This article reports 13 cases of pneumococcal septic arthritis and reviews another 177 cases reported since 1965. Of 2407 cases of septic arthritis from large series, 156 (6%) were caused by Streptococcus pneumoniae. Mortality was 19% among adults and 0% among children. Pneumococcal bacteremia was the strongest predictor of mortality. At least 1 knee was involved in 56% of adults. Polyarticular disease (36%) and bacteremia (72%) were more common among adults with septic arthritis caused by S. pneumoniae than among adults with other causative organisms. Only 50% of adults with pneumococcal septic arthritis had another focus of pneumococcal infection, such as pneumonia. Functional outcomes were good in 95% of patients. Uncomplicated pneumococcal septic arthritis can be managed with arthrocentesis and 4 weeks of antibiotic therapy; most cases of pneumococcal prosthetic joint infection can be managed without prosthesis removal. A fatal case of septic arthritis caused by a b-lactam-resistant strain of S. pneumoniae is also presented.Pneumococcal septic arthritis is described as "rarely encountered" [1] or "unusual" [2]. However, Streptococcus pneumoniae causes septic arthritis more often than is generally thought. Ispahani et al.[3] last reviewed pneumococcal septic arthritis in this journal, reporting 32 cases and reviewing 58 cases from large series published since 1965. We present 13 previously unreported cases and review 177 cases of pneumococcal septic arthritis reported in the English-language literature since 1965 , emphasizing the frequency of bacteremia and polyarticular disease among adults, the absence of extra-articular infection in many patients, and the emerging problem of pneumococcal antibiotic resistance. We report 2 cases of pneumococcal prosthetic joint infection and a case of pneumococcal arthritis in an adult that was caused by a strain of S.

The indistinguishable patient and cockatoo isolates strongly suggest that the patient's infection resulted from exposure to aerosolized cockatoo excreta. Although the incidence of cryptococcal infection due to such exposure is unknown, it may be prudent to advise immunocompromised patients to avoid pet birds and avian excreta.

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Treatment of K562 cells, a human erythroleukemia cell line, with desferrioxamine raised the levels of the receptor for transferrin (Tf) two-to threefold over that of the control cells. The levels of receptor were reduced by at least 50 and 35% of that of the control in cells treated with diferric Tf and ferric ammonium citrate, respectively. These changes were of total cellular receptors with no alteration in the proportion of receptors found on the cell surface. The half-lives of the receptor were identical in cells treated with desferrioxamine, diferric Tf, or ferric ammonium citrate. Cells metabolically labeled with [35S]methionine showed a 2.5-fold increase in the rate of receptor synthesis when treated with desferrioxamine and a 35 and 65% decrease when treated with ferric ammonium citrate and diferric Tf, respectively. In vitro translations of. polyadenylated mRNA isolated from cells incubated with desferrioxamine showed a 2.5-fold increase in translatable mRNA for the receptor, whereas treatment of cells with ferric ammonium citrate and diferric Tf resulted in a 25 and 50% reduction, respectively, in translatable mRNA for this receptor.Iron is an essential constituent of all cells. It is required for the normal functioning of a wide array of cellular enzymes, including those of the respiratory pathway (2, 4, 6). Cells receive iron via the receptor-mediated endocytosis of irontransferrin (Tf). Large amounts of iron can be stored in cells in ferritin and as hemosiderin. The iron needs of cells vary and are high in fetal, erythropoietic, and rapidly proliferating cells. Concomitant with these needs is a high level of expression of Tf receptors in placental cells, reticulocytes, and proliferating cells (1,8,10). It is not known exactly how cells regulate their iron uptake, but clearly the modulation of the number of Tf receptors can play a role in such regulation. Recently, Bridges et al. (Fed. Proc. 42:2193 and Mattia et al. (9) showed that K562 cells can alter Tf receptor numbers in response to intracellular iron chelation by desferrioxamine. The locus of this regulation was shown to be at the level of mRNA for the receptor (9). Ward et al. (12) reported a down regulation of Tf receptors in HeLa cells that were treated with iron salts. In this paper we report the extension of our studies on the regulation of Tf receptor biosynthesis in K562 cells. We show that delivering iron to cells results in a twofold decrease in specific synthesis of the Tf receptor. A decrease in the levels of mRNA is responsible for this drop. Furthermore, we compare the efficacy of Tf with that of ferric ammonium citrate in lowering receptor biosynthesis and establish the range of receptor regulation achievable with iron depletion or iron introduction without causing observable cellular toxicity.

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A rapidly fatal case of pulmonary tularemia in a 43-year-old man who was transferred to a tertiary care facility is presented. The microbiology laboratory and autopsy services were not notified of the clinical suspicion of tularemia by the service caring for the patient. Despite having a laboratory bioterrorism procedure in place and adhering to established laboratory protocol, 12 microbiology laboratory employees were exposed to Francisella tularensis and the identification of the organism was delayed due to lack of notification of the laboratory of the clinical suspicion of tularemia. A total of 11 microbiology employees and two persons involved in performing the patient's autopsy received prophylactic doxycycline due to concerns of transmission. None of them developed signs or symptoms of tularemia. One microbiology laboratory employee was pregnant and declined prophylactic antibiotics. As a result of this event, the microbiology laboratory has incorporated flow charts directly into the bench procedures for several highly infectious agents that may be agents of bioterrorism. This should permit more rapid recognition of an isolate for referral to a Level B laboratory for definitive identification and should improve laboratory safety.Francisella tularensis, a fastidious gram-negative coccobacillus, is an uncommonly encountered organism in most clinical microbiology laboratories. Nevertheless, the need for diagnostic laboratories to be familiar with this organism has taken on increased importance due to its possible use as a bioterrorism agent (4,7,8,10,13). F. tularensis has been classified as a Category A critical biological agent because it can be disseminated easily, causes high mortality with the potential for major public health impact, might cause public panic and social disruption, and requires special action for public health preparedness (3). It was reportedly developed as a weapon by both the United States (10) and the Soviet Union (1).Despite the presence in the clinical microbiology laboratory of a written procedure for working with agents of bioterrorism, including F. tularensis, the identification of F. tularensis isolated from a fatal case of pulmonary tularemia was delayed, resulting in the manipulation of the organism at the bench by laboratory workers, many of whom subsequently began taking prophylactic antibiotics. Although tularemia is rare, with approximately 200 cases annually in the United States, in Pike's study of 3,921 cases of laboratory-associated infections, it ranked second in the United States as a cause of laboratory-associated infections, behind only brucellosis, and third worldwide, behind brucellosis and typhoid (15).We report a fatal case of culture-proven tularemia and the associated laboratory investigation prompted upon learning of the cause of the patient's demise. We provide guidelines that will assist other laboratories in suspecting and more safely dealing with infections caused by this organism. Case report.A 43-year-old man with no significant past medical history pr...