Other Gram-Positive Bacilli

Microbiology

E. rhusiopathiae is a gram-positive, pleomorphic, non–spore-forming, nonmotile, encapsulated, aerobic or facultatively anaerobic bacillus. Older colonies can lose cell wall integrity, making them look like gram-negative or gram variable bacteria. The organism grows readily on standard media and in conventional blood culture systems. Both the rough and smooth colonies are noted on blood agar. Smears from rough colonies can show granular and nonbranching filaments. Some strains can cause α-hemolysis in 48–72 hours. E. rhusiopathiae is easily distinguished from other similar shaped, gram-positive bacteria ( Listeria species and Corynebacteriaceae) by an absence of motility, a negative catalase reaction, and hydrogen sulfide (H ₂ S) production. E. rhusiopathiae is oxidase and urease negative; it produces acid from glucose and lactose. A growth pattern in gelatin stab cultures that resembles a test-tube brush or a pipe cleaner is highly characteristic.

Epidemiology

E. rhusiopathiae, a ubiquitous organism, is primarily a pathogen of animals. It has been isolated from wild mammals; various fowl, fish, and shellfish; and from domestic animals, such as pigs, sheep, cattle, and horses. ^, Contaminated soil is thought to be a source. Human infections are often the result of occupational exposure to infected animals or contaminated animal products. People at risk include slaughterhouse workers, butchers, poultry workers, fishermen, fish marketers, veterinarians, farmers, and housewives. The incidence of human infection is higher in the summer months. A 4:1 male preponderance may reflect occupational exposure.

Clinical Manifestations

The three major types of clinical disease are (1) the most common form, a localized, recurring but usually self-limited, cutaneous form, known as erysipeloid, which resembles streptococcal erysipelas; (2) a diffuse cutaneous form, which manifests with multiple skin lesions and systemic symptoms; and (3) a systemic form, which is marked by septicemia and endocarditis. Erysipeloid is a painful, inflammatory lesion of the skin that usually involves the hands and fingers and commonly occurs at the site of a scratch contaminated through contact with animals or other infectious material. The incubation period is 1–7 days (usually <4 days) after inoculation. The lesion appears with a characteristic purplish red hue and irregular, raised borders that spread peripherally as central clearing occurs. The lesion can spread proximally to involve an adjacent joint. Erysipeloid lesions usually recover in 1–4 weeks.

The diffuse cutaneous form of E. rhusiopathiae infection, with progression of violaceous lesions remote from the initial site, is rarely reported; it is associated more frequently with systemic symptoms, such as fever, malaise, arthralgia, myalgia, and severe headache. Although this form of the infection is not accompanied by bacteremia, its clinical course is more protracted and often complicated by recurrences.

Septicemia and endocarditis are rare complications of E. rhusiopathiae infections, including occupationally acquired diseases. Of >50 reported cases of bloodstream infection (BSI) caused by E. rhusiopathiae, approximately 90% were associated with endocarditis, which manifests as an acute or subacute process and is preceded by erysipeloid lesions in only one third of cases. The infection commonly affects people of normal health. It also affects native heart valves, involving the aortic valve in 70% of reported cases. Approximately 40% of patients have had previous heart disease. Valvular degeneration and abscess are common, and intracranial complications have been reported. Some experts have questioned whether E. rhusiopathiae bacteremia has a predilection for association with endocarditis. Bacteremia without endocarditis has been reported in 26 humans with varied co-morbid conditions ranging from apparently healthy to diabetes, kidney disease, and malignancies requiring chemotherapy, or animal exposure.

A variety of other infections associated with E. rhusiopathiae have been reported, such as BSI resulting from colonic perforation by a toothpick, and BSI in patients with lupus nephritis, HIV infection, and Crohn disease. Conditions associated with E. rhusiopathiae infection have included chronic meningitis, vertebral osteomyelitis, pyogenic arthritis, infected arthroplasty, pneumonia, peritonitis associated with peritoneal dialysis, intra-abdominal abscess, spinal abscess, necrotizing fasciitis, and infection from cat bite. ^,

Reported pediatric infections include cutaneous infections, endocarditis; BSI with acute leukemia, systemic lupus erythematosus, and HIV infection; systemic disease and pleural effusions; empyema, septic arthritis, pyomyositis, osteomyelitis, and localized infection of the knee. ^{, ,}

Diagnosis

The diagnosis of erysipeloid relies on clinical recognition and an epidemiologic link to animal exposure. The organism is located deep in the reticular layer of the dermis; successful isolation from a skin lesion requires a full-thickness biopsy obtained from the peripheral quadrant of the lesion. E. rhusiopathiae is isolated from blood in patients with septicemia or endocarditis. An Erysipelothrix selective broth can be used to increase the yield. A high index of suspicion is necessary because these isolates occasionally are misidentified as streptococci or considered insignificant diphtheroids. ^, Serologic diagnostic methods are unreliable; however, polymerase chain reaction (PCR) methods and mass spectrometry have improved diagnostic accuracy, although not yet widely used in human disease. ^,

Treatment

Penicillin is considered the drug of choice for E. rhusiopathiae infections, based on exquisite susceptibility in vitro and limited clinical experience. Imipenem also has excellent activity against E. rhusiopathiae in vitro, followed by cefotaxime, clindamycin, and ciprofloxacin. Resistance was noted to aminoglycosides, chloramphenicol, erythromycin, teicoplanin, tetracycline, trimethoprim-sulfamethoxazole and vancomycin. E. rhusiopathiae’s resistance to vancomycin is noteworthy because this drug is frequently used as empiric therapy for endocarditis, especially in patients allergic to penicillin. Oral penicillin therapy usually is adequate for erysipeloid. E. rhusiopathiae BSI and endocarditis are best treated with aqueous penicillin G, 12–24 million units intravenously daily, in divided doses every 4 hours for 4–6 weeks. ^, No data are available to evaluate in vitro synergy with an aminoglycoside. Surgical intervention often is indicated for endocarditis. Alternative drugs for patients allergic to penicillin include cephalosporins, imipenem, and fluoroquinolones. ^{, , ,}

Microbiology

Rothia dentocariosa is a nonmotile, non–spore-forming, non–acid-fast, gram-positive bacillus with a variable morphology that includes coccoid and branching filamentous forms. Preferring aerobic conditions, R. dentocariosa grows less well in microaerophilic environments. The organism is slow growing and occasionally is isolated from anaerobic cultures that have been held longer than aerobic cultures. Colonies are either smooth and convex or rough with a “spoke-wheel” surface with scalloped edges. R. dentocariosa produces acid from glucose, sucrose, maltose, and glycerol; it is catalase positive and oxidase, indole, and urease negative (although urease-positive and catalase-negative strains have been identified). R. dentocariosa hydrolyzes esculin, reduces nitrate, produces hydrogen sulfide, and typically is identified correctly by commercial identification systems. Microbial identification also has been confirmed by 16S (small subunit) ribosomal RNA (rRNA) gene sequencing.

Epidemiology

R. dentocariosa, part of the normal flora of the human mouth, was first isolated from dental caries in 1949 and remains a constituent of carious teeth and adenoids. This organism’s pathogenic potential has been confirmed by a growing body of case reports, predominantly of infective endocarditis.

Clinical Manifestations

The first human infection involving R. dentocariosa, a periappendiceal abscess, was reported in 1975. Since then, rare R. dentocariosa infections in people of normal health have been reported: BSI, periodontitis, pericoronitis, maxillary cyst, pilonidal cyst, and endocarditis. Endocarditis associated with R. dentocariosa is reported most commonly. It typically involves native valves with preexisting cardiac abnormalities in patients with carious dentition or periodontitis, or who have undergone dental manipulation; occasionally prosthetic valves are involved. ^{, ,} Complications of endocarditis include valvular abscess, brain abscess, multiple intracranial hemorrhages, mycotic aneurysms, subarachnoid hemorrhages, and aneurysm, and vertebral osteomyelitis, spondylodiscitis. ^{, ,} A few patients also had an underlying malignancy. ^, Additionally, R. dentocariosa has caused pneumonia and BSI in patients with underlying lung cancer and leukemia; peritonitis associated with peritoneal dialysis; septic arthritis in an immunosuppressed patient with rheumatoid arthritis; and arteriovenous fistula infection in a diabetic patient undergoing hemodialysis. A proposed etiologic association with cat-scratch disease has not been verified.

Few R. dentocariosa infections have involved children. Reported cases include BSI without endocarditis (in a neonate) and complicating lymphoproliferative disease after renal transplantation, congenital heart disease, and herpangina. Case reports also include severe exudative tonsillitis in a healthy 4-year-old child and corneal abscess in an 11-year-old boy who licked his fingertip before rubbing his eye. ^, Fetal blood cultures grew R. dentocariosa in an intrauterine fetal death.

Treatment

Penicillin appears to be the drug of choice for R. dentocariosa infections, based on clinical experience of cure in patients with endocarditis. ^{, , , ,} Most treatments also included an aminoglycoside. Although data are limited, the organism consistently is susceptible in vitro to penicillins, cephalosporins, erythromycin, rifampin, and vancomycin; it is variably susceptible to clindamycin, aminoglycosides, tetracycline, and trimethoprim-sulfamethoxazole. Resistance to ciprofloxacin have been reported. ^{, ,} Determination of in vitro susceptibility is advisable because individual instances of β-lactam resistance and other variable resistance patterns have been described. Treatment failure has been observed in a few patients with endocarditis who initially were treated with vancomycin.