Human Infections And Disease

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pathgenicity

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the ability for an organism to cause disease

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4 requirements

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1. access to a host/portal of entry

2. adhere to host tissues: must be able to stick to the host

3.penetrate/evade: penetrate tissue and evade defenses

4. directly damage to tissues or through accumulation of enough waste products

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1. portals of entry

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1.mucous membrane: most common* food, sexual transmission, breathing in resp most common

2.skin: tougher* puncture injection bit cut wound surgery

splitting of mm/skin due to swelling or drying

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2.adherence

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adhesins-some sort of protein sticking off surface, specific to host tissue

MM: part of glycocaylx, spikes on flagella, biofilms group of microbes work together seen in mouth(plaque).

if cannot stick to host cell it may stick to invading bacterial cell forming a clump of bacteria

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3. penetrating host defenses

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-now it needs to cause damage, some have 1.capsules:avoid detection organized glycocalyx

2.M-proteins: can live in acid and fever

3. enzymes: trick host, kinase dissolves blood clots, collagenase which allows it to move thru collagen and into the blood.

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4. damage to the host

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1. use all of the nutrients of the host, cause anemia use all iron in blood, tapeworm eats everything host eats.

2.directly: endotoxins and exotoxins

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exotoxins

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gram +

made by living bacteria exits the body of the living bacteria cell and binds to the host by phagocytosis the exotoxin breaks off

1. one part stays in cell and damages cell

2. neurotox bind to the nerve and a portion stays in cell and eventially kill the cell

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exotoxin

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lyse(kill) host cells making protein channels in plasma membrane, disrupt phospholipid bilayer

-cause basic discomfort nause and vomiting to shock and death

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endotoxin

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only in gram -

bacteria needs to die to release the endotoxin

immune system macrophages come in and kills it, endotoxin released immune system responds causing fever,chills, weakness, large amount can cause anaphylactic shock

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5. port of exit

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not required though for pathogen to truly exist it must be able to leave one host and enter another

-resp: cough, sneeze, breathing, speaking

-GI: feces, saliva

-GU: penile, vagina, urine

skin: only some worms can push out of the skin

blood: cut , needle, a mosquito

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innate immunity

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present at birth

1. 1st line of defense:skin/mm

2. 2nd line: NKcells, phagocytes, imflamm, fever, interferon, complement

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adaptive immunity

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-slower but more effective, respond to a single type of pathogen w/ specific types of cells

memory component: develop immunity to things that have been exposed previously

-T and B lymphocytes

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activation of innate immunity

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-self vs nonself

toll like receptors"TLR": proteins found on surfaces of a defense cell sticking out goes thru the body and checks other cell to be sure theyre self.

-PAMPS: on bacteria, TLR will bind and cytokines released

-cytokines: chemical signals sent my immune cells into the blood and activate every other immune system cell this process is called

chemotaxis (call for help)

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immune system cells

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Leukocytes WBC

-high WBC count means some pathogen present the body increases the numbers to fight infection

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4 types of WBC

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1. neutriphil: phagcytic first to arrive

2. monocytes: phagocytic, in blood turn into macrophageswhen leave blood and go into tissue in the skin, mm,stomach,liver

3. basohphils: releases hisamines to signal other cells to come and fight, they dont fight only call

reason for allergy

4. eosinpohils: one job,to fight worm infections find worm attach and secrete a protein that will kill it

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Lympohocytes

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-Natural killer cells(NK: kill self and tumor cells tumor cells are self go into mitosis too fast, NK gram and release perforins which tell cell to start self death called apoptosis

-a way to tell cell to die and save the parts that can be reused

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lymphatic system

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-collection of channels(lymphnodes) that run thru the body draining excess fluid and returning it to the blood so it can be filtered thru kidneys

-lymph nodes part of immune response not immune system

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lymph nodes

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-found: groin, axilla, neck in large consentrations

-tonsils and nodes: sites where the lymphoctes and phagocytic cells stay when they are not involved in an immune response

-swollen node is working to kill the pathogen

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phagocytosis steps

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1. chemotaxis: release of chemicals that have made the phagocytic cell atrracted to the area

2. adherence: TLR binds to PAMP on bacteria cell

(self finds nonself and binds)

3.reaches out w/ pseudopods and starts pulling it into cell

4. pathogen in and phagosome formed

5. phagosome fuses w/ lysosomes and phagolysosome

6. lysosome enzymes break down digest it

7. before expelled takes a piece of it and attaches it to cell wall

8. rest of digest particles are expelled out the cell and into blood stream for B-cells to use

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microbes that can trick the phagocyte for invasion

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thick capsule- phage cant adhere/stick

inhibit digestion or destruction

-prevent fusion of phagos, ingested but hide inside the phagocyte

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inflammation

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cardinal signs: reddness, heat, pain,swelling

-chemotaxis cause vessels in the area to expand and clots at edges of vessels prevent bacteria to get into bloodstream

-vessels swell increase blood flow bring in more WBC-stick to edge of vessels squeeze out vessels move toward patho to get it & destroy after skin will form scab

-swelling causes pressure on the pain receptors

-inflamm good sign bacteria is being attacked

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fever

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systemic inflamm occurring throughtout the body response to infection or production of toxins

-fever wont kill but slow growth enough to allow body to kill pathogen

-fever isnt necessarily bad in an adult

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complement

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-group of proteins made in liver, new ones found all the time

-they secrete in blood and patrol the body and help other parts of immune system

-help inflamm in phagocytosis

-get a signal they will grab the patho and hold it for ingestion

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interferon

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-set of proteins that stop virus from replicating

-produces antiviral protein that disrupt some stages of viral replication

-antiviral meds work this way doesnt kill but stops it from replicating

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lines of defense overview

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innate: skin and mucus membranes

2nd: phagocytosis, neutrophils, macrphages inflamm fever complement

-1st and 2nd must be activated to get 3rd

-3rd line: humeral immunity and cellular immunity

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humeral immunity

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production of B cells, antibodies are secreted into the blood where they become active

(third line of defense)

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cellular immunity

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response of cells, T cells Helper which give permission and cytotoxic that kill

-t and b come from marrow stem cells

-stem cells migrate from the marrow and become b cells, grown in the bone marrow other cells go to the thymus and then end us as T cells

-adult: stem cells become b or t and live in lymphoid tissue, spleen, and bone marrow

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antigens

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-protein that the IS recognizes as foreign

-anything that is exposed on the surface of the pathogen that the b and t cells can respond to

-bacteria have a lot different types of antigens that only one B cell can recognize

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Epitope

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the specific portion that the B or T cell recognizes antibodies bind to epitope

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other ways the cells respond

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-free antigen: that was broken down into pieces after phagocytosis

-other cells respond to the antigen on the bacterial cell or something that is presents by another cell

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Antigen-presenting cells

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reaching out and grab a patho and pull it in once in once inside a cell a piece of the path is place on the surface of the microbe surface

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antibody aka immunoglobulins (Ig)

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-have a y-shape -5 different types

constant region(base): never changes every antibody in the body has the same constant region its how the body recognizes self.

-Variable region: changes depending on antigen the AB specific for.

-light and heavy chains made of di-sulfide strongest known

-if theres an antibody that binds to E.coli there will be 5 diff classes of AB that will bind

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1. IgG

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-80% of antibodies

-helps phagocytosis

-bind to antigen and send out signal to phagocytes to come and kill it

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2.igM

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-pentamers 5-Ys stuck together. first AB produced in initial response

-part of memory cell

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3. IgA

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in all secretions mucus membranes esp in eyes.

part of the first line of defense where first exposure occurs

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4. igD

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hard to understand but largely able to substitutes for igM functions in B-cells

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5. IgE

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linked to allergic reactions, specifically help esinophils

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b cells and humeral immunity

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AB come from B cells, make up humeral immunity

immature B cells, recieve signlas in form of cytokines from phagocytes

-recognize the antigen, bind and undergo clonal expansion (profilferation)

-stem cells make B cells and theyre just waiting for activation in lymphoid tissue each b cell responds to a different antigen

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clonal expansion

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b cell recognizes and attaches
displays it on its cell surface
receptor on the tcell recognizes it and antigen fragment it activated produces cytokines which activate bcell begin clonal expansion
some become anitbody producing plasma cells

activated bcells: expand and proliferate( multiply)

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t helper cells

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comes and checks the antigen to make sure it is not self gives permission to kill and then there is clonial expansion, proliferation, antibody production

they also release cytoklines that make the bcell proliferate

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anitgen and antibody binding

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1.aggultination: AB cause AG to clump and fall out of blood/solution

2.opsonization: AG is coated w/ AB to enhance digestion by phagocytic cells

3.neutralization: AB inactivate microbes by blocking attachment to host cell; wont let it attach

4. compliment: makes holes on the AG for it to die

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t cells

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2 types: t-helper and t-cytotoxic cells

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t helper cells

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regulate give b cells permission to make the AB

replicated different than Bcells they cant respond to free antigen

-they require presentation from ATC

once it recognizes bad on the presentation from phagocyte surface,

-tcell will produce cytokines and bring other cells to site or tell bcell o make ab or tell t cyto to kill

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cytotoxic T cells

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become capable of killing a virus or patho infected cell

-AG to a cytotoxic t cell CTC will now send out perforins that make the infected cell shrivel and die

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overview B and T cells

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-humeral: free ag patho made it pass the first defense 2nd line patho is ingested by phagocyte broke it down and spit it out (free ag)

-b cells bind to the spit out "Free ag"proliferates makes plasma cell and plasma cell makes ab the ab can go back and bind to the ag

-helper T cells have to give Bcells permission

at the same time the phagocyte will present some of the ag to the helper, it will give permission to the cytotoxic tcell to start killing

-activated b cells make memory cells to get a faster response if 2nd exposure

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types of immunity natural

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-exposed to ag naturally

1.naturally acquired: person exposed to ag, becomes ill and recovers thru activation of immune system lifelong/shortlived

t/b cells activated and make the ab

2.passive:transfer from mother to infant,

(full ab no b/t cells made)

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artificially acquired

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-from an injecition, man made

1. active:result of vaccination, person i intentionally exposed to ag resulting in activation of immune response

2.passive: ab being introduced into the body, IG shot is just pure ab given to person

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memory cells

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we only hold a limited number of them

booster: given to keep the bacteria/virus in the memory pool