1例Q热肺炎诊治报告北大核心CSCD

Q热是一种重要的人兽共患病,病原体为贝氏柯克斯体(Coxiella burnetii),其经呼吸道吸入进入体内,引起急性Q热,严重急性Q热可出现肺炎、肝炎或心肌炎并发症。部分患者治疗不彻底转为慢性Q热。慢性Q热为贝氏柯克斯体在机体局部持续感染,常需要外科手术及数年抗感染治疗,其严重危害患者身体健康及加重家庭经济负担;。追其原因是临床医生对该病认识不足,导致延误治疗所致。本文旨在报告1例Q热肺炎的诊治和体会,以提高临床医生对该病认识。     

Q fever in children

Q fever is a zoonosis caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection, and transmission to human beings is mainly accomplished through inhalation of contaminated aerosols. This illness is associated with a wide clinical spectrum, from asymptomatic or mildly symptomatic seroconversion to fatal disease. Q fever in children has been rarely reported. We reviewed published work on this topic. Seroepidemiological studies show that children are frequently exposed to C burnetii. However, children are less frequently symptomatic than adults following infection, and may have milder diseases. Using the standard diagnostic criteria, we identified 46 published paediatric cases only. Self-limited febrile illness and pneumonia were the most common manifestations of acute Q fever. Chronic disease manifested as endocarditis and osteomyelitis. A history of exposure to possible sources of infection with C burnetii in a child with a compatible infectious syndrome should prompt testing for Q fever. Studies are required to determine the spectrum of morbidity associated with Q fever during childhood.     

Q fever in children in Greece

The aim of this study was to investigate the incidence, epidemiology, and clinical manifestations of Q fever among hospitalized children in Greece. During a two-year period, 1,200 children with various clinical manifestations were prospectively tested for Coxiella burnetii infection by indirect immunofluorescence. Acute Q fever was diagnosed in eight (0.67%) patients. No chronic case of infection was detected. Multivariate analysis showed that children 11-14 years old and children reporting consumption of cheese from rural areas were at increased risk for this illness. Clinical manifestations of acute Q fever were pneumonia (two patients), meningitis (two), prolonged fever (two), hepatitis (one), and hemolytic-uremic syndrome (one). Q fever accounted for 2.9% of the cases with prolonged fever, 1.2% of the cases of meningitis, and 0.5% of the cases of pneumonia. Fever and headache were the most common symptoms at presentation. Our study indicates that Q fever is a rare cause of hospitalization during childhood.     

Q fever pneumonia

PURPOSE OF REVIEW: In this era of emerging infectious diseases and bioterrorism it is important to be up to date with the diagnosis and management of Q fever pneumonia. RECENT FINDINGS: A considerable amount of new information has emerged regarding the pathogenesis of Coxiella burnetii infection. The complete genome of this microorganism has now been sequenced and there are several unique features. The spectrum of manifestations of infection due to C. burnetii continues to expand. Some of the more recently described findings are acalculous cholecystitis, rhabdomyolysis, long-term persistence of Coxiella, post Q fever fatigue syndrome, and hemolytic uremic syndrome. Pneumonia as a manifestation of acute Q fever shows tremendous geographic variation, being common in one area of a country such as Spain but not in another area. SUMMARY: Pneumonia continues to be an important manifestation of infection with C. burnetii. It responds to treatment with doxycycline, quinolones or macrolides.     

Cellular immunity in Q fever: specific lymphocyte unresponsiveness in Q fever endocarditis

Human infection with the rickettsia Coxiella burnetii presents as acute influenza-like primary Q fever, subacute granulomatous hepatitis, or chronic endocarditis with hepatitis. To investigate whether persistent infection is associated with a possible immunologic defect, we tested lymphocyte proliferation specific for Coxiella in vitro in peripheral blood mononuclear cells from patients and controls. All four patients with endocarditis had profound lymphocyte unresponsiveness to Coxiella antigens with normal proliferation to control antigens. Hepatitis and primary Q fever were associated with vigorous responses in vitro to Coxiella antigens. Suppression of lymphocyte unresponsiveness was in part mediated by an antigen-nonspecific, glass-adherent cell. We hypothesize that specific T cell unresponsiveness is an important factor in persistent infection with C. burnetii and offer in vitro lymphocyte stimulation as a more specific diagnostic test to distinguish cases of endocarditis among those with chronic hepatitis due to Q fever.     

Q fever bioprosthetic aortic valve endocarditis (PVE) successfully treated with doxycycline monotherapy

Q fever is a zoonotic infection caused by Coxiella burnetii. The most common clinical manifestation of acute Q fever infection is as an atypical community-acquired pneumonia. The pulmonary findings are accompanied by extrapulmonary findings, most typically an increase in serum transaminases and splenomegaly. Because C. burnetii is difficult to culture, the diagnosis of Q fever is usually made serologically. The diagnosis of acute Q fever atypical community-acquired pneumonia is made by demonstrating a fourfold or greater increase in titer between acute and convalescent specimens or by demonstrating elevated immunoglobulin (IgM) (phase II) titers. Chronic Q fever is manifested as granulomatous hepatitis or more commonly as culture-negative endocarditis (CNE). Chronic Q fever (CNE) is a difficult diagnosis because of difficulty in culturing the organism from the blood and the vegetations with Q fever CNE are small or absent. The diagnosis of chronic Q fever CNE is based on serology. Such patients commonly have highly elevated IgM and IgG titers (phase I/II) titers. Chronic Q fever CNE may involve native or prosthetic heart valves. Q fever prosthetic valve endocarditis is rare compared with native valve Q fever endocarditis. Q fever prosthetic valve endocarditis usually requires valve replacement for cure. We present a case of chronic Q fever bioprosthetic aortic valve endocarditis that was successfully treated with doxycycline monotherapy that did not require aortic valve replacement.     

Cynomolgus monkey model for experimental Q fever infection.

A subhuman primate model was developed for study of the pathogenesis of infection with Coxiella burnetii. Cynomolgus monkeys (Macaca fascicularis) that were exposed to 10(5) mouse median infectious intraperitoneal doses of C. burnetii in a small-particle aerosol developed clinical signs of illness and pathologic changes characteristic of Q fever infection in humans. All monkeys had radiologic evidence of pneumonia by day 9. Antibodies to C. burnetii were detectable by the indirect fluorescent antibody test by day 7. These data indicate that the cynomolgus monkey is a suitable model for study of the pathogenesis of Q fever infection and may prove valuable in the evaluation of C. burnetii vaccines.     

Acute Q fever lobar pneumonia: a case report

Q fever is a zoonotic disease caused by Coxiella burnetii-an obligate, Gram-negative, intracellular bacteria. Acute febrile illness, hepatitis, and atypical pneumonia are the three most common manifestations, whereas lobar pneumonia is rarely reported among acute Q fever patients. We report a case of acute Q fever with lobar pneumonia and multi-organ involvement.     

Clinical manifestations of Q fever in adults and children

Q fever is a common zoonosis with almost a worldwide distribution caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection and transmission to humans is usually via inhalation of contaminated aerosols, which may be carried by the wind far from the original source of infection. Occupational groups with close association with farm or wild animals are most at risk, however travellers occasionally become infected. The disease is associated with a wide spectrum of clinical manifestations and symptoms, ranging from asymptomatic infection to fatal disease. Awareness of the disease and newer diagnostic methods led to increase of recognition and detection in cases with various or multiple symptoms in adults and children. However, children seem to be less frequently symptomatic and may have milder disease. This review of Q fever cases examines clinical manifestations and symptoms of Q fever in both adults and children and shows that certain symptoms and their severity have altered presentation in children with acute and chronic Q fever when compared to adults.     

Clinical manifestation of Q fever and tuberculosis, similarly caused by intracellular parasites

Q fever is a generic term for pneumonia, bronchitis, etc. caused by infection with Coxiella burnetii, a rickettsia-related species of bacteria, in humans. Q-fever is a transient and acute febrile illness that takes a course similar to influenza, and its clinical picture greatly differs from that of tuberculosis that takes a chronic course. The reason for this is thought to be because the generation time of C. burnetii is extremely short (several tens of minutes) compared with Mycobacterium tuberculosis, though those are similar intracellular parasites. Q fever is fourth- or fifth-ranked among the community-acquired pneumonias in the United States and Europe but has a good prognosis with 1-2% of mortality even in the cases that follow a natural course without treatment. Meanwhile, there is a chronic type that follows a protracted course or has a poor prognosis. Therefore, cases definitely diagnosed with Q fever or strongly suspected of Q fever should seek aggressive treatment. Q fever is definitely diagnosed by confirming significant increase in serum antibody titer, but the patients should be followed because in many cases it takes a long time before serum antibody titer increases. Beta-lactams are ineffective against C. burnetii, an obligate intracellular parasite. Although tetracyclines, macrolides, quinolones, rifampicin, etc. are used effectively in the treatment of Q fever, many cases appear to improve by beta-lactam administration because the illness often takes a natural course.     

Bichat guidelines for the clinical management of Q fever and bioterrorism-related Q fever

Q fever is a zoonotic disease caused by Coxiella burnetii. Its interest as a potential biological weapon stems from the fact that an aerosol of very few organisms could infect humans. Another route of transmission of C. burnetii could be through adding it to the food supply. Nevertheless, C. burnetii is considered to be one of the less suitable candidate agents for use in a bioterrorist attack; the incubation is long, many infections are inapparent and the mortality is low. In the case of an intentional release of C. burnetii by a terrorist, clinical presentation would be similar to naturally occurring disease. It may be asymptomatic, acute, normally accompanied by pneumonia or hepatitis, or chronic, usually manifested as endocarditis. Most cases of acute Q fever are asymptomatic and resolve spontaneously without specific treatment. Nevertheless, treatment can shorten the duration of illness and decrease the risk of complications such as endocarditis. Post-exposure prophylaxis is recommended after the exposure in the case of a bioterrorist attack.     

Spontaneous splenic rupture complicating acute Q fever.

Q fever is usually a self-limited febrile illness that involves the lungs and the liver. Acute complications are rare. We present the case of a 30-yr-old patient with spontaneous splenic rupture during the course of acute Q fever infection. He was admitted to the hospital with high temperature and the radiological signs of an atypical pneumonia. Forty-eight hours after admission, he developed shock. Because of free intraabdominal liquid, a laparatomy was performed that revealed a tear in the enlarged spleen. A splenectomy was performed. The diagnosis of Q fever was established by a significant titer increase in complement fixation test and IgM-ELISA. Serological investigations into the patient's surroundings revealed evidence of Q fever infection in 10 additional persons. Q fever should be taken into account as a possible differential diagnosis in patients with unexplained febrile illness and symptoms of pneumonia. The acute course of Q fever infection can be complicated by splenic rupture. The diagnosis of an acute infection with Coxiella burnetii often requires serologic testing of a second serum sample obtained at least 10 days after the onset of symptoms. Q fever should be ruled out in cases of unexplained splenic rupture particularly in Q fever endemic areas.     

Q fever 1985-1998. Clinical and epidemiologic features of 1,383 infections

In order to describe the clinical features and the epidemiologic findings of 1,383 patients hospitalized in France for acute or chronic Q fever, we conducted a retrospective analysis based on 74,702 sera tested in our diagnostic center, National Reference Center and World Health Organization Collaborative Center for Rickettsial Diseases. The physicians in charge of all patients with evidence of acute Q fever (seroconversion and/or presence of IgM) or chronic Q fever (prolonged disease and/or IgG antibody titer to phase I of Coxiella burnetii > or = 800) were asked to complete a questionnaire, which was computerized. A total of 1,070 cases of acute Q fever was recorded. Males were more frequently diagnosed, and most cases were identified in the spring. Cases were observed more frequently in patients between the ages of 30 and 69 years. We classified patients according to the different clinical forms of acute Q fever, hepatitis (40%), pneumonia and hepatitis (20%), pneumonia (17%), isolated fever (17%), meningoencephalitis (1%), myocarditis (1%), pericarditis (1%), and meningitis (0.7%). We showed for the first time, to our knowledge, that different clinical forms of acute Q fever are associated with significantly different patient status. Hepatitis occurred in younger patients, pneumonia in older and more immunocompromised patients, and isolated fever was more common in female patients. Risk factors were not specifically associated with a clinical form except meningoencephalitis and contact with animals. The prognosis was usually good except for those with myocarditis or meningoencephalitis as 13 patients died who were significantly older than others. For chronic Q fever, antibody titers to C. burnetii phase I above 800 and IgA above 50 were predictive in 94% of cases. Among 313 patients with chronic Q fever, 259 had endocarditis, mainly patients with previous valvulopathy; 25 had an infection of vascular aneurysm or prosthesis. Patients with endocarditis or vascular infection were more frequently immunocompromised and older than those with acute Q fever. Fifteen women were infected during pregnancy; they were significantly more exposed to animals and gave birth to only 5 babies, only 2 with a normal birth weight. More rare manifestations observed were chronic hepatitis (8 cases), osteoarticular infection (7 cases), and chronic pericarditis (3 cases). Nineteen patients were observed who experienced first a documented acute infection, then, due to underlying conditions, a chronic infection. To our knowledge, we report the largest series of Q fever to date. Our results indicate that Q fever is a protean disease, grossly underestimated, with some of the clinical manifestations being only recently reported, such as Q fever during pregnancy, chronic vascular infection, osteomyelitis, pericarditis, and myocarditis. Our data confirm that chronic Q fever is mainly determined by host factors and demonstrate for the first time that host factors may also play a role in the clinical expression of acute Q fever.     

Pneumonia and meningo-encephalitis due to Coxiella burnetii

We describe the case of a 35-year-old man who presented with pneumonia and encephalitis due to Coxiella burnetii. The neurological manifestations of Q fever are discussed and we suggest that C. burnetii be included in the differential diagnosis of patients with pneumonia and encephalitis.     

Acute Q fever: an emerging and endemic disease in southern Taiwan

Acute Q fever is a worldwide zoonosis caused by Coxiella burnetii infection. In Taiwan, cases of acute Q fever increased during 3 y of observation, especially at Kaohsiung County and City in southern Taiwan. From 15 April 2004 to 15 April 2007, a total of 67 cases of acute Q fever were identified at E-Da hospital located at Kaohsiung County. 19 (28.4%) patients had a history of travel in rural areas and only 1 had been outside southern Taiwan. 21 (31.3%) patients had a history of animal contact. 20 (30.8%) of the 65 examined patients had underlying chronic hepatitis B or hepatitis C virus infection. Fever (98.5%), chills (79.1%), headache (79.1%), relative bradycardia (44.8%), elevated aminotransferases (100%), and thrombocytopenia (74.6%) were common manifestations. 12 (19.0%) cases had abnormal findings on chest X-ray. Fatty liver (50.0%) and hepatomegaly and/or splenomegaly (41.9%) were found by abdominal image examinations. 42 (76.4%) of 55 cases had defervescence within 3 d after treatment, whereas 4 (7.3%) had spontaneous remission. Acute Q fever is an endemic infectious disease with hepatitis rather than pneumonia as the major presentation in southern Taiwan and the emergence of Q fever is due to increased alertness for the disease by physicians.     

Dysregulation of cytokines in acute Q fever: role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines. Their amounts were higher in patients with hepatitis than in patients with fever or pneumonia. In patients with valvulopathy, who exhibited the highest risk of chronic evolution, the amounts of TNF and IL-10 were higher than in patients without valvulopathy. TNF production was specifically enhanced in patients who developed Q fever endocarditis. These results show that acute Q fever is associated with cytokine overproduction. Persistent TNF amounts were associated with the occurrence of endocarditis in patients with valvulopathy, and that may be a marker of chronic evolution of Q fever.     

Q fever: current concepts

Persons with Q fever usually present with severe retrobulbar headache, a fever to 104 degrees F or higher with shaking chills, general malaise, myalgia, chest pain, and sometimes pneumonia and hepatitis. Cattle, sheep, goats, and ticks are the primary reservoirs of the etiologic agent, Coxiella burnetii. Humans are usually infected by inhaling infectious aerosols. Because C. burnetii can survive for long periods in the environment, it poses a continuing health hazard once it is disseminated. Q fever usually occurs sporadically, but large outbreaks are frequently observed throughout the world, particularly among abattoir workers and personnel working in research centers. Q fever endocarditis follows a chronic course and is frequently fatal. Tests for antibodies to C. burnetii are required for confirmation of the diagnosis. Tetracyclines remain the mainstay of treatment for acute Q fever, and tetracyclines in combination with other antibiotics have been advocated for patients with Q fever endocarditis. Vaccines for Q fever have been proven effective in clinical trials.     

Q fever in an American tourist returned from Australia

Q fever was diagnosed in a previously healthy man who had recently traveled to the East Coast of Australia. The patient experienced fever and headache accompanied by lymphopenia and elevated liver enzymes but not pneumonia. He had no known direct exposures to animals, exhibited IgM and IgG seroconversion to phase II antigen of Coxiella burnetii and IgM only to phase I antigen, and responded to doxycycline treatment. This case serves as a reminder to clinicians to consider Q fever in the differential diagnosis of acute febrile illness in travelers returning from endemic areas.     

Q fever as a biological weapon

Q fever is a bacterial zoonosis caused by Coxiella burnetii, a unique intracellular coccobacillus, adapted to live within the phagolysosomes of macrophages and monocytes. It is highly infectious, with as little as one organism needed to cause clinical infection, making it an attractive organism for use in biowarfare. Despite its high infectivity, it has low virulence, and most patients undergo only asymptomatic seroconversion. Acute clinical manifestations are a nonspecific febrile illness, pneumonia, hepatitis, and neurologic abnormalities ranging from headache to meningoencephalitis. Chronic Q fever can result in endocarditis, hepatitis, or a chronic fatigue syndrome. Diagnosis usually is made by serology because culture of the highly contagious organism is potentially hazardous. Tetracyclines are the antibiotics of choice. When individualized therapy is possible, a 14- to 21-day course of doxycycline usually is used. In a mass casualty situation, a 5- to 7-day course of doxycycline is recommended, both for therapy and prophylaxis. For chronic infections such as endocarditis, 18 months of doxycycline supplemented with hydroxychloroquine is currently the best therapy.     

Coxiella burnetii and acute exacerbations/infections in patients with chronic lung disease

The aim of the present study was to determine the incidence of Q fever in patients with an acute exacerbation of a chronic lower respiratory tract infection. Eighty patients treated for acute exacerbation of chronic lower respiratory tract infections during a 30-month period were studied. Q fever was diagnosed by ELISA. Two elderly woman with pre-existing bronchiectasis (2.5%) were diagnosed as having an acute infection by Coxiella burnetii. The acute illness was considered to be a result of mixed infection with Pseudomonas aeruginosa and Haemophilus influenzae with C. burnetii. Co-infection with C. burnetii can occur during a bacterial exacerbation of a chronic lower respiratory tract infection.