Microbiology

Unit 3

Serology

Study of blood serum and its disease fighting chemicals

Immunology

study of body’s defenses

Antigen

foreign substance that requires an immune response

APCs

B cells, dendritic cells, macrophages (presents antigens to the T-helper cells)

Cytokines

communication, chemicals (proteins/glycoproteins)

MHC glycoproteins

holds fragments of pathogen’s antigens (epitopes) for display to immune cells in lymph nodes

First line of defense

nonspecific, immediate, (skin, mucous membranes, lacrimal glands, microbiota)

Second Line of Defense (innate)

leukocytes (granulocytes- N,E,B) (agranulocytes-M,L, macrophages and dendritic cells), inflammation, fever, antimicrobial proteins

PRISH

pain, redness, immobility, swelling, heat

acute inflammation

develops rapidly, last few days/weeks, mild-self limiting

chronic inflammation

develops slowly, months/years, severe-progressive

function of inflammation

destroys agent, limit effects, repair/replace damaged tissue

Fever

enhances interferon action, inhibits growth microbes, improves cell function and tissue repair

complement system

30 proteins produced by the liver, destroys gram (-) by cytolysis, enables opsonization of pathogens and enhances inflammation.

interferons

proteins produced by virus-infected cells that help to inhibit viral replication and activate immune cells.

iron binding proteins

keeps iron levels low, bacteria (siderophores) steal iron

antimicrobial peptides

small proteins that can kill bacteria, fungi, and viruses by disrupting their cell membranes.

Class 1 MHC proteins

on all mammalian nucleated cells (identifies cell as ‘self’)

class 2 mhc

on apcs (b cells, macrophages, dendritic cells)

epitopes

specific regions on antigens that are recognized by antibodies or T cell receptors. to trigger an immune response

Cytotoxic T cells

A type of T cell that kills cancer cells, cells that are infected (particularly with viruses), or cells that are damaged in other ways.

T helper cells

A subset of T cells that help activate B cells and cytotoxic T cells, playing a crucial role in the immune response. regulates activity of other immune cells and enhances their functions.

T helper 1 cell

assists CD8 cells and regulates innate immunity

T helper 2 cells

functions with b cells

T helper 17 cells

a subset of T helper cells that play a role in the immune response against extracellular pathogens and are involved in inflammation and autoimmunity.

T regulatory cells

combats autoimmune reactions, protect normal resident microbiota

humoral immunity

the aspect of immunity that involves B cells and the production of antibodies to neutralize pathogens.

IgG

a type of immunoglobulin that is the most abundant antibody in the blood and extracellular fluid, playing a crucial role in the body's immune response.

IgM

large, made first

IgA

good for protection of GI, respiratory, urinary, and reproductive tractsand is found in mucosal areas, saliva, tears, and breast milk.

IgE

a type of immunoglobulin associated with allergic reactions and responses to parasitic infections.

IgD

a type of immunoglobulin involved in B cell activation and maturation.

Antibody functions

activation of complement and inflammation, Neutralization (neutralize toxins/prevent adhesion), opsonization (phagocytosis), Killing by oxidation (direct/chemicals), Agglutination (lumps),Antibody Dependent Cellular Cytoxicity (binding causes lysis by natural killer cells

primary immune response

cannot be immune before first exposure, memory b and t cells formed—immunity

secondary immune response

faster, more effective, immunization after first exposure

attenuated vaccine

weakened live, closely mimics natural infection—lifelong immunity, rare potential=disease

inactivated vaccine

cannot=disease

naturally acquired immunity

natural response to infection by organisms

naturally acquired passive immunity

Mom’s IgG antibodies across placenta, breast milk

Artifically acquired active immunity

vaccine

Artficially acquired passive immunotherapy

given antibodies made in humans or animals.

sterilization

elimination of all harmful microbes including viruses and bacterial endospores, but not prions

aseptic

free of contamination by pathogens

aseptic technique

procedures conducted to prevent contamination of individuals, cultures, and the surrounding environment

disinfection

destructive of vegetative cells and many viruses on inanimate objects

antisepsis

disinfection of skin/tissues

suffix -stasis/-static

inhibits microbial growth

suffix -cide/-cidal

=agents that destroy or permanently inactivates microbes

microbial death

permanent loss of reproductive ability

biosafety levels

BSL1- many student micro labs (not ours)

BSL 2- moderate risk, gloves, goggles, lab coats

BSL 3- highly infectious airborne pathogens

BSL 4- The “hot zone”, sealed lab, space suits, negative pressure

antimicrobials

encompasses drugs against all types of microbes

antibiotics

reserved for drugs against bacteria only

Selective Toxicity

drugs more toxic to pathogen than host (6 methods)

• inhibits cell wall synthesis, protein synthesis, disrupt cell membranes, inhibits metabolic pathways, inhibits nucleic acid synthesis, blacks viral activities

1) inhibits cell wall synthesis

cell wall protects against osmotic pressure effects, inhibits cell wall formation-weakens cell wall-lysis, targets only actively growing cells (beta-lactams, polypeptide antibiotics, antimycobacterial antibiotics)

2) inhibit protein synthesis

pro(70s) euk(80s) ribosomes, can -activate liver and bone marrow cell problems in ribosmes, if affect large subunit-distorts mRNA-total stoppage of protein synthesis, is small subunit affected then causes misreading of mRNA (aminoglycosides, tetracyclines, macrolides, axazolidinones)

3) disrupt cell membranes

some antifungal drugs combine with sterols in fungal plasma membrane, ineffective against bacteria (no sterols in membrane, may bind to cholesterol in human membranes) some antiparasitic drugs, polypeptide antibiotics

4) inhibit metabolic pathways

interferes with electron transport, inactivates of enzymes with heavy metals, blocks viral activation

5) inhibits nucleic acid synthesis

rifamycins block bacterial topoisomerase or RNA polymerase activity, reverses transcriptase inhibitors

6) blocks viral activity

may blocks attachment, entry, uncoating, genome integration, nucleic acid synthesis, exits, viral DNA polymerase uses more easily and replication more rapid

Antiprotozoan drugs

some interfere with anaerobic metabolism, some mechanisms unknown, quinine’s synthetic chloroquine, metronidazole

Anthelminthic drugs

sushi- tapeworm incidence increased, treated with miclosamide or praziquantel, some inhibit microtubule formation, some membrane permeability

the perfect antimicrobial

available, inexpensive, stable, easily administrated, nontoxic/nonallergenic, selectively toxic against pathogens

Broad spectrum

affects wide range of pathogens, streptomyocin,tetracycline, erythromycin

narrow spectrum

affects only a few kinds of pathogens, isoniazid, penicillin

microbial antagonism

competes with check growth of pathogens and other microbes, if certain organisms in normal flora not destroyed by antibiotics but their competitions are normal flora-opportunistic pathogens

superinfection

growth of target pathogen that has developed antibiotic resistance

The 6 mechanisms of resistance; the first three

1- make enzymes (destroy/inactivates drugs)

2- slow/prevent penetration of antibiotic to target (block entry into cell, especially gram negatives do this-modify porins)

3- targets modifications (alters target/metabolic chemistry, reduces amount of target overproduce target or stop producing target)

The 6 mechanisms of resistance: the last three

4) pump antibiotic out with efflux pumps\

5) biofilms

6) protects metabolic target of antibiotics with decoy molecule

cross resistance

some resistant to one drug gain resistance to another

The price of resistance

higher disease, higher mortality rates, combats resistance, new drug development, development of 2nd 3rd generation

side effects of antibiotic use

liver/kidney damage, toxicity, synergism(2 drugs together-greater effect), antagonism (neither effect when together better when acted alone), allergy response, therapeutic index

pathology

study of disease

pathogenesis

how disease develops

pathogen

microorganism able to cause disease

pathogenicity

ability to cause disease in another organism, called a host

etiology

cause of infectious disease

infection

invasion of body by a pathogen and it begins multiplying

disease

if infection causes departure from health and signs/symptoms appear

opportunistic pathogens

some normal flora, some not

obligate pathogens

rarely in host without disease

Resident microbiota

Microorganisms that normally live in a specific environment in the body.

Transient Microbiota

present days, weeks, months, but disappears, competition, body defenses dislodged

Microbial antagonism

prevents overgrowth of harmful organisms, nutrient competition, if upset it can cause disease

commensalism

2 organisms interact, one benefits, one unaffected

Mutualism

both organisms benefit

Parasitism

one organism benefits and other is harmed

Koch’s postulates

A set of criteria established by Robert Koch to identify the causative agent of a particular disease. The postulates include: 1) The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms. 2) The microorganism must be isolated from a diseased organism and grown in pure culture. 3) The cultured microorganism should cause disease when introduced into a healthy organism. 4) The microorganism must be re-isolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

Limits of Koch’s postulates

some cannot be cultured on artificial media, multiple pathogens can cause same symptoms, more than 1 organism or environmental factor needed to cause disease, some pathogen can cause several disease, ethical considerations

classifying infectious disease

manifestations of disease, behavior within host/population, occurence of disease, severity or duration of disease, extent of host environment, timing

symptoms

changes in body function - subjective

signs

observable and/or measurable changes -objective

syndrome

group of symptoms or signs accompanying a disease-helps with diagnosis

communicable disease

disease can spread from one host to another either directly or indirectly like chicken pox

contagious disease

easily spread from one person to another

noncommunicable disease

not spread from one host to another, caused by normal flora or other environmental microbes that must be inside body to cause disease

incidence

number of new cases of specific disease during specified time interval, rate of occurrence of new cases, indicates spread of specific disease, risk of contracting

prevalence

number of cases (already existing) of specific disease at specified time, how serious it is and how widespread the disease is

sporadic disease

occurs occasionally

endemic disease

constantly present in a population- like a common cold

epidemic disease

many get the disease in short amount of time- influenza