Moraxella lacunata or Morax-Axenfeld bacillus1 is a gram-negative, aerobic, and oxidase- and catalase-positive diplococcobacillus. Moraxella species are considered to be commensals of the upper respiratory tract, but they can be associated with otitis media in children and pharyngitis, sinusitis, conjunctivitis in adults. Moraxella lacunata has been previously reported most commonly to cause chronic follicular conjunctivitis and keratitis.5 In rare situations, it has also been known to cause endocarditis,2 septic arthritis4 and acute meningitis. Although Moraxella-related invasive infections have been exceedingly rare, we describe here the first case of M. lacunata causing septicemia and acute tubular necrosis in an immunocompetent patient.
A 34-year-old white man was referred to the emergency room by the family physician because of elevated blood urea nitrogen and creatinine. The patient presented to the primary care doctor with fever, chills, and rigors for 5 days. He also had nausea, vomiting, and loose watery nonbloody diarrhea without abdominal pain for 3 days before presentation. The patient had no significant medical history and returned from a trip to Israel 8 days before admission. He spent 12 days in Israel to attend to a wedding and bathed once in "holy water" from a natural warm water source. The patient's wife traveled with him but remained healthy. The patient was not taking any medications and had no known drug allergies. He worked in the food and nutrition department of an airline company as a supervisor. He denied smoking, alcohol abuse, and illicit drug use. The patient lived at home with his wife and 7 children, all of whom were healthy and did not have any gastrointestinal or upper respiratory symptoms. The patient denied contacts with sick people or pets. On admission, vital signs were stable, and temperature was 102.7°F. Physical examination was unremarkable except for bibasilar lung crackles. His blood urea nitrogen and creatinine were significantly elevated at 72 and 8.7 mg/dL, respectively (normal, 0003C13 and 1.3 mg/dL, respectively), respectively. His white cell count was 18,000/μL with 26% bands. He also had thrombocytopenia (platelet count, 29,000/μL), whereas his coagulation parameters were within normal limits. The urine sediment showed muddy brown casts, coarse granular casts, 5 to 10 white blood cells, and 10 to 20 red blood cells. Liver function tests suggested cholestasis with alkaline phosphatase of 177 U/L (normal, 0003C107 U/L), mild rise in both AST and ALT, and albumin of 2.1 mg/dL. Cardiac enzymes showed troponin I of 3.94 ng/mL (normal, 0003C0.08 ng/mL), creatine kinase of 25 U/L (normal, 24-170 U/L), and creatine kinase-MB of less than 4 ng/mL. Troponin I elevation was attributed to acute renal failure and sepsis. Electrocardiogram showed sinus tachycardia at 112 beats per minute without ST-segment or T-wave abnormalities. Chest radiograph suggested fluid overload and bilateral pleural effusions. Blood cultures were sent, and the patient was admitted to a medical floor. Empiric therapy with ciprofloxacin and ticarcillin-clavulanate was started. In 12 hours, blood cultures showed growth of gram-negative rods in the aerobic bottles. Echocardiogram was within normal limits with ejection fraction of 0.55 and no evidence of endocarditis. On hospital day 3, the patient suddenly became hypotensive, tachycardic, and disoriented. He was transferred to the intensive care unit with sepsis and acute tubular necrosis. His therapy was changed to imipenem-cilastatin and ciprofloxacin. Hepatitis serologies and autoimmune workup for renal failure were negative. Stool cultures grew normal enteric flora, and no ova and parasites were identified. The hospital microbiology laboratory had difficulty identifying the gram-negative organism in the blood culture, and the specimen was sent to the New York State Department of Health. Eleven days later, the organism was reported as M. lacunata. On hospital day 7, his fever resolved, diarrhea persisted, and renal function started to improve. By the time the causative organism was identified on day 11, antibiotics were discontinued because of the development of pruritic skin rash. The patient was discharged home on day 24 with normal blood cell count, blood urea nitrogen, and creatinine.
Moraxella strain identified in this patient was a gram-negative coccobacillus, oxidase- and catalase-positive, indole-negative, with relatively rapid growth on blood and chocolate agar, and no growth on MacConkey agar.1 It was identified as a Haemophilus-like organism by the rapid Neisseria-Haemophilus identification kit. The blood sample was then sent to the New York State Department of Health, where it was finally confirmed to be M. lacunata.
Bacteremia and, more importantly, sepsis due to Moraxella species are rare events. Moraxella is usually associated with conjunctivitis, keratitis, pharyngitis, otitis media, sinusitis, pneumonia, occasionally with endovascular infection or endocarditis,2 and very rarely with meningitis and septic arthritis.4 Moraxella bacteremia and sepsis have been documented mainly in immunocompromised and malnourished patients. Bacteremia complicated by sepsis syndrome in an immunocompetent patient is an unusual occurrence. In this case report, there are 3 points of interest: first, M. lacunata is an exceedingly rare cause of sepsis in a previously healthy person; second, acute tubular necrosis and gastroenteritis as presentation of invasive M. lacunata infection have never been reported in literature; and third, the geographic association of all reported M. lacunata cases.
On PubMed search and on review of literature within the past 25 years, we found only 5 documented cases of M. lacunata bacteremia, and none showed evidence of acute tubular necrosis. In Table 1, we summarize the cases of sepsis due to different Moraxella species, their clinical characteristics, complications, and outcomes. Table 2 shows presentation of M. lacunata infection without clinical sepsis. Majority of sepsis cases were caused by Moraxella catarrhalis (4 cases), next being M. lacunata (2 cases) and Moraxella osloensis (1 case). Of all reported cases, only M. osloensis sepsis was complicated by an acute renal failure.6,10 When the search was narrowed down to M. lacunata infection, we identified 6 cases. Five of them were cases of bacteremia,2 and one was a case of septic arthritis.4 The patient in the latter case also had vasculitis and nephrotic syndrome and subsequently developed chronic renal insufficiency 2 years later. However, the relationship of vasculitis and chronic kidney disease to Moraxella infection remained unclear. Our patient had an acute tubular necrosis and acute renal failure which completely resolved after successful treatment of sepsis. Most patients had underlying comorbidities, including prosthetic valves, malignancies, and autoimmune diseases unlike our patient who was immunocompetent. Moraxella organisms are usually susceptible to amoxicillin-clavulanate, piperacillin, ticarcillin, second- and third-generation cephalosporins, macrolides, fluoroquinolones, aminoglycosides, and trimethoprim-sulfamethoxazole and resistant to penicillin, ampicillin, methicillin, vancomycin, and clindamycin. The optimal duration of therapy is unknown and depends on the source of infection. Usual length of antibiotic treatment was found to be 6 to 8 weeks (range, 6-12 weeks). In our case, treatment continued only for 11 days with resolution of bacteremia and sepsis.
The literature details 2 fatal outcomes as in M. catarrhalis and M. osloensis sepsis. All patients with M. lacunata infection survived. Overall mortality rate due to invasive Moraxella infection in the described cases was 17%. Interestingly, the literature review revealed that 4 of 5 cases of M. lacunata endocarditis were reported from Israel. The significance of this information is not clear. It suggests 2 possibilities: either there may be a more virulent strain of M. lacunata circulating in that geographic area, or these rare infections are more efficiently diagnosed in Israel and subsequently reported in literature. Our patient, although born and raised in the United States, developed invasive M. lacunata infection after a trip to Israel. However, according to the Israeli Microbiology Surveillance Services that we contacted, there have been no cases of Moraxella infection identified in Israel within the proceeding 6-month period.
Based on the recent review of literature, invasive Moraxella infections are very rare and occur in persons with comorbidities. We describe the only case of M. lacunata sepsis presenting as acute tubular necrosis in a previously healthy person. The majority of M. lacunata endocarditis cases are reported from Israel. There were no similar cases reported as we contacted the department of health in Israel. Literature review on M. lacunata endocarditis shows 4 cases were reported from Israel, and this may be of geographical significance, suggesting a more virulent strain in the area. The optimal choice of antibiotics and the duration of treatment have not been defined, but a short 11- to 14-day course may be adequate for bacteremia without endocarditis. Prognosis in Moraxella sepsis depends mostly on the underlying medical condition.
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