In this prospective, randomized study fluconazole and amphotericin B/5-flucytosine were compared in the treatment of systemic candidiasis. Seventy-two non-neutropenic intensive care patients with systemic Candida infections were enrolled. Thirty-six patients were randomly assigned to receive fluconazole (400 mg on the first day then 200 mg) and 36 were randomized to amphotericin B/5-flucytosine (1.0-1.5 mg/kg body weight every other day and 3 x 2.5 g flucytosine/day) for 14 days following the diagnosis. There was no statistically significant difference in clinical outcome in regard to the treatment of pneumonia and sepsis: 18/28 of the patients were treated successfully with fluconazole and 17/27 with amphotericin B/5-flucytosine. For the treatment of peritonitis, however, amphotericin B/5-flucytosine was more effective than fluconazole (55% vs. 25%). Furthermore, amphotericin B/5-flucytosine was found to be superior to fluconazole with regard to pathogen eradication (86% vs. 50%). Fluconazole was associated with less toxicity than amphotericin B/5-flucytosine.
A small-colony variant (SCV) of Staphylococcus aureus was cultured from a patient with a persistent wound infection (abscess and fistula) 13 months after herniotomy. The strain was nonhemolytic, nonpigmented and grew only anaerobically on Schaedler agar. As it was coagulase-negative, it was initially misidentified as a coagulase-negative Staphylococcus. In further analysis, however, the microorganism was shown to be an auxotroph that reverted to normal growth and morphology in the presence of menadione and hemin (Schaedler agar) and could be identified as a SCV of Staphylococcus aureus. Surgery and antibiotic treatment of the patient with flucloxacillin and rifampicin for 4 weeks resulted in healing of the chronic wound infection.
As compared to phenotypically normal (nu/+)NMRI mice showing the typical course of an experimental listeric infection, that of congenitally hypothymic (nude, nu/nu)NMRI mice was found to be characterized from the outset bya chronic trend. During the early phase of the infection, significantly reduced numbers of Listeria monocytogenes were observed in the spleens of nude mice.
Congenitally dysthymic nude (nu/nu) NMRI mice showed increased resistance to viable Listeria monocytogenes cells during the initial phase of infection as compared with euthymic control mice. The intravenous mean lethal dose (LD50), as determined for euthymic mice after an observation time of 7 and 14 days, amounted consistently to 6 X 10(4) Listeria. The corresponding values determined in nude mice were found to be increased by either 20-fold (1.2 X 10(6) Listeria after an observation time of 7 days) or 4-fold (2.4 X 10(5) Listeria after an observation time of 14 days). The transfer of spleen cells from immune euthymic donor mice into chronically infected nude mice caused almost complete elimination of Listeria within 1 week. The injection of dextran sulfate 24 h before a secondary infection with L. monocytogenes caused loss of antibacterial resistance in both chronically infected nude mice and Listeria-immune euthymic mice, this being expressed by a rapid increase in the numbers of bacteria in the spleens as well as the occurrence of serious signs of illness.
Young adult (6–12 weeks old) and aged (20–24 months old) NMRI mice were infected with various intracellular parasites. The following results were obtained: (1) After a sublethal infection with Listeria monocytogenes, aged mice were found to show a resistance similar to that of young adults. A challenge infection with this pathogen was followed by specific immunity of long duration in both age-groups. (2) On the other hand, young animals were significantly more resistant to Salmonellatyphimurium than aged mice. It was concluded that this was due to the LD50 which was 14 times greater for 2-month-old than for 20-month-old mice. Furthermore, during 7 weeks after infection there were more S. typhimurium in the spleens of senescent mice than in those of young adult controls. (3) Aged mice showed highly increased susceptibility to the weakly virulent DX strain of Toxoplasma gondii. Almost all aged animals died whereas the control mice survived. When death of the aged mice was prevented by treatment with sulfadiazine after infection with the DX strain, the aged mice were found to be as well protected against subsequent infection with the strongly virulent BK strain as the young adult mice. These results suggest that the susceptibility of the aged animal to infectious agents may considerably vary from one pathogen to another.
A 13-year-old patient developed severe shock due to administration of a Yersinia enterocolitica-contaminated red blood cell concentrate. Y. enterocolitica (serotype O:9, biotype II) was cultivated from the residual blood in the blood bag and from a stool sample of the blood donor. In the donor's plasma immunoglobulin M (IgM), IgA, and IgG antibodies against Yersinia outer proteins (YopM, -H, -D, and -E) were found. Since the donor remembered a short-lasting, mild diarrhea 14 days prior to blood donation, a transient attack of Yersinia enteritis may be associated with a longer than expected period of asymptomatic bacteremia that causes contamination of donor blood. Serological screening for IgM antibodies against Yersinia outer proteins might offer a way to reduce the risk of transfusion-associated Y. enterocolitica sepsis.
Parenteral injection of dextran sulfate 500 (DS 500; 50 mg/kg of body weight) into mice caused a complete loss of resistance to a sublethal (2 x 103 to 5 x 103) infection with Listeria monocytogenes. Such loss could be prevented by pretreatment of animals with 3 x 109 heat-killed Bordetella pertussis organisms (PO) 5 to 30 days before the administration of DS 500. The increased phagocytic capacity induced by PO was only exhausted when a fourfold dose of DS 500, effecting complete loss of antibacterial resistance (50 mg/kg of body weight), was administered. Listeriosis in mice treated with DS 500 is characterized by rapid-progressive necro-purulent inflammation of liver and spleen, lack of mononuclear phagocyte response, and 100% lethality within 72 h after infection. In contrast, the time course, extent, and morphological characteristics of listeriosis in animals pretreated with PO before the DS 500 application were not significantly different from those of nonpretreated controls. Evidence is presented that the protective effect of PO is due to activation of the mononuclear phagocyte system, which without such treatment is blocked by the DS 500 administration. The data presented indicate that the protective effect of PO is due only in part to the endotoxic moiety of these bacteria. Differences in the course and morphology of listeriosis in animals with dysfunction of the mononuclear phagocyte system and in animals with deficiency of the cellular immune system are discussed.
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