A comparative histopathological study of systemic candidiasis in association with experimentally induced breast cancer

Abstract

Abstract. systemic candidiasis is a fungal infection which coupled with solid malignancies places patients at high risk of succumbing to the disease. Few studies have shown evidence of the relationship between systemic candidiasis and malignancy-induced immunosuppression disease especially in breast cancer. At present, animal studies that exclusively demonstrate this relationship have yet to be conducted. the exact causative mechanism of systemic candidiasis is currently under much speculation. this study therefore aimed to demonstrate this relationship by observing the histopathological changes of organs harvested from female Balb/c mice which were experimentally induced with breast cancer and inoculated with systemic candidiasis. the mice were randomly assigned to five different groups (n=12). The first group (group 1) was injected with phosphate buffer solution, the second (group 2) with systemic candidiasis, the third (group 3) with breast cancer and the final two groups (groups 4 and 5) had both candidiasis and breast cancer at two different doses of candidiasis, respectively. Inoculation of mice with systemic candidiasis was performed by an intravenous injection of Candida albicans via the tail vein following successful culture methods. Induction of mice with breast cancer occurred via injection of 4T1 cancer cells at the right axillary mammary fatpad after effective culture methods. the prepared slides with organ tissues were stained with hematoxylin and eosin, periodic acidic schiff and gomori methenamine silver stains for a histopathological analysis. grading of primary tumour and identification of metastatic deposits, as well as scoring of inflammation and congestion in all the respective organs was conducted. statistical tests performed to compare groups 2 and 4 showed that group 4 exhibited a highly statistically significant increase in organ inflammation and congestion (p<0.01). The median severity of candidiasis in the kidneys and liver also increased in group 4 as compared to group 2. In conclusion, based on the above evidence, systemic candidiasis significantly increased in mice with breast cancer.

Tocotrienol-Adjuvanted Dendritic Cells Inhibit Tumor Growth and Metastasis: A Murine Model of Breast Cancer

“…Table 2 shows the differentiation of the primary breast tumor as well as lung and liver metastases in each group analyzed using the Kruskal-Wallis test for global comparison of organ metastases among group that was previously described [24]. From the test conducted, we found the p -value to be 0.005 ( p <0.05) for the lungs and liver.…”

“…The images showing the gross morphology of the lungs were captured digitally and the number of tumor nodules on the lungs were counted and recorded in all specimens. The analysis was done using Kruskal-Wallis Test for global comparison of organ metastases among the groups [24]. …”

“…For each group, sections from a minimum of three mice (n=3) were examined for histopathological changes. The analysis was done using Kruskal-Wallis Test for global comparison of organ metastases among the groups [24]. …”

Identification of airborne microbiota in selected areas in a health-care setting in South Africa

“…In addition, the presence of fungi in the health-care environment has also been implicated in numerous HAI cases. Although aerosolised fungi have been known mainly to cause food spoilage, literature has shown that airborne fungi may result in infectious diseases such as aspergilloses, candidoses, coccidioidomycosis, cryptococcosis, histoplasmosis, mycetomas and paracoccidioidomycosis [ 9 ].…”

Dectin-1 plays an important role in host defense against systemicCandida glabratainfection

“…The development of systemic candidiasis is the result of an imbalance between pathogen invasion and host defense response. 10 Fungi are recognized by the innate immune system via pattern recognition receptors (PRRs) which are predominantly expressed on myeloid cells, such as Toll-like receptors (TLRs) and C-type lectin receptors (CLRs). 11 Although all of the PRRs are involved in antifungal immune recognition, only CLR pathway mutations are associated with the spontaneous human fungal infections development.…”