth rate due to BRD amounted to $3.41 per calf with clinical or subclinical BRD, or $1.79 per animal entering the feedlot.

Intravenous versus nebulized ceftazidime in ventilated piglets with and without experimental bronchopneumonia: comparative effects of helium and nitrogen.

BACKGROUND: Lung deposition of intravenous cephalosporins is low. The lung deposition of equivalent doses of ceftazidime administered either intravenously or by ultrasonic nebulization using either nitrogen-oxygen or helium-oxygen as the carrying gas of the aerosol was compared in ventilated piglets with and without experimental bronchopneumonia. METHODS: Five piglets with noninfected lungs and 5 piglets with Pseudomonas aeruginosa experimental bronchopneumonia received 33 mg/kg ceftazidime intravenously. Ten piglets with noninfected lungs and 10 others with experimental P. aeruginosa bronchopneumonia received 50 mg/kg ceftazidime by ultrasonic nebulization. In each group, the ventilator was operated in half of the animals with a 65%/35% helium-oxygen or nitrogen-oxygen mixture. Animals were killed, and multiple lung specimens were sampled for measuring ceftazidime lung tissue concentrations by high-performance liquid chromatography. RESULTS: As compared with intravenous administration, nebulization of ceftazidime significantly increased lung tissue concentrations (17 +/- 13 vs. 383 +/- 84 microg/g in noninfected piglets and 10 +/- 3 vs. 129 +/- 108 microg/g in piglets with experimental bronchopneumonia; P < 0.001). The use of a 65%/35% helium-oxygen mixture induced a 33% additional increase in lung tissue concentrations in noninfected piglets (576 +/- 141 microg/g; P < 0.001) and no significant change in infected piglets (111 +/- 104 microg/g). CONCLUSION: Nebulization of ceftazidime induced a 5- to 30-fold increase in lung tissue concentrations as compared with intravenous administration. Using a helium-oxygen mixture as the carrying gas of the aerosol induced a substantial additional increase in lung deposition in noninfected piglets but not in piglets with experimental bronchopneumonia.

Diagnosis by ultrasonography of congestion of the caudal vena cava secondary to thrombosis in 12 cows.

This paper describes the clinical, ultrasonographic, radiographic and postmortem findings in 12 cows with thrombosis of the caudal vena cava. The principal clinical signs were chronic bronchopneumonia and fever in 11 cows; one cow had epistaxis and one cow bled from the mouth; eight cows had anaemia and leucocytosis, and the clotting time for the glutaraldehyde test was markedly decreased in all the cows; in nine of the cows the activity of gamma-glutamyltransferase was high, suggesting chronic hepatic congestion. The most important ultrasonographic finding was congestion of the caudal vena cava attributable to thrombosis of the vein. In all the cows the caudal vena cava was round to oval on cross-section, rather than the normal triangular shape. The hepatic, splenic and portal veins were dilated in five, three and one cow, respectively. The results of radiography and endoscopy supported a diagnosis of bronchopneumonia, but there were radiographic changes in the diaphragmatic lung lobes that supported a diagnosis of vena caval disease in only four cows. Postmortem there was a thrombosis of the caudal vena cava in all the cows, and the thrombi were located in the thoracic, subphrenic and abdominal part of the caudal vena cava at the level of the liver in four, one and seven cows, respectively. In three cows, the thrombus was situated where a hepatic abscess had broken into the caudal vena cava, and in one cow it was at the site of a diaphragmatic abscess. In another cow, there was a fistula between the major bronchus of the right diaphragmatic lung lobe and the caudal vena cava where the thrombus was situated. Three cows had liver abscesses that had not broken into the caudal vena cava. There was severe bronchopneumonia in 11 of the cows, some of which also had multiple pulmonary abscesses.

Sudden death of an infant with 'an early epileptic encephalopathy'.

This article reports an autopsy case of sudden death of an infant with an infrequent encephalopathy involving epileptic episodes. The infant was a 1-year and 10-month-old boy, who had a history of the first convulsive seizures in the third month after birth. The clinical diagnosis was described as 'an early infantile epileptic encephalopathy with suppression-bursts' (Ohtahara syndrome). On a winter day, he was collapsed following a high fever and was already dead on the arrival at a hospital. The body was small for the age and poorly nourished. The autopsy and postmortem magnetic resonance imaging scan (MRI) of formalin-fixed brain revealed advanced unsymmetric brain atrophy with cortical dysplasia, which were prominent in the left temporal and right occipital lobes, and sclerotic atrophy of the parahippocampal gyri, additionally showing a feature of the olivo-ponto-cerebellar atrophy. However, the cause of death was pathologically and microbiologically determined as bacterial bronchopneumonia following pulmonary infection of the influenza A virus. In sudden death cases of physically handicapped infants, the investigation of viral infection in consideration of an epidemiological survey is important even when the death can be pathomorphologically explained.

Deficiencies in lung surfactant proteins A and D are associated with lung infection in very premature neonatal baboons.

Surfactant proteins A (SP-A) and D (SP-D) are important in the innate host defense against pathogenic microorganisms. A deficit in these proteins in premature infants, either because of immaturity or as a consequence of superimposed chronic lung disease (CLD), could increase their susceptibility to infection. The study reported here examined infection in CLD in the premature newborn baboon, and correlated it with the amounts of SP-A and SP-D in lung tissue and lavage fluid. Two groups of baboons were delivered prematurely, at 125 d gestational age (g.a.), and differed principally in whether they developed naturally acquired pulmonary infections and sepsis. Group I animals were ventilated with clinically appropriate oxygen for 6 d and 14 d without clinical incident. Group II animals were ventilated for 5 to 71 d, but differed from those in Group I in that most developed pulmonary infection and/or sepsis. In Group I animals, tissue pools of both SP-A and SP-D were equal to or exceeded those in adults, and lavage pools of SP-A increased progressively with the time of ventilation to about 35% of adult levels after 14 d. In contrast, most Group II animals had concentrations of lavage SP-A that were less than 20% of that in adult animals. A low concentration of lavage SP-A correlated with the release of interleukin-8, and with a high "infection index" based on histopathology, microbiologic cultures, and clinical indications of sepsis. Our data suggest that the amounts of SP-A and SP-D in lavage fluid are indicators of the risk of infection in the evolution of neonatal CLD. Deficits in the amount of lavage SP-A, even after 60 d of ventilation, may have inhibited the resolution of infection and thereby contributed to the developing injury among our Group II animals.