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Unusual dual infection in an immunocompetent young man with community-acquired pneumonia.
Daniele Torres¹ MD, Gaspare Parrinello¹ MD, Salvatore Paterna¹ MD and Giuseppe Licata¹ MD.
¹ Department of Internal and Specialistic Medicine, University Hospital of Palermo.
Address for correspondence:
Dott. Daniele Torres
Via SS. Cosma e Damiano 14 ,
Partinico 90047, Palermo, Italy
Tel. 39.333.2152198; Fax 39.91.8781895;
M.pneumoniae is one of the most bacterial causes of community acquired pneumonia in young adults and mixed viral–bacterial infections are frequent in childhood but uncommon in immunocompetent adults. A combination of M.pneumoniae infection and mononucleosis-like illness due to cytomegalovirus (CMV) have not been reported in adults with community-acquired pneumonia. We describe a 29-year-old immunocompetent patient admitted to our hospital with thirteen days history of continuous-remittent fever, with dry cough and shortness of breath from four days. He had epato-splenomegaly with inguinal and axillary lymphadenopathy. Laboratory findings revealed elevated transaminases and absolute lymphocytosis with atypical lymphocytes on peripheral blood film. High-resolution computer tomography showed bilateral multiple small consolidations with air bronchogram of left lower lobe, lingual, right mean and lower lobe with paratracheal and pulmonary lymphadenopathy. Antibodies to M. pneumoniae and cytomegalovirus titred on ELISA were significantly elevated. Negative the other serologies. We discuss the hypothesis that M.pneumoniae and CMV coinfection may act as cofactors in community-acquired pneumonia also in immunocompetent patients. This infectious event may be secondary to a transient decrease in the immune function due to a primary CMV infection or to a viral reactivation triggered by bacterial pneumonia.
Few cases of mononucleosis-like illnesses are accompanied by pneumonia and are mostly described in children (1). Mycoplasma pneumoniae (M.p) and cytomegalovirus (CMV) coinfection have still not reported in adults with community-acquired pneumonia. In healthy subjects acquired CMV infections are frequently chiefly asymptomatic and pathological manifestations include, uncommonly, mononucleosis-like syndrome without pharyngitis and respiratory symptoms (2). Recently, we observed a 29-year-old married patient admitted to our hospital with thirteen days history of continuous-remittent fever (39,5°C) and with dry cough and shortness of breath from four days. His past medical history not included significant clinical events. He was immunocompetent and not a drug addict. He was treated before hospital admission with amoxicillin+acid clavulanic ineffectively. On clinical examination we observed a significantly decreased vesicular murmur at the pulmonary basis and mild-to-moderate epato-splenomegaly with inguinal and axillary lymphadenopathy. Cardiac examination and trans-thoracic echocardiography were normal. Laboratory findings revealed elevated serum GOT (78 U/L), GPT (181 U/L), γ-GT (123 U/L) and lactate dehydrogenase (640 U/L) levels. Inflammatory markers were increased and white-cell count was 9110/µl with 26,6% of neutrophils and absolute lymphocytosis (54,4%) and monocytosis (15,8%). Peripheral blood film confirmed the absolute lymphocytosis with finding of 11% of atypical lymphocytes. Chest x-ray showed basal linear and reticular infiltrates in both lung fields while and at high-resolution computer tomography bilateral multiple small consolidations with air bronchogram of left lower lobe, lingual, right mean and lower lobe without diffuse interstitial pattern and with paratracheal and pulmonary lymphadenopathy were detected. Arterial oxygenation was normal. A mild elevation of cold agglutinins (titre 1:102) was observed. Antibodies to M.p and CMV titred on ELISA were significantly elevated. Negative the other serologies (toxoplasmosis, EBV infection, HHV-6 infection, viral hepatitis, HIV), PPD test and blood cultures. Typisation of circulating lymphocytes was revealed normal. In the suspicion of pneumonia due to M.p the patient was treated with clarytromycin with rapid clinical response, resolution of fever, dry cough and shortness of breath. After hospital discharge he continued a course of treatment with clarytromycin for twenty days. The laboratory parameters and radiological findings reintered after three weeks.
M.p is one of the most bacterial causes of community acquired pneumonia in young adults (3,4), but mixed viral–bacterial infections, common in childhood, are uncommon in immunocompetent adults. Two hypotheses should be considered in this case: - the patient has either coinfection: a CMV infection with suprainfection of M.p or a CMV reactivation during M.p primary infection or a non-specific antibody response during pneumonia. We believe that, if serological cross-reaction is relatively common between these two microbes, the clinical findings of absolute lymphocytosis with atypical lymphocytes, lymphadenopathy (Sumaya’s diagnostic criteria for infectious mononucleosis), hepatosplenomegaly with hepatic dysfunction, bilateral pulmonary consolidation and cold agglutinins had confirmed the true co-infection: M.p infection secondary to a transient decrease in the immune function due to a primary cytomegalovirus infection or CMV reactivation (5) triggered by M.p. To conclude, we suggest that M.p and CMV may act as cofactors in community-acquired pneumonia in immunocompetent patients. So the routine CMV and M.p screening in immunocompetent patients presenting with an infectious mononucleosis-like syndrome and with respiratory symptoms is recommended. Further studies are needed to clarify the relationships of these infectious agents in the pathogenesis of community-acquired pneumonia.
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2. Foti G, Hyeraci M, Kunkar A et Al. Cytomegalovirus infection in the adult. Minerva Med. 2002;93:109-17.
3. Waites KB, Talkington DF. Mycoplasma pneumoniae and its role as a human pathogen. Clin Microbiol Rev. 2004;17:697-728
4. Schneeberger PM, Dorigo-Zetsma JW, van der Zee A. Diagnosis of atypical pathogens in patients hospitalized with community-acquired respiratory infection. Scand J Infect Dis. 2004;36:269-73.
5. Hummel M, Abecassis MM. A model for reactivation of CMV from latency. J Clin Virol. 2002;25:S123-36
Copyright Priory Lodge Education Limited 2007
First Publsihed October 2007