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PubMed1977

A seriological investigation of Q fever in clinical patients.

Results of a serological survey of 507 patients, 301 males and 206 females at the Ahmadu Bello University Teaching Hospital indicated a total 20.5 per cent, or 21.3 per cent in males and 19.4 per cent females, had been exposed to Q fever agent and had circulating antibody against Coxiella burnetii. Most of the positive sera were from patients whose clinical diagnoses were typhoid and pyrexia of unknown origin though these generally are the commonest clinical diagnoses in the hospital. Titres varied from 1:4 to 1:1028 indicating old infections in some patients and acute in others. The results of normal blood donors also showed a 22 per cent positive. It is suggested that the presumptive evidence of the serological tests results be substantiated by isolation of the agent so that a correlation between clinical signs and evidence of Q fever infection be established.

Agglutination Tests↗

PubMed2004

Causative organisms of infective endocarditis according to host status.

A prospective study of infective endocarditis (IE) was conducted between 1994 and 2000 in Marseilles, France, and included 170 definite cases diagnosed with the use of modified Duke criteria. Classification of IE based on the aetiological agent was related to epidemiological characteristics, including age, gender and the nature of the injured valve. Enterococci and Streptococcus bovis were identified more frequently in older subjects (p 0.02), and S. bovis was also associated with mitral valve infection (p 0.03). Streptococcus spp. were found to be associated with native valves (p < 10(-3)), whereas coagulase-negative staphylococci and Coxiella burnetii were associated with intracardiac prosthetic material (p < 0.05). S. bovis and Staphylococcus aureus were the predominant species associated with presumably healthy valves (p < 0.05), whereas oral streptococci caused IE exclusively in patients with previous valve damage. The basic host status of IE patients has been linked to specific microorganisms, and this may be of value when empirical treatment is needed in patients who have received previous antibiotic therapy and whose blood cultures are negative.

Adolescent↗

PubMed1981

Q fever in Finland: clinical, immunological and epidemiological findings.

Clinical, immunological and epidemiological features of 14 human cases of Q fever diagnosed at Aurora Hospital are presented. All patients had an acute febrile disease and 9 (64%) had respiratory symptoms, 4 (29%) verified pneumonia, and 9 (64%) hepatitis, which in 4 biopsied cases proved to be granulomatous. Presence of circulating immune complexes was shown in 10/11 patients investigated by the platelet aggregation test (PAT) and the platelet iodinated protein A (PIPA) test. Q fever is not known to be endemic in the Nordic Countries. However, the causative agent, Coxiella burnetii, should tolerate our climate and there is a rich potential animal reservoir. All patients had visited some endemic area shortly before they were taken ill. In 3 cases the interval between arrival in Finland and the onset of symptoms was more than double the reported maximal incubation period, namely 69, 75 and 88 days. We suggest that these patients acquired the infection after their return to Finland from their clothing or from souvenirs. If so, Q fever could be acquired by this mechanism by persons who have never visited an area where the disease is endemic.

Adult↗

PubMed1982

Q fever endocarditis.

Despite a worldwide distribution of Coxiella burnetii, only single cases of Q fever endocarditis have been reported outside Great Britain and Australia. We present 10 patients; five were female, only four had a history of environmental exposure, and the mitral valve was involved as commonly as the aortic stenosis, and three patients had a prosthetic valve. We confirm the importance of hepatic involvement, thrombocytopenia and hypergammaglobulinemia as diagnostic features. Diagnosis was established by finding and elevated complement-fixing antibody to Phase I C. burnetii antigen. Tetracycline, with or without lincomycin or cotrimoxazole, was used in nine patients, and one patient received cotrimoxazole as as the sole antibiotic agent. Optimal duration of therapy is unknown. In one patient, relapse followed when treatment was stopped after 18 months. Valve replacement was necessary in five patients, because of hemodynamic problems. Five patients died, and the means survival is 36 months with a range of five to 66 months. We suggest that Q fever endocarditis is frequently missed, and we recommend clinicians to consider the diagnosis in all cases of culture-negative endocarditis.

Adult↗

PubMed1989

Q fever pneumonia.

Pneumonia is one of several clinical syndromes that results from inhalation of Coxiella burnetii. This microorganism, the etiologic agent of "Q" (query) fever, infects a wide range of animals and insects. Cattle, sheep, goats, and cats are the reservoirs whereby this agent is spread to humans. High concentrations of C burnetii are present in the placenta and at parturition, the organism is shed into the environment to be inhaled by humans. Following an incubation period that ranges from four to 30 days (mean 14 days), fever, headache, malaise, and cough ensue. The clinical presentation of pneumonia may range from a mild to a severe illness--the latter with the clinical picture of rapidly progressive pneumonia. There are no characteristic features of Q fever pneumonia but the severe headache and the epidemiological history should serve as clues. Treatment with tetracycline or rifampin for two weeks usually results in cure. Many cases of Q fever pneumonia remit without antibiotic therapy. The diagnosis is usually confirmed serologically using a complement fixation or microimmunofluorescence test.

Animals↗

PubMed1988

Markers of cell-mediated immunity after vaccination with an inactivated, whole-cell Q fever vaccine.

A clinical trial of Q fever vaccine in four South Australian abattoirs showed apparently complete protection against natural infection; however, only 50%-60% of vaccinees developed complement-fixing or immunofluorescent antibody after vaccination. Cell-mediated immunity to Coxiella burnetii antigens, as measured by an index of lymphoproliferative responses (LSI) of peripheral blood mononuclear cells, was therefore assessed. Eighty-five percent of 13 subjects with "low risk" of exposure to Q fever and with an initially negative LSI converted to a positive LSI after vaccination; conversion was noted nine to 13 days after vaccination, and positive values were obtained for at least 96 d. Only 35% of this group seroconverted. In a "high-risk" group (abattoir workers), higher rates of positive LSI (greater than 95%) and of antibody (50%-70%) were observed after vaccination; greater than 95% of vaccinees in this group, who had been vaccinated five years previously, had positive LSI values.

Antigens, Bacterial↗

PubMed1986

Q fever vaccination of sheep: challenge of immunity in ewes.

Adult ewes (17 months of age) were vaccinated against Coxiella burnetii, using a formalin-inactivated whole cell (WC) phase I Henzerling strain vaccine or a chloroform methanol residue (CMR) vaccine. Nineteen pregnant ewes were placed in 3 categories [(i) unvaccinated, (ii) WC vaccine, and (iii) CMR vaccine] and were challenge exposed at approximately the 100th day of gestation with 210,000 plaque-forming units of C burnetii inoculated subcutaneously. Shedding of rickettsiae was measurably reduced, but was not prevented in vaccinated groups, as shown by inoculating ewes' placental tissues, amniotic fluid, and colostrum into mice, as well as by histopathologic lesions of placental tissues. The rickettsiae were shed in the placenta, amniotic fluid, or colostrum in 6 nonvaccinated ewes. In comparison, rickettsiae were detected in placental inoculations from 2 of 6 ewes in the WC vaccine group and 1 of 6 in the CMR group. In contrast to those in the vaccinated ewes, placentitis, high concentrations of rickettsiae in microscopic preparations, and weak lambs were typical for the nonvaccinated ewes.

Animals↗

PubMed1985

Immunofluorescence serology. A tool for prognosis of Q-fever.

The indirect immunofluorescence antibody test is currently the method of choice for Q-fever laboratory diagnosis. It permits the detection of IgG-, IgM-, and IgA-specific antibodies against the two phases of Coxiella burnetii. Sera from 20 cases of C. burnetii infection have been examined. Only total IgG against phase II were detected in cryptic infections. In acute Q-fever cases, the appearance of total IgG antibodies against phase I was a sign of aggravation, while IgM titers remained low. In subacute cases of Q-fever, anti-phase-I IgG titers were equal to or higher than anti-phase-II titers, and IgM against both phases were produced over a long time. Particularly high IgM titers were found in cases of granulomatous hepatitis. IgA antibodies against phase I were found in cases of Q-fever endocarditis, although the two cases that died had few or no IgA antibodies, despite very high IgG and IgM titers.

Acute Disease↗

PubMed1985

Seroepidemiology of Q fever among domestic animals in Nova Scotia.

We used the indirect microimmunofluorescence test to determine the presence of antibodies in sheep, cattle, goat, cat, and dog sera to phase I and II Coxiella burnetii antigens in Nova Scotia. Only 6.7 per cent of the 329 sheep tested had antibodies to phase II antigen and none had antibodies to phase I. Of 29 goats tested, 7 per cent and 3.5 per cent had antibodies to phase II and phase I antigens, respectively. In contrast, 23.8 per cent of the 214 cattle tested had antibodies to phase II antigen, and 24.2 per cent had antibodies to phase I antigen; 24.1 per cent of 216 cats tested had antibodies to phase II antigen and 6 per cent had antibodies to phase I antigen. None of the 447 dogs tested had antibodies detected. We conclude that cattle and cats may be reservoirs for human Q fever in Nova Scotia.

Animals↗

PubMed1989

Development of local morphological changes after intradermal inoculation of Q-fever chemovaccine.

Development of morphological changes was studied in the site of intradermal inoculation of Q-fever chemovaccine. The chemovaccine was obtained by trichloroacetic acid extraction from Coxiella burnetii, strain Nine mile, phase I cells. The effect of two vaccine doses (0.2 mg and 1.0 mg) was compared in two groups of guinea pigs (each consisting of 21 animals). After inoculation of 1.0 mg vaccine abscesses formed in the dermis and in subcutaneous tissue along with dystrophic changes of skeletal muscles. Reparation of these lesions progressed sufficiently slowly and was not completed before 60 days after vaccine inoculation. The regeneration of skeletal muscles was of budding type. After inoculation of 0.2 mg of chemovaccine minimal lesions occurred in the subcutaneous tissue only. However, already within 48 hr this vaccine dose evoked a strong reparation response. Interesting was the finding of Kurloff cells in the haemorrhagic foci. The results suggest that the low-reactogenic chemovaccine dose of 0.2 mg might be sufficiently immunogenic after subcutaneous administration.

Abscess↗

PubMed1989

[Q fever infectious endocarditis. Apropos of a new case].

We report a case of Coxiella burnetii endocarditis in a 42-year old man presenting with a long-known cardiac murmur and an infectious syndrome of several months duration. The aetiological diagnosis, delayed by the lack of knowledge of a primary Q fever, was established by serology. The infection responded to tetracycline combined with cotrimoxazole, but a valve replacement performed for haemodynamic reasons was followed by serious complications. We remind the readers that Q fever endocarditis must be considered as a possible diagnosis in all cases of endocarditis with negative blood cultures and that specific serological examinations in search of anti-phase I antibodies of the IgA type should be performed as soon as possible, using the indirect immunofluorescence technique. Attention is drawn to the different serological responses of the three clinical types of Q fever infection and to the cellular immunity associated with that disease.

Adult↗

PubMed1990

The immune response in a cat-related outbreak of Q fever as measured by the indirect immunofluorescence test and the enzyme-linked immunosorbent assay.

The isotypic immune response of 16 individuals who developed Q fever pneumonia following exposure to an infected parturient cat was studied. The enzyme-linked immunosorbent (ELISA) test was used to detect IgM, IgA, and IgG antibodies to phase I and phase II Coxiella burnetii whole-cell antigens and to the phase I lipopolysaccharide. The indirect immunofluorescent antibody (IFA) test was also used to detect antibodies to phase I and phase II whole cells. None of the 16 subjects developed antibodies to the phase I lipopolysaccharide. The ELISA was more sensitive than the IFA test. IgM antibodies to phase II antigen were detectable by ELISA in 80% of the subjects at the time of onset of symptoms and were still present in 7 of the 8 tested at 32 weeks following the onset of symptoms. In all instances (ELISA: IgG, IgM; IFA: IgG, IgM) phase II antibodies developed earlier and reached higher levels than did phase I antibodies. The absence of antibodies to phase I lipopolysaccharide in acute Q fever combined with our unpublished findings of antibodies to phase I lipopolysaccharide in chronic Q fever suggests that this test may be used to distinguish acute from chronic Q fever.

Adult↗

PubMed1999

Enhanced interaction of HLA-DM with HLA-DR in enlarged vacuoles of hereditary and infectious lysosomal diseases.

Following biosynthesis, class II MHC molecules are transported through a lysosome-like compartment, where they acquire antigenic peptides for presentation to T cells at the cell surface. This compartment is characterized by the presence of HLA-DM, which catalyzes the peptide loading process. Here we report that the morphology and function of the class II loading compartment is affected in diseases with a phenotypic change in lysosome morphology. Swollen lysosomes are observed in cells from patients with the hereditary immunodeficiency Chediak-Higashi syndrome and in cells infected with Coxiella burnetii, the rickettsial organism that causes Q fever. In both disease states, we observed that HLA-DR and HLA-DM accumulate in enlarged intracellular compartments, which label with the lysosomal marker LAMP-1. The distribution of class I MHC molecules was not affected, localizing disease effects to the endocytic pathway. Thus, cellular mechanisms controlling lysosome biogenesis also affect formation of the class II loading compartment. Analysis of cell surface class II molecules revealed that their steady-state levels were not reduced on diseased cells. However, in both disease states, enhanced interaction between HLA-DR and HLA-DM was detected. In the Chediak-Higashi syndrome cells, this correlated with more efficient removal of the CLIP peptide. These findings suggest a mechanism for perturbation of Ag presentation by class II molecules and consequent immune deficiencies in both diseases.

Antigens, CD↗

PubMed1991

Rickettsiae and rickettsioses in Portugal.

The only rickettsiae recorded in Portugal till now were Rickettsia conorii and Coxiella burnetii. Boutonneuse fever is one of the most important transmissible diseases in Portugal. Though the annual number of cases is not exactly known, it is estimated to be not far from 20,000 in some years. Q fever is the other rickettsiosis widely disseminated throughout the country. The serological prevalence and the incidence of those rickettsioses in Portugal are presented in this communication. In recent research in southern Portugal, about 4,000 adult ticks of nine species were screened by the haemocyte test for rickettsiae and rickettsia-like organisms (RLO). In addition to R. conorii three microscopically different RLO were observed. Two of them, i.e. ovoid and bacillary-like, were positive in the immunofluorescence test with spotted fever (R. conorii) antiserum. The first occurred mainly in Rhipicephalus sanguineus ticks, the second one also in other tick species. The latter agent was cultivated in half-engorged R. sanguineus females and in Vero cells. The third organism was found in R. sanguineus, where it exhibited a massive infestation in haemocytes resembling that seen in experimentally infected ticks with C. burnettii, but not being this agent. The investigation of the isolates and their identification and characterization are being continued.

Animals↗

PubMed1986

Onset and duration of immunity in guinea pigs and mice induced with different Q fever vaccines.

Protective effects of different types of Q fever vaccines, namely untreated Coxiella burnetii phase I cells (Cb I) or Cb I cells treated with chloroform-methanol (CM) mixture (Cb I-CM) and of a Q fever chemovaccine obtained by trichloroacetic acid extraction (TCAE) from intact Cb I cells, were compared in mice and guinea pigs at different intervals after intraperitoneal (i.p.) or subcutaneous (s.c.) immunizations. The highest degree of protection at all intervals studied was achieved with Cb I cells, irrespective of the route of immunization and i.p. or aerosol challenge. This vaccine exerted a protective effect in guinea pigs and mice as early as after one or two weeks post-immunization, the effect lasting for at least 40 weeks in mice (i.p. challenge) and 12 months in guinea pigs (aerosol challenge). Addition of small amount of Cb I cells to TCAE increased resistance of guinea pigs to aerosol challenge. Degree, onset and duration of protection to either type of virulent challenge afforded by Cb I-CM cells and TCAE was similar, but when compared with that of Cb I cells it was lower, started later (from the 2nd week in guinea pigs and the 3rd week in mice), and in mice it lasted for a shorter period (20 weeks only). The resistance to virulent challenge in guinea pigs did not depend on the levels of microagglutination (MA) antibodies and in mice it was reflected by delayed type hypersensitivity (DTH) reaction and adoptively transferred splenocytes, rather than by MA antibody titres and passive transfer of immune sera to recipient mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Urban zoonoses caused by Bartonella, Coxiella, Ehrlichia, and Rickettsia species.

The last half of the 20th Century witnessed an increase in the occurrence and recognition of urban zoonoses caused by members of the genera Bartonella, Coxiella, Ehrlichia, and Rickettsia, all traditionally considered to be members of the family Rickettsiaceae. In recent years, new human pathogens (Bartonella elizabethae, Bartonella henselae, and Rickettsia felis) have been recognized in urban environments. Other newly recognized pathogens (Ehrlichia chaffeensis and Ehrlichia phagocytophila in the United States) have sylvan zoonotic cycles but are present in urban areas because their vertebrate hosts and associated ectoparasitic arthropod vectors are able to survive in cities. Still other agents, which were primarily of historical importance (Bartonella quintana) or have not traditionally been associated with urban environments (Rickettsia rickettsii), have been recognized as causes of human disease in urban areas. Some diseases that have traditionally been associated with urban environments, such as rickettsialpox (caused by Rickettsia akari) and murine typhus (caused by Rickettsia typhi), still occur in large cities at low or undetermined frequencies and often go undetected, despite the availability of effective measures to diagnose and control them. In addition, alternate transmission cycles have been discovered for Coxiella burnetii, Rickettsia prowazekii, and R. typhi that differ substantially from their established, classic cycles, indicating that the epidemiology of these agents is more complex than originally thought and may be changing. Factors leading to an increase in the incidence of illnesses caused by these bacteria in urban areas include societal changes as well as intrinsic components of the natural history of these organisms that favor their survival in cities. Transovarial and transstadial transmission of many of the agents in their arthropod hosts contributes to the highly focal nature of many of the diseases they cause by allowing the pathogens to persist in areas during adverse times when vertebrate amplifying hosts may be scarce or absent. Domesticated animals (primarily cats, dogs, and livestock) or commensal rodents [primarily Norway rats (Rattus norvegicus) and house mice (Mus musculus)] can serve as vertebrate amplifying hosts and bring these agents and their ectoparasitic arthropod vectors into direct association with humans and help maintain transmission cycles in densely populated urban areas. The reasons for the increase in these urban zoonoses are complex. Increasing population density worldwide, shifts in populations from rural areas to cities, increased domestic and international mobility, an increase in homelessness, the decline of inner-city neighborhoods, and an increase in the population of immunosuppressed individuals all contribute to the emergence and recognition of human diseases caused by these groups of agents. Due to the focal nature of infections in urban areas, control or prevention of these diseases is possible. Increased physician awareness and public health surveillance support will be required to detect and treat existing urban infections caused by these agents, to determine the disease burden caused by them, to design and implement control programs to combat and prevent their spread, and to recognize emerging or resurging infections caused by members of these genera as they occur.

Animals↗

PubMed1999

Treatment of Q fever endocarditis: comparison of 2 regimens containing doxycycline and ofloxacin or hydroxychloroquine.

BACKGROUND: Q fever endocarditis, caused by Coxiella burnetii, is fatal in 25% to 60% of patients. Currently, treatment with a long-term tetracycline and quinolone regimen for at least 4 years is recommended, although relapses are frequent. METHODS: Between January 1987 and December 1997, the reference treatment of Q fever endocarditis was compared with one of doxycycline and hydroxychloroquine sulfate. Patients were treated by conventional therapy until May 1991 and then by the new regimen. Microimmunofluorescence was used for antibody-level determination for diagnosis and follow-up. RESULTS: Thirty-five patients were included in the study, 26 males and 9 females. Of 14 patients treated with a doxycycline and quinolone combination, 1 died, 7 relapsed (3 were re-treated and 4 switched to the new regimen), 1 is still being treated, and 5 were considered cured using this regimen only. The mean duration of therapy for cure in this group was 55 months (median, 60 months). Twenty-one patients received the doxycycline and hydroxychloroquine regimen: 1 patient died of a surgical complication, 2 are still being treated, 17 were cured, and 1 is currently being evaluated. Two patients treated for 12 months but none of the patients treated for longer than 18 months relapsed. The mean duration of treatment in this group was 31 months (median, 26 months). No significant differences were observed between the 2 regimens in terms of death, valve surgery, or tolerance. The mortality rate for both regimens in this study was 5%. CONCLUSION: Prescription of the doxycycline and hydroxychloroquine combination for at least 18 months allows shortening of the duration of therapy and reduction in the number of relapses.

Adult↗

PubMed2002

Neurological involvement in acute Q fever: a report of 29 cases and review of the literature.

BACKGROUND: Q fever is characterized by its clinical polymorphism; neurological involvement has occasionally been described. In the course of acute Q fever, neurological manifestations may include aseptic meningitis, encephalitis or encephalomyelitis, and peripheral neuropathy. OBJECTIVE: To review and evaluate cases of acute Q fever with neurological symptoms diagnosed in our laboratory. METHODS: A total of 1269 acute Q fever cases were recorded from January 1985 to January 2000 in our laboratory and were reviewed for neurological complications. Patients were considered to have acute Q fever when serological procedures showed Coxiella burnetii phase II titers of 1:200 or higher for IgG and 1:50 or higher for IgM. Those patients who underwent a lumbar puncture for cerebrospinal fluid analysis or who had abnormal neurological symptoms were selected for this study. We describe the clinical, epidemiological, and biological features of these cases. We also review the literature and compare our cases with those previously reported. RESULTS: Among the 45 patients selected, 14 were excluded because they had normal cerebrospinal fluid and no neurological symptoms. Two were excluded because there were no clinical or epidemiological data. Three major clinical syndromes were observed: meningoencephalitis or encephalitis in 17 cases; meningitis in 8; and myelitis and peripheral neuropathy in 4. Encephalitic signs were not specific, but behavior or psychiatric disturbances were common. CONCLUSIONS: Q fever should be included in the differential diagnosis of acute neurological disease in a patient with a fever. Serological testing should be performed in cases of meningoencephalitis, lymphocytic meningitis, and peripheral neuropathy, including Guillain-Barré syndrome and myelitis.

Acute Disease↗