Acute Lobar Pneumonia Research Articles

Inhalation Toxicity of Humidifier Disinfectants as a Risk Factor of Children’s Interstitial Lung Disease in Korea: A Case-Control Study

BackgroundThe occurrence of numerous cases of interstitial lung disease in children (chILD) every spring in Korea starting in 2006 raised suspicion about a causal relationship with the use of humidifier disinfectants (HDs). The aim of this study was to evaluate the association between HD use and the risk of chILD.MethodsThis retrospective, 1∶3 matched case-control study consisted of 16 cases of chILD that had developed between 2010 and 2011. The three groups of parallel controls (patients with acute lobar pneumonia, asthma, and healthy children) were matched by age, gender, and index date. Indoor/outdoor environmental risk factors, including HD use, were investigated by asking the guardians to complete a questionnaire.ResultsThe median age of the affected children (43.8% male) was 26 months (18.25–36.25). The chILD group did not differ significantly from the control groups with respect to socio-demographic and clinical variables. Indoor and outdoor environmental factors were not associated with a risk of chILD. However, the previous use of HDs (OR; 2.73. 95% CI; 1.41–5.90, P = 0.00) were independently associated with an increased risk.ConclusionsThis study showed that HDs, which are widely used in South Korea in the winter season, independently increased the risk of chILD in spring. Therefore, continuous monitoring and, if needed, changes in policy are essential to prevent and control pediatric diseases caused by toxic chemicals.

Cross protection of a Mannheimia haemolytica A1 Lkt-/Pasteurella multocida ΔhyaE bovine respiratory disease vaccine against experimental challenge with Mannheimia haemolytica A6 in calves

Bovine respiratory disease causes significant economic losses in both beef and dairy calf industries. Although multi-factorial in nature, the disease is characterized by an acute fibrinous lobar pneumonia typically associated with the isolation of Mannheimia haemolytica. M. haemolytica A1 and A6 are the two most commonly isolated serotypes from cattle, however, the majority of vaccines have not demonstrated cross-serotype protection. In the current study, the efficacy of a novel, attenuated live vaccine, containing both M. haemolytica serotype A1 and Pasteurella multocida, was evaluated in calves challenged with M. haemolytica serotype A6. Although the challenge was more severe than expected, vaccinated calves had reduced clinical scores, lower mortality, and significantly lower lung lesion scores compared to the placebo-vaccinated control group. The results demonstrate that vaccination with an attenuated live vaccine containing M. haemolytica serotype A1 can protect calves against clinical disease following challenge with M. haemolytica serotype A6.

Pattern of deaths in females in a tertiary health center, south-west Nigeria

PurposeThe aim of this study was to review autopsies to determine the pattern of deaths in females at Wesley Guild Hospital, Ilesa, Nigeria.MethodsA 9-year retrospective study was done of all autopsies done on females in the Department of Morbid Anatomy and Forensic Medicine, Obafemi Awolowo University Teaching Hospitals Complex, Wesley Guild Hospital, Ilesa, Nigeria, from January 2002 to December 2010. Records of all autopsies done on females during the period were reviewed.ResultsDuring the study period 215 cases of female death were autopsied. The age range was 0–75 years (mean = 32.9). Deaths due to trauma were most common (57.2%), followed by obstetric deaths (15.8%). Deaths due to infections and cardiovascular diseases accounted for 13% and 5.6%, respectively. Injuries sustained from automobile accidents were responsible for 88.6% of all trauma deaths. Gunshot injuries accounted was 4.9% of these trauma deaths. The causes of death from automobile accidents included multiple injuries (49.5%), head injury (38.5%), and hypovolemia (8.3%). Obstetric deaths were predominantly due to uterine sepsis (51.5%) and hemorrhagic shock (39.4%). About 39% of deaths from infection were due to septicemia. Acute bacterial meningitis, acute lobar pneumonia, and malaria caused 23.1%, 15.4%, and 7.7% of deaths from infections, respectively. Four cases of sudden unnatural deaths (other than trauma) were recorded.ConclusionTrauma was the most common cause of death in women autopsied in our hospital, and automobile injuries were the most common causes of these trauma deaths. Obstetric deaths ranked second. Sepsis and hemorrhage were the most common causes of these obstetric deaths. Deaths from eclampsia were low. Requests for autopsies on women who died from cancer were few. There is a need for clinicians to ascertain the actual cause of death in women who die from cancer.

Membranoproliferative Glomerulonephritis in a Nigerian Adolescent with Congenital Solitary Kidney: Unraveling the Cause of Mortality

Background: Unilateral renal agenesis (URA) or solitary kidney usually presents as non-ectopic solitary functioning kidney (SFK) with absent contra-lateral kidney. Although it is compatible with normal longevity, recent studies indicate that arterial hypertension, proteinuria, impaired renal function as well as glomerulosclerosis are potential complications. Case Report: We report a male adolescent patient who presented pre-mortem with features of acute renal failure and lobar pneumonia. Post-mortem examination revealed a solitary kidney with light microscopic findings suggesting membranoproliferative glomerulonephritis (MPGN) as the fundamental disease. The short duration of hospitalization and paucity of diagnostic facilities precluded a more accurate confirmation and classification of the glomerular disease. This report however highlights possible pathological scenarios, as well as the handicaps in the practice of Nephrology in this environment. Key words: Renal agenesis; acute renal failure; lobar pneumonia

Right congenital diaphragmatic hernia a well-known pathology?

In right congenital diaphragmatic hernia (RCDH), several clinical diagnostic pitfalls are possible and should be known to those caring for infants and children with this disorder. The records of the 18 patients at Hotel Dieu de France Hospital with a history of CDH between 1990 and 1999 were collected; those of the ten who had a RCDH were reviewed retrospectively. The mean age at diagnosis was 6 months; the male-to-female ratio was 2:3. The delay between the first symptom and the diagnosis ranged between 0 and 10.5 months (mean 4.5 months). An acute presentation was observed in four cases, consisting of respiratory distress in three; the 4th presented with gastric volvulus and intestinal obstruction. The presenting symptoms were mild in four cases; recurrent respiratory infections in three and failure to thrive in one. The diagnosis was incidental in two cases during the evaluation of respiratory symptoms attributed to an atrial septal defect. The radiologic findings provided by a chest radiograph (CxR) were sufficient to make an accurate diagnosis in eight cases and peritoneography was useful in one. In six cases, the presenting CxR had been misinterpreted as normal or acute lobar pneumonia. Pathologic findings at surgery consisted of lateral and posterior right diaphragmatic defects in nine cases; the defect was lateral and anterior in one. A hernia sac was found in seven cases; malrotation was present in three. Surgical correction was done by an abdominal approach in nine cases and a thoracic approach in one. The diaphragmatic defect was repaired by transverse closure in six cases, diaphragm plication in three and prosthetic closure in one. The postoperative outcome was uneventful in eight cases. Two patients died. Thus, RCDH seems to cause less severe symptoms than left-sided LCDH. It usually manifests beyond the neonatal period as respiratory or gastrointestinal symptoms. The diagnosis should be made easily by a CxR. The presence of a hernia sac correlated with a mild presentation. An abdominal surgical approach is preferred.

The concept of organizing pneumonia.

At the beginning of the 19th century, Laennec described the sequential gross pathological stages of acute lobar pneumonia, which was later related to pneumococcal infection [27]. The first stage is congestion, in which the involved lobe is heavy and congested. During the next stage, called red hepatization, the lobe becomes red and dense, much like the liver. After a stage of gray and airless lung (grey hepatization), resolution of pneumonia usually occurs with eventual complete healing.

Dissociation of neutrophil emigration and metabolic activity in lobar pneumonia and bronchiectasis

In animal models of pulmonary inflammation, neutrophils exhibit a dramatic influx of glucose in periods of high metabolic activity. This information was utilized to develop a technique, involving positron emission tomography (PET) of 2-[18F]-fluoro-2-deoxy-D-glucose (18FDG), which measures neutrophil activity in situ. This technique was applied in a comparative study of neutrophil function in patients with acute lobar pneumonia or bronchiectasis. Neutrophil emigration was measured by gamma-scintigraphy of intravenously injected 111In-labelled granulocytes and neutrophil activity determined by PET of 18FDG. Neutrophil emigration was evident in 4 out of 5 bronchiectasis patients, whilst no emigration was apparent in the two pneumonia patients studied, consistent with animal studies showing maximum emigration soon after challenge. In contrast, 18FDG uptake was markedly increased in 4 out of 5 pneumonia patients but not in the patients with bronchiectasis. Localization of radioactivity to neutrophils was confirmed by microautoradiography of lavage fluid in a patient with pneumonia. These results suggest that the elevated uptake of glucose by neutrophils during the inflammatory response is a postmigratory event, most likely reflecting the respiratory burst, and that high levels of neutrophil emigration are not necessarily associated with significantly increased metabolic activity of these cells.

Invasion of Eukaryotic Cells byLegionella Pneumophila: A Common Strategy for all Hosts?

Legionella pneumophila is an environmental micro-organism capable of producing an acute lobar pneumonia, commonly referred to as Legionnaires' disease, in susceptible humans. Legionellae are ubiquitous in aquatic environments, where they survive in biofilms or intracellularly in various protozoans. Susceptible humans become infected by breathing aerosols laden with the bacteria. The target cell for human infection is the alveolar macrophage, in which the bacteria abrogate phagolysosomal fusion. The remarkable ability of L pneumophila to infect a wide range of eukaryotic cells suggests a common strategy that exploits very fundamental cellular processes. The bacteria enter host cells via coiling phagocytosis and quickly subvert organelle trafficking events, leading to formation of a replicative phagosome in which the bacteria multiply. Vegetative growth continues for 8 to 10 h, after which the bacteria develop into a short, highly motile form called the 'mature form'. The mature form exhibits a thickening of the cell wall, stains red with the Gimenez stain, and is between 10 and 100 times more infectious than agar-grown bacteria. Following host cell lysis, the released bacteria infect other host cells, in which the mature form differentiates into a Gimenez-negative vegetative form, and the cycle begins anew. Virulence of L pneumophila is considered to be multifactorial, and there is growing evidence for both stage specific and sequential gene expression. Thus, L pneumophila may be a good model system for dissecting events associated with the host-parasite interactions.

Aspects de pneumopathies de la Fièvre Q

We report two different aspects of Q Fever pneumonia in two patients coming back from the same guided tour in Crete. The first patient presented with an influenzae-like syndrome associated with an interstitial pneumonia. The second patient presented with acute lobar pneumonia and hepatitic cytolysis. Mild thrombocytopenia was observed in both patients. Diagnosis was confirmed by evidence of seroconversion for Coxiella burnetii . Recovery was observed after treatment including fluoroquinolones.

Granulocyte/macrophage colony-stimulating factor-deficient mice show no major perturbation of hematopoiesis but develop a characteristic pulmonary pathology.

Mice homozygous for a disrupted granulocyte/macrophage colony-stimulating factor (GM-CSF) gene develop normally and show no major perturbation of hematopoiesis up to 12 weeks of age. While most GM-CSF-deficient mice are superficially healthy and fertile, all develop abnormal lungs. There is extensive peribronchovascular infiltration with lymphocytes, predominantly B cells. Alveoli contain granular eosinophilic material and lamellar bodies, indicative of surfactant accumulation. There are numerous large intraalveolar phagocytic macrophages. Some mice have subclinical lung infections involving bacterial or fungal organisms, occasionally with focal areas of acute purulent inflammation or lobar pneumonia. Some features of this pathology resemble the human disorder alveolar proteinosis. These observations indicate that GM-CSF is not essential for the maintenance of normal levels of the major types of mature hematopoietic cells and their precursors in blood, marrow, and spleen. However, they implicate GM-CSF as essential for normal pulmonary physiology and resistance to local infection.

Pathogenesis ofActinobacillus pleuropneumoniae infections

Pathogenesis ofActinobacillus pleuropneumoniae infections

A study of acute community-acquired pneumonia, including details of cardiac changes.

We prospectively studied 102 patients, aged 15-50 years, with acute community-acquired lobar pneumonia without underlying cardiorespiratory illness, admitted to Baragwanath Hospital May 1990-April 1991. Demographic, clinical, microbiological and laboratory data and negative prognostic features of these patients are described. In particular, we documented electrocardiographic changes and studied their possible relevance in patients with pneumonia. Electrocardiographic changes occurred in 32 patients (31%). The commonest changes were clockwise rotation (16%), followed by P. pulmonale (9.8%) and S1 Q3 T3 pattern (7.8%) Other changes included right axis deviation (n = 6), right bundle branch block (n = 3), ventricular extrasystoles (n = 2), atrial fibrillation (n = 1) and nodal rhythm (n = 1). These changes returned to normal in survivors after a mean of 2 days. The S1 Q3 T3 pattern was associated with cardiac enzyme leak (CK-MB fraction), hypoxia and a high Simplified Acute Physiology Score (SAPS). In addition, P. pulmonale, right axis deviation and clockwise rotation correlated with hypoxia and a high SAPS score. Clockwise rotation also correlated with serum (including cardiac fraction) enzymes leak (LDH and CK-MB fraction), and pulmonary artery pressure. The overall mortality rate was 10.8%, with no association between electrocardiographic changes and mortality. The negative prognostic factors documented were hypoxia (p < 0.0001), multilobar pulmonary consolidation (p < 0.0001), tachycardia (p = 0.0001), tachypnoea (p = 0.0002), renal dysfunction function (p = 0.0009), hypotension (systolic p < 0.02, diastolic p < 0.003), bacteraemia (p = 0.003), and serum (including cardiac fraction) enzymes leak: LDH (p < 0.02), CK (p < 0.002) and CK-MB fraction (p = 0.0002). These factors, with the exception of renal dysfunction, also correlated with the need for intensive care unit admission. Acute and reversible electrocardiographic changes are common in acute community-acquired lobar pneumonia. Electrocardiographic changes, especially those compatible with acute cor pulmonale and accompanied by cardiac enzyme (CK-MB fraction) leak, correlated with severity of illness but not with mortality.

Clinical pharmacokinetics of iron preparations.

The principle of iron conservation is the basis of iron metabolism; the normal basal loss of iron from the body is about 1 mg daily in a 70 kg man and 0.8 mg in a 55 kg woman. Iron is lost mainly by the menstrual and gastrointestinal routes. The total iron requirement during pregnancy is 800 mg; in the last month the requirement may amount to 7 to 8 mg/day. Supplementary iron is recommended for many menstruating women, and during the latter part of pregnancy. Correct fetal iron metabolism is ensured by proper maternal iron status, although there are contradictory opinions and findings about the relationship between maternal and fetal iron metabolism. Preterm infants fed on breast milk have a negative iron balance, and require an iron intake of about 0.6 mg/kg/day, and 3.4 mg/1 g haemoglobin, to compensate for intestinal and venesection iron losses, respectively. The absorption of supplementary iron by the preterm infant is a linear function of intake. Preterm infants do not require iron supplements when given repeated blood transfusions. During lactation the total iron losses of the mother are 1 mg/day, and thus no supplementary iron is needed if the iron metabolism has been in balance during the pregnancy. Serum ferritin concentration decreases continuously when iron stores in the body are reduced, and totally empty iron stores are the only known reasons for low serum ferritin concentration. Despite depleted iron stores, serum ferritin concentration can be normal or higher than normal in protein-energy malnutrition, up to 3 months after major surgery, in acute liver damage, in some patients with prolonged hyperglycaemia due to diabetes mellitus, in acute lobar pneumonia, active pulmonary tuberculosis and rheumatoid arthritis on gold therapy, in sepsis secondary to marrow hypoplasia induced by chemotherapy, in heavy drinkers and for a few days after myocardial infarction. In haemochromatosis, iron is deposited in liver (producing fibrosis), pancreas, endocrine glands and heart. The rise in the level of iron in the body is due to increased absorption and/or increased intake. This pathology may occur in transfusions, in alcoholism (especially when alcoholic beverages are contaminated with iron and the diet is low-protein), in several liver diseases, in congenital transferrin deficiency and in idiopathic disease. Patients susceptible to haemochromatosis should receive a low-iron diet. Serum ferritin determination may be helpful in early identification of susceptible members of a family with idiopathic familial haemochromatosis, but transferrin saturation is not a good indicator of either iron depletion or iron overload.(ABSTRACT TRUNCATED AT 400 WORDS)

Indomethacin and acetylsalicylic acid reduce intrapulmonary shunt in experimental pneumococcal pneumonia.

Arterial hypoxemia in acute experimental pneumococcal pneumonia is caused primarily by persistence of pulmonary blood flow to lung regions consolidated by pneumonia, which results in an intrapulmonary shunt. In order to test the hypothesis that in acute pneumonia indomethacin or acetylsalicylic acid (ASA) would improve gas exchange, as has been observed in some other disease models, 15 pentobarbital-anesthetized dogs with acute lobar pneumonia caused by Streptococcus pneumoniae type 3 were studied. After baseline measurements of pulmonary gas exchange, central hemodynamics and radionuclide-labeled microsphere determination of regional distribution of pulmonary blood flow, the dogs were randomly assigned to receive an intravenous infusion of indomethacin (2 mg/kg, n = 5), ASA, (100 mg/kg, n = 5) or a saline infusion (control, n = 5). All measurements were then repeated 30 and 60 min after infusion. Although there were no significant changes in the control group, PaO2 during O2 ventilation increased from a mean +/- SD value of 104 +/- 46 mmHg at baseline to 180 +/- 73 mmHg after ASA and from 262 +/- 173 to 361 +/- 134 mmHg after indomethacin. These improvements in PaO2 were associated with a decrease in shunt from 0.38 +/- 0.12 to 0.23 +/- 0.03 with ASA and from 0.29 +/- 0.21 to 0.21 +/- 0.08 with indomethacin. The reduction in shunt in both treatment groups was attributable to a fall in the fraction of the pulmonary blood flow perfusing the consolidated lung regions, from 33 +/- 8 to 21 +/- 5% after ASA and from 33 +/- 12 to 22 +/- 9% after indomethacin.(ABSTRACT TRUNCATED AT 250 WORDS)

The non-immune inflammatory response: Serial changes in plasma iron, iron-binding capacity, lactoferrin, ferritin and C-reactive protein

The interrelationships between various components of the non-immune inflammatory response (white cell count, plasma lactoferrin, C-reactive protein, ferritin, iron and iron-binding capacity), were studied serially in a variety of inflammatory conditions including acute lobar pneumonia, active pulmonary tuberculosis, rheumatoid arthritis on gold therapy and sepsis in the face of marrow hypoplasia induced by chemotherapy. Lactoferrin concentrations paralleled the white count in all groups. They were highest in pneumonia and tuberculosis, mildly elevated in rheumatoid arthritis and markedly decreased in neutropenic sepsis. Very high initial lactoferrin concentrations were associated with a poor prognosis in acute pneumonia. C-reactive protein and ferritin concentrations remained elevated through the period of study in acute pneumonia and neutropenic sepsis, while they gradually normalised over weeks in subjects with tuberculosis or rheumatoid arthritis on therapy. In pneumonia and tuberculosis moderate hypoferraemia and a reduced iron-binding capacity were evident. In contrast, a raised percentage saturation was present in neutropenic sepsis, probably related to erythroid marrow suppression. Comparisons between ferritin, lactoferrin and C-reactive protein in the various groups supported the concept that ferritin behaves in part as an acute phase reactant and that hypoferraemia in inflammation is due to deviation of iron into ferritin stores. The suggestion that lactoferrin is responsible for the hypoferraemia and hyperferritinaemia was not supported by the present data. Iron deficiency appeared to limit the hyperferritinaemic response in rheumatoid arthritis, while erythropoietic inhibition by chemotherapy dampened the hypoferraemic response in neutropenic sepsis.

Electron microscopy of the organism of Legionnaires' disease.

LEGIONNAIRES' disease, an acute lobar pneumonia with a considerable fatality rate, gained its name from the explosive outbreak which followed an American Legion convention in Philadelphia in July 1976 (ref. 1). Since then, some smaller outbreaks and an increasing number of sporadic cases have been recognised in the USA2. There have also been reports of cases in the UK, from Glasgow, mainly associated with holiday travel3,4, and, as an indigenous occurrence, from Nottingham5,6 and London7. The causative organism, a small Gram-negative bacillus, has been cultured with some difficulty, its size being 0.3–0.5 µm in width and 2–3 µm in length, though longer forms up to 20 µm are not uncommon8. We present here electron micrographs showing the organism in post mortem lung tissue.

Blood flow in pulmonary and bronchial arteries in acute experimental pneumonia and pulmonary embolism.

Acute lobar pneumonia and pulmonary embolism were induced in rabbits and the blood flow in the pulmonary artery and bronchial arteries was determined using isotopic microspheres. In acute pneumonia the pulmonary artery flow to the involved lung was reduced 8.5 times and the bronchial artery flow was reduced 5.0 times compared to flow in the normal lung. In acute pulmonary embolism, both the pulmonary artery flow (2.3 times) and the bronchial artery flow (2.5 times) were also reduced. For all animals, the reduction in pulmonary artery flow paralleled the reduction in bronchial artery flow (r=0.65).

Nitroblue Tetrazolium Test in Pulmonary Thromboembolism and Pneumonia

The histochemical nitroblue tetrazolium (NBT) test was performed in 88 patients with acute pulmonary thromboembolism or lobar pneumonia and in 88 healthy control subjects. In the control group, the mean NBT score was 5.4%. In the group of 55 patients with pulmonary thromboembolism the mean NBT score was 6.5% which is insignificantly different from the control mean. Only 3 of these patients had scores above normal. 35 embolism patients were followed by repeated examinations for 1 week after admission. The NBT scores remained within normal limits. 29 of the 33 patients with lobar pneumonia had elevated scores, and the mean NBT score was 33.5%. Endotoxin stimulated NBT test disclosed normal enhancement of NBT reduction by neutrophils from patients in either group as well as controls. The NBT test is of value in the differential diagnosis of pulmonary infection and thromboembolic disease. However, the results should be interpreted in the light of other pertinent laboratory and clinical findings.

Drug Treatment of Infants and Children Suffering from Pneumonia

vomited when administered, penicillin should be given intramuscularly. From 1,000,000 units at 2 years to 2,000,000 units at 5 years of age should be sufficient. In either case no further specific treatment should be necessary for acute pneumococcal lobar pneumonia. Attention thereafter is directed solely to the child's general condition and not to the physicial signs in the lungs: these will follow the normal course, and their disappearance is in no way expedited by the stoss therapy. In other words, the continued presence of slight fever and the persistence of bronchial breathing for two to three days are not an indication for further treatment, provided the child's general condition is steadily improving. If, in the early stages, a frequent, irritable and painful cough is present, Gee's linctus (linctus scillae opiatus B.N.F.) may be given in doses of 30-60 minims (1.7-3.5 mi.) until relief is obtained. No other drug therapy is required.

Dehydroascorbic acid level in blood of patients suffering from various infectious diseases.

Summary1. Dehydroascorbic acid and ascorbic acid values of blood were estimated in healthy subjects and in patients suffering from meningococcal meningitis, tetanus, acute lobar pneumonia, typhoid fever and tubercular meningitis. These values were also determined in surviving patients during convalescence. 2. There was statistically significant increase in dehydroascorbic acid and a diminution in ascorbic acid values of blood of patients suffering from above mentioned diseases. During convalescence, the dehydroascorbic acid level diminished with a concomitant increase in the ascorbic acid level of the blood. 3. Significance of the rise of de-hydroascorbic acid level of blood in acute infectious diseases has been discussed. It has been suggested that the estimation of dehydroascorbic acid content of the blood should be undertaken for prognostic purpose.