Livestock grazing impact on soil wettability and erosion risk in post-fire agricultural lands.

Fires in agricultural areas are common, modifying the functioning of agro-ecosystems. Such fires have been extensively studied, and reported to considerably affect soil properties. Yet, understanding of the impact of livestock grazing, or more precisely, trampling, in fire-affected lands is limited. The objective of this study was to assess the impact of low- to moderate-fire severity and livestock trampling (hoof action) on the solid soil's wettability and related properties, and on soil detachment, in burnt vs. non-burnt croplands. The study was implemented by allowing livestock to access plots under high, medium, and low stocking rates in (unintentionally) burnt and non-burnt lands. Also, livestock exclusion plots were assigned as a control treatment. Results showed that fire slightly decreased the soil wettability. At the same time, water drop penetration time (WDPT) was negatively related to the stocking rate, and critical surface tension (CST) was ~13% smaller in the control plots than in the livestock-presence treatments. Also, the results showed that following burning, the resistance of soil to shear decreased by ~70%. Mass of detached material was similar in the control plots of the burnt and non-burnt plots. At the same time, it was three-, eight-, and nine-fold greater in the plots of the burnt×low, burnt×medium, and burnt×high stocking rates, respectively, than in the corresponding non-burnt ones. This study shows that livestock trampling in low- to moderate-intensity fire-affected lands increased the shearing of the ground surface layer. On the one hand, this slightly increased soil wettability. On the other hand, this impact considerably increased risks of soil erosion and land degradation.

Fast method for physical optics propagation of high-numerical-aperture beams.

A method is presented that expands the scheme of physical optics propagation beyond the Fresnel approximation to include beams that are nonparaxial. The formalism retains most of the calculation advantages of the Fresnel approach; i.e., it is based on a single Fourier transform step. The kernel of the new transformation is no longer separable in Cartesian coordinates; thus the formalism can account for astigmatic coupling effects originating purely from diffraction. The validity limits of the proposed algorithm are explored. Analytical expressions, numerical simulation results, and experimental data are compared.

Serological evidence of Mycoplasma pneumoniae infection in acute exacerbation of COPD.

A prospective study was conducted to identify and characterize hospitalizations for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) with serologic evidence of infection with Mycoplasma pneumoniae (Mp). Two hundred forty hospitalizations for AECOPD were included in a 17-month prospective study. Paired sera were obtained for each of the hospitalizations and were tested serologically for Mp using a commercial enzyme immunoassay (EIA) kit. Only significant changes, according to the formula in the manufacturer's instructions, in antibody titers for IgM and/or IgG and/or IgA were considered diagnostic for Mp infection. In 34 hospitalizations (14.2%) the serologic tests for Mp were positive (MpH). In 29 of these hospitalizations (85%) a significant change in IgA was found. In 11 of these hospitalizations (32%) the only change identified was in IgA. In 24 MpH (71%) there was serologic evidence for infection with at least one other respiratory pathogen. In comparison to the 206 hospitalizations without serologic evidence of infection with Mp, MpH had higher rates of inhaled steroid therapy (41% vs. 24%, p = 0.033) and a longer time interval between the appearance of dyspnea and hospitalization (6.6 +/- 3.8 days vs. 5.0 +/- 3.5 days, p = 0.012). There were no significant differences between these two groups in a broad spectrum of patient- and exacerbation-related clinical variables. Specific antibiotic therapy for Mp in the MpH group did not shorten the hospital stay. Serologic evidence of Mp infection is common in patients hospitalized for AECOPD, and is usually based on changes in specific IgA antibody titers. In most MpH another respiratory pathogen can be identified. The vast majority of clinical characteristics are the same in patients with and without serologic evidence of infection with Mp. The practical implications of these findings should be clarified in further studies.

Prevalence of antibodies to Chlamydia pneumoniae in an Israeli population without clinical evidence of respiratory infection.

AIMS: To estimate the occurrence of recent, past, and "persistent" infections with Chlamydia pneumoniae--as indicated by serology--in an Israeli population without clinical evidence of respiratory infection. METHODS: Serum samples from 402 subjects (172 children and 230 adults), without known respiratory symptoms, were collected. Antibodies to C pneumoniae (IgG, IgA, and IgM) were evaluated using the microimmunofluorescence (MIF) assay. Antibody prevalence and indication of recent, past, and persistent infections were calculated and their distribution determined according to age, sex, and season. RESULTS: Antibodies to C pneumoniae were detected in 53 children (31%) and 171 adults (74%). Recent infection was indicated in only one of 50 children under 5 years of age, in nine of 122 older children, and in 19 of 230 adults. IgM antibodies were detected in nine children, but only in three adults. Past infection was indicated in six of 96 young children (aged 1-10 years), in 28 of 76 teenagers, and in 128 of 230 adults. Persistent infection was indicated in three young children, in six teenagers, and in 24 adults, with a significantly higher frequency (p = 0.012) in men (18 of 117) than in women (six of 113). No seasonal differences could be detected. CONCLUSIONS: Infection with C pneumoniae was detected serologically in children and adults without clinical signs of respiratory disease. These results should serve as a basis for studies on the role of C pneumoniae infections and their sequelae in Israel and contribute to the general understanding of asymptomatic infection with C pneumoniae.

Serological evidence of Legionella species infection in acute exacerbation of COPD.

A prospective study was conducted to identify and characterize hospitalizations for acute exacerbations of chronic obstructive pulmonary disease (AECOPD) with serological evidence of infection with Legionella spp. (Lsp). Two-hundred and forty hospital admissions for AECOPD of 213 patients were included in the study. Paired sera were obtained for each of the admissions and were tested for 41 different serogroups of Lsp, using microimmunofluorescence-serology. Only a significant change in immunoglobulin-G and/or immunoglobulin-M antibody titres was considered diagnostic. In 40 admissions (16.7%) there was serological evidence of infection with Lsp (LspH). Legionella pneumophila 1 was identified in nine admissions, L. pneumophila 3-15 in 19 and nonpneumophila in 22. In 26 LspH (65%) there was serological evidence of infection with at least one other respiratory pathogen. Compared to the 200 admissions without Lsp (NLspH), the LspH patients were younger (p<0.05) and more hypoxaemic (p<0.04). None of the cases in the LspH group had an abrupt onset of disease, compared to 58 (29.0%) in the NLspH group (p<0.0001). The incidence of myalgia/arthralgia was 55% for LspH compared to 37% for NLspH (p<0.03). To conclude, serological evidence of infection with Legionella spp. is common among patients hospitalized with acute exacerbations of chronic obstructive pulmonary disease. In most hospital admissions with serological evidence of infection with Legionella spp. an additional respiratory pathogen can be identified. Acute exacerbation develops gradually in these patients and is characterized clinically by more systemic manifestations than hospital admissions without serological evidence of infection with Legionella spp. The true interpretation and practical relevance of these findings should be determined in further studies.

Infectious etiologies in acute exacerbation of COPD.

Acute exacerbation (AE) is a frequent episode during the prolonged chronic course of chronic obstructive pulmonary disease (COPD), which entails significant morbidity and mortality. The purpose of this study was to determine the frequency distribution of infectious etiologies in these episodes. Two hundred forty hospitalizations for AECOPD were included in a prospective, purely serologically based study. Paired sera were obtained for each of the hospitalizations and were tested using immunofluorescence or EIA methods to identify 13 different pathogens. Only significant changes in antibody titers were considered diagnostic. The mean age ( +/- SD) of the patients was 66.8 +/- 9.0 years and 179 (84%) were males. In 175 (72.9%) hospitalizations at least one infectious etiology was identified. In 117 (48.8%) hospitalizations at least one of 7 viral etiologies was identified. In 72 (30.0%) hospitalizations at least one of the following atypical bacteria was identified: Legionella spp. in 40 (16.7%), Mycoplasma pneumoniae in 34 (14.2%), and Coxiella burnetii in a single hospitalization. In 58 (24.2%) hospitalizations at least one classic bacterial etiology was found: Streptococcus pneumoniae in 48 (20.0%), Hemophilus influenzae in 10 (4.2%) and Moraxella catarrhalis in 9 (3.8%). More than one etiology was found in 72 (30.0%) hospitalizations. There were no significant differences in the etiologic distribution when the patients were classified by severity of airway obstruction or the clinical type of the exacerbation. We conclude that in most cases of hospitalization due to AECOPD the infectious etiology is viral or atypical bacteria and is classic bacteria in only a minority of cases. More than one etiologic cause can be identified in a third of the cases. The frequency distribution of the etiologies is not associated with the severity of airway obstruction or the clinical type of the exacerbation. The results of our study suggest that atypical bacteria should be covered in antibiotic regimens recommended for AECOPD. This issue should be addressed in future studies.

Chlamydia pneumoniae infection in acute exacerbations of chronic obstructive pulmonary disease: analysis of 250 hospitalizations.

Two hundred fifty hospitalizations were included in a serologically based prospective study to assess the role of Chlamydia pneumoniae in episodes of acute exacerbation of chronic obstructive pulmonary disease (AECOPD) and the percentage of COPD patients chronically infected with this pathogen. Chlamydia pneumoniae-specific IgG, IgA and IgM antibody titers were determined using a commercial kit with the microimmunofluorescence method. A significantly higher geometric mean titer in the COPD patients compared to the control group was found for IgG (P<0.00001) and IgA (P<0.000001). The serological criterion for chronic Chlamydia pneumoniae infection (IgG > or = 28 concomitant with IgA > or = 64) was positive in 73 (33.3%) COPD patients compared with 7 (7%) controls (P=0.000001). No difference was found in any serological parameter when the study population was divided by severity of COPD. When the serological profiles were compared between the first and second of 31 pairs of hospitalizations, 7 of the 62 (11.3%) hospitalizations showed evidence of acute infection with Chlamydia pneumoniae around one of the episodes of AECOPD. It is concluded that compared with the control group, the COPD patients had a significantly higher prevalence of chronic Chlamydia pneumoniae infection. In the COPD group, there was no correlation between the severity of the disease and the rate of chronic Chlamydia pneumoniae infection. In a substantial percentage of AECOPD cases, there is serological evidence of acute Chlamydia pneumoniae infection around the time of the exacerbation. The clinical and pathophysiologic implications of these findings should be clarified by further studies.

Increased typability of multiresistant Staphylococcus aureus by reverse phage typing.

Sixty percent of Staphylococcus aureus isolates from patients in Israeli hospitals proved to be non typable by the conventional phage typing method. Heat pretreatment improved typability only to 54% while reverse typing increased typability to 75%. In general isolates typable by conventional phages belonged to group V, II, III, I, or to mixed groups. While isolates typable only by reverse typing belonged to group III, II, the extended group III + IIIa, or to mixed groups, but seldom to group I. Although most isolates were resistant to penicillin G, only one half were resistant to other antibiotics as well. While one third of these isolates could by typed by conventional phage typing, typability was significantly improved to over 80%, by the use of reverse typing as the additional typing method. Two main groups of oxacillin resistant isolates were identified. The partial resistant group consisting of isolates resistant to penicillin G and oxacillin with no or few other resistances. These isolates were mostly typable by conventional phage typing (group V) and dominated in the first study period (1989-1990) but were only seldom isolated in the second one (1991-1992). The multiresistant group consisted of isolates resistant to penicillin G and oxacillin accompanied by resistances to 3-5 other antibiotics (chloramphenicol, clindamycin, erythromycin, gentamicin and tetracycline). These isolates were mostly typable by reverse typing (the extended group III + IIIa) and showed no change in isolation frequencies during the entire study period. Reverse typing is proposed by us as a typing tool for these multiresistant S. aureus isolates.

Etiology of respiratory tract infection in adults in a general practice setting.

A prospective study was conducted over a 3-month winter period in three general practice clinics in an urban population in southern Israel to identify the etiological agents of respiratory tract infections (RTI) in adults. RTI was defined as an acute febrile illness with cough, coryza, sore throat or hoarseness. Serum samples were taken from all patients in both the acute and convalescent phases of their illness. Tests were conducted for detection of 17 microorganisms known to cause RTI, including serological tests for 16 known pathogens. An etiological diagnosis was established in 80 (66%) of the 122 patients who participated in the study. The distribution of the etiological agents was as follows: influenza B virus in 27 (22%) patients. Chlamydia pneumoniae in 22 (18%), Legionella spp. in 15 (12%), Mycoplasma pneumoniae in 13 (11%), influenza A virus in 11 (9%), Bordetella pertussis in 9 (7%), adenovirus in 4, Epstein Barr virus in 4, Haemophilus influenzae in 3, beta-hemolytic streptococci in 3, Streptococcus pneumoniae in 2, respiratory syncytial virus in 2, parainfluenza 1 virus in 2 and parainfluenza 2 virus in 1. No patients were found to be infected with Coxiella burnetii, Moraxella catarrhalis or parainfluenza 3 virus. More than one pathogen was identified in 27 (34%) patients in whom an etiological diagnosis was established. It is concluded that RTI is caused by a broad spectrum of etiological agents, a considerable number of patients having evidence of infection with more than one pathogen. The therapeutic significance of these findings should be elucidated in further studies.

Molecular cloning of a novel human gene encoding a 63-kDa protein and its sublocalization within the 11q13 locus.

A human cDNA previously isolated by virtue of its ability to complement partially the ultraviolet sensitivity of a xeroderma pigmentosum cell line was further characterized. The transcription unit is expressed as a single 4.0-kb mRNA that encodes a novel 63-kDa cytoplasmic protein, possibly initiating from an internal AUG codon. The gene encoding this protein, named UVRAG, has been extremely well conserved during evolution, implying an important role for this gene product in cell metabolism. The transcribed mRNA is constitutively expressed in a wide variety of human tissues. The protein encoded by this gene is predicted to contain a coiled-coil structure and is likely to be metabolically unstable based on the occurrence of a strong PEST domain. UVRAG was assigned to human chromosome 11 by Southern hybridization to a somatic cell hybrid panel. Fluorescence in situ hybridization coupled with PCR analysis of human/rodent somatic cell hybrids containing segments of human chromosome 11 has localized this gene to a subregion of 11q13 in between the D11S916 and the D11S906 loci. Importantly, this region has been shown to be amplified in a variety of human malignancies, including breast cancer.

Chlamydia pneumoniae community-acquired pneumonia: a review of 62 hospitalized adult patients.

In a prospective study, Chlamydia pneumoniae was identified as the etiological agent in 62 (17.9%) of 346 adult patients hospitalized over the course of one year for community-acquired pneumonia at the Soroka Medical Center in Beer-Sheva, Israel. The diagnosis of C. pneumoniae infection was based on serological testing of antibodies by the MIF technique. In 43 of these patients (69.4%), at least one other etiological agent, in addition to C. pneumoniae for community-acquired pneumonia was identified. Streptococcus pneumoniae was identified in 34 patients with C. pneumoniae (54.8%), as an additional causative factor in infection. Community-acquired pneumonia patients with C. pneumoniae were significantly older than non-C. pneumoniae patients (p = 0.03), had a higher APACHE II score on admission (p < 0.05), a higher rate of positive blood cultures (p = 0.02), and longer periods of hospitalization (p = 0.022). Seven patients with pure C. pneumoniae infection recovered, despite treatment which is not considered to be specific for C. pneumoniae. It was concluded that C. pneumoniae is a common etiological agent for community-acquired pneumonia in our region, particularly in the elderly, and is characterized by a high rate of concomitant infections with other pulmonary pathogens. No specific clinical or radiological pattern was discerned that could distinguish between C. pneumoniae community-acquired pneumonia and non-C. pneumoniae community-acquired pneumonia.

[Serodiagnosis of atypical bacterial respiratory infections].

Since prevalence of antibodies to bacteria causing atypical respiratory infections in Israel is as yet unknown, a 5-year antibody prevalence study was performed. Seroreactivity to Chlamydia pneumoniae (TWAR), with titers > or = 1:16 by microimmunofluorescence assay (MIF) was detected in 725/1305 (55.5%) of patients. 47/1012 ((4.6%) of adult patients had MIF results indicating recent infection with TWAR, (IgG titers of > or = 1:512, and/or IgM titers of > or = 1:16, and/or seroconversion). Antibody prevalence and titers were low in children aged 1-10 years, increased in teenagers, and peaked in adults and the elderly, in whom prevalence was up to 79% and mean geometric titer up to 1:163. Unlike the consistency in TWAR antibody prevalence and serological evidence of recent infection during the study period, a significant decrease in those variables was observed for Chlamydia trachomatis during the first 3 study years. Antibodies to M. pneumoniae were detected in 53 and to Legionella sp. in 47 out of 763 patients. There was serological evidence of recent infection with M. pneumoniae in 10 (including 7 children) and with Legionellae in 8. Improved diagnosis of atypical respiratory infection might be achieved by the combined use of these proposed serological procedures.

Prevalence of Chlamydia pneumoniae antibodies in patients with acute respiratory infections in Israel.

AIMS: To evaluate the prevalence of antibodies to Chlamydia pneumoniae (TWAR) in relation to other aetiological agents of acute respiratory infections in Israeli patients. METHOD: Serum samples from 604 patients (183 children and 421 adults) were collected over three years. Antibodies to C pneumoniae, C trachomatis, and Legionella sp were evaluated using the microimmunofluorescence (MIF) assay. Antibodies to Mycoplasma pneumoniae were detected using the Serodia Myco II test. RESULTS: Antibodies to TWAR were detected in 319 (51.3%) sera. Twenty one patients had MIF results indicative of recent infection. TWAR prevalence and antibody titres in children (aged 1-10 years) were low, gradually increased in teenagers (11-18 years), and were highest in adults and elderly patients. In contrast to the consistently noted TWAR antibody prevalence and serological evidence of recent infection during the study period, a significant decrease in those variables was recorded for C trachomatis. Six patients had serological evidence of recent infection with both C pneumoniae and C trachomatis. The presence of antibodies to Mycoplasma pneumoniae and Legionella sp was tested in 473 of the patients; 29 had antibodies to M pneumoniae and 23 to Legionella sp. Six patients (including five children) had serological evidence of recent infection with M pneumoniae and four with Legionella sp. CONCLUSION: C pneumoniae should be considered in patients with acute respiratory diseases. MIF is the preferred method for monitoring the presence of antibodies to this organism.

Activation of human eosinophil and neutrophil functions by haematopoietic growth factors: comparisons of IL-1, IL-3, IL-5 and GM-CSF.

We compared the effect of haematopoietic growth factors granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-1, IL-3, and IL-5 on the functional activation of human eosinophils and neutrophils from the same donor. All four colony-stimulating factors (CSF) enhanced the phagocytosis of Candida albicans by eosinophils and increased staphylococcal, but not Candida, killing. GM-CSF and IL-5 had a profound stimulating effect on eosinophil staphylocidal activity. GM-CSF and IL-3 enhanced the generation of leukotriene C4 (LTC4) induced by calcium ionophore A23187 and the release of arylsulphatase and beta-glucuronidase from specific and small granules of eosinophils. In contrast, IL-1 and IL-5 had no effect on degranulation. GM-CSF and IL-1 enhanced phagocytosis of C. albicans by neutrophils, and GM-CSF stimulated degranulation and the release of the enzymes beta-glucuronidase and arylsulphatase from neutrophils while IL-1 stimulated the release of arylsulphatase only. This study indicates that the eosinophil-active colony-stimulating factors can markedly enhance the host defence function of the eosinophil and even make it the equal of the neutrophil in staphylocidal activity. The CSF-activated eosinophil, however, may cause inappropriate inflammation and normal tissue damage.

Immediate and late airway response of allergic rhinitis patients to segmental antigen challenge. Characterization of eosinophil and mast cell mediators.

Segmental antigen bronchoprovocation was used to define the nature of the inflammatory process in allergic airway disease. Bronchoalveolar lavage fluid obtained from allergic rhinitis patients 12 min after segmental antigen instillation (immediate response) revealed a significant increase in histamine and tryptase, but no cellular response. Repeat segmental lavage 48 h later (late response) showed marked and significant increases in both low and normal density eosinophils as well as striking elevations of eosinophil granular protein levels (major basic protein, eosinophil-derived neurotoxin, eosinophil cationic protein, and eosinophil peroxidase). Leukotriene C4, but not tryptase, concentrations were also consistently elevated in late lavage samples. Further, the late lavage samples showed a significant increase in interleukin-5 concentrations that correlated with the presence of eosinophils and eosinophil granular proteins. Neither eosinophils nor soluble mediators of eosinophils increased when normal subjects were similarly challenged with antigen. These data suggest that eosinophils are attracted to the airway during the late-phase allergic reaction and that IL-5 may produce changes in airway eosinophil density and promote the release of granular proteins to cause airway injury.

Immunologic characteristics in relation to high and low leukemogenic activity of radiation leukemia virus variants. I. Cellular analysis of immunosuppression.

Infection of adult C57BL/6 mice with variants of the radiation leukemia virus resulted in variable leukemia incidence. One variant, designated D-RadLV, induced lymphatic leukemia in 0 to 25% of mice after virus inoculation directly into the thymus of young adult mice. The leukemia incidence could be increased to 80 to 100% by host exposure to x-rays. The second variant, A-RadLV, induced lymphatic leukemia in 80 to 100% of similarly inoculated mice without the need for additional radiation treatment. Adult mice were inoculated with D-radLV or A-RadLV. Both variants reduced the immune response to sheep erythrocytes whereas only D-RadLV had an immunosuppressive effect after immunization with a thymus-independent immunogen polyvinyl-pyrrolidone (PVP). Results of transfer experiments indicated that the immunosuppressive effects were expressed at the immunocompetent cell level. Thymus-derived cells were affected by A-RadLV since their immunocompetent function was impaired, whereas D-RadLV affected the marrow cell population of immunocytes. Exposure of D-RadLV-inoculated mice to x-rays induced functional impairment of both thymus and marrow cells. Since the radiation leukemia virus induces "T" lymphatic leukemia it could be proposed that the initial tropism of the virus to thymocytes would lead to high leukemia induction potential, whereas virus tropism to bone marrow cells would yield a low leukemia incidence. The coleukemogenic effect of x-rays could perhaps be related with its capacity to alter and introduce a change in virus-lymphoid cells interaction.

Enhancement and retardation of spontaneous reticulum cell neoplasm development in SJL/J mice.

The enhancement or delay in the appearance of spontaneous reticulum cell neoplasms (RCN-B) in SJL/J mice was tested. Immunosuppressive treatment with antithymocyte serum and prolonged antigenic stimulation by repeated injections of sheep erythrocytes, leukemogenic cell-free centrifugates, and multichain synthetic polypeptides had no effect on the incidence or latency of spontaneous tumor appearance. Treatment with mineral oil or incomplete Freund adjuvant markedly enhanced tumor appearance (though the abundance of plasma cells induced by these treatments did not evoke the development of plasmacytomas, nor did it affect the incidence of serum paraproteinemia among mice with spontaneous tumors). Treatment with cortisone acetate, however, markedly retarded spontaneous tumor development. Tumors occurring early due to mineral oil and adjuvant treatment all had the characteristics of "RCN-B plasma cell type," and tumors occurring late due to cortisone treatment were all of the "RCN-B reticulum cell type." The possible involvement of the stem cell pool size in the enhancement or delay of spontaneous tumor development was discussed.