Immunology (C3) Flashcards

1
Q

Pathogen/pathogenic definition

A

pathogenic: an ORGANISM that causes DAMAGE to its HOST

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2
Q

Infectious definition

A

infectious: a DISEASE that may be passed or

TRANSMITTED from one individual to ANOTHER

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3
Q

Carrier definition

A

carrier: a person who shows NO symptoms when
infected by a disease organism but can PASS the
disease on to another individual

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4
Q

Disease reservoir definition

A

disease reservoir: where a PATHOGEN is normally found; this may be in HUMANS or another ANIMALS and may be a SOURCE of infection

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5
Q

Endemic definition

A

endemic: a disease, which is ALWAYS present at LOW

levels in an AREA

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6
Q

Epidemic definition

A

epidemic: where there is a significant INCREASE in the
usual number of cases of a disease often associated
with a RAPID spread

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7
Q

Pandemic definition

A

pandemic: an EPIDEMIC occurring WORLDWIDE, or over a very wide area, crossing INTERNATIONAL BOUNDARIES and usually affecting a LARGE number of people

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8
Q

Vaccine definition

A

vaccine: uses NON-PATHOGENIC forms, PRODUCTS or
ANTIGENTS of micro-organisms to stimulate an immune RESPONSE which confers PROTECTION against SUBESQUENT infection through MEMORY CELLS

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9
Q

Antibiotics definition

A

antibiotics: substances produced BY microorganisms

which AFFECT the GROWTH of other microorganisms (BACTERIA)

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10
Q

Antibiotic resistance

A

antibiotic resistance: where a microorganism, which
SHOULD BE affected by an antibiotic, is NO LONGER
susceptible to it

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11
Q

Vector definition

A

vector: a LIVING organism which TRANSFERS a disease from one individual to another

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12
Q

Toxin definition

A

toxin: is a CHEMICAL produced by a MICROORGANISM

which causes DAMAGE to its host

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13
Q

Antigenic types definition

A

antigenic types: organisms with the SAME or very
SIMILAR ANTIGENS on the SURFACE. Such types are SUB groups or STRAINS of a microbial species which may be used to TRACE infections. They are usually IDENTIFIED by using antibodies from SERUM

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14
Q

Antigen definition

A

antigen: a molecule that CAUSES the immune system to PRODUCE ANTIBODIES against it. These may be INDIVIDUAL molecules or those on the SURFACE of cells

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15
Q

Antibody definition

A

antibody: a PROTEIN produced by IMMUNE cells (B cells/ b lymphocyte cell - a type of WBC) which BINDS to a SPECIFIC antigen

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16
Q

What type of disease if cholera?

A

Cholera is caused by a Gram negative bacterium

*an endemic in some areas

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17
Q

Cholera: tissue affected , symptoms , mode of transmission

A
  • Its toxins affect the gut lining
  • causing watery diarrhoea leading to severe dehydration and frequently death
  • ## humans act as reservoirs or carriers and contaminate water supplies in which the organism is transmitted, (although it only multiplies in the human host)
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18
Q

Cholera: prevention , treatment , vaccine?

A
  • prevention is by the treatment of water, good hygiene and the provision of clean drinking water
  • antibiotic treatment is possible but treatment is largely by rehydration
  • vaccine (killed organism or possibly genetically engineered) may provide temporary protection
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19
Q

What type of disease is Tb?

A
  • Tuberculosis is a bacterial disease

* that is again on the increase, partly due to the link with the HIV epidemic

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20
Q

Tb: tissue affected , symptoms , mode of transmission

A
  • The most common form of TB attacks the
    lungs and neck lymph nodes
  • Symptoms include coughing, chest pain and coughing up blood
  • It can be spread rapidly in overcrowded conditions and is transmitted in airborne droplets when infected people cough and sneeze
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21
Q

Tb: prevention , treatment , vaccine?

A
  • good hygiene and ventilation
  • Tuberculosis is prevented by a BCG vaccination programme for children
  • Treatment involves a long course of antibiotics
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22
Q

What type of disease is smallpox?

A
  • It is caused by the virus Variola major
  • can have a 30 to 60% fatality rate
  • Smallpox is the only organism that humans have intentionally made extinct
23
Q

Smallpox: prevention/vaccine?, success?

A
  • successful immunisation program was based on its low rate of antigenic variation and the highly immunogenic nature of its component antigens.
  • this meant that the vaccine was highly effective.
  • in addition, there was no animal reservoir and people were keen to be immunised because of the devastating effects of the disease.
24
Q

What type of disease is influenza?

A
  • influenza is caused by a virus
  • of which there are three main sub-groups
  • within each subgroup there are many different antigenic types
25
Q

Influenza: tissue affected, symptoms, mode of transmission

A
  • it infects cells lining the upper respiratory tract
  • causing sore throat, coughing and fever
  • sufferers spread the disease by droplet infection
26
Q

Influenza: prevention, treatment, vaccine?

A
  • prevention includes quarantine and hygiene but influenza’s mode of spread is difficult to
    control
  • antibiotics are ineffective against influenza and are only used to treat the symptoms of
    secondary bacterial infection
  • annual vaccination programmes are available but due to the number of types, together with the emergence of new types, they are not always effective.
27
Q

What types of disease is malaria?

A
  • malaria is caused by Plasmodium spp. , a protoctistan parasite
  • endemic in some sub-tropical regions.
28
Q

Malaria: tissue affected, symptoms, mode of transmission

A
  • the organism initially invades liver cells and then multiplies in red blood cells which burst, releasing more parasites
  • causing severe bouts of fever
  • female mosquitoes, feeding on blood taken, act as vectors to transmit the parasite to new victims
29
Q

Malaria: prevention

A
  • prevention of malaria relies on knowledge of the life cycle of both the vector and the parasite in order to exploit their weak points
  • a variety of methods are used either to prevent
    transmission (prevent biting by use of nets, clothing, insect repellent) or to destroy populations
    of the vector.
  • the mosquito larvae are aquatic and can be eaten by introduced fish, or killed by drainage of breeding sites or the spraying of oil on the water surface. The adults are killed with insecticides, with bacterial infections or by sterilization

*each of these control measures has
advantages and disadvantages

30
Q

Malaria: treatment, vaccine?

A
  • drug treatment is available but mainly to reduce the chances of infection
  • vaccines have proved difficult to develop because the malarial parasite mutates and there are different antigenic types.
  • plasmodium is affected by drugs when outside the cells in the blood but these have limited effectiveness and have side effects; resistance is an increasing problem.
  • antibodies also are only effective against the parasite when outside body cells so limiting the
    target stages for a vaccine
31
Q

Are viruses intra or extra cellular?

and method of virus reproduction

A

viruses are INTRACELLULAR parasites that use a cell’s METABOLIC PATHWAY to produce more virus particles

32
Q

How do viruses cause damage to the host/ there pathogenic effects? (x4)

A
  • CELL LYSIS when they escape from cells to infect other cells/ organisms (shedding)
  • production of TOXIC substances
  • cell TRANSFORMATION where they can trigger cells to become CANCEROUS
  • SUPPRESS the immune system (e.g. HIV)
33
Q

Lytic cycle in virus reproduction

A

LYTIC: cells IMMEDIATELY reproduce using hosts metabolism to copy nucleic acid and synthesis new capsid (encloses genetic material)
leave via… LYSIS of host cell (common cold) OR
BUDDING from hosts cell membrane (influenza)

34
Q

Lysogenic cycle in virus reproduction

A

PENETRATION of hosts cell, the viral nucleic acid is integrated into host cell genome and may remain DORMANT and enter the LYTIC cycle some time later and symptoms are then produced

35
Q

What disease do antibiotics treat?

A

BACTERIAL

36
Q

Bacteriostatic vs bactericidal antibiotics

A
BACTERIOSTATIC = antibiotics  PREVENT growth
BACTERICIDAL = KILL bacteria 

**chosen type depends on which aspect of bacterial metabolism is affected. Antibiotics used medically, affect bacterial metabolism but do NOT interfere with the host cell metabolism

37
Q

Structure of gram negative bacteria cell walls (linking? advantages?) and what certain features provide protection against which antibiotic action

A

cell wall of bacteria’s has a unique structure:
• it contains PEPTIDOGLYCAN consisting of molecules of POLYSACCHARIDE CROSS LINKED BY AMINO ACID SIDE CHAINS. The cross linking provides STRENGTH and the wall protects AGAINST OSMOTOC LYSIS.
• gram negative bacteria - surrounded by an outer layer of LIPOPROTIEN and LIPOPOLYSACCHARIDE.
• the presence of such extra layers protects the cells from the action of some antibacterial agents e.g. lysozyme and penicillin

38
Q

How does penicillin affect bacteria? Which bacteria is penicillin more effective against?

A
  1. Penicillin affects the FORMATION of cross linkages in the peptidoglycan layer of the cell wall during the GROWTH and DIVISION of bacterial cells.
  2. It does this by binding to and INHIBITING the ENZYME responsible for the formation of cross-links between molecules of peptidoglycan.
  3. The wall is weakened so when osmotic changes occur, the cells lyse.
  4. Penicillin is more effective against Gram positive organisms than Gram negative due to the difference in the structure of the cell wall (thick peptidoglycan, no lipopolysaccharide)
39
Q

How tetracycline affect bacteria?

A
  1. Tetracycline is an antibiotic that affects protein synthesis specifically translation and is effective against a broader range of bacteria.
  2. It acts as a competitive inhibitor (binding to the active site, less ESC form) of the second anticodon-binding site on the 30S of bacterial ribosomes (responsible for protein synthesis)
  3. Preventing the binding of a tRNA molecule to its
    complementary codon (codon-anticodon complex’s cannot form)
  4. In this way tetracycline inhibits the translation
    stage of protein synthesis
40
Q

Why do antibiotics not effect viruses?

A

viruses are not affected due to the absence of metabolic pathways which can therefore not be inhibited

41
Q

How has the overuse of antibiotics resulted in the spread of antibiotic resistance amongst pathogenic bacteria?

A

• because bacteria divide rapidly under optimum conditions and have a high mutation rate;
naturally occurring mutations that give resistance to antibiotics have given these bacteria a selective advantage in the presence of antibiotics

• overuse of antibiotics has resulted in the accidental selection of bacterial strains that are completely unaffected by some antibiotics;
in the absence of antibiotics they no longer have an advantage over non-mutated forms BUT if they cause an infection they become increasingly difficult to control

42
Q

Name the natural barriers in the body which reduce the

risk of infection (x7)

A

• the SKIN is a tough barrier - vitamin C is needed to
maintain STRONG CONNECTIVE TISSUE
• SKIN FLORA offer protection by competing with pathogenic bacteria and unlike these bacteria, the flora is not easily removed by washing
• BLOOD CLOTTING to seal wounds
• INFLAMMATION to localise breaks in the barrier
• PHAGOCYTOSIS to destroy invading microbes
• CILIATED MUCOUS MEMBRANES trapping microbes in inhaled air
• LYSOZYME in tears, saliva and stomach acid that kills
bacteria - breaks peptidoglycan cell wall

43
Q

What are the specific immune responses of the body? when?

A

a specific immune response (adaptive) develops as a result of ANTIGENS being recognised as FOREIGN to the body - lymphocytes provide this response (sub group of leucocytes/WBCs)

  1. HUMORAL response
  2. CELL MEDIATED immune response
44
Q

What is the humoral response? lymphocytes? clonal expansion to produce?

A
  1. B LYMPHOCYTES, originate from STEM CELLS in the BONE MARROW, and mature in the blood, SPLEEN and LYMPH NODES
  2. each B lymphocyte has SPECIFIC RECEPTORS for the detection and binding to its specific antigen (individual or on a pathogens)
  3. activation (by binding to foreign antigen) stimulates the COLONAL EXPANSION/proliferation by MITOSIS then differentiation forming PLASMA CELLS and MEMORY CELLS
45
Q

Antibodies; origin, structure/shape, role?

A

origin:
• B LYMPHOCYTES undergo clonal expansion producing plasma cells and memory cells - the PLASMA CELLS secrete antigen specific antibodies which BIND to specific antigens

structure:
• antibodies are Y - SHAPED GLOBULAR PROTIENS, made from FOUR POLYPEPTIDE CHAINS (also held together by DISULPHIDE BRIDGES) and have TWO antigen BINDING SITES (bind two at once)

role:
• antibodies are SPECIFIC to the antigen with which they bind (at tips of variable region) to form an ANTIGEN-ANTIBODY COMPLEX
• an antigen-antibody complex renders the antigen INACTIVE in ways, such as through
AGGLUTINATION (clumping together), which increases the rate of engulfment by PHAGOCYTES

46
Q

What is the cell mediated response process? lymphocytes? clonal expansion to produce?

A
  1. T LYMPHOCYTES, which also originate from STEM cells in the BONE marrow, but are activated in the THYMUS GLAND
  2. PHAGOCYTES engulf a pathogen, LYSOSOMES release hydrolytic enzymes to digest pathogen into component parts, phagocyte can then PRESENT some parts (antigens) on its membrane SURFACE becoming an ‘ANTIGEN PRESENTING CELL’
    * (b lymphocytes and infected body cells can also become antigen presenting cells)
  3. t lymphocyte with SPECIFIC RECEPTOR detects and binds to specific antigen on antigen presenting cell stimulating COLONAL EXPANSION/ proliferation by MITOSIS
  4. clonal expansion of t lymphocytes into T HELPER CELLS, T MEMORY CELLS and T KILLER CELLS/CYTOTOXIC CELLS
47
Q

What are the roles/functions of; t helper cells, t memory cells and t killer/cytotoxic cells?

A

T HELPER CELLS - secrete CYTOKINES, chemicals stimulating B LYMPHOCYTE ACTIVATION to produce more PLASMA cells thus secreting more ANTIBODIES by which AGGLUTINATION can occur for phagocytic cells to engulf

T MEMORY CELLS - remain DORMANT in blood dividing rapidly by clonal expansion to T LYMPHOCYTES if same antigen encountered in future

T KILLER CELLS/CYTOTOXIC CELLS - KILL infected BODY cells by LYSING

48
Q

What are the roles/functions of; plasma cells and b memory cells?

A
  • PLASMA cells - SECRETE ANTIBODIES specific to foreign antigen for binding - AGGLUTINATION of pathogens for phagocytes
  • MEMORY cells - remain DORMANT in the blood circulation ready to divide by clonal expansion to form B LYMPHOCYTES/plasma cells if the SAME antigen is encountered again in FUTURE
49
Q

What is the process of PRIMARY immune response?

A
  1. following FIRST exposure to a foreign antigen there is a LATENT period during which ANTIGEN PRESENTING CELLS (including macrophages) carry out phagocytosis and incorporate foreign antigen into their cell membranes
  2. T lymphocytes activated by specific antigen to mitotically produce T HELPER cells which secrete CYTOKINES which stimulate B lymphocyte activation
    • activated b lymphocytes undergo clonal expansion (mitosis and differentiation) producing more PLASMA cells and thus more ANTIBODIES for agglutination by phagocytosis
    • also producing long lived MEMORY cells that retain the ability to undergo mitosis on detection of same antigen in future
    • PLASMA b cells secrete a LOW level of ANTIBODIES over a period of 2 – 3 weeks, which CLEARS the infection and symptoms DISAPPEAR
50
Q

What is the process of SECONDARY immune response?

A
  1. following RE-EXPOSURE to the SAME antigen there is a very SHORT LATENT period due to the presence of MEMORY cells
  2. only a very SMALL amount of ANTIGEN is required to stimulate RAPID production of PLASMA cells
  3. ANTIBODY levels INCREASE to between 10 and 100x greater than the INITIAL response and in a very SHORT time
  4. antibody levels stay HIGH for LONGER and NO symptoms develop
51
Q

What is active immunity? acquired? length?

A

ACTIVE immunity is where the individual produces own
antibodies either
- NATURALLY; if it follows natural infection
- ARTIFICIALLY; when it follows vaccination e.g. against
Rubella.

• protection is LONG-LASTING due to the production of
antigen-specific MEMORY cells.

52
Q

What is passive immunity? acquired? length?

A

PASSIVE immunity is where the individual RECIEVES
antibodies produced by ANOTHER individual either

  • NATURALLY; when antibodies are transferred to the
    FEOTUS via the PLACENTA, or to the baby in BREAST MILK
  • ARTIFICIALLY; when PRE-SYNTHESISED antibody is INJECTED into an individual e.g. tetanus antitoxin

• protection is SHORT LIVED because the antibodies are recognised as NON-SELF and are DESTROYED, NO
MEMORY cells are produced

53
Q

What are some ethical considerations of vaccines? x4

A

• COST vs EFFECTIVENESS of the vaccine

• protection of the INDIVIDUAL compared to
protection of the COMMUNITY

• the RIGHTS of the individual when considering
MANDATORY compared with voluntary programmes

• SIDE EFFECTS, whether real or perceived