• 1

    Kaplan MM, Bertagna P, 1955. The geographical distribution of Q fever. Bull WHO 13 :829–860.

  • 2

    Kazar J, 1993. Q fever is absent from New Zealand. Int J Epidemiol 22 :945–949.

  • 3

    Hunt JG, Field PR, Murphy AM, 1983. Immunoglobulin responses to Coxiella burnetii (Q fever). Single serum diagnosis of acute infection using an immunofluorescence technique. Infect Immun 39 :977–981.

    • Search Google Scholar
    • Export Citation
  • 4

    Hart RJC, 1973. The epidemiology of Q fever. Postrgrad Med J 49 :535–538.

  • 5

    Zeman DH, Kirkbride CA, Leslie-Steen P, 1989. Ovine abortion due to Coxiella burnetii infection. J Vet Diagn Invest 1 :178–180.

  • 6

    Derrick EH, 1937. “Q” fever, a new fever entity: clinical features, diagnosis and laboratory investigation. Med J Aust 2 :281–299.

  • 7

    Robbins FC, Ragan CA, 1946. Q fever in the Mediterranean area: Report of its occurrence in allied troops. Clinical features of the disease. Am J Hyg 44 :6–22.

    • Search Google Scholar
    • Export Citation
  • 8

    Derrick EH, 1973. The course of infection with Coxiella burnetii. Med J Aust 1 :1051–1057.

  • 9

    Marrie TJ, 1995. Coxiella burnetii (Q fever) pneumonia. Clin Infect Dis 21 (Suppl 3):S253–S264.

  • 10

    Maurin M, Raoult D, 1999. Q fever. Clin Microbiol Rev 12 :518–553.

  • 11

    Turck WPG, Howitt G, Turnberg LA, Fox H, Longson M, Matthews MB, Das Gupta R, 1976. Chronic Q fever. Q J Med 45 :193–217.

  • 12

    Ellis ME, Smith CC, Moffat MAJ, 1983. Chronic or fatal Q fever infection: a review of 16 patients seen in North-East Scotland (1967–80). Q J Med 52 :54–66.

    • Search Google Scholar
    • Export Citation
  • 13

    Atienza P, Ramond M-J, Degott C, Lebrec D, Rueff B, Benhamou J-P, 1988. Chronic Q fever hepatitis complicated by extensive fibrosis. Gastroenterol 95 :478–481.

    • Search Google Scholar
    • Export Citation
  • 14

    Fournier P-E, Marrie TJ, Raoult D, 1998. Diagnosis of Q fever. J Clin Microbiol 36 :1823–1834.

  • 15

    Morbidity Mortality Weekly Report, 2004. Summary of provisional cases of selected notifiable diseases, United States, cumulative, week ending January 3, 2004 (53rd week). 52: 1291.

  • 16

    Biberstein EL, Behymer DE, Bushnell R, Crenshaw G, Riemann HP, Franti CE, 1974. A survey of Q fever (Coxiella burnetii) in California dairy cows. Am J Vet Res 35 :1577–1582.

    • Search Google Scholar
    • Export Citation
  • 17

    DeForge J, Cone LA, 2006. The serologic prevalence of Q fever (Coxiella burnetii) complement fixing antibodies in the Peninsula bighorn sheep of Southern California. Am J Trop Med Hyg (in press).

  • 18

    Davis GE, Cox HR, 1938. A filter-passing infectious agent isolated from ticks. I. Isolation from Dermacentor andersoni, reactions in animals, and filtration experiments. Public Health Rep 53 :2259–2261.

    • Search Google Scholar
    • Export Citation
  • 19

    Dyer RE, 1939. Similarity of Australian “Q” fever and a disease caused by an infectios agent isolated from ticks in Montana. Public Health Rep 54 :1229–1238.

    • Search Google Scholar
    • Export Citation
  • 20

    Marie TJ, Raoult D, 1997. Q fever—a review and issues for the next century. Int J Antimicrob Agents 8 :145–161.

  • 21

    Oliphant JW, Gordon DA, Meis A, Parker RR, 1949. Q fever in laundry workers, presumably transmitted from contaminated clothing. Am J Hyg 49 :76–82.

    • Search Google Scholar
    • Export Citation
  • 22

    Stoenner HG, Lackman DB, Benson WW, Mather J, Casey M, Harvey KA, 1961. The role of dairy cattle in the epidemiology of Q fever in Idaho. J Infect Dis 109 :90–97.

    • Search Google Scholar
    • Export Citation
  • 23

    D’Angelo LJ, Baker EF, Schlosser W, 1979. Q fever in the United Staes 1948–1977. J Infect Dis 139 :613–615.

  • 24

    Guigno D, Coupland B, Smith EG, Farrell ID, Desselberger U, Caul EO, 1992. Primary humoral antibody response to Coxiella burnetii, the causative agent of Q fever. J Clin Microbiol 30 :1958–1967.

    • Search Google Scholar
    • Export Citation
  • 25

    Raoult D, Marrie T, 1995. Q fever. Clin Infect Dis 20 :489–496.

  • 26

    Yebra M, Marazuela M, Albarran F, Moreno A, 1988. Chronic Q fever hepatitis. Rev Infect Dis 10 :129–130.

  • 27

    Geddes AM, 1983. Q fever. Br Med J 287 :927–928.

  • 28

    Spelman DW, 1982. Q fever: a study of 111 consecutive cases. Med J Aust 1 :547–553.

  • 29

    Maurin M, Raoult D, 1993. In vitro susceptibilities of spotted fever group Rickettsiae and Coxiella burnetii to clarithromycin. Antimicrob Agents Chemother 37 :2633–2637.

    • Search Google Scholar
    • Export Citation
  • 30

    Raoult D, Yeaman MR, Baca OG, 1989. Susceptibility of Coxiella burnetii to perfloxacin and ofloxacin in ovo and in persistently infected L929 cells. Antimicrob Agents Chemother 33 :621–623.

    • Search Google Scholar
    • Export Citation
  • 31

    Raoult D, Houpikian P, Tissot–Dupont H, Riss JM, Arditi-Dijiane J, Brouqui P, 1999. Treatment of Q fever endocarditis: comparison of two regimens containing doxycycline and of-loxacin or hydroxychloroquine. Arch Int Med 159 :167–173.

    • Search Google Scholar
    • Export Citation
  • 32

    McQuiston JH, 2002. Childs. Q fever in humans and animals in the United States. Vector Borne Zoonotic Dis 2 :179–191.

  • 33

    Cone LA, Saeed S, 2000. Q-fever presenting with intractable diarrhea and fever with both responding to indomethacin. Anti-microb Infect Dis Newsletter. 18 :38–40.

    • Search Google Scholar
    • Export Citation
 
 
 
 

 

 
 

 

 

 

 

 

 

Q FEVER IN THE SOUTHERN CALIFORNIA DESERT: EPIDEMIOLOGY, CLINICAL PRESENTATION AND TREATMENT

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  • 1 Department of Medicine, Eisenhower Medical Center, Rancho Mirage, California; Department of Medicine, Palo Verde Hospital, Blythe, Bighorn Institute, Palm Desert, California

Despite the absence of a natural reservoir for Q fever in the desert of Southern California, six cases have been identified during the past 32 years. During that period of time, two areas have been used by northern sheep ranchers from Idaho and Wyoming to import sheep to an area in the Coachella Valley through 1985. Thereafter, because of housing development, the sheep area was moved to Blythe along the Colorado River. All but two of these patients probably acquired infection by Coxiella burnetii by living or working in close proximity to these grazing areas but not directly involved with the sheep. The shift of infected patients from the Coachella Valley to Blythe (100 miles distant) seems to support that supposition. All patients with acute Q fever developed antibodies primarily to phase II antigen, whereas the only person with chronic Q fever developed phase I antibodies. All patients presented with granulomatous hepatitis. One also had a pulmonary infiltrate, and the single individual with chronic Q fever also had a mitral valve prosthesis, although echocardiography could not define endocarditis. All patients with acute infections responded to 3–5 weeks of therapy with doxycycline, whereas the patient with chronic disease failed 3 years of therapy with combination regimens. Further studies at the Eisenhower Medical Center on the prevalence of infection in Blythe, CA, and elsewhere are anticipated.

INTRODUCTION

Coxiella burnetii, a member of the tribe Rickettsiaceae, exists globally except for in Antartica1 and New Zealand2 and has been identified in > 50 countries.3 It infects ticks, reptiles, and other vertebrates including humans, but causes natural disease only in humans.4 In goats, and less often in sheep and cattle, infection by C. burnetii may result in abortion in females and reduced fertility in males.5

The diseases was first described in Australia in 1937 by Derrick6 as “Q(uery)” fever and is characterized acutely by fever, pneumonia (in 50% of patients), pleuro-pericardial symptoms, and hepatitis, which ordinarily disappear in 2–3 weeks.79 Moreover, about 60% of individuals seroconvert without significant clinical manifestations after primary infection. In ~ 5% of those infected, a chronic syndrome ensues expressing itself as endocarditis or hepatitis and hepatosplenomegaly, at times leading to hepatic fibrosis.1013 It is interesting to note that in Canada, Spain, and Switzerland, pneumonitis is the most commonly recognized form of Q fever, whereas in France, California, and Australia, hepatitis is more frequent.14 Despite a large animal reservoir of domestic sheep, goats, and cattle throughout the United States, few cases of Q fever have been described. In 2002, only 61 cases were reported, and in 2003, 75 cases were reported to the US CDC because it is a notifiable disease in many states.15 Furthermore, nearly 90% of all cattle in Southern California are infected by Coxciella burnetii16 without manifesting signs of illness, whereas in Northern California, a similar situation exists with domestic sheep.

The Eisenhower Medical Center (EMC) is a 275-bed general hospital located in the arid Coachella Valley of Southern California. It provides medical care to about 300,000 permanent residents in its catchment area, which extends to the Arizona state line on the east, to the border with Mexico to the south, to the Nevada state line to the north, and to the Peninsula mountains to the west. There is virtually no large-scale animal husbandry in this area. However, for at least four decades, sheep from Montana, Wyoming, and Idaho have been exported to the Coachella Valley in the fall and kept there until the spring when they deliver their young. That locale was changed in 1985 to an area about 100 miles southeast around Blythe, CA, along the Colorado River.

Although there are ~ 500 native desert Peninsular bighorn sheep that range within the Santa Rosa and San Jacinto mountains of the Coachella Valley, human contact is uncommon, and these animals have been shown to demonstrate antibody to C. burnetii in < 10% of their population.17 However, this observation does not exclude the bighorn sheep as playing a role in human infection nor does it exclude other possible animal reservoirs. Six cases of Q fever seen at EMC during the past 33 years are described below.

CASE 1

A 52-year-old Mexican-American male farm worker supervisor developed fever, chills, and anorexia and malaise a week before hospitalization at EMC on June 12, 1978. He was found to have abnormal liver function studies, and because a rather extensive workup failed to disclose an etiology, a liver biopsy was performed. Granulomatous hepatitis was identified, and the patient was empirically begun on tetracycline at a dose of 2 g daily. He promptly became afebrile, and on July 13, 1978, Q fever antibodies were reported to be positive at a titer of 1:1,024 by complement fixation. It was later learned that he lived only a block away from where sheep had been kept and had their lambs born just a few months earlier.

CASE 2

A 67-year-old white, female grade school teacher was hospitalized at EMC on February 23, 1984, complaining of fever, chills, night sweats, myalgia, headache, anorexia, and a non-productive cough for more than a week. Aside from mild hypertension treated with diuretics and propranolol hydrochloride, she enjoyed excellent health.

Laboratory studies revealed abnormal liver function tests and borderline neutropenia. Both a bone marrow aspiration and liver biopsy revealed non-caseating granulomata. On March 16, 1984, Q fever complement fixing antibodies were reported positive at a titer of 1:1,024. Therapy with tetracycline was begun at a dose of 4 g daily in four divided doses for 10 days, and she improved promptly. However, after only 10 days of treatment, she relapsed with malaise and afternoon fever, A second 10-day course of tetracycline resulted in a permanent cure. The patient denied any contact with domestic sheep or cattle. She did, however, work and live within three blocks of the imported sheep in Palm Desert.

CASE 3

A 50-year-old white housewife of a retired butcher was hospitalized in 1979, 1980, and 1982 for fever and chills. A definitive diagnosis was never made, and she stated that all cultures and x-rays were normal. On September 30, 1983, she developed fever and rigors and was found to have hepatosplenomegaly. She was consequently hospitalized at EMC.

Of significance in her past medical history was an episode of rheumatic fever at age 9 while living in Israel and a Starr-Edwards valve replacement at a Los Angeles hospital in 1976 for mitral valve disease. She had since been maintained on warfarin anticoagulation.

All blood cultures were sterile, while liver function studies revealed abnormal transaminases, alkaline phosphatase, and lactic dehydrogenase. Although her white count, hemoglobin, and hematocrit were normal, the platelets were decreased to 108,000/mm3. Platelet-bound IgG antibody was markedly elevated. An IgG hypergammaglobulinemia was also noted, but circulating immune complexes were not defined. A transthoracic echocardiogram failed to define any vegetation. A liver biopsy was performed. A few doughnut type granulomata and a diffuse interstitial lymphocytic infiltrate were seen, suggesting Q fever, On October 9, 1983, phase 1 complement fixing antibody to C. burnetii was elevated to a titer > 1:5l2; IgA was > 128 and IgM was > 128. The patient was started on doxycycline 100 mg twice daily and trimethoprim/sulfamethoxazole (200/800 mg) twice daily and a concomitant reduction of warfarin dose. Despite this precaution, she developed gastrointestinal bleeding secondary to a prolonged prothrombin time.

After 6 months of therapy, she was feeling well, and the anti-microbials were discontinued. Hepatosplenomegaly was nearly gone, and her liver function studies had improved significantly, Four months later she again noted malaise, headache, and anorexia. These symptoms were accompanied by a worsening of the liver function studies and reappearance of hepatosplenomegaly, Oral therapy with doxycycline 100 mg twice daily and clindamycin 300 mg four times daily were prescribed, and after 2 months of therapy she felt well. There was improvement in the liver function studies. Phase 1 antibody to C. burnetii remained significantly elevated, however. In June 1989, the patient moved to Florida, and contact was lost. This patient’s source of infection was felt to be caused by her husband, a butcher who wore his work clothes when he was at home.

CASE 4

A 59-year-old white male engineer lived in Blythe and was always well until April 10, 2000, when he developed a fever and a cough. The cough improved somewhat, and he subsequently developed diarrhea that became intractable. Because of fever and diarrhea lasting 10 days, he was referred for admission to EMC on April 21, 2000. The patient had no recent travel abroad but liked to fish in the Colorado River in Blythe and often had to cross fields containing wastes and placentas from imported sheep to reach the river.

Physical examination was unremarkable, but laboratory studies revealed abnormal liver function studies with elevation of the transaminases, alkaline phosphatase, and the gamma glutamyl transpeptidase. Additionally, a chest x-ray revealed a mediastinal mass. Stool studies for the cause of his diarrhea were unremarkable. Because of his chest mass and diarrhea, a diagnosis of a probable neoplasm was made, assuming the diarrhea was caused by a paraneoplastic syndrome.

Thus, indomethacin was given, and within 24 hours, the diarrhea and fever had disappeared, consistent with a diagnosis of paraneoplastic syndrome. However, a needle biopsy of the lung lesion revealed granulomata and a liver biopsy defined a doughnut granulomatous pathology. Special stains for fungi and acid fast bacilli were negative. After the liver biopsy suggested doughnut granulomata, serologies were sent for C. burnetii antibody. They proved to be strongly positive for phase 2 IgG, IgM, and IgA globulins. Treatment with doxycycline at a dose of 100 mg, twice daily for 2 months, resulted in the disappearance of the mediastinal mass, abnormal liver function studies, and diarrhea. The etiology of the diarrhea and fever were both thought to be caused by cytokine overproduction, which has been described in patients with Q fever.14

CASE 5

A 42-year-old white male farm supervisor from Blythe had been an insulin-dependent diabetic for 15 years. He had otherwise been well, and his diabetes was well controlled. About a week before admission to EMC, he developed a fever without any cardiopulmonary, gastrointestinal, or genitourinary symptoms. He was hospitalized at the Palo Verde Hospital on July 23, 2004, in Blythe, where cultures, x-rays, and laboratory tests were unremarkable other than for elevated liver function tests, including the transaminases, alkaline phosphatase, and the gamma glutamyl transpeptidase. He experienced a headache when his body temperature rose. As a result, a lumbar puncture was performed and was unremarkable. He was transferred to EMC, where the physical examination noted a palpable liver 3 cm below the right costal margin. A computerized tomographic scan of the abdomen revealed a fatty liver. A serologic study of C. burnetii was positive at 1:16 for phase 2 IgG and IgM antibodies. A liver biopsy revealed typical doughnut granulomata. Treatment with doxycycline at 100 mg twice daily lowered his temperature to near normal. The doxycycline was discontinued after 2 weeks, and he became afebrile immediately. However, after 2 weeks, his fever recurred and he additionally received a month of doxycycline and then felt well. The liver function studies are now normal.

The patient and his family live adjacent to a field in Blythe where imported sheep live and deliver their lambs.

CASE 6

A 60-year-old retired Hispanic American rancher had enjoyed good health other than for hypertension, for which he took atenolol, and type II diabetes, for which he uses glyburide, until 2.5 weeks before admission to EMC when he developed fever and chills. He noted some associated anorexia and malaise. After a few days, he was seen by his personal physician, who obtained several laboratory tests as well as blood and urine cultures but was unable to establish a diagnosis. He was empirically placed on amoxicillin/clavulanate and then gatifloxacin, but he remained ill, with temperatures as high as 40°C. After hospitalization in April 2005, a physical examination was within normal limits, and laboratory studies revealed only slight elevations of the transaminases and an elevated C-reactive protein and sedimentation rate. A computerized tomographic scan of the abdomen revealed a fatty liver, and a gallium scan was unremarkable.

The patient stated that he raised chickens on his ranch but had no exposure to domestic cattle, sheep, or goats. He also drank 10 bottles of beer daily. A liver biopsy was performed that revealed doughnut granulomas, and a Q fever IgG phase I screen was negative, but the IgM phase 1 screen was positive. A Q fever phase 2 screen was positive with IgM and IgG titers ≥ 1:1,024. The phase 1 titer was 1:16. These serologies confirmed the diagnosis of acute Q fever hepatitis. The patient had ceased to be continuously febrile with the use of celecoxib, and he remained afebrile when doxycycline was initiated. After discontinuation of celecoxib and 3 weeks of doxycycline, the patient was well. Five months after treatment, he feels well, and liver function studies are normal. Phase 2 antibodies remain quite elevated, but phase 1 antibodies are positive at 1:16.

DISCUSSION

Nearly 70 years ago, a filter-passing agent was isolated by Davis and Cox18 from the Rocky Mountain wood tick, Dermocenter andersoni, collected near Nine Mile Creek about 32 miles west of Missoula, Montana. The agent, C. burnetii, was subsequently identified as the rickettsial organism responsible for Q fever.19

This organism is commonly found in domestic ungulates and a variety of wildlife mammals worldwide, who when infected generally remain asymptomatic.20 Livestock handlers and those that work in slaughter houses dealing with contaminated laundry or wool as well as textile workers, butchers, laboratory technologists, and veterinarians21 are occupationally at risk and are most commonly infected. Sheep seem to be more infectious than cattle and goats, and most cases in Idaho occur during the post-lambing period, which lasts about 4 months.22 Idaho is second only to California in reporting clinical cases of Q-fever in the United States.23

However, as exemplified in this communication, a direct association with infected material often can not usually be incriminated.

The acute disease often resembles influenza, leptospirosis, or brucellosis and thus requires serologic studies as the mainstay of clinical diagnosis, particularly because an attempt to isolate the organism is particularly hazardous to laboratory technologists.

In most primary infections, IgM antibodies to phase II antigen appear early (from the second week onward) in Q fever and remain detectable for short periods of time (10–17 weeks) after the onset of the disease. Thereafter, IgA and IgG (usually IgG1) antibodies are measurable and are generally present 5–10 days later.24 These antibodies can be detected by complement fixation (CF; the least sensitive), indirect immunofluorescence (IFA), and enzyme-linked immunosorbent assay (ELISA).25 Antibodies to phase I antigens are generally elevated more than phase II antibodies in patients with chronic Q fever infection.25

We have diagnosed six cases of Q fever at EMC during the past 32 years. All but two patients had lived adjacent (< 0.25 mi) to the imported sheep habitat in the Coachella Valley or in Blythe near the Colorado River. One patient was married to a butcher and another raised chickens on his rural ranch in the desert. None drank unpasteurized milk. Unpasteurized cheese is brought into California from Mexico, but none of our patients consumed these cheeses, making ingestion of contaminated food an unlikely source of Q fever hepatitis.

All but one patient in our group had antibody directed at phase 2 antigen, and all patients responded to between 1 and 2 months of antimicrobial therapy with doxycycline. Only a single patient with Q fever chronic hepatitis who also carried a Starr-Edwards mitral valve prosthesis manifested greater phase 1 than phase 2 antibodies. This individual had undergone at least three trans-thoracic echocardiograms and a single trans-esophageal echocardiogram that failed to show vegetations on the mitral valve but does not definitely exclude concomitant endocarditis. She had received at least three courses of multi-drug anti-microbial therapy for each as long as 6 months without curing her Q fever or reducing her markedly elevated antibody titers.

Chronic Q fever was originally thought to be associated with endocarditis, which developed on abnormal or prosthetic valves. However, patients without obvious endocarditis have been reported,26,27 and it has been assumed that the liver could serve as a reservoir for C. burnetii.28 Indeed, hepatic fibrosis in conjunction with chronic Q fever hepatitis has been described,26,27 as well as recurrent episodes of granulomatous hepatitis. Although in our experience Q fever hepatitis occurs more commonly than pneumonitis, the hepatic lesions of chronic Q fever have been microscopically documented in only a small number of cases (< 10%) in patients with chronic Q fever. Our patient’s > 3-year course of fever and abnormal liver function studies with a liver biopsy 3 years later revealing granulomas and lymphocytic infiltrates certainly speaks for chronic hepatitis and not endocarditis as the etiology of her chronic Q fever. Other causes of chronic Q fever include endovascular infections of aneurysms or prostheses, osteomyelitis, infection during pregnancy, pseudotumor of the lung, and pulmonary fibrosis.9

The granulomas of Q fever are histologically characterized by a central lipid vacuole and or a dense fibrin ring termed a doughnut granuloma. These granulomas are thought to be characteristic of Q fever hepatitis and were noted in all of our patients described in this communication. Because of the characteristic histopathology in the liver, we felt confident that patient 5 was infected by C. burnetii despite a borderline low antibody titer.

Treatment of acute infection by C. burnetii is best achieved with doxycycline28 at a dose of 200 mg daily for 2 weeks. Macrolides and quinolones have been successfully used as alternative therapy.29,30 Antimicrobial therapy for chronic Q fever usually uses doxycycline in conjunction with clindamycin, trimethoprim-sulfamethoxazole, rifampin, or a quinolone. More recently, hydroxychloroquine was added to doxycycline to alter the pH in the acid phagolysosome that the organism needs for growth in the treatment of Q fever endocarditis.31 At least 3 years of therapy are recommended for chronic Q fever.

Although Q fever seems to be an uncommon clinically diagnosed disorder in the desert of Southern California, an unusual epidemiologic situation involving imported domestic sheep to graze and give birth to lambs during the fall and winter months in a warm climate is able to overcome the lack of a presumed natural reservoir in the area. Although coyotes, gray foxes, skunks, raccoons, rabbits, deer, and mice have been shown by serosurvey to have been infected in California,32 we still believe that imported domestic sheep likely causes the disease in humans in the Coachella Valley. Seroprevalence amongst farmers in Idaho is 19%,32 indicating significant exposure to Q fever occurs in that state with a large domestic sheep population that are imported into Southern California annually for several months to feed and lamb. It is likely that aerosolized dust from sheep excrement and placentas are the sources of infection in humans in this area of California.

All six patients manifested hepatitis as a major illness, and only one patient presented with a pulmonary lesion as well. A single patient manifested chronic Q fever. All patients with acute Q fever responded to doxycycline, and two instantly became afebrile with non-steroidal anti-inflammatory drugs.33

*

Address correspondence to Lawrence A. Cone, Eisenhower Medical Center, Probst Professional Building, Suite 308, 39000 Bob Hope Drive, Rancho Mirage, CA 92270. E-mail: laconemedico@aol.com

Authors’ addresses: Lawrence A. Cone, Noel Curry, Phillip Shaver, and Barbara E. Potts, Department of Medicine, Eisenhower Medical Center, Rancho Mirage, CA 92270, E-mail: laconemedico@aol.com. David Brooks, Department of Medicine, Palo Verde Hospital, Blythe, CA. James DeForge, Bighorn Institute, Palm Desert, CA.

REFERENCES

  • 1

    Kaplan MM, Bertagna P, 1955. The geographical distribution of Q fever. Bull WHO 13 :829–860.

  • 2

    Kazar J, 1993. Q fever is absent from New Zealand. Int J Epidemiol 22 :945–949.

  • 3

    Hunt JG, Field PR, Murphy AM, 1983. Immunoglobulin responses to Coxiella burnetii (Q fever). Single serum diagnosis of acute infection using an immunofluorescence technique. Infect Immun 39 :977–981.

    • Search Google Scholar
    • Export Citation
  • 4

    Hart RJC, 1973. The epidemiology of Q fever. Postrgrad Med J 49 :535–538.

  • 5

    Zeman DH, Kirkbride CA, Leslie-Steen P, 1989. Ovine abortion due to Coxiella burnetii infection. J Vet Diagn Invest 1 :178–180.

  • 6

    Derrick EH, 1937. “Q” fever, a new fever entity: clinical features, diagnosis and laboratory investigation. Med J Aust 2 :281–299.

  • 7

    Robbins FC, Ragan CA, 1946. Q fever in the Mediterranean area: Report of its occurrence in allied troops. Clinical features of the disease. Am J Hyg 44 :6–22.

    • Search Google Scholar
    • Export Citation
  • 8

    Derrick EH, 1973. The course of infection with Coxiella burnetii. Med J Aust 1 :1051–1057.

  • 9

    Marrie TJ, 1995. Coxiella burnetii (Q fever) pneumonia. Clin Infect Dis 21 (Suppl 3):S253–S264.

  • 10

    Maurin M, Raoult D, 1999. Q fever. Clin Microbiol Rev 12 :518–553.

  • 11

    Turck WPG, Howitt G, Turnberg LA, Fox H, Longson M, Matthews MB, Das Gupta R, 1976. Chronic Q fever. Q J Med 45 :193–217.

  • 12

    Ellis ME, Smith CC, Moffat MAJ, 1983. Chronic or fatal Q fever infection: a review of 16 patients seen in North-East Scotland (1967–80). Q J Med 52 :54–66.

    • Search Google Scholar
    • Export Citation
  • 13

    Atienza P, Ramond M-J, Degott C, Lebrec D, Rueff B, Benhamou J-P, 1988. Chronic Q fever hepatitis complicated by extensive fibrosis. Gastroenterol 95 :478–481.

    • Search Google Scholar
    • Export Citation
  • 14

    Fournier P-E, Marrie TJ, Raoult D, 1998. Diagnosis of Q fever. J Clin Microbiol 36 :1823–1834.

  • 15

    Morbidity Mortality Weekly Report, 2004. Summary of provisional cases of selected notifiable diseases, United States, cumulative, week ending January 3, 2004 (53rd week). 52: 1291.

  • 16

    Biberstein EL, Behymer DE, Bushnell R, Crenshaw G, Riemann HP, Franti CE, 1974. A survey of Q fever (Coxiella burnetii) in California dairy cows. Am J Vet Res 35 :1577–1582.

    • Search Google Scholar
    • Export Citation
  • 17

    DeForge J, Cone LA, 2006. The serologic prevalence of Q fever (Coxiella burnetii) complement fixing antibodies in the Peninsula bighorn sheep of Southern California. Am J Trop Med Hyg (in press).

  • 18

    Davis GE, Cox HR, 1938. A filter-passing infectious agent isolated from ticks. I. Isolation from Dermacentor andersoni, reactions in animals, and filtration experiments. Public Health Rep 53 :2259–2261.

    • Search Google Scholar
    • Export Citation
  • 19

    Dyer RE, 1939. Similarity of Australian “Q” fever and a disease caused by an infectios agent isolated from ticks in Montana. Public Health Rep 54 :1229–1238.

    • Search Google Scholar
    • Export Citation
  • 20

    Marie TJ, Raoult D, 1997. Q fever—a review and issues for the next century. Int J Antimicrob Agents 8 :145–161.

  • 21

    Oliphant JW, Gordon DA, Meis A, Parker RR, 1949. Q fever in laundry workers, presumably transmitted from contaminated clothing. Am J Hyg 49 :76–82.

    • Search Google Scholar
    • Export Citation
  • 22

    Stoenner HG, Lackman DB, Benson WW, Mather J, Casey M, Harvey KA, 1961. The role of dairy cattle in the epidemiology of Q fever in Idaho. J Infect Dis 109 :90–97.

    • Search Google Scholar
    • Export Citation
  • 23

    D’Angelo LJ, Baker EF, Schlosser W, 1979. Q fever in the United Staes 1948–1977. J Infect Dis 139 :613–615.

  • 24

    Guigno D, Coupland B, Smith EG, Farrell ID, Desselberger U, Caul EO, 1992. Primary humoral antibody response to Coxiella burnetii, the causative agent of Q fever. J Clin Microbiol 30 :1958–1967.

    • Search Google Scholar
    • Export Citation
  • 25

    Raoult D, Marrie T, 1995. Q fever. Clin Infect Dis 20 :489–496.

  • 26

    Yebra M, Marazuela M, Albarran F, Moreno A, 1988. Chronic Q fever hepatitis. Rev Infect Dis 10 :129–130.

  • 27

    Geddes AM, 1983. Q fever. Br Med J 287 :927–928.

  • 28

    Spelman DW, 1982. Q fever: a study of 111 consecutive cases. Med J Aust 1 :547–553.

  • 29

    Maurin M, Raoult D, 1993. In vitro susceptibilities of spotted fever group Rickettsiae and Coxiella burnetii to clarithromycin. Antimicrob Agents Chemother 37 :2633–2637.

    • Search Google Scholar
    • Export Citation
  • 30

    Raoult D, Yeaman MR, Baca OG, 1989. Susceptibility of Coxiella burnetii to perfloxacin and ofloxacin in ovo and in persistently infected L929 cells. Antimicrob Agents Chemother 33 :621–623.

    • Search Google Scholar
    • Export Citation
  • 31

    Raoult D, Houpikian P, Tissot–Dupont H, Riss JM, Arditi-Dijiane J, Brouqui P, 1999. Treatment of Q fever endocarditis: comparison of two regimens containing doxycycline and of-loxacin or hydroxychloroquine. Arch Int Med 159 :167–173.

    • Search Google Scholar
    • Export Citation
  • 32

    McQuiston JH, 2002. Childs. Q fever in humans and animals in the United States. Vector Borne Zoonotic Dis 2 :179–191.

  • 33

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