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

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1 2.2.2 (Chapter 11) – Health and Disease Lesson Objectives: To define the terms ‘health’ and ‘disease’ To discuss different categories of disease

2 So what is ‘health’? What do we mean by ‘health’? What are the characteristics of health? Healtha person’s physical, mental andsocial condition World Health Organisation (WHO): ‘a state of complete physical, mental and social well-being and not merely the absence of disease and infirmity’

3 Healtha person’s physical, mental andsocial condition Good Poor Happiness Fulfilling life More than just the absence of disease! Positive outlook Well adjusted to society Can undertake physical and mental tasks without difficulty

4 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

5 So what is ‘disease’? What do we mean by ‘disease’? Diseasea disorder or malfunction of the mind or body which leads to a departure from good health

6 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: malariaMultifactorial eg: heart disease Signs (symptoms) – physical and/or mental ACUTE eg: influenzaCHRONIC eg: TB

7 The 9 categories (types) of disease ‘Miss D. Pind’ M I S S D P I N D ental nfectious hysical on-infectious ocial elf-inflicted eficiency egenerative nherited

8 Name this infection. The infection is…. ….. a cold or flu This infection is caused by…. …..a virus

9 Name this infection. The infection is…. …..athletes foot This infection is caused by…. …..a fungus

10 Name this infection. The infection is…. …..warts This infection is caused by…. …..a virus

11 Name this infection. The infection is…. …..chicken pox This infection is caused by…. …..a virus

12 Name this infection. The infection is…. …..food poisoning This infection is caused by…. …..bacteria

13 Name this infection. The infection is…. …..measles This infection is caused by…. …..a virus

14 Name this infection. The infection is…. …..fungal nail infection This infection is caused by…. …..obviously a fungus

15 Name this infection. The infection is…. …..impetigo This infection is caused by…. …..bacteria

16 Name this infection. The infection is…. …..oral thrush This infection is caused by…. …..a fungus

17 Single celled organisms Types of pathogenic organisms … Bacteria Virus Fungi Protozoa

18 = 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

19 So how are diseases spread? Vectors (eg: insects) Contaminated food/water Air Contaminated needles Direct contact Indirect contact

20 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

21 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

22 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.

23 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

24 STARTER – Read the fact sheet from the WHO about TB

25 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)

26 What do you already know? Cause? Prevalence? Treatment? Prevention? Impact? TB Symptoms? Basic Summary Better!!

27 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)

28 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 p on TB

29 TB – treatment

30 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

31 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

32 TB – impact Quite hard to catch - spreads most rapidly when there is overcrowding, especially if people are: HHomeless LLiving in poor, substandard housing PPrisoners HHave low immunity eg: malnutrition, HIV positive IIV drug users, alcoholics or have diabetes ‘The biggest killer of women in the world’ - WHO Deaths in women aged years: 9% TB, 3% war, 3% HIV, 3% heart disease

33 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 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: ~800,000 deaths in the UK Now very few in developed countries TB – prevalence

34 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

35 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

36 TB – prevention Prevention Break the lifecycle! Isolation of infected people Address social issues such as overcrowding Better treatment (maybe not antibiotics?) Vaccinations

37 TB – prevention Vaccinations – Injected: BCGBacille Calmette Guérin – some protection Vaccinations update: 2004Contains 2 TB proteins that stimulate a strong immune response in humans (taken from naturally immune individuals)

38 So what do we know now? Cause? Prevalence? Treatment? Prevention? Impact? TB Symptoms?

39 Think, Pair, Share How can we prevent TB, now and in the future?

40 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

41 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 s/Introduction.aspx Basic SUMMARYhttp://www.nhs.uk/conditions/HIV/Page s/Introduction.aspx

42 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.

43 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

44

45 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 symptoms Fever Headache Tiredness Enlarged lymph nodes Months to years after infection

46 HIV – symptoms AIDS: 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

47 HIV – symptoms HIV develops into AIDS due to opportunistic infections such as: ooral thrush (Candida albicans) p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 alnutrition TB + HIV: A dual Epidemic e.com/watch?v= MnvdYfgb2DA

48 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

49 HIV – impact Affects economic development of countries as it affects primarily year olds (potentially the most economically productive) Drugs expensive eg: major impact on the growth of some African states HIV leaving a cell

50 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 million Americans may be infected, ¼ of whom don’t know Leading killer of year old African-American males

51 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

52 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

53 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

54 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?

55 Microbicides protecting against HIV

56

57 r4gs/Queen_Days_of_Our_Lives_Episode _2/http://www.bbc.co.uk/iplayer/episode/b011 r4gs/Queen_Days_of_Our_Lives_Episode _2/

58 Lesson Objectives: To explore the causes, transmission and effects of Malaria n.aspxhttp://www.nhs.uk/Conditions/Malaria/Pages/Introductio n.aspx Summary Malaria

59 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

60 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 (25 th April) om/watch?v=O0Fsw- 0_ldM

61 Malaria – the cause Protozoan parasite Plasmodium: Plasmodium falciparum Plasmodium vivax Plasmodium ovale Plasmodium malariae Eukaryote (RBC) bursting after infection

62 Malaria – method of transmission Vector = female Anopheles mosquitoes feeding on human blood (to get protein to develop their eggs!)

63 Heineman Text Page 162

64 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.

65 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.

66 Malaria – prevalence 1/3 of the global population are at risk from malaria (~2 billion) Incidence = million per year Causes million deaths per year (3,000 in the under 5s) 5 people per minute die of Malaria Endemic in – South America Africa Indonesia 90% of clinical malaria cases India, Brazil, Sri Lanka, Vietnam, Colombia, Solomon Islands

67 Think, Pair, Share How can we prevent the spread of malaria?

68 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

69 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

70 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 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 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

71 Summary – copy and complete the following table (from memory!) Pathogen Vector (Definitive host) Main stages of development Intermediate host Features Incidence

72 Key word Bingo! Pathogen Plasmodium Vector Transmission Liver RBCs SCA Immunity Definitive Intermediate Gametes Sexual Asexual Anticoagulant Sporozoite Erythrocyte Saliva Symptoms Endemic Malaria

73 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

74 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?

75 What is blood made up of? 55% plasma = water proteins other chemicals 45% cells= RBCs WBCs Platelets What is the structure and function of each of these cells?

76 Blood cells Red 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

77 Defending ourselves against pathogens First line of defence (non- specific)

78 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

79 Oh no! A cut! Damaged cells produce Thrombokinase This stops a chemical called Heparin from working … which allows Thrombin to work … FibrinogenFibrin + Platelets BLOOD CLOTS!

80 Heparin Thrombokinase ProthrombinThrombin Fibrinogen Fibrin + Platelets BLOOD CLOTS! What happens when you get cut

81 Heparin Thrombokinase ProthrombinThrombin Fibrinogen Fibrin + Platelets ‘Normal’ (non-cut!) cells NO BLOOD CLOTS!

82 What happens if a pathogen gets past the first line of defence?

83 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

84 Phagocytosis Body recognises invaders and releases chemicals eg: HISTAMINE NEUTROPHILS move towards the pathogen (chemotaxis) Release digestive enzymes (lysosomes) … afterwards the neutrophils die 

85 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!)

86 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

87 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

88 White blood cells – fight disease Phagocytes Lymphocytes T cells Recognise antigens, stimulate B cells B cells Make antibodies Memory B cells ‘remember’ antigens (immunity)

89 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)

90 Write down all the key words you have met in today’s lesson – with a brief definition! Lymphocytes

91 Lesson Objectives: To work independently To find out more detail about leukocytes (white blood cells) Leukocytes

92 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

93 Your task … 1.B cells and memory cells Where 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!)

94 Lesson Objectives: To give our presentations To recap our learning from this chapter so far! Mini review

95 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 …

96 Lesson Objectives: To summarise our learning from the previous lessons To look at our agar plates Immunity

97 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

98 Answers … 1.Definitions: a)Immune response the way in which lymphocytes respond to infection by pathogens b)Antigena molecule or cell that is recognised as foreign by the immune system c)AntibodyA small protein secreted by B lymphocytes in response to a particular antigen

99 2. Phagocytosis Body recognises invaders and releases chemicals eg: HISTAMINE NEUTROPHILS move towards the pathogen (chemotaxis) Release digestive enzymes (lysosomes) … afterwards the neutrophils die . ‘Waste’ material egested.

100 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!

101 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!)

102 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

103 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

104 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!)

105 Lesson Objectives: To discuss immunity To find out about antibiotics and antibodies Antibiotics and preventing illness

106 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!

107 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%)

108 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

109 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 Penicillin Amoxicillin Streptomycin Erythromycin Neomycin Vancomycin

110 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)

111 Antibiotics – how do they work? Broad spectrumeffective against a wide range of bacteria Narrow spectrumactive against a few

112 Antibiotics – how do they work? What it doesExamplesEffect on bacteria Inhibits cell wall synthesis Penicillin, cephalosporin, vancomycin Bactericidal Inhibits transcription RifampicinBactericidal Inhibits protein synthesis Chloramphenicol, tetracycline Erythromycin, streptomycin Bacteriostatic Bactericidal Interferes with metabolic reactions Sulpha drugsBacteriostatic Inhibits membrane functions PolymyxinBactericidal

113 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

114 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

115 SUMMARY OF DISEASES MalariaTBHIV Cause Symptoms Treatment Prevention Prevalence Impact

116 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

117 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 years Pandemic in 1918 – if a similar strain emerged today it would kill million people Influenza (flu)

118 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

119 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

120 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 First introduced in England

121 Cigarettes Nicotine Addictive Affects the brain, nervous system and the cardiovascular system Tar Carcinogenic Carbon monoxide Produced by incomplete oxidation which reduces oxygen carrying capacity of the blood Particulates Tiny particles (eg: C) which irritate lungs and airways

122 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)

123 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

124 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

125 Lung diseases associated with smoking 1.COPD – Chronic obstructive pulmonary disease (includes emphysema) 2.Lung cancer 3.Infectious organisms

126 Lesson Objectives: To think about the effects of smoking on health To review Chapter 11 Finishing off the unit! Sir Richard Doll ( )

127 Smoking and lung cancer … the results Why the difference between males and females? Why is there a time lag between the peaks?

128 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

129 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

130 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

131 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 % caused by smoking

132 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 COPD – Chronic Obstructive Pulmonary Disease

133 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)


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