Microbiology Exam 3

the study of where and when diseases occur and how they are transmitted

changes in disease date like if diseases are occuring, spreading, and if control methods are working

the penetration of the host defenses and colonization by a pathogen

a state of unhealth, the loss of homeostasis, or the presence of signs and symptoms

diabetes

the period of time between the initial infection and disease and when symptoms first appear

pathogens are adjusting metabolism, reproducing, attempting to evade the immune system, and producing toxins

the number of cases of disease that occur

the number of new cases reported during a period of time

the total number of cases during a period of time (includes new cases and old cases from an older period of time)

number of cases per 100,000 - this allows for comparison of areas with different populations

they allow authorities to track where and when diseases occur, the changes can tell if control measures are working or if they require intervention

sporadic, endemic, epidemic, and pandemic

disease occurs infrequently

the disease is constantly present

a sudden increase in the incidence of a disease over the normally expected amount of time

epidemic on more than one continent

They are the same to an epidemiologist, they both indicate a sudden increase in number of cases

where the microbe normally lives

a continuous source of the pathogen or infection

the human

animals, soil, water, enviromental

direct, indirect, or aerosols

when a pathogen is temporarily transferred to an object by one person and picked up by a second person when they handle the same object

fomites - door knobs, phone buttons, tissues, clothing, bedding, food, dishes, money

when pathogens travel on tiny droplets (aerosols) of fluid from person to person - when we talk, cough, or sneeze

arthropods that transport pathogens from one host to another

fleas, ticks, mosquitoes

Flies and Roaches - spread them as they crawl around carrying pathogens on their surface

zoonotic diseases

hospital visit

10%

pathogens in the hospital environment, presence of compromised hosts, and a chain on transmission

people often come to the hospital carrying pathogens, and sanitation efforts leave behind resistant microbes with little competition

people often have immune systems that are compromised due to drugs or disease, and medical procedures often bypass the body's defenses

medical personnel and instruments move microbes from person to person, and ventilation systems move air and microbes around

they have an epidemiologist or infection control officer on staff

bypassing a normally intact defense

urinary tract infection - surgical site infection

use of catheters - they carry microbes into the urinary tract if it's contaminated or it prevents normal flush of urine and microbes in tract multiply

expose normally protected tissues to microbes in the environment

gram-positive cocci, gram-negative rods

Staphylococcus

E. coli, Psuedomonas

Clostridium difficile

following antibiotic therapy (when competing microbes in the intestinal tract are eliminated)

following antibiotic therapy (when competing microbes in the intestinal tract are eliminated)

following antibiotic therapy (when competing microbes in the intestinal tract are eliminated)

diarrhea to death

after antibiotic theraphy (when antibiotics kill bacteria and leave fungi without any competition for nutrients, which result in overgrowth of fungi)

yeast infection - Candida albicans

Koch's Postulates

• 1) The organism you suspect must be present in every instance of the disease.
• 2) The organism must then be isolated and grown in pure culture.
• 3) The organism you isoled must cause the disease when it's inoculated into healthy individuals.
• 4) The organism must be present in newly infected individuals.

Robert Koch - germ theory of disease - 1876

Bacillus anthracis - anthrax

many diseases are caused by microbes

must be capable of causing disease, must be transmitted to the host and have a route of entry, host must be susceptible

traits of a ohst that increase the risk of developing a disease

the severity of the disease the pathogen causes

traits of a pathogen that contribute to its ability to cause disease

Attachment, Toxins, Evading immune system

E. Coli and Neisseria gonorrhoeae require fimbriae to attach to the cell of the urinary tract, Streptococcus pnuemoniae requires a capsule to stick to cells of the respiratory tract

flagella allows cells to move away from immune cells - the mycolic acid in the cell walls of mycobacteria is resistant to many chemicals immune defenses

infectious dose for 50% of the population

low (low numbers of cells)

through airborne transmission (the air we breathe)

portal of entry

respiratory tract - gastrointestinal tract

Mucous membranes, Skin, Parenteral route

respiratory tract, gastrointestinal tract, genitourinary tract, conjunctiva (inside of eye and white)

only if the microbe can penetrate the skin, which few can, but they can penetrate damaged skin

Parenteral route

injections (iv's), animal bites (insect bites), surgery, and injuries (scrapes, tacks, nails, silvers)

fimbriae and capsules

if cells produce enough capsule slime

a thick layer of slime inhabited by numerous slime-producing and non-slime-producing cells

slime on spoiled food or slime that develops on dirty dishes soaking in the sink

biofilm

has a protective effect on cells

toxins that are released from the cell - always proteins

on plasmids

held in or on the cell and are released only when the cell dies or breaks apart - lipopolysaccharide in the outer membrane of gram-negative bacteria

lipid A

fever and chills - shock and death

• 1) phagocytes engulf and digest gram-negative cells
• 2) digestion breaks the cells apart which releases the LPS
• 3) LPS stimulates the phagocyte to produce IL-1 (interleukin-1)
• 4) IL-1 travels through the bloodstream and stimulates the hypothalamus to produce prostaglandins
• 5) prostoglandins stimulate the hypothalamus to re-set the body temperature to a higher level
• 6) fever develops and continues as lonas as the level of prostaglandins remains high in the hypothalamus

block the production of prostaglandins

life-threatening drop in blood pressure

blood flow to various organs decreases or even stops, which results in organ failure followed by death if the condition isn't corrected

the presence of bacteria in the blood and the complex toxic condition that occurs as a result

Bacteremia

sepsis

chemicals our immune system produce during the fight against the bacteria in the blood

• 1) phagocytes engulf and digest the gram-negative bacteria
• 2) digestion breaks the cells apart which releases the LPS
• 3) LPS stimulates the phagocyte to produce TNF (tumor necrosis factor)
• 4) a series of events initiated by TNF results in damage to capillaries
• 5) the damaged capillaries leak excessive fluid from the circulatory ystem
• 6) the loss of fluid caues blood pressure to drop

fluid replacement and epinephrine

causes blood vessels to constrict

the innate immune system and the adaptive immune system

at birth or soon after

as we are exposed to more microbes throughout our lives

skin, mucous membranes, ciliary escalator, peristalsis, fluid flow in various locations

the major protein of skin is keratin, few microbes produce enzymes that can break down keratin so as long as the skin is not damaged microbes can't go through it

they line the respiratory, digestive, and genitourinary tracts, the membranes trap invading cells and prevent contact with host cells

the cilia on the cells in the respiratory tract move mucus (and microbes trapped in it) out of the lungs and into the throat

rhythmic contractions that move materials along the digestive tract

fluids flowing across the surfaces of the mouth (saliva), urinary tract (urine), and eyes (tears) rinse away microbes

low pH, lysozyme, digestive enzymes, and transferrins

the pH of the skin is often around 3-5, which is low enough to inhibit microorganisms, the pH of the stomach is about 2, and the pH of the vagina is very low

due to fatty acids in sebum as well as acids produced by bacteria on our skin

acids produced by a species of Lactobacillus

an enzyme produced in tears, sweat, and saliva that breaks down peptidoglycan and ruining that peptidoglycan layer make the cell vulnerable to damage and death

enzymes in our saliva, stomach, small intestine, and pancreas break down the carbohydrates, proteins, and lipids in bacterial cells as easily as the food we eat

iron-binding proteins in the blood, saliva, milk, and tears work by preventing iron from floating free in our fluids which prevent nutrients for microbes

they produce their own iron-binding proteis called siderophores that help them grab available iron

bacteria we pick up and drop off during the day when we come into contact with dust and other things

in the colon

innate immune system

crowd out pathogens and produce acids

Bacteroides

colon

Staphylococcus epidermidis

• Propionibacterium acnes
• Brevibacterium linens

major contributor to the acidity of the skin

major contributor to foot and body oder due to sulfer compounds it produces (methanethiol)

live microbes consumed for a benficial effect

lactobacillus (Lactobacillus acidophilus or Bifidobacterium - colon)

a good population of normal microbiota will always be present in the intestinal tract

neutrophils, basophils, eosinophils, monocytes, natural killer cells, B cells, and T cells

neutrophils

phagocytic, first responder

histamine

allergic and inflammatory responses

helminths

macrophages (which are phagocytic)

attack infected cells

PMNs (polymorphonuclear leukocytes)

anaphylactic shock - they histamine they release when stimulated cause capillaries to expand and become leaky all over the body - the loss of fluid from the blood is shock (anaphylactic bc of the things that enter the blood)

they live under skin and mucous membranes

vesicles of histamine - basic allergic reactions that affect they eyes and respiratory passages where their histamine cause a more local reaction that involves redness and swelling

No, they don't live in the blood

releasing toxins and reactive oxygen species (like peroxide)

they leave the circulatory system when stimulated and mature into macrophages

they come second (after neutrophils) and act as clean up crew

they wander through our tissues and respond to infection where they find it

a specific organ - Kupffer cells, microglial cells, and alveolar macrophages

macrophages found in blood vessels of the liver where they kill bacteria that flow by

macrophages found in the central nervous system (spinal cord, brain) where they migrate around and kill bacteria they find

passageways and alveoli of the lungs where they digest bacteria or particles that enter

they release perforin and granzymes - the perforin creates pores in the cell membrane which allows granzymes to enter then stimulate cell suicide

apoptosis

kill the host cell and then phagocytes (neutrophils and macrophages) kill any bacteria/viruses released

cytokines

chemicals (cytokines)

phagocytosis

phagocytosis, fusion of the vesicle with a lysozome, and digestion

initial ingestion of an invader, after the microbe is contained in a vesicle inside the cell

the vesicle merges with a lysozome (another vesicle filled with digestive enzymes)

various digestive enzymes begin breaking down all parts of the microbe (proteins, lipids, DNA, carbs) and other enzymes produce acids, hypochlorite, and an oxidative burst

the sudden production of various toxic forms of oxygen (ROS) - cause numerous undesirable reactions and interfere with all cell functions

virus-infected cells

the stimulate neighboring cells antiviral proteins (hopefully before it becomes infected), these proteins prevent viral biosynthesis and limit the spread of infection

therapeutically in combination with other drugs to treat chronic viral infections and some types of cancer

a set of proteins found in the blood, when damage or inflammation occur they enter the affected area and activate

form pores in the cell membrane of invading cells, resulting of the death of the invader

when the level of prostaglandins increase in the hypothalamus, which causes the hypothalamus to reset the body temp to a higher temp

infection

increases our metabolism and effectiveness of immune cells (the high temp does not kill pathogens)

• heat
• redness
• swelling
• pus
• pain

• injury causes mast cells to release histamine, prostaglandins, and other materials
• histamine increases vasodilation, vascular permeability, and phagocyte chemtaxis
• damage, sweeling, and prostaglandins all stimulate pain nerves

expansion of the blood vessels

increases blood flow to the area which results in heat and redness

allows fluids, phagocytes, complement, and antibodies to escape from capillaries - the accumulation of these fluids causes swelling

phagocytes flowing in the bloodstream sense histamine and other cytokines and they migrate to the damaged area

phagocytize dead neutrophils and damaged host cells

prostaglandins sensitize pain nerves

the adaptive immune system improves throughout the life as each person is exposed to more microorganisms

lymphocytes - they spend most of their time in the lymph system and the lymphoid tissues (but are also considered leukocytes because they spend part of their time in the blood)

collect fluids that leave the circulatory system and return them to the circulatory system near the heart

near lymphoid tissues

lymph nodes, tonsils, Peyer's patches, spleen

enlarged pockets that occur along the vessel of the lymph system

numerous lymphocytes that detect invaders that flow by in the lymph fluid

they fill up with large numbers of reproducing lymphocytes during infection

constantly sample materials on the surface and present the material to the immune cells under the surface which allows immune cells to respond to pathogens before they have time to penetrate the body

the small intestine

trap and destroy damaged red blood cells

CD4 cells

a molecule on the surface of helper t cell's that is important to their function

ringleaders of the immune system, they stimulate and regulate oher immune cells with the cytokines they release

antigens displayed on the surface of other immune cells, once stimulated they release cytokines that stimulate the immune cell

antibodies - each are identical and grab the same antigen

initial stimulation by an antigen and then stimulation by a helper t cell

plasma cells, memory cells

release large quantities of antibodies, all of which are identical and bind to the antigen that stimulated its production

they wait and multipy and release antibodies when we become infected again with the same pathogen, these cells help us react more quickly the second time

days

IgM - first stages of infection

IgG

they are both produced but IgG are much higher

to mimic the initial infection of a pathogen and stimulate the adaptive immune response (without causing sickness) so that the immune system can respond faster and stronger when exposed to the actual pathogen

proteins produced by plasma cells in response to an antigen and able to bind to the antigen

immunoglobulin

any molecule that stimulates the production of antibodies

proteins or polysaccharides on the surface of a pathogen

Y

IgG, IgM, IgA

immunoglobulin

a monomer

IgG

IgG

crosses the placenta and protects the fetus

a pentamer

IgM

agglutination

a dimer

IgA

IgA

IgA

• agglutination
• enhanced immune cell grip
• complement activation

antibody binding causes clumps of the pathogen to form

immobilizes them until immune cells can destroy them

CD8 cells

molecule of the surface of cytotoxic t cell's that is important to their function

infected cells

humoral immunity and cell-mediated immunity

immunity provided by antibodies

extracellular pathogens

immunity provided by cytotoxic t cells

intracellular pathogens

the study of the immune system

preparations designed to induce adaptie immunity

• whole agent vaccines
• subunit vaccines
• toxoids

whole cells or whole virions, but these may be weakened or killed

antigenic pieces of a pathogen, usually proteins or polysaccharides rom a cell membrane or viral capsid

they only contain necessary cell parts, so they're less likely to cause disease or have side effects

inactivated toxins

they reproduce in the host and mimic an actual infection

establish herd immunity and prevent outbreaks - if a large enough population is immune the risk is reduced because the chances of susceptible people coming into contact with someone infected is decreased

85-90% of population becomes vaccinated

antibodies against a toxin

after exposure to a toxin (like a snake bite) in order to provide immediate relief by neutralizing the toxin

toxins that cause botulism or tetanus

Serological tests

indentifying bacteria or diagnosing disease

agglutination and immunofluorescence

clumping

microscopic latex beads - they can be coated with antibodies - latex agglutination

hemagglutination

blood typing

bonded with fluorescent dye

Mycobacterium tuberculosis and Treponema pallidum (causes syphillus)

an inability to produce a normal immune response

AIDS (acquired immunodeficiency), SCID (severe combined immunodeficiency syndrome)

an enveloped retrovirus

CD4 cells - a protein in the envelope called gp120 attaches to the CD4 cells

• the first stage is usually asymptomatic
• as infection progresses, cell numbers drop, and susceptibility increases
• when tH cell count reaches 200/mm3 the CDC diagnoses AIDS

persistent yeast infections (oral in males, vaginal in females)

1000/mm3

10 years

Candida albicans (yeast infections that can spread to esophagus and lungs), Pneumocystis jiroveci (yeast that causes severe pnuemonia), and humans herpesvirus (causes Kaposi's sarcoma, a skin cancer)

sub-saharan africa

contact with the blood of monkeys killed or food

reverse transcriptase inhibitors, usually in combination with other drugs

Antibiotics

penicillin

Alexander Fleming - 1928

World War II

in animal feeds to encourage weight gain

species of Streptomyces

molds or species of Bacillus

they are soil microbes, and their antibiotics are useful in eliminating competition in the crowded soil environment

Spectrum of Action

tetracycline

gram-postive, gram-negative, and obligate intracellular bacteria

penicillin

only gram-positive bacteria

when the agent is unknown - normal microbiota

when the agent is known so the antibiotic can be targeted against a specific pathogen in the location of infection

selective toxicity

we don't want to harm the host when we're trying to heal them

bacterial pathogens - eukaryotic pathogens - viruses

prokaryotic cells have numerous differences from our cells that can be taken advantage of

human cells are eukaryotic and have many similarities to the cells of eukaryotic pathogens (fungi, protozoa, helminths)

viruses use host cells to reproduce, which makes it hard to inhibit viral production without inhibiting normal cell function

disk-diffusion test

Kirby-Bauer test

MIC - minimum inhibitory concentration

you have to reach the MIC in the body for the antibiotic to be effective at treatment but if the levels get too high the risk of side effects is high

using dose regimens in safe levels (above MIC, under toxic level)

inhibit production of an essential cell component or injure the cell membrane

peptidoglycan, proteins, nucleic acids, nutrients

provides protection against physical damage and osmotic pressure

they are required for nearly all active functions of a cells

cells can't reproduce or make proteins if they can't make nucleic acids

lack of essential nutrients eventually causes death of a cell

penicillin (all of the -cillins), bacitracin

they make proteins and proteins are needed for all cell function

tetracycline (all of the -cyclines), neomycin, and erythromycin

prevents cell from dividing - prevents transcription and protein production

rifampin, chloroquine, acyclovir, and reverse transcriptase inhibitors

trimethoprim and sulfamethoxazole (sulfa drugs) inhibit folic acid synthesis

polymyxin B, clotrimazole, and miconazole

bacitracin (inhibits peptidoglycan synthesis), neomycin (inhibits protein synthesis), and polymyxin B (injures cell membranes)

mutations or genetic recombination

late 1940's

prevent entry of the drug, inactivate the drug, alter the target of the drug, or eject the drug from the cell

using the outer membrane of gram-negative bacteria

enzymes produced by the cell break down the antibiotic - penicillinase

the cell begins producing an altered version of the antibiotic target, the altered version still accomplishes its task but is resistance to antibiotics

pumps in the cell membrane quickly remove an antibioitc and send it to the exterior

TSS (toxic shock syndrome), Necrotizing fasciitis, and Inflammatory acne

Warts, Cold Sores, Genital Herpes, Chickenpox/Shingles, and Kaposi's sarcoma

tinea, candidiasis, and dandruff

dracunculiasis

pediculosis

neonatal conjunctivitis and trachoma

staphylococcus aureus (usually)

streptococcus pyogenes (usually)

propionibacterium acnes

HPV

herpes simplex virus 1

herpes simplex virus 2

vericella zoster virus

human herpesvirus 8 (HHV-8)

dermatophytes (usually Trichophyton)

Candida albicans

malassezia globosa

dracunculus medinensis (guinea worm)

pediculus humanus (lice)

neisseria gonorrhoeae or chlamydia trachomatis

chlamydia trachomatis

superantigen

fever, vomiting, rash, fatigue, and shock

exotoxin A

superantigen

destruction of local tissues

digestion of sebum oils releases fatty acids

virus stimulates cell division

sacral nerves, reactivation causes eruption on the outer genitalia

trigeminal nerves, reactivation causes eruption usually on the edge of the lips

nervous, reactivation causes shingles

raised dark red lesions on the skin

keratinases (and other proteases) which permits infection of skin, hair, and nails

whitish patches on surface

disgestion of sebum lipids releases fatty acids that irritate the skin

increase in cell division (flaking)

an emerging worm causes a blister and burning sensation

lice feed on blood, skin is sensitized to louse saliva, causes itching

infection of the conjuctiva, eventual damage to cornea leads to blindness

infection of conjunctiva, long term inflammation leads to scarring under eyelid, scards abrade the cornea

nosocomial

tampons

25%, nose

A strep, beta strep

the beta-hemolysis it causes on blood agar

10%, throat

skin acidity, adolescents (produce more sebum)

skin or cervical cancer

90%, infancy

25% of US adults over the age of 30

HHV-3, direct contact or respiratory route

AIDS

jock itch, athlete's foot, ringworm, and nail infections

tenea cruris

tinea pedis

tinea capitis, if on the head - tinea corporis, if on the body

tinea unguium

failing immune system in an HIV infection (decrease in number of helper t cells)

normal microbiota of scalp

contaminated drinking water, humans only

dracunculiasis

head/body lice, not pubic lice (crabs)

pubic lice - Phthirus pubis

erythromycin (US) - iodine solutions (rest of world)

same species that causes STD chlamydia, but non-sexually (touching, fomites, vectors)

trachoma

obligate intracellular parasites