Infectious Diseases in Clinical Practice:
A Severe Community-Acquired Pneumonia Caused by Dual-Culprit Pathogens, Streptococcus pneumoniae and Klebsiella pneumoniae
Toala, Iván MD*; Christensen, Diana MD†; Huang, Anna MD†; Ramírez, Julio MD, FACP†
*Division of Infectious Diseases, Hospital "Dr Arnulfo Arias Madrid," Panama City, Panama; and †Division of Infectious Diseases, University of Louisville Hospital, Louisville, KY.
Address correspondence and reprint requests to Julio Ramirez, MD, FACP, Division of Infectious Diseases, 512 South Hancock St, Carmichael Bldg, Room 208-D, Louisville, KY 40202. E-mail: firstname.lastname@example.org.
Abstract: A case of Streptococcus pneumoniae combined with Klebsiella pneumoniae as a mixed infection in a patient with community-acquired pneumonia is presented. Community-acquired pneumonia due to combined etiology should be considered in patients who develop clinical deterioration on pathogen-specific therapy against S. pneumoniae.
Streptococcus pneumoniae as etiology of community-acquired pneumonia (CAP) can produce single or mixed infections.1,2 The organisms most frequently reported in the literature in combination with S. pneumoniae are the atypical pathogens Legionella pneumophila, Chlamydia pneumoniae, and Mycoplasma pneumoniae.3-6 The association of S. pneumoniae with typical pathogens as etiology of CAP is considered a rare clinical event. Here, we report a case of S. pneumoniae CAP combined with Klebsiella pneumoniae.
A 52-year-old white man with a history of squamous cell carcinoma of the floor of the mouth (stage IV, T2/T3 N2 MO) was admitted to the Veterans Affairs Medical Center of Louisville with a 3-day history of cough and shortness of breath. He completed treatment 3 months before admission (weekly taxol and carboplatin along with radiation) and has a performance status of 100% with a general condition grade 1, according to the scale of the Eastern Cooperative Oncology Group. Because of problems with swelling and tongue pain, he has a percutaneous enteral gastrostomy tube. On physical examination, his temperature was 99.7°F; heart rate, 136 beats per minute; respiratory rate, 32 breaths per minute; blood pressure, 126/66 mm Hg with an oxygen saturation of 55% while breathing room air. Lung examination revealed decreased breath sounds in the left lung. The rest of the physical examination was unremarkable. Laboratory tests at admission showed a white blood cell count of 3600/mL with 72% neutrophils and 5% bands (reference range, 4.8-10.8 × 103/μL) and a platelet count of 215,000/mL (reference range, 130-430 × 103/μL). Sodium was 130 mmol/L (reference range, 133-150 mmol/L); potassium, 2.9 mmol/L (reference range, 3.5-5.1 mmol/L); and creatinine, 1.2 mg/L (reference range, 0.5-1.5 mg/dL). Chest x-ray on the day of admission showed opacification of the left hemithorax, and the computed tomography (CT) scan revealed left pleural effusion with alveolar infiltrates on the left lower and upper lobes (Fig. 1A). On the day of admission, a chest tube was inserted for treatment of empyema. The patient's prognosis was evaluated at the time of hospitalization using the pneumonia severity index. The patient was risk class V with an estimated risk of mortality of 26.7%. The patient was admitted to the intensive care unit, placed on mechanical ventilation, and treated with intravenous fluids and vasopressors. Microbiological workup on the day of admission included cultures from bronchoalveolar lavage fluid, pleural fluid, and blood. Because the patient had severe CAP, was admitted to intensive care unit, and was immunocompromised, it was considered that Pseudomonas aeruginosa was a likely pathogen. Because in the Louisville area we have recently treated several cases of severe CAP caused by methicillin-resistant Staphylococcus aureus, this organism was also considered in the list of likely pathogens. Due to the previously mentioned considerations, the patient was started on a combination of piperacillin/tazobactam, ciprofloxacin, and vancomycin.
The bronchoalveolar lavage fluid grew S. pneumoniae and K. pneumoniae; the pleural fluid grew S. pneumoniae, and 2 sets of blood cultures grew S. pneumoniae and K. pneumoniae. The S. pneumoniae was fully susceptible to penicillin, and the K. pneumoniae was susceptible to fluoroquinolones, aminoglycosides, third-generation cephalosporins, carbapenems, and piperacillin/tazobactam. After reports of cultures, ciprofloxacin and vancomycin were discontinued. A second chest x-ray on day 11 was without change compared with admission. The third CT scan on day 11 showed decreased alveolar infiltrate with development of multiple cavities compatible with necrotizing pneumonia (Fig. 1B). The patient was extubated on day 15 and transferred to the general medical floor on day 21. The characteristics of our patient compared with 3 previously reported cases of combined S. pneumoniae and K. pneumoniae CAP are depicted in Table 1.
This case represents only the fourth reported case of definitive combined etiology of CAP that is caused by S. pneumoniae plus K. pneumoniae.7,8 Although reported cases of combined etiology of CAP as a result of typical bacteria are scarce, the real incidence of combined typical etiology is difficult to estimate. When typical pathogens are isolated from sputum cultures, they are considered only presumptive etiology of CAP, and these cases do not qualify as definitive combined etiology. Etiologies for typical pathogens in CAP are considered definitive when the pathogens are isolated from sterile body sites.9 Our case fulfills criteria for definitive etiology because of the isolation of S. pneumoniae and K. pneumoniae in blood cultures. Because positive blood cultures occur in approximately 10% of all hospitalized patients with CAP,1 it can be speculated that the diagnosis of combined etiology can be easily missed in a significant number of patients. Reported cases of CAP with S. pneumoniae combined with typical pathogens have been characterized by affecting hosts with severe underlying diseases and abnormal host defenses. In our case, the patient has cancer of the mouth and had received recent chemotherapy. In a prior report of 3 cases of definitive combined etiology of S. pneumoniae CAP associated to S. aureus, 2 of the patients had decompensated hepatic disease at admission to the hospital.10 The high mortality rate associated to CAP as a result of combined typical pathogens may be explained by the host immune deficiencies as well as the added virulence of 2 typical pathogens causing CAP.
When S. pneumoniae is identified as etiology of CAP, national guidelines for the management of CAP recommend de-escalating antibiotic therapy and performing pathogen-directed therapy.1,2 In our clinical case, directed therapy to S. pneumoniae with penicillin G would have produced a clinical failure because of the lack of treatment of the second bacterial etiology, K. pneumoniae. In summary, we report a case of definitive combined etiology of CAP caused by S. pneumoniae and K. pneumoniae. The possibility of a second organism combined to S. pneumoniae should be considered in patients who develop clinical deterioration on pathogen-directed therapy against S. pneumoniae.
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