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Results for “RICKETTSIAL DISEASES”

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At least 1,135 records · Page 63Linked to original sources
PubMed1989

[Treatment of pneumonia caused by Legionella, Mycoplasma, Chlamydiae and Rickettsia using ofloxacin].

To asses the efficacy and the safety of ofloxacin as therapy of pneumonia caused by intracellular pathogens, 35 patients were studied (26 male, 9 female, mean age: 52.5 +/- 16.6 years). Causative pathogens were Chlamydia psittaci (n = 13), Legionella pneumophila (n = 10), Mycoplasma pneumoniae (n = 7) and Coxiella burnetii (n = 5). Ofloxacin was administered orally in 32 cases (200 mg b.i.d. in 80% of cases) and by I.V. route in 3 cases. All patients were cured without any side effects. In conclusion, ofloxacin appears, in our study, as an efficient therapy for these pneumonias. It could be considered as a valuable alternative to other antimicrobial agents with intra-cellular activity.

Adult↗
PubMedDate not supplied

[Vascular rickettsiosis].

The authors discuss the problem of rickettsial and para-rickettsial etiopathogeny of some types of angiopathies earlier characterized by a febrile state. They are especially interested in vasculopathies occurring in endemia areas. The disease may involve the entire vascular system and the pathogenic agent remains in the mid membranes and in the adventitia, as can be seen by seriologic and anatomo-pathologic tests. There are diffuse or nodular lymphoblastic infiltrations (pan-vascular condition). The authors also demonstrate that treatment with higher tetracyclines (Reverin) is absolutely advised, and draw attention to the need to do systematic seriologic research on all patients hospitalized for cardio-vascular diseases.

Animals↗
PubMed1991

Isolation and continuous culture of Neorickettsia helminthoeca in a macrophage cell line.

Experimental evidence is presented supporting the development of a system for the isolation and propagation of a Neorickettsia sp. in a continuous canine macrophage cell line (DH82). To isolate a Neorickettsia sp. pathogenic to the canine species, three naive dogs were fed metacercaria-encysted kidneys of salmon caught in a river where infection of metacercariae with Neorickettsia helminthoeca has been circumstantially known for decades. Clinically, the classic course of salmon poisoning disease developed in all of the dogs. Parasitemia began on day 8 to 11 postinfection, when the dogs developed a febrile peak, and continued until euthanasia. At necropsy, characteristic gross and microscopic lesions of the disease were present. A Neorickettsia sp. was also isolated from liver and spleen samples of these animals. The isolates have been continuously propagated and passed in DH82 cells for more than 6 months. Electron microscopic examination confirmed that the rickettsial organisms multiplied in the membrane-bound compartment of DH82 cells and that they morphologically closely resembled rickettsia belonging to the genus Ehrlichia. An indirect fluorescent antibody test using Neorickettsia organisms cultured in DH82 cells showed that all dogs seroconverted 13 to 15 days postinfection. Finally, inoculation of the cell-cultured Neorickettsia organisms into a naive dog reproduced clinically typical salmon poisoning disease which was of greater severity and had a more rapid time course than that in the dogs from which the original isolation was made. On the basis of the clinical and pathologic responses of the dogs in our study, we believe that virulent N. helminthoeca was isolated and cultured in a continuous cell line.

Animals↗
PubMed2005

Changes in the adherens junctions of human endothelial cells infected with spotted fever group rickettsiae.

Rickettsiae of the spotted fever group are obligately intracellular bacteria that primarily infect the vascular endothelium, invade adjacent cells propelled by actin polymerization, and cause severe systemic diseases. Endothelial dysfunction and vascular leakage develop as a consequence; this effect is the pathophysiological mechanism that explains most clinical manifestations. Here we report that rickettsial infection of cultured primary human endothelial cells is associated with the formation of gaps in the interendothelial adherens junctions, occurring late during the course of in vitro infections but not early, even when rickettsial loads are significant.

Adherens Junctions↗
PubMed1978

Wild rodents as laboratory models and their part in the study of diseases.

The paper describes the use of 14 South African wild rodent species as experimental models and demonstrates the proven value of many of these as laboratory animals in research on bacterial infections (plague, relapsing fever), rickettsial infections (tickbite fever, louse typhus), viral infections (poliomyelitis. Rift-Valley fever and other arbovirus infections, Lassa fever), fungal infections (histoplasmosis), parasitic infections (schistosomiasis) and in diabetes mellitus and cancer research.

Animal Husbandry↗
PubMed2003

Rickettsia rickettsii infection in the pine vole, Microtus pinetorum: kinetics of infection and quantitation of antioxidant enzyme gene expression by RT-PCR.

The pine vole, Microtus pinetorum, was evaluated as a laboratory animal model for infection with Rickettsia rickettsii. Voles demonstrated signs of acute disease, and 45% of infected animals died following intraperitoneal infection with 3 x 10(6) plaque forming units of R. rickettsii. Spleen, liver, kidney, lung, brain, testes and blood were analyzed for rickettsial burden by a quantitative PCR assay. The distribution of rickettsiae in tissues during the course of infection was determined by immunohistochemical staining and pathological changes in tissues were correlated with the clinical severity of infection. Quantitative RT-PCR assays were designed to measure the mRNA levels of the antioxidant enzyme genes for catalase, glutathione peroxidase, glutathione reductase, heme oxygenase, Cu-Zn superoxide dismutase (SOD) and Mn-SOD, and 2 housekeeping genes, actin and glyceraldehyde phosphate dehydrogenase. Tissues from acutely ill animals on days 2 to 6 of infection, convalescent animals, and uninfected control animals were studied. The number of transcripts of each enzyme gene was determined and compared to the degree of rickettsial infection present. These studies demonstrate that the pine vole is a valuable experimental model for studying infection with R. rickettsii. Our results provide the first experimental evidence that R. rickettsii causes alteration(s) of the anti-oxidant system in vivo.

Animals↗
PubMed2002

Clinical manifestations and complications of rickettsiosis in southern Taiwan.

BACKGROUND AND PURPOSE: Taiwan is an endemic area for scrub typhus. Recent increases have been noted in two other infectious diseases caused by obligate intracellular organisms, Q fever and murine typhus. These diseases usually present as an acute febrile illness with non-specific symptoms and are difficult to distinguish. This study describes the clinical manifestations and complications of cases of rickettsial infections treated at a medical center in southern Taiwan. METHODS: Serum samples from patients with acute febrile illness with or without shock, but without a clinical diagnosis of localized bacterial infection after a preliminary work-up, were collected for serologic study. Medical records of cases with serologic evidence of infection were reviewed and their clinical manifestations were analyzed. RESULTS: From October 1992 to July 2000, 51 serologically diagnosed cases of rickettsiosis were studied. Q fever predominated (28 cases). All cases of acute Q fever presented with hepatitis during the course of the illness and more than half (54%) reported an animal contact history. Most patients with Q fever (96%) and murine typhus (86%) were male, Serious complications, especially pneumonitis, occurred more frequently with scrub typhus than with acute Q fever. Spontaneous remission frequently occurred with acute Q fever. Administration of tetracycline or its analogues usually resulted in defervescence by the third day of treatment of scrub typhus. CONCLUSIONS: In our study, serious complications including pneumonitis, meningitis/meningoencephalitis, shock, acute renal failure, and disseminated intravascular coagulation were not uncommon in patients with scrub typhus. Physicians should include scrub typhus in the differential diagnosis of suspected cases of community-acquired febrile illness with multiple organ dysfunction in this endemic area. As Q fever is an emerging infectious disease in southern Taiwan, further large-scale epidemiologic surveillance and clinical data are needed.

Adult↗
PubMedDate not supplied

Dual infection with Ehrlichia chaffeensis and a spotted fever group rickettsia: a case report.

Well-documented cases of simultaneous human infection with more than one tick-borne pathogen are rare. To our knowledge only two dual infections have been reported: simultaneous human infection with the agent of human granulocytic ehrlichiosis and Borrelia burgdorferi and simultaneous human infection with B. burgdorferi and Babesia microti (1-2). Rocky Mountain spotted fever has long been known to be endemic in North Carolina; cases of human ehrlichial infection were recognized there soon after Ehrlichia chaffeensis was recognized as an important cause of tick-borne disease in the southeastern United States. Because both Rocky Mountain spotted fever and ehrlichiosis are prevalent in North Carolina, occasional cases of simultaneous human infection by rickettsial and ehrlichial agents would not be surprising; however, no such cases seem to have been reported.

Adult↗
PubMed2001

Kawasaki disease: is it caused by an infectious agent?

Kawasaki disease (KD) is an acute systemic febrile illness of unknown aetiology, predominantly affecting children under five years of age. Initially described in 1967 by Tomisaku Kawasaki, it is now the most common cause of acquired heart disease in children in the developed world. Although normally self-limiting, KD is associated with a range of complications, the most important of which is the development of life-threatening coronary artery abnormalities. Here, we examine the evidence supporting the concept that KD is caused by an infectious agent. Various infectious agents--including bacterial, viral and Rickettsial organisms--have been implicated as potential causes, as have certain immunological agents such as bacterial toxin-mediated superantigens, allergens such as anionic detergents and house-dust mites, and some chemicals (including heavy metals). Following extensive research, however, no links between any of these individual agents and the disease have been established irrefutably. Despite this, most of the epidemiological and immunological evidence currently available indicates that the causative agent is most likely to be infectious in nature; and additional evidence highlights the likelihood that development of KD is multifactorial in nature, requiring certain genetic and immunological factors, and possibly a vector.

Bacterial Infections↗