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Coxiella burnetii and lobar pneumonia.

To the Editor: A 32-year-old woman was admitted to our department with high fever, headache, myalgia, back pain and dry cough of three days' duration. Her past history was unremarkable. On physical examination, the patient was very ill, febrile to 39.5[degrees]C and with inspiratory coarse crackles at the base of the right lung. Admission laboratory findings included a WBC of 11,600/[mm.sup.3] (86% polymorphonuclear cells), ESR: 82 mm/h and increased C-reactive protein (182 mg/L). Serum biochemistry, coagulation tests and urinalysis were normal. Chest x-ray showed dense consolidation in the right lower lobe (Fig.). Community-acquired pneumonia (CAP) was diagnosed and the patient was treated with clarithromycin plus cefuroxime. Despite the antibiotic therapy, on the following days, her symptoms showed no improvement. Blood cultures were negative. In addition, she had progressive worsening of her liver function tests. On the 5th day after admission, AST was 118 IU/L, ALT 262 IU/L, ALP 433 IU/L, and [gamma]GT was 154 IU/L). Although the latter were attributed to possible adverse reaction to antibiotics, further evaluation was decided. Serologic markers for hepatitis B and C, EBV, CMV, HSV, Mycoplasma pneumoniae, Legionella pneumophila, Leptospira and Toxoplasma were all negative. However, immunofluorescence antibody revealed positive antibodies against C burnetii, compatible with acute infection (IgM 1/3200 and IgG 1/1920). The patient had a dog as a pet, but without recent parturition. Cefuroxime was substituted by oral doxycycline 100 mg b.i.d. The patient became afebrile two days later and she was discharged in good condition. The patient was followed up in the clinic, with normalization of her liver tests and positive conversion of IgG antibody (IgM 1/1600 and IgG 1/2840), 20 days after discharge.

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C burnetii is the causative agent of Q fever. (1,2) Although there are some reports of person-to-person spread, most Q fever infections result from inhalation of infectious aerosol particles from parturient ruminants derived from a wide variety of animals, such as cows, goats, sheep, cats and occasionally dogs, due to the fact that the organism has high concentrations in the placenta of infected animals. (3,4) However, this contact may be indirect, and other animals' products may be involved. In our case, the patient had a domestic dog, but was not around the breeding period.

It is estimated that C burnetii infection is asymptomatic in 60% of the cases and only 2% of the acute infected patients need hospitalization. (3) Hepatomegaly with abnormal liver function tests is also common. (2) Pneumonia, with (similar to our case) or without hepatitis, is usually mild, but respiratory distress needing mechanical ventilation occasionally occurs. (1) Generally, the clinical feature of Q fever pneumonia varies greatly and depends on the geographic origin of the infection and host factors. (2)

Although C burnetii is considered a causative agent of atypical pneumonia (range: 0.8%-5.8% of CAP), (5) in our case, radiological (lobar pneumonia) and laboratory (86% polymorphonuclear cells) findings at admission were compatible with typical bacterial CAP. It is estimated that 17 (6.3%) of 272 patients with Q fever pneumonia had segmental consolidation. (1) However, it has been suggested that there is a second type of acute Q fever pneumonia presenting as bacterial CAP due to a mixed infection with S pneumoniae or H influenzae. (5) However, in our case, clinical and laboratory findings as well as treatment responsiveness were not able to establish a case of mixed infection.

In conclusion, prompt diagnosis, based on epidemiologic (geographic characteristics, exposure to risk factors), clinical and serologic data, is essential, since acute Q fever pneumonia may present with atypical laboratory and radiological findings.

Evangelos Cholongitas, MD

Chrysoula Zouli, MD

Chrysoula Pipili, MD

Konstadinos Katsogridakis, MD

Konstadinos Rellos, MD

Maria Dasenaki, MD

Department of Internal Medicine

General Hospital of Sitia

Crete, Greece

References

1. Marrie TJ. Coxiella burnetii pneumonia. Eur Respir J 2003;21:713-719.

2. Parker NR, Barralet JH, Bell AM. Q fever. Lancet 2006;367:679-688.

3. Raoult D, Marrie T, Mege J. Natural history and pathophysiology of Q fever. Lancet Infect Dis 2005:5:219-226.

4. Marrie TJ. Q fever pneumonia. Curr Opin Infect Dis 2004;17:137-142.

5. Okimoto N, Asaoka N, Osaki K. et al. Clinical features of Q fever pneumonia. Respirology 2004;9:278-282.
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Author:Dasenaki, Maria
Publication:Southern Medical Journal
Article Type:Letter to the editor
Date:Nov 1, 2006
Words:719
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