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what are 4 basic microbes that can cause pathogens?
what kingdom are they each/
- bacteria: prokaryote
- viruses: non living
- fungi: eukaryote
- protoza: eukaryote
differences between bacteria and eu cells?
- nucleus: eukaryotes - membrane-bounded, bacteria: floating (also plasmids)
- RB: eukaryotes: 80S (60S & 40S), bacteria: 70S (50S & 30S)
- organelles: eukaryotes - mitochondria, golgi apparatus, lysosomes, peroxisomes and ER, bacteria: not those
bacteria divide by binary fission
what are the unifying princples of a) viral structures b) viral replication?
a) viral structures: all viruses package their genomes inside a particles that mediates transmission of the viral genome from host to host
b) viral replication: the viral genome contains the info for initiating and completing an infectious cycle within a susceptible, permissve cell.
what are capsids?
what is nucleocapsid?
The capsid surrounds the virus and is composed of a finite number of protein subunits known as capsomeres, which usually associate with, or are found close to, the virion nucleic acid.
nucleocapsid: capsid protein + viral nucleic acid
what is the baltimore classification system?
dsDNA viruses
ssDNA viruses
dsRNA viruses
(+)ssRNA viruses
(-)ssRNA viruses
ssRNA-RT viruses
dsDNA-RT viruses
what type of virus (from baltimore classification) is:
- coronavirus
- influenza
- HIV?
- coronavirus: (+)ssRNA viruses
- influenza:(-)ssRNA viruses
- HIV: ssRNA-RT viruses
Role of:
Reverse transcriptase ?
Integrase ?
Protease ?
RNA polymerase ?
Reverse transcriptase – turns +ssRNA into DNA
Integrase – integrates viral DNA with host genome
Protease – help create viral building blocks
RNA polymerase – forms mRNA before going to ribosome
basal cells of epidermis cells are attached to what?
what do adherens and desmosomes, tight junctions and gap junctions do in epidermis basal lamina?
basal cells of epidermis cells are attached to what?
what do adherens and desmosomes, tight junctions and gap junctions do in epidermis basal lamina?
how do you differentiate betweeen melanocytes and keratinocytes?
- *melanocytes**: smaller nucleus, cytoplasm looks like halo
- *keratinocytes**: brown looking
what do merkel cells do ? found? appearance?
- *merkel cells:**
- location: **stratum basale
- appearance:lobed nucleusanddenser cytoplasm.** looks like a bean. (hard to differentiate with melanocytes)
- function: underlying sensory nerve endings - light touch sensory. aso possess antigenic markers
what do merkel cells do ? found? appearance?
- *merkel cells:**
- location: **stratum basale
- appearance:lobed nucleusanddenser cytoplasm.** looks like a bean. (hard to differentiate with melanocytes)
- function: underlying sensory nerve endings - light touch sensory. aso possess antigenic markers
explain the major ways microbe adherence can occur [3]
adhesive hair-like structures
- *1. pili or fimbriae**: adhesive hair-like structures formed of proteins
subunits: major subunit - pili. minor subunit - tip - *2. afimbrial adhesin:**
- membrane or membrane anchored protein, interacting directly with host cell receptors.
- indirect interaction with hosts cell receptors via bridging molecules (e.g. fibronectin binding proteins)
- *3. biofilms:** adhesion to solid surfaces and infections
- community of bacteria that produce sugar polymer, known as extrapolymeric substance (EPS), allows biofilm to attach to a surface
what are the different stages of disease caused by a microbe?
- *1. incubation period**
- asymptomatic period
- *2. prodromal stage**
- vauge feelings of non-specific complaints
- *3. period of illness (invasion)**
- sympotmatic and more specific signs
- effects of toxins
- *4. convalescences**
- persons of immune system responds to infection (or medical intervention)
label these pls xoxo
why are biofilm associated infections really problematic? (2)
extreme resistance to antiobiotics and other anti-microbrial agents
- high resistance to host immune defences
whats hypersensetivity? give example of type II, III and IV?
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
Type II: IgG/IgM to patients own RBCs due to M. pneumonia
Type III: complement activation causing inflammation e.g. S. pyogenes causing glomerulonephritis
Type IV: T cell mediated e.g. TB granulomas
how does invasion of host cell oocur by bacterial invasion of host cells?
some bacteria promote their entry into non-phagocytic cells:
- *1. triggered invasion:**
- bacteria inject virulence factors into host cell cytoplasms to activate uptake by cell
- bacteria force the cell to extend local protrusion that engulf the bacterium
- = type 3 secretion system-dependent
- Salmnoella spp, Shigella flexneri
- *2. Zippered invasion:**
- bacteria produce outer membrane protein, with extracellular part exposed
- recognises receptor on target cell
- taken up by the cell
- specifc high affinity interaction between bacteria molecule and host cell receptor.
what is the complement system?
what are the three main functions?
- *group of blood soluble proteins:**
- 30 proteins circulate in inactive forms
- activated by pathogens detection
- chain reaction: activated proteins activate other proteins by cleavage
- *functions:**
- opsonisation (C3b and IGG): opsonins tag foreign pathogens for elimination by phagocytes
- membrane attack complex (MAC) (C5b): formation at surface of invading microbes of clustering of complement molecules. create a pore in microbe. leads to lysis and death
- enhance inflammation: activation and recruitment of phagocytic cells by anaphylatoxins (C5a & C3a), released by digestion of complement components
what is the complement system?
what are the three main functions?
- *group of blood soluble proteins:**
- 30 proteins circulate in inactive forms
- activated by pathogens detection
- chain reaction: activated proteins activate other proteins by cleavage
- *functions:**
- opsonisation (C3b and IGG): opsonins tag foreign pathogens for elimination by phagocytes
- membrane attack complex (MAC) (C5b): formation at surface of invading microbes of clustering of complement molecules. create a pore in microbe. leads to lysis and death
- enhance inflammation: activation and recruitment of phagocytic cells by anaphylatoxins (C5a & C3a), released by digestion of complement components
how do some microbes destory antibodies?
- create IgA proteases
- these destroy IgA (IgA coat foreign microbes with mucous)
which bacteria produce lipooploysaccharide (LPS)?
where located in bacteria?
made of? which part is toxic?
gram negative bacteria
location: outer membrane of bacteria cell wall
structure: lipid A, core polysaccharide, O antigen
lipid A = toxic
what are the 3 main type of exotoxins?
1. toxins that damage membranes: cytolysines and pore forming toxins. help spread of bacteria
2. toxins that act as enzymes: A/B toxins, more diverse group of toxins
- toxins that activate immune response: superantigens
cholera toxin:
- *-** produced by?
- what does it do in the body?
- does it induce ^?
Cholera toxin
produced by: Vibrio cholerae
effect: speeds up normal excreotry process in gut epithelium: massive fluid loss. diarrhoea
induces diarrhoea by:
- A-B toxin
- A part activates cell’s G-protein, modifies G-protein and keeps it in active state
- causes more and more production of adenylate cyclase: causes more cAMP
- this stimulates CFTR channel to have more Cl- leave cell: imbalance of electrolytes
- water follows Cl- and electrolytes
- causes severe diaarhea
- treatment: fluodsa and electroyltes
explain how A/B toxins work
what are the different subunits and what are their functions?
act as enzymes: most toxins acting as enzymes are A-B toxins
- 2 subunits: A&B
- A = enzymatic activity
- B = binds to cell membrane (allows A to go into cell(
