Extradural abscess has been described infrequently as a complication of extradural anaesthesia and analgesia. We describe an abscess that developed 5 days after operation in a patient who had extradural anaesthesia for Caesarean section and postoperative analgesia, and review the literature on extradural abscess complicating extradural catheterization, including a discussion on pathogenesis, clinical presentation, diagnosis and management. There have now been 16 reported cases of extradural catheter-related extradural abscess. Only one previous case has been in obstetric practice, despite the widespread use of these techniques in this specialty. A disproportionate number of cases have involved thoracic catheters. Duration of catheterization ranged from 40 h to 6 weeks, the majority of catheters being in place for 5 days or less. The time from catheter placement to development of symptoms ranged from 72 h to 5 months. The causative organism was isolated in 11 cases: Staphylococcus aureus was identified in nine (82%) and Staphylococcus epidermidis in two (18%). Outcome was reported in 15 cases, of which seven (47%) had a full or near full recovery and eight (53%) had a persistent neurological deficit. One case was managed successfully without surgery. Fifty percent of all cases have been reported in the past 5 years. With the increasing use of extradural techniques for anaesthesia and analgesia, this serious complication may be seen more frequently in the future.
"Eradication of methicillin-resistant Staphylococcus aureus from a neonatal intensive care unit by active surveillance and aggressive infection control measures. " Infection Control and Hospital Epidemiology.26,7. 616-621. (2005).
Human infection with Rhodococcus equi is apparently rare with most published reports describing the development of lung abscesses in immunocompromised hosts. Of only 18 cases of infection previously recorded, four have recently occurred in patients with the acquired immune deficiency syndrome (AIDS). In Australasia, R. equi has frequently been isolated from soil and infected farm animals yet no human infections have been reported thus far. Three cases of R. equi infection have occurred in New Zealand and, collectively, they cover a wider spectrum of disease than that previously recognised. The natural history of R. equi infections, their clinical features and treatment are described in the light of our recent experience.
INTRODUCTIONA fundamental concept in the ecology of ectoparasite-borne disease is that of the reservoir, or the wellspring of the infection in nature during interepidemic periods. In the case of chigger-borne rickettsiosis (scrub typhus), it has often been argued that chiggers (larval trombiculid mites) are not only the vectors but also the true reservoirs of the infection and that the small mammals (theraphions) that serve as hosts of the chiggers are of no importance as a source of rickettsiae for the chiggers.' This point of view has been based largely upon several factors, namely, the known transovarian transmission of the causative agent, Rickettsia tsutsugamushi. from mother to progeny in certain species of chiggers,' the demonstration of the efficiency of the mechanism of transovarian transmission by Rapmund and his colleagues,+-" the difficulty or impossibility to show that chiggers can acquire R . tsutsugamushi while feeding on infected hosts in the laboratory,'. c -l l the fact that chiggers are unique among vectors in that in their lifetime, they are parasitic only in one stage (i.e., as larvae) and normally attach to, and feed upon, only one vertebrate and therefore could not acquire an infection from one such host and transmit it later directly to a second, and, finally, the widespread belief that chiggers do not imbibe blood but, instead, feed solely on serum exudate when in the parasitic stage and thus are unlikely to come in contact with pathogens that circulate in the blood of the host.', In the present paper, it is shown that, contrary to general belief, chiggers can acquire R . tsutsugarnushi while feeding on rickettsemic mice and that, when tested by pools of chiggers, this acquisition is relatively frequent. Persistence of acquired rickettsiae for at least 1-2 weeks in the chiggers is demonstrated, and a single case of presumed transovarian transmission to the next generation is reported. The preliminary data presented suggest, somewhat surprisingly, that in nature, under certain conditions, a small but perhaps significant proportion of chiggers may partially feed on one host and then later feed to repletion on a second one, raising the possibility that such "reattached" chiggers may * 91 92 Annals New York Academy of Sciences transmit acquired rickettsiae. These points, coupled with the observation in our laboratory that chiggers may, indeed, imbibe blood on o c~a s i o n ,~~ 5 , l2 indicate that theraphions may perhaps truly be of significance as a source of R. tsutsugumushi infection in chiggers in nature, even though the trombiculids themselves apparently constitute the prime reservoir of chigger-borne rickettsiosis.The approach in this study has primarily been concerned with the acquisition of R. tsrrtsugamushi by chiggers that were presumably free of natural infection; we utilized colonies of six species of chiggers that are known or suspected vectors of chigger-borne rickettsiosis and fed the chiggers on mice that had been inoculated with R. tsutsugumushi. The absence of natural infect...
The infection cycle of Rickettsia rickettsii, studied in slide chamber cultures of chicken embryo and L-929 cells, was found to be complex and did not conform to a one-step growth cycle. Initial uptake kinetics resembled those established for Rickettsia prowazekii, but subsequent events showed very marked differences. Intracytoplasmic growth commenced exponentially without measurable lag. However, very soon after infection, intracytoplasmic rickettsiae began to escape from the host cell into the medium in large numbers, resulting in (i) failure of large numbers of rickettsiae to accumulate in the cytoplasm, (ii) sustained rapid division of the organisms in the cytoplasm, (iii) substantial accumulation of extracellular rickettsiae, and (iv) rapidly spreading infection in the culture, with most cells infected in 48 to 72 h. In the occasional cell, rickettsiae were found in the nucleus, where they multiplied to form compact masses. Thus, analysis of the growth characteristics of R. rickettsii must consider the entire culture as a unit in which the rickettsiae are distributed among three compartments in which they behave in different ways: (i) intranuclear, (ii) intracytoplasmic, and (iii) extracellular. The rickettsial traffic is bidirectional across the host cell plasma membrane and dominantly monodirectional across the nuclear membranes. The implications of this behavior with respect to location and range of receptors and substrates involved in membrane penetration are discussed. In older cultures, unique intracytoplasmic ring or doughnut colonies were common, indicating a change in the intracytoplasmic environment. The possible significance of the growth characteristics in cell culture to the characteristics of infection in humans and animals is discussed.
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