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Citrobacter koseri (formerly classified as Citrobacter diversus ) is a gram-negative bacillus (GNB) that occurs as an opportunistic pathogen in neonates and immunocompromised patients. Citrobacter species have been implicated in nosocomial settings leading to infections involving the urinary tract, respiratory tract, liver, biliary tract, meninges, and even in rarer conditions-blood stream infection and infective endocarditis (IE). Gram-negative bacilli are responsible for 3% to 4% of all IE cases and have been traditionally associated with intravenous drug users. Patients with non-HACEK (species other than Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, or Kinglella species) GNB IE have poor clinical outcomes with higher rates of in-hospital mortality and complications. The American Heart Association (AHA) and Infectious Diseases Society of America (IDSA) both recommend the use of combination antibiotic therapy with a beta-lactam (penicillins, cephalosporins, or carbapenems) and either an aminoglycoside or fluoroquinolones for 6 weeks (about 1 and a half months) to treat IE due to non-HACEK GNB. Citrobacter koseri is becoming more recognized due to its inherent resistance to ampicillin and emerging drug resistance to beta lactams and aminoglycosides requiring carbapenem therapy. Our case is of a 75-year-old male with no previously reported history of primary or secondary immunodeficiency disorders who developed C koseri blood stream infection. His infectious work-up revealed mitral valve IE and septic cerebral emboli resulting in ischemic infarcts. This case illustrates the importance of recognizing GNB organisms as rising human pathogens in IE cases even without active injection drug use or nosocomial exposure., Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Odontogenic bacteremia, most commonly involving gram-positive oral flora, can result from daily self-care practices or professional dental procedures. Though usually transient and quickly cleared by the immune system, the presence of periodontal disease increases the frequency of exposure and risk of persistence of oral-systemic infections. Comorbidities such as asplenia, alcoholism, and immunocompromise increase the risk of complications of hematogenous spread and severe systemic illness. Capnocytophaga is a genus of anaerobic fastidious gram-negative bacilli, which is a common member of human oral flora, and its density is proportional to mass of dental plaques and periodontal diseases. Capnocytophaga spp that colonize humans are less virulent and are uncommon causes of bacteremia when compared with the Capnocytophaga typical of canines. C gingivalis has been rarely reported as a cause of disease in immunocompromised or immunocompetent hosts. In this article, we present a case of an immunocompromised 70-year-old man with poor oral hygiene, on methotrexate and prednisone for rheumatoid arthritis and sarcoidosis, who was admitted for chronic obstructive pulmonary disease exacerbation and developed C gingivalis bacteremia and septic shock after an episode of upper gastrointestinal bleeding. Poor oral hygiene in our patient is believed to have increased his risk as an immunocompromised patient to developing C gingivalis bacteremia. This case highlights the importance of oral care in immunocompromised patients especially while hospitalized, and those about to receive transplant, chemotherapy, or on immune modulators.

Soft tissue infections occur in over 30% of patients with chemotherapy-induced neutropenia. Gram-positive bacterial infections predominate early in neutropenia, and likelihood of infection by resistant bacteria and fungi increases with prolonged neutropenia. Prior infections and exposures influence the risk of rare pathogens. A 55-year-old woman with chemotherapy-induced neutropenia was scratched on her forearm by a dog. She cleaned the wound with isopropanol and was treated empirically with amoxicillin-clavulanate. Over the next 4 days, she developed fever along with erythema, edema, and mild tenderness of the forearm without purulence or crepitus. She was hospitalized and received empiric treatment with intravenous vancomycin, piperacillin-tazobactam, tobramycin, and voriconazole. Despite therapy, her fevers persisted and the cellulitis progressed for over a week. After 10 days of hospitalization, her neutrophil count began to recover and a bulla developed at the wound site. Culture of the bullous fluid grew Serratia marcescens, and antibiotics were switched to cefepime based on susceptibility. She defervesced and showed substantial improvement of cellulitis within 48 hours and was discharged on oral ciprofloxacin. Serratia marcescens skin infections are rare, and this may be the first report of Serratia cellulitis associated with trauma from dog contact. This case highlights the need to consider unusual pathogens based on exposure history and immune status and to obtain cultures from fluid collections or tissue in cases of treatment-resistant soft tissue infections.