Horizontal gene transfer

Define and name two ways that this can happen. 

• genes are passed to other microbes of the same generation.

-donor cell gives a portion of its DNA to a recipient cell, or

-donor DNA incorporated into recipient’s chromosome

•Transformation

•conjugation

•transduction.

•It was discovered in Streptococcus pneumoniae.

•Took a pathogenic strain w/capsule and a non-pathogenic strain w/o capsule and injected them into mice. Injected non-encapsulated strain into mouse, and it remained healthy. Isolated bacteria that was non-encapsulated from that healthy mouse.

•When encapsulated strain injected into mouse, it would die. They isolated capsule containing bacteria from the dead mice. Took that encapsulated bacteria, heat killed it and injected mice, and mouse remained healthy.

•But when they injected a mouse with living non-encapsulated and heat-killed encapsulated strains, the mouse died. The bacteria isolated from the dead mouse were encapsulated. This showed that the genes from dead bacteria entered the live cells of the non-encapsulated strain, and made it encapsulated.

•Nutrients (food in GI tract, material in body fluids/dead cells, waste products of cells)

•Chemical and physical factors (temp, pH, O2 and CO2 availability, salt)

•Host defenses (role in determining and regulating normal flora is unclear)

•Mechanical factors (tongue/teeth, flow of digestive secretions, urination)

•Age, nutritional status, diet, health, disabilities, stress, geography, hygiene

1) competing for nutrients

2) producing substances harmful to other microbes

3) affecting the pH and available oxygen

•commensalism

•mutualism

•parasitism

Commensalism

Define and give an example.

Mutualism

Define and give an example.

•benefits both organisms

• Bacteria in large intestine produce vitamin K; we provide them with nutrients

parasitism

Define and give an example.

•one organism benefits at the expense of the other

• Example: tapeworm

opportunistic pathogens

Define and give an example.

•don’t cause disease in their normal habitat. Normal flora.

•Ex: E.coli is mutualistic in intestine, but disease causing in urinary tract, lungs, spinal cord.

1) The same pathogen must be present in every case of the disease

2) The pathogen must be isolated from diseased host and grown in pure culture

3) The pathogen from pure culture must cause disease when inoculated into healthy animal

4) Pathogen must be isolated from inoculated animal and shown to be original organism.

1) microbes that can’t be cultured on artificial media: Mycobacterium leprae, and Treonema pallidum (syphilis)

2) microbes that only multiply inside cells: Rickettsia and viruses

3) microbes that only infect humans: HIV

•subjective changes not apparent to observer

(like pain)

•By behavior in a host or population

•By frequency of occurrence

communicable

Define and give an example.

contagious

Define and give an example.

non-communicable

Define and give an example.

Incidence

Define, and tell what it helps indicate. 

•number of people who develop the disease in a specific time period.

•Helps indicate the spread of disease.

Prevalence

Define, and tell what it helps indicate. 

•number of people who develop disease, no matter when it first appeared

•Helps indicate how seriously and how long it affects a population 

sporadic

Define, and give example.  

endemic

Define and give example. 

epidemic

Define and give an example. 

pandemic

Define and give an example. 

acute

Define and give an example. 

chronic

Define and give an example. 

latent

Define and give an example. 

herd immunity

Define and tell how it can occur. 

 •many immune individuals present in a population

This can happen by getting enough people vaccinated and protected against rapid spread of disease

sepsis

•toxic inflammatory condition from spread of microbes from an infected area (big umbrella word)   

 local infection

Definition and give an example. 

systemic infection

Define and give an example. 

 focal infection

Define and give an example. 

•first there’s a reservoir, or source of pathogens for an infectious disease that allows for

•transmission from the source to the susceptible host.  This can happen through direct contact, indirect contact or through some other vector like a flea. 

•During invasion, microbes enter host and multiplies.  •Pathogenesis occurs as the microbe injures the host.

    pathogens.

2) factors that make the body more susceptible to         disease or alter the  course of disease such as             gender, genes, climate and weather, preexisting         illness, age, fatigue, lifestyle, occupation.   

•Incubation period

•Prodromal period

•Period of illness

•Period of decline

•Period of convalescence 

•Human reservoirs: people with S&Ss, or carriers who transmit w/o showing signs and symptoms     

•Animal reservoirs: who spread zoonoses by direct contact, waste, contaminated water, insect vectors.  

• Non-living reservoirs like soil, water, foods.       

• Contact transmission

•Vehicle transmission

•Vectors 

•direct or indirect contact, or through droplet transmission (spread in mucus droplets that travel in short distances).         

•Kissing, sexual intercourse (staphylococcal infections),or fomites like tissues, towels, bedding, money, cups, needles (HIV, tetanus).  Sneezing, coughing, talking (flu,pneumonia).

•disease transmitted by a medium; food, H2O, blood, etc.            

•Water: cholera, shigellosis.

•Food: food poisoning.

•a hospital acquired infection. 

It is said to be the cause of 2 million infections a year, causing 20K deaths and being the 8th leading cause of death

• Microbes in the hospital

• Chain of transmission

• Compromised host

•include the normal flora like E.coli and P.aeruginosa.

•Antibiotic resistant infections are now a major concern as P.aeruginosa carries R-factors.  Normal microbes like these can then form a threat to compromised hosts if transmitted.

•cannot resist infection due to disease, therapy or burns.      

•Either compromised by broken skin or mucous membranes, or by suppressed immune system by drugs or disease.   

•by reducing the number of pathogens patients are exposed to.

•by using aseptic techniques, hand-washing, and education.

•they study etiology (cause of disease)

•disease data (history of immunization, age, occupation, common history of infected individuals, etc)

•site of contact with disease agent

•methods of controlling disease (vaccines, drugs, control of vectors)

•frequency of disease in the population

•health care workers have to report specified diseases. 

•This helps in establishing a chain of transmission (AIDS, gonorrhea, tetanus, etc.), and once chain of transmission is found, a control measure can be applied to stop the disease (vaccine development, education

 •is the infectious dose for 50% of the population

•This is used to compare relative virulence.

• is the lethal dose for 50% of the population

•This is used to compare relative toxicity 

1) gain access to host                 

2) bind to tissues

3) evade defenses

4) damage tissues

1)  Mucous membranes

2) openings in skin like glands, ducts                     

3) parenteral route: directly entry into tissues like a bite, injection, cut, surgery.              

•Many have a preferred portal of entry and don’t cause disease if enter elsewhere.   

• how a pathogen binds to tissues. 

•Surface molecule on pathogen (called adhesin or ligand-- mostly glyco- or lipo--protein) binds to surface receptor on specific host cell tissues, mostly sugars.

Define invasin

and explain how a pathogen can penetrate into host cell cytoskeleton.

Name one genera of microbes that can do this. 

coagulase

Name an organism that produces these. 

An exoenzyme. Converts fibrinogen in blood to fibrin=blood clots.

Some Staph sp. do this.

kinase

Name an organism that produces this. 

hyaluronidase

Name an organism that produces this. 

collagenase

Name an organism that produces this. 

IgA protease

Name an organism that produces this. 

Antigenic variation

Name an organism that does this. 

• Alteration of surface antigens by some pathogens. Our bodies produce antibodies to inactivate or destroy antigens (foreign substances/microbes).               

Example Neisseria gonorrhoeae.

1) using host cell nutrients

2) direct damage in immediate vicinity of invasion

3) Production of toxins (poison produced by microbes) that damage sites distant from site of invasion 

4) Induce hypersensitivity reactions 

• enzymatic damage to host cell during entry/release.  

•Rupture cells during multiplication and release.       

•Damage due to toxins.  They can use cell nutrients and produce wastes or alkaline products, causing harm.

Production of toxins (poison produced by microbes) that damage sites distant from site of invasion.

What types of toxins can these be?  What can they cause? 

Exotoxin

•What is it made out of?

• Found in gm (+) or gm (-)?

•How do they get around body?

•How is it named? 

• poison produced inside and secreted outside.

Proteins, mostly enzymes.  part of microbial metabolism.  Small amounts can be harmful and since its an enzyme, can act over and over.  Can be very lethal.  Both Gram (+) and (-) can produce them although mostly gm (+).  Genes can be         carried on plasmids or phages.  They are soluble in body fluids and easily diffuse in blood.  Destroy specific part of host cell or inhibit metabolic functions.  Disease caused by exotoxin, not microbe itself.  Like in case of Staphylococcal food poisoning.  Named after what it attacks or disease caused like neurotoxin, or tetanus toxin.                 

1) A-B toxins

2) Membrane-disrupting toxins

3) Superantigens 

A-B toxin

Describe and name an organism that produces this.

Membrane-disrupting toxins

Describe and give example. 

 • lyse host cells by disrupting plasma membrane.              Forms holes or pores in membrane (S.aureus) or disrupt phospholipids (C. perfringens).

•Hemolysins:  lysis of red and white blood cells.            (Streptococci sp. and Staphylococci sp.)

Superantigens

Describe, name results of superantigens, and give an organism that produces them. 

•bacterial proteins that provoke intense immune response.  Result in fever, nausea, vomiting, diarrhea, shock and death.     

(Staphyloccocus aureus toxin: toxic shock)

Endotoxin

• What is it made out of?

• When is it released?

•What signs and symptoms result?

• 

•Lipopolysaccharides (not proteins like exotoxins). Part of LPS in gm(-) cell wall; Lipid A is the endotoxin.

• Released when gm (-) cells lyse or replicate (some toxins release with fission).

•Produce same S&Ss regardless of species of microbe.  Results in: chills, weakness, aches, shock and death.

[Exotoxins, S&Ss differ- diptheria diff from tetanus] Activate blood clotting proteins; block capillaries that can cause tissue death.

Describe how septic shock can be caused by bacteria.

What does TNF do? 

Name an organism that can cause this? 

• as phagocytosis of gm (-) bacteria causes release of tumor necrosis factor (TNF). 

•TNF damages capillaries: permeability increased and large loss of fluids. 

•Salmonella typhi.

• Plasmid genes may be the cause of some virulence factors rather than an outer membrane or an enzyme (tetanus neurotoxin. S. aureus - adhesins                 and coagulase). 

•Some bacteriophage genes also encode virulence factors (Diptheria toxin).                                 

•Keep microbes out.

•Remove microbes if they get in

• Fight them if they remain inside. 

•Immunity that does not involve specific recognition. 

•Compared to adaptive (specific) immunity, it's the rapid responder that acts against microbes in the same way

•has no memory component

•consists of the 1st and 2nd lines of defense.

•1st line of defense includes the skin and mucous membranes.           

•2nd line of defense includes formed elements in the blood, two categories of WBCs (granulocytes and agranulocytes for phagocytosis)

• adaptive (specific) immunity also responds to foreign microbes, but is slower to respond (is the 3rd line of defense)

• has a specific response to a microbe

• has a memory component

• involves T cells (T lymphocytes) and B cells which are types of WBCs

Describe the structure of the mucous membranes and how it can defend against microbes.

Where is it found? 

• Lacrimal apparatus: structure that make and drain tears.   

•Saliva- dilutes number of microbes; washes teeth and mouth membranes     

•GI, urinary and respiratory tracts- mucus, nose hair, cilia and upward mucus                 movement.  Ciliary escalator = 1-3 cm hour.   

•Sebaceous (oil) glands- coats surface of skin, lowers pH that inhibit pathogens.

•Sweat glands- produce sweat that flushes microbes from surface of skin.  Contains         lysozyme - enzyme that breaks down bacterial cell walls.

•Gastric juice: produced by glands in stomach.  HCl, enzymes and mucus, low                 pH, but still some pathogens are protected by food particles. 

• Normal microbiota- contribute to innate immunity. 

Formed elements

Name the 3 major types of formed elements. 

•cells and cell fragments.

Major types: RBCs, WBCs, platelets.

•neutrophils

•basophils

•eosinophils

•dendritic cells 

Agranulocytes

Which cells are considered agranulocytes? 

• granules not visible under microscope

•includes monocytes, macrophages (fixed and wandering).

Perforin

• What cells produce these? 

 •makes channels in membrane that cause cells to lyse (cytolysis)

•natural killer cells 

Granzymes

Which cells produce these? 

•cause target cell suicide (aptosis)

•natural killer cells 

• During Initial phase: granulocytes seen, mostly                 neutrophils.                  

• Later in infection: macrophages dominate.          

• Viral and fungal infections: macrophages                         predominant throughout.   

• sac surrounding the microbe.

= phagosome fused with lysosome (organelle containing degradative enzymes). 

•begins with chemotaxis where phagocyte and microbe are attracted

•adherence-attachment of phagocyte to microbe-that may happen thru opsonization. 

•ingestion where projections of phagocyte plasma membrane engulf microbe- complex becomes a         phagosome when inside cell.

1) structures that inhibit adherence. Ex: capsules (S. pneumoniae).

2)ingested but not killed- they may release substances that kill the phagocyte (Staphylococcus sp)

3)survival inside pathogens- escape phagosome before it fuses with lysosome (Shigella) 

• defensive response to damage to body tissues (by microbial infection, physical agents, or chemical agents).   

•1) redness    2) pain         3) heat        4) swelling     (5) sometimes loss of function 

1) Vasodilation and increased permeability of blood vessels.

2) Phagocyte migration & phagocytosis

3) Tissue repair 

•Chemicals released by damaged cells (kinins, histamine,               prostaglandins).               

•Blood vessel dilation; increased flow to damaged area.                   Defensive substances in blood move to injured area, and         you get edema, or swelling caused by fluid build up.        • Cause of redness and heat.                                       

• Clot forms around site which prevents microbes/toxins from         spreading.               

•Localized collection of pus (dead cell, body fluids); abscess.

 What happens during phagocyte migration & phagocytosis in inflammation?

Define  margination and emigration. 

• Phagocytes destroy invading microbes.

• margination: phagocytes stick to inner surface of blood vessels 

•emigration: collected phagocytes squeeze between cells of blood vessels to injured area.     

• replacement of dead/damaged cells. (formation of a scab)         

• ability to repair depends on the types of tissue.

1) gm (-) endotoxins             

2) Chemicals released by damaged cells                

3) Chemicals released by phagocytes   

1) rapid heart rate

2) dehydration

3) electrolyte imbalances 

4) seizures

• defensive system made up of over 30 proteins. 

• produced in the liver, circulate in blood and body            tissues.                       

• destroy microbes and prevent excess tissue damage.

•9 inactive proteins (C1-C-9) that become active when split.        

•Compliment proteins act in a “cascade”-- one  activates another, and then an other.                      

•Activation of C3 triggers a cascade that results in three outcomes.    

•There are three pathways through which complement can be activated: 1) Classical pathway 2) Alternative pathway 3)  Lectin Pathway

1) Phagocytosis thru Opsonization- C3 is split into C3a and C3b.   C3b binds to microbe surface and phagocyte can attach to C3b.         

2) Cytolysis (bursting of microbe due to inflow of extracellular fluid) C5b,C6,C7 + [C8 an C9] = membrane attack complex (MAC) that creates channels in membrane.     

3) Inflammation- C3a and C5a bind to mast cells which leads to increase of blood vessel permeability and chemotactic attraction of phagocytes.

1) Capsule may prevent compliment activation                           

    -Prevents opsonization                                        

    -Prevents membrane attack complex formation (MAC)

2) Some gm (-) bacteria lengthen lipid-carb complex   

    -Prevents MAC  formation 

3) Gm (+) cocci produce enzyme breaks down C5a                 

    - C5a: chemotactic factor that attracts phagocytes.     

• Interferons - (IFNs) are antiviral proteins.

• Interfere with viral multiplication

• Not virus specific

• Different interferons produced by different cell types

• antiviral proteins- (AVPs) = interrupt different stages of viral multiplication.

• Found in viral infections. 

•Three main groups of interferons:

IFN-α,

IFN-β, and

IFN-γ.

•IFN-α and IFN-β produced by virus infected cells, which trigger neighboring, uninfected cells to make AVPs.

•IFN-γ is produced by lymphocytes which induces phagocytosis in macrophages and neutrophils. 

Define transferrins.

Where is it found? 

•Iron-binding proteins.

•Found in blood, milk, saliva, and tears. 

• Inhibit bacterial growth by limiting available iron in our bodies.

•Excess iron suppresses chemotaxis and phagocytosis

•Limiting iron increases effectiveness of immune cells.