Fungi and parasites Flashcards
How does morphology aid pathogenicity of Candida albicans ? (dimorphic switch)
Candida is a unicellular yeast that reproduces asexually by budding. It switches to filamentous form when there is a change in pH, cell density, exposure to serum and iron deprivation. Yeast form is more easily disseminated through the bloodstream. FIlamentous form facilitates invasion and evasion of phagocytosis
What causes innate recognition of fungi?
recognition is mediated by interactions with conserved cell wall constituents: glucans, mannans and galactans (sugars)
What dendritic cell and macrophage receptor recognise fungal PAMPs?
Dectin-1 a highly conserved receptor on dendritic cells and macrophages.
activation of Dectin-1 results in tyrosine phosphorylation of ITAMs
TLR2 acts synergistically with dectin-1 that leads to sythesis and secretion of proinflammatory cytokines
Types of parasites
Nematodes (roundworms), trematodes (flukes) and cestodes (flatworms or tapeworms)
Schistosomes life cycle
In fresh water eggs hatch to form motile miracidia that infect snails. The miracidia undergo maturation and multiplication in the snail to release cercariae back into fresh water. The motile cercariae infect humans where they mature into male and female within the liver and lay eggs which are released into the bladder and secreted. They penetrate the skin using proteases and muscular action of their oral sucker
How does schistosoma infection lead to liver damage?
Pairs of worms release eggs int the bladder and intestines. laid eggs initatie immune resposne that encapsulates them in a granuloma and is excreted in urine or stool. Some eggs can be swept back into the liver, where granulomas slowly dissapate causing collagenous scars to coalesce and cirrhoisis develops, leading to obstruction of blood flow and creation of vascular by-pass channels called varices that can bleed and cause death.
Example of a protozoa parasitic infection?
Malaria
Trypanosome variable antigen types (VATs), best known in T. brucei
Trypanosomes can escape the hosts defences by antigenic variation of a series of variable antigen types. Each time the hosts antibodies are sucessful in eliminating infection, the parasites express a new VSG thus becoming a new VAT that the host has no antibodies against. Once the immune system produces an antibody to the new VAT the VSG changes again. This cycle repeats itself until the host dies or becomes asymptomatic
VSG - variant-specific surface glycoprotein
VSG coats the outside of the parasite to form a capsule. Large amount of the genome is dedicated to VSG. Only one VSG is transcriptionally active at one time and the rest is silent - another gene is switched on during change of VAT.
As VSG levels decrease the pathogen switches VAT
Asymptomatic trypanosome patients
They are asymptomatic as they have deveoped T cell-dependent immune response to invarient (protein part of the glycoprotein-VSG) components of VSG molecule associated with resistant hosts