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PubMed2001

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.

Adult↗

PubMed2002

Diagnostic methods current best practices and guidelines for identification of difficult-to-culture pathogens in infective endocarditis.

Culture-negative endocarditis currently represents a diagnostic challenge for physicians. Traditional methods such as histology, serology, and culture have been improved and new molecular techniques have been developed to improve the detection of difficult-to-culture agents. Serologic tests for the two most frequent etiologic agents, Coxiella burnetii and Bartonella spp, should be performed first because they can usually be identified easily in this way. The sensitivity of culture for intracellular bacteria has been improved by inoculation of samples in shell vials and by the use of novel tissue cell lines. Recently, universal and species-specific primers have been designated to amplify bacterial DNA directly from resected valves, allowing positive identification.

Bacteria↗

PubMed1994

An epidemiological study on Q fever in the Emilia-Romagna Region, Italy.

A seroepidemiological survey was carried out in cattle from an Apenninic area of the Emilia-Romagna Region, Italy, in order to assess the prevalence and to analyze the epidemiology of Coxiella burnetii infection. The complement fixation test was performed on 711 animals from 99 herds. The prevalence rate was 13.1% with respect to the herds and 4.4% with respect to the animals. The positive titres ranged from 1:8 to 1:256. Significant differences in positivity were found between animals of different age and breed and between animals from herds of different types of production and management. The infection seems to be linked also with infertility and with replacement from the outside.

Animals↗

PubMed2002

Cytoskeletal proteins and resident flora.

Recent observations demonstrate that enteropathogenetic and enterohaemorrhagic bacteria, as well as other non enteropathogenetic bacteria (Listeria, Coxiella Burnetii), may subvert the host cell cytoskeleton. Models from enteropathogenic bacteria demonstrate that cytoskeletal proteins are required for bacteria binding to the enterocytes and that they play a role in the immune response of the host to intestinal bacteria. The cytoskeletal protein family Tropomyosins is present in all eukaryotic cells, with multiple isoforms regulated by multiple genes. Of the different Tropomyosin isoforms, TM5 has been shown to be expressed in colonic and jejunal epithelial cells, while TM1 in colonic and jejunal smooth muscle. In vitro studies have shown the presence of serum and mucosal IgG against TM5 in almost two thirds of patients with ulcerative colitis, suggesting: a. a possible autoimmune response to Tropomyosin in these patients; b. the hypothesis that the development of pouchitis may be related to the expression of TM5 in the ileal pouch; c. the use of probiotics in the treatment of pouchitis. Overall, the new expression of cytoskeletal proteins on the cell surface appears to be possibly induced by several mechanisms, including intestinal bacteria and apoptosis. The expression of cytoskeletal proteins on the cell surface may induce tolerance or autoimmune response on target cells. Further investigations are, however needed on the possible role of cytoskeletal proteins in human diseases.

Cytoskeletal Proteins↗

PubMed2005

Diffuse abdominal uptake mimicking peritonitis in gallium inflammatory scan: an unusual feature of acute Q fever.

The clinical features in patients with acute Q fever are variable. We present a patient with fever, abdominal distension, pericardial effusion, and diffuse gallium uptake in the abdominal cavity, mimicking peritonitis or peritoneum carcinomatosis. Serologic surveys revealed acute infection by Coxiella burnetii. The patient responded poorly to doxycycline and improved with oral levofloxacin. During the afebrile period, gallium inflammatory scan showed resolution of previous diffuse uptake in the abdomen, and cardiac echo resolution of pericardial effusion, which was suggestive of peritoneal inflammation related to acute C. burnetii infection. Therefore, clinicians in Taiwan should be alert to the possibility of acute Q fever in patients with fever of unknown cause, especially with clinical evidence of peritoneal and/or pericardial inflammation.

Abdominal Cavity↗

PubMedDate not supplied

Q fever control measures: recommendations for research facilities using sheep.

Q fever (Query Fever) is a zoonosis caused by the rickettsia Coxiella burnetii. domestic ungulates such as sheep, cattle, and goats serve as the reservoir of infection for humans and shed the desiccation-resistant organism in urine, feces, milk, and especially in birth products. In humans the illness is generally mild; however, Q fever hepatitis is often seen and Q fever endocarditis is an uncommon, but frequently fatal complication. Q fever long has been recognized as an occupational hazard among persons working with animals or animal products, and in laboratories working with C. burnetii. Recently, Q fever outbreaks have occurred in medical research facilities using sheep as research animals. Recommendations are presented for reducing the risk of exposure to Q fever in persons not working with sheep in research facilities that use sheep. In addition, recommendations are presented for reducing the risk of infection in persons who work with sheep in research facilities.

Animals↗

PubMed1990

Q fever in Plymouth, 1972-88. A review with particular reference to neurological manifestations.

Between 1972 and 1988 we have serologically confirmed 103 Coxiella burnetii infections: 46 were acute, 5 were chronic, 52 represented past infections. Details of 61 cases are presented. Of acute cases 80% had respiratory involvement; at least 63% had pneumonias. The incidence (22%) of neurological complications was of particular interest; 40% of these patients had prolonged sequelae. One acutely ill patient died of fulminating hepatitis. Patients with pre-existing pathology or immunosuppression were especially susceptible to C. burnetii. In the absence of acute sera, the complement fixation test alone provided inadequate differentiation between recent and past Q fever: phase II titres persisted at greater than or equal to 80 for more than 1 year after the acute infection in 15 cases; maximum duration of persistence was 14 years. Three patients acquired high phase I titres. Only 5% of cases had chronic Q fever, but in view of the diverse sequelae observed in this series, we suggest that long-term serological and clinical follow-up of all cases of Q fever is fully justified.

Acute Disease↗

PubMed2003

Variation in immune response genes and chronic Q fever. Concepts: preliminary test with post-Q fever fatigue syndrome.

Acute primary Q fever is followed by various chronic sequelae. These include subacute Q fever endocarditis, granulomatous reactions in various organs or a prolonged debilitating post-infection fatigue syndrome (QFS). The causative organism, Coxiella burnetii, persists after an initial infection. The differing chronic outcomes may reflect variations within cytokine and accessory immune control genes which affect regulation of the level of persistence. As a preliminary test of the concept we have genotyped QFS patients and controls for gene variants spanning 15 genes and also examined HLA-B and DR frequencies. QFS patients exhibited a significantly increased frequency of HLA-DR-11 compared with controls and also significant differences in allelic variant frequencies within the NRAMP, and IFNgamma genes. These results indicate a possible genetic role in the expression of overt chronic Q fever. Further studies will be undertaken to increase sample sizes, to survey other forms of chronic Q fever and to examine Q fever patients who have recovered without sequelae.

Cation Transport Proteins↗

PubMed2003

Infective endocarditis not related to intravenous drug abuse in HIV-1-infected patients: report of eight cases and review of the literature.

OBJECTIVES: To add to the limited information on infective endocarditis (IE) not related to intravenous drug abuse (IVDA) in HIV-1-infected patients. METHODS: We have reviewed the characteristics of eight cases of IE in non-IVDA HIV-1 infected patients diagnosed in our institution between 1979 and 1999 as well as cases in the literature. RESULTS: All our patients were male, and the mean age was 44 years (range 29-64). HIV-1 risk factors were: homosexuality in five, heterosexuality in two, and the use of blood products in one. HIV stage C was found in six cases, and the median (range) CD4 cell count was 22/microL (4-274 cells/microL). IE was caused by Enterococcus faecalis in three cases, staphylococci in two cases, and Salmonella enteritidis, viridans group streptococci and Coxiella burnetii in one case each. Three patients acquired IE while in the hospital. All IE cases involved a native valve, and underlying valve disease was found in three patients. The aortic valve was the most frequently affected (five cases). Two patients underwent surgery, with a good outcome, and one patient died. Fourteen cases of IE not related to IVDA in HIV-1-infected patients were found in the literature review. The most common causative agents were Salmonella spp. and fungi (four cases each). Two patients had prosthetic valve IE, and the mitral valve was the most frequently affected (10 cases). The remaining clinical characteristics and the outcome were similar to those in the present series. CONCLUSIONS: IE not related to IVDA is rare in HIV-1-infected patients. In more than half of the cases, IE develops in patients with advanced HIV-1 disease. A wide etiologic range is found, reflecting different clinical and environmental conditions. None of the patients who underwent surgery died, and the overall mortality rate was not higher than in non-HIV-1-infected patients with IE.

AIDS-Related Opportunistic Infections↗

PubMed2000

[Q-fever outbreak in Dortmund in the summer of 1999. Results of an epidemiological outbreak study].

In the summer of 1999, the health department of the City of Dortmund registered an increased incidence rate of reported Q-fever-diseases. Q-fever is a zoonosis caused by the Coxiella burnetii bacterium which typically multiplies within cells. To investigate the cause of this outbreak, an investigation was initiated. Clinical and veterinary examinations, investigations of the environment and an epidemiological case-control-study were combined. Patients as well as healthy persons interviewed for comparative purposes were asked to complete a questionnaire on their habits of life and the answers compared. The results of this study show a clear connection between an exposition with sheep, dung (OR = 14.9; 95% CI: 4.9-47) and manure (OR = 18.7; 95% CI: 3.5-180) of infected sheep and the Q-fever outbreak. The study confirmed the assumption that a local sheep farm was the source of infection for the epidemic outbreak of Q-fever in the same quarter of Dortmund.

Adolescent↗

PubMed2003

Active self-splicing group I introns in 23S rRNA genes of hyperthermophilic bacteria, derived from introns in eukaryotic organelles.

Group I introns are common in the 23 rRNA genes of mitochondria and chloroplasts. Often, they encode "homing endonucleases," which target highly conserved gene sequences and drive interorganellar intron mobility, even across species and genus lines. Most bacterial 23S rRNA genes show these same endonuclease-sensitive target sequences. However, only two bacterial 23S rRNA genes are known to contain group I introns: that of Simkania negevensis [Everett, K. D., Kahane, S., Bush, R. M. & Friedman, M. G. (1999) J. Bacteriol. 181, 4734-4740], where the intron is not spliced and probably limits growth, and that of Coxiella burnetii [Seshadri, R., et al. (2003) Proc. Natl. Acad. Sci. USA 100, 5455-5460], where no direct evidence of splicing exists. Both bacteria are intracellular parasites and might have acquired introns from eukaryotic hosts. Here we provide direct evidence for splicing, and evolutionary evidence for mobility, of group I introns in the 23S rRNA genes of several free-living hyperthermophilic bacteria of the genus Thermotoga. These bacteria do not live closely with eukaryotes, but phylogenetic analyses suggest that their introns were also acquired from eukaryotic (probably algal) organelles. In vivo, their introns must be spliced at temperatures approaching 90 degrees C, making them the most thermostable natural ribozymes so far described. We demonstrate that at least some of these introns can also self-splice in vitro.

Bacteria↗

PubMed1998

Membrane association of active plasmid partitioning protein A in Escherichia coli.

QsopA and SopA, proteins essential for stable maintenance of low copy number plasmids and encoded on plasmid QpH1 of Coxiella burnetii and the F plasmid of Escherichia coli, respectively, are shown to be membrane associated using three independent approaches: isolation of hybrid protein A-PhoA proteins that display PhoA (bacterial alkaline phosphatase) activity indicating a periplasmic location, biochemical fractionation by flotation gradient centrifugation, and subcellular localization by immunoelectron microscopy. These data provide insight into the mechanism by which partitioning protein A spatially directs plasmids into daughter cells at bacterial division.

Bacterial Proteins↗

PubMed2006

Jaundice of unknown origin: Remember zoonoses!

Zoonotic diseases are randomly remembered in the differential diagnosis of jaundice of unknown origin. We present four characteristic cases of jaundice attributed to brucellosis and Coxiella burnetii infection and discuss the various pathogenetic pathways implicated in each case. We present a brief review of the relevant literature and, in an era of increasing subspecialization, underline the importance of viewing the "whole picture".

Aged↗

PubMed1989

Chlamydial disease pathogenesis. The 57-kD chlamydial hypersensitivity antigen is a stress response protein.

Chlamydia trachomatis infection of humans is commonly a localized inflammation that can result in infertility, blindness, and perhaps arthritis. The pathogenic process(es) that cause these sequelae are thought to be immunological. A 57-kD protein that is common among Chlamydia elicits ocular inflammation when introduced onto the conjunctivae of guinea pigs or nonhuman primates previously sensitized by chlamydial infection. This protein is thought to mediate the immunopathology that follows chlamydial infection. To more thoroughly characterize this chlamydial component, we cloned its gene from a C. psittaci strain and identified a particular recombinant that produced the 57-kD polypeptide. The recombinant gene product was immunoreactive with a monospecific anti-57-kD serum, and elicited an ocular inflammation similar to that produced by the 57-kD antigen isolated from chlamydiae. Sequencing identified two ORFs that encode polypeptides of 11.2 and 58.1 kD and are co-transcribed. These two polypeptides show homology with Escherichia coli groE and Coxiella burnetii htp heat-shock proteins. Striking homology (greater than 50%) was found between the 57-kD protein and the HtpB, GroEL, 65-k Mycobacterium tuberculosis and Hsp60 proteins. Thus, the 57-kD chlamydial protein, previously implicated as mediating a deleterious immunologic response to chlamydial infections, is a stress-induced protein similar to those that occur universally in both prokaryotic and eukaryotic organisms.

Amino Acid Sequence↗

PubMed2001

Risks factors and prevention of Q fever endocarditis.

Coxiella burnetii causes acute and chronic Q fever. To evaluate the risk factors of development of chronic endocarditis following Q fever and to assess the best preventive therapy, a retrospective study of patients diagnosed as having Q fever during 1985-2000 was conducted. Twelve patients with acute Q fever who developed endocarditis and 102 patients with Q fever endocarditis were included in the study. When compared to 200 control patients with acute Q fever, preexisting valvular disease (P<10(-7)), especially a prosthetic valve (P=.01), were encountered more often among patients with endocarditis. Among patients with valvular defects, we estimate the risk of developing endocarditis to be 39%. A combination of doxycycline plus hydroxychloroquine was better at preventing the development of endocarditis than doxycycline alone (P=.009). Our results should encourage physicians to detect valvular lesions in patients with acute Q fever and to search for acute Q fever in patients with a valvulopathy and unexplained fever. A proper treatment for such patients and a scheduled follow-up should reduce the risk of developing endocarditis.

Aged↗

PubMed2004

Three cases of Q fever osteomyelitis in children and a review of the literature.

Q fever is a common zoonosis worldwide. Awareness of the disease and newer diagnostic modalities have resulted in increasing recognition of unusual manifestations. We report 3 cases of Q fever osteomyelitis in children and review the literature on 11 other reported cases. The cases demonstrate that Coxiella burnetii can cause granulomatous osteomyelitis that presents without systemic symptoms and frequently results in a chronic, relapsing, multifocal clinical course. Optimal selection and duration of antimicrobial therapy and methods of monitoring therapy are currently uncertain.

Adult↗

PubMed2006

Role of sex, age, previous valve lesion, and pregnancy in the clinical expression and outcome of Q fever after a large outbreak.

BACKGROUND: Q fever is a zoonosis caused by Coxiella burnetii. After a large outbreak occurred in the Chamonix Valley in the French Alps in 2002, an extensive surveillance was conducted, to describe the variations in the clinical expression of acute Q fever according to host factors, as well as to monitor the risk of evolution of acute Q fever to chronic Q fever in patients at risk. METHODS: Three groups of patients with risk factors for evolution of acute Q fever to chronic Q fever were considered: 376 pregnant women, 19 immunocompromised patients, and 91 patients with valvular or vascular abnormalities. A group of 578 people without risk factors for evolution of acute Q fever to chronic Q fever was also tested. Diagnosis of Q fever was based on serologic testing by immunofluorescence assay. RESULTS: Between 30 August 2002 and 31 July 2003, a total of 1946 serum samples obtained from 1064 persons were tested. A total of 101 patients (9.3%) had acute Q fever diagnosed, and 5 patients (0.5%) had chronic Q fever diagnosed. A diagnosis of acute Q fever was established for 11 pregnant women (2.6% of 379 pregnancies), 5 patients with valvular disease (5.5%), and 85 people without risk factors (14.7%) (71 [27.9%] of 254 symptomatic patients and 14 [4.3%] of 324 asymptomatic patients). A new pregnancy in a woman with negative results of serologic tests for Q fever exposes the woman to a new risk for acute Q fever able to evolve to chronic Q fever. The rates of clinical expression were 90.6% in adult men, 75% in adult women, and 33.3% in children, and they were significantly lower (9.1%) in pregnant women. Evolution to chronic Q fever was observed in 5 patients. CONCLUSION: This study emphasizes the importance of active surveillance in postepidemic conditions, especially among patients at risk, as well as the importance of systematic serologic testing during pregnancy.

Adolescent↗

PubMed1999

Use of corticosteroids in glomerulonephritis related to infective endocarditis: three cases and review.

We report the cases of three patients treated for infective endocarditis (IE) for whom corticosteroids were added to the antibiotic treatment. They all had clinical and biological evidence of immune-mediated glomerulonephritis. The microorganisms responsible for IE were Coxiella burnetii, Streptococcus bovis, and Cardiobacterium hominis. Median duration of IE before antimicrobial therapy was 7 months. In all patients, renal function deteriorated despite appropriate antimicrobial treatment for a mean duration of 16 days, but it improved after addition of corticosteroid therapy. All patients were cured of IE. A literature review revealed four additional cases of IE-related glomerulonephritis in which adjunctive immunosuppressive therapy was considered to be effective. Although corticosteroid therapy is generally not recommended for IE, it should be considered for patients whose renal dysfunction secondary to glomerulonephritis does not improve with appropriate antimicrobial treatment, especially if the duration of the illness is long.

Aged↗