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1. Compare prokaryotes and eukaryotes Prokaryotes -do not have membrane bound nucleus hereditary material suspended in a portion of cytoplasm ( nucleoid/nuclear region ) devoid mitochondria and organelles eg: mycoplasma, ricketsia, Chlamydia, bluegreen algae Eukaryotes -have distinct nucleus membrane-bounded nucleus contain mitocondria and organelles eg: algae, protozoa, slime moulds, fungi
a) viroids : protein free fragments of single stranded circular RNA that cause disease in plants b) prions : infectious proteins devoid of nucleic acid. c) virions : complete virus particle that is composed of a nucleic acid core (DNA or RNA) surrounded with a protein coat(capsid)
Chapter 2 BACTERIAL STRUCTURE
1) Enumerate the functions of:
a) Ribosomes -site of protein synthesis -selective target for antibiotic action b) Mesosomes -involved in cell division and sporulation -membranous support for respiratory enzymes c) Cytoplasmic membrane -selective transport -excretion of extracellular enzymes
-respiration -cell wall biosynthesis -reproduction -chemotactic system d) Cell wall –maintain characteristic shape of bacterium -support against high internal osmotic pressure of protoplasm(5-25atm) -cell division -staining affinity of organism e) Capsule -protection against antibacterial agents -protection from phagocytosis (considered as virulence factor) -attachment to target surface to establish infection
f) Flagella -movement of bacteria towards regions with higher concentration of nutrients and solutes or away from disinfecting substances (negative chemotaxis) g) Fimbriae (pili) -adherence and attachment to host surfaces to establish infection -conjugation
2) Compare : a) The composition of Gram positive and Gram negative cell wall Gram positive -peptidoglycan and teichoic acid Gram negative -peptidoglycan,outer membrane and periplasmic space
b) Mycoplasm and L-forms of bacteria Mycoplasm L-form of bacteria
-exist without cell wall
-wall deficient or defective bacteria
c) Flagella and fimbriae (pili) Flagella -consist of protein called flagellin which are highly antigenic -function: for movement of bacteria
d)Short pili and sex pilus
pili -composed of structural protein subunits called pilins -function: adherence and conjugation
Short pili -enable bacteria to attach to host surfaces and establish infection
sex pili -involved in transfer of DNA between bacteria by process of conjugation
3) Give reasons for : a) The impressive strength of cell wall -it is formed of peptidoglycan b) Mycoplasm do not assume a defined shape -lack of rigid cell wall c) Mycoplasm are resistant to penicillin -it exists without cell wall and resistant to cell wall inhibitors as penicillin d) The capsule is considered an important virulence factor -protect bacterial cell from phagocytosis
e) Fimbriae are considered a virulence factor -enable bacteria to attach to host surfaces and establish infection f) The marked resistnce of spores -thermal resistance is due to high content of Ca and dipicolinic acid -impermeability of cortex and outer coat -low content of water
smaller than the 80S ribosomes of eukaryotes. permanently lose the capacity to produce a cell wall -they may survive antibiotic therapy. -they present in isotonic medium -some L-forms resynthesize their walls once the inducing stimulus is removed.others. b) Axial filaments -composed of two groups o fibers that originate within the opposite ends of the cell and overlap in the middle. .their reversion to the walled state can produce relapses of the overt infection. streptococci -the cocci that divide on many planes produce clusters eg.L-forms of bacteria -they are wall defective or wall deficient bacteria -they loose their cell wall when exposed to hydrolysis by lysozyme or by blocking peptidoglycan biosynthesis with antibiotics. -the cocci that divide along a single plane produce diplococci or chains eg. d) the cause and effect of the cell wal rigidity cause: primarily due to peptidoglycan effect: maintains the characteristic shape of the bacterium 5) Give an account: a.-very low metabolic and enzymatic activity 4) Comment : a) The arrangement of cells is determined by the planes of cell divisions. staphylococci b) bacterial ribosomes are a selective target for antibiotic actions -prokaryotic ribosomes have a sedimentation constant of 70S. such as penicillin. c) the mesosomes have a function analogous to the mitochondria in eukaryotes -they provide a membranous support for respiratory enzymes.
Flavobacterium spp. in Vibrio cholerae and may reach 24 hours in Mycobacterium tuberculosis.-called “endoflagella” because it is structurally and chemically similar to flagella. as they can not synthesize complex organic substances from simple inorganic sources.Give reasons for a) obligate anaerobes die in presence of O2 : because obligate anaerobes lack superoxide dismutase and catalase and so they cannot grow in presence of of O2. c)Most bacteria of medical importance are mesophils : because they can grow within range of 20-40oC which can replicate on or in human body at optimum temperature of 37oC which is the normal body temperature. b)Most bacteria of medical importance are heterotrophs : because they require organic sources for carbon.Pathogens which replicate on or in humanbody are able to grow within this range. Chapter 3 BACTERIAL GROWTH 1.and flexes and bends along its length.g.It may be as short as b) c) d) e) f) g) h) 13 min. Eg:spirochaetes-move by means of axial filaments by rotating along its longitudinal axis.g: Clostridium perfringens Capnophilic bacteria: microorganisms which thrive in the presence of high concentrations of carbon dioxide (CO2) or which require the presence of carbon dioxide to survive. Mesophiles: organisms that grow within a temperature range of 20-40oC.g. Colony: macroscopic products of 20-30 cell divisions of a single bacterium on solid media. . Psychophiles: (cold loving) are capable of growth at refrigeration temperature (0-8oC) e. Thermophilus: (heat loving) grow best at high temperature (>60oC). Bacillus stearothermophilus. with an optimum temperature of 37oC which is the the normal body temperature. e. Growth: is an increase in the size and number of organisms. 2. Define a) The generation time: is the time between two successive divisions. Aerotolerant anaerobes: have an anaerobic pattern of metabolism but can tolerate the presence of oxygen because they possess superoxide dismutase e.
Chapter 4 BACTERIOPHAGES 1.Define: a)Lysogenic bacteria: :bacteria carrying the integrated phage genome ( the phage DNA integrated with the bacterial chromose and divides with it to pass into daughter cells ) :the phage DNA integrated with the bacterial chromosome and divides with it to pass into daughter calls. b)Prophage c)Lysogenic conversion d) Eclipse phase . ( integrated phage genome ) :acquisition of a new character coded for by a prophage DNA :no phage components are detected inside the cells. Structure of bacteriophage 2.
to specific receptors on the bacterial cell.3. by its tail. 2. Induction maybe spontaneous or achieved by an inducer. phage typing. Intracellular synthesis: of phage nucleic acids.Give an account on: a) Lytic cycle of phage replication cycle: this cycle ends in lysis of the bacterial host cell and release of a newly formed phages 1. capsids and tails.the prophage may be carried inside the bacterial cell indefinitely passing to daughter cells. 5. Penetration: The tail sheath contracts and the nucleic acid is injected into the cell.Give reason: Lysogenic diphtheria bacilli are toxigenic -only capable to produce toxic when lysogenized. 3. The empty head and the tail are left outside the cell.the prophage may be induced to detach from the bacterial chromosome and start a lytic cycle. 4. research elements in some biological n genetic studies 4. cloning vectors in recombinant DNA technology 2. Several hundreds of phage components are synthesized. Release: The bacterial cell bursts liberating a large number of phage particles to infect new cells. Eclipse phase: in which no phage components are detected inside the cell. Assembly: The phage components aggregate to form a complete phage particles which mature into typical infectious phage. 6. 2. . It takes a short time ( minutes to hours ) during which viral nucleic acid directs the host cell metabolism to synthesize the enzymes and proteins required for phage synthesis. Adsorption: The phage attaches.g: UV light. b)Outcome of the temperate phage cycle 1. 3. c)Practical uses of bacteriophages 1. The specificity of this process determines the susceptibility of bacteria to different phages. E.
2. The bacterial genome Total set of genes present inside the bacterial cell.cell Large Non-conjugative Plasmids Usually small >30 Absent By the help of conjugative plasmid Common in Gram+ve cocci Cannot conjugate Size Copy number F factors Transfer among bacteria Host bacteria Conjugation .Chapter 5 BACTERIAL GENETICS 1. Plasmid curing The experimental kicking off of the plasmids using physical agents or chemical agents. d. Compare: Replication Copy number Size a. e. transposable genetic elements and bacteriophage DNA (prophage). Define: a. Bacteriocins Bactericidal substances produced by certain bacterial stains and are active against other strains of the same closely related species. Plasmid copy number Multiple copies of the same plasmid that may exist in the same cell c.Relaxed Plasmids Absence of protein 30-50 copies/cell Small b.Conjugative Plasmids Large 1-2 Present By conjugation Common in Gram-ve bacilli Can conjugate Stringent Plasmids Acquired protein synthesis 1-5 copies. Gene cassettes Genes that can be clipped out of one integron and inserted into another.plasmids. b. It comprises bacterial chromosome.
adhesins or invasion factors. They are capable of replicating independently of the bacterial chromosome and plasmid is generally dispensable. This is evidenced by spontaneous loss of plasmid during cell division and plasmid curing. They are much smaller than the bacterial chromosome. replication or survival of the host bacterium. Integrons .Insertion sequence Simplest type of transposable elements Encode enzyme necessary for : a) Recombination (transposition) b) The control of frequency of transposition Transposons Complex transposable elements Encode specific genes. Antibiotic resistance Some plasmid carry genes for resistance (R-factors) to one or several microbial drugs. double-stranded DNA molecules dispersed in the cytoplasm. Other function includes nitrogen fixation. They are also capable of mediating their own transfer from one location to another on the same chromosome or between the chromosome and plasmids. 4. circular. resistance to heavy metals and degradation of aromatic compounds. iv. H2S production. They often comtrol the formation of enzymes capable of destroying the antimicrobial Drugs iii. v. Virulence plasmids May code for exotoxins. ii. This results in the rapid spread of drug-resistance among bacterial populations and the development of multiple drug-resistant straints e. flanked by two IS elements. Transposable genetic elements These are non-replicating DNA segments (units) that are capable of inserting themselves into other DNA molecules. Give a short account on: a. 3. Bacteriocin production Bactericidal substances produced by certain bacterial stains and are active against other strains of the same closely related species. R-factors R-factors are usually conjugative plasmids that can be transferred among bacteria by conjugation. b. Plasmid can be transfer from one bacteria cell to another. Sex pilus formation. Functions of plasmid i. antibiotic production. This indicates that most plasmids encode properties that are essential for growth. Some plasmid carry fertiliy (F) factors that code for the formation of sex pilus which mediates the process of conjugation . d. sugar fermentation. Properties of plasmid Plasmids are extra chromosomal. c.c. Comment: Plasmids are dispensable.
b. Multiple copies of the same plasmid may exist in the same cell Plasmids are capable of replicating independently of the bacterial chromosome. Compare between phenotypic and genotypic variation.They are specific class of transposons caapable of capturing and mobilizing genes contained in mobile elements called gene cassettes. Loss of flagella upon exposure to phenol It occurs through: a. Plasmid especially virulence plasmid may code for exotoxins .Compare between generalized and specialized transduction Generalized transduction • Type of phage Lytic phage Specialized transduction Temperate phage . Phenotypic variation • It occurs in respond to changes in the environmental condition without change in the genetic constitution Reversible Not-heritable • Genotypic variation It occurs as a result of a change in the underlying genetic constitution irreversible Heritable • • • • Example: a. Give reason for: a. adhesions or invasion factor. Gene transfer: • • • Transformation Transduction Conjugation b. Chapter 6 BACTERIAL VARIATIONS 1) a. 5. Plasmid may render the bacteria pathogenic. L-forms bacteria b. Mutation b.
2) Give an account on: a.• • Replication cycle Lytic cycle The transfer DNA fragment Any piece of bacteria DNA(chromosomal or plasmid) Lysogenic cycle A specific piece of DNA adjacent to the site of the insertion of the phage. Mutation. • It results from a change in the nucleotide sequence of DNA that may occur either spontaneously as replication error or induced by radiation or chemical agents Classified according to the nucleotide substitution. Eg: a. and it may carry genes that transform the recipient bacteria. Missense mutation- When the mutant base change the coding sequence so different amino acid is produced b. insertion of transportable elements • • mutation-When its code for the same amino acid b. insertion or deletion into: • Single-base mutation • It involves in the replacement of a single nucleotide in the coding sequence. . Eg: a. Transformation • Dying bacteria release DNA which can taken up by other bacteria that may be chromosomal or plasmid in origin. Same sense(Silent) Frame-shift mutation • Occurs when the nucleotide is inserted into or deleted fro the coding sequence.
Specialized transduction: - Occur when phage contained lysogenized bacterial cell is induced to detach . Generalized transduction: During the lytic phage cycle. Conjugation. Involves 2 cell types : donor (F+) which processed the fertility (F) factor and recipient (F-) factor which lack the F factor.• • It may become integrated with bacterial chromosome or re-established extrachromosomally in the recipient’s cells. The phage particle can then transfer the incorporated DNA into another bacteria. The 2 DNA strands of the F factor separated. - d. • It is transfer of DNA from one cell to another cell by bacteriophage. It depend upon competence which is the ability of the recipient bacterial cell to take up DNA and competence depends upon the presence of protein in the cell membrane that have the ability to bind DNA and transport it into the cell c. Transduction. the bacterial DNA fragmented and any fragment of DNA may be incorporated into the phage head. Enumerate: a) Methods of gene transfer among bacteria • • Transformation Conjugation . and one of them is transfer into recipient cell. Such prophage may carry with it the adjacent piece of the DNA and transfer to another bacterial cell. Each strand form the complementary. thus the recipient cell acquires a copy of the F plasmid and become F+ factor • • • 3. The F factor carries genes for the synthesis of the sex pilus which acts as conjugation tube between the donor and recipient cells. • • It is a part of mechanism of DNA transfer.
Silent mutation b. • Single-base mutation a.• Transduction a. Generalized transduction b) Types of mutation. Missense mutation • Frame-shift mutation 4) Define a) phenotypic variations -changes in bacterial characters in response to changes in the environmental conditions without change in the genetic constitution. Specialized transduction b.change in the nucleotide sequence of DNA that may occur spontaneously or induced by chemical agents or radiation. b) Genotypic variations -changes in bacterial characters as a result of a change in underlying genetic constitution c) Mutation . d) Competence -ability of the recipient bacterial cell to take up DNA .
Enumerate: a)requirements for an ideal cloning vector -as small as possible -well characterized regarding gene location and nucleotide sequence -possess a single cleavage site for at least 1 restriction endonuclease -capable of autonomous replication within the host cell -carry selective marker . Define: a)cloning vectors-vehicles used to carry and introduced foreign DNA fragments into a host cell b)cosmids-artificially constructed cloning vectors formed of plasmoids and cohesive end (COS) of lambda phage DNA c)restriction endonucleases-enzymes that recognized specific nucleotide sequences within DNA molecules and catalize the cleavage of both DNA strands at internal position within the sequence d)genetic probes-short single stranded DNA or RNA fragments used for diagnosis of infections as well as genetic diseases 2.Chapter 7 GENETIC RECOMBINATION 1.
production of recombinant vaccines -preparation of genetic probes -gene therapy d)the properties of host organisms used for cloning properties -strains used should be free of any restriction activity -nucleic acid of host easily saparable from that of cloning vector 3.activity is restricted to unmodified foreign DNA because own DNA is methylated in specific manner to be protected from cleavage by own enzymes produce b)the ideal cloning vector must be small . hormones . Give reasons for: a)the restriction endonucleases are so-called .g.b)commonly used cloning vectors -plasmids -bacteriophage -cosmides -animal viruses c)applications of recombinant DNA technology -mapping of microbial genome -production of biological product of medical importance.to contribute as little as possible to the overall size of recombinant molecule c)the ideal cloning vector must be carry a selectable marker .e.to distinguished between the host cells transformed with the vector from non-transformed cells .
to achieve the desired properties. or it may depend on the inhibition of a biochemical event essential for the organism but not for the host.they fulfill most of the requirements for ideal cloning vector Chapter 8 ANTIMICROBIAL THERAPY 1. Selective toxicity : is the ability of an antimicrobial agent to harm a pathogen without harming the host. and a few moulds (Penicillium and Cephalosporium) Antibiotics that are made synthetically Chemical modification of certain antibiotic. an antimicrobial agent that is capable of inhibiting bacterial multiplication an antimicrobial agent that is capable of killing bacteria antibiotics which kill or inhibit the growth of a wide range Gram-positive and Gram-negative bacteria C Synthetic antibiotics D Semisynthetic antbitics E Bacterostatic agent F Bacteriocidal agent G Broad spectrum bactercidal agent 2. especially Streptomyces. Define : A Antimicrobial chemotherapeutic agents B Antibiotics chemically synthesized substance that are used to treat infectous disease by killing or inhibiting the growth of microorganisms low molecular weight antmicobial substance that are produce as secondary metabolites by certain groups of microorganism.It may be function of a specific receptor for the drug found in the microb but not in the human body (eg. b.d)the relaxed plasmids are among the best cloning vectors . Peptidoglycan). mechanism of action of antimicrobial drugs inhibition of cell wall synthesis interference with cell membrane function inhibition of bacterial protein synthesis inhibition of bacterial nucleic acid . Give a short account on : a. Bacillus.
g. Target elimination by developing new metabolic pathways: the bacteria createa new metabolic pathways that bypass the original target. c. efflux pumps : the antibiotic is pumped out across the cytoplasmic membrane faster than it can diffuse in b. e. Gram-negative cell membrane has pores too small to allow large antibiotic molecules. Mechanism of acquired drug resistance : One or more of the following mechanisms used by bacteria: a. resistance to trimethoprim e. It is consistent and can be expected once the organism is known.c. Aureus strains with intermediate susceptibility to vancomycin (VISA) d. Intrinsic resistance: refer the bacteria that are insensitive. eg: production of β-lactamase leads to hydrolysis of the β- lactam rings. An organism lack the target or receptor for the antibiotic as in case of resistance of enterococcus species to cephalosporin.referred as limited spectrum. Target overproduction : used by S. thus inactivates penicillins and cephalosporins c. Spectrum of activity : range of action of microorganism that are affected by a certain antibiotics is expressed as its spectrum of action. . to penetrate. If effective against one of them. Inactivation of the antibiotic. If effective mainly against either Gram-positive or Gram-negative bacteria they are narrow spectrum. Target modification : modification of the target site for the antibiotic reduces its affinity for its receptor d. eg. e. decrease in influx of antibiotic through reduction of permeability of the outer membrane by modification or loss of porin ii. nafcillin. Streptomyces are protected from the antibiotics they produce. b. Intrinsic resistance occurs in the follwing situations : a. Antibiotic that kill both Gram-positive and Gram-negative said to be broad spectrum. reduction of the intracellular concerntration of the antibiotic by: i.
thus preventing development of a disease.g. : cefepime+ vancomycin d.f. Synergistic effect(1+1=>2) : the combined action is greater than the sum of both effect.:Vancomycin+gentamicin in treatment of methicillin-resistant staphylococci b. h. Indifference (1+1=1) : the combined action is no greater than that of the more effective agent when used alone.g. Complication of chemotherapy : a. Antagonistic effect (1+1<2) : the combined action is less than that of the more effective agent when used alone. Antimicrobial chemoprophylaxis : is the administration of an effective antimicrobial agent to prevent rather than to treat infection with a certain microbe. allergy(hypersensitivy) c.e. j. Empiric therapy : is a best guess.e.g.e.g. Depending on the type of bacteria.e. Superinfection : it occurs as a result of outgrowth of resistance members of normal flora when the sensitve ones are eradicated during antibiotic therapy.: Pseudomembranous colitis caused by outgrowth of the yeast Candida. emergence of resistant strains d. Best guess treatment is not always successful as many bacteria have unpredictable susceptibilities to antimicrobial agents.e. . then treating the infection. Indication : in seriously and if no sample is available. Addition (1+1=2) : the cobined action is equivalent to the sum of the action of each drug when used alone. By indicating type of infection.pyogens. g. there will be an antibiotic that can acts on the bacteria. Effects of combined therapy a. superinfection i. a short list of bacteria can be identified. : Long acting penicillin is given to rheumatic patient to prevent reinfection with S. Toxicity b. : penicillin + Chlorompenicol in treatment of meningitis c.g.
tube broth dilution) • Gradient diffusion (E test) method b. macrolides 4. Vancomycin could be used successfully in infections caused by β-lactam resistant bacteria • the mechanism of resistance to β-lactam antibiotics is different from that of glycopeptides (vancomycin). Methods for in vitro susceptibility testing: • Disc Diffusion method • Dilution method (eg. Antibiotics which interfere with the cytoplasmic membrane function are highly toxic • they have narrow margin of selective toxicity c. MIC : the lowest concerntration of a drug that prevents growth of a test organism b. Enumerate: a. β-lactam antibiotics are bactericidal with minimal host tissue toxicity . Indications for empiric therapy: • in seriously ill patient after collecting specimens for culture • in closed lesion (no available sample) 5. b. Define: a. while organisms with MICs above the breakpoint are considered resistant 6. > agents acting on the 30S ribosomal subunit : eg. Possible indications for combined therapy • severely ill patient suspected of having serious infection • febrile neutropenia • to delay the emergence og drug-resistant mutants • to achieve bactericidal action through synergistic effect • mixed infections c. Comment : Bacterial ribosomes are a selective target for antimicrobial agent Bacteria have 70S ribosomes (30S & 50S subunits) differ from mammalian cell ribosomes.3. β-lactam drugs inhibit the last step of peptidoglycan synthesis while vancomycin inhibit early steps in the biosynthesis of peptidoglycan which occur inside the cytoplasmic membrane. Give reason for: a. Breakpoint of antimicrobial agent: the concerntration that can be achieved in the serum with optimal dose -then mention their impact in determining susceptibility Organisms with MICs at or below breakpoint are considered susceptible. tetracycline > agents acting on the 50S ribosomal subunit : eg.
and other foreign materials.Define :a)Sterilization . viruses. Chapter 9 DISINFECTION AND STERILIZATION 1. organic load. destruction or inactivation of all forms of microbial life including bacteria. and fungi.it is the elimination of most. The process removes some microorganisms. Antibiotic resistance is more prolonged in hospitals • due to the higher antibiotic use. . if not all. b)Disinfection . c)Antiseptics . d)Cleaning . Cleaning must always precede disinfection and sterilization. pathogenic microorganisms including spores.it is a process of removal of the visible dust.special types of chemical disinfectants which can be safely applied to skin and mucous membranes but are not suitable for systemic administration.it is complete removal. It is advisable to use as narrow antibiotic spectrum as possible • the use of broad spectrum antibiotics is likely to induce resistance to antibiotics and may be complicated by superinfection e. detergents or enzymatic products.• β-lactam antibiotics inhibit the last step of pepyidoglycan synthesis by binding to penicillin binding proteins d. dirt.spores. It is usually done with water and soap. Undue prolonged therapy should be avoided • may result in drug toxicity and antibiotic resistance f.
or at 72oC for 20 sec. 2. II. f)Critical items . Heat 1. Low temperature (“cold”) sterilization methods: A-Chemical 1. 3Ultraviolet Radiation: Ultraviolet Radiation(UV) is a low energy. in operating rooms and laboratory safety cabinets. and Coxiella burnetti. cavities. Mycobacterium tuberculosis. 2.Enumerate a) Main methods of disinfection 1Boiling water : Boiling at 1000C for 20 minutes achieves high disinfection.objects that contact intact skin only but not mucous membranes. followed by rapid cooling. h)Non critical items .objects that come in contact with mucous membranes or non intact skin.it is a general term that is applied to any procedure by which pathogenic microorganisms are reduced to a level where items are safe to handle. g)Semicritical items . 4Chemical disinfection b)Main methods of sterilization I. 2.Moist heat or steam sterilization. Brucella.Dry heat sterilization. Therefore UV rays can be used only for air and surface disinfection. non-ionizing radiation present in sun rays or artificially produced by mercury lamps.instruments that enter sterile tissues. or vascular system.e)Decontamination . 2Pasteurization: (hot water at temperatures lower than 100o C) e. UV radiations have extremely weak penetration power.g pasteurization of milk by heating at 63oC for 30 min. destroys important pathogenic organisms e. It can be useful in emergencies if no sterilizer is available.ethylene oxide gas.liquid sterilization process: commonly used liquid sterilants include: -Glutaraldehyde . Salmonella.g..
c)Advantages and disadvantages of: advantages 1.Microwaves. disadvantages 1. 3.Filtration.Low costs.Ionizing radiation. Other sterilization methods 1.-Liquid peracetic acid -hydrogen peroxide 6% B-Plasma sterilizers III.Liberation of latent heat of 2.Steam sterilization is not vaporization after cooling due suitable for sterilizing to condensation of the steam.Absence of toxicity 4.Some items cannot withstand steam at high temperatures.The capability of being used 1.Slow and uneven . 3. Hot air sterilization 1.A good ability of saturated steam to penetrateinto loaded porous items. Steam sterilization 2. powders and oils. 2.
for sterilizing powders, penetration of heat into the waterless oils and glassware. materials to be sterilized. 2.Absence of a corroding effect. 3.Low costs. Gas (E.O) 2.A necessity for prolonged exposure.
3.Damage to the rubber items and some fabrics Capability of the instrument 1.long duration of the that cannot be subjected to the sterilization cycle steam/hot air sterilization 2.high costs without any damage 3.toxicity
1.filter more rapidly 2.they don’t affect the filtrate in any way 3.they adsorb very little of the substances being filtered 4.remove microorganism from air supplied to critical areas
3.Give an account on: Monitoring of steam sterilizers(autoclaves) a. Physical measurement of the tracts of the time,temperature and pressure b. Chemical indicators:chemically impregnated strips which change their colour at certain temperature should be used with each cycle of sterilization c. Biological indicators: - use paper strip containing Bacillus stearothermophilus - the biological indicator are placed in the depth of the load to be sterilized -after that,spore strips are incubated in a fluid medium and checked for viability -absence of bacterial growth indicates an efficient sterilization cycle 4. Mention one method used for sterilization (disinfection) of a. skin-chemical (biguanides-chlorhexidine) b.air in operation room-ultraviolet radiation c. milk-pasteurization d. disposable plastic syringes@glove-irradiation e. glassware-sterilization (dry heat) f. hormones,vitamins@blood products-filtration g. floor,walls@furnitures-chemical (quaternary ammonium compound) 5.Mention one use for each of the following methods a. Incineration
-For dead animal bodies, infectious hospital waste such as used surgical dressing and needles. b. Hot air sterilizers -Sterilization of powders, waterless oils and glassware. c. UV radiation -For air and surface disinfection, in operating rooms and laboratory safety cabinets. d. Alcohol -Disinfection of thermometers, external surfaces of stethoscopes and as skin antiseptics (by themselves or in mixture with iodine or chlorhexidine) e. Iodophores -For antiseptic purposes f. Hydrogen peroxide -Disinfection of endoscopes and antiseptic for open wound g. Glutaraldehyde -For high level disinfection or sterilization of the instruments such as endoscopes, respiratory and anaesthesia equipments. h. Red heat -Sterilization of inoculating wires, loops and point of forceps. i. Bacteria filters -Sterilization of fluids which would not withstand heat such as antibiotic solutions, blood products, hormones and vitamins j. Ionizing radiation -Sterilization of prepacked heat-sensitive power items such as bone grafts, surgical sutures, disposable plastics syringes, gloves, catheters, plastics Petri dishes and intravenous infusion set. k. Chlorine-active compounds -Decontamination of the blood splashes and laboratory working surfaces.Linen bleaching. Disinfection of water for domestic use. l. Phenolics -Cleaning of floors ,walls and furnitures m. Peracetic acid -High level disinfection or sterilization of the instruments such as endoscopes n. Biguanides (chlorhexidine) -Disinfection of the skin and mucous membrane (as a mouth wash).It is often combined with detergents for hand washing or with alcohol as a handrub. 6. Give reason. a. Moist heat is much more efficient than dry heat as a method of sterilization. - Because it kills microorganism by coagulating and denaturing their enzymes as structural proteins also it is quicker in heating up the article to be sterilized. b.Steam sterilization is the most preferred method of sterilization. - It is suitable method for those items that can withstand high temperature and moisture. c. In steam sterilization, it is essential to make steam free of any residual air.
- Because air acts as an insulator, reduces temperature and hinders penetration. 7. Give an account on plasma sterilizers. - Plasma describes any gas that consists of electrons, ions or neutral particles. Plasma sterilizers with the use of liquid peracetic acid or hydrogen peroxide or a mixture of both are commercially available.
Chapter 10 BACTERIAL PATHOGENESIS
1.Define: a)saprophytic bacteria= bacteria which live freely in nature,on decaying organic matter,in soil or water.They do not require a living host. b)parasitic bacteria= bacteria which live on or in aliving host.They are classified according to their relation to the host into pathogenic,non pathogenic and opportunistic pathogen. c)opportunistic bacteria= potentially pathogenic bacteria that do not cause disease under normal conditions but can cause disease in immunocompromised patients or when they find another site other than their normal habitat. d)toxoid= a preparation of the poisonous toxin that has been treated to removes its toxicity and retains its antigenicity.Are used in vaccines.
g. pertussis (chromosomes) H.g. pylori (PAI) nature protein Lipopolysaccharide (lipid A) antigenicity Highly antigenic Poorly antigenic Heat stability Unstable to temp. diphteriae (phage) E. above 60 ̊c detoxification Can be converted into toxoid Can not Specificity Every toxin has specific action Same generalized effect.These criteria are as follows: 1)The organism must be isolated from every patient with the disease 2)The organism must be isolated free fromall other organisms and grown in pure culture in vitro 3)The pure organism must cause the disease in an healthy.Compare: a)pathogenicity and virulence pathogenicity=A qualitative description of a species of bacteria denoting ability to produce disease virulence=A quantitative character (degree of pathogenicity) of a strain belonging toa pathogenic species b)exotoxins and endotoxins Endotoxins Integral part of the cell wall of Gram –ve organisms. toxins) that enables the organism to cause disease. capsule) or a product(e.plasmids. 2)The glycocalyx of Staphylococcus epidermidis and certain viridians streptococci their adherence strongly to the heart valve c)Invasion factors of virulence= One of main mechanisms by which bacteria can cause disease is through invasion of tissue followed by inflammation.bacteriophages chromosomes or PAI exampes C. coli help their attachment to the urinary tract epithelium.susceptible animal 4)The organism must be recovered from the inoculated animal b)Adherence factors of virulence= They enable bacteria to attach to the host surfaces.Liberated upon cell disintegration Coding genes Encoded by Encoded by genes on the chromosomes.all give fever and shock (non specific action) toxicity high low source Exotoxins Secreted by living oraganisms both Gram +ve(mainly) and Gram -ve 3. above 60 ̊c Stable to temp.For examples: 1)The fimbriae of Neisseria gonorrhoeae and E. 2.This invasion is helped by: 1)Enzymes: a-collagenase:degrade collagen ------------------>allow bacteria to spread through Hyaluronidase:degrade hyaluronic acid ----->subcutaneous tissues .Give an account on: a)Koch’s postulates= These are criteria that were proposed by Koch in order to determine if the organism isolated from the patient actually caused the disease. coli Cl. tetani (plasmid) Meningococcal endotoxins B.e)virulence factors= A structure(e.
Pyogenes) : protein A(Staph.g: M protein(Strept. NK cells Absent Less efficient Acquired Following exposure to pathogens Relatively delayed B&T lymphocytes Present More efficient and improves with each exposure .b-IgA protease:degrades IgA c-Leukocidin:destroy both polymorphonuclear leucocytes and macrophages d-Deoxyribonuclease:breaks down DNA e-Lecithinase:breaks down lecithin of cell membrane 2)Antiphagocytic factors: a-capsule:prevents phagocytes from attachment to bacteria. e.This clot protect bacteria from phagocytosis e. Aureus) c-coagulase:accelerates the formation of a fibrin clot from fibrinogen. Strept.Compare: A)innate& acquired immunity Innate Presence Onset of action Main cells Memory Efficiency Since birth Immediately after infection Granulocytes. Staph. pneumoniae b-cell wall proteins of Gram +ve cocci e. aureus Chapter 11 OVERVIEW OF THE IMMUNE SYSTEM 1.g. monocytes / macrophages.g.
Antigen presentation: Macrophages help to show or present part of the foreign agents they have eaten to T cells. -thus. Enumerate: a. 3. antigen specificity is maintained in the daughter cells 3.Define naive lymphocytes : small B and T lymphocytes that have matured. Against a particular pathogen Interact with innate immunity through: e. all having identical receptors. B)The clonal selection theory -T & B lymphocytes are very specific -they recognize the antigen by the receptor present on the surface of antigen-each naive lymphocyte have single type of receptor of certain specificity -only the lymphocytes which meets the antigen which their receptor recognize. against all microorganisms Interact with acquired immunity through: e.g. so that the T cells can start responding to them. will undergo activation.-antigen presentation Specific: Occur in a given person.Direct cytotoxicity: They may kill target without engulfing them.Specificity Interaction Non specific: Present in all individuals.They leave bone marrow n thymus respectively..e. g.Give an account on: A)functions of macrophages 1. proliferation and differentiation -the result is a clone family of identical daughter cells. the different lymphoid organ -there are 2 types of lymphoid organ: . they are among a group of cells called antigen presenting cells(APCs). interleukins 4.g. which can bind the same antigens wherever they find it. Tumor cells can also be killed in a similar way.phagocytosis 2. Helminthic parasite which are too large to be engulfed can be killed by macrophages releasing their toxics contents onto them.Secretion: They secrete chemical mediators called cytokines .and circulate continually to secondary lymphoid organ such as lymph node 4. Thus.opsonization B)T&B cell receptor B cell receptor It is an antibody molecule Has 2 antigen recognition site Can be active even after detachment Can recognize the antigen directly T cell receptor It is a dipeptide molecule 1 antigen recognition site Cannot be active after detachment-always need cell surface receptor Recognize the antigen only when presented by antigen presenting cells 2. but have not yet met antigen .
where the B cells complete their maturation =>the thymus . adenoids.includes the tonsils. sneezing.saliva.the sticky mucous covering mucous membrane traps any foreign material.cilia of respiratory tract epithelium sweep foreign material out.forming the white pulp. 4. 1. while the T lymphocytes are more diffusely distributed in the paracortical area =>the spleen .where the T cells complete their maturation 2-secondary(peripheral) lymphoid organ -places where lymphocytes meet the antigens. tears. Enumerate a) Mechanical barriers and surface secretions as a mechanism of innate immunity. 2. alimentary and genitourinary tracts contain lysozyme which is bactericidal. 3. and coughing reflexes expel foreign particles. appendix and Payer's patches in more diffusely organized collections of lymphocytes which protect the respirator epithelium =>other mucosal sites b) changes which occurs when a naive lymphocyte recognizes an antigen -the changes which occur are: 1-activation : become lymphoblast 2-proliferation : rapid multiplication 3-differentiation : change into effector cells ~B cells changes into plasma cells. and mucous secretions of respiratory. adenoids. appendix and Payer's Patches =>BALT .includes the tonsils. . from the blood they reach the peripheral tissue where they start functioning to eliminate the specific infection which started their activation Chapter 12 INNATE IMMUNITY 1.the B lymphocytes are localized in follicles and in the cortex of the lymph node.1-primary(central) lymphoid organ -places where lymphocytes complete their maturation -they are: =>the bone marrow . leading to activation of the lymphocytes -they are: =>the lymph node .sweat and sebaceous secretions contain substances that inhibit microorganisms. the inner part of this called periarteriolar lymphoid sheath. 5. capable of secreting antibody ~cytotoxic T cells becomes capable of killing infected cells ~helper T cells becomes capable of producing cytokines -they leave the lymph nodes through efferent lymphatic vessels and return to the blood trough the thoracic duct.the lymphocytes surrounds the arterioles entering the organ.blinking.intact skin and mucous membrane constitute a barrier that cannot be penetrated by most microorganisms. containing mainly T cells and is surrounded by a Bcells corona =>GALT . 6.
7. 8.acute phase protein: present at very low levels in normal serum but rise dramatically after onset of infection. Give an account on: . 2.the flushing action of saliva. b) humoral defence mechanism.complement: group of plasma protein that act to attack extracellular pathogen. tears and urine helps in washing microbes from the body. 4. 1. 3.lysozyme: enzyme that lysis bacteria by destroying the peptidoglycan of their cell wall.gastric and vaginal acidity inhibit growth of microorganism. Type 1 is innate immunity and type 2 is part of acquired immunity 2.interferon: 2 types of interferons.
microorganism digested by lysosomal enzymes c) Respiratory burst • • • • one of killing mechanism in phagocytosis due to rise in o2 consumption accompanied by increase activity of enzymes & leads to production of reactive o2 intermediates which lethal to mocroorganism e. Phagocytosis Low level in normal serum Rise immediately after onset of infection E. b) Attachment : • Phagocytes have receptors on their surface that can recognize non-specific molecules common to many pathogens.g fibrinogen & C-reactive protein. • Some microorganisms may lack these molecules @ having thick capsule that not recognized by any phagocyte receptor. allowing attachment to them. • Lysosomes fuse with phagosome forming phagolysosomes • Engulf material killed & digested d) Killing: O2 dependent mechanism : respiratory burst consist of steep rise in o2 consumption.g H2O2 . they act to limit spread of infectious agent or stimulate host response. • Substance that help phagocytosis is called opsonin c) Engulfment : • Cytoplasmic membrane of phagocyte surround organism and encloses it in a vacuole termed phagosome.This is called opsonization. E.1. O2 independent mechanism : Once ingested. • Attachment may still occur if microorganism coated by molecules which phagocyte can recognize.g endotoxins stimulate macrophage to release IL-1 & IL-6 which stimulate liver to produce large no. of enzymes lead to generation reactive o2 intermediates which lethal to organism. Acute phase proteins 2. help in complement activation a) Migration : microorganisms & injured tissue elaborate chemotactic factors that attract phagocytic cells to site of infection. accompanied by increase activity of no. of APP.
Compare: Innate immunity Presence Onset of action Main cells Since birth Immediately after infection Granulocytes Monocytes/macrophage NK cells Absent Less efficient Non-specific : Present in all individuals against Acquired immunity Following exposure o pathogens Relatively delayed B & T lymphocytes Memory Effeciency Specificity Present More efficient and improves with each exposure Specific : . they compete with pathogens for essential nutrients.3. they produce bacteriocins and acids that destroy microorganism. 2. 1. 4.Give reason: normal body flora act as a mechanism of/play role in innate immunity.
low molecular weight substance . Give an account on adjuvants -non specific potentiatiors of the immune response. Give reasons: a) Adjuvants are added to toxoids during human immunisation . c) Hapten .substance that can stimulate the immune system to produce an immune response .all microorganisms Interaction Interact with acquired immunity through : . b) Epitopes -small. -one of the commonly use adjuvants is aluminium hydroxide which is added to diphtheria and tetanus toxoids (used for human immunization) -aluminum hydroxyde delays the absorption of toxoids and prolongs the period of their exposure to the immune system. Define: a) Immunogen / Antigen . limited parts present on antigen molecule which is recognized by immune system specifically. 4.to delay the absorption of toxoids and prolongs the period of their exposure to the immune system b) The most potent immunogens are proteins .incapable of inducing immune response alone .Antigen presentation Occurs in given person.act as antigen when coupled with a carrier molecule (protein) 2.reacs specifically with the product of this response.against a particular pathogen Interact with innate immunity through : -Opsonization Chapter 13 ANTIGENS 1. Enumerate: Factors affecting immunogenicity a) Foreigness b) Molecular size c) chemical nature d) route of administration e) dosage f) adjuvants g) host factors 3.
Chapter 14 T-CELL MEDIATED IMMUNITY 1. Among them are: 1)T cell receptor (TCR) -2 plypeptide chain: alpha and beta -constant part and variable region -all are identical and recognize the same antigen.(3)markers in identifying T cells and divide them into subsets.help immune system by secreting cytokines CD8.helper T cells (Th)…. other cells recognized by T cells.cytotoxic T cells (Tc)…kill infected cells. Give an account on : a) T cell surface surface molecules Their roles are. tumour cells.present on all T cells -binds to B7 on APC>>delivers second signal (for T cells activation) >>>= ‘co-stimulatory molecule’ 5)CD40L. the more complex the molecule.(1)antigen recognizer. the more immunogenic it is. 4)CD28.present on activated Th cells -involved in B cells activation by T cells -binds to CD40 .(2)interact with other cells. 2)CD3 -close to TCR on all T cells -transmitting signals from TCR inside the cells 3)CD4 and CD8 –T cells carry either of them CD4. Both are associated with TCR…= ‘CO-RECEPTORS’ *SIGNAL DELIVERED THROUGH TCR WITH THE HELP OF THE ABOVE MENTIONED IS THE ‘FIRST SIGNAL’ FOR ACTIVATION OF T-CELL.proteins are complex molecules.
b)the professional APCs -the only cells that capable of activating naïve T cells -in the peripheral lymphoid tissues 1)dendritic cells…most important So called because > have dendrites(cytoplasmic projections) In nearly all tissues Most efficient Antigen presentor 2)macrophages…important phagocytic cells Essentials for innate immune system Contribute to acquired immune system 3)B cells…humoral immunity Also as APCs c)MHC restriction -they code production of certain cell-surface gycoproteins -another name > human leucocyte antigen (HLA)…first discovered on leucocytes -two classes(important in T cells activation): 1) Class | (MHC |) 2) class || ( MHC ||) -all people have both classes 2) Compare: endogenous and exogenous pathogens Cytosolic “endogenous” Vesicular “exogenous” .
B cells and others 3) Give reason: a) CD3 found close to the TCR on all T cells -involves in transmitting signals from TCR to the inside of the cells b) CD28 is called CD-stimulatory molecules -its binding to B7 molecules delivers the second signals for activation of T cells.few bacteria cytoplasm MHC I CD8 Cytotoxic killing of presenting cell by CD8 -intracellular bacteria -extracellular bacteria and their products when internalized Vesicles MHC II CD4 -Secretion of cytokines by CD4 -help macrophages.cytokines Cytokines are peptide or glycoprotein mediators that are produced by cells of the immune system and have an effect on the behaviour and properties of many cells b. Not specific to antigen that produce them . They are highly potent being acting at very low concentration II.General characteristis of cytokines I.Examples Degraded in Peptides bind to Presented to result All viruses. Chapter 15 CYTOKINES 1) Define a.LAK It is the NK cells which is being activated by IL-2 to enhance their killing ability 2) Enumerate a.
IL-1 c. Give reason: .increase effect of other(synergy) or as antagonist b. Act through high affinity cell surface receptor IV. They are pleiotropic-same cytokines may have multiple effects VII. Chemokines h. IFN-α b.α e. • Induces synthesis of nitric oxide and other bactericidal • Induces macrophages to secrete cytokines b) IL-4 in development of allergy (hypersensitivity) • Promotes production of IgE • Promotes growth and function of eosinophils • Helps activation and growth of the B-cells 6. Explain the role of: a) IFN-α in activation of macrophages • Promotes fusion of pagosomes containing bacteria to lysosomes containing antibacterial substances.TNF-β b. Cytokines that mediated acquired immunity a.α b. GM-CSF e. IL-6 5. Different cytokines may have same activity(redundancy) VIII. IL-12 d. They act in an autocrine or paracrine manner VI. TH-2 – IL-4. TH-1 – IL-1. Pro-inflammatory cytokines a. IL-10 c. Cytokines that mediate innate immunity a. IL-3 b. TNF. d. They may act sequentially(network interaction). Their action is transient V.TGF-β c. IL-7 c. Cytokines that stimulate haematopoiesis a. IL-1 f. TNF.IL-5.IFN-γ. IL-6 g.III. IFN-β c.
promotes local inflammation.surface immunoglobulin which act as antigen receptor -all BCR on a single B cell are identical specificity -then B cell then secrete antibody of the same specificity -immature B cell express only IgM on their surface. induces synthesis of acute phase protein) • When enters blood stream causing systemic effects such as fever. but mature B cell bear both Igm n IgD 1) CD40: essential for the interaction between B n T cells 2) MHC II: antigen presentation to T helper cell (b) -mature naïve B cell leaves the blood stream and enters secondary lymphoid organ .a) GM-CSF is used in treatment of leucopenia • Promotes development of granulocytes and monocytes b) IFN-α has shown success in treatment of viral infections • Inhibition viral replication by causes cells to synthesize a number of enzymes that interfere with translation of viral mRNA • Activation NK cell • Increased expression of MHC I molecules leads to more recognition of viral peptides and more efficient killing of virally-infected cells by Tc cells c) INF-α has been used in trials to treat malignancies • Inhibition of cell proliferation d) IL-2 is shown as autocrine growth factor of T-cells • Produced by activated Th1 cells which then promote activation of T cells and cytokine production of T cells. e) IL-2 is not used in large scale as a therapeutic agent • Due to severe toxic side effect f) TNF α is not used on large scale to treat tumors • Induces IL-1 production.Give an account on: (a) B cell surface molecules B cell receptor receptor(BCR) -This is membrane bound antibody molecule. shock and even death welcome Chapter 16 THE HUMORAL IMMUNE RESPONSE 1. and both have pro-inflammatory action (produces fever.
-The B cell has received both signal.short segments in the variable domains of light(LC) & heavy chain(HC) that have variability in a.this regions r folded & brought together creating a single hypervariable surface or paratope . Other complement proteins may lyse the pathogen directly by forming pores in its membrane.the Bcell binds it specific antigen via the surface igs(BCR) and full activation of B cell occur.genitourinary) . This is another example for opsonization.Bcell traverses this region rapidly and enters the circulation -in the presence of it antigen.g. And produce CD 40 Ligand and IL-4. NK cells possess receptors for the Fc portion of antibodies. e. thereby preventing their attachment to their specific receptors on their target cells.constant amino acid Light chain = constant of an VL and CL Heavy chain = consist of an VH and 3 to 4 CH (f)Sec IgA -produced by submucosal plasma cell n found n mucosa secretions(saliva. Phagocytosis) • Neutralization: antibodies can inhibit the infectivity of a pathogen (viruses or bacteria) or the toxicity of a toxin molecule by binding to them.tears.colostrums. may also exert ADCC.-in the absence of it target antigen.IL-5.IL-10 which are B cell stimulatory cytokines. • Second signal is delivered by activated T helper cell.wide variation of amino acid b) Constant domain . sequence . Bacteria) results in clumping of the pathogen which prevents its dissemination and stimulate its removal by other mechanisms (e. An antibody bound to an antigen on a target cell can also bind to the NK cell through its Fc portion facilitating adhesion of the NK cell to the target cell and triggering its cytotoxic activity.g. -to become fully activated naïve B cell must receive 2 signal: • First signal is delivered by binding of antigen to BCR. that can recognize and bind Fc portion of antibody molecules coating a pathogen.not spread evenly over entire length of variable domains of LC & HC . Some of these complement proteins become deposited on the pathogen and also bind to complement receptors on phagocytes.IL-6. favoring the uptake and destruction of the pathogen by the phagocyte. d) hypervariable regions ~pg 75 .degrades it into peptides and persents this peptide on the cell surface in association with MHC II.to divide repeatedly(proliferation) and ti differentiate into antibody secreting plasma cell.To receive this signal. This facilitates the engulfment and subsequent intracellular killing of the pathogen by the phagocytic cells.g.paratope is da antigen(Ag)-binding site~complementary to & interacts with epitope of Ag e) Immunological domain Immunoglobulins consist of light and heavy chain and each chain is subdivided into domains which are: a) Variable domain .T Helper cell will recognize the peptide –MHC class II complex.these stimulate Bcell to become a lymphoblast(activation).Bcell engulfs the bound antigen. macrophages. • Antibody –dependent cell-mediated cytotoxicity (ADCC): it is the destruction of antibody –coated cells by natural killer (NK) cells.a.GIT. • Opsonization: phagocytic cells have Fc receptors on their surface. • Complement activation: antibodies bound to the surface of a pathogen may activate proteins of the complement system. Other cells possessing Fc receptors. (c) functions (effector mechanisms) of antibodies • Agglutination: binding of antibodies to an antigen (e.
immunosuppressive therapy in graft rejection. determination of lymphocytes markers e. Enumerate: applications of monoclonal antibodies(Ab) ~pg 81 a) diagnostic applications –widely used in different kinds of serological reaction for Ag detection i. It is complementary to and interact with the epitope of the antigen b)Heterophil Ab: because of the similarity that may be found between different antigens.Compare . detection of HLA Ag (tissue typing) iii.g CD markers ii. da use of monoclonal Ab against CD3 on T cells iii.IL-5. hormonal assays v.antibodies produced in response to an antigen may cross react with another one.There is no alteration in the Lchain or the variable domain of heavy chain(VH). da use of monoclonal anti-Rh D 3.g digitalis iv. Define a) Paratope: is the antigen-binding site. antitumor therapy.its main function is neutralization as it prevent attachment of organism to mucosal surface (g)Immunoglobulin class switching -class switching is mediated by a change in constatant domain of the heavy chain(CH). a short peptide chain that join the 2 unit together In a secretory component -the secretory component help the passage of IgA through the epithelial cell n protect the molecules from Proteolytic digestion -secretory IgA provides local immunity at the mucosal surface. -IL-4 increase IgE -IL-4.-the dimeric form of secretory is composed of two basic units. detection of tumor Ag b) therapeutic applications i.Such cross-reacting antibodies are called heterophil antibodies. prevention of Rh incompatibility. c) monoclonal Ab these are highly specific antibodies against a single epitope produced by a single clone of B cells. detection & typing of viruses iv.IL-6 increase IgG -TGF-B increase IgA -IL-5 increase IgA 2.so that the immunoglobulin produced later has the same specificity as the original IGM but differs in biological characteristic. They can be artificially produced to be used in diagnosis and therapy. ttt of drug toxicity e. da use of tumor specific monoclonal Ab linked to cytotoxic drugs (magic bullet therapy) ii. -Class switching is dependent on cytokines release from T cell. d) immunoglobulins(Igs) ~pg 73 glycoproteins that bind specifically to da Ag that induced their formation 4. passive immunotherapy in some viral diseases v.
no class switching Memory cell absent Fast and earlier IgM 5 bassic unit(pentamer) held together by disulphide bond n a single J(joining) chain 8-10% circulating Igs in blood Major antibody of the primary immune respone Cannot cross placental barrier Biological activities: Agglutination Complement activation IgM found on the surface of B cell forming BCR Secondary response Short(few hours to gew days) High(10 times greater) Long (month) Predominantly IgG Present Major antibody of the secondary immune respone Only Igs which can cross placental barrier Biological activities: Neutralization Opsonization Complement activation ADCC Primary response Induction(lag)period Antibody level Duration Ig class Memory cell Long (7-10 days) Low Short (antibody declines rapidly) Predominantly IgM Absent 5.Thymus dependent 1)Requires second signal from t cell 2)Activation of t cell Small antigen IgM then IgG production.Give reasons: a)Most vaccines are given in more than one dose .can change to other isotype with same immunological specificity Memory cell is produced Fast IgG Single basic unit (monomer) 75 % circulating Igs in blood T cell antigen Ig Memory cell Duration Thymus independent 1)No need of second signal from t cell 2)no t help Large antigen Bacteria pathogen IgM only.
---Therefore.The response can be boosted to higher levels by further exposures.-The antibody level is 10 times greater than during primary response. Type of pathway Type of immuniti lectin Initiation Role of antibody Role of faotor B.g. Ig M is the only antibody made to thymus-independent antigens d)Presence of IgM in newly born blood indicates intrauterine infection -IgM cannot passes placenta from the mother to the fetus.provides passive protection to the newborn during the first few months of life c) IgM is the only antibody made to ABO blood group antigens -this is because. b) IgG is the only Ig that can pass the placenta to the foetus ~pg 77 . Chapter 17 COMPLEMENT 1) Compare : a) The classical and alternative complement pathways.For this reason. its presence in newborn blood indicates intrauterine infection.IgG interacts with Fc receptors in the placenta & is. endotoxin) No role Have a role .most vaccines are given more than one dose. It is produced in primary immune response. b) The 3 complement pathways. therefore the only Ig that can pass the placental barrier to the foetal circulation(placental transfer) .D and properdin Classical pathway Acquired(specific) Antigen-antibody complex Needed for initiation (activation of C1) No role Lectin pathway Innate(non-specific) Lectin bindind to pathogen surface No role No role Alternative pathway Innate(non-specific) Microbial components (e.
7. III.e.8.6.RBCs transport them to the organ that rich in fixed pgagocytes. Direct cytolysis : insertion of MAC into the cell surface lead to killing of many cells through osmotic lysis.The molecules are called anaphylatoxins.Role of mannosebinding lectin The involved component No role C1. 3) Give reason : Host cells are protected from damage by complement. Degranulation of mast cells and basophils to release mediators of inflammations.2.8.Phagocytes removed the immune complexes from the red cells by their own C3b and Fc receptors.3. C3b receptors also found on RBCs. I.Phagocytes removed the immune complexes from the red cells by their own C3b and Fc receptors. Recruitment of phagocytic cells to the site of inflammation (chemotaxis_and stimulate of their phagocytes power and intracellular killing.RBCs transport them to the organ that rich in fixed pgagocytes. II. .Phagocytic cells recognize C3b bound to the pathogen via their C3b receptors.6.This help clearance of soluble immune complexes from the circulation and prevents the development of immune complex diseases.Phagocytic cells recognize C3b bound to the pathogen via their C3b receptors.9 Has a role C4.6.These recognize C3b bound to soluble immune complexes and the RBCs bound to them.188.8.131.52 No role C3.These recognize C3b bound to soluble immune complexes and the RBCs bound to them. Immune complex clearance : C3b receptors also found on RBCs.5.C1 inhibitor binds to and inactivates C1 preventing further cleavage of C4 and C2.This facilitate the attachment and subsequent uptake and killing of the C3bcoated pathogen by the phagocytes cell. b) Opsonization.9 2) Give on account on : a) Functions of complement.8.5. Inflammatory response : by-product C3a and C5a are produced during complement activation. C3b become deposited on the surface of the pathogen during complement activation.3.This help clearance of soluble immune complexes from the circulation and prevents the development of immune complex diseases. Opsonization : C3b become deposited on the surface of the pathogen during complement activation. c) Immune complex clearance. b. IV.This facilitate the attachment and subsequent uptake and killing of the C3b-coated pathogen by the phagocytes cell.7.They have following biological activities: a. This because the host cells are protected by series of complement regulatory proteins.g.5.
helper is stimulated.more tissue destruction and death occur. Enhance phagocytic and microcidal activity of macrophage. Thus. T cells response: main protective: Bacteria induce production of IL-12 b macrophage and IFN-y by NK cells……… development of Th-1 ………. T. • In LEPROMATOUS LEPROSY…Th-2 is induced… no intracellular digestion….has intracellular digestion of bacteria and some is living In tissue. Antibody function: opsonization. neutralization of bacterial toxin (prevent it bindin to host cell). activate macrophage to kill the bacteria inside them.Immunity to extracellular bacteria Innate immunity Phagocytosis by neutroils. Induce local inflammation. the T. The organism grow abundantly…. activate macrophage to kill intracellular bacteria. produce IFN-y. BUT… • In TUBERCULOID LEPROSY…Th-1 is induced…. binding to pilin protein f bacteria (prevent it adhesion to host). T cell response: Extracellular bacteria are internalized by APC and peptides are presented at MHC 11. moncyte or tissue macrophage. activation of complement through classical pathway. b. Give an account on: a. . Activation of complement by alternative pathway: Complement is activated by pptidoglycan and polysaccharide of bacteria cell wall..helper secrete cytokine that leads to: Stimulate antibody production.secrete IFN-y…………. recruitment and activation phagocytes and lysis of bacteria. disease is under control. Innate immunity: INEFFECTIVE: bacteria are resistant to degradation within phagocytes. agglutination of bacteria(prevent spread). Specific immunity Humoral immune response: Main protective against extracellular bacteria. Specific immunity Humoral immune response: dont play a role… because inaccessible to circulating antibody. NK cells provide early defense. Leads to production o opsonin.Chapter 18 IMMUNITY TO MICROBES 1.Immunity to intracellular bacteria. Skin and peripheral nerve is damaged but.
and not specific againsts certain virus. Th cell… contribute by secretion of cytokines: • IL-2 promote proliferation and activation of Tc cell and also activates NK cells.. It is immediate immunity but temporary. Opsonization to enhance phagocytosis. e. Neutralize virus pass in the blood stream.c. prophylaxis or treatment against bactria that produced exotoxins… as in diphtheria / tetanus. Specific immunity Humoral immune response: by antibody…(before the virus enter the target cell or during viruses released from infected cell…. Activation of complement.made antibodies or lymphocyte to an individual.. Antibody function: Bind to virus. transfer must between genetically identical individuals to avoid rejection reactions. Better presentation of viral peptide. 2-IgM and IgG…. Passive acquired immunity involves transfer of ready. It is 2 type: Humoral immunity. . Administration of convalescent serum to protect from disease (infectious hepatitis). Cell-mediated immunity. against extracellular viuses and specifis in action.. is produced by virally infected cell.. 3-Type 1 IFN…act early during viral infection. 1-Secretory IgA… neutralize virus that enter mucosa. 4-antibodies… act on late stage.artificial passive immunity. T cell response: Major defense against fungal: Fungi induce production of IL-12 b macrophage and IFN-y by NK cells………development of Th-1 ……….Immunity to viruses Innate immunity: NK cells. on viruses intracellularly. activate macrophage to kill the fungi inside them. Its function: • Inhibit viral replication and produce anti viral state • Activate NK cells • Increase expressin of MHC-1…. Transfer of antibodies (Passive immunization): Administration of antitoxic serum..secrete IFN-y…………. • IFN-y activate NK cells. killing virally infected cell in early infection..Immunity to fungi. promote phagocytosis and lysis of viruses. d.Transfer of lymphocyte.main mechanism where the infected cell is killed. Specific immunity: Humoral immune response: antibody are often produced againdt fungi…BUT it is not useful because fungi act as intracellular bacteria. Type 1 interferons(IFN-a and IFN-B)…. T-cell response: Tc cell. Th1 response is protective while Th2 response is harmful. Innate imunity: Neutrofil is the most important. thus prevent their attachment or entrance to host cell. It liberate fungicidal substance and phagocytose Macrophage can also combat fungal infections. Administration of gamma globulin to immunodeficient person.
-The result is there is intracellular digestion of the organisms that found in the tissues. this is still under control and patient survives -But with Th2 cells in humoral immunity. -Thus. -Neutrophil is the most important cell of the innate immune system in combating fungi. 3. with decreasing number of neutrophil cell in body. innate immunity is usually ineffective in controlling infections by these organisms. b) People with neutropenia are extremely sensitive to fungal infections. Although inflammatory responses associated with macrophage activation occur. c) In case of fungal and intracellular bacteria infections.2. -Th1 activates macrophages for combating these organisms. Give reasons for : a) Intracellular bacteria tend to cause chronic infection -Intracellular bacteria are resistant to degradation within phagocytes. -Neutrophil liberate fungicidal substances and phagocytose fungi as well. -Thus. Then these organisms can grow abundantly in macrophages causing much more destruction and eventually death. -Th1 cell in cell-mediated immunity is the main protective immune response against intracellular bacteria and fungal infections. -That is why these organisms tend to cause chronic infections that last for years and may recur after apparent cure.Compare: a)Type 1 IFN with antibobies in immunity against viruses Type 1 IFN Act early in viral infection Again intracellular viruses Not specific agains certain viruses Antibodies Act at a later stage in viral infection Again extracellular viruses Specific in action b)active and passive acquired immunity Active Role of immune system Mechanism Onset of protection Important role Stimulate B/t cell Delayed Passive No role Transfer of ready made antibobies/lymphocytes immediate . this is useless in combating against intracellular bacteria and fungal infections because antibodies cannot reach the organisms. Th1 response is protective and Th2 response is harmful. that people will be very sensitive to fungal infections.
Duration of protection Memory cell Examples Longer yes -Natural infection -Acive immunization with vaccines Shorter no -maternally –acquired antibodies -passive immunization with antitoxin serum c)immunity to extracellular and intracellular bacteria Immunity to Extracellular bacteria Innate immunity Process start with phagocytosis then degradation Activation of complement by alternative pathway Humoral immunity play role Both Th1 and Th2 play role Immunity to Intracellular bacteria Only phagocytosis no degradation(bacterial resistance) NK cell produce IFNγ then activate macrophage Humoral immunity no role Only Th1 play role Acquired immunity Chapter 19 TUMOR IMMUNOLOGY 1. Give an account on . 2.Define -Immuno –surveillance:ability of the immune system to prevent the development of most tumors through early recognition and destruction of tumor cell.
tumor-specific Ag (TSAs).present mainly on tumors produced by oncogenic viruses . An ideal tumour marker is: • Release only from tumour tissue • Specific for a given tumour type • Detect antibodyle early upon tumour formation • Its concentration in the blood is proportional to the tumour mass • Present in all patients with the tumour Most tumour marker are antigenic.e. no tumour markers has definite specificity or sensitivity for application in early diagnosis.e.2 groups of tumor Ag i. may not be able to stimulate an effective response . induce an active immune response(IR) ii. alpha foeto-protein(AFP) in hepatoma carcinoembryonic Ag (CEA) in colon carcinomas ii. oncofoetal Ag.virally derived peptides associated with surface MHC on tumor cells . tissue-specific differentiation Ag . TATA on virally-induced tumors .present during normal foetal development .g.origin of tumor Ag. and can be detected by immunoassays. tumor-associated Ag (TAAs).g Epstein-Barr virus (EBV) in lymphomas.tumor arising from a particular tissue may express normal differentiation Ag specific for that tissues .any tumor Ag from either this group that contributes to tumor rejection is referred to as tumor associated transplantation Ag (TATA) .reappear with development of tumors . circulating in the blood.g prostate-specific Ag(PSA) (b) Tumour markers Tumour markers are substance that present which indicating tumour. Tumour antigens can be very useful tumour markers in the diagnosis and follow-up of various tumours. i. Examples of tumour markers are: • Carcinoembryonic antigen (CEA): in colon carcinomas • α-Foetoprotein (AFP): in primary hepatoma • β-Subunit of human chorionic gonadotrophin (β-HCG): in choriocarcinoma • prostate-specific antigen (PSA): in cancer prostate • CA 125: in ovarian cancer • CA 19-9: in colonic and pancreatic tumours • CA 15-3: in breast cancer .behv as powerful transplantation Ag .Ag that are expressed on tumor cells but not on normal cells & might. Although useful in monitoring patients for tumour recurrence after therapy. therefore.lost during adult life .e.Ag that are relatively restricted to tumor cells but may also present on normal tissue & therefore. hepatitis B virus (HBV) in hepatic carcinoma iii.a) tumor Ag ~pg 92 .
b. stimulated in vitro using IL-2 n tumor antigen and then reinfused 2. Passive cellular immunotherapy -term used when activated cells are directly infused to a patient a)therapy with lymphokine-activated killer(LAK) cells: the patient lymphocyte are cultured in vitro with IL-2 then reinfused b)therapy with T cells:lymphocytes that have infiltrated tumors are excreted from tumor biopsies.NK cells (d) Approaches to Tumor Immunotheraphy 1.NK cells and B cell.Enumerate i.Evasion of the Immune Response a.macrophages. cytotoxic.Passive cellular and humoral(combined) immunotherapy -links 1 antibody reacting with the tumor cell to a second antibody reacting with a cytotoxic cell 4.B cell = process and present tumour antigen to Th cells tumour specific antigen which leads to tumour cell lysis fix complement on tumour cell membrane. toxins or cytokines.Active specific immunotherapy a)Allogeneic tumor cells: tumor taken from other patients.Nonspecific immunotherapy a)interferons b)bacterial adjuvants 3. -coupling has the advantages of delivering high doses of cytotoxic drugs to the site of tumor 3. irradiated n then injected with BCG vaccine or other adjuvants b)Tumor antigen vaccines: cellular immunity to antigens can be induced by using short synthetic peptide 5.related to tumour antigens: -tumours lack antigens that can stimulate immune response -tumours can’t be processed and presented with MHC .membrane attack complex leads to lysis of tumour cell Antibody dependent cell mediated cytotoxicity (ADCC) c. drug. Passive humoral immunotherapy-monoclonal antibodies directed against tumors antigens -may be used either alone or coupled to radioisotopes.T cell = cytotoxic T-cell : recognize the tumor antigen then kill them helper T-cell recognize sheded tumor antigen which is internalized and presented on Antigen Presenting Cell (APC) which will secrete cytokines that will activate Tc cells.• Bence-Jones proteins: in myeloma Pancarcinoma antigen (TAG-72): is used to localized occult tumour secondaries by using radiolantibodyelled monoclonal antibody (c) ) Effector mechanism in tumor immunology Innate and specific (humoral and cellular) immune system can effect the growth and progression of tumor: a.immunocompromised host b.
-amount too small to stimulate immune response -sheded antigens block antibodies and T cells from reacting with tumour cell c.poor in expressionof MHC 1 molecules e. Give reason: Th cells play a role in immunity to tumors.fibrin coating.Characteristic of ideal tumor makers 1) Released only from tumor tissue 2) Specific for a given tumor type 3) Detectable early upon tumor formation 4) Its concentration in the blood is proportional to the tumor mass 5) Present in all patients with the tumor 2. NK cells & B cells . macrophages.until resistant is built up . gradually increasing doses of the allergen.tumours located at inaccessible to the immune system d.masking of tumour antigens f. although tumor cells express class I MHC & not class II MHC molecules ~pg 93 .they secrete cytokines which activate Tc cell.tumours secrete substances that suppress the immune response -ii. over a period.Th cells are activated by shed tumor Ag which become internalized & presented on the surface of APC in association with MHC II .Define: a) hypersensitivity reactions : inappropriate immune responses to certain antigens causing tissue damage b) desensitization : a method for reducing the effects of a known allergen by injecting.produce TNF~directly toxic to tumor cells Chapter 20 HYPERSENSITIVITY 1.
C 3a and C5a(anaphylatoxin) -react with receptor on mast cells and basophil -release of vasoactive amines -increase vascular permeability -C 5a also chemotactic to neutrophils that infiltrate the area. a)Preformed mediators -histamine and PAF(platelet activating factor) -during early phase. -TH2 cell will release IL-4 which is critical stimulus for changing production IgM into IgE.basophils which contribute to inflammatory respond and tissue damage.2. b)Newly formed mediators -leukotriens and prostaglandin -during late phase.typicaly occur 5-6 hours after exposure and persist longer. . -this induce degranulation of mast cell and release two types of mediators. TH2.which occur witin 15-20 minutes after exposure. -neutrophils engulf this comlex and release lysosomal enzymes that destroy basement membrane. (4)Platelet aggregation -release vasoactive amines -form microthrombi that cause local ischemia and further tissue damage. -TH2 lymphocytes are responsible for production of IgE. (2)Degranulaton of mast cell -upon 2nd exposure to the same allergen. -recruitment of other effector cells e.Give an account on: A)mechanism of hypersensitivity: Type I (1)Sensitization -in normal person only low level of IgE are relesed when exposed to antigen. (3)Lysis of target cell by ADCC(antibody dependant cell mediated cytotoxicity) Type 3 (1)Formation of immune complex(antigen with IgG/IgM) (2)Penetration of complex to the endotelial wall and become deposited on the vascular basement membrane. -IgE bind to mast cells and basophils via its Fc receptor.IgE on the mast cell cross link by the allergen. (2)Opsonization with or without complement activation. -Now. (3)Activation of complement .g. Type 2 (1)Lysis of target cell by complemet activation.mast cells and basophils are sesitized during first exposure.eosinophils. -but high levels of IgE are produced in individuals having this type of hypersensivity.
corticoseroid. -inflammatory reaction leads to local tissue damage. (b)Atopy management -AVOIDANCE of responsible allergen -DESENSITIZATION by giving gradually increase dose of injection against the allergen. -produce larger amount of IgE than oter individuals in response to allergen. -T cytotoxic may also play role.Its aim is at shifting the immune response from TH2 to TH1 thus down regulate IgE -DRUG that inhibit mediator release/couteract their effect e.and oxygen inhalation. and inflammatory response occur -resulting in local erythema. C)Arthus reaction -local immune complex disease -due to repeated subcutaneous injection of low dose of foreign antigen -e. *Therapeutic measures (a)anaphylactic shock management -an emergency case -immediate admininstraton of adrenaline.g insulin and rabies vaccine -occur at the site of inection -immune complex deposit in the blood vessel wall. antihistaminic.Type 4 (1)TH 1 cells recognize antigen -release po-inflammatory cytokines.g. D)Diagnosis & therapeutic measures of type 1 reaction *Diagnosis (1) -detection of antigen by skin test -introduce various antigen to the patient skin -Wheal flare reaction proves positive case -it appears within 15-25 minutes at the site where the patient is allergic to certain antigen. -attract and activate monocytes.corticosteroid. and more T cells.macrophages.oedema. (2) -Measurement of total IgE levels and specific IgE for particular antigen.and necrosis. -increase vascular permeability leads to leakage of flid ito the tissue.activation of comlement. B)Atopy -hereditary tendancy to type 1 hypersensitivity.antileukotriens .
g in AIDS patient with mycobacterial infection since Th level is very low -central core is infected macrophages.arthralgia. mycobacteria) -when the intracellular bacteria resist to microbicidal effect of activated macrophages. -Formed immune complex deposite at certain site cause disease manifestation.Enumerate the clinical forms (examples) of: a)Type I Hypersensitivity : -Systemic anaphylaxis -Localized anaphylaxis ( Atopy ) b)Type II Hypersensitivity : -Blood group incompatibility -Autoimmune disease -Drug interact -Graft rejection c)Type III Hypersensitivity : -Serum sickness -Arthus reaction -Post-streptococcal glomerulonephritis -Viral infections -Autoimmune disease -Hypersensitivity pneumonitis d)Type IV Hypersensitivity : -The tuberculin skin test -Contact dermatitis -Granuloma formation -Autoimmune disease -Graft rejection . -It leads to fever.may include fused macrophages(multinucleated giant cell).lymphadenopathy. -antibodies bind with remnants of antigen.splenomegaly(develop few days-2 weeks after time of injection) F)Granuloma formation -can be seen especily in chronic infectious disease caused by intracellular bacteria (e.g.E)Serum sickness -systemic immune complex disease -due to injection of large dose of : *foreign serum-horse antitetanic / antidiphtheritic serum *drug-penicillin -antigen slowly cleared form the body while antibody production starts. -Continous release of cytokines by Th 1 accumulate activated macrophages forming GRANULOMA *granuloma: -protecive mechanism to isolate pathogen that resist destruction -prevent from dissemination of infection -are fatal with its absence -e.the antigen persistently give rise to chronic antigenic stimulus.urticaria.surronded by large macrophages (epitheloid cell) -Th cell surrond the central core -The cells in the center of granuloma undergo necrosis (caseation necrosis) 3.
depending on genetic disparity. Not foreign and do not elicit rejection 2) Isograft – graft between genetically individual (eg: identical twins). Antigen responsible for immune rejection 1) Blood group antigen of the ABO system 2) MHC antigen 3) Minor histocompatibility complex antigens. HLA-DR b. HLA-C Locus : HLA-DP.Chapter 21 TRANSPLANTATION IMMUNOLOGY 1) Classify Class I MHC and Class ll MHC 2) Enumerate. HLA-DQ. 4) Xenograft – represent maximal genetic disparity and rapidly reected. Types of rejection 1) Acute rejection – takes days or weeks to develop because of the time taken for T cell activation 2) Hyperacute rejection – take place within minutes. c. a. MHC l Found on surface of all nucleated cell MHC ll Found on surface of the professional antigen presenting cell.This allograft express antigen which are recognized foreign by the recipient. .graft from one part of body to another. Composed of 2 glycoprotein chain ( alpha chain and beta chain ) Composed of 2 polypeptide chain ( alpha chain and beta-2 microglobulin chain ) Locus : HLA-A. HLA-B.Types of graft 1) Autograft . Do not express antigen and not rejected. caused by preformed anti-donor antibodies 4) Chronic or late rejection – take place months or years after transplantation. 3) Allograft – one person donates organ to genetically different individual of the same species.
-Tc cell causes direct destruction of transplanted cells -Th cells release a number of cytokines which lead to activation of the immune response. significance of MHC 1) antigen presentation 2) enables virus infected cell to be a target for Tc cell ( MHC I) 3) mismatching of donor and recipient MHC causes graft rejection 4) certain MHC alleles affect the susceptibility of an individual to certain diseases. proliferation and migration into the donor graft. systemic erythematosus and DR3) 5) used in forensic medicine e. ankylosing spondylitis and B27. -The antibodies attach to the endothelial cells of the donor organ and fix complement -Causing damage to the vascular endothelium. It takes days or weeks to develop because of the time taken for T cell activation.g. rheumatoid arthritis and DR4. -IL-2 is required to activate Tc cells -TNF-α and IFN-γ activates macrophage 2) hyper acute rejection -caused by performed anti-donor antibodies binding to either ABO blood group or HLA class I antigen on the graft.g. It take place whithin months to years after transplantation depends on • genetic disparity between donor and recipient • success of immunosuppressive therepy more prominent with patient having • chronic viral infection • cytomegalovirus (especially) • pre-existing autoimmune disease c.3. Give an account on a. graft versus host disease -it occurs when the graft react against the recipient tissue not vice versa -e. mechanism of graft rejection 1) acute rejection -it is type IV hypersensitivity (cell mediated) delayed. disputed paternity b. leading to • haemorrhage • platelet aggregation within the vessels • graft thrombosis • lytic damage to cells of transplant • release of pro inflamatory complement compenents C3a and C5a 3) chronic or late rejection caused by low grade cell mediated rejection or the deposition of antibodies or antigen-antibody complexes in graft.g. -To reduce the risk • careful typing • careful use of immunosuppresive drugs • careful removal of mature T cells from the donor stem cell . It take place within minutes of transplantation. These diseases are often inflammatory or autoimmune in natur (e. in bone marrow transplantation -immunological competent T cells are transplanted into a genetically non-matching immunosuppressed recipient.
d. thus prevent lymphocyte proliferation • monoclonal antibodies: monoclonal antiCD# antibodies block the function of T cells 3) antigen specific induced tolerence still under trial~ 4. prevention of rejection 1) selection of donor • ABO matching Perform antibodies against ABO blood group system • Histocompatibility testing Leucocytes carry all known HLA antigen. Tissue typing by lymphocytoxicity test Purified suspension of lymphocyte + antisera + complement If complement fixed = cell damaged n dye enters If complement not fixed = cell remain viable. Give reasons: a) cyclosporin is used to prevent graft rejection it inhibits T cell cytokine production mainly IL-2 and TNF-γ b) azathioprine is used to prevent graft rejection it inhibits DNA production. unstained Compatibilty testing by the mixed lymphocyte reaction (MLR) Donor and recipient cells are incubated together If recipient cell recognize foreign HLA on donor cell. 2) immunosupressive therapy prevent and/or treat graft rejection n GVHD these drugs carry risk of infection • corticosteroids: potent anti-inflammatory • cytokine producer inhibitor: cyclosporine n tacrolimus inhibit T cell cytokine production mainly IL-2 and TNF-γ • antiproliferative drugs: azathioprine and methotraxate inhibit DNA production.Define : . so it can be used for tissue typing to identify HLA and test compatibility between donor and recipient i. thus prevent lymphocyte proliferation Chapter 22 Tolerance and Autoimmunity 1. it will proliferate Proliferation is measured by the extent of radioactive thymidine uptake Molecular HLA typing PCR Accurate and sensitive ii. iii.
due to uptake in immune complexes b. Self-reactive B cells may mature and migrate to the secondary lymphoid organ but due to lack of T cell help. Decreased level of serum complement. Interference with the mechanism which normally suppress surviving self-reactive T cells ii. It is because some of the self-antigens are not expressed in them. Exposure of the immune system to antigens that are normallly hidden within organs e. Breakdown of immune network which occur due to: i.Spectrum of autoimmune diseases .peripheral tolerance : i. Structural modification or alteration of tissue proteins f. it occurs if the elimination of self-reactive cells in primary lymphoid organ is not complete.Detection of autoantibodies in the serum iii. Self-reactive T cells are also unable to respond due to various mechanism 2.Interference with cytokine network(under trial) 4.Aetiology of autoimmune diseases d.Give an account on : 1. ii.A Tolerance absence of specific immune response againsts some antigen in fully immunocompetent person B Autoimmunity adaptive immune response to self-antigens C Clonal elimination of immature self-reactive lymphocytes during their deletion maturation 2.Diagnosis and management of autoimmune diseases a.Detection of immune complexes in the serum and in tissue biopsy iv. they cannot do their function iii.central tolerance : it is the phase in the primary lymphoid organ in which B and T lymphocytes undergo permanent inactivation after being in contact with self-antigen b.Diagnosis i.Elevated level of serum immunoglobulins ii. Over production of IL-2 by Th1 cells 3.Imunosuppressive drugs iii. Polyclonal activation of lymphocytes iii.Anti-inflammatory drugs ii. Cross reactivity g.Plasmapheresis iv.Mechanism of auto-tolerance : a.Management i.
immune complex deposition (type III) iii. high doses of antigen tolarize B-cells while minute doses given repeatedly tolarize T-cells ii. there are the organ-spesific diseases where the immune response is directed against components spesfic to the organ involved. in Grave’s disease. eg. . prenatal or neonatal period b. leading to thyrotoxicosis. antibodies formed are non-organ-spesific but the lesion tends to localize to a single organ eg. increasing the response of cell receptors to TSH. non-organ-spesific diseases. anti-thyroid antibodies react with thyroid gland cells. antimitochondrial antibody in 1ry billiary cirrhosis 3. the tolerogen must persist or repeatedly admnistered iv. protein antigen are more tolerogenic in soluble form than in aggregated or particulate form iii. giving the antigen together with immunosuppresant v.SLE In between. Grave’s disease At the other end. thus stimulates secretion of excess thyroxin. Mechanism of tissue damage in autoimmune disorders i. to maintain acquired tolarance.Enumerate a. cell-mediated reactions (type IV) iv. Factors influencing the induction tolerance i. The lesion is not confined to one organ eg. cytotoxic reactions (type II) ii.At one extreme.
fungal and protozoal infections k) Combined T and B cell deficiency(SCID) o patients present during the first few months with failure to thrive.continuous diarrhea.but with little pus formation.bacterial.and respiratory tract.bronchitis. c) Defect of early component of classical pathway o accumulation of immune complex and local tissue damage d) Defect of early component of alternative pathway o pyogenic infection e) Defect of terminal complement (C5-C9)of complements(MAC) o increased susceptibility to capsulated organism Neisseria meningitides f) Defect of complement C1 inhibitor uncontrolled activation of the classical pathway of complement activation o C2 activation and generation C2a(vasoactive amine)-fluid accumulation in tissues and swelling of epiglottis which may lead to suffocation and death. and pneumonia. i) Deficiency of natural killer cell o patients suffer from certain viral diseases and malignancies j) Thymic aplasia and hypoplasia(Di George Syndrome) o develop recurrent and chronic viral. b) Defects intracellular killing of phagocytic cells o phagocytes cannot produce reactive oxygen radicals.mouth. . h) Transient hypogammaglobunaemiaof infancy o infants have recurrent infections and poor response to the vaccines taken routinely at that age.Chapter 23 IMMUNODEFICIENCY DISEASES 1. o patient present with infections of skin.despite their presence in large numbers in the blood.as well as viral and fungal infections. Mention the patient presentation in(or the effect of): a) Defects of migration of phagocytic cells o defects in migration leads to failure of neutrophils and monocytes to migrate from blood stream to sites of infection.”Hereditary Angioedema” g) X-linked agamaglobulinemia o infants:symptomatic and natural loss of antibodies at the age 5-6 months They suffer from chronic bacterial infection such as otitis.lead to decrease ability to kill intracellular as well as ingested bacteria o male children present with chronic bacterial infections-some cases lead to formation of granules.
investigation of B cell deficiency Quantitation of cells using flurescein-labelled monoclonal antibodies against B cell markes. e.the result is the patients develop recurrent and chronic viral.Leucocyte adhesion deficiency It is defect of phagocytic function on migration that involves adhesion molecules.Chronic granulomatous disease It is defect of phagocytic function on intracellular killing. d. In George syndrome is a severe form T cells deficiency caused by congenital aplasia or hypoplasia of the thymus. b. Patient – infections of skin.fungal and protozoa infection. respiratory tract with little pus formations.g.Defective T-cells immunity(without affection of humoral immunity) is rare: As the collaboration between T cells and B cells in the process of antibody formation.Investigations of T cell deficiency Quantitation of cell by fluorescein-labelled monoclonal antibodies against cell markers. Thus. b. ( mitogens are substances that can nonspecifically stilmulate proliferation of lymphocyte. Assessment of cytokine production.Give an account on: a.Patients suspected of suffering immunodeficiency never be given live vaccine: the patient may die as the result of immunodeficiency due to lack of T-cells and B-cells action which are very important in protection of the body from the foreign body(live vaccine) organism.g. - . c. Some stimulate T cell only.bacteria. mouth. Measure ability of T cells to proliferate in response to mitogens. with antibodies against CD3 ( to quantitate total T cells ) and against CD4 and CD8 ( to quantitate T cell subsets ). candidin test. Give reasons a. 3. Lead to failure of neutrophils and monocytes to migrate from blood stream to sites of infection although there are in huge amount. e. production of antibodies against T-dependent antigens in particularly can be affected in cases of T cell immunodeficiency. Determination of serum level of immunoglobulin classes as well as IgA in saliva. Delayed type hypersensitivity test to test functional activity of T cells using extracts from organism to which people are frequently expose. some B cell and others stimulate both ). Usually an X-linked disease and male children with chronic bacterial infections that may lead to granulomas. Immunization with commonly used vaccines such as tetanus toxoid followed by measuring the antibody response.2. Phagocyte cant produce reactive oxygen radicals – decreased ability to kill intracellular and ingested extracellular bacteria.
steroids. 1. • Treatment with cytokines such as GM-CSF.immunosuppressive drugs and burn with severe loss of body fluids. Tuberculosis 5. cytotoxic drugs. • Administration of suitable immunization. development of certain kinds of tumour . IL-2. • Prompt treatment of infections with antibiontics. occurrences of opportunistic infection 5. Other virus infection lead to transient ID eg. • Immunoglobulin therapy for cases of antibody deficiencies. Malnutrition in poor and under development country 2. Others eg. Human Immunodeficiency Virus (HIV) causes Acquired Immune Deficiency Syndrome (AIDS). Enumerate a. Malignancies specially Hodgkin’s disease and leukaemias 7. failure to thrive in infant and children 6. IFN-gamma 4. Causes of secondary immunodeficiency(ID) may acquired a transient or permanent immunologic impairment later in life. Specific measures according to defect • Transplantation of foetal thymus or bone marrow in SCID and other deficiencies. Schistosomiasis 6. increased in frequency of infection 2.e. Causes in which immunodeficiency is suspected 1. Severe bacterial infection eg. Treatment with X-rays. Patient with immunodeficiency should never be given vaccines contain living organism since it maybe fatal.the virus infects CD4 Th cells 3. Parasitic manifestation eg. dissemination of local infection to distant sites 4. Diabetes and renal failure b. failure clearance of infection rapidly despite adequate therapy 3. chronic debilitating disease eg. Measles 4.management of the immunodeficient patient General measures – minimize infections by avoidance. 8.
The diameter of the ring is proportional to the concentration of the antigen in the well e. mumps viruses etc) or other substances.Give an account for each principle of Ag-Ab reaction and give one application. Eg. If no haemagglutination occur. Serum is mixed with known influenza virus and RBCs.Haemagglutination inhibition To see the agglutination of the RBCs by antibodies. The antibodies are mixed with the agar before it was poured into the plate. Use for diagnosis certain viral diseases because specific anti-viral antibodies bind to the viral particles and block their ability to agglutinate RBCs. – a person suspected of having influenza so his serum is examined for specific antibodies.Chapter 24 ANTIGEN-ANTIBODY REACTION 1. certain virus particles (influenza.Used to quantitate antigens b.Single radial immunodiffusion a. Quantitation of IgG by using agar gel mixed with anti IgG antibody . With antibodies = no agglutination No antibodies = agglutination b. Precipitation will occur as a ring around the antigen well d. so the antibody is present and vice versa. Then the antigen is placed in wells punched in the agar gel c. (Illustrate with diagram) a. Routinely used to quantitate various Ig classes in human samples eg.
diphtheriae c. Eg. Antibodies against bacterial toxin will neutralize its hazardous effects b. For the diagnosis of rabies in brain of rabid animals Fluorescein tagged antibody unknown antigen binding observed by UV microscopy e. In-vivo toxin neutralization test for determination of toxicity of C. Presence of antigen will be bonded and be visualized as a green stain specimen under the UV light d. Diagram as haemagglutination test d. Toxin neutralization a. Used to detect certain antigen in tissue sections fixed in microscopic slide b. Specific fluorescein-labelled antibody is used c. ELISA a. Detection of the conjugation is by adding proper colorless substrate that in the presence of the enzyme it'll be converted into a colored product . Direct immunofluorescence a.Sample 2 Sample 1 Ag standard 2 Ag standard 1 Petri dish containing antibody in agar c. The principle is conjugation of the antibodies or antigens to an enzyme b.
Complement Fixation Test Sensitive test.c. Iodine125 replaces the enzyme in ELISA technique to label antigen or antibody b. Degree of color change can be measured by spectrophotometrically. Direct Differences Indirect Red cell of newbornsSample Serum of Rh –ve mother sensitize erythroblastosis fetalis with Rh antigen Hemolytic anemia patients Method 1-Patient’s RBC washed 2-Add anti human globulin to cell suspension Positive result 1-Serum + Rh +ve + group O red cells => incubated 2-Washing 3-Add anti-human globulin Agglutination Positive result h. Used to quantitate many biological substances eg. Coombs’s Test: Function: To detect non-agglutinating antibodies. i. tumour markers. FlocculationFunction : Detect small insoluble particulate antigen Example: Syphilis Antigen: Water insoluble cardiolipin (not treponemal-difficult to obtain) Result : Microscopical aggregates => heterophil antibody(reagin) in serum of +ve syphilis. A radioactive assay eg. Hormones. drugs g. Accompanied by hazards of radiation d. In antigen-antibody interaction – complement is fixed(consumed) Function : Detect and quantitate antigen-antibodies Source of complement: Guinea pig serum-rich in complement Method: (a) Test system: 1-Heat the serum 56°-inactivate native complement 2-Add measured amount of antigen & complement +ve-antigen-antibody complexes will form(cannot be seen) (b) Indicator system: 1-Add sheep RBC+hemolysin => test presence of free complement . Examples and diagrams of technique that could be used will be referred to page 125 and 126 vol III f. considered as an indicator of the amount of antigen or antibody in the sample d. ~in RPR-carbon particles added => result seen by naked eye. Ag-Ab reaction will be measured by radioactivity c. RIA (Radioimmunoassay) a.
l.Result +ve . -ve CPE : serum antibody + virus + target cell => antibodies present. Result: +ve – agglutination occur. Method: 1-Serum of patient (unknown antibody) + Treponema pallidum (known antigen) on slide 2-Washing 3-Overlay flourecein-labelled antihuman antibody on the slide 4-Examine with UV microscope Result: +ve-green fluorescence => antigen antibody complexes binding. 2-Inoculate susceptible cell culture into (1) Result: +ve CPE : virus + target cell ONLY =>no neutralizing antibodies.g: Latex particles or RBC ) ~if RBC is used= Passive heamagglutination. Examples: 1.Rheumatoid arthritis (IgM vs IgG) Antibody: Rheumatoid Factor(RF) Latex coated particles + IgG = agglutination [RF present] 2.all complement are used -ve -hemolysis . Viral neutralization Cytopathogenic Effects(CPE) :Virus + app. cell culture => observable cell destruction Function: searching virus neutralizing antibodies in a serum sample Method: 1-Serum containing antibody + known virus suspension.Inflammation Antibody: C-reactive protein Serum + latex + anti C-reactive protein = agglutination [ C-reactive ptn present] . k. Indirect immunoflourecence Function: Detect presence of antibody against certain organism.no hemolysis .Passive agglutination Method: Adsorbing the known reactant (soluble antigen or antibody) passively on suface of inert particle (e.free complement exist => lyse the sheep RBC Example: -Diff bacterial -Rickettsial -Viral -Fungal -Parasitic diseases j.
3. Diagnosis of newborns with erythroblastosis fetalis – Coomb's (antiglobulin) test 6. Detection of viral infections – Haemagglutination inhibition test 10. VDRL test for syphilis – Flocculation 8. Blood grouping – Slide agglutination 2.Mention the type of Ag-Ab reaction in each of the following tests 1. Quantitation of hormones – Radioimmunoassay 9. Detection of anti-Rh in the mother's serum – indirect Coomb's (antiglobulin) test . Diagnosis of rabies in brain of rabid animals – Complement fixation 5. Immunologic pregnancy test – Passive agglutination 7.Immunologic pregnancy test Antibody: HCG Drop of urine + latex + anti-HCG = agglutination [ +ve pregnancy test] 4. Elek's test – Precipitation 3. Antistreptolysin O – Passive agglutination 4.
Lipid A of LPS forms the endotoxin. 1-2 sheets Comprising 5-10% of cell wall material Absent Outer surface is composed of molecules of lipopolysaccharide (LPS).EXAM : GENERAL BACTERIOLOGY 1) Compare : a)compare gram +ve and gram –ve cell wall Gram +ve As many as 40 sheets Comprising up to 50% of cell wall material Teichoic acid and cell wall associated protein are major surface antigen Gram –ve Thin. while polysaccharides are major surface antigen Space between cytoplasmic and outer membrane containing peptidoglycan layer and gel-like solution of protein Peptidoglycan layer Teichoic acid Outer membrane Absent Periplasmic space Absent b)compare obligate aerobes and obligate anaerobes Obligate Aerobes Oxygen requirement Example Require oxygen for growth Pseudomonas aeruginosa Obligate Anaerobes Require complete absence of oxygen Bacteroides fragilis c)compare conjugative and non-conjugative plasmids Conjugative Size Copy number F factors Large 1-2 (stringent) Present Non-Conjugative Usually small >30 (relaxed) Absent .
. Toxicity-may be dose dependent or independent Tetracycline may cause staining of teeth in infants Streptomycin may affect the 8th cranial nerve leading to vestibular dysfunction. The prophage may be induced to detach from the bacterial chromosome and start a lytic cycle.pertussis (chromosome) h. it passes this fragment to it giving it new characters.pylori (PAI) Protein Higly antigenic Unstable to temperature >60 Can be converted into toxoid Every toxin has specific action high Endotoxins Integral part of cell wall of gram –ve organisms. the prophage may carry with it few genes of the bacterial chromosome.plamids.V light 3.g U. When it infectes another bacterium. 2. >60 for several hours Can not Same generalized effect ( non specific action).Sex pilus formation Transfer among bacteria Host bacteria d)exotoxins and endotoxins Yes By conjugation Common gram –ve bacilli No By the help of conjugative plasmid Common in gram +ve cocci Exotoxins Source Coding genes Examples Nature Antigenicity Heat stability Detoxificati on Specificity Toxicity Secreted by living organism both garm +ve( mainly ) and – ve Encoded by chromosomes. During the process of induction.bacterio phages and PAI c. This is known as “specialized transduction”.tetani (plasmid) b. The prophage may be carried inside the bacterial cell indefinitely passing to daughter cells.all give fever and shock. e.diptheriae (phage) cl.coli and meningococcal endotoxins Lipopolysaccharide (lipid A) Poorly antigenic Stable temp. Induction may be spontaneously or achieved by an inducer. Low 2) Give an account on : a) Outcome of temperate phage cycle 1. b) Complication of chemotherapy 1.liberated upon cell disintegration Encoded by genes on the chromosome e.
• Local application of sulphonamides may result in contact dermatitis. anaphylactic shock or serum sickness. It is recommended that in vitro susceptibility testing should be performed to guide the selection of antibacterial drugs. adhesions or invasion factors. 3. . Bacterial genome.total set of genes present inside the bacterial cell. Superinfection • It occurs as a result of outgrowth of resistant members of normal flora when the sensitive ones are eradicated during antibiotic therapy: eg:pseudomembranous colitis caused by outgrowth of clostridium difficile. These mutants will overgrow and replace the originally susceptible bacteria. no real indication and improper choice) encourages the emergence of resistant mutants.integrated phage genome. Opportunistic pathogens.the ability of the recipient bacterial cell to take up DNA. interrupted course. Allergy (Hypersensitivity): usually not dose dependent • Penicillins may cause urticaria. c) The ideal cloning vector should carry a selectable marker It must carry a selectable marker so that the host cells transformed with the vector can be distinguished from non transformed cells. Competence. 4.It is the elimination of most. Aminoglycosides may cause nephrotoxicity Chloramphenicol can cause bone marrow depression 2. e) Disinfection. 4) Define: a) b) c) d) Prophage. • -oral thrush caused by overgrowth of the yeast candida 3) Give reason for : a) Mycoplasma are resistant to penicillin Mycoplasma is the only group of bacteria that exist naturally without cell wall so they are naturally resistant to cell wall inhibitor like penicillin. if not all. Emergence of resistant strains: • The abuse of antibiotics ( low dosage.These are potentially pathogenic bacteria that do not cause disease under normal condition but can cause disease in immunocompromised patients or when they find their way to another site other than their normal habitat. pathogenic microorganism excluding spores. b) Plasmid may render the bacteria pathogenic Plasmid may render the bacteria pathogenic as it has fuction as virulence plasmid that may code for exotoxins.
is the ability of an antimicrobial agent to harm a pathogen without harming the host. CH 14-T cell mediated immunity 1) Compare : a) Effector and naïve T cells Effector T cells Ability to respond quickly and efficiently when encounter antigen an target cells Can be trigger to act without need costimulation Naïve T cells Yes No Yes No b) Ordinary antigen and superantigen Ordinary Antigen Processing inside APCs Presentation by MHC molecules Site of binding to MHC molecule Binding to TCR Yes Yes Peptide-binding cleft Variable portion of α and β chains Superantigen No No Outside peptide-binding cleft Variable portion of β chain .f) Selective toxicity.
Give an account on a) Sequence of events in activation of naïve T cells • • Any cytosolic peptide is delivered on a MHC1 molecule to the surface of the APC. . any vesicular peptide is delivered on an MHC 2 molecule to the surface of the APC. A CD8 (cytotoxic) T cell with TCRs specifics for that peptide binds he MHC1 peptide complex.Specificity of TCR to it Acquired immune response Development of memory Result of T cell stimulation Very specific Stimulated Yes Usually beneficial to host Not very specific Supressed No Usually harmful to host c) NK cells and Tc cells Tc cells MHC restriction Antigen specificity Mechanism of killing Direct killing Resticted to MHC I Specific to certain antigen NK cells No restriction Not specific Direct killing Antigen dependant cellular cytotoxity (ADDC) 2. A CD4 (helper) T cell with receptor specific for that peptide binds the MHC 2 peptide complex. Similarly.
The second signal is delivered by binding of CD28 on the T ell to B7 on the APC(costimulation). a state called anergy. During this events. certain molecules called adhesion molecules. acting as a clamp between both molecules The type of binding to TCR is not very specific as in ordinary activation a T cells and. but have the ability to bind directly to the MHC 2 molecules on the surface of the APC without entering the cell. which not beneficial to the host and even causes systemic toxicity. a cytokine secrete by the T cell itself.This signal is very important and without it the T cell ‘shuts down’ and becomes non-responsive. There is supprson of the normal acquired immune response and no memory cells are produced Superantigens are produced by any different bacteria and viruses and are afctive at very low concentratins Examples of superantigens are staphylococcal enerotoxins and toxic shock syndrometoxin. consenquently very large numbers of Th cells can be activated by one kind of suprantigen. The result is release of huge amounts of cytokines. Overproduction of cytokines in response to these toxins accounts for many of their toxic effects on the body c) Functions of effector CD4 T cells (helper Tcells) (or mechanismof activation of macrophages by Th1) The main function of of effector CD4 T cells is to secrete cytokines Classified to Th1 or Th2 cells according to cytokines they secrete . divides repeatedly (proliferation or clonal expansion) and its progeny (daughters) finally become interleukin-2 (IL2). The T cell become a lymphoblast (activation). and at the same time to the variable portion of the β chain of the TCR. b) Superantigens • • • • • • • • Superantigen is certain protein that secreted by some pathogens do not act by ordinary antigens They are not processed and presented to T cells like ordinary antigens. this leads to delivery of first signal required for T cell activation. Present on the T cell and APC help to hold the two cells together.• • • • In either case.
nitric oxide and antibacterial enzymes bymacriphage.Ther is more efficient fusion between the phagosomes containing the bacteria and the lysosomes containing the acterial enzmes -There is also increased producton of oygen radicals. the Tc cell detaches and search for other target cells to kill.displays on its surface viral peptide in conjugation in an MHC 1 molecule. However. its absence can lead to serious consequences of disseminated infection.making more capable of killing the bacteria it harbous: . d)Functions of effector CD8 Tcels (cytotoxic T cells) (or mechanism of killing by Tc cells) The main function of effector CD8 T cells is to eliminate abnormal cells. Mechanism of activation of macrophages by Th1 cells • • An infected macrophage displays a peptide MHC 2 complex to an effector T cell If the TH1 cell is specific for that peptide MHC2complex. Activation of Th1 cells and consequent macrophage activation can sometimes cause significant tissue damage. which could be dangerous to the body as a whole. Such as virus-infected cells or tumor cells.γ).Th2 cells Produced cytokines which predominantly help B cells and promote humoral immunity. 2. it is induced to secrete cytokines. This is typically seen in AIDS patients with microbacterial infection.Th1 cells Produced cytokines which predominantly help macrophages and promote inflammation. An effector T cell with TCR specific for that peptide MHC2 complex recognizes it and delivers a lethal hit. After inducing death of target cell.most important of which is interferon-γ (IFN.Induction of apoptosis . • • • The target cell.1. leading to death of target cell.This causes activation of the macrophages. Mechanism of killing by Tc cells Two mechanisms: 1. since the number of Th cells in this patients is very low.such as avirus-infected cell.
Apoptosis is a clean death in which the cell destroys itself from within. 3) Give reason : a) superantigens cause systemic toxicity Superantigens are non specific protein that attaches to the MHC II and TCR without the need of presentation by APC. giving a signal for apoptosis in the target cell. The perforins create perforations( holes) in the Cytoplasmic membrane of the target cells. leading to death of the target cell by osmotic lysis. pesent normally on many cells.Osmotic lysis The pores produced in the target cell membrane by the perforins may allow entrance of fluid into cell. present on cytotoxic cells. b)apoptosis is a suitable mechanism of killing virally infected cells Through apoptosis. binds to a molecule called FAS-ligand. it will stimulate humoral immune response. Thus the elimination occurs through antibodies present in plasma and extracellular fluid. leading to degradation of cells’s DNA. a state called T-cell anergy. they activate a very large number of Th cells leading to release of huge amount of cytokines. thus preventing release of viral particles to infect other cells. This process of suicide is called Apoptosis. Through those holes granzymes enter The target cell and cause activation of enzymes naturally present in it. such as bacteria and its toxin. shrinking and degrading itself until little is left. 4) Explain : a) significance of 2nd signal of activation of naïve T-cells Absence of the 2nd signal of activation will cause T-cells to become non-responsive. which cause systemic toxicity. shrinking and degrading itself.The T cell induces the target cell to undergo suicide. The enzymes which are activated to destroy cellular DNA can also degrade viral DNA. The cytotoxic cell releases two kinds of graules Called perforins and granzymes. the cell dies by destroying itself from within. 2. The enzymes which are activated to destroy cellular DNA can also degrade viral DNA. b) the lifestyle of the pathogen decides the type of immune response if it is extracellular pathogen. . Being non-specific. A receptor called FAS. thus preventing release of viral particles to infect other cells. It may occur one or two mechanisms • release of cytoplasmic granules. • Interaction of cell surface molecule. Death apoptosis is faster than osmotic lysis and is probably the main mechanism involved n killing of target cells by Tc cells.
it will stimulate cell-mediated immune response (antibodies are not accessible to the pathogens). d) the significance of present of MHC II on only a few cells of the immune system presentation of antigen to Th cells result in production in cytokines.in many consequences. Otherwise it would escape killing. which would be dangerous to body. These cause activation of many cells of the immune system.there is no need for the present of MHC II on all cells of the body. In fact this would lead to over stimulation of Th cells and over production of cytokines.But if it is intracellular such as viruses and some bacteria. so all cell must possess MHC I molecules in order to be able to show viral peptides to the Tc cells so that it can kill that infected cell. c) the significance of the present of MHC I on all nucleated cells of the body any cell on the body is liable to be infected by a virus. e)CD8 T cells are MHC I restricted CD8 T cells recognize peptides bound to MHC I molecule only f) CD4 T cells are MHC II restricted CD4 T cells recognize peptides bound to MHC II molecule only . The presence of MHC I molecules on all body cells is necessary so that these cell can be targets for the Tc cells if the need arise. The destruction of these pathogens is the function of T lymphocytes.
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