Severe adenovirus community-acquired pneumonia mimicking Legionella

Dear Editor, I read with interest the report of Drs. Hakim and Tleyjah on severe adenovirus pneumonia in your journal [1]. Their literature review reminds us of the reemergence of adenoviral community-acquired pneumonia (CAP) and that it may mimic other causes of CAP, particularly the atypical pneumonias, e.g., Legionnaire’s disease [2, 3]. As the authors correctly state, adenovirus is the only viral cause of CAP that may resemble bacterial pneumonia with focal/ lobar infiltrates or consolidation. However, as with other viral causes of pneumonia, early the chest X-ray in adenoviral CAP may be normal, even when the patient is short of breath and hypoxemic. The two most likely radiologic presentations of adenovirus is a completely normal chest X-ray with hypoxemia and symptoms of pneumonia or with lobar infiltrate/consolidation. Unlike influenza, routinely associated with leukopenia, adenoviral CAP is associated with a normal or elevated white blood cell (WBC) count, excluding viral influenza. An important clue noted by the authors, which has been our experience as well is the presence of conjunctival suffusion when present. Another important point is that viral pneumonias are ordinarily not accompanied by loose stools/diarrhea [4]. Adenovirus is most likely to be confused in this respect with Mycoplasma pneumoniae or Legionnaire’s disease, which is a common feature of both. Adenoviral CAP in patients with lobar infiltrates mimic Legionnaire’s disease, which may be differentiated from Legionella by the absence of hyponatremia, hypophosphatemia, and highly elevated serum levels [5]. As with conjunctival suffusion, an important clue to adenoviral pneumonia is wheezing, more common in children that, if present, should suggest adenovirus [1]. Recently, we have had a case of adenoviral CAP in a normal host different to that reported by the authors. The patient was a 36-year-old immunocompetent male who presented with severe CAP with a prominent dry cough and headache. On physical examination, he had a questionable faint truncal rash and conjunctival suffusion. Auscultation of the chest revealed no rales. His WBC count was 7.3 K/ mm with monocytosis. Relative lymphopenia was not present. His platelet count was 280,000 K/mm. Because of his headache and possible rash, the question of aseptic meningitis was raised and a lumbar puncture was performed. His cerebrospinal fluid (CSF) showed 8 WBCs/hpf with a normal glucose, protein, and lactic acid level. Head magnetic resonance imaging (MRI) was negative. He was hypoxemic on room air. Both his erythrocyte sedimentation rate (ESR) and liver function tests (LFTs) were unelevated and cold agglutinin titers were negative. His creatine phosphokinase (CPK) was unelevated. Titers for Legionella, M. pneumoniae, and Chlamydia pneumoniae were negative. His Legionella urinary antigen test was negative. His adenovirus titer was elevated 1:128 (normal<1:8). As the authors suggest, adenoviral CAP is probably more common than recognized. It is an easily missed diagnosis and should be included in the differential diagnosis of severe CAP in patients. Early on, in immunocompetent CAP patients without pulmonary infiltrates, the differential diagnosis should include influenza and cytoEur J Clin Microbiol Infect Dis (2009) 28:313–315 DOI 10.1007/s10096-008-0611-6