SUMMARY Bacillus cereus is a Gram-positive aerobic or facultatively anaerobic, motile, spore-forming, rod-shaped bacterium that is widely distributed environmentally. While B. cereus is associated mainly with food poisoning, it is being increasingly reported to be a cause of serious and potentially fatal non-gastrointestinal-tract infections. The pathogenicity of B. cereus, whether intestinal or nonintestinal, is intimately associated with the production of tissue-destructive exoenzymes. Among these secreted toxins are four hemolysins, three distinct phospholipases, an emesis-inducing toxin, and proteases. The major hurdle in evaluating B. cereus when isolated from a clinical specimen is overcoming its stigma as an insignificant contaminant. Outside its notoriety in association with food poisoning and severe eye infections, this bacterium has been incriminated in a multitude of other clinical conditions such as anthrax-like progressive pneumonia, fulminant sepsis, and devastating central nervous system infections, particularly in immunosuppressed individuals, intravenous drug abusers, and neonates. Its role in nosocomial acquired bacteremia and wound infections in postsurgical patients has also been well defined, especially when intravascular devices such as catheters are inserted. Primary cutaneous infections mimicking clostridial gas gangrene induced subsequent to trauma have also been well documented. B. cereus produces a potent β-lactamase conferring marked resistance to β-lactam antibiotics. Antimicrobials noted to be effective in the empirical management of a B. cereus infection while awaiting antimicrobial susceptibility results for the isolate include ciprofloxacin and vancomycin.

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Yersinia enterocolitica, a gram-negative coccobacillus, comprises a heterogeneous group of bacterial strains recovered from animal and environmental reservoirs. The majority of human pathogenic strains are found among distinct serogroups (e.g. O:3, O:5,27, O:8, O:9) and contain both chromosome- and plasmid (60 to 75 kb)-mediated virulence factors that are absent in "avirulent" strains. While Y. enterocolitica is primarily a gastrointestinal tract pathogen, it may produce extraintestinal infections in hosts with underlying predisposing factors. Postinfection sequelae include arthritis and erythema nodosum, which are seen mainly in Europe among patients with serogroups O:3 and O:9 infection and HLA-B27 antigen. Y. enterocolitica is acquired through the oral route and is epidemiologically linked to porcine sources. Bacteremia is prominent in the setting of immunosuppression or in patients with iron overload or those being treated with desferrioxamine. metastatic foci following bacteremia are common and often involve the liver and spleen. Of particular concern is blood transfusion-related bacteremia. Evidence has accumulated substantiating the role of Y. enterocolitica as a food-borne pathogen that has caused six major outbreaks in the United States. The diagnosis of Y. enterocolitica gastroenteritis is best achieved through isolation of the bacterium on routine or selective bacteriologic media. When necessary, serogrouping, biogrouping, and assessment for plasmid-encoded virulence traits may aid in distinguishing virulent from "avirulent" strains. Epidemiologically, outside of identified food-borne outbreaks, the source (reservoir) of Y. enterocolitica in sporadic cases is speculative. Therefore, prevention and control measures are difficult to institute.

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A 57-year-old male with a history of hypercholesterolemia and anxiety but otherwise in good health volunteered to donate the right lobe of his liver to his brother. The operation was performed uneventfully, without transfusion. Postoperatively he did well, until he developed tachycardia, profound hypotension, and coffee ground emesis on postoperative day 3. Despite resuscitative measures, he arrested and expired. Autopsy demonstrated gas gangrene of the stomach as the underlying cause of the hemorrhage and numerous colonies of Gram-positive bacilli were identified. Subsequent polymerase chain reaction (PCR) analysis identified these bacteria to be Clostridium perfringens (C. perfringens) type D. This patient's death was devastating, both to his family and his medical team. The impact of his death has transcended that of an individual occurrence. In conclusion, herein we present the facts and discuss this extraordinary example of florid clostridial infection and toxin-mediated shock. It was completely unexpected and probably unpreventable, and its cause was almost inconceivable. L iving donor liver transplants have been performed with increasing frequency. Formally and informally, 9 donor deaths have been reported. 1 -3 After performing more than 175 living donor liver transplants, we report the death of a donor in our program.The patient was a 57-year-old male with a history of hypercholesterolemia and anxiety but otherwise in good health, who volunteered to donate the right lobe of his liver to his brother. He had allergies to penicillin and bee venom. He took atorvastatin daily and clonazepam as needed. Preoperative evaluation followed our protocol. 4 Preoperative liver biopsy was normal. He was admitted the morning of surgery and received preoperative vancomycin and aztreonam.The operation was performed using previously described techniques. 5 The donor remained hemodynamically stable, required no transfusion, and was extubated in the operating room. Postoperative medications included epidural fentanyl, an H 2 -blocker, prophylactic antibiotics for 48 hours, and intravenous fluids. He stayed overnight in the recovery room and was transferred to the inpatient floor the following morning. Table 1 shows postoperative laboratory results. He was given liquids on postoperative day 1. Later, he felt so well that he asked his family for a lobster dinner from a local restaurant. The next morning, he felt well and sat in a chair. Temperature was 37.2°C, pulse was 79 beats per minute, and blood pressure was 126 / 69 mmHg. That evening, he complained of nausea and hiccups and was given metoclopramide and later thorazine. At midnight, his temperature was 36.8°C, his pulse was 115 beats per minute, and his blood pressure was 145 / 103 mmHg.Early on postoperative day 3, he was without complaints and sat in a chair. That afternoon, he again felt nauseated and had a small amount of guaiac-positive emesis. His tachycardia progressively worsened; 2 hours later he vomited again. Shortly thereafter, he became hypoxic and hypotens...

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