Journal of Infection (2005) 51, e89–e91
www.elsevierhealth.com/journals/jinf
CASE REPORT
Acute Q fever lobar pneumonia: a case report Maria Tsironi*, Panagiotis Andriopoulos, Spiros Fokas, George Nikokiris, Marina Mantzourani, George Assimakopoulos, Athanassios Aessopos Department of Internal Medicine, Sparta General Hospital, 23100 Sparta, Greece Accepted 6 September 2004
KEYWORDS Q fever; Pneumonia; Hepatitis; Doxycycline
Abstract 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. Q 2005 The British Infection Society. Published by Elsevier Ltd. All rights reserved.
Introduction Q fever, a zoonosis, is due to infection with Coxiella burnetii. This spore-forming microorganism is a small Gram-negative coccobacillus that is an obligate intracellular parasite. The most common animal reservoirs are goats, cattle, sheep, cats, and occasionally dogs. The organism reaches high concentrations in the placenta of infected animals. Aerosolisation occurs at the time of parturition and infection follows inhalation of this aerosol.1–3 Persons at risk from Q fever include farmers, veterinarians, abattoir workers, those in contact with dairy products, and laboratory personnel performing C. burnetii culture. However, there has been an increase in reports of sporadic cases in people living in urban areas after occasional contact with farm animals or after contact with infected pets. The disease is usually mild—up to 60%
* Corresponding author. Tel.: C30 693 248 3226; fax: C30 273 108 1140. E-mail address:
[email protected] (M. Tsironi).
of initial infections are asymptomatic1 —and resolves spontaneously within 2–3 weeks. Q fever is divided into acute and chronic infection characterized by different evolution and serological profiles. There are three distinct clinical syndromes of the acute form of the illness: nonspecific febrile illness, pneumonia, and hepatitis. The pneumonic form of the illness can range from very mild-to-severe pneumonia, presenting commonly with the usual features of atypical pneumonia. We present a patient with acute Q fever lobar pneumonia, pleural effusion and hepatic dysfunction, who was first misdiagnosed as a typical bacterial community acquired pneumonia, according to the radiographic findings.
Case report A 32-year old white man, living in an urban area, sought treatment for acute onset of fever, chills, and non-productive cough. Community acquired pneumonia (CAP) of the right base was diagnosed and amoxycillin and roxythromycin were
0163-4453/$30.00 Q 2005 The British Infection Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.jinf.2004.09.003
e90
M. Tsironi et al.
prescribed. The patient’s symptoms persisted and when retroorbital headaches, abdominal pain (especially in the right hypochondrium), nausea and night sweat appeared 5 days later, he sought further treatment at the emergency department. He was a tall, thin pale young man, with a 10-pack years history of cigarette smoking. His temperature was 39.5 8C, pulse rate 100 beats per minute, arterial pressure 90/60 mmHg. Hypoxemia was recorded and on lung auscultation inspiratory coarse crackles were heard in the right base, along with diminished bronchial sounds. Tactile fremitus was decreased and dullness upon chest percussion was present in the same area. The white-cell count was within the normal range but markedly shifted to the left with toxic granulations. Erythrocyte sedimentation rate (ESR) was 82 mm (first hour). The biochemical profile was: serum glucose 101 mg/dl, BUN 27 mg/dl, alkaline phosphatase (ALP) 123 U/l, SGOT 125 U/l [normal: 9–40 U/l], and SGPT 132 U/l [normal: 7– 45 U/l]), ferritin 2472 ng/ml. Renal function was normal, direct Coombs test was negative and coagulation tests were within the normal ranges. Sputum and two sets of blood cultures were obtained. The chest X-ray showed consolidation of the right lower lobe and pleural effusion (Fig. 1) and sonographic examination of the abdomen revealed a slight enlargement of the spleen. He was admitted to the internal medicine department with the diagnosis of CAP, possibly due to Streptococcus pneumoniae. The patient was administered penicillin and ciprofloxacin in high doses, in order to cover a wide spectrum of typical and atypical pathogens. Fever decreased in the next 4 days, but a persistent increase of liver function tests (SGOT 132 U/l, SGPT 274 U/l) along with acanthocytes on the peripheral blood smear were observed. They were both attributed to a liver dysfunction caused
Figure 1
either by septicaemia or by adverse effects of roxythromycin and/or ciprofloxacin. Despite of the latter possibility, treatment was continued because of clinical amelioration. As blood and sputum cultures were negative for common pathogens, serum samples were tested for atypical pathogens and the indirect immunofluoresence antibody (IFA) assay demonstrated IgG antibodies reactive with C. burnetii phase II antigens at reciprocal titers of R1.680, confirming a diagnosis of Q fever. Treatment was changed to oral administration of doxycycline 100 mg twice a day and the patient was discharged 5 days later with clinical and laboratory improvement. The patient owned a female dog, but there had been no recent animal births.
Discussion Acute Q fever can manifest as a relatively mild, self-limited febrile illness, or a more severe disease characterized by sudden onset of one or more of the following: high fever, severe headache, general malaise, myalgia, confusion, sore throat, chills, sweat, non-productive cough, nausea, vomiting, diarrhea, abdominal pain, and chest pain. Hepatitis and pneumonia can coexist,while myocarditis, pericarditis, and meningoencephalitis are rare. The most frequent clinical presentation of acute Q fever may vary from one area to another. Pneumonia is the major clinical presentation in Nova Scotia and in Switzerland.3,4 In contrast, hepatitis is observed more frequently than pneumonia in California, Ontario and France,4–6 and febrile illness was the most frequent manifestation of acute Q fever in a series of 111 consecutive patients in Australia.7 Atypical pneumonia is a major clinical presentation. In Greece, a study performed in 1990 in
Chest X-ray showing consolidation of the right lower lobe and pleural effusion.
Acute Q fever lobar pneumonia: a case report northern Greece demonstrated that 4.7% of 3686 patients with ‘atypical pneumonia’ had antibodies against C. burnetii antigens.8 From 1989 to 1993, 1998 Q fever cases were diagnosed and most patients were men (73.5%).9 The frequency of Q fever pneumonia among cases of communityacquired pneumonia varies, being certainly low. Clinical symptoms may range from clinically asymptomatic pneumonia diagnosed on the chest X-ray to, rarely, acute respiratory distress.10 Complications associated with acute Q fever pneumonia include encephalitis, renal failure, congestive heart failure, respiratory failure, and myocarditis. Hypoxemia was recorded in up to 26.6% in a series of patients with Q fever pneumonia.11 Abnormal liver function tests are the primary manifestation of Q fever hepatitis but are also common in patients presenting with Q fever pneumonia. They are usually mildly elevated two to three times of the normal levels.12 Fever, pulmonary signs, and elevated liver enzyme levels can coexist, as in our case, and they may be misinterpreted. Since, symptoms of Q fever can vary, fixing diagnosis is done by serology with the phase I and the phase II antibody.13 Q fever usually is diagnosed by evaluating paired acute and convalescent phase serum samples. In humans, the antibody response is directed against phase I and phase II antigens of C. burnetii. Patients with acute Q fever typically produce an antibody response primarily to C. burnetii phase II antigen; chronic C. burnetii infections typically elicit a higher antibody response to phase I antigens.13 Tetracycline is the drug of choice for treatment of C. burnetii infection. Some reports support the clinical effectiveness of erythromycin and quinolones,14,15 and this could explain the apyrexia of our patient under ciprofloxacin treatment. Because antibiotic treatment is most effective during the early phase of the illness, treatment should not be withheld pending results of confirmatory laboratory antibody tests, which provide a retrospective diagnosis. The objective of this case report is to increase the physician’s awareness of the different clinical presentations of Q fever and discuss the possible diagnostic misinterpretation of community acquired pneumonia. Atypical pneumonia, in our
e91 case Q fever pneumonia with lobar consolidation, peural effusion and hepatic dysfunction such as our patient’s, represents a diagnostic puzzle, especially when there is no typical occupational history. Therefore physicians should be aware of the often dubious and misinterpreted appearance of community acquired pneumonia
References 1. Raoult D, Mege JL, Marrie T. Q fever: queries remaining after decades of research. In: Scheld WM, Craig WA, Hughes JM, editors. Emerging infections 5. Washington, DC: ASM Press; 2001. p. 29–56. 2. McQuiston JH, Childs JE, Thompson HA. Q fever. J Am Vet Med Assoc 2002;221:796–9. 3. Marrie TJ. Q fever, 1979–1987 Nova Scotia. Can Dis Weekly Rep 1988;14:69–70. 4. Dupuis G, Peter O, Pedroni D, Petite J. Clinical aspects observed during an epidemic of 415 cases of Q fever. Schweiz Med Wochenschr 1985;115:814–8. 5. Clark WH, Lennette EH, Railsback OC, Romer MS. Q fever studies in California. VII. Clinical features in one hundred and eighty cases. Arch Intern Med 1951;88:155–67. 6. Vellend H, Salit IE, Spence L, McLaughlin B, Carlson J, Palmer N, Van Dreumel AA, Hodgkinson JR. Q fever in Ontario. Can Dis Weekly Rep 1982;8:171–3. 7. Spelman DW. Q fever: a study of 111 consecutive cases. Med J Aust 1982;1:547–53. 8. Alexiou-Daniil S, Antoniadis A, Pappas K, Doutsos J, Malisiovas N, Papapanagiotou I. Incidence of Coxiella burnetii infections in Greece. Hell Iatriki 1990;56:251–5. 9. Tselentis Y, Gikas A, Kofteridis D, Kyriakakis E, Lydatakis N, Bouros D, Tsaparas N. Q fever in the Greek island of Crete: epidemiologic, clinical, and therapeutic data from 98 cases. Clin Infect Dis 1995;20:1311–6. 10. Marrie TJ. Coxiella burnetii pneumonia. Eur Respir J 2003; 21(4):713–9. 11. Marrie TJ. Coxiella burnetii (Q fever) pneumonia. Clin Infect Dis 1995;21(Suppl. 3):5253–64. 12. Okimoto N, Asaoka N, Osaki K, Kurihara T, Yamato K, Sunagawa T, Fujita K, Ohba H, Nakamura J, Nakada K. Clinical features of Q fever pneumonia. Respirology 2004; 9(2):278–82. 13. Fournier PE, Marrie TJ, Raoult D. Diagnosis of Q fever. J Clin Microbiol 1998;36:1823–34. 14. Bertrand A, Janbon F, Jonquet O, Reynes J. Infections par les rickettsiales et fluoroquinolones. Pathol Biol (Paris) 1988; 36:493–5. 15. Perez-del-Molino A, Aguado JM, Riancho JA, Sampredo I, Matorras P, Gonzales-Macias J. Erythromycin and the treatment of Coxiella burnetii pneumonia. J Antimicrob Chemother 1991;28:455–9.
