A practical method for monitoring bacterial contamination of inhalation therapy machines.
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Biomedical subjects
Publications and source records attributed to D M Musher.
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Candidal infection after prosthetic arthroplasty has been reported in six previous cases, to which four cases are now added. Candida albicans was the offending organism in four patients, Candida parapsilosis in three, Candida tropicalis in two, and Candida (Torulopsis) glabrata in one. None of the 10 patients had evidence of disseminated candidiasis, and, except for the uniform presence of a prosthesis, other underlying factors that are generally associated with candidal infections were present in only three. Clinical features that distinguished periprosthetic from natural bone and joint infection included an older patient population, the usual lack of predisposing factors other than the prosthesis, and the absence of evidence of disseminated candidiasis. All patients were treated with removal of the prosthesis and antifungal therapy, consisting of amphotericin B alone (six patients) or combined with 5-fluorocytosine (three patients) or ketoconazole (one patient). Infection appeared to be cured in nine of the 10 patients, but the follow-up was less than 1 year in five cases. Replacement with a new prosthetic joint was attempted in only two cases and successful in only one. Direct inoculation of organisms during surgery or transient unrecognized candidemia may initiate periprosthetic infection, which might then be promoted by favorable local factors, both mechanical and molecular. The role of prosthetic materials, candidal adhesins, and human factors such as fibronectin in initiating these infections has yet to be characterized.
Between 1971 and 1987, 97 patients with polymicrobial bacteremia (PMB) were seen by a consulting infectious disease service. Seventy-four had severe underlying illnesses, and infection was hospital acquired in 80. PMB resulted from intraabdominal, urinary tract, or soft tissue infection in 45 patients, but a wide range of sources were implicated in the rest. Eleven patients had more than one source for the bacteremia, and, despite intensive diagnostic efforts, 24 had no identifiable source for at least one blood isolate. Bacteremia due to gram-negative bacilli most commonly occurred in intraabdominal, urinary tract, and wound infections; Escherichia coli and Klebsiella species were most frequently isolated. Streptococcus faecalis and Staphylococcus aureus were the predominant gram-positive isolates. Certain bacterial combinations seemed to provide a clue for predicting the source of PMB: for example, S. aureus together with gram-negative facultative rods usually arose from a skin or soft tissue source, whereas S. faecalis together with a gram-negative bacillus could often be traced to an intraabdominal infection. No unique clinical features appeared to predict the occurrence of bacteremia due to multiple rather than to a single organism. The mortality in patients was 21%, lower than has previously been described in PMB but similar to that reported for bacteremia due to a single organism.
Clostridium septicum is a major cause of spontaneous, nontraumatic gas gangrene. Unlike Clostridium perfringens, C. septicum is relatively aerotolerant and thus appears to be more capable of initiating infection in the absence of obvious damage to tissues. Six cases illustrate the clinical setting and fulminant nature of spontaneous gangrene caused by C. septicum. A lesion in the colon such as carcinoma is often present and is presumed to serve as a portal of entry to the bloodstream. Diabetes and leukopenia are also common predisposing conditions; compromise of vital host responses may facilitate proliferation of those organisms that settle out in the tissues. Acute lymphoma or leukemia during a course of chemotherapy is accompanied by damage to bowel mucosa and granulocytopenia, thus predisposing to spontaneous clostridial gangrene. Infection progresses in a fulminating manner; the majority of patients die within 24 hours of onset. Characteristic symptoms and signs include excruciating pain (although a sense of heaviness may be the only early symptom), swelling of tissues, crepitance, and bulla formation. A hallmark of C. septicum infection is the absence of acute inflammatory cells in involved tissues or in bulla fluid. A series of laboratory investigations demonstrated that fluid obtained from a bulla adversely affected the viability, morphology, and function of polymorphonuclear leukocytes (PMNs), which may explain the paucity of PMNs in involved tissues and may in part contribute to the fulminant progression observed in infection due to this organism.
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Four patterns of tissue involvement can be distinguished in sepsis due to gram-negative enteric bacilli. When intense local inflammation predominates, cellulitis or thrombophlebitis results, often with venous or arterial obstruction. Bacteria are present in the affected tissues, but not in sufficient numbers to be seen microscopically. When bacterial proliferation is unchecked by an appropriate leukocyte response, ecthyma gangrenosum, erythema multiforme, or diffuse bullous lesions may occur with minimal clinical or histologic signs of inflammation. In symmetric peripheral gangrene associated with disseminated intravascular coagulation, bland fibrinous deposits are seen in small vessels but neither inflammatory cells nor bacteria are present. The fourth kind of lesion is that seen in bacterial endocarditis. In all four patterns a vascular component is prominent clinically and histologically. The pathogenesis of these lesions is multifactorial; in each individual case the interaction between bacterial and host factors probably determines which clinical picture will result. The appearance of symmetric soft tissue lesions of the extremities in the absence of predisposing local conditions suggests the possibility of sepsis due to gram-negative bacilli, especially if other clinical features indicate that sepsis might be present.
This study involved cases of unexplained fever for which an infectious disease consultation was requested and for which an untoward drug reaction was thought responsible. Twelve cases that met strict criteria for drug-induced fever are presented. Antimicrobial agents were responsible for eight cases; other causes included antihypertensive and anticonvulsant drugs and allopurinol. The duration of drug administration before fever appeared was highly variable. Most patients had no history of previous drug reaction. Seven patients had fever with on other symptoms or signs that would suggest a diagnosis of drug-induced fever. Consultations are generally not requested for adverse drug reactions with more typical findings, such as skin rashes and eosinophilia; therefore, the true incidence of drug-induced fever is probably greater than indicated by the 12 definite cases seen in this general hospital during a six-year period.
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Technologic advances in thermometer design and conceptual advances in the understanding of homeostasis between 1700 and 1850 led to recognition of the usefulness of measuring body temperature in human disease. These advances took place in Europe and Great Britain, culminating in the publication in 1868 of the seminal work on fever in human disease by Carl Wunderlich. In the United States thermometry was popularized by a number of distinguished American physicians who used European data that had appeared in British and American journals even before 1868. Thus Edward Seguin and Austin Flint included fever curves and vital signs in articles that appeared in 1866. Flint and Jacob DaCosta added sections on thermometry to their medical textbooks in 1866-1867, and Edouard Seguin (the father of Edward) encouraged the use of thermometry by the public at large in a series of articles in the medical and lay press. Within just two decades thermometry became recognized as an indispensable medical tool, which it remains to the present time.
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