Microbio exam 4

Infection is invasion/colonization of the body by pathogenic microorganisms

Disease occurs when an infection results in any change from a state of health

Pathogenesis

etiolology = study of cause of disease

• Symptoms are subjective e.g. pain, malaise
• Signs are objective which can be measured/observed eg blood pressure, swelling, lesions

• Communicable is any disease that spreads from one host to another (directly or indirectly)
• Contagious means it EASILY spreads

• Source! AKA Reservoirs - can be....
• humans, animals, or nonliving

• Transmission! can be via...
• -direct contact e.g. touching, kissing
• -indirect contact (via fomite= a general term for nonliving object involved in spread of infection) e.g. tissues, towels, bedding
• -droplet e.g. coughing, sneezing, talking
• -vehicle e.g. water, food, air, bodily fluids
• -vectors e.g. mosquitos, flies, ticks, fleas

The number of people that develops the disease in a time period

Prevalence= ALL the cases (both old n new)

• Acute- a disease of short duration, develops rapidly eg influenza
• Chronic- long lasting disease, develops slowly (no convalescent period eg TB or hepatitis B
• Latent- the causative agent remains inactive (or dormant) for long periods eg shingles

the presence of immunity in most of a population

• -there must be a reservoir as a source
• -pathogen must be transmitted to host (can occur by direct, indirect or by vectors)
• -invasion, pathogen enters & multiplies
• -injury to host, pathogenesis

1. Incubation period- interval between initial infection & 1st appearance of signs/symptoms

2. Prodromal period- short interval, early & mild symptoms of disease e.g. aches & malaise

3. Period of Illness- most severe signs & symptoms (if disease not txed pt dies)

4. Period of Decline- signs & symptoms subside (pt vulnerable to secondary infection)

5. Period of Convalescence- recovery, return to prediseased state

****Note that human can spread infection (act as a reservoir) AT ANY STAGE, even convalescence****

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• *NOTE- Infection can be spread at ANY stage!!

entrances to the human body for a pathogen to enter

eg. mucous membranes, skin, or parenteral route (spots where skin/membranes are injured, like punctures, bites, cuts etc)

specific routes that microbes use to leave the body e.g. secretions, excretions, discharges or tissue

In general these routes are related to part of the body infected & will use the same portal for entry & exit

Certain bacteria must gain access in a particular route in order to cause disease

e.g. Salmonella typhi causes typhoid fever IF the bacteria is swallowed, if rubbed on skin, no disease.  Note that some bacteria have multiple preferred routes

Adherence- means of attachment of the pathogen to a host's tissues 

Pathogens have surface molecules called adhesins or ligands that bind specifically to complementary surface receptors on cells of host's tissue

capsules- bacteria that are encapsulated are more difficult for the body to destroy

M protein- can reside in cell wall, it is a heat-resistant & acid-resistant protein.  It mediates attachment & resists phagocytosis by WBCs

Also production of extracellular enzymes or antigenic variation (ability of pathogens to alter their surface antigens therefore evading host antibodies)

• 1. using host's nutrients
• e.g. siderophores- proteins secreted by the bacteria that steal iron away from the host in various ways
• 2. cause direct damage in immediate vicinity 
• 3. produce toxins (which get transported all over the body via blood or lymph)  *Most common way*
• 4. inducing hypersensitivity reactions

toxin- poisonous substances produced by certain bacteria

exotoxins & endotoxins

• exotoxin- produced INSIDE the bacteria then secreted or released following lysis. A PROTEIN
• *they have an enzymatic nature, so small amount is dangerous b/c it can be used over and over again. mostly found in Gram + but also Gram - too

endotoxin- Gram - only!  present in the outer part of cell wall, the LPS layer, specifically lipid portion (called lipid A).  They get released when bacteria dies.  A LIPOPOLYSACCHARIDE

• neurotoxins- attack nerve cells
• enterotoxins- attack GI tract
• cytotoxins- attack a wide variety of cells

1. A-B toxins-- two parts, one binds and helps "break in", the other acts similar to an enzyme and disrupts protein synthesis

2. Membrane-disrupting toxins-- cause lysis of host cells by disrupting their plasma membranes

3. Superantigens-- antigens that provoke very intense immune response

• fever, chills, weakness, general aches, and sometimes shock and/or death.  can also induce miscarriage
• also activation of blood-clotting proteins

• Shock = decrease in blood pressure
• septic shock= shock caused by bacteria

Gram - can cause endotoxic shock

1. Gram - bacteria ingested by phagocytes

2. As bacteria degrade, LPS layer is released (endotoxins too).  Endotoxins cause macrophages to produce cytokines-Interleukin 1 

3. Cytokines are carried to hypothalamus

4. Once at hypothalamus, lipids called prostaglandins are released, which reset the thermostat at a higher temp. Result is fever

immunity- resistance to infection

innate- defenses that are present from birth, responds rapidly

adaptive- once innate lines of defense are breached, this 3rd level adjusts to handle microbe.  It's slower to response but has a memory

Protein receptors that hang in the plasma membrane of defensive cells (such as macrophages).  They activate the innate system.

Basically they are detectors on the surface of macrophages & dendritic cells, they detect incoming Gram - bacteria by LPS or endotoxin

proteins that regulate intensity & duration of immune responses.

basically they are chemicals that get released by WBCs & trigger different responses in diff. types of WBCs

• Physical factors:
• -intact skin, mucous membranes, (e.g. GI, respiratory & genitourinary system), and lacrimal apparatus 

• Chemical factors:
• -Sebum (oily substance produced by skin), and lysozyme capable of breaking down cell wall. Lysozyme is found in  mucous, perspiration, tears and urine.

system of tear ducts that protect the eye, washes over the eye and lysosyme in the tears destroys pathogens

Ciliary escalator- wave like cells in lung that push out particles & pathogens trapped in mucous

-phagocytes (e.g. neutrophils, eosinophils, dendritic cells, & macrophages)

• -inflammation
• -fever
• -antimicrobial substances

Leukocytes

Leukocytosis

Leukopenia

• Granulocytes- WBCs that stain grainy under light microscope
• e.g. Neutrophils, Basophils, & Eosinophils

• Agranulocytes - don't stain grainy under microscope
• e.g. Monocytes, Lymphocytes, Dendritic cells

• polymorphonuclear leukocytes (PMNs)  
• aka polymorphs

highly phagocytic & motile, active in initial response of infection

• Neutrophil- most active/motile
• Basophil- releases histamine

• Eosinophils- smaller, makes toxic proteins which damage parasites
• Monocytes- are NOT phagocytic until they leave the blood & turn into MACROPHAGES

• Dendritic cells- derived from monocytes, initiation of adaptive immune
• Lymphocytes- Natural Killer (NK) cells, T cells and B cells; destroy target cells by cytolysis (cell bursts from too much ECF) and apoptosis (self destruction)

a phagocytic cell, a mature monocyte

enhancement of phagocytosis by coating microorganisms with certain serum proteins (opsonins); also called immune adherence

2nd line of defense, natural triggered response to damage done to body

• 1. Redness
• 2. Pain
• 3. Heat
• 4. Swelling
• 5. Loss of Function

• 1. damage
• 2. vasodilation & increased permeability of blood vessels
• 3. phagocyte migration & phagocytosis by macrophages & neutrophils
• 4. repair

proteins that are released from damaged tissue.  induce both local & systemic responses (for example cause fibrinogen for blood clotting and kinins for vasodilation)

dilation of blood vessels  (it increases blood flood to area and is responsible for redness & heat associated with inflammation)

It increases permeability this allows defensive substances normally held in blood to pass thru the vessels and enter injured area  AKA Vasopermeability

the process by which phagocytes stick to the lining of blood vessels (endothelium)

Diapedesis- WBCs gather up and squeeze through to reach injured site

system of proteins that assist in destroying microbes.  Not adaptable, but sometimes is recruited and brought into action by adaptive immune system

1. cytolysis (pokes holes in membrane, ECF flows in and cell bursts)

2. inflammation (vasodilation, margination of phagocytes, diapedesis)

3. phagocytosis (via opsonization)

*note complement proteins also prevent excessive damage to tissues

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designated with upper case C (C1-C9)

they are inactive until split into fragments (products).  They act in a cascade.  various C proteins will cause opsonization, cytolysis, & inflammation

This cascade is called complement activation & may occur three ways

1 of the 3 ways complement activation occurs.

1. antibodies attach to antigens, forming complexes.  This complex bind & activate C1

2. C1 in turn activates C2 & C4 (by splitting them).  They get split into C2a / C2b; C4a / C4b

3. C2a and C4b combine and activate C3 by splitting it into C3a / C3b.  This fragments then initiate cytolysis, inflammation, and opsonization

• B cells
• T cells
• NK [natural killer] cells

immunity produced by antibodies dissolved in body fluids, mediated by B cells

B lymphocytes making antibody

immunity from T lymphocytes

Cell mediated

Humoral

anything that provokes the immune response, usually a protein or polysaccharides

Name is short for "antibody generators"

An antibody (Ab), also known as an immunoglobulin (Ig), is a large Y-shape protein produced by plasma cells.  

It is used to identify and neutralize foreign objects such as bacteria and viruses.

• IgG
• IgM
• IgA
• IgD
• IgE

IgG

80%

IgM  (from macro, to reflect large size)

• 5-10%
• due to large size they generally stay in the blood cells, they are short lived

IgA

10-15%

IgG is most abundant in serum, while IgA is most abundant in the whole body

IgE

.002%

a cell that an activated  B cell differentates into; plasma cells manufacture specific antibodies

a small set of B cells that stays with us for life & will secrete the antibody we have previously made against a known pathogen

CD4+

works with macrophage & B cells to help produce antibody

APC encounters antigen, it gets broken down inside APC (eg dendritic cell) and these fragments combine with MHC complex which puts a signal at cell's surface.  This signal "calls" and binds to T helper cell which releases cytokines to stimulate immune systems

they process antigens so that T cells may recognize them.  T cells then become activated and release Interleukin 1 and B cells become primed to make antibody

• CD8+
• subset of T cells that kill already infected cells

Active in NATURALLY ACQUIRED: antigens enter body naturally, body responds

Passive in NATURALLY ACQUIRED: antibodies pass from mom to baby (via placenta or moms milk)

Active in ARTIFICIALLY ACQUIRED: antigens are introduced via vaccines, body responds

Passive in ARTIFICIALLY ACQUIRED: premade antibodies in serum get injected

whole agent vaccines where pathogen has been weakened so it's not strong enuff to cause a rapid/quick infection.  This gives body time to respond and make antibodies.   We keep these antibodies as protection in case we encounter the pathogen in nature

similar to attenuated vaccines, except instead of a weakened pathogen, it's KILLED and only the shell remains to prime the immune system into response.

when a polysaccharide vaccine is joined to a protein to make it more potent.