2.2.2 (Chapter 11) – Health and Disease Lesson Objectives: To define the terms ‘health’ and ‘disease’ To discuss different categories of disease

2.2.2 (Chapter 11) –

Health and Disease

Lesson Objectives:

To define the terms ‘health’ and ‘disease’

To discuss different categories of disease

So what is ‘health’?

What do we mean by ‘health’?

What are the characteristics of health?

Health a person’s physical, mental and social condition

World Health Organisation (WHO):

‘a state of complete physical, mental and social well-being and

not merely the absence of disease and infirmity’

Health a person’s physical, mental and social condition

Good

PoorHappiness

Fulfilling life

More than just the absence of disease!

Positive outlook

Well adjusted to society

Can undertake physical and mental tasks without difficulty

EVERYONE is born with the genetic potential for growth and development … they need good health to grow and realise their potential both as humans and within society.

World Health Organisation (WHO; an agency of the UN):

“Good health is a fundamental human right”

What do we NEED for good health?

-Shelter

-Nutrition

-Exercise

-Sleep and rest

-Good hygiene

-Access to medical and social care

So what is ‘disease’?

What do we mean by ‘disease’?

Disease a disorder or malfunction of the mind or body

which leads to a departure from good health

Disease a disorder or malfunction of the mind or body which leads to a departure from good health

What are the causes of disease?

How do you know if you have a disease? (what are the characteristics?)

Single cause eg: malaria

Multifactorial eg: heart disease

Signs (symptoms) – physical and/or mental

ACUTE eg: influenza CHRONIC eg: TB

The 9 categories (types) of disease

‘Miss D. Pind’MISS

D

P

IND

ental

nfectious

hysical

on-infectious

ocial

elf-inflicted

eficiency

egenerative

nherited

Name this infection.

The infection is….

….. a cold or flu

This infection is caused by….

…..a virus



…..athletes foot


…..a fungus



…..warts


…..a virus



…..chicken pox


…..a virus



…..food poisoning


…..bacteria



…..measles


…..a virus



…..fungal nail infection


…..obviously a fungus



…..impetigo


…..bacteria



…..oral thrush


…..a fungus

Single celled

organisms

Types of pathogenic organisms …

Bacteria

Virus

Fungi

Protozoa

= An organism that causes a disease= a kind of parasite (an organism that lives in a very close relationship with another organism, the host, and does it harm … a well adapted pathogen will not kill its host)

Pathogen

Pathogens can enter the body in a number of ways ...

…or other natural openings…

They can be breathed in through the mouth or nose

They can enter through cuts or bites in the skin

HOST

So how are diseases spread?

Vectors (eg: insects)

Contaminated food/water

Air

Contaminated needles

Direct contact

Indirect contact

So how are diseases spread?

Vectors (eg: insects)

Contaminated food/water

Air

Contaminated needles

Direct contact

Indirect contact

Micropredator that actively delivers the parasite to the next host

What have you learnt today?

Define ‘health’ Define ‘disease’

What is the WHO? What do we need for good health?

What are the 9 categories of disease?

a person’s physical, mental and social condition

a disorder or malfunction of the mind or body which leads to a departure from good health

Shelter, nutrition, exercise, sleep and rest, health and social care, good hygiene

World Health Organisation

MISS D PIND

Homework

Go to WHO website:1.Write a brief description of what the WHO is and it’s remit.2.Then choose one disease of your choice to research, write a 200 word review of the information on that website on your chosen disease.

Lesson Objectives:

To describe the causes & means of transmission of TB

To assess the worldwide importance of this disease

To describe the roles of different factors in the prevention and control of TB

Tuberculosis

STARTER – Read the fact sheet from the WHO about TB

KEY WORDS

Incidence

Prevalence

Mortality

Endemic

Epidemic

Pandemic

The number of NEW cases in a population occurring in a given time period

The number of people in a population with a disease within a given time period

The number of people who have died of a certain disease in a given time period

An infectious disease that is always present in a population

When a disease suddenly spreads rapidly to affect many people (eg: influenza)

When a disease spreads over a very large area (eg: a continent or the whole world; we are having pandemics of AIDS and TB at present)

What do you already know?

Cause?

Prevalence?

Treatment?Prevention?

Impact?TB

Symptoms?

http://www.youtube.com/watch?v=JtyX694ubio Basic Summaryhttp://www.nhs.uk/conditions/Tuberculosis/Pages/Introduction.aspx Better!!

TB – symptoms

Some people become infected and develop TB quite quickly whilst others harbour the bacteria for many years …

… it may become active when the immune system is weakened eg: malnutrition, HIV/AIDS

persistent cough

coughing up blood

fever

loss of appetite

emaciation

tiredness

night sweats

(caused by release of hormone-like compounds)

TB – treatment

Antibiotic – Streptomycin (1940s) has been used to decrease incidence of TB

Samples of sputum (pus and mucus) taken from lungs for analysis – identified using a microscope

Chest x-rays (fibrosis, calcification, pneumonia)

Skin tests

Sufferers isolated for most infectious stage (2-4 weeks)

Treated for 9 months to a year with antibiotics – bacteria are slow growing and not sensitive to the drugs

Drug resistance – found after 1950s

READ p167-168 on TB

TB – treatment http://www.youtube.com/watch?v=XvxCs8IlyQk

TB – the cause

Two bacteria:

Mycobacterium tuberculosis

Mycobacterium bovis

Live inside human cells, particularly the lungs, though can spread through the entire body (even bone tissue)

Also occurs in cattle – spreads to humans through meat and milk

first isolated in 1882 by a German physician named Robert Koch who received the Nobel prize for this discovery

SECONDARY TB

TB – the cause

Cough, sneeze, talk, spit

Bacilli in air in tiny droplets of liquid

Inhaled

Infectious stage: 2-4 weeks

Taken into the lungs

Macrophages (phagocytic WBCs) coat the TB bacilli in thick waxy coat (‘walled off’)

Local lung infection (pneumonia)

Lymph nodes become enlarged

Leads to scar tissue forming (fibrosis)

PRIMARY TB

Kidneys

Bone

Lining of the brain

Spinal cord

TB – impact

Quite hard to catch - spreads most rapidly when there is overcrowding, especially if people are:

Homeless

Living in poor, substandard housing

Prisoners

Have low immunity eg: malnutrition, HIV positive

IV drug users, alcoholics or have diabetes

‘The biggest killer of women in the world’ - WHO Deaths in women aged 15-44 years:

9% TB, 3% war, 3% HIV, 3% heart disease

Estimated that 30% of the world’s population is infected with TB (~1.8 billion)

8-10 million people infected per year

2-3 million die per year (eg: in 2002 - 2 million deaths due to TB)

~1 person per second contracts TB

By 2020 nearly 1 billion will be newly infected, of which 70 million will die (WHO)

M. bovis – spread from cattle to humans:

1850-1950 ~800,000 deaths in the UK

Now very few in developed countries

TB – prevalence

TB – prevalence

The leading cause of death of HIV positive people.

Has been prevalent for thousands of years …

evidence in 4000 year old Egyptian mummies

Found primarily in: eastern Europe (250,000 cases/year)

Asia (3 million cases/year)

Africa (28% of all cases)

A worldwide pandemic

Those with HIV are 100x more likely to develop TB than other members of the population

Bangladesh, China, India, Indonesia, Pakistan, Philippines

TB – prevalence

Incidence in the UK decreased BEFORE introduction of the vaccine (1950s) due to improvement in housing and diet … showing a resurgence now

Resistant strains

HIV/AIDS pandemic

Poor housing in inner cities

Rising homelessness

Breakdown of TB control programmes (partial treatment)

Migration

TB – prevention

Prevention Break the lifecycle!

Isolation of infected people

Address social issues such as overcrowding

Better treatment

(maybe not antibiotics?)

Vaccinations

TB – prevention

Vaccinations – Injected:

BCG Bacille Calmette Guérin – some protection

Vaccinations update:

2004 Contains 2 TB proteins that stimulate a strong immune response in humans

(taken from naturally immune individuals)

So what do we know now?

Cause?

Prevalence?

Treatment?Prevention?

Impact?TB

Symptoms?

Think, Pair, Share

How can we prevent TB, now and in the future?

Lesson Objectives:

To describe the causes & means of transmission of HIV/AIDS

To assess the worldwide importance of this disease

To describe the roles of different factors in the prevention and control of HIV/AIDS

HIV/AIDS

What’s the difference?

• HIV means human immunodeficiency virus – so it’s the name of the pathogen that causes the disease

• AIDS means Acquired immune deficiency syndrome – so it’s the name of the disease

• http://www.nhs.uk/conditions/HIV/Pages/Introduction.aspx Basic SUMMARY

The nature of HIV• Viruses are very small!• HIV is a ball of protein and lipid

around RNA and reverse transcriptase (an enzyme). It’s a member of the group of viruses called retroviruses

• Once inside a cell the enzyme makes a ‘DNA version’ of the virus’s RNA

• The infected cell then follows the code on the ‘new’ DNA to make new viruses.

HIV – the cause

HIV only reproduce when inside a host cell.

HIV infects T lymphocytes.

Dr Robert Gallow, National Cancer Institute, 1984 – isolated HTLVIII

which causes AIDS

AIDS is not a disease – it is a collection of opportunistic diseases associated with acquired immunodeficiency

HIV – symptoms

Later symptoms:

Lack of energy

Weight loss

Frequent fevers and sweats

Yeast infections (oral or vaginal)

Skin rashes or flaky skin

Pelvic inflammatory disease in women

Short-term memory loss

Shingles

Children grow slowly or are sick frequently

Initial infection:Flu-like symptomsFeverHeadacheTirednessEnlarged lymph nodes

Months to years after infection

HIV – symptomsAIDS:

Coughing and shortness of breath

Seizures and lack of coordination

Difficult/painful swallowing

Forgetfulness

Confusion

Diarrhoea

Fever

Vision loss

Nausea, abdominal cramps and vomiting

Weight loss and extreme fatigue

Severe headaches

Coma

HIV – symptoms

HIV develops into AIDS due to opportunistic infections such as:

oral thrush (Candida albicans)

pneumonia (Pneumocystis carinii) – an unusual form of pneumonia

Leads to collapse of the immune system, meaning the body cannot detect and deal with:

cancer (eg: Kaposi’s sarcoma – a rare skin cancer caused by a herpes-like virus)

dementias

TB

malaria

malnutrition

TB + HIV: A dual Epidemic

http://www.youtube.com/watch?v=MnvdYfgb2DA

HIV – the cause

Spread by intimate human contact:

direct exchange of bodily fluids (eg: sexual intercourse, blood donation, sharing of needles, over the placenta)

may pass through breast milk – viral particles and infected lymphocytes are found in breast milk

high risk individuals – haemophiliacs treated with Factor VIII from many donors

HIV – impact

Affects economic development of countries as it affects primarily 20-30 year olds (potentially the most economically productive)

Drugs expensive eg: major impact on the growth of some African states

HIV leaving a cell

HIV – prevalence

Pandemic in early 1980s

47 million infected with HIV by 1998 of which 14 million had already died

980,000 cases reported in USA since 1981

1 million Americans may be infected, ¼ of whom don’t know

Leading killer of 25-22 year old African-American males

HIV – prevalence

Initial epidemic in North America (first reported in 1981) in male homosexuals that practised anal intercourse with many partners (high risk as the mucous lining of the rectum is not as thick as that of the vagina and less natural lubrication … virus can pass from semen into blood)

Transmission through heterosexual intercourse on the rise especially in Africa

Endemic in: sub-Saharan Africa

USA

Europe

Asia

HIV – treatment

No cure as yet and no vaccine

Anti-HIV drugs eg: zidovudine (AZT) works by blocking the viral reverse transcriptase

Not sure if 100% of HIV positive patients will develop AIDS – some appear to be symptomless carriers

Antiretroviral drug therapy slows onset of AIDS but have side-effects:

rashes

headaches

diarrhoea

nerve damage

abnormal fat distribution

Mild and temporary

Severe and permanent

HIV – treatment

AIDS = advanced HIV infection with significant loss of CD4 cells,

weakening the immune system to a point where the body is at risk of ‘AIDS-defining’ illnesses (ones that mark the onset of AIDS)

= CD4 count below 200 cells per cubic mm of blood

CD4 cells are the host cells that aid HIV in replication.

Test identifies presence of antibodies to HIV – several weeks after the initial infection

HIV – prevention

Prevention Education

Spread of AIDS difficult to control – long latent stage means that carriers may not know that they have HIV

Virus changes its surface proteins making it hard to detect and the production of a vaccine difficult

Protection Condoms,

femidoms and dental dams, screen blood

Clean needles

Testing people –

cheap but does it infringe your

rights?

Microbicides protecting against HIV

• http://www.bbc.co.uk/iplayer/episode/b011r4gs/Queen_Days_of_Our_Lives_Episode_2/

Lesson Objectives:

To explore the causes, transmission and effects of Malaria

http://www.nhs.uk/Conditions/Malaria/Pages/Introduction.aspx Summary

Malaria

STARTER – quick recap

1. What type of pathogen causes TB and HIV/AIDS?

2. What is the means of transmission of TB and HIV?

3. What is the leading cause of death of HIV+ patients?

4. What is the main cause of a resurgence of TB in the last 20 years?

5. Define the following:

a)Pathogen

b)Incidence

c) Mortality

d)Endemic

Malaria – symptoms

Fever

Anaemia

Nausea

Headaches

Muscle pain

Shivering

Sweating

Enlarged spleen

Symptoms in cycles – related to the asexual cycle of Plasmodium in RBCs – periodically burst open and reinfect RBCs

Causes the RBCs to become sticky – obstruct blood vessels

World Malaria Day (25th April)http://www.youtube.com/watch?v=O0Fsw-0_ldM

Malaria – the cause

Protozoan parasite Plasmodium:

Plasmodium falciparum

Plasmodium vivax

Plasmodium ovale

Plasmodium malariae

Eukaryote (RBC) bursting after

infection

Malaria – method of transmission

Vector = female Anopheles mosquitoes feeding on human blood (to get protein to develop their eggs!)

Heineman Text Page 162

Step by Step Life Cycle

1. If the host already has malaria, the mosquito will such the parasite gametes into it’s stomach.

2. Gametes fuse, zygotes develop in mosquito's stomach.

3. Infective stages are formed move to mosquito’s salivary glands.

4. Mosquito bites another person, saliva injected as anti-coagulant.

5. Infective stage of parasite transmitted, travels to liver, multiplies and enters blood.

6. In blood they enter RBCs, gametes produced.

Malaria – impact

A widespread and dehabilitating disease for the human population over thousands of years leaving a mark on our genome.

One of the world’s biggest threats to health – over 40% of the population live in areas where there is risk of Malaria.

Accounts for 1 in 10 deaths of children in the developing world.

Recent resurgence of the disease in sub-Saharan Africa.

Malaria – prevalence

1/3 of the global population are at risk from malaria (~2 billion)

Incidence = 400-500 million per year

Causes 1.5-2.7 million deaths per year (3,000 in the under 5s)

5 people per minute die of Malaria

Endemic in – South AmericaAfricaIndonesia

90% of clinical malaria cases

India, Brazil, Sri Lanka, Vietnam, Colombia, Solomon Islands

Think, Pair, Share

How can we prevent the spread of malaria?

Malaria – prevention

Plasmodium still retains a ‘relict’ chloroplast (fatty acid biosynthesis) complete with a genome – a possible target for anti-malarial drugs?

CONTROL

Reduce number of vectors Avoid

being bitten

Use drugs to prevent infection

Better testing?

Vaccines

Malaria – anti-malaria drugs – more information!

Prophylactics (preventative drugs – stops infection if you are bitten by an infected mosquito)

1.Chloroquinine – inhibits protein synthesis and prevents the parasite from spreading within the body – problems with resistance to this drug

2.Proguanil – also inhibits sexual reproduction of Plasmodium inside the mosquito

3.Mefloquine – a newer drug. Expensive and sometimes causes side effects such as restlessness, vomiting, dizziness and disturbed sleep

Read p172 on anti-malaria drugs (prophylactics) and make your own

notes

Malaria – immunity

Sickle Cell Anaemia

A disease that alters the shape of red blood cells (into a sickle shape), thereby reducing their oxygen capacity, causing weakness, cramps, organ damage and anaemia especially during high activity.

CAUSE – single point mutation in the Hb gene, recessive disease

Typically in black Africans/Afro-Americans

Homozygous HbS - lethal

Heterozygous - selective advantage

Continuous Reinfection-Become immune to malaria if they survive the first 5 years of life

-Immunity only lasts for as long as you are in contact with the disease

Sickle Cell Anaemia




Homozygous HbS - lethal

Heterozygous - selective advantage

Sickle Cell Anaemia




Summary –

copy and complete the following table (from

memory!)

Pathogen

Vector (Definitive host)

Main stages of development

Intermediate host

Features

Incidence

Key word Bingo!

PathogenPlasmodium

Vector

Transmission

Liver

RBCsSCA

Immunity

Definitive

Intermediate

Gametes

Sexual

Asexual

Anticoagulant

Sporozoite

Erythrocyte

SalivaSymptoms

Endemic

Malaria

Lesson Objectives:

To be able to name and give the functions of the different parts of blood

To describe the lines of defence against disease in humans

Blood and the immune system

Where are blood cells made?

-From blood stem cells

-In bone marrow in various places around the body

How much blood?

How much blood is found in the

average human?

What is blood made up of?

55% plasma =

water

proteins

other chemicals

45% cells =

RBCs

WBCs

PlateletsWhat is the structure and function of each of these

cells?

Blood cellsRed Blood Cells

-Erythrocytes (‘red cells’)

-Contains haem groups (Fe)

-Transport oxygen

Platelets

-Thrombocytes

-Anuclear in mammals

-Functions – blood clotting, cell adhesion, signalling

White Blood Cells

- Leukocytes

-Immune response

Defending ourselves against pathogens

First line of defence

(non-specific)

What is the body’s first line of defence?

Skin (sebum)

Nasal hairs

Tears, saliva (lysozymes and salt)

Lungs (cilia & mucus)

Stomach - HCl

The virus that causes warts can pass through unbroken

skin!

Staphylococcus aureus

The skin harbours a ‘flora’ of bacteria – most pathogenic

bacteria cannot survive there

Blood clotting

Helps to seal wounds rapidly until more permanent repair by mitosis

Oh no! A cut!

Damaged cells produce Thrombokinase

This stops a chemical called Heparin from working

… which allows Thrombin to work …

Fibrinogen Fibrin + Platelets

BLOOD CLOTS!

Heparin

Thrombokinase

ProthrombinThrombin


BLOOD CLOTS!

What happens when you get cut

Heparin

Thrombokinase

ProthrombinThrombin


‘Normal’ (non-cut!) cells

NO BLOOD CLOTS!

What happens if a pathogen gets past the first line of

defence?

White blood cells – fight disease

Phagocytes Lymphocytes

SECOND LINE of defence - engulf and digest microbes

THIRD LINE of defence – recognise invaders and make antibodies and anti-toxins

Neutrophils Macrophages

PhagocytosisBody recognises invaders and releases chemicals eg: HISTAMINE

NEUTROPHILS move towards the pathogen (chemotaxis)

Release digestive enzymes (lysosomes) … afterwards the neutrophils die

What is pus?

White blood cells (neutrophils) and dead bacteria!

Inflammation?

Areas become red and hot due to extra blood being taken there … extra white blood cells and the higher temperature also help to kill microbes (second line of defence!)



SECOND LINE of defence - engulf and digest microbes

THIRD LINE of defence – recognise invaders and make antibodies and anti-toxins

Neutrophils Macrophages

Lymphocytes

Key points:

Smaller than phagocytes

A large nucleus

2 types, both produced before birth in the bone marrow

Contain receptor proteins which bind to antigens



T cells

Recognise antigens,

stimulate B cells

B cells

Make antibodies

Memory B cells

‘remember’ antigens

(immunity)

T cells

Recognise antigens,

stimulate B cells

B cells

Make antibodies

Lymphocytes

Mature in the bone marrow

Concentrate in lymph nodes and spleen

Mature in the bone marrow

Collect in the thymus (in the chest just below the sternum)

Write down all the key words you

have met in today’s lesson –

with a brief definition!

Lymphocytes

Lesson Objectives:

To work independently

To find out more detail about leukocytes (white blood cells)

Leukocytes

YOUR TASK

Get into 8 groups (maximum 3 students per group)

Select a theme from below (maximum 2 groups per theme)

1. B cells and memory cells

2. T helper cells and killer cells

3. Primary and secondary response and its role in immunisation

4. Active and passive immunity

YOUR TASK – using the questions set on the next slide as prompt, produce a 5 minute overview of your theme suitable for the rest of the class to make notes from. You may produce handouts if needed (including diagrams or slides etc. – maximum 1 side of A4 paper)

You have the rest of the lesson and homework to prepare this – due in NEXT LESSON

Your task …1. B cells and memory

cellsWhere do they develop? How do

they respond to antigens? Why do they clone themselves? What is the difference between plasma and memory cells?

2. T helper cells and killer cells

Where do they develop? What do they respond to? What is the difference between helper and killer cells? How do they work?

3. Primary and secondary response and its role in immunisation

What is this? How does immunity develop? What is the difference between the two responses? Show diagrams detailing both.

4. Active and passive immunity

What is this? How do you get both active and passive immunity? Where is it important? How does it work? How long do both types last for?

An OUTSTANDING presentation will address AT LEAST these questions and will involve background reading (ie: reading the text

book is NOT ENOUGH!)

Lesson Objectives:

To give our presentations

To recap our learning from this chapter so far!

Mini review

YOUR TASK - what is lurking on your skin?!

1 agar plate per person

Split into 4 sections by drawing lines on the back

Place a finger gently onto a section

Now run your hand under my desks (yuck!) and place a finger in another section

Now wash your hands and place a (‘clean’) finger on another section

What about my door handle? Or your text book?!

Label the sections and write on your name. Tape the top on (2 pieces of sellotape only). Put in the tray at the front …

Lesson Objectives:

To summarise our learning from the previous lessons

To look at our agar plates

Immunity

YOUR TASK

In your notes:

1. Define the terms immune response, antigen and antibody

2. Describe (with diagrams) the structure and mode of function of phagocytes

3. Describe (with diagrams) the structure and mode of action of T lymphocytes and B lymphocytes including the significance of cell signalling and the role of memory cells

4. Compare and contrast the primary and secondary immune responses

EXTENSION:

Complete SAQ 5 and 6 from page 180

Answers …

1. Definitions:

a) Immune response the way in which lymphocytes respond to infection by pathogens

b)Antigen a molecule or cell that is recognised as

foreign by the immune system

c) Antibody A small protein secreted by B lymphocytes in

response to a particular antigen

2. PhagocytosisBody recognises invaders and releases chemicals eg: HISTAMINE

NEUTROPHILS move towards the pathogen (chemotaxis)

Release digestive enzymes (lysosomes) … afterwards the neutrophils die . ‘Waste’ material egested.

3. Lymphocytes

Stimulated when they detect ANTIGENS (‘free’ or as part of a cell wall for example).

Lymphocytes detect SPECIFIC antigens only – so we have many different types in our blood.

As they mature, lymphocytes produce ANTIBODIES (small globular glycoproteins) which are specific to an antigen.

They are placed into the plasma membrane of the lymphocyte – act as receptors for an antigen.

If bacteria enters the body it is detected and the immune response is triggered!

3. Lymphocytes – B lymphocytes

Triggered into action when an antigen binds to a receptor (could be found on a macrophage – an antigen presenting cell, APC, which might be in the lymph nodes)

-Divides by mitosis (clones are formed)

-Some clones DIFFERENTIATE into plasma cells (short lived) which develop extra ER, ribosomes and golgi apparatus to make loads of antibodies to be released by exocytosis (up to 2000 molecules per second!)

-Antibodies secreted into the blood – bind with antigens on bacteria

-Some clones do not secrete antibodies – they remain as MEMORY CELLS (long lived, circulate, secondary response!)

3. Lymphocytes – T lymphocytes

Triggered by binding of an antigen to glycoproteins on the plasma membrane ONLY when this is found in the plasma membrane of another cell (eg: APC or virus particles found on the outside of an invaded body cell)

T helper cells with complementary receptors bind to the antigen then divides. The clones secrete CYTOKINES which stimulate other cells (eg: macrophages, B lymphocytes, T killer cells)

T killer cells destroy the cell (including infected body cells) using chemicals such as hydrogen peroxide

Some cells remain as MEMORY CELLS

The ways in which lymphocytes work …

1.Antibodies make microbes stick together in clumps … then phagocytes ingest them!

2.Some antibodies stick to microbes to make it easier for phagocytes to find them

3.Some even stick to TOXINs produced by the microbes and make them harmless (ANTI-TOXINs!)

4.Antibodies stick to microbes and make them burst open

4. Primary and Secondary Response

Only a few lymphocytes with receptors that fit the antigen in the body – takes time to form clones and produce antibodies – delay when pathogen can divide and damage body tissues

Memory cells remain in the blood – a faster response when the pathogen invades again preventing any illness (immunity!)

Lesson Objectives:

To discuss immunity

To find out about antibiotics and antibodies

Antibiotics and

preventing illness

STARTER

Grab a mini whiteboard, pen and rubber and sketch the following:

1.A graph showing the primary and secondary immune response (with explanations)

2.Phagocytosis

Compare your pictures with your partner!

Active Immunity

Your immune system is stimulated to make a particular type of antibody – fast secondary response

1. Due to first infection

2. By vaccination

Natural immunity

Artificial immunity

Herd immunity (80-85%)

Passive Immunity:

Short lived immunity

Natural immunity - Babies get antibodies via the placenta and breast milk, giving them immunity to the same diseases as their mother.

Only present during growth in the womb and when breast feeding.

Artificial immunity – injections of antitoxins eg: in A&E against tetanus after a cut

Antibiotics – what are they?

Drugs used to treat/cure infections

Show selective toxicity

A wide variety available to treat bacterial and fungal and infections

Only a few available to treat viral infections

Sir Alexander Fleming 1928

PenicillinAmoxicillin

Streptomycin Erythromycin

Neomycin Vancomycin

Penicillin works by destroying

bacteria's ability to maintain the rigidity

of their cell wall.

Antibiotics – where do we get them from?

Derived from living organisms

Can be synthetic (eg: isoniazid)

Antibiotics – how do they work?

Broad spectrum effective against a wide range of bacteria

Narrow spectrum active against a few

Antibiotics – how do they work?

What it does Examples Effect on bacteria

Inhibits cell wall synthesis

Penicillin, cephalosporin, vancomycin

Bactericidal

Inhibits transcription

Rifampicin Bactericidal

Inhibits protein synthesis

Chloramphenicol, tetracyclineErythromycin, streptomycin

Bacteriostatic

Bactericidal

Interferes with metabolic reactions

Sulpha drugs Bacteriostatic

Inhibits membrane functions

Polymyxin Bactericidal

Antibodies

Glycoproteins – amino acid chain with sugar units

Also known as IMMUNOGLOBULINS – different types eg: IgG and IgA

The ways they work:

Antibodies make microbes stick together in clumps … then phagocytes ingest them!

Some antibodies stick to microbes to make it easier for phagocytes to find

them Some even stick to TOXINs produced

by the microbes and make them harmless (ANTI-TOXINs!)

Antibodies stick to microbes and make them burst open

Some may stop pathogens from attaching to cells or tissues

Lesson Objectives:

To recap HIV/AIDS, TB and Malaria

To discuss the response to the threat of new strains of influenza each year

New diseases, and old

SUMMARY OF DISEASES

Malaria TB HIV

Cause

Symptoms

Treatment

Prevention

Prevalence

Impact

SARS

Severe acute respiratory syndrome (SARS)

Caused by a virus

Respiratory disease in humans

One near pandemic (Nov 2002 – July 2003; 8,096 known cases, 774 deaths (9.6% fatality))

Started in China and rapidly spread

An RNA virus which constantly mutates (antigenic drift) meaning that if you are immune to it one year, you may not be immune the next year

Spreads easily and rapidly

Peak outbreaks in winter months (ie: twice a year across the globe due to seasonal differences – one per hemisphere)

Typically 3-5 million severe cases per year with 500,000 deaths worldwide

A pandemic every 10-20 years

Pandemic in 1918 – if a similar strain emerged today it would kill 50-80 million people

Influenza (flu)

Influenza (flu) – H5N1

Easily transmissible between birds

Enzootic in many bird populations esp. Southeast Asia

Epizootic (epidemic in nonhumans)

Panzootic (affecting many birds of different species over a wide area)

Transmitted through saliva, nasal secretions, faeces and blood

Lasts in the environment (without a host) for weeks

New hope?

Few drugs work against viruses

Antibiotic resistance

Sponges

One of the earliest multicellular animals on Earth (up to 600 million years old)

Found in seas over the world

Animals – no cell walls, fixed permanently to sea bed or coral reef

Absorb food across cells with flagella which beat rhythmically creating currents

Contain specialised cells but no true tissues or organs

Interest from pharmaceutical companies – they have evolved a defence mechanism to deter predators

Our changing attitudes to smoking …

With all of the information that we now have about the effects of smoking on our health, is it a good idea to smoke?

Used since 500 AD

1565 - First introduced in England

1875

1921

Cigarettes

NicotineAddictive

Affects the brain, nervous system and the cardiovascular system

TarCarcinogenic

Carbon monoxideProduced by incomplete oxidation which reduces oxygen carrying capacity of the blood

ParticulatesTiny particles (eg: C) which irritate lungs and airways

Nicotine-A neurotoxin (chemical that damages the nervous system)

-Used as an INSECTICIDE (!)

-Addictive

-Relatively small molecules which move into every part of the body including the brain

-Increases amount of dopamine (feeling of pleasure)

-Causes the release of adrenaline into the blood (increased heart rate, breathing rate and blood pressure)

Carbon monoxide

-Diffuses into capillaries from alveoli

-Forms carboxyhaemoglobin

-Hb has a very high affinity for CO

-Less Hb available to transport oxygen

-SMOKING REDUCES THE AMOUNT OF OXYGEN DELIVERED TO TISSUES (including heart tissue)

-Less energy available to muscles during exercise

Knock on effects

Increased blood pressure (nicotine)

Atherosclerosis and CHD

Blood clots/blood vessel bursts = stroke

Left hemisphere – language skills, memory

Right hemisphere – movement, spacial awareness, memory

Lung diseases associated with smoking

1.COPD – Chronic obstructive pulmonary disease (includes emphysema)

2.Lung cancer

3.Infectious organisms

Lesson Objectives:

To think about the effects of smoking on health

To review Chapter 11

Finishing off the unit!

Sir Richard Doll (1912-2006)

Smoking and lung cancer … the results

Why the difference between males and females?

Why is there a time lag between the peaks?

Smoking and lung cancer

Cells in the lungs divide uncontrollably and form a tumour

Mortality rate in England and Wales: ~35,000/year (30% of smoking related deaths)

Smokers are almost 20x as likely to die from lung cancer than non-smokers

Smoking and lung cancer

Cigarette smoke contains CARCINOGENS

A lump of disorganised cells (tumour) forms

This tumour can be almost anywhere in the gas exchange system (most often where bronchi begin or at other branching points)

The tumour will displace other tissues as it grows – leading to blockage of airways or part of the lungs

Other lung illnesses

Tuberculosis

Bronchitis

Cause: Inflammation of the trachea and bronchi due to infection (or other causes)

Tobacco smoke has been linked to acute bronchitis

Smoking has been shown to increase risk of infection, risk of progression from infection to disease and risk of death

COPD – Chronic Obstructive Pulmonary Disease

Airflow into and out of the lungs gradually and progressively becomes more obstructed

~600 million worldwide suffer from COPD

Mortality rate: 300 million/year

Approx. 80-90% caused by smoking

Some chemicals from cigarette smoking stimulate NEUTROPHILS

They come to the lungs and CAUSE illness by secreting NEUTROPHIL ELASTASE (a protease that breaks down elastin; forms the elastic fibres in tissues of the airways)

Inhibitors prevent enzyme from doing too much harm – in smokers the balance between inhibitor and enzyme tips towards the enzyme (bad!)

Proteases gradually break down the elastin tissues in the lungs – irreversible damage esp. to alveoli



Emphysema

Bronchitis

Beta antagonists widen airways

Severe cases – use oxygen cylinders

Pathology of lung showing centrilobular emphysema characteristic of smoking. Closeup of fixed, cut surface shows multiple cavities lined by heavy black carbon deposits. (CDC/Dr. Edwin P. Ewing, Jr., 1973)

Documents

2.2.2 (Chapter 11) – Health and Disease Lesson Objectives: To define the terms ‘health’ and ‘disease’ To discuss different categories of disease