Cardiac tamponade secondary to acute Q fever

Dear Editor,

Q fever, described in 1935 by Derrick,¹ is a zoonosis with worldwide distribution, with an incidence of three cases per 100,000 inhabitants/year. It is caused by Coxiella burnetii, a small gram-negative intracellular coccobacillus, resistant to heat and desiccation, which explains its ability to withstand adverse environmental conditions. Domestic ruminants, sheep and goats, are considered the main reservoir of the bacteria and inhalation is its main route of transmission. On rare occasions, cases of infection have been reported after the consumption of unpasteurised and contaminated dairy products.²

We present the case of a young woman with an unusual presentation of acute Q fever, diagnosed with acute pericarditis with cardiac tamponade and liver damage.

The patient was a 34-year-old woman of Moroccan origin, with no relevant family or personal history. Epidemiologically, the consumption of unpasteurised dairy products (fresh cow's cheese) was noted. She consulted for progressive dyspnoea with intolerance to decubitus and chest pain in the right hemithorax with pleuritic characteristics of two days evolution. She reported no fever, cold sensations or other symptoms in the clinical history of organs and systems. The physical examination revealed a tendency to arterial hypotension (84/66 mmHg), with an elevated heart rate and jugular venous engorgement. On auscultation, there were no murmurs or friction, although there were symptoms of right pleural effusion. The electrocardiogram showed sinus tachycardia with decreased voltages and electrical alternation. The tests showed raised total bilirubin (1.9 mg/dl; direct 1.18 mg/dl) and transaminases (GOT 392 U/l, GPT 339 U/l), as well as marked elevation of acute phase reactants (CRP 287 mg/dl, procalcitonin 2.21 ng/ml and fibrinogen 455 mg/dl). Brain natriuretic peptide was determined showing figures of 412 pg/ml, as well as ultra-sensitive troponin I, which was normal. A transthoracic echocardiography was carried out that confirmed the presence of severe pericardial effusion with signs of tamponade, performing percutaneous pericardiocentesis with pericardial fluid with characteristics of exudate with neutrophilic predominance and high levels of adenosine deaminase (ADA: 40 U/l). Both the cytology and the mycobacteria culture were negative. Viral (parvovirus B19, HBV, HCV, HIV) and bacterial (Mycoplasma pneumoniae, Chlamydia pneumoniae, Brucella) serological tests were performed, all negative except for being positive for antibodies against phase II of C. burnetii (1/512) and minimal against phase I (1/64), by indirect immunofluorescence. This was confirmed with a second test, after two weeks, obtaining the same antibody levels against phase II and with no detection of antibodies against phase I. Abdominal ultrasound was performed, which showed no significant alterations. Targeted treatment was established, with doxycycline 200 mg per day for three weeks, with the patient becoming asymptomatic after finishing treatment, with normalisation of transaminases and acute phase reactants, and without segmental alterations, ventricular dysfunction or pericardial effusion on follow-up echocardiography.

Both myocarditis and acute pericarditis are rare manifestations of acute Q fever, reported in less than 1% of all cases.³ In an aetiological analysis of pericardial effusion in 204 patients over four years, it was observed that 10 cases were due to infection by C. burnetii.⁴ Continuing with the experience obtained over four more years, a similar aetiological incidence was obtained.⁵ Echocardiographic findings can be nonspecific and range from normal ventricular function to wall motion abnormalities with severe systolic dysfunction.⁶ Patients are considered to have pericarditis due to this pathogen if they show an apparently infectious syndrome; pericardial effusion and an antibody titre consistent with acute Q fever (phase II IgG titre of 200 and IgM titre of 50) is demonstrated.⁷ In those cases where pericardial drainage is performed, the fluid must be analysed by culture and PCR analysis, since it can provide an accurate and fast diagnosis. Díaz-Morant et al. noted that such tests are performed in cases with unsatisfactory evolution, because the incidence is likely to be underestimated.⁸ The treatment of choice is doxycycline 200 mg daily for three weeks.⁹ In patients with a diagnosis of pericarditis or myocarditis, we must always take this pathology into account, although it is infrequent, since the delay in diagnosis and treatment can cause a worsening of morbidity and mortality.

Funding

No funding was received for this study.

Conflicts of interest

The authors declare that they have no conflicts of interest.