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Note On Infectious Disease

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Published in: Biology
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AS Biology Infectious Disease

Areesha A / Dubai

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Qualification: IGCSE-AS Level-A level

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  1. Human Health & Disease ot
  2. Infectious Disease cholera Disease malaria HIV/AIDS Antibiotics Antibiotic resistance
  3. Infectious Disease An infectious disease is a transmissible disease resulting from the presence of pathogens including viruses, bacteria, fungi, protozoa and multicellular parasites. These pathogens are able to cause disease in animals and/or plants.
  4. Infectious pathologies are usually contagious diseases due to their potentiality of transmission from one person or species to another. Transmission vectors can be a variety of things, from drinking water to sexual contact.
  5. • The four diseases you are required to know are relevant because they are the ones of current concern - they are all in epidemic or pandemic status. Due to international travel, diseases can be spread round the entire world very quickly, as in the SARS incident of 2002/2003. Some bacteria are growing resistant to the use of antibiotics, which used to be an effective way of stopping disease spreading.
  6. Transmission cycle is the way in which a pathogen passes from one host to another. The control methods attempt to break the transmission cycle.
  7. Infectious Disease cholera Disease malaria HIV/AIDS Antibiotics Antibiotic resistance
  8. Endemic: a disease that exists permanently in a particular region or population. Malaria is a constant worry in parts of Africa Epidemic: an outbreak of disease that attacks many people at about the same time and may spread through one or several communities Pandemic: When an epidemic spreads throughout the world; a worldwide epidemic; an epidemic occurring over a wide geographic area and affecting a large number of people
  9. Cholera • Caused by the bacterium Vibrio cholerae Cholera is endemic in the west &east Africa as well as Afghanistan. lectron micrograph of Vibrio cholerae. The faeces of the victims are full of these bacteria.
  10. Cholera is a disease of acute intestinal tract infection the bacterium Vibrio cholerae, enter the body through contaminated food or beverages The bacteria release enterotoxin (poison)/choleragen in the intestinal tract so that there is an acute diarrhea accompanied by vomiting and severe, resulting in a person in just a few days lost a lot of body fluids and get in on the condition of dehydration.
  11. Vibrio cholera attachment and population.
  12. How cholera is transmitted from person to person • Infected individuals pass out large numbers of Vibrio cholerae in their faeces. The bacteria contaminate the water supply Uninfected persons come into contact with the contaminated water supply through drinking, bathing, washing • Eating contaminated food by vectors (e.g. flies) or prepared by infected people.
  13. How does an uninfected person get The site of infection (portal of entry) is the small intestine When bacteria pass through the stomach, the acidic condition (pH < 4.5) should be able to kill the bacteria
  14. How does an uninfected person get • If the bacteria do reach the small intestine, they will multiply, colonize the lining of the small intestine and secrete a toxin, choleragen. Choleragen is a protein that chemically modifies a protein involve in regulating salt and water secretion.
  15. How does an uninfected person get infected? As a result, intestinal cells release salts into the intestines and water follows by osmosis The infected person develops diarrhea The loss of fluid can be fatal if not treated as a result of dehydration and the loss of mineral salts. Oral rehydration solution/ORS therapy.
  16. Com»on cause No sewage treatment or clean water in growing populations of developing countries No financial resources to tackle large municipal projects such as providing drainage system and clean water supply. Inadequate cooking or washing in contaminated water.
  17. Features.o Pathogen Transmission method Incubation choler Vibrio cholerae food and water borne 1-5 days Symptoms Annual incidence/mortality worldwide Site of infection Global distribution Severe diarrhoea, loss of water and salts, dehydration. 5.5 million/ 120,000 Walls of small intestines Asia, Africa, Latin America
  18. Mä aria Malaria is caused by the protoctist Plasmodium • It is transmitted by the Anopheles mosquito Confined to tropical areas
  19. Mä aria The female Anopheles mosquito feed on human blood to obtain protein • If the person they bite is infected with the Plasmodium, they will take up some of the pathogen's gametes. These gametes fuse and develop in the mosquito's gut to form the infective stage, which then move to the mosquito's salivary glands.
  20. Mä aria When the infected mosquito feeds again, it injects an anti-coagulant into the blood meal so that it flows out from the host into the mosquito. The infective stages of the Plasmodium enter the red blood cells, where they multiply @ The female Anopheles is therefore the vector of malaria and she (it) transmits the disease when she passes the infective stages into an uninfected person.
  21. infective Stages Of parasite invade mosquito's salivary glands infected mosqui to takes blood nmeal infective Stages of parasite enter bloodstream and then liver cells parasites leave liver cells and enter red blood cells maturation and production of parasite's male and female sex cells (gametes) cell division produces thousands of immature malarial parasites 6—12 days male and female gametes fuse in mosquito's stomach 24 hours mosquito takes infected blood meal 48—72 hours
  22. Oocysts dewlop gut wall sucked up u In mosquitoes Sporozoites develo in oocy?t Sporozoites rn• rate to safvary glands Sporozoite injected wiå mosquito bite Liver stage '4b cell stage sickle.bwh.harvard.edu *laria le.ht In humans
  23. Infection Transmission to mosquito Sporozoites Merozoites Gametocvtes Merozoite, Infected RBC Merozoite invasion Red cell Adhesion in placenta Adhesion to endothelium Infected RBC 'urn
  24. Zygote Fomah garnoto 1. Moswito suds fron infectuf 01 gametocytes Microgametocyte Macrogametocyte Oocysts in mosquto stomach En 2. Then feeds an uninfected thus transmitti sp Red blood Spcgozotes in ito vary glands zones injected saliva disease $otozoitos Ever cens Metozoites released trom red NOOd Schtzont containing merozoites Red blood cell merozoites
  25. Features of Malaria Pathogen Transmission method Incubation Symptoms Annual incidence/mortality worldwide Site of action of pathogen Global distribution Plasmodium falciparum Insect vector/Anopheles mosquito 1 week- 1 year Fever, nausea, headaches, sweating, spleen enlargement, muscle pain, anaemia, 300 million/ 1.5-3 million Liver, red blood cells, brain Tropics and subtropics.
  26. The three main ways to control malaria: (i) Reduce the number of mosquitoes (destruction of breeding ground, stagnant water, the use of insecticides) (ii) Avoid being bitten by mosquitoes (using fly screens, mosquito repellents) (iii) Using prophylactic drugs to prevent parasites from infecting people (chloroquine and quinine, proguanil, mefloquine) Ahnia•' ,44in.1'
  27. • Two biological control measures that can be used are: i) Fish which can feed on mosquito larvae ii) Spraying bacillus thuringiensis which kills mosquito larvae, but is not toxic to other forms of life. too
  28. Anti-malarial drugs • Quinine and choloquine are used to treat infected people. • Taken before, during and after visiting an area where malaria is endemic. Chloroquine inhibits protein synthesis and prevents the parasite spreading within the body. Chloroquine resistance is widespread in parts of South America, Africa and New Guinea. Mefloquine is used in these areas but is expensive and sometimes caused unpleasant side effects.
  29. Malaria Eradication programme • Coordinated by WHO in 1950s. Although malaria was cleared from some countries, it was not generally successful.
  30. Malaria Eradication • • programme Plasmodium became resistant to the drugs used to control it Mosquitoes became resistant to DDT (dichlorodiphenyltric hloroethane) Malaria was temporarily eradicated
  31. The programme had not been tackled more sensitively. preventing malaria infections and, preventing the transmission of resistant parasites.
  32. Worldwi e concern • An increase in drug- resistance forms of of cases caused by Plasmodium falciparum • Difficulties in developing a vaccine • An increase in the number of epidemics because of climatic and environmental changes that favours the spread of mosquitoes • the migration of people as a result of civil unrest and war.
  33. Tuberculosis An invasive disease - it starts with a primary infection in the lungs and quickly spreads to the lymph nodes, bones and gut. It often strikes HIV-positive people when their immune system begins to weaken. Tubercle Bacillus (T B)
  34. Scanning Electron Mcrograph of Wcobatterium tuberculosis Pathogen • Tuberculosis is caused by two types of bacteria: Mycobacterium tuberculosis and Mycobacterium bovis.
  35. Tuberculosis Affects Many Parts Of the Body Midle ear Alrenal Sands CNS (brain and meningo To opposite Lung Tonsi TO other pætS of same lung bones. spire, psoa:s muscle intestine Li',er. NIeen. peritoneum Genial especi y Adnexa Ureter aadder Prod ate. semnal wsctes Pericarcium • most commonly affects the lungs (pulmonary TB) but can also affect the central nervous system, lymphatic system, circulatory system, genitourinary system, bones, joints, and even the skin.
  36. • • Some people become infected and develop TB quite quickly, whilst in others the bacteria remain inactive for many years. People with this inactive infection do not spread the disease to others. But the bacteria become active when these people are weaken by other diseases, suffer from malnutrition or become infected with HIV.
  37. Methods of transmission Generally, it is spread via airborne droplets, and is particularly prevalent in overcrowded areas, and people suffering malnutrition are more susceptible. Can also spread via unpasteurized milk
  38. A person may contract pulmonary tuberculosis from inhaling droplets from a cough or sneeze by an infected person Granuloma in lung tissue
  39. Airborne droplets TB is spread when infected people with the active form of the illness cough or sneeze The bacteria are carried in the air in tiny droplets of liquid. • Transmission occurs when uninfected people inhale this droplets. • TB spreads most rapidly among those in overcrowded areas, homeless, poor substandard housing, having low immunity because of malnutrition or being HIV positive.
  40. Unpasteurized milk M. Bovis also causes tuberculosis and occurs in cattle, it can be spread via their meat and milk, but both bacterium infections have fallen now because of vaccine introduction in the 1950s. People can also catch TB from cattle through airborne droplets
  41. hio R—piratory bro droplets Alveol - Blood
  42. Pathogen Transmission method Incubation Symptoms Mycobacterium tuberculosis, M. bovis airborne droplets 2-6 weeks Coughing up blood, shortness of breath, fever, chest pain and sweating. Annual incidence/mortality 8 million/ 2 million worldwide
  43. Symptoms of Tuberculosis (Established) pulmonary tuberculosis Productive cough Primary pulmonary tuberculosis Structural abnormalities Tuberculous pleuritis Chest pain ast Weigh ointestinal s m m specific Colored lines Overlapping Miliary tuberculosis Return of dormant tuberculosis Cough with increasing mucus Coughing up blood Extrapulmonary tuberculosis Common sites: Meninges Lymph nodes Bone and joint sites Genitourinary tract
  44. Treatment Sufferers are isolated after diagnosis (samples of sputum collected for analysis and identification of the tuberculosis bacteria by microscopy. The treatment involves using several drugs to ensure that all bacteria are killed, especially the drug resistant strain of the bacterium.
  45. Treatment The treatment is a long one. (9 months to a year) It takes a long time to kill the bacteria. People who do not complete a course of treatment are very likely to infect others with drug-resistant forms of TB. WHO promotes a scheme (DOTS: Direct Observation, Treatment and Shortcourse) to ensure that the patient complete their course of drugs
  46. Treatment The drugs widely used are isoniazid and rifampicin, often in combination with other drugs. Drug resistance occurs as a result of mutation in the bacterial DNA. Stopping treatment early means that the M. tuberculosis can develop resistance to all sorts of drugs. Every year, nearly half a million new cases of multidrug-resistant tuberculosis (MDR-TB) are estimated to occur worldwide.
  47. Isoniaz.d 1952 Inhibits cell wall synthesis Ethambutol 1961) Inhibits cell wall synthesis PyrazinamiOe (1952) Exact Target unclear Disrupts Plasma Membrane Disrupts Energy Metabolism Cell Wall Synthesis Acyl Lipids M olic Acid Ritarn •n 1966 Inhib.ts RNA synthesis DNA Coiling, Transcription, and Translation DNA G rase DNA Ribosome Arabinogalactan e id can Plasma Membra Mycobacterium tuberculosis ATP cell Våii ATP Synthesis
  48. Resistance • Tuberculosis is unfortunately showing a comeback, and this is thought to be due to a variety of factors. These include; a) b) c) d) Breakdown in the tuberculosis vaccination and control program Poor housing causing overcrowding The AIDS epidemic weakening immune systems and allowing it to be more prevalent Some strains are now resistant to antibiotics
  49. Control • Spread of disease to among children is prevented to a large extent by vaccination BCG (Bacillus Calmette-Guérin) vaccine is derived from M. bovis 80% effective in preventing tuberculosis for a duration of 15 years; however, its protective effect appears to vary according to geography. • Protection decreases with age
  50. Control Contact tracing — screening for TB bacterium. Cattles are routinely tested for TB and any food found to be contaminated/infected with the bacterium are destroyed Pasteurize milk to kill TB bacteria.
  51. AIDS • Acquired Immune Deficiency Syndrome, is a syndrome caused by the retrovirus Human Immunodeficiency Virus (HIV).
  52. protein capsorneres protein core protease gp 41 gp 120 outer lipid rnernbrane transcriptase Figure 13.5 Hurnan inununodeficiency virus (HIV). The outer envelope contains tvvo glycoproteins gp120 and gp 41. The protein core contains genetic rnaterial (RNA) and tvvo enzylnes. a protease and reverse transcriptase. Reverse transcriptase uses the RNA as a ternplate to produce DNA (page 237) once the virus is inside a host cell.
  53. Figure 136 A series of transmission electron micrographs showing HIV budding from the surface of an infected lymphocyte, becoming surrounded by a membrane derived from the plasma membrane ofthe host cell. a The viral particle first appears as a bump, b which then buds outand c iseventuallycutoff, d The outer shell of dense material and less dense core are visible in the released virus. (x 176000)
  54. Human Immunodeficiency Virus 3 Medscape http:Ihnmnm.medscape.com HIV pathogens infect and destroy the T helper lymphocytes cells of the immune system, and without these the immune system does not respond adequately to infection.
  55. Human Immunodeficiency Virus When T-Cell numbers are low, the body is particularly vulnerable to infection by anything from the common cold to tuberculosis (opportunistic infections) Thus, AIDS is not a disease, HIV is the virus that causes AIDS which is a syndrome — a collection of rare opportunistic disease.
  56. 1 . The HIV virus attaches toa helper T cell via CD4 proteins. 2. Viral RNAand reverse tranæriptase enter the cell. Helper T Cell 8. New viral particles ar mbled. 9. The cell is killed, and the viruses leave infect nevoi cells. 3. Reverse transcriptase nukes a DNA copy of the viral RBI.A. 4. en an d into s thral DNA s the nucleus corporates eceu•s DNA e viral A rep tes... 6. and m Nuc leus e HIV proteins. 7. Protæse cuts the proteins to tieir proper size.
  57. N/A
  58. HIV— human immunodeficiency virus HIV is a retrovirus of the lentivirus group. Viral RNA is converted to DNA. which htegrates into the cellular Enzyme e Discovery Of HIV in paüents Vrus prodißtion T cells by rev«æ activty. 10 o Etiviy 10 18 (p24) Discovery of an unknown virus Patient with Swollen lymph —2 weeks T cells from ph nodes Cu Electron rnicroscopy identifies retrovial budding from infected T cells. Infect«i cells fuse and many die. O The Nthel Comrnittee for Physdoqy Medicine 2CX)8 Illustration: Annika ROhl
  59. 1200 1100 900 800 600 400 300 200 100 Primary InfectiOn / Acute HIV syndrome Wide dissemination of vit-us Seeding Of lymphoid organs Clinical latency Symptoms of AIDS Opportunistic Constitutional Symptoms 107 106 105 104 102 6 9 12 Weeks 1 2 3 4 5 6 7 8 9 10 11 Years A generalized graph of the relationship between HIV copies (viral load) and CD4 counts over the average course of untreated HIV infection; any particular individual's disease course may vary considerably. CD4+ T Lymphocyte count (cells/mm3) plasma HIV RNA copies per mL of
  60. Methods of transmission The most common methods of transmission of HIV are: Unprotected sex with an infected partner Sharing needles with infected person Almost eliminated as risk factors for HIV transmission are: Transmission from infected mother to fetus Infection from blood products HIV spread by intimate human contact No vector The virus in unable to survive outside the human body Transmission is possible by direct exchange of body fluid
  61. Methods of transmission HIV can be spread most easily through Unprotected sexual intercourse - Blood donation - Sharing of needles - The placenta from the mother to the fetus - Anal intercourse Multiple sex partners.
  62. Symptoms HIV is a slow virus Flu-like symptoms for several weeks after becoming infected HIV positive but does not have AIDS Condition to develop AIDS - Oral thrush - A rare form of pneumonia
  63. Symptoms When immune system collapse further - less effective in finding and destroying cancers like Kaposi's sarcoma, a skin cancer caused by a herpes-like virus. • Degenerative diseases of the brain (dementia).
  64. Pathogen Transmission method Incubation Symptoms Annual infected/new incidence/mortality worldwide Human immunodeficiency virus (HIV) Exchange of body fluids (sexual intercourse, intravenous needle sharing, blood transfusions) HIV has a few weeks, but AIDS may not develop for up to ten years HIV - fever and then none AIDS - hugely increased susceptibility to disease, such as pneumonia and TB. 33.4 million/6 million/2.5 million
  65. Social an' conomj ole HIV infection is a serious public health problem because it makes people more vulnerable to malnutrition, TB and malaria. AIDS cause an adverse effect on the economic development of countries • Purchase of expensive drugs drains government funds AIDS reverse 10-15 years of economic growth for some African states.
  66. Trea ment • No cure and no vaccine for HIV Drug therapy can slow down the onset of AIDS The drugs have side effects and are expensive. • Two or more drugs (combination therapy) can prevent the replication of the virus inside the host cells. The pattern and timing of medication through the day must be strictly followed.
  67. Control Spread of AIDS is difficult to control The virus can have a long latent stage The virus can change its surface protein The present control measures - Education - Condoms, femidoms, (barrier between body fluid) - Contact-tracing (HIV test) - Needle exchange schemes - Screen-donated blood for HIV (ELISA) - HIV positive women are advised to not breast-feed.
  68. Antibiotics :-D Chemicals produced by microorganism which are capable of destroying or inhibiting the growth of other microorganisms.
  69. ! kid! a cf ido Even be de They can be synthetic (isoniazid) or derived from living organisms. Antibiotics are selective toxins, killing or disabling the pathogen without harming the host. @ÖriönaiAnist I Reproduction rights obtåinable from www.CartoonStock.com "It's a prescription for one of those new super-antibiotics. You won't just get better, you'll get even."
  70. Antibiotics interfere with some aspects of growth or metabolism of the target microorganism: Enzyme function Synthesis of bacterial walls Antibiotic's action mechanism Protein synthesis Plasma membrane function
  71. Cell wall synthesis inhibitors penicillin (b) cephalosporin (b) vancomycin (b) Membrane inhibitor polymyxin (b) DNA Transcription inhibitor rifampicin (b) RNA polymerase a — bacteriostatic (stops bacterial growth) b bactericidal (kills bacteria) Protein synthesis inhibitors chloramphenicol (a) erythromycin (b) tetracycline (a) streptomycin (b) ribosome Interfere with metabolic reactions sulpha drugs (a) The sites of action of antibiotics in bacteria
  72. Different diseases are treated with different antibiotics. • Some kinds of bacteria are completely resistant to particular antibiotics E.g. Mycobacterium tuberculosis is resistant to penicillins Other bacteria have certain strains that are resistant.
  73. Broad spectrum antibiotics EXAMPLES: 3rd gen«atbn ftMomÅnolones 2r4 3rd 4th gaEratim Cephalæporins Penicilin Lhcosami&s Rta-nycin
  74. Penicillin • In 1928, bacteriologist Alexander Fleming made a chance discovery from an already discarded, contaminated Petri dish. The mold that had contaminated the experiment turned out to contain a powerful antibiotic, penicillin. Though Fleming was credited with the discovery, it was over a decade before someone else turned penicillin into the miracle drug for the 20th century.
  75. Penicillin • In 1928, bacteriologist Alexander Fleming made a chance discovery from an already discarded, contaminated Petri dish. The mold that had contaminated the experiment turned out to contain a powerful antibiotic, penicillin. Though Fleming was credited with the discovery, it was over a decade before someone else turned penicillin into the miracle drug for the 20th century.
  76. Penicillin • Penicillin is a group of antibiotics derived from Penicillium fungi. CH3 CH3 COOH
  77. Penicillium colony Bacteria inhibited Bacteri Education. as
  78. cell wall/ synthesis inhibitor in growth medium Spherop a • Bacteria that attempt to divide in the presence of penicillin fail to do so and end up shedding their cell walls in the process.
  79. Penicdln binding protan +9, Penicillin and other ß-lactam antibiotics act by inhibiting penicillin-binding proteins, which normally catalyze cross-linking of bacterial cell walls
  80. Penicillin's ode ofA tion Penicillins functions by preventing the synthesis of the cross links between the peptidoglycan polymers in the cell walls of bacteria. They are only active against bacteria and only when they are growing. Many types of bacteria have enzymes for destroying penicillins (penicillinase) and are therefore resistant to these antibiotics.
  81. o disc impregnated with antibiotic clear area where bacteria grow bacteria growing on agar • o Figure 13.11 An antibiotic sensitivity test for a pathogenic strain of Escherichia coli. Table 13.5 shows the inhibition zone diameters for the six antibiotics. Result of an antibiotic sensitivity test carried out on a pathogenic strain of the human gut bacterium Escherichia coli. Various antibiotics are absorbed onto discs of filter paper and placed on the agar plate. The most effective antibiotics are chosen based on the diameter of the inhibition zones.
  82. Antibiotic Inhibition zone diameter (mm) Resistant s 11 12 s 11 s 12 14 Sensitive 2 14 218 2 14 22 215 19 • Table 13.5 Inhibition zone diameters for the antibiotics of figure 13.11. If the diameter of the inhibition zone for an antibiotic is equal to or less than the figure given in the first column, the bacteria are resistant to it. If the diameter is equal to or greater than the figure in the right hand column, the bacteria are sensitive and the antibiotic may be chosen for treatxnent.
  83. Antibiotics should be chosen carefully Screening antibiotics against the strain of the bacterium or fungus isolated from sufferers ensures that most of the effective antibiotics can be used in treatment.
  84. • An example of this is MRSA, (Methicillin Resistant Staphylococcus aureus) which is a bacteria that is resistant to four of the most popular antibiotics due to their inappropriate use and people not finishing their course of antibiotics — leaving antibiotic resistant bacteria to grow and spread. reslsnnce Is Futile methicillin-reslstönt Staphylococcus dureus
  85. • It is advisable to keep some antibiotics for use as the last resort when everything else has failed to lessen chances of more such resistant organisms.
  86. Antibiotic Misuse and Resistanc ÄRø•r the introduction Of ant.bZtiCS@ forms Of bacteriä rney survive. Use of antlblotlcs to treat Viral Infections Inadequate pathogen coverage Excessive use of broad-spectrum agents Sub-optimal dosing Poor adherence to antlblotlc therapy Retammg unfimshed antlblotlc for later use