Microbio Exam 3 comprehensive study guide

Disinfectants

Destroys harmful microorganisms (99.9% of bacteria and viruses)

antiseptics

destroys harmful microorganisms from living tissue (mouth wash)

Sterilants

removes and destroys ALL microbial life through sterilization

Biocides

(germicide) are treatments to KILL microbes but not necessarily endospores.

Biostatics

inhibiting microbial and fungal growth

Bio. Safety level 1:

microbes that don’t cause many diseases, low risk microbes

Bio safety Level 2:

microbes are where they generally belong and have varying severity in diseases. 

Bio safety level 3:

Microbes are indigenous or exotic and could potentially be lethal, spread through respiratory system

Bio. safety level 4:

Very hard to kill, lethal high-risk microbes

• require treatment or vaccines

Dry heat

Kills by oxidation

• Flaming is very common in sterilizing loops

• incineration used to deal with lots of garbage

• hot air steer is usually electrical reaches high temps

Boiling (moist heat)

denatures enzymes and proteins

• easiest at home or industry method

Pasteurization

Heat treatment that kills harmful pathogens and spoilage microorganisms in food

• enhances food safety and extends shelf life

Autoclave

Applies steam under pressure

• combo of heat and pressure

• Kills ALL organisms and endospores

• Hospitals use strips to know if somethings sterile

Application of filtration

Passage of liquids and air through a filter

• Used for heat sensitive materials

• HEPA air filters can remove endospores, microbes, and viruses as air flows through

• Membrane filters deal with larger units and use a vacuum to draw out the solution

• Smaller membrane filters use syringes

What conditions affect the activity of a antimicrobial agent

• Population size; larger vs. smaller populations

• Composition of population; microorganisms and sensitivity to antimicrobial agents

• Concentration or intensity of an antimicrobial agent; higher concentrations kill faster

• Duration of exposure; longer exposure = more organisms killed 

• Temperature; higher temp usually increases killing

• Local environment; many factors impact effectiveness depending on the thing (pH, organic matter conc.)

Surfactant

• Surface active agents; group of chemical Compounds that lower the surface tension of water. 

  • Major ingredients in soaps and detergents

Goal of antimicrobial drugs

synthetic substances made to interfere with microbial growth

Chemotherapy

the use of chemicals to treat disease

antibiotics

Substance made by a microbe that inhibits another microbe in small amounts

Selective toxicity

selectively finding and destroying pathogens without hurting the host

Spectrum of activity of antimicrobial drugs

• Narrow spectrum of microbial activity: drugs affect a narrow range of microbial types 

• Broad spectrum antibiotic: affects a broad range of graph positive or gram-negative bacteria

Compare regular toxicity to selective toxicity

• Toxicity: side effects caused by drug

• Selective toxicity: selectively kills or inhibits growth of microbial targets while causing minimal or no harm to the host

What is the significance of dosage?

amount of medication given during a certain time interval

• ensures that optimum therapeutic drug levels are reached at the site of the infection without causing significant side effects

Whats the significance of the route of drug administration

• Orally; pros are that patients can more conveniently take these drugs at home. Cons are that some drugs aren’t easily bodied by GI tract into bloodstream

• Parenteral route (injection); pro is short time it takes to reach high concentrations in plasma. Is typically performed in health care settings.

What are factors and variables that can influence the side effects of a drug

• Half life of drug: rate at which 50% of a drug is eliminated from plasma 

• Toxicity: side effects caused by drug

• Selective toxicity: selectively kills or inhibits growth of microbial targets while causing minimal or no harm to the host

Bacteriostatic vs bactericidal activities

Bactericidal kills directly while bacteriostatic just inhibits growth

• Synergism (+): 2 antibacterial drugs may be administered together to improve efficacy

• Antagonism (-): can occur between 2 antimicrobials or between antimicrobials and non-antimicrobial used to treat other conditions. Interactions may cause loss of drug activity, decreased therapeutic levels due to increased metabolism and elimination, or increased potential for toxicity

How do drugs inhibit cell wall biosynthesis

• cell wall made of peptidoglycan and proteins. Forming a beta-lactam ring stops peptidoglycan from being made

  • Natural penicillin; susceptible to penicillinases

  • Semisynthetic penicillin; contain chemically added side chains that make them resistant to penicillinases

How do drugs inhibit protein synthesis

• targets different steps in bacterial translation. 

  • Chloramphenicol: binds to 50S subunit of 70S ribosome to stop peptide bond formation. Can suppress bone marrow and affect blood cell formation

  • Tetracyclines: interfere with tRNA attachment to ribosomes

How do drugs inhibit membrane function

polypeptide antibiotics change membrane permeability. The membrane targeting mechanism isn’t a selective toxicity

How do drugs inhibit nucleic acid synthesis

• Interferes with DNA replication and transcription. Stops DNA replication by inhibiting DNA polymerase and DNA helicase, and blocks transcription by inhibiting RNA polymerase

  • Not selective toxic for DNA, but is selectively toxic for RNA

How do drugs inhibit metabolic pathways

Antimetabolites compete with normal substrates for an enzyme.

• Sulfanilamide competes with para-aminobenzoic acid (PABA), stopping the synthesis of folic acid

Explain drug resistance

Antimicrobial resistance happens when microbes develop the ability to defeat drugs designed to kill them

How do microbes use an efflux pump in drug resistance

transports antibiotics or other poisonous substances out of bacteria

• uses transport proteins

• builds resistance to multiple drugs at once

How do microbes use blocked penetration in drug resistance

just doesn’t let anything in

How do microbes use inactivation of enzymes in drug resistance

stops needed metabolic processes, which causes structural breakdown and death

How do microbes use target modification in drug resistance

changes the composition of structures like enzymes or ribosomes to stop antibiotics from binding

• spontaneous mutations can change the targets of antibiotics and build drug resistance

Describe tests used to determine microbe susceptibility to an antibacterial drug.

• Give drug in appropriate concentrations to destroy susceptible microbes

• Give two or more drugs at same time

• Use drugs only when necessary

• Possible future solutions:

  • continued development of new drugs

  • use of bacteriophages to treat bacterial disease

How do microbes fight drugs

• Microbes are constantly evolving

• widespread clinical use of antibiotics has also provided selective pressure for microbes to evolve

  • overuse and misuse of antimicrobials,

  • inappropriate use of antimicrobials,

  • Sub-therapeutic dosing, and

  • patient noncompliance with the recommended course of treatment

• once resistance originates in a population it can be transmitted to other bacteria

  • a particular type of resistance mechanism is not confirmed to a single class of drugs

• Microbes in abscesses or biofilms may be growing slowly and not be susceptible

• Resistance mutants arise spontaneously and are then selected

How do you test the effectiveness of an antimicrobial drug

• Kirky-baur disc diffusion test: Paper disks with a chemotherapeutic agent are placed on agar containing the test organism

  • Zone of inhibition around the disk determines the sensitivity of the organism to the antibiotic

• Dilution test measures the minimal bactericidal concentration of a drug

• E test: gradient diffusion method that determines antibiotic sensitivity and estimates minimal inhibitory concentration

What happens if you stop an antibiotic prescription early?

It will leave the toughest microbes that were harder to kill remaining, and those microbes will come back with a resistance to the antibiotic and be tougher to kill

Disease

Any condition in which normal structure or functions of the body are damaged or impaired

• infection by a pathogen,

• genetics (as in many cancers or deficiencies),

• noninfectious environmental causes, or

• inappropriate immune responses

Infection

successful colonization of a host by a microorganism

Pathogenicity

potential ability to cause disease 

• it’s qualitative; either an organism can or cannot cause a disease

Virulence

disease producing power of an organism or the degree of pathogenicity when compared within a group

• quantifies pathogenicity: Median infectious dose (ID) is the number of pathogen cells needed to cause active infection in 50% of inoculated animals.

• Median lethal dose is number of pathogenic cells or amount needed to kill 50% of the infected animals

What features protect cells against phagocytosis (come back to)

• Capsule production and proteases to protect against phagocytosis and destruction of antibodies

• Use a variety of virulence factors. 

What’re the 2 types of infectious diseases

disease caused by direct effect of a pathogen

• Communicable: contagious disease easily spread from person to person

• Non-communicable: infectious disease not spread from person to person

iatrogenic infectious diseases

contracted as result of medical procedure

• wounds/flesh-eating Clostridium

Nosocomial infectious diseases

disease acquired in hospital settings

• MRSA

Zoonotic infectious diseases

transmitted from animals → humans

• rabies, yellow fever, flu

What’re the stages of acute infectious disease in terms of number of pathogens present and severity of signs and symptoms.

1. Incubation period: low pathogen #, very few symptoms

2. prodromal period: mid pathogen #s, average symptoms

3. Illness period: sick and getting sicker. Pathogen #s rise and symptoms worsen to a peak

4. Decline period: pathogen #s start to decline and symptoms lessen

5. convalescence period: symptoms stop quickly before the pathogen #s eventually do

Koch’s postulates

• 1. Suspected agent must be gone in all healthy organisms, but present in the diseased organisms

• 2. Isolate causative agent from infected organism and grow it in culture

• 3. Cultured agent must cause same disease when put into healthy regular patient

• 4. Same agent must be reisolated from inoculated diseased organism

What are the limitations of kochs postulates

• many pathogens aren’t culturable

• some only cause disease in certain hosts

• Some diseases are asymptomatic

• Some diseases involve multiple pathogens

What determines outcome of host parasite relationship (come back to)

• if they’re primary or opportunistic (attack when immune system compromised)

How do virulence factors contribute to signs and symptoms of infectious diseases

• pathogens may make exoenzymes or toxins that work as virulence factors to let them colonize the host

  • Production of toxins contributes to signs and symptoms of diseases

• Virulence factors used for adhesion to attach to receptors on the host cell. They use adhesin (protein or glycoprotein)

• Bacteria use virulence factors to evade phagocytosis

Explain toxins

Poisonous substances produced by microorganisms. 

• Produce fever, cardiovascular problems, diarrhea and shock 

• Endotoxins

• Exotoxins

• Toxigenicity: ability of microorganism to make toxin

• toxemia: presence of toxin in hosts blood

• intoxication: presence of toxins without microbial host

Endotoxins

• Built into the structure of a bacterium and released when the cell is damaged. 

  • Often cause fever, inflammation, sometimes serious septic shock

Exotoxins

• Proteins made inside pathogenic bacteria as part of their growth and metabolism. The exotoxins are then secreted into the surrounding medium during the log phase. 

Virulence factors of eukaryotic pathogens

• Fungal virulence: production of adhesins and proteases (Candida), capsule production (Cryptococcus), exotoxins (Claviceps purpurea – ergotism)

• Protozoan virulence: unique features for attaching to host cells like flagella, antigenic variation, formation of capsules.

• Helminth virulence: proteases to penetrate skin, large size to evade the immune system, and destruction of antibodies.

Epidemiology

Study of where and when diseases occur, and how they’re transmitted in populations 

Notifiable disease (noteworthy)

diseases that physicians are required to report occurrences of

• considered to be important for public health on national scale

Mortality

deaths from a notifiable disease

Morbidity

incidence (number of new cases) of a specific notifiable disease.

• incidence measures risk of developing disease

Sporadic diseases

uncommon, occurs only occasionally and affect relative number of persons.

Endemic diseases

constantly present in certain percentage of population

Epidemic diseases

Disease acquired by many people in each area, causing damage to living organisms in short period of time

Pandemic diseases

affect large geographical area, often global scale

What’re the types of epidemiological studies?

• observational: data gathered from study participants through questions or measurements

• Experimental: Uses lab or clinical studies to manipulate the subject and study connections between diseases and potential causative agents or assess treatments

Which factors would increase the spread of a communicable disease? (comeback to?)

• High population density

• quick global travel

• poor hygiene and sanitation

How can diseases be transmitted

• Direct contact transmission: requires close association

• Indirect contact transmission; spreads to a host by a nonliving object called a fomite

• Droplet transmission: transmission via airborne droplets less than 1 meter

• Vehicle transmission; transmission by inanimate reservoir. (waterborne, foodborne, or airborne)

• 2 general methods of disease transmission:

  • Mechanical transmission: arthropod carries pathogen on its feet

  • Biological transmission: pathogen reproduces in vector; transmitted through bites or feces

What’re nosocomial infections

• A healthcare associated infection that was acquired while receiving treatment in a health care facility; got sick by being in hospital

  • Mostly upper respiratory tract infection

  • 1/25 in hospital patients are infected

  • 2 mil people per year infected, leads to 20,000 deaths

What’s a compromised host

An individual whose resistance to infection is impaired by disease, therapy, or burns

What factors contribute to re-emerging and emerging diseases

• If they’re zoonotic, need a vector, or are viral

• Population growth, migration, international air travel

• Poverty wars and destructive ecological changes

What’s innate immunity

Ability to fight infection or toxins. If not immune then they’re susceptible to disease

• Present at birth, protect against any pathogen, doesn’t discriminate between what’s you and what’s not you. Has no memory. 

What is adaptive immunity

specific; responds to specific pathogens, discriminates between self/non-self memory. 

• T cells and B cells

What’re the main anatomical features of the lymphatic system

• lymph: carries microbes to lymph nodes where lymphocytes and macrophages destroy the pathogen

• lymphatic vessels

• lymphoid tissue

• red bone marrow

what’re some of the functions of antimicrobial peptides

• a special class of broad-spectrum antimicrobial mediators

  • nonspecific (can interfere with different pathogens)

• Some AMPs are secreted by microbiota, macrophages, or other parts to inhibit pathogens such as bacteria, viruses, or fungi by disrupting their cell membranes

What’s the complement system

• Complement is a group of over 30 proteins circulating in serum that are activated in a cascade: one complement protein triggers the next

• Complement activation is the process by which circulating complement precursors become functional

• Process triggered by classical, alternative, or lectin pathways

What’re the outcomes of complement activation

• Cytolysis: Proteins create a membrane attack complex (MAC). Microbes burst as extracellular fluid flows in through transmembrane channel formed by membrane attack complex.

• opsonization: Coating microbes with C3b promotes attachment of a phagocyte to a microbe

• inflammation: Blood vessels become more permeable, and chemotactic agents attract phagocytes to area.

What’re interferons

• cytokines (proteins) made by cells that have antiviral activity

• made in response to viral infections, cause neighboring cells to make antiviral proteins to inhibit viral replication

• some cause neutrophils and macrophages to kill bacteria

• induce apoptosis in viral cells

• activate and stimulate immune cells in response to viruses

What’re the signs of acute inflammation and fever?

• symptoms: redness, swelling, pain, and heat

• destroys harmful agents or limits their effect on the body

• replaces and repairs tissue damaged by harmful agent

• Inflammation activates acute-phase proteins by the liver that cause vasodilation and increased permeability of blood vessels

What’re the cellular and molecular mediators of inflammation

• histamine: stimulates vessels to open further.

  • Blood plasma and platelets are released into area.

• Kinins: Bradykinin – causes heat, promotes extravasation (diapedesis), stimulates mast cells to degranulate, and release histamine

• Prostaglandin: promotes histamine release, contribute to fever

• Leukotrienes: pro-inflammatory mediators produced by leukocytes

• Cytokines: small proteins important in cell signaling

What’re the signs of chronic inflammation

Some pathogens resist host defenses

• Remain in body stimulating inflammatory response

• Body “walls off” site of inflammation forming a granuloma

  • Fibrotic lesion around bacteria

Identify and describe components of blood

Cells and cell fragments suspended in plasma

• Erythrocytes (red blood cells): transport oxygen from lungs to body tissue, and bring CO2 back to lungs

• Leukocytes (white blood cells): immune system response cells that travel through bloodstream to attack foreign pathogens

• Platelets: stop bleeding by adhering to blood vessel walls

• Created in red bone marrow stem cells via hematopoiesis

What’re the possible outcomes of the inflammation process (come back to?)

Explain the process of phagocytosis and the mechanisms by which phagocytes destroy and degrade pathogens.

Phagocytosis: cells capacity to seek, ingest, and kill pathogens

• phagocytes squeeze between endothelial cells of blood vessels through diapedesis

• trans endothelial migration: sticking of phagocytes to blood vessels in response to cytokines at site of inflammation