Disseminated Candidiasis in Leukopenic Dogs

Ehrensaft, Daniel V.; Epstein, Robert B.; Sarpel, Suleyman; Andersen, Burton R.

doi:10.3181/00379727-160-40377

Cited by 24 publications

(13 citation statements)

References 5 publications

(10 reference statements)

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“…This is evidenced by the high incidence of invasive and systemic candidiasis in neutropenic patients and those with qualitative neutrophil disorders (Odds, 1988). Experimentally, numerous studies in a variety of animal models have confirmed the critical role of phagocytic cells, especially PMNL, in resistance to systemic infections caused by Candida (Holm and Marwin, 1967; Elin et al , 1974; Ehrensaft et al , 1979). Additionally, PMNL are highly effective at killing C. albicans in vitro (Odds, 1988) and are considered to play a role in innate resistance against candidal infection at any mucosal site.…”

Section: Host Defense Mechanisms Against C Albicansmentioning

confidence: 99%

Immunity to Candida

2002

Oral Diseases

137

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Candida species are commensal fungal organisms as well as opportunistic pathogens of mucosal tissues. From the commensal relationship, most healthy individuals have demonstrable Candida-specific immunity. In immunocompromised persons, however, fungal infections caused primarily by C. albicans often occur. In HIV disease, up to 90% of HIV+ persons will have a symptomatic episode of oropharyngeal candidiasis (OPC) sometime during progression to AIDS, many of which become recurrent. In contrast, vulvovaginal candidiasis (VVC) and systemic Candida infections (candidaemia) are much less common during HIV disease, indicating the diversity and compartmentalization of the host response to Candida. Both innate resistance and acquired immunity play some role in maintaining C. albicans in the commensal state and protecting the systemic circulation. Polymorphonuclear leukocytes (PMNL) are critical for protection against systemic infections, whereas cell-mediated immunity (CMI) by Th1-type CD4+ T-cells is important for protection against mucosal infections. However, there is a discordant role for CMI at the vaginal versus oral mucosa, whereas little to no role for local or systemic CMI is evident at the vaginal mucosa. In contrast, there is a strong correlation between reduced blood CD4+ cells and the incidence of OPC, but it remains unclear whether systemic or local CMI is more important. Evaluation of systemic CMI in a cohort of HIV+ individuals with and without mucosal candidiasis revealed that Candida-specific CMI is not different between HIV+ persons with OPC or VVC and HIV- persons. Thus, the correlation of reduced CD4+ cell numbers to OPC may be explained by the requirement for a threshold number of systemic CD4+ cells to protect the oral mucosa together with the status of local immunity. Indeed, HIV+ persons with and without OPC had a Th2-type salivary cytokine profile suggestive of susceptibility to Candida infection compared with a protective Th0/Th1-type profile in HIV- persons. Candida-specific antibodies, although present, are controversial relative to a role in protection or eradication of infection. While studies of mucosal innate resistance are limited, we recently found that epithelial cells from saliva and vaginal lavages of healthy individuals inhibit the growth of Candida in vitro. This epithelial cell anti-Candida activity requires cell contact by viable cells with no role for soluble factors, including saliva. Interestingly, oral epithelial cells from HIV+ persons with OPC had significantly reduced activity, indicating some protective role for the epithelial cells. Taken together, these data suggest that immunity to Candida is site-specific, compartmentalized and involves innate and/or acquired mechanisms from systemic and/or local sources.

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Section: Host Defense Mechanisms Against C Albicansmentioning

confidence: 99%

Immunity to Candida

2002

Oral Diseases

137

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“…Although they were affected in the number as well as in the functional activity of several immune cells [12,16], the cyclophosphamide-immunodepressed mice might maintain some ability to cope with non-pathogenic species. Experiments were therefore conducted to test the candidacidal activity in-vitro of PMN and SC effectors obtained from either untreated or Cytreated donors.…”

Section: In-vitro Anti-c Aibicans and Anti-c Parapsilosis Activity mentioning

confidence: 99%

In-vitro killing ofCandidaspecies by murine immunoeffectors and its relationship to the experimental pathogenicity

Vecchiarelli¹,

Bistoni²,

Cenci³

et al. 1985

Med Mycol

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Killing of yeast cells of several species of Candida by murine phagocytic cells was assessed in vitroby a radiolabel release microassay and measurement of colony forming units. The most effective candidacidal phagocytes, i.e. polymorphonuclear and bone marrow ceils, were able to kill equally well cells of any species or isolate tested, given sufficient time (4 h) and an appropriate effector: target ratio. However, C. guilliermondii, C. krusei and C. parapsilosis were killed by polymorphonuclear and bone marrow ceils much more promptly (1 h) and at a significantly lower effector:target ratio than C. albicans, C. tropicalis and C. viswanathii. Moreover, there were immune effectors such as peritoneal resident macrophages and, mostly, spleen ceils which were practically ineffective against C. albicans and C. tropicalis but showed significant activity against C. guilliermondii, C. krusei and C. parapsilosis, even in mice immuno-depressed with cyclophosphamide. Three isolates of C. albicans, differing in the capacity to form germ tubes, also differed in mouse virulence: the germ-tube forming isolate was the most virulent. However, they showed an identical pattern of susceptibility to killing by mouse immunoeffectors, suggesting that virulence is probably not due to the resistance of hyphal cell to phagocytosis.In a previous study on the experimental pathogenicity of Candida species, we observed that isolates of C. albicans, C. tropicalis and, to a lesser degree, C. viswanathii were distinctly pathogenic in comparison with isolates of C. parapsilosis, C. krusei and C. guilliermondii, which showed no significant pathogenicity for untreated or cyclophosphamide-immuno-depressed mice [5]. The host-Candida interaction is complex and many factors may contribute to the expression of the pathogenic potential of any given species or isolate. Production of mycelium [26,28,31,33] release of toxic substances or virulence enzymes [6,7,19,23,27] and modulation of adherence properties [17,18] are examples of factors that specifically affect virulence. The capacity of Candida species to resist destruction by host phagocytes has also been emphasized by several authors [22,30,32; for a review, see Odds, 26].

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“…A number of studies have focused on the role of granulocytes in disseminated candidal infection (16)(17)(18) and in experimental cutaneous candidiasis (25). Both in dogs (16) and in mice (17) a marked increase in the severity of a candidal infection was found after treatment with cyclophosphamide, while in nitrogen mustard-treated granulocytopenic mice, pulmonary clearance of Candida albicans was delayed with subsequent dissemination of the infection (18).…”

Section: Discussionmentioning

confidence: 99%

“…Most investigators have concentrated primarily on T celldependent cellular immunity and the role of activated macrophages (1)(2)(3)(4)(5)(6)(7)(8)(9), although in the acute phase of an experimental candidal infection in mice the infiltrate in the kidneys consists predominantly of granulocytes (10). Although a number of studies have shown the enhancing effect of cytostatic treatment on experimental candidal infections, these studies do not elucidate the relative contributions of granulocytes and monocytes to natural resistance against systemic candidiasis (16)(17)(18)(19). Although a number of studies have shown the enhancing effect of cytostatic treatment on experimental candidal infections, these studies do not elucidate the relative contributions of granulocytes and monocytes to natural resistance against systemic candidiasis (16)(17)(18)(19).…”

mentioning

confidence: 99%

Contribution of granulocytes and monocytes to resistance against experimental disseminatedCandida albicans infection

Wout

Linde

Leijh

et al. 1988

Eur. J. Clin. Microbiol. Infect. Dis.

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The aim of the present study was to investigate the contribution of granulocytes and monocytes to resistance against an acute systemic candidal infection in mice. To this end granulocytopenia and monocytopenia were induced by irradiation or treatment with cyclophosphamide, and monocytopenia was obtained by treatment with VP-16. After intravenous injection of 1 X 10(4) Candida albicans into mice irradiated with 8 GY, the number of Candida albicans cultured from the kidneys, expressed as the geometric mean of the number of CFU/g tissue, was 5.4 X 10(4), 7.1 X 10(6) and 5.8 X 10(7) on days 1, 3 and 5 of infection respectively (p less than 0.001 compared to normal mice). The number of Candida albicans cultured from the liver and spleen was also significantly higher for irradiated animals than for normal mice (p less than 0.001). For cyclophosphamide-treated mice the number of organisms in the kidney (1.7 X 10(4) CFU/g on day 1, 1.9 X 10(6) on day 3 and 3.8 X 10(6) on day 5 of infection) and spleen was significantly higher (p at least less than 0.02) than for normal mice after injection of 1 X 10(3) Candida albicans. Monocytopenia induced by VP-16 did not result in an increase in the number of Candida albicans cultured from the kidney or spleen after infection. From these studies it is concluded that granulocytes and not monocytes or exudate macrophages play an important role in resistance against Candida albicans during the first five days of a systemic infection.

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Disseminated Candidiasis in Leukopenic Dogs

Cited by 24 publications

References 5 publications

Immunity to Candida

Immunity to Candida

In-vitro killing ofCandidaspecies by murine immunoeffectors and its relationship to the experimental pathogenicity

Contribution of granulocytes and monocytes to resistance against experimental disseminatedCandida albicans infection

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