Lactobacillus endocarditis is hardly a new entity. A PubMed literature search using the term "lactobacillus endocarditis" uncovered a case report from the German literature dating back to 1955.1 Scattered case reports and several case series have been published over the ensuing years.2-8 New mechanisms of disease pathogenesis have altered the clinical appearance of lactobacillus infections. Probiotic agents, serving as an entry vehicle for lactobacillus, are a relatively new risk factor identified in the genesis of these infections. Clearly, lactobacillus infections are not emerging infections, but could they be re-emerging, given this new mechanism of disease pathogenesis?
A 42-year-old white man, with a history of mild mental retardation and surgery during childhood to remove a vascular ring surrounding the great vessels which compressed the trachea and esophagus, was admitted to the hospital after an outpatient transthoracic echocardiogram revealed posterior mitral valve vegetation and an atrial secundum defect. All historical information was confirmed by the patient's mother. The patient had been feeling unwell over the past several months, complaining of fatigue, 10-lb unintentional weight loss, intermittent fever (unmeasured), chills, right upper quadrant abdominal pain, shortness of breath, occasional heartburn, and a poor appetite. He was treated for sinusitis twice before admission: 8 weeks prior with azithromycin and 6 weeks prior with trimethoprim-sulfamethoxazole. He had not been to the dentist in the past year and denied ingestion of probiotics, vitamins, or excessive amounts of dairy products as part of his diet.
Upon admission, the patient was afebrile; temperature, 97.2°F; pulse rate, 108 beats per minute; respiration rate, 20 breaths per minute; and blood pressure, 81/55 mm Hg. There were no cutaneous stigmata of endocarditis. His dentition was in a poor state of repair, with numerous missing, broken, and carious teeth. A II/VI soft early systolic murmur became crescendo as systole ended without a diastolic component. His chest was clear. There was mild right upper quadrant abdominal tenderness without hepatosplenomegaly, masses, guarding, or rebound. Normoactive bowel sounds were ascultated. There was no peripheral edema. Laboratory examinations demonstrated a white blood cell count of 8300/μL with a normal differential; hemoglobin, 10.7 g/dL; and platelet count, 129,000/μL. Blood chemistry evaluation showed sodium of 129 mEq/L; chloride, 95 mEq/L; potassium, 3.2 mEq/L; bicarbonate, 23 mEq/L; blood urea nitrogen, 13 mg/dL; and creatinine, 0.9 mg/dL. Westergren erythrocyte sedimentation rate was measured as 30 mm/h (normal, 0-30 mm/h). Rheumatoid factor was significantly elevated. Urinalysis was unremarkable without proteinuria or hematuria. Three sets of blood cultures were obtained.
Seventy-two hours after admission, all blood cultures grew gram-positive bacilli, which were identified as Lactobacillus casei (Fig. 1). The patient had low-grade, nonsustained, intermittent temperature elevations, never above 101°F, during the first week of hospitalization. He was initially started on ampicillin/sulbactam but was switched to ertapenem. After susceptibility testing demonstrated resistance to ceftriaxone, vancomycin, and the carbapenem class, he was prescribed ampicillin and gentamicin. Repeat blood cultures eventually became negative. A transesophageal echocardiogram confirmed the presence of the mitral valve vegetation, severe mitral insufficiency, atrial septal defect, and moderate tricuspid regurgitation. Because of his poor dental health, a full extraction was performed 13 days after admission. Three days after his dental work, he underwent a mitral valve replacement with repair of the atrial septal defect (Figs. 2 and 3).
Six days after his valve replacement, the patient was discharged to home, where he completed a 6-week course of intravenous antibiotic therapy administered through a peripherally inserted central catheter. He had no complications during his outpatient treatment and currently remains well.
Lactobacillus species are gram-positive, facultative anaerobic bacteria that are normally found in the oral cavity, gastrointestinal tract, and female genitourinary tract. Although they are uncommon causes of infection and bacteremia, Lactobacillus species fortunately are associated with low mortality rates.2,9 These bacteria account for less than 1% of recovered organisms from blood cultures overall and have been implicated as pathogens in bacteremia, dental caries, infective endocarditis, endometritis, urinary tract infection, liver abscess, meningitis, and splenic abscess.2,9 Immunocompromised patients are more vulnerable to infection with Lactobacillus species, and bloodstream infections have been described in AIDS patients3 and in patients with carcinoma and accompanying neutropenia.10 Published reports demonstrate lactobacillus bacteremia occurring after endoscopy,5 colonoscopy,6 appendectomy,7 after dilatation and curettage,11 and continuous ambulatory peritoneal dialysis.12 Lactobacillus overgrowth may occur in patients with short bowel syndrome and may lead to D-lactic acidosis.13 Lactobacilli are commonly isolated from polymicrobial infections; moreover, the presence of lactobacillemia may be a marker of serious or fatal disease. However, identification of lactobacillus to the species level occurs only in half of all isolates, whether microscopic studies, colony morphology, growth on agar medium, or molecular methods are used.
Lactobacillus endocarditis was first described in 193814 and is estimated to represent 0.05% to 0.4% of all endocarditis cases.15,16 There have been many attempts to determine predisposing risk factors leading to infection. Classically, lactobacillus endocarditis has been linked to structural heart disease, invasive procedures, prosthetic valves, heart transplantation, and dental infection or procedures.4,17 It has been postulated that those Lactobacillus species causing endocarditis have shown a greater ability to bind collagen and fibrinogen, aggregate platelets, and produce both glycosidases and proteases which allow for survival and colonization of vascular surfaces.18
Even with appropriate antimicrobial treatment, lactobacillus endocarditis may lead to recurrent infection or death. Many strains are naturally resistant to vancomycin, and case reports have documented endocarditis caused by vancomycin-resistant Lactobacillus species, additionally resistant to cephalosporins and quinolones.19,20 Lactobacillus bacteremia and endocarditis are effectively treated using synergistic therapy with penicillin and gentamicin. On occasion, valve replacement may be necessary.21
Aside from preventing the spoilage of food, lactobacilli play an important role in preventing the overgrowth of pathogenic microorganisms in the human gastrointestinal and genitourinary tracts. Probiotic administration diminished Helicobacter pylori colonization of the stomach22 and decreased nasal colonization of potentially pathogenic bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, β-hemolytic streptococci, and Haemophilus influenzae.23 Probiotics have been studied for the prevention and therapy for antibiotic-associated diarrhea and diarrhea caused by infectious agents. Treatment with lactobacillus has been shown to reduce the duration and frequency of infectious diarrhea24,25 and decrease the severity of diarrhea.26
There has been a renewed interest focused on the use of probiotics, specifically the role of lactobacillus as a pathogen.27,28 With the recent changes in dietary habits, vitamin usage, and consumption of over-the-counter supplements, a prudent physician, as a matter of routine, would probe their patients' history and background for these epidemiological links to uncover the potential source of uncommon infectious diseases. Common food sources where lactobacilli are found include milk, cheese, sauerkraut, yogurt, and other fermented items. For several years, probiotics (such as those containing Lactobacillus spp) have been considered beneficial and safe to humans. Although pathogenesis and infection are extremely rare, there has been much debate about whether probiotics may lead to infection.29 In Finland, where there has been strong consumption of these agents, there has not been an elevation from the baseline rate of lactobacillus infections.30 However, there have been clinical isolates recovered that are indistinguishable (using molecular methods) from the probiotic strain of lactobacillus, but differ on their phenotypic properties.31 Whether lactobacilli will become a more prominent pathogen remains undecided at this time.
The presence of lactobacillus in a blood culture should not be routinely considered a contaminant, and careful analysis of the patient's clinical status is required. When determined to be the cause of either bacteremia or endocarditis, it should be treated aggressively and accordingly. With the isolation of lactobacillus from infected sources, linkages to diet and probiotic consumption should be sought.
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