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197 Cards in this Set

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what can activate the complement pathway?
peptidoglycan layer in bacterial cell walls
-techoic acids & PG fragments of gram positive
-LPS of gram negative
The complement system is part of the _____ system and consists of many _____ that act as a cascade.
-innate
-proteins
individuals with deficiencies in complement activity have increased susceptibility to two types of disease:
1.recurrent infections by pyogenic bacteria
2.illness characterized by production of autoantibodies and immune complexes
The most important component of complement is _____ which is present in circulation in amounts similar to immunoglobulins.
C3
The two main pathways for complement activation reflect:
the innate and adaptive immune response
best known and most successful application of immunological principles to human health
vaccination
vaccination involves ____ immunity.
adaptive
the antigens of the vaccine must induce ______ and ____ leaving behind a population of _____.
-clonal expansion in specific B cells
-T cells
-memory cells
Consideration in producing a vaccine are: (3)
1. safe to administer
2. induce the right sort of immunity
3. must be affordable
which type of organisms tend to be more effective when making a vaccine?
-living organisms are more effective than killed organisms
-exception: toxin vaccine
Live vaccines can be ____ or ____ organisms.
natural or attenuated
Cowpox Vaccine
-only example of a NATURAL LIVE VACCINES
-to protect against human smallpox virus
Problem with NATURAL LIVE VACCINES
safety issue: high potential of being pathogenic
Attenuated Live Vaccines
-highly successful
-attenuated pathogen
-diminishes virulence while retaining desired antigen
Examples of Attenuated Live Vaccines
a) bacterial
b) viral
a)BCG (bacille-Calmette-Guerin) for TB - low efficacy
b)yellow fever virus, polio, rubella,mumps & measles
Origin of Attenuated Live Vaccines
-1908 to 1921: Calmette & Geurin grew cultures of bovine strain of M.tuberculosis in vitro for 13 years
-resulted in bacterial strain much less virulent than wild type strain
-BCG Vaccine for TB
How can attenuation be achieved?
mutation - purely random series of mutation induced by unfavorable conditions of growth, then constant selection for antigen retention & loss of virulence
Three types of Polio (Sabin) Virus
-Type 1: 57 mutations, almost never reverts to WT
-Type 2 & 3: 2 key mutations, reverts back to WT frequently - some have led to outbreaks of paralytic poliomyelitis
Why do Type 2 & 3 polio vaccines revert back to WT while Type 1 rarely does?
easy to revert back to WT when there are only a few mutations as in Type 2 and 3 vaccines. Type 1 has high number of mutations.
Current Polio Vaccine
Killed, Inactivated (Salk)
Advantages of Live, Attenuated Vaccines
-able to replicate in body as if a normal virus/bacteria but is less virulent
-immune system will be activated in the same way it is when a foreign antigen is present
-yields high # of memory cells
Disadvantages of Live, Attenuated Vaccines
reversion to wild type
Killed Vaccines
-intact but non-living or deactivated
-incapable of replication in host
-Salk Polio Vaccine, Typhoid,Cholera,Influenza,
Plague,Typhus
How is the pathogen killed/inactivated to form Killed Vaccines?
-heat: protein denaturing alters epitopes
-chemical: formaldehyde or alkylating agents
Effective Killed Vaccines
Salk Polio Vaccine
Moderately effective Killed Vaccines
typhoid, cholera, influenza
Low Efficacy Killed Vaccines
plague, typhus
Advantages to Killed Vaccines
no reversion
Disadvantages to Killed Vaccines
-incomplete inactivation
-low # of memory cells,no replication in host
-needs repeated booster shots, potential allergy
Most Successful Bacterial Vaccines
Inactivated Toxins and Toxoids
Toxins and Toxoids
-inactivate the toxin of bacteria vs. bacteria itself
-toxin is the pathogen
-purify & inactivate exotoxin to form toxoid
Vaccination with TOXOID induces _____ which are able to _____.
-antitoxoid antibodies
-bind toxin and neutralize its effect
Subcellular Fragments & Surface Antigens
(Subunit Polysaccharide Vaccines)
-safe & effective vaccines
-immune system sees surface antigens of most organisms first and responds
-lack infectious portion, purified
-polysaccharide vaccines
Advantages of Subunit Vaccines
-risks associated with attenuated and killed vaccines are eliminated
Disadvantages of Subunit Vaccines
-may activate B cells in a T cell independent manner
Vaccine for Streptococcus Pneumoniae (causes pneumococcal pneumonia)
-Pneumovax 23(Merck)
-Pnu-Immune 23(Lederle Labs)
-23 antigenically different capsular polysaccharides
-administered to high risk groups
Limitation of Polysaccharide Vaccines (Subunit Type)
-inability to activate TH cells
-activate B cells in a T cell independent manner (not presenting to T cells)
-results in production of IgM w/little class switching to IgG to form memory cells
Recombinant Antigen Vaccines
-introduction of gene encoding a major antigen of a virulent pathogen into attenuated virus/bacteria
-attenuated organism serves as vector replicating w/in host & expressing gene product of pathogen
Examples of Recombinant Antigen Vaccines
Vaccinia virus,attenuated polio virus,adenovirus, attenuated strains of Salmonella and BCG strain of M.bovis
-Hep B (gene is cloned & expressed)
A modification of recombinant antigen vaccine:
-clone major antigen gene of virulent pathogen into yeast
-then, purify large quantities of antigen
-ex. Hepatitis B
Vaccine for Streptococcus Pneumoniae (causes pneumococcal pneumonia)
-Pneumovax 23(Merck)
-Pnu-Immune 23(Lederle Labs)
-23 antigenically different capsular polysaccharides
-administered to high risk groups
Limitation of Polysaccharide Vaccines (Subunit Type)
-inability to activate TH cells
-activate B cells in a T cell independent manner (not presenting to T cells)
-results in production of IgM w/little class switching to IgG to form memory cells
Recombinant Antigen Vaccines
-introduction of gene encoding a major antigen of a virulent pathogen into attenuated virus/bacteria
-attenuated organism serves as vector replicating w/in host & expressing gene product of pathogen
Examples of Recombinant Antigen Vaccines
Vaccinia virus,attenuated polio virus,adenovirus, attenuated strains of Salmonella and BCG strain of M.bovis
-Hep B (gene is cloned & expressed)
A modification of recombinant antigen vaccine:
-clone major antigen gene of virulent pathogen into yeast
-then, purify large quantities of antigen
-ex. Hepatitis B
Tolerance
-a very high dose of antigen in the body results in lack of response by body
-experimental methods test to see if body is constantly making the antigen, will it develop immunity?
Future Vaccine
-DNA Vaccines: plasmid DNA encoding a viral antigen directly injected in muscle of recipient
-muscle cells take up DNA and express encoded protein
-leads to humoral & cell-mediated immune response
Limitations of DNA Vaccines (Future Vaccine)
-no one knows the consequences of long term antigen expression
-could chronic persistent expression lead to tolerance or autoimmunity?
Future Vaccine
-Anti-idiotype Vaccine:can be used when original antigen is unsuitable
-anti-idiotype Ab is internal image of the antigen
-HIV
Living Vaccines have the advantage of:
1.providing an increasing antigenic challenge that lasts for days or weeks & inducing it at the right site
2.containing greatest # of microbial antigens
Killed Vaccines: since they do not replicate in the host, what is needed?
repeated boosters are needed to maintain the immune status of the host
Acceptable side-effects after immunization
-minor pain or swelling at the site of injection
-mild fever
Serious complications after immunizations
-vaccines may be contaminated w/unwanted proteins or even live viruses
-attenuated viruses may rever to wild type
-patient may be hypersensitive to minute amounts of contaminating protein
-immunocompromised are susceptible to full blown infection
Adjuvants
-greatly enhance Ab production
-aluminum salts have this non-specific property
-added to antigen
The effect of adjuvants is:
1.concentration of antigen in a site where lymphocytes are exposed to it
2.induction of cytokines which regulate lymphocyte fxn
Passive Immunization
-injecting preformed antibody can be life saving where toxins are already circulating (non-immunized individual)
-ex. tetanus,diphtheria,snake-bite
normal flora
-refers to the large number of microorganisms inhabited by the human body
-most members are bacteria, but fungi & protozoa can inhabit the body,too
are viruses part of the normal flora?
no
where do normal flora reside?
-some microbes occur on the skin but most live on the inner surfaces of the body which are lined with mucous membranes
-nose,mouth,URT,GI, genitourinary tract
do normal flora reside in the internal organs, tissues, blood or CSF?
no
the term normal flora implies...
that the inhabitants are harmless/do not cause disease/are residents of the healthy human body and are permanent occupants
transient microorganisms
those that may establish themselves within the body briefly but are excluded by competition from the normal flora and by the host's immune system
are transients considered part of the normal flora?
no
commensals
-most residents of the normal flora
-def: they benefit from the association with host, but the host is not adversely affected.
mutualistic
-both the organism and the host benefit from the relationship
normal flora as opportunistic pathogens
-cause infection if tissue injury occurs at specific parts of the body or if the resistance in the body is low
-ie.due to prolonged exposure to antibiotics & use of immunosuppressive drugs
-ex.Candida albicans
Origin of the human flora
-before birth, healthy fetus is free of microorganisms
-acquired them by surface contact, swallowing or inhaling
-organisms that compete the best will predominate and form stable flora
do eating habits and hygiene contribute to what normal flora will be present on the body?
yes
germ-free animals have an underdeveloped immune system and require ____.
vitamins B and K
Effect of antimicrobial agents on the normal flora: suppression of normal flora with the use of antibiotics
-indicated that normal flora defend the host against potential pathogens
-Pts. on antibiotics may lose the normal flora of large bowel & develop pseudomembrane colitis from the excessive toxin released by C.dificile
-C.dificile is normally a minor resident of the bowel & antibiotic treatment causes its overgrowth
-C.albicans causes diarrhea,inf.of mouth, vagina & anal area this way
What gives the normal flora a selective advantage over other bacteria allowing them to become residents of the body?
1.adherence to surface of host epithelial cells
2.production of antimicrobial substances that can inhibit other microbes
adherence of the normal flora to host cells
-adhere to surface of host epithelial cells
-result of interaction btw.microbial cell surface & receptor on body cell
-proteins,polysacch.,pili on microbial surface help
what does adherence to host cells do for normal flora?
-adherence allows the bacteria to avoid being removed by the flushing of surface fluids & peristalsis
-allows bacteria to multiply
desquamation
the detachment of host epithelial cells from the body surfaces and replacement of the lost cells by new cells
Where does desquamation occur and what does it result in?
-occurs in intestine at high rate
-results in elimination of microorganisms which are not part of the normal flora (transients) & are only weakly attached to the cell surface
-normal flora have ability to reattach to fresh epithelial surface and persist at these sites
production of antimicrobial substances
some resident microorganisms produce metabolic products that can inhibit other microbes
transient bacteremia
-occasionally, microbes can cross protective barriers as a result of trauma such as tooth extraction or childbirth and for a brief time, may be found in the blood stream before they are filtered out by immune system
-can cause infection
-ex. subacute endocartitis in individuals w/damaged heart valves
Blood, body fluids, tissues & the normal flora
-in a healthy individual, the blood, CSF and other body tissues are normally free of microorganisms
"first line of defense" against microorganisms
the skin: forms an effective barrier against most microorganisms
in order for microorganism to enter body,
there must be a cut
T/F: the outermost layer of the epidermis is made of dead, non-nucleated horny cells that are constantly in contact with microorganisms.
True.
hostile environment of the skin for pathogens
1.dryness
2.low pH
3.inhibitory substances
Pathogens and dryness of skin
-relatively dry surface of skin is inhibitory to microorganisms
-enter dormancy or die within a few hours
-moist areas of skin (armpit,btw.toes/thighs) have higher # of normal flora
-fungi prefer
Pathogens and low pH
-skin has pH between 3 and 5 due to organic acids such as lactic acid, produced by normal skin microorganisms
-low pH inhibits growth
Pathogens and inhibitory substances
-sweat glands secrete lysozyme that destroys bacterial cell wall
-sebaceous glands secrete complex lipids that are partially degraded by Propionibacterium acnes to produce long chain fatty acids such as oleic acid - which is highly inhibitory to other bacteria
T/F: some bacteria can survive on the skin despite hostility of the environment (antimicrobial factors)
True
How can some microorganisms surive on the skin despite its hostile environment (antimicrobial factors)
-secretions of sweat & sebaceous glands provide water,amino acids,urea,salt & fatty acids which serve as nutrients
Most of organisms that are able to survive on skin are members of which genera?
-Staphylococcus (S.epidermis)
-Micrococcus
-Propionibacterium
-Cornyebacterium
-Candida (fungi)
Where do most of the normal bacterial flora of the skin reside?
-openings of hair follicles
To sterilize the skin:
-an antiseptic must enter the openings of the hair follicles
Eye
-lining eyelid and eyeball conjunctiva
-contiuously washed with tears to remove microbes
-tears contain lyzozymes, which cleave peptidoglycan
T/F: Staphylococcus & Streptococcus species are found on the eye
True.
Upper Respiratory Tract
-portion above larynx
-as you breathe, microbes stick to the epithelial lining where continuous beating action of cilia push them downward
-this allows them to be swallowed & possibly destroyed by HCl in stomach
-lyzosome in nasal mucous kills microbes
Residents of the Upper Respiratory Tract
-despite antimicrobial factors, numerous organisms inhabit the nasopharynx by ability to adhere to epithelial surface
-S.epidermis, S.aureus, S.pneumoniae & other alpha-hemolytic streptococci
Lower Respiratory Tract
-should be entirely free of flora
-mucous membranes of trachea & bronchi do not have flora
-microbes are usually removed by upward cilia driven flow of mucous
-if bacteria do enter, usually taken up by phagocytic cells in body
Mouth
-abundant moisture and dissolved foods would make mouth a great place for growth
-however, saliva flushes microbes and leads to swallowing
-desquamation of epithelial cells also occurs here
Microbial flora of the teeth
-until eruption of the teeth, most organisms in the mouth are aerobes or facultative aerobes
-when teeth are erupted, tissue surround the teeth provides an anaerobic environment
Streptococcus mutans
-major cause of dental caries
-produces glycan that sticks bacterial cells together & to teeth
-glycan is produced only in presence of sucrose which splits into glucose & fructose
dental plaque
-aggregation of bacteria and organic matter on the surface of the teeth
-contains high numbers of bacteria
healthy human gingiva is inhabited by
-gram positive bacteria
-Streptococcus sanguis, Actinomyces
In diseased gums, there is a shift in the type of flora to:
-gram negative bacteria
-Porphyromonas,Prevetolla, Bacteroides, Fusobacterium
gingivitis inflammation results in:
redness and bleeding
periodontis
-inflammation where the cement between the gum and enamel comes apart resulting in pockets that become filled with anaerobic bacteria
-Porphyromonas gingivalis is suspected cause
Several commensalistic protozoa inhabit the oral cavity
Trichomonas tenox
-may occur in gum margins and in plaque
-associated with poor oral hygiene
some of highest concentration of normal flora are found in which part of the body
gastrointestinal tract
when there is no food in the stomach, the numbers of normal flora are ____
low
After ingestion of food into the stomach, the number of bacteria _____
-rises (1000 - 1 million) but soon falls as the pH of the stomach drops
Normal flora of the small intestine
-1000 bacteria survive here because of combined action of acid of stomach and inhibitory action of bile from gallbladder
In the third and last portion of the small intestine, facultative anaerobes such as ____ live in large numbers.
E.coli
What portion of the gastrointestinal tract has the largest microbial population?
-colon or large intestine
-25% of feces made up of microorganisms
Factors that remove microorganisms from the large intestine
1.continual movement of the intestinal contents
2.desquamation of surface epithelial cells
-mucus aids in mechanical removal of microbes from intestine
What may influence the composition of normal flora in the intestine?
-antibiotic treatment
-diet
-starvation
-stress
Gram negative bacteria of the intestine
E.coli,Bacteroides, Fusobacterium
Gram positive bacteria of the intestine
Lactobacillus, Clostridium perfringens
Yeast of the intestine
Candinda albicans
Protozoa of the intestine
Trichomonas hominis, Entamoeba
Antibiotics and the normal intestinal flora
-antibiotic treatment may eliminate many normal intestinal microorganisms
-this permits antibiotic resistant organisms to thrive
-may result in GI disturbance such as diarrhea, constipation
Genitourinary Tract
-in a healthy person, the kidneys, ureters and urinary bladder are free from microorganisms
-however, bacteria are commonly found in the lower portion of the urethra in both males and females
Common residents of the lower portion of the urethra
-S.epidermis,Strep.faecalis, Neisseria,E.coli (occassionally present)
Residents of the adult vagina
-lactobacilli: breakdown glycogen produced by epithelium to form lactic acid
-pH 4.4 to 4.6
Pathogenicity
the ability of microorganism to cause disease
Virulence
extent of pathogenicity
Contagious or communicable
diseases that are spread from an infected animal or person
Endemic
disease is constantly present in a geographic area
Epidemic
when the occurrence of the disease exceeds the expected levels
Pandemic
when an epidemic of a disease becomes worldwide
Sporadic
disease occurs only occasionally
Incubation Period
the interval between infection and appearance of the first symptoms of the disease. This period is followed by illness and then by the period of convalescence (infectious organisms can be spread to others during these stages)
Periods of Illness and Convalescence
-following incubation period
-time during which organism can be spread to others
Carriers
-individuals that have acquired sufficient immunity to the disease producing organism to prevent occurrence of symptoms
-however, they are unable to eliminate the agent from their bodies
-spreading the agent to others for months or years
Virulence Factors
1. adhesins
2. host cell invasion
3. antiphagocytic mechanisms
4. siderophores
5. toxins
Adhesins
-virulence factors that are responsible for adherence
Two types of Adhesins
1. bacterial fimbriae
2. cell-surface structures - specifically bind to receptors on the surface of host's cell
Host Cell Invasion
-virulence factor
-many organisms are able to invade and grow inside host cells
-here, they are protected from the host's humoral immune response
-ex. bacterium is able to prevent phagosome-lysosome fusion
-ex. Brucella abortus releases 5'GMP and adenine which prevents degranulation of peroxidases from PMNs
Most Common Antiphagocytic Mechanisms
Capsules
-made of polysaccharide and are not toxic alone
-make organism slippery preventing leukocyte from making intimate contact to engulf microorganism
-ex.pneumococci, meningococci
Additional Antiphagocytic Mechanism
(virulence factor)
Fimbriae
-can impede phagocytosis by binding to a surface component of the phagocyte
-preventing close contact necessary for phagocytosis to occur
Siderophores
-low MW compounds with high affinity for iron (higher than transferrin) thus binding iron from host
-microorganisms as well as vertebrates require iron for growth
-competing successfully for iron is an important virulence factor
lactoferrin & transferring
-vertebrates have evolved different ways of retaining iron in a soluble state for synthesis of new cell components
-lactoferrin: milk,tears, saliva, mucus,intestinal fluid
-transferrin: plasma
Toxins
-virulence factors
-toxic substances excreted from bacterial cell or released after lysis of the bacterium
-ie. strep.,staph.
Toxins
hyaluronidase,streptokinase, coagulase,collagenase, hemolysins,leukocidins, enterotoxins,neurotoxins, pyrogenic toxins, endotoxins
Hyaluronidase
-toxin (virulence factor)
-enzyme capable of breakding down hyaluronic acid (the IC glue that keeps connective tissue together)
-helps in the spread of microbe
Streptokinase
-toxin (virulence factor)
-activates proteolytic enzyme called plasmin which is present in host's plasma
-plasmin causes dissoluation of blood clots
-allows spread of streptococci & staphylokinase (streptococci)
Coagulase
-toxin (virulence factor)
-causes coagulation of plasma producing fibrin clot
-this allows microbe to lay down thin layer of fibrin around each cell
-preventing phagocytosis
-produced by Staphylococci
Collagenase
-toxin (virulence factor)
-causes breakdown of collagen
-helps spread organism
-produced by Clostridia (gas gangrene)
Hemolysins
-toxin (virulence factor)
-induce lysis of host's RBC
-does not kill leukocytes but probably provides essential iron for growth
Leukocidins
-toxin (virulence factor)
-kill host's leukocytes
-mechanism is unknown
Enterotoxins
-toxins (virulence factors)
-interact with GI system to cause diarrhea/dysentary
Two types of Enterotoxins
1.stimulators of synthesis of cyclic AMP causing electrolyte imbalance-results in flow of water into intestine (V.cholera,E.coli,B.cereus)
2.inhibitors of protein synthesis-kills epithelial cells lining intestine (Shigella,E.coli)
Two types of Neurotoxins
(virulence factors)
1.spastic paralysis- block inhibitory nerve impulses causing neurons to fire continuously (tetanus)
2.flaccid paraylysis- preventing release of acetylcholine (botulism)
Pyrogenic Toxins
-virulence factors
-termed superantigens
-Streptococci,Staphylococci
-part of large family of toxins that include:
-strep.pyrogenic toxins, staph.enterotoxins,staph. exoliatin, TSS toxin
Superantigens
-induce the secretion of large quantities of TNF-alpha and IL-1
-induce inflammation, irreversible shock, death
-pyrogenic toxins
Enterotoxins
-virulence factors
-lipid A portion of Gram negative cells
-presence in bloodstream can result in fever,inflamm, irreversible shock
-often called septic shock
-Salmonella,N.meningitidis
-Lipid A binds to macrophages causing synthesis of TNF-α & IL-1
Two main reasons why microbes that cause systemic infections leave the relatively safe environment of the body surface to spread through the body where they will be attacked by host defenses:
1.temperature:one
-ex.rhinovirus infections are restricted to URT because they are temp. sensitive replicating efficiently at 33 but not at 37 in the throat
2.site of budding
-refers to how the viruses spread when they infect the cell (lateral vs. through basal membrane)
Directions of Spreading
a)laterally
b) through basal membrane
Viruses that spread laterally tend to stay _____.
localized (surface)
Viruses that spread through the basal membrane tend to spread _____.
into deeper tissues - systemic
Mechanisms of microorganism spread through the body
1.spread to lymph and blood
2.spread from blood
3.spread via nerves
After microbes go through the body surface, they face the following defense:
-tissue fluids containing anti-microbial substances, local macrophage, physical barrier of local tissue structure
Spread of microbes to lymph and blood
-lymphatic system brings the microorganisms to phagocytic & immunologic defenses
-infection may be halted at any stage
-but, by multiplying locally or in the lymph nodes & evading phagocytosis, the microrbes can finally reach the blood stream
-will encounter Ab, complement, phagocytes
The fate of microbes in the blood depends on...
whether they are free or associated with circulating cells.
associated
-microorganisms are "associated" with circulating cells
-these cells can protect them from host defenses & carry them around the body
free
-microorganisms that are not associated
-free in blood & exposed to body defenses such as Abs and phagocytes
Microbial Spread via Nerves
-peripheral nerves from peripheral parts of body to CNS and vice versa
-ex.rabies,herpes simplex virus, varicella zoster virus
-travel in axon
Viruses and bacteria in the nasopharynx generally spread to the CNS via ____
blood
Microbial spread via cerebral spinal fluid
-once in CNS, pathogen can travel via CSF
-pathogens can then invade neural tissue (mumps) or multiply locally (Neisseria meningitidis, Haemophilus influenza, S.pneumoniae) and infect meningeal cells
free
-microorganisms that are not associated
-free in blood & exposed to body defenses such as Abs and phagocytes
Microbial Spread via Nerves
-peripheral nerves from peripheral parts of body to CNS and vice versa
-ex.rabies,herpes simplex virus, varicella zoster virus
-travel in axon
Viruses and bacteria in the nasopharynx generally spread to the CNS via ____
blood
Microbial spread via cerebral spinal fluid
-once in CNS, pathogen can travel via CSF
-pathogens can then invade neural tissue (mumps) or multiply locally (Neisseria meningitidis, Haemophilus influenza, S.pneumoniae) and infect meningeal cells
Genetic Determinants of spread replication
-ability of microbe to infect and cause dz in host is influenced by genetic constitution of the host
-ie. malaria, sickle cell anemia
Susceptibility due to genetic determinants often operates at the level of _____
immune response
Genetic determinants:
Susceptibility to Leprosy is strongly influenced by ______ genes.
MHC 2 genes
Other factors affecting spread and replication
-brain
-stress causes excess release of glucocorticoids which have powerful action on immune cells
A shortage of glucocorticoids or an excess, as with steroid therapy, results in
increased susceptibility to infection
latent
-those that are shed intermittently, such as herpes simplex virus, polyoma viruses, typhoid bacilli, malaria parasites
Persistent Microbes fall into two categories:
1.shed continuously
-ex.EBV into saliva, HepB into blood
2.latent-shed intermittently
-ex.HSV,Polyoma viruses,typhoid bacilli, malaria parasites
Some microbes are able to persist in host for many years. Persistence is worthwhile only if...
shedding occurs during the persistence
Viruses can thwart immune defenses by:
1.silent invasion of tissues & cells
2.some viruses can infect for time w/o adverse effects
3.interfering w/molecular mechanisms of host cell
4.latency
5.viruses do not produce toxins-avoid detection
Silent invasion by viruses
-thwart immune defenses
-invasion of tissues/cells is often silent
-unlike bacteria,do not form toxins
-therefore, no damage
-therefore, no sign of illness
Infection of cells for long periods of time without adverse effects
-some viruses can infect cells for long periods of time without adverse effects
-rubella,wart,Hep B, EBV
Viral Interference
-as a method of thwarting immune defenses
-viruses establish intimate relationships with infected cell
-ex.interfering with production or action of interferon
Latency of Viruses
-viral genome continues to be present in the host without producing antigens or infectious material
-do so only occassionally when virus reactivates
Productive Infection
-rapid hit and run infection used by viruses
-microbe invades, multiplies and is shed w/in a few days
-occurs w/in 7 days
-after 7 days, adaptive immune system kicks in
-too late:virus already shed, infection in other cells
Principle Strategies used by parasites to evade the immune system are:
1.concealment of antigens
2.antigenic variation
3.immunosuppression
Shedding
-shed viral particles and infect more hosts
Concealment of Antigens
a)virus displays proteins secretly inside cells and not on cell surface
b)colonize privileged sites keeps out of reach of circulating lymphocytes
c)concealment by taking up host molecules to cover their surface
d)avoid inducing an immune response
Three main mechanisms for antigenic variation
1.mutation-antigenic drift
-Influenza
2.recombination-antigenic shift
-Influenza A
3.gene switching
The best known example for mutation is ___
influenza virus
Definition: Antigenic Variation
-to confuse the host by repeated changes in appearance
-ex. African trypanosome
-small mutations in genome result in loss of recognition even of pathogens that body has already seen and has already made memory cells against
When can antigenic variation occur?
-during course of infection; ex. HIV mutates w/in body of one individual;can see different strands of HIV in one person
-during spread of microbe through host community ie. Influenza
-mutations occur as virus moves throughout population
Recombination
-antigenic shift
-Influenza A
-appears to occur every 30yrs
-avian flu
-wild birds, pigs, poultry
-most have occured in Asia and then spread pandemically
The classic example of recombination is
Influenza A virus
Gene switching was first demonstrated in
African Trypanosome
-these organisms carry genes for about 1000 distinct surface molecules which are immunodominant
-trypanosome can switch from use of one gene to another w/effect on host of having a persistent infection
Recombination takes place by exchange of genetic material between two different microbes. For example, between...
human and avian virus strains with result of a completely new strain of Influenza A virus
Immunosuppression
-many viral infections cause general temporary immunosuppression
-allows microbe time to grow, spread, shed
Different microbes have different immunosuprressant effects. This involves actual infection of:
immune cells
-T cells: HIV, measles
-B cells: EBV
-macrophage: HIV,leishmania
-dendritic cells: HIV
Three types of Persistent Infections
1.represent a failure of host defenses
-microbe can persist in infectious form(Hep B)
2.low infectivity (adenovirus in tonsils)
3.latency