Streptococcus viridans is usually considered to be nonpathogenic in healthy patients. Some strains become penicillin-resistant and cause life-threatening infections in immuno-compromised patients. We report an immunocompetent boy who had community-acquired S. viridans pneumonia that was resistant to penicillin. Clinicians should note local patterns of virulence and antibiotic resistance in S. viridans and adjust treatment strategies accordingly.

Key words: Community-acquired pneumonia, Drug resistance, Immunocompetent,

Streptococcus pneumoniae is the most commonly identified pathogen in community-acquired pneumonia. S. Viridans is not commonly related to community-acquired pneumonia. Most S. viridans strains are sensitive to penicillin; nevertheless, the rate of penicillin resistance has increased steadily worldwide. Herein, we report the case of an immunocompetent 4-year-old boy who presented with cough, intermittent fever, and dyspnea attributed to penicillin-intermediate-resistant S. viridans-related community-acquired pneumonia.

A 4-year-old boy presented with intermittent fever and productive cough for 2 weeks. He was given medications to alleviate the symptoms; however, high fever and shortness of breath were noted 4 days later. The parents stated that the boy had no history of aspiration, dental caries, or dental extraction. He had previously received a four-dose pneumococcal 7-valent vaccination. There was no history suggestive of food or drug allergy, chest pain, or oliguria.

On initial examination, the patient had fever with a temperature of 39ºC, a heart rate of 143/min, a respiratory rate of 28/min, blood pressure of 101/65 mmHg, and oxygen saturation on room air of 98%. Coarse breathing sounds combined with rhonchi over the right lung field were audible, and no heart murmur was revealed by physical examination. No skin rash was found over any part of the body. The remainder of the physical examination was unremarkable.

We prescribed empiric antibiotics with cefuroxime and azithromycin at first. However, spikes fever persisted over 2 days. Two blood culture specimens grew S. viridans that were intermediately resistant to penicillin (MIC = 0.5 µg/mL) but sensitive to ceftriaxone and vancomycin (MIC <0.5 µg/mL in both). Accordingly, the antibiotics were switched to ceftriaxone (600 mg every 6 hours; 100 mg/kg/day). Subsequently, we performed an echocardiogram that showed no regurgitation of the valves, no obvious vegetations, and normal left ventricular systolic function. The patient became afebrile and subjectively showed improvement within 24 hours of commencing intravenous ceftriaxone treatment. Blood culture, done 48 hours after beginning antibiotic treatment, was sterile. A recheck chest radiography 5 days after ceftriaxone therapy revealed only residual and small focal parenchymal consolidations over the right upper lobe. The species from our patient is identified as S. mitis. Therapy with ceftriaxone was changed to oral ceftibuten (200 mg daily), which was continued for 9 days. Consequently, the patient totally recovered without sequelae on follow-up, 1 month after discharge.

Viridans streptococci are often regarded as nonpathogenic bacteria; clinical isolation of S. viridans is usually attributed to specimen contamination. However, the organism is recognized as a cause of infective endocarditis in patients with valvular disease. In particular, it is commonly associated with dental caries followed by an episode of bacteremia and dissemination to remote sites. The lower respiratory tract is the most common site of infection [1]. In addition, S. viridans is recognized as an important cause of pneumonia and sepsis in neutropenic individuals [2]. Nevertheless, S. viridans is rarely reported to be the cause of pneumonia in immunocompetent patients, such as the case illustrated here.

In children with fever and neutropenia, Paganini and colleagues demonstrated an increasing incidence of viridans bacteremia paralleling the increasing use of histamine type 2 antagonists, the presence of oropharyngeal mucositis, prophylactic antibiotic treatment with cotrimoxazole or quinolones, severe neutropenia, and chemotherapy involving high doses of ARA-C [3]. Gingivitis and toothbrushes can play potential roles in viridans streptococcus bacteremia in immunodeficient patients [4]. However, no obvious predisposing factor has been identified in immunocompetent hosts with viridans bacteremia.

Gaudreau, et al. first reported the clinical relevance of bacteremia caused by S. viridans in 71 children in 1981 [5]. However, the report did not mention about the immune status of the children. In 1989, the first case series of primary pneumonia caused by S. viridans with bacteremia in healthy adults was reported and all of the cases were sensitive to penicillin [6].

In Brazil, Freitas, et al. reported that viridans streptococci rank as the second most frequent causal agent of community-acquired pneumonia in children under 5 years of age and that all of the affected patients appeared to be without underlying disease; in that study, other causes, such as degree of malnutrition or dental cavities, could not be excluded [7]. In our report, the patient did not have poor dental hygiene, malnutrition, or evidence of immune deficiency. Nevertheless, pneumonia was proved from chest radiography, and S. viridans bacteremia was identified from blood culture.

The overuse of antibiotics may increase the incidence of infection by formerly nonpathogenic organisms such as viridans streptococci and may be a potential cause of bacteremia and pneumonia in the absence of other pathogens. Clinicians should note any increased local incidence of community-acquired pneumonia due to viridans streptococci and should select empiric antibiotic therapy based on the local pattern of antibiotic susceptibility among recent clinical isolates.

Contributors: All authors were involved in all aspects of manuscript preparation.

Funding: None; Competing interests: None stated.

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