A 5-Year-Old Girl With High Fever and Nonproductive Cough

Nicholas J. Bennett, MB BChir, PhD


May 08, 2020

Severe infections with adenovirus, particularly those from serotype 7, are associated with a hyperlucent lung.[2] The hyperlucency affects the lung in a lobar distribution or the entire lung and is not a result of cystic lung destruction. In this case, the area of hyperlucency was clearly cystic rather than lobar, and it included an air-fluid level consistent with an abscess. In addition, the hyperlucent lung disease seen in severe adenovirus infections is considered a long-term complication of infection and not part of the acute illness.

Aspergillus is a mold that can cause cavitary lung lesions and may be seen as a "fungal ball" on radiography or CT. Aspergillus species are ubiquitous in the environment but rarely cause disease in immunocompetent hosts. In patients with cancer and those receiving chemotherapy, especially those with prolonged neutropenia or who are receiving steroids, aspergillosis should always be considered as a cause of lung pathology.

This patient had no history suggestive of immune deficiency or cancer and was not receiving any immunosuppressive medications. In addition, CT showed an air-fluid level rather than an air-filled cavity with a round density, which would be more typical of a fungal ball. Aspergillus in the lung may also present as multifocal disease.

Although Staphylococcus aureus has a well-deserved reputation for causing both postviral secondary pneumonia and complex pneumonia with parenchymal destruction and abscess formation, S pneumoniae is capable of causing similarly severe disease, as is highlighted in this case. Pneumococcus is the most common bacterial infection in community-acquired pneumonia, particularly in young children. The clinical picture and imaging studies were strongly suggestive of a bacterial lung abscess caused by S aureus or S pneumoniae.

Highly resistant S pneumoniae infections are becoming more frequent.[3] Pneumococcal resistance to penicillin and cephalosporins is caused by modified penicillin-binding proteins and is not amenable to beta-lactamase inhibitors. Macrolide resistance among pneumococci is also prevalent, and macrolides such as azithromycin are poor choices for first-line empirical treatment of moderate or severe pneumonias unless there is a strong suspicion of atypical pneumonia with mycoplasma or Chlamydophila pneumoniae. Familiarity with local patterns of antimicrobial sensitivity is important.

Severe infections with suspected pneumococcus or staphylococcus should include vancomycin as empirical therapy until formal identification and sensitivities are available. The choice to use linezolid in this case was made on the basis of difficulty obtaining high vancomycin levels despite doses of 80 mg/kg/d divided every 6 hours. Current recommendations are for vancomycin troughs between 15 and 20 mg/L to treat infections of the lung, blood, bone, and central nervous system, based in part on less apparent toxicity than was traditionally thought for vancomycin and in part on concerns regarding the development of vancomycin resistance.[4] The pharmacokinetics of vancomycin are different in children compared with adults, and more frequent dosing is often required to obtain therapeutic drug levels.

Linezolid is an expensive medication that should be considered only in unusual situations. Many microbiology labs will not release susceptibility testing results for linezolid to reduce the likelihood of widespread use, but if testing is performed, the results can usually be obtained by contacting the laboratory. Linezolid has excellent oral bioavailability, making for an easy transition from intravenous to oral therapy for discharge. This option is not available for vancomycin, which has almost no oral bioavailability.


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