Adherence, Colonisation and Invasion Flashcards

1
Q

Virulence steps

A

contact
adhesion
Invasion
infection

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2
Q

adherence

A

It is the enhanced ability of M to attach to host tissues
-it is neccessary but not suffficient to start a disease
-There are many different receptors coating the P and the tissue where it binds

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3
Q

Adhesions

A

Glycoproteins or lipoproteins found on P surface that enable it to bind to host cells

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4
Q

Virus adhesion

A

Viruses attach to receptor molecules on cell surface, these can be proteins, carbs or lipids
-they have a single primary receptor as well as co-receptor ( HIV-1: CD4 and CCR5, CXCR4)

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5
Q

Attachment factors

A

Low affinity receptors that are involved and facilitate an initial low affinity binding which is initial step

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6
Q

Heparan sulfate

A

-Found in ECM
-Serves as an attachment factor for many viruses, therefore these receptors have low specificity

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7
Q

Binding NB

A

serves to overcome repulsive electrostatic forces

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8
Q

Viral receptors

A

-diverse
-Have own cellular function ( cytomegalovirus binds to epidermal growth factor, EGF is a powerful mitogen)
-Viruses (V) subvert cell receptors/proteins to utilise them to gain entry
-dictate cell tropism

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9
Q

E. B binding

A

S.aureus binding is facilitated via fibrinogen using the N2 and N3 domains of its SDrG adhesion protein
-Opa adhesion proteins of Neisseria species attach to carcinoembryonic antigen related adhesion molecules (CEACAM) on epithelial surface

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10
Q

Capsules

A

It is a thick hydrated polysaccharide-based( or peptide based) coating outside the plasma membrane and celll wall

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11
Q

Capsule function

A

-Sticky and contains specific receptors to facilitate attachment on host tissues
-Capsules found in encapsulated strains of Streptococcus pneumonia protect from phagocytosis

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12
Q

Fimbriae, Flagella and Pili

A

surface protein structures that function in attachment
-pili are longer and fewer in number than fimbriae
-pili used in horizontal gene transfer (conjugation)

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13
Q

Fimrbia and flagella adhesion

A

-Flagella facillitate adherence to host cells
-Fimbriae possess adhesins which alow for attachment to cells or ECM
-E.coli use them to attach to mannose receptors

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14
Q

Colonization

A

Growth of micro-organisms after they’ve gained access to host tissue

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15
Q

Biofilms

A

A hydrogel composed of polysaccharides, proteins, lipids and DNA that comprises a consortium of bacteria/M that adhere to one another within the gel matrix

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16
Q

Biofilm phenotype effect

A

-B within biofilm are physiologically distinct from planktonic cells
-They are more protected, exhibit communal behaviour
-undergo a phenotypic shift and express/regulate different protein sets
-antibiotic resistance

17
Q

E. biofilms

A

Pseudomonas aeruginosa are opportunistic P that form biofilms on hospital equipment and on damaged tissue surfaces (burns)

18
Q

Invasion

A

-Dissemination of a P throughout local tissues or body
-P may produce exoenzymes or toxins which allow them to colonise and damage host tissue as they spread deeper
-P may also produce virulence factors (mainly enzymes) to protect them against immune system defences
-A P’s specific virulence factors determine degree of tissue damage

19
Q

E. specialised enzymes

A

H.pylori
-Contact with stomach acid keeps the mucin lining the epithelial cell layer in spongy-like state that is impermeable to H.pylori
-B releases urease which neutralises stomach acid by forming ammonia from urea hydrolysis
-This causes mucin to liquify which allows B to swim through it

20
Q

exoenzymes

A

-Virulence factors that facilitate invasiveness
-Invasiveness requires P to break down host tissues to gain access to deeper or distal tissues
-includes: Hyaluronidase, Coagulase and streptokinase

21
Q

Hyaluronidase

A

-catalyses the hydrolysis of hyaluronan, a constituent of the ECM which increases tissue permeability
-Other enzymes that degreade ECM include collagenase, chondroitin sulfatase, neuramidase
-streptococcus pyogenes

22
Q

Coagulase and streptokinase

A

-When staphylococus aureus enter cut, they produce coagulase
-Clot walls off pathogen, blocking access to immune cells
-When P has produced enzymes to fight immune system, streptokinase dissolves clot which release P to bloodstream and deeper tissues
Streptococcus pyogenes

23
Q

Local infection

A

-Confined to small area of body, typically near point of entry (like boil with staphylococcus)
-P is largely contained to location
-Include urinary tract infections confined to bladder or pneumonia to lungs

24
Q

Focal infection

A

Localised P and toxins it produces goes to secondary location

25
Q

E. Focal

A

Bacilus anthraxis or Clostriudium Bascilium

26
Q

Systeminc infection

A

P spreads throughout body of organism
-E: Yersinia pestis

27
Q

Secondary infection

A

Primary infection can lead to secondary by another P
eg. influenza and pneomonia

28
Q

Mechanisms of viral spread

A

-V may remain localised to body surface through which they entered (skin, respiratory tract, intestine, etc)
-Or they can cause generalised infections associated with viremia (V in blood)
-papilloma V cause warts and repliacte in skin epithelia and spread through neighboring cells
-Cells that infect mucosal layer, like coronaviruses, spread in similar way. Infection is limited to mucosa probably due to limited cell tropism in other tissues

29
Q

Lymphatic system

A

Complex network of tissues, organs and vessels in vertebrates that is part of immune system and complementary to circulatory system
-Lymph nodes, lymphoid organs and lymphoid tissues such as bone marrow make up this system
-excess fluid from blood is carried in lymph to heart

30
Q

V and Lymph

A

Many V will move from a localised site and disseminate within host, firstly through lymphatic system and then into blood stream and to other organs
-Polio goes from gut to nervous system
-rabies
-smallpox