In this teaching case we used the format of presentation of successive parts of the history, physical examination, and management accompanied by discussion (in bold characters) of a commentator.
A 64-year-old male presented to the Emergency Room of the local hospital in a rural area of Greece complaining of fever, shortness of breath, productive cough, and mild low back pain. He had no previous hospitalizations.
The patient's symptoms suggest a lower respiratory tract (LRT) infection as the most likely diagnosis. Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis are common etiologic agents in patients with community acquired LRT infections. In addition, atypical bacteria including Mycoplasma, Chlamydia, Legionella, and Rikketsiae species are the cause of a considerable proportion of lower respiratory tract infections that varies in different age groups. Also, several viruses including influenza, parainfluenza, and adenoviruses may cause LRT infection, especially during the winter session.
The patient was a farmer. His past medical history was significant for a work-related injury in the lower back 10 years ago. He consumed alcohol, about half a liter of wine per day, for 20 years. He did not smoke. He never traveled outside Greece.
The details of the medical history and the habits of the patient suggest additional possible pathogens for his LRT infection, mainly Klebsiella pneumoniae, given the history of alcoholism. Because of his occupation, leptospirosis should be considered in thedifferential diagnosis. In addition, brucellosis should be also considered given that the patient lives in a rural area in Greece where the infection is endemic. It should be noted that brucellosis may cause manifestations from the respiratory system.
The patient's condition deteriorated despite the administration of antimicrobial treatment (ceftriaxone 1 g every 12 hours i.v. and clarithromycin 500 mg every 12 hours p.o.) at the local hospital. He was transferred to a tertiary hospital in Athens, two days after his admission at the local hospital. He presented with temperature 38.5 oC, heart rate 108/min, and tachypnea (45 breaths/min). Physical examination on admission revealed crackles in the base of the left lung and the upper right lung. Routine laboratory testing showed white blood cell count 8,800/mm 3, neutrophils 88%, erythrocyte sedimentation rate 104 mm/1st hour, serum urea 57 mg/dl and creatinine 1.4mg/dl. Gram stain of a sputum specimen showed about 20 neutrophils per optic field. Chest x-rays on admission showed infiltrates in the left lower and the right upper lobe (figure 1). Arterial gas testing showed PaO2/FiO2=240, arterial pH = 7.48, and PCO2=28 mmHg.
The patient's worsening condition despite the use of appropriate antimicrobial treatment for community-acquired pneumonia suggests several possibilities. First, that the pathogen responsible for his pneumonia was indeed one of the most commonly implicated micro-organisms in LRT infections, namely Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, or an atypical pathogen that was however resistant to the administered agents. There is an increasing proportion of pneumococcal isolates with full resistance to penicillin in several countries during the last years. Although still a controversial issue, it seems that the majority of evidence supports that the outcome of patients who receive treatment with ceftriaxone for pneumonia due to Streptococcus pneumoniae with full resistance to penicillin is worse than with vancomycin or other agents with activity against this pathogen. Second, the pathogen may be one not included in the above list of microorganisms. Someone should also consider other etiologic agents such as staphylococci, streptococci other than Streptococcus pneumoniae, anaerobes, and Gram-negative bacteria other than Klebsiella pneumoniae. In addition, mycobacteria, mainly Mycobacterium tuberculosis, should be always considered in the differential diagnosis in patients with LRT infection. It should be also noted that antibacterial agents would not influence the natural history of a viral LRT infection, except if a secondary bacterial infection had already developed. Non-infectious causes of lung infiltrates should also be included in the differential diagnosis at this stage.
Because of deterioration of his condition, antimicrobial treatment with vancomycin 1 gr every 12 hours i.v. and ciprofloxacin 400 mg every 12 hours i.v. was started. Treatment with ceftriaxone continued, while clarithromycin was stopped. Despite the change of the regimen of antibiotics, the patient's condition continued to deteriorate and he was transferred to the intensive care unit (ICU), after a three-day hospitalization in the medical ward. On admission to the ICU, he was intubated due to severe respiratory failure (PaO2/FiO2 ratio 175, arterial pH 7.21, PaCO2=59 mm Hg). Laboratory testing showed white blood cell count =11,100/mm3 (polymorphonuclear cells = 89%), hemoglobin = 9.9 g/dl, hematocrit = 32%, platelets = 103,000/ mm3, serum urea 131 mg/dl, serum creatinine 1.7 mg/dl, C-reactive protein = 16.4 mg/dl, fibrinogen 935 mg/dl, and D-dimmer 544 ìg/l. A CT-scan of the chest showed extensive infiltrates in both lungs with pneumoceles (figure 2).
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