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Second video discussion  (Zoom)-VM3_Group5

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Uploaded by Sofiah Tajuddin on 2017-05-05.

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1. Several low virulent Candida albicans mutant strains: CM1613 (deleted in the Mitogen Activated Protein (MAP) Kinase MKC1), CNC13 (deleted in the MAP-kinase HOG1) and the morphological mutant 92’ were used as vaccines employing a murine model of systemic candidiasis

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1. HYR1 gene reduced phagocytic killing activity of C. albicans in vitro and increased tissue fungal burden in vivo.
2. Concordant with its positive regulation by the transcription factor Bcr1p, autonomous expression of HYR1 complemented the hypersusceptibility to phagocyte-mediated killing of a bcr1 null mutant of C. albicans in vitro
3. Vaccination with a recombinant Hyr1p significantly protected mice against hematogenously disseminated candidiasis
4. Anti-rHyr1p polyclonal antibodies enhanced mouse neutrophil killing activity by directly neutralizing rHyr1p effects in vitro. Thus, Hyr1 is an important virulence factor for C. albicans, mediating resistance to phagocyte killing

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1. Development of a vaccine against Candida spp. should induce both cellular and humoral immune responses. While the TLRs are strong inducers of inflammatory responses, it seems that the CLRs have the potential to modulate these responses by enhancement or inhibition of cytokine production
2. Three signals are critical for effective stimulation of an adaptive immune response: (a) the presentation of antigens by antigen-presenting cells (APC) on MHC-II to T-cell receptor (TCR) on naïve CD4+ T-cell, (b) the up-regulation of co-stimulatory molecules, and (c) production of cytokines that direct differentiation of a certain type of helper T-cell (Th) response
3. in experimental models of candidiasis in which it has been shown that the T-cells lead to protection against mucosal [28,29] and disseminated [30] C. albicans infections

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1. Vaccination with the recombinant N
terminus of Als1p (rAls1p-N) protects mice against disseminated and oropharyngeal candidiasis.
2. Vaccination of mice with a related candidate, rAls3p-N, induces
a broader antibody response than rAls1p-N and a similar cell-mediated immune response
3. The rAls3p-N vaccine was
equally as effective as rAls1p-N against disseminated candidiasis
but was more effective than rAls1p-N against oropharyngeal
or vaginal candidiasis
4. Immunization with the recombinant N terminus of Als1p (rAls1p-N) markedly improved survival of immunocompetent or immunocompromised mice infected via the tail vein with C. albicans

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Q.10--Describe the types & mechanism(s) of action for the antimicrobial drug

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Q.10--Describe the types & mechanism(s) of action for the antimicrobial drug

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Q.10--Describe the types & mechanism(s) of action for the antimicrobial drug

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Q.10--Describe the types & mechanism(s) of action for the antimicrobial drug

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Q.10-Describe the types & mechanism(s) of action for the antimicrobial drug

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Q.10-Describe the types & mechanism(s) of action for the antimicrobial drug

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How does the pathogen transmitted from host to host?

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How does the pathogen transmitted from host to host?

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1.part of normal flora in human body but can be transmitted from mother to child during birth and rarely spread through sexual intercourse.
2.People-to-people acquired infections mostly happen in hospital settings where immunocompromised patients acquire the yeast from healthcare workers

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Vaccines in the treatment of invasive candidiasis

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Recognition of Fungi and Activation of Immune Response

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Developed and produced for http://www.MechanismsinMedicine.com Animation Description: The initial steps in antifungal host defenses are recognition of invading fungal pathogens and activation of the immune response. This animation reveals how these pathogens make it into our system, and the subsequent immune response our body elicits to get rid of them.

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Immune defense againts C. albicans infection 

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Immune defense againts C. albicans infection 

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1)    Candida cell which normally reside at the gastrointestinal tract can invade the perotonium and blood stream when there is mucosal injury.

2)    Candida cell bind into opsonin. Candida may bind to the opsonin such as compliment and antibody.

3)    Recognition of Candida is facillitate by pattern recognition and opsonic receptor. Opsonized and non-opsonized Candida fungal particle bind to dendritic cell and macrophages.

4)    Candida fungal particle bind to cell surface pattern recognition receptors and activated. Intracelluar signaling cascade.

5)    MAPK are activated and additionally NFĸB is translocated to the nucleus. At the nucleus, gene for the cytokines and chemokines are transcribed.

6)    Cytokines and chemokines are synthesized and release from the macrophages and dendritic cell into the blood stream.

7)    Cytokines and chemokines activated monocytes and neutrophil for innate immune response. Activated monocytes and neutrophils are recruited to the area of the infected and damage tissue and will ingest or kill the pathogens.

8)    Activations of dendritic cells will also lead to antigen presentation and activation of T-helper responses that. This will lead to activation of second line defense which involved T cell and B cell which in turn will aid in pathogen elimination.

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- long-term usage of antibiotics.
(opportunist commensal C. albicans population increased significantly as the resident microflora populations knocked out by pro-longed usage of antibiotics)
- sexual intercourse with infected partner.
(contact transmission)
- immunocompromised patients such as AIDS patients and cancer patients receiving chemotherapy.
(patients with low immune system easily infected by C. albicans)
- diabetic patients.
(high blood glucose level favours C. albicans growth)
reference: http://cmr.asm.org/content/23/2/253.full

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- creamy white patches, thrush and may inflamed in mouth tongue or throat.
- reddish inflmmation on skin, sometimes scally.
- white or yellowish vaginal discharge ( "cottage cheese-like" vaginal discharge).
- feels of itchy and burning in genital area.
- itchy rash on the penis.
- high fever, chills, anemia (when infections had enter bloodstream).
reference:
http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0507.2012.02185.x/full