Israel Medical Association Journal

Background: Chlamydia pneumoniae has previously been associated with higher prevalence of valvular and cardiac calcifications.

Objectives: To investigate a possible association of seropositivity for C. pneumoniae and the presence of cardiac calcifications (mitral annular or aortic root calcification, and aortic valve sclerosis).

Methods: We retrospectively analyzed serological data (immunoglobulin G TWAR antibodies) from the AZACS trial (Azithromycin in Acute Coronary Syndromes), and correlated the serological findings according to titer levels with the presence of cardiac calcifications as detected by transthoracic echocardiography.

Results: In 271 patients, age 69 ± 13 years, who underwent both serological and echocardiographic evaluation, we found no significant association between the "calcification sum score" (on a scale of 0–3) in seropositive compared to seronegative patients (1.56 ± 1.15 vs.1.35 ± 1.15, respectively, P = 0.26). The median "calcification sum score" was 1 (interquartile range 0–3) for the seronegative group, and 2 (interquartile range 0–3) for the seropositive group (P = 0.2757). In addition, we did not find a significant correlation of any of the individual sites of cardiac calcification and Chlamydia pneumoniae seropositivity.

Conclusion: Our findings suggest that past C. pneumoniae infection may not be associated with the pathogenesis of valvular and cardiac calcifications.
 

Objectives: To determine whether there is an association between the presence and severity of adult calcific aortic stenosis and Chlamydia pneumoniae seropositivity

Methods: Forty adult patients (23 women, 17 men) were divided into three groups according to echocardiographic aortic valve area: Group A – 7 symptomatic subjects (age 67 ± 7 years) with normal aortic valve and normal coronary angiogram, Group B – 16 patients (age 73 ± 6) with moderate ACAS[1] (AVA[2]> 0.8 £ 1.5 cm²), and Group C – 17 patients (age 76 ± 7) with severe ACAS (AVA £ 0.8 cm²). We tested for immunoglobulins M, G and A as retrospective evidence of C. pneumoniae infection using the micro-immunofluorescence method. Past C. pneumoniae infection was defined by IgG titer > 16 £ 512.

Results: No patients in Group A showed positive Ig[3] for C. pneumoniae. IgM was not detected in any of the patients with ACAS (groups B and C) while 2 of 17 patients (12%) in group C showed IgA for the pathogen. High titers of IgG were found in 14 of 33 (42%) of the patients with moderate or severe ACAS: 5 of 16 (31%) in group B and 9 of 17 (53%) in group C (P = 0.2). Both groups had the same prevalence of coronary artery disease (66%). AVA was lower in IgG-seropositive patients than in the seronegative group (0.88 ± 0.3 cm² vs. 1.22 ± 0.4 cm², respectively, P = 0.02).

Conclusions: Past C. pneumoniae infection may be associated with a higher prevalence and greater severity of ACAS.

Objectives: To compare leukocyte counts and blood levels of various inflammatory cytokines in children and adults diagnosed with community-acquired bronchopneumonia.

Methods: We prospectively evaluated all pediatric and adult patients admitted for bronchopneumonia based on clinical and chest X-ray findings.. Blood was drawn for complete blood count and serum concentration of the following cytokines: granulocyte colony-stimulating factor, interleukins-6, 8 and 10, interferon-gamma, tumor necrosis factor, as well as matrix metalloproteinase-9 and intercellular adhesion molecule-1.

Results: There were 31 children and 32 adults. The patients in both groups had similar parameters of infection severity. None of them required admission to the Intensive Care Unit. Mean (± SD) leukocyte counts in the pediatric and adult groups were 21,018/mm (± 10,420) and 12,628/mm (± 6735) respectively (P = 0.02). Age was inversely correlated with leukocytes in the pediatric group (P = 0.0001). A significant inverse correslation was also found between age and platelet counts. Although cuytokine levels in both groups were not significantly different, age was

Conclusions: The immune response in community-aquired bronchopneumonia is, at least partly, age-dependent.

Background: Lipoid pneumonia is a pneumonitis resulting from the aspiration of lipids, and is commonly associated with the use of mineral oil as a laxative. LP[1] is relatively unfamiliar to clinicians and is probably underdiagnosed.

Objectives: To increase physicians' awareness of LP, its diagnosis and prevention.

Methods: We present two illustrative cases of LP and review the literature.

Results: Two cases of LP were diagnosed within half a year in an internal medicine ward. Both cases were elderly patients, and LP was associated with the use of mineral oil as a laxative agent. Computerized tomography revealed bilateral low attenuation infiltrates, associated with a "crazy paving" pattern in one case. Sudan Black staining was diagnostic in both cases – in one on a transbronchial biopsy specimen, and in the other on sputum cytologic examination. Both patients suffered from neurologic diseases and were at risk of aspiration. In both cases clinical symptoms and signs continued for several months prior to diagnosis but resolved after the mineral oil was discontinued.

Conclusions: LP often occurs in elderly patients who are at risk of aspiration. The condition may be underdiagnosed. Since in most cases mineral oil cathartics are the causative agent, an effort at primary prevention is indicated. It is suggested that the licensing of mineral oil for internal use be changed.

Objectives: To present a variety of radiologic findings on high resolution computerized tomography in eight sequential patients with COP[1], together with clinical and pathologic correlation.

Methods: Sequential HRCT[2] examinations of eight patients (four males) aged 53–80 years (mean 65.5 years) with pathologically proven COP were retrospectively analyzed by a consensus of two experienced chest radiologists for the existence and distribution of airspace consolidation, ground-glass opacities, nodular thickening along bronchovascular bundles, small (<1 cm) and large (>1 cm) nodules. The distribution of radiologic findings was classified as unilateral or bilateral, located in the upper, lower or middle lobe, and central or peripheral. Also recorded was the presence or absence of mediastinal lymphadenopathy and pleural effusion. Correlation with clinical symptoms was analyzed.

Results: All eight patients had bilateral airspace consolidations: in two cases consolidations were limited to central fields, in four they were peripheral, and in the remaining two cases they were both central and peripheral. Small nodules were noted in six cases and large nodules in three. Ground-glass opacities were found in four cases. All patients had enlarged lymph nodes (1–1.5 cm) in the mediastinum. Radiologic abnormalities resolved or improved after steroid treatment in all patients.

Conclusions: HRCT findings of bilateral multiple heterogenic lung infiltrates and nodules associated with mild mediastinal lymphadenopathy in a patient with non-specific clinical symptoms are suggestive of COP; in such cases, lung biopsy is indicated. Radiologic resolution of abnormalities correlates well with clinical improvement under adequate steroid treatment.

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[1] COP = cryptogenic organizing pneumonia

[2] HRCT = high resolution computerized tomography

Background: Recent studies have suggested a possible association between Chlamydia pneumoniae infection and coronary heart disease.

Objectives: To determine titers of antibodies to Chlamydia pneumoniae in patients with acute  myocardial infraction compared with titers in several control groups.

Methods: This prospective case-control study investigated 209 individuals. We assessed the serum IgG antibody titers to Chlamydia pneumoniae in 57 consecutive patients admitted with AMI to our intensive coronary care unit during a 4 month period. A serum sample was drawn upon admission after 6 weeks. Results were compared with those of four control groups: a) patients admitted with community-acquired pneumonia (n=18), b) patients with community-acquired urinary tract infection (n=42), c) patients with angiographically normal coronary artery disease (n=44), and d) patients with stable coronary artery disease (n=48). Serum immunoglobin G antibody titers to C. pneumoniae were determined using standard micro-immunofluorescene technology.

Results: Of 57 patients with AMI, 32 (56%) had a high lgG titer to C. pneumoniae (>=1:256) on the initial test, which remained unchanged (62%) after 6 weeks. The percentage of patients with high titers was significantly lower in the control groups: 5 of 18 patients (28%) in the pneumonia group (P<0.01), 11 of 42 (26%) in the urinary tract infection group (P<0.01), 11 of 44 (25%) with normal coronary arteries (P<0.01), and 17 of 48 (35%) with stable chronic ischemic heart disease (P<0.05).

Conclusion: The detection of high titers of lgG antibodies to C. pneumoniae in many patients with AMI, compared to control groups, suggest that chronic Chlamydia pneumoniae infection plays a role in the pathogenesis of atherosclerosis and acute ischemic events.

Objective: To describe the epidemiology of ceftazidime-resistant K. pneumoniae in our medical center, as representing the situation in tertiary care hospitals in Israel.

Methods: We vigorously restricted the use of ceftazidime in the ICU and enforced barrier precautions. The susceptibility rate of K. pneumoniae was surveyed in the ICU and throughout the hospital before and after the intervention in the ICU.

Results: Following the intervention, the susceptibility rate of K. pneumoniae increased from 11% (3/28) to 47% (14/30) (P0.01) among ICU isolates, from 55% (154/280) to 62% (175/281) (P=0.08) among total hospital isolates, and from 61% (50/82) to 74% (84/113) (P0.05) among total hospital blood isolates, although no additional control measures were employed outside the ICU.

Conclusions: The epidemiology of ceftazidime-resistant K. pneumoniae in our medical center is similar to that reported from other centers around the world. Early awareness to the emergence of this resistance, identification of the source of the epidemic, and prompt action at the putative source site may reduce the rate of acquisition and spread of such resistance inside and outside of the source unit.

Objectives: To evaluate the association between chronic infection with C. pneumoniae, as measured by a high titer of IgG antibody, and CAD. Our study was designed to explore the relationship between seropositivity to C. pneumoniae and serious coronary events, and to assess whether or not there may be an additional association between established cardiovascular factors and infection with this organism.

Methods: The serum of 130 patients with proven CAD was tested for the presence of IgG antibodies to C. pneumoniae using an ELISA test. A titer ≤1:64 using the microinfluorescence method, the recognized "gold standard," correlates with a positive result when using the ELISA method. The mean age was 57 (40-65 years). The patients, 82% male and 18% female, had either myocardial infarction (n=109) or unstable angina (n=21) 6 months before the investigation (range 3-24 months). The serum for the control group was obtained from 98 blood donors from the same area matched for age 52 (40-58 years) and sex. The donors had no known cardiac history.

Results: In the CAD group 75% of patients were positive for C. pneumoniae compared to 33% in the control group (P=0.001). No increased correlation could be demonstrated between traditional risk factors and C. pneumoniae infection, except in those patients with diabetes mellitus. We found a lower prevalence of IgG antibody to C. pneumoniae in the diabetes subgroup than in other subgroups (P<0.006), but a higher prevalence than in the control group.

Conclusions: We demonstrated a more than twofold increase in seropositivity to C. pneumoniae among patients suffering serious coronary events, and this trend was independent of gender, age or ethnic group. These findings suggest that chronic C. pneumoniae infection may be a significant risk factor for the development of CAD, but this correlation should be investigated further.

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CAD= coronary artery disease