Describe the causes and means of
transmission of malaria, HIV/AIDS
and TB.
Malaria
• Caused by 4 different Plasmodium species,
these are parasitic protozoa,(eukaryotic)
• Each spends part of its life cycle in female
Anopheles mosquitoes. These act as vectors
they transfer the Plasmodium to and from the
human host.
• Female mosquitoes need a blood meal to help
their eggs develop, male mosquitoes only feed
on plant sap
More than 40% of global population
are at risk of Malaria
Plasmodium life cycle
Plasmodium
reproduces,
bursts out of
RBCs and infects
more RBCs
Bites usually occur
in the evening on
exposed skin
Mosquitoes
breed in
stagnant water
Gametes fuse in the
mosquito’s
intestine and
produce more
plasmodium
Malaria Control Measures
• Destroy mosquito breeding sites, clear stagnant
water
• Prevent mosquito bites, use nets for sleeping,
wear cover-up clothing, use insecticide spray on
skin
• Introduce predators of mosquito larvae
• Use insecticide to control populations of
mosquitoes
• Use anti-malarial drugs to prevent people being
infected by the parasite. Most work by inhibiting
enzymes in the parasite and preventing normal
metabolism and reproduction
Problems with control
• Insecticides kill useful pollinating insects too
• Mosquitoes become resistant to insecticides
• Plasmodium mutate and become resistant to anti-malarial drugs eg
chloroquine,
• New anti-malarials have unpleasant side – effects, so they are not
always taken
• No effective vaccine- Plasmodium (protoctist) surface antigens
change due to mutation, many different antigens on cell surface
• Plasmodium only exposed in blood stream for a short time, spends
most of time in human in liver cells or RBCs
• Mosquito larvae predators get out of control and become pests
• Global warming may extend Anopheles mosquito territories
• Political unrest in many malarial areas prevents adoption of effective
control measures
Tuberculosis (TB)
• Contagious, pandemic disease caused by the
bacteria Mycobacterium tuberculosis or
Mycobacterium bovis
• In 1993 WHO declared the situation with TB a
global emergency
• By 1998 WHO estimated that about 1/3 of the
world’s population were infected
• Between 2002 and 2020 approx 1000 million
people will be newly infected, over 150 million
will become ill, 36 million will die
Global TB deaths 1990-1999
Tuberculosis
• Spread by droplets from an
infected person, produced when
they cough, sneeze, talk or spit.
• Most easily spread when people
live and sleep in over-crowded
conditions
• M. bovis spreads in meat and milk
from infected cattle
Control measures
• BCG vaccine reduces chance of developing
disease
• Multi antibiotic treatment, ie DOTS (direct
observation therapy, short course) for 6 – 12
months
• TB testing of cattle, destruction if infected
• Pasteurising milk to kill the bacteria
• Isolate people while they are still infectious
• Contact tracing to find others likely to be infected
Problems with control
• Many people with TB live in LEDCs so medical facilities are
inadequate to ensure vaccination and /or DOTS takes place
• Contact tracing expensive and time-consuming, unlikely
where funding for medical treatment and control is limited
• Many people stop treatment when they feel better,
bacteria are still present in lungs and will reproduce and
spread to other tissues and be passed on to others
• Repeated use of a range of anti-biotics is leading to
development of resistant strains
• Inadequate housing and overcrowding means infection is
passed on within these populations
• Poor populations reluctant to kill infected cattle
HIV/ AIDS Pandemic
• Caused by Human Immunodeficiency Virus
• Passed on by sexual intercourse, infected blood and
blood products, sharing or re-using hypodermic
needles used by an infected person, across HIV
particles passing across placenta from mother to
foetus
• Global spread, highest prevalence in Africa and
South-east Asia
Prevalence of HIV/AIDS
HIV /AIDS
• Initial HIV infection may cause swollen lymph glands or
a short-lived viral illness
• Initial level of HIV in blood spikes and then falls again
• Over time HIV causes number of T helper cells
(important components of the immune system that
activate other cells) to fall dramatically
• Eventually the immune system starts to fail and AIDS
(aquired immuno deficiency syndrome) develops
• AIDS is recognised by the range of opportunistic
infections and unusual cancers that occur in patients,
these are usually kept in check by a healthy immune
system
Control measures
• Using condoms during sexual intercourse
• Health education about “Safe Sex”
• Contact tracing to find sexual partners and
people likely to be infected
• Blood donations screened for HIV
• Blood and blood products heat treated to prevent
virus infecting
• Drug treatment to prevent HIV replicating in cells
and slow AIDS development
Problems with control
• Limited success changing sexual practices
and increasing condom use by education
programs
• Limited success with preventing drug
users sharing needles
• Long latent period when HIV+ person can
continue to pass on virus to others
• No successful vaccine yet, HIV mutates
quickly, hides inside body cells
• Drugs to delay onset of AIDS are
expensive
• Lack of funds in LEDCs for education
programs and drug treatment
• Reluctance to know if HIV+ due to
discrimination
Learning Outcomes
Describe the primary lines of defence against
pathogens and parasites (including skin and
mucous membranes) and outline their
importance (no details of skin structure are
required).
Describe the structure and mode of action of
phagocytes.
Define the term immune response
Describe the primary lines of defence
against pathogens and parasites and
outline their importance
• Carry out the card sort activity and then
complete the fill in the blanks sheet.
(10 minutes total)
Different types of blood cells
• Phagocytes eg:
Neutrophils ,
monocytes and
macrophages
• Lymphocytes eg:
B cells, plasma cells, B
memory cells
T cells, T killer, T helper
and T memory cells
Work in groups to make a table about the
structure and roles of the following cells (10 mins)
Be prepared to feedback to class
•
•
•
•
•
•
•
•
Phagocytes
Neutrophils
Monocytes
Macrophages
B plasma cells
T killer cells
T helper cells
T and B memory cells
Functions
Functions
of
White
Blood
Cells
Phagocytes
engulf pathogens (usually a non-specific response)
Cells
Neutrophils
Multi-lobed nucleus, travel in blood, may migrate to tissue fluid between
cells. Short-lived, take part in phagocytosis, attracted to sites by
histamine and monokines (released by macrophages and monocytes)
Monocytes
Made in bone marrow, travel in blood and become macrophages. Take
part in phagocytosis and release monokines
Macrophages:
large phagocytes permanently in lymph nodes and organs, long lived,
may become APCs (antigen presenting cells) after ingesting a pathogen.
Release monokines to attract neutrophils and stimulate B cells to turn
into plasma cells
B plasma cells
differentiate from B cells (made and mature in bone marrow) produce
antibodies specific to an antigen from a pathogen
T killer cells
Made in bone marrow mature in thymus,kill infected body cells and
destroy pathogen at same time
T helper cells
Release cytokines that cause B cells to turn into plasma cells and
stimulates phagocytosis by phagocytes
T and B memory
cells
Remain in blood long-term to react swiftly to second infection by same
pathogen
Phagocytosis
Describe in detail and illustrate the 4 stages of
phagocytosis
(use AS vocabulary and knowledge of cell
ultrastructure)
•
•
•
•
Recognition
Engulfing
Digesting
Release of waste products
• Describe and illustrate what happens at the end
of phagocytosis if the phagocyte becomes an APC
(Antigen Presenting Cell)
Immune response
• The specific response to a
pathogen which involves the
action of the lymphocytes and
the production of antibodies.
Learning Objectives
• Define the terms antigen and antibody.
• Describe, with the aid of diagrams, the
structure of antibodies.
• Outline the mode of action of antibodies, with
reference to the neutralisation and
agglutination of pathogens.
• Compare and contrast the primary and
secondary immune responses.
Definitions
• ANTIGEN
Any molecule that can stimulate an immune response.
Usually proteins, carbohydrates or glycoproteins of cell
membranes or virus coats
• ANTIBODY
Molecules made of protein, produced by plasma cells in
response to antigens found on pathogens. Each has a
binding site with a complementary shape to its specific
antigen.
Plasma cells can produce thousands of antibody molecules
per second. What difference is there between an
undifferentiated B lymphocyte and a plasma cell?
Describe with the aid of diagrams, the
structure of antibodies.
A polypeptide is a long chain of
amino acids joined by peptide bonds
(ref to other module of AS spec)
• 4 polypeptide chains (2 light+ 2
heavy) held together by disulphide bonds
• Constant region that helps the
antibody be recognised by and
attach to phagocytes
• Variable region that is specific
and complementary to each
antigen. Millions of different
ones are possible due to the
huge variability of protein
structures
• Hinge region that allows
flexibility and attachment to
more than one antigen molecule
Antibody structures
Antibody action
• Antibody molecules can:
• Bind to antigens preventing pathogens entering
cells (neutralisation)
• Immobilise bacteria by sticking them together in
clumps (agglutination)
• Immobilise bacteria by binding to flagella
• Bind to pathogens “flagging them up” to
phagocytes
• Bind to toxins preventing them having an effect
on cells
Outline the mode of action of antibodies, with
reference to the neutralisation and agglutination of
pathogens.
• Antibodies bind to the antigens on
the outside of pathogens. These
antigens may usually be used to
bind to the host cells. The pathogen
is “neutralised” and cannot infect
the host cells
• Large antibodies with many antigen
binding sites can bind to many
pathogens at the same time. The
pathogens clump together
“agglutination”
Compare and contrast primary ad
secondary immune response
Compare and contrast primary ad
secondary immune response
• PRIMARY RESPONSE
• Few cells with specific
receptors for antigen
• Slow growth of specific
lymphocyte population
• Slow production of
required antibody
• Slow elimination of
pathogen
• Symptoms of
infectiondevelop
• SECONDARY RESPONSE
• Many cells with specific
receptors for antigen
(memory cells from
previous infection)
• Fast production of
antibody
• Fast elimination of
pathogen
• Symptoms of infection
rarely develop
Complete the cloze exercises on cell
mediated and humoral responses
• Humoral
• Disease, mitosis,
plasma, pathogen,
vesicles, selection,
expansion, antigenpresenting cells,
interleukins, RER,
phagocytosis, plasma
membrane, decrease,
antigen,
• Cell mediated
• Short, antigen,
symptoms, antibodies,
replicating, selection,
proteins, plasma,
enzymes, expansion