|Organism||Antibiotic (Ab) (alternative Ab)||Route||Dosage||Duration|
|IV||12 million U||(10–14 d)a|
|IV||≥12 million U||(10–14 d)a|
4 to 6 wk for endocarditis
Penicillin G and gentamicin
|12 million U daily|
20–24 million U daily for endocarditis
1.0 mg/kg q8h
|Oerskovia||Penicillin G, TMP–SMX|
|IV||(Moderate to high dosage)a||4–6 wk for endocarditis|
|IV||20 million U daily for endocarditis||6 wk|
Penicillin G ± aminoglycosides
|40 mg/kg (4 divided doses)|
250–500 mg QID
2 million U q4h (for endocarditis)
Until clinical response
|Rhodococcus||Vancomycin (V) or|
rifampin (AIDS) or
|1 g q12h|
500 mg q6h
500 mg–1 g QID
|Ampicillin or penicillin + gentamicin|
a Suggested by some authorities.
Abbreviations: TMP–SMX = trimethoprim–sulfamethoxazole; AIDS = acquired immunodeficiency syndrome.
Leuconostoc species are catalase-negative, gram-positive coccobacilli that have been increasingly recognized as human pathogens over the last decade. These organisms are normally found in dairy products and vegetable matter and are used in the production of wine, dairy products, and dextrans. Leuconostoc species are not considered part of the normal human flora, but they have been isolated from the feces, vagina, and gastric fluid, primarily in hospitalized patients. Immunocompromised patients and those treated with vancomycin, to which leuconostocs are intrinsically resistant, may have gastrointestinal colonization with these organisms.
Leuconostoc species may cause bacteremia in otherwise healthy neonates. At least four Leuconostoc species (including Leuconostoc mesenteroides, Leuconostoc paramesenteroides, Leuconostoc cremoris, and Leuconostoc citreum) may cause human infections. Risk factors for Leuconostoc infection include lengthy hospitalization requiring tracheostomy or parenteral nutrition, intravascular catheters, prior antibiotic therapy, prematurity, short gut syndrome, and serious underlying disease. Leuconostoc infections have been associated with pancreatitis, necrotizing enterocolitis, meningitis, and chylothorax to name a few.
Diagnosis is based on identification of the organism from cultures of blood or other sterile body fluids. On Gram stain the organisms appear as pairs or chains of slightly elongated gram-positive cocci that may appear rod-like. They may be difficult to distinguish from viridans streptococci, enterococci, lactobacilli, or pediococci. Helpful tests include the production of gas from glucose; a negative catalase, oxidase, and PYRase test; and the absence of arginine hydrolysis.
Leuconostoc isolates, like pediococci, are uniformly resistant to vancomycin and other glycopeptides. Most strains are susceptible to penicillin, clindamycin, and gentamicin. Susceptibility to the cephalosporins, quinolones, and trimethoprim–sulfamethoxazole (TMP–SMX) is variable. Daptomycin and linezolid show activity against Leuconostoc spp. Resistance to quinupristin/dalfopristin has been demonstrated. Penicillin, the drug of choice, should be given at relatively high dosages (≥12 million units daily). In the case of penicillin allergy or resistance, therapy should be based on results of susceptibility testing. Appropriate therapy may also include removal of potentially infected devices such as indwelling intravascular catheters.
Lactobacillus species are gram-positive rods that normally inhabit the human mouth, vagina, and gastrointestinal tract. More than 50 species of lactobacilli are recognized, many of which are used in the production of cheese, yogurt, pickles, and fermented beverages. Lactobacilli are widely considered to have low pathogenicity, and over the last decade have been used as probiotic factors (e.g., immunomodulation, microbe–microbe interactions, epithelial barrier protection), as part of prevention and treatment protocols for post-antibiotic enteric infections, vehicles for oral immunization, and as part of treatment policies called ecoimmunonutrition. Nevertheless, they have been reported to cause infections, including bacteremia, endocarditis, intra-abdominal and hepatic abscesses, meningitis, and pneumonia. Risk factors for serious infections caused by Lactobacillus species include underlying immunocompromised state (including human immunodeficiency virus [HIV] disease) and gastrointestinal surgery. Prior antibiotic therapy, particularly with vancomycin (to which most lactobacilli are resistant), has also been identified as a clinical risk factor. In patients with Lactobacillus bacteremia and endocarditis, cancer, recent surgery, and diabetes mellitus were identified as underlying risk factors. Additional history of dental infection or manipulation is common.
Diagnosis is based on identification of the organism from sterile body fluids. Lactobacilli are gram-positive rods, but they may appear coccoid if grown on solid media. Cultures grown in broth are more reliable for assessing morphology. Some Lactobacillus isolates may be difficult to distinguish from Leuconostoc species and streptococci. The combination of tests for gas production from glucose, arginine hydrolysis, PYRase, and carbohydrate fermentations should allow proper identification.
Intravenous penicillin (≥12 million units daily) is generally the drug of choice for serious infections. Endocarditis should be treated with penicillin 20 million to 24 million units daily plus gentamicin for 6 weeks. Lactobacilli are usually resistant to glycopeptides such as vancomycin. Susceptibility to cephalosporins and quinolones is variable, and most isolates are resistant to tetracycline and TMP–SMX. Most strains are susceptible in vitro to clindamycin, a possible alternative therapy in penicillin-allergic patients, but few clinical data are available. Lactobacilli are usually susceptible in vitro to linezolid but may be resistant to daptomycin and quinupristin–dalfopristin. Because of variable activity, susceptibility testing is critical in developing a treatment regimen. In the patient allergic to β-lactams who has endocarditis, penicillin desensitization should be considered.
Oerskovia and Cellulosimicrobium species
Oerskovia species are yellow, gram-positive, non-acid-fast organisms with extensively branched filaments. They were first described by Orskov in 1938 as “motile Nocardia.” Their usual habitat is soil, although they have also been isolated from decaying plant materials and grass cuttings. Two species of Oerskovia were originally recognized: Oerskovia turbata and Oerskovia xanthineolytica. Recently, O. xanthineolytica has been reclassified as Cellulosimicrobium cellulans, and O. turbata has been proposed for reclassification as a novel Cellulosimicrobium species. Both are rare causes of opportunistic infection in humans but should be considered as potential pathogens of low virulence, especially in the setting of indwelling devices. Reported infections caused by Oerskovia and Cellulosimicrobium species include native and prosthetic valve endocarditis, peritonitis, central venous catheter infections, bacteremia in immunocompromised hosts (including patients with acquired immunodeficiency syndrome [AIDS]), acalculus cholecystitis, prosthetic joint infection, keratitis, and endophthalmitis due to a penetrating eye injury. Several reported cases have been associated with exposure to soil, marine sediment, and bacterial contamination of hydrophilic contact lens solutions.
The diagnosis of Oerskovia and Cellulosimicrobium