SK320 Q & A - Block One
Block 1 Unit 9 Diagnosing Infection Question 9.1 (This question relates to unit learning objectives 1, 2 and 4.) A displaced person arrives at a refugee camp and complains of severe diarrhoea. Briefly suggest what diagnostic tests might be carried out to determine the cause of their condition, and any public health measures that should be adopted in the refugee camp.
Answer There are many causes of diarrhoea, and distinguishing between them may be difficult. A history should be taken from the patient, detailing any food they have recently eaten, and any contact with other people with diarrhoea. A visual examination of the stools might suggest a diagnosis: e.g. blood in the stools might mean infection with enterohaemorrhagic E. coli, whereas rice-water stools would suggest cholera. There are unlikely to be any laboratory facilities available in a refugee camp, so the patient should be isolated as far as possible from others, and strict hygienic measures applied to them. In particular, their faeces should be prevented from contaminating the drinking water. Since dehydration is a problem with all cases of diarrhoea, attempts should be made to have a rehydration solution available to any sufferers. If vaccination measures are available, they should be offered initially to vulnerable groups (the young and the elderly) and then, if resources permit, to everybody.
Block 1 Unit 2 Pathogenic Organisms. Question 2.2 (This question relates to unit learning objectives 1, 4 and 5.) List the main points of entry to the body of infectious agents and the first-line host defences for each infection route.
Answer. The main routes of infection and the corresponding first-line host defences are shown in Table 2.4. (Note that this is the same information as appears in Table 2.2 in Section 4.2.2.) View Table 2.4 Points of entry into the body by pathogens, and the body's firstline defence mechanisms.
Block 1 Unit 8 Parasitic Invertebrates Question 8.5 (This question relates to unit learning objectives 1 and 3.) Figure 8.21 outlines the life cycle of a theoretical parasitic fluke of humans. (a) List all the possible larval stages that may occur between A and B, B and C, and C and A. (b) Indicate where, and by what means, measures might be applied to exert control and/or prevention of the transmission of this parasite from one human host to another.
Answer (a) Between A and B: miracidium; between B and C: sporocyst, redia, cercaria, metacercaria; between C and A: metacercaria (this develops into the adult worm, which produces eggs that are released in the faeces into water). (b) A: prevent human faeces from contaminating the water supply. B: attempt to kill the snail by the use of molluscicides, or introduce a predator of the snail. C: clear the vegetation, or avoid eating it. If it is to be eaten, clean and cook it properly beforehand
Block 1 Case Study - Cholera Question 1.4 (This question relates to case study learning objectives 6 and 7.) A patient presents with rice-water stools and severe dehydration. (a) Explain in fewer than 150 words what patient samples (and what techniques) could be used to diagnose cholera. (b) What short-term treatment could be used to combat cholera in this patient?
Answer (a) A stool sample will show motile curved rod-shaped Vibrio bacteria if the patient is infected with cholera. These bacteria can be typed by adding Inaba or Ogawa antisera to the wet-mount sample and observing if the bacteria cease moving (a positive result, due to antibodies binding the H antigens present in the flagella). Also, a faecal sample can be grown in peptone water and then used in an oxidase test, as V. cholerae is oxidase positive. In parallel, a bacterial sample in peptone water can plated on a TCBS agar plate: V. cholerae produces yellow colonies (with no blackening) on TCBS agar plates. (105 words) (b) Immediate treatment with oral rehydration salts is a cheap and very effective treatment against cholera.
Block 1 Case Study - Cholera Question 1.2 (This question relates to case study learning objectives 3 and 4.) (a) Explain, in a few words, the main symptoms of cholera. (b) What is happening at the cellular level in the gut of somebody with cholera to cause these symptoms? (Answer in less than 200 words.)
Answer (a) The main symptom is profuse, cloudy, watery diarrhoea; often called 'rice stools', and related severe dehydration. (b) Rice stools occur because of an osmotic imbalance in the gut that causes water and electrolytes to be drawn out of the epithelial cells into the lumen. The mechanism of this process is as follows: (1) Cholera toxin binds GM1 ganglioside on gut epithelial cells and is internalised. The clustering of GM1 ganglioside on the apical surface causes neighbouring potassium ion channels to open, allowing K+ ions to escape from the cell. (2) The A subunit of the toxin catalyses the addition of ADP-ribose to a G protein, altering its function so that it can no longer switch off adenylate cyclase. (3) The increased adenylate cyclase activity raises cAMP levels in the cell, causing dysregulation of ion channels in the apical membrane, preventing the entry of Na+ ions, and allowing Cl- and HCO3 - ions to escape from the cell. (4) The accumulation of Na+, K+, Cl- and HCO3 - ions on the gut side of the epithelium draws water out of the epithelial cells by osmosis, resulting in copious amounts of water in the gut lumen. (5) This process also causes the gut lumen to become more alkaline, creating the optimum growth conditions for the vibrios.
Block 1 Unit 8 Parasitic Invertebrates Activity 8.1 Digital Microscope 'Parasites II' slides Allow 1 hour Access the Digital Microscope section of the module website or access the appropriate part of the module DVD. When you have the application open select the 'Parasites II' slide set from the 'Catalogue' box at the top right of the screen. This set comprises 22 slides, including examples of: Ascaris, Fasciola, Clonorchis, Schistosoma, Paragonimus, Taenia, Trichuris, Trichinella, and a calibration slide for measurement purposes. Work through the slides from top left to bottom right, reading the descriptions of each one. Please feel free to browse around the images too. Where necessary you may wish to review the relevant section(s) of this unit in order to put the microscopy into a broader context. For the purposes of discussing these slides with your tutor and other students, we recommend you quote the X and Y coordinates of any objects or features that interest you and the magnification that you are using. After viewing the 'Parasites II' slides, you should be able to use the Digital Microscope to answer the following questions. Question 8.1 Examine Slides 1-3 (nematode) 6, 7, 13, 16 (flukes) and 17 (tapeworm) in the 'Parasites II' set. Describe how each group of parasites obtains nutrients and removes waste.
Answer . Nematodes: ingest food by mouth only and expel waste via the anus. . Flukes: suction by mouth and some by absorption across the metabolically active tegument. Most have bifurcate caeca. Waste via the mouth. . Tapeworms: absorb all nutrients across the tegument. No waste.
Block 1 Unit 5 Bacteria Question 5.7 (This question relates to unit learning objectives 1 and 8.) List the routes of infection used by the following pathogens: . Yersinia pestis, . Staphylococcus aureus, . Corynebacterium diphtheriae, . Neisseria gonorrhoea, . Salmonella typhi, . Escherichia coli.
Answer . Yersinia is transmitted by an insect bite or via the air as pneumonic plague. . Staphylococcus enters via broken skin. . Corynebacterium is an airborne respiratory pathogen. . Neisseria is sexually transmitted. . Salmonella is a gut pathogen that is transmitted by infected food and water. . E. coli can be food-borne, but may also be a commensal that becomes an opportunistic pathogen.
Block 1 Unit 9 Diagnosing Infection Question 9.2 (This question relates to unit learning objectives 1, 3 and 4.) Imagine that your child complains of a headache and has a rash on their chest. Assuming you live in a developed country with health advice readily available, describe the events that might take place to help your child recover. What steps might also be taken to protect the health of other individuals?
Answer As an anxious parent you would probably begin by taking your child to the family doctor. The doctor would examine the child to assess her symptoms, and would take a history from you both to establish whether you had recently travelled to an area with particular endemic diseases, or been in contact with infected persons. This information, together with features like the appearance and location of the rash, would allow the doctor to make an initial diagnosis. The doctor's initial diagnosis might also depend on their knowledge of any current local epidemics, such as measles in local schools. If the doctor was confident in diagnosing a straightforward childhood illness, you would be sent home with appropriate therapeutic advice, to wait for your child to recover. However, in less certain cases the doctor could take samples to send to the local clinical microbiology laboratory, making sure that they were labelled correctly. If a bacterial infection was suspected, the laboratory would culture the samples using non-selective and selective media, and would assess the antibiotic sensitivity profile of any identified pathogen. This information would be conveyed back to the doctor, who could then quickly prescribe a suitable antibiotic. For non-bacterial diseases the culture period would be longer, and therapy might begin before the diagnosis was finalised (this might happen anyway if the child was seriously ill). If the infection was notifiable, the laboratory would contact the authorities.
Block 1 Unit 4 Prions Question 4.2 (This question relates to unit learning objectives 1-4.) Dog carcases are usually destroyed by incineration, but an unscrupulous dog food manufacturer believes that they could be economically recycled into dog food. Assuming the scenario in Question 4.1, how would you advise the government on this matter?
Answer As in the cases of scrapie and BSE, the industrial processes involved in rendering carcases and preparing animal feed from them are insufficient to destroy prions. Therefore if MDD-infected dog carcases were fed to other dogs, many more MDD cases might be expected to appear. Dogs have a fairly short lifespan, and TSEs are generally slow diseases, but quicker onsets are possible, as with vCJD. Thus from an animal-welfare perspective you would probably advise the government not to allow this recycling process. However, governments are pragmatic, and may consider that there is no danger to humans, as dogs do not often (in the UK at least) enter the human food chain. You might counter this argument by pointing out that there remains a danger to people who handle the processed meat, including many dog owners who are also voters. Moreover, there are well documented cases when prions have unexpectedly arisen, such as in the original transmission of the mutant prion to cows. Events such as this are unpredictable, all the more so since prions are relatively poorly understood. In the circumstances, you would probably advise the government to legislate as quickly as possible against the use of infected carcases of any species in any food production system. Whether your advice would be heeded is another matter!
Block 1 Unit 6 Protists Question 6.2 Using the ×40 objective of the Digital Microscope, estimate the percentage parasitaemia in the 'Malaria 36 hour' sample (Slide 3 of the 'Parasites I' set) and the 'Malaria 48 hour schizonts' sample (Slide 4). For the purposes of this question, observing the number of parasites per 250-300 RBCs should be adequate to calculate percentage parasitaemia. We suggest you move around the slide to about five or six different (non-overlapping) fields of view and record the number of parasites and RBCs that you see until you have counted at least 250 RBCs and can then more reliably determine what percentage of these contain Plasmodium parasites. Note: a RBC infected with multiple parasites only counts as one parasitised red cell. Hints: to avoid miscounting, it's a good idea to mask the field of view with a piece of paper and count cells that appear as you slowly reveal the image; using the 'grid' on the microscope will also help you.
Answer Because the RBCs are not dense enough to be touching, there are small regional differences in cell density that mean that your values are unlikely to be exactly the same as ours, below. 'Malaria 36 hours' (Slide 3) Five fields of view counted: . Field 1: 62 red blood cells (RBCs), 3 infected . Field 2: 73 RBCs, 4 infected . Field 3: 65 RBCs, 8 infected . Field 4: 55 RBCs, 4 infected . Field 5: 63 RBCs, 4 infected Total: 318 RBCs, 23 infected. So the percentage parasitaemia in the sample is 100/318 × 23 = 7.2%. 'Malaria 48 hour schizonts' (Slide 4) Five fields of view counted: . Field 1: 46 RBCs, 5 infected . Field 2: 47 RBCs, 5 infected . Field 3: 42 RBCs, 5 infected . Field 4: 48 RBCs, 2 infected . Field 5: 39 RBCs, 4 infected . Field 6: 51 RBCs, 1 infected Total: 273 RBCs, 22 infected. So the percentage parasitaemia in the sample is 100/273 × 22 = 8.1%. Summary The percentage parasitaemia is quite similar in both slides, but slightly more in the 48-hour sample. Percentage parasitaemia in non-falciparum malaria rarely exceeds 2%, whereas in falciparum malaria (shown in Slides 3 and 4) it can exceed 50%. However, in falciparum malaria RBCs can become stuck in capillaries, giving a falsely low count of the 'visible' parasitaemia in the peripheral blood. For this reason, the developmental stage of the parasite also gives important information, since a higher proportion of more mature stages (>20% late trophozoites and schizonts) indicates a more advanced disease and worse prognosis.
Block 1 Unit 7 Fungi Question 7.2 (This question relates to unit learning objectives 1-3.) How does Candida cause balanitis?
Answer Candida is a frequent commensal of the skin, mouth, gut and vagina. If the fungus is transferred to, and grows on, the penis, its feeding mechanism means that extracellular enzymes will be poured onto the tissue. This results in tissue breakdown and inflammation, and general redness and soreness.
Block 1 Unit 5 Bacteria Question 5.3 (This question relates to unit learning objectives 1 and 5.) Lactobacillus acidophilus (Doderlein's bacillus) colonises the vagina and metabolises glycogen, produced by the action of circulating oestrogen hormones. In doing so, it protects the female genital tract from infection. Briefly research this bacterium and explain (in 4-5 sentences) how it protects the vagina from infections, and how this mechanism could be affected by antibiotic treatment.
Answer Doderlein's bacillus is a commensal species that lives in the vagina of women of reproductive age. The bacillus metabolises glycogen in the vaginal epithelial cells, producing lactic acid. This reduces the vaginal pH to around 5.0, which is too low for many other species, including many pathogens. If antibiotic treatment kills the Doderlein's bacilli, the vaginal pH rises, allowing opportunistic or exogenous infections to take hold.
Block 1 Unit 9 Diagnosing Infection Question 9.4 (This question relates to unit learning objectives 1 and 5.) Suppose you are a medical laboratory technician in a well-equipped and well-funded laboratory. What tests would you carry out on samples from a patient with a respiratory disease?
Answer In the absence of any further information about the patient, you do not know whether the suspected cause of the infection is viral (e.g. influenza), bacterial (e.g. TB) or something more unusual. Being pragmatic, you would test for the more obvious things first. To test for influenza you could try to identify viral antigens in the sample by immunofluorescence. You might also carry out a haemagglutination test. If the presence of influenza virus was confirmed, you could identify the type by doing a haemagglutination inhibition assay and a neuraminidase inhibition assay, or a PCR test followed by sequencing to determine any strain variations. To test the sample for TB, the first approach is to analyse the sample microscopically. You could try to detect TB bacilli by immunofluorescence microscopy, or you could do a Ziehl-Neelsen stain to identify any mycobacteria in the sample. A positive identification by Ziehl-Neelsen is conclusive, but you might also wish to identify mycobacterial DNA by PCR analysis. Mycobacterium tuberculosis is difficult to grow in culture, and needs to be grown in egg-based media. The cultures are very slow-growing, so screening for drug resistance is a slow process. If neither of these approaches yielded a firm diagnosis, you would look further afield, and culture any microbes in the patient's sample on a non-selective medium. Any that grew, and were not part of the normal flora, could then be selectively cultured, and, hopefully, identified.
Block 1 Unit 5 Bacteria Question 5.8 (This question relates to unit learning objectives 1 and 10.) What is the rationale of phage therapy?
Answer Like all organisms, bacteria are subject to attack by viruses: in this case bacteriophages or phages. Phages target specific bacterial strains, so the use of particular phages against known infections leaves the commensal biota unaffected. Moreover, phages target only bacteria so the human cells are also unaffected. Phages show particular promise where the infecting bacteria are antibiotic resistant, or living in a biofilm. However, bacterial resistance to phages via the CRISPR system may limit the effectiveness of phage therapy.
Block 1 Case Study - Tuberculosis Question 1.2 (This question relates to case study learning objective 8.) What is multidrug-resistant TB (MDR-TB)? How does it differ from extensively drug-resistant TB (XDR-TB)?
Answer MDR-TB is active TB involving M. tuberculosis bacteria that are resistant to at least isoniazid and rifampicin: the two most powerful anti- TB agents. XDR-TB is resistant to isoniazid and rifampicin, but also to fluoroquinolones and any of the second-line drugs: amikacin, kanamycin or capreomycin.
Block 1 Unit 9 Diagnosing Infection Question 9.3 (This question relates to unit learning objectives 1 and 6.) Why is it necessary to flame the necks of bottles when transferring microbial material in and out of them?
Answer Microbes are readily carried in tiny droplets in aerosols, and can easily spread to the environment. Flaming the necks of bottles in a Bunsen burner flame causes an updraft which carries away any aerosols and microbes. As the microbes are carried into the flame by the updraft, they are destroyed, thus protecting both the operator and the surroundings from microbial contamination
Block 1 Case Study - Tuberculosis Question 1.4 (This question relates to case study learning objective 8) Imagine that a pharmaceutical company plans to launch a new combination product containing two new active ingredients, for the treatment of pulmonary TB. Suppose that trials have shown that the treatment is effective, and the company plans to launch the product in Europe and in North America. Below are listed four features of the hypothetical product and the characteristics of three imaginary patients (A-C). For each patient, identify those product features that are particularly relevant and in each case explain your reasoning. (Note: no detailed information is needed on the drugs incorporated in the new product or on other drugs these patients may be taking concurrently.) Product features: (1) The product demonstrates some interactions with some other medicines. (2) One of the drugs included in the product is metabolised (inactivated) in the liver. (3) One of the drugs in the combination has shown slight fetal toxicity in animal tests. (4) The product is available in two strengths as a skin patch (similar to nicotine patches for smoking cessation). The stronger strength is used for six weeks, and the weaker strength for four months. A fresh patch needs to be applied every 12 hours. (Note: this is a hypothetical product and any resemblance to any product already on the market or in development is accidental.) Patient descriptions: (A) A 70-year-old woman with high blood pressure and osteoarthritis. (B) A 29-year-old mother of a child aged 18 months. (C) A homeless alcoholic man.
Answer Patient A: This patient will already be taking several other medicines, so the possibility of drug interactions (feature 1) would need to be checked. The skin patch (feature 4) would probably be an asset, because usage will be simpler for a patient with disability to manage and she will already be taking other medicines in the form of tablets or capsules. Patient B: The principal concern of this patient would be the evidence that one of the drugs might be toxic for a developing fetus (feature 3) and is unlikely to be prescribed for pregnant women. So the issue of any possible further pregnancies would have to be addressed. Patient C: The main issues for this patient are the metabolism of the drugs and compliance. His alcoholism is likely to have damaged his liver, so he will probably not metabolise drugs in the 'normal' way and doses might have to be adjusted, but one drug in this product (feature 2) may present a particular problem. The patient's lifestyle would seem to make the skin patch (feature 4) the simplest way of delivering therapy, but replacing it every 12 hours would still present a serious problem for compliance.
Block 1 Case Study - Malaria Activity 1.2 Host responses to malaria Allow 1 hour Watch the immunology interactive malaria mini-lecture by David Male and make notes on it. To fully understand this mini-lecture, you will need to have studied Block 2 Unit 2, but there are elements that offer further insights into the content in Block 1. Video 1.2 Malaria and immune responses mini-lecture You should be able to answer the following questions after watching this mini-lecture. (1) What types of immune defence are appropriate for dealing with sporozoites? (2) What immune defences can recognise parasitised red cells? (3) How does Plasmodium falciparum produce the symptoms of cerebral malaria? (4) What role does the circumsporozoite (CS) antigen have in evading immune responses? (5) Do T cells have any role in protective immunity? Explain your answer in a few sentences. (6) What evidence is there that genetic polymorphisms affect susceptibility to malaria?
Answer Question 1 Antibodies can intercept sporozoites in the bloodstream. Question 2 Antibody-dependent cell-mediated cytotoxicity, effected by large granular lymphocytes (K cells). The parasitised cells may also be targeted by antibody against surface molecules, and complement. Question 3 Antigens of P. falciparum insert into the membrane of the parasitised red cell and cause it to attach to endothelial cells in the brain. This can cause local obstruction of the vessels, but also induces local inflammation. Question 4 CS antigens are shed in the presence of immune serum, thereby acting as a decoy for the immune system. Question 5 Yes, both CD4 and CD8 T cells are involved, possibly by releasing IFNγ and activating macrophages. If T cells had no role, then we would not see the genetic association with particular MHC haplotypes. Question 6 Human populations in endemic malaria areas have a higher proportion of MHC haplotypes, which confer immunity, than in non-endemic areas (e.g. HLA-B53). The sickle cell anaemia gene is also partially protective in heterozygotes and this helps to maintain an otherwise disadvantageous gene in the population of malarial areas.
Block 1 Case Study - Malaria Activity 1.1 Introduction to malaria Allow 1 hour Watch the video mini-lecture by David Warhurst of the London School of Hygiene and Tropical Medicine. It will be useful for you to have a diagram of the lifecycle of Plasmodium (Figure 1.1) nearby to help you understand the first half of the mini-lecture (up to Slide 23). If you wish to make notes on this lecture, you can find a printable slide handout sheet in the 'Study resources' section of the module website. Be aware that while Slides 47-54 (which deal with cell adhesion molecules and the genetic adaptations of human populations against malaria infection) are very interesting, their content is not an essential part of this activity. Video 1.1 Malaria introduction mini-lecture You should be able to answer the following questions after watching this minilecture. (1) What is the usual reservoir of infection for malaria parasites and how is this different for Plasmodium knowlesi? (2) In endemic areas, which two groups of people are at greatest risk of death from malaria? (3) What climatic conditions favour malaria transmission? (4) What human behaviours can help limit or prevent malaria transmission?
Answer Question 1 Humans are the normal reservoir and the intermediate host of Plasmodium (thus the disease is an anthroponosis). The exception is P. knowlesi, for which monkeys are the reservoir of infection for human transmission (i.e. a zoonosis). (See Slide 3.) Question 2 Pregnant women and infants are at greatest risk of death from malaria in endemic areas. (See Slide 24.) Question 3 Factors include a required relative humidity above 45% (mosquitoes do not feed below this limit) and sufficiently warm temperatures. The time required for the parasite to mature in the mosquito is temperature dependent. Below a threshold temperature, the maturation time of the parasite exceeds the lifespan of the mosquito, so transmission becomes impossible. (See Slides 25-26.) Question 4 Public health education programmes and knowledge of the malaria cycle. Also, the use of insecticides, insecticide-impregnated bed nets, and the draining or covering of pools where the mosquitos could otherwise lay eggs and hatch. (See Slides 31-35.)
Block 1 Unit 9 Diagnosing Infection Activity 9.1 Antimicrobial susceptibility testing Allow 2 hours Watch the mini-lecture by Alan Johnson from the Health Protection Agency (Video 9.6), in which he describes in some detail the widely used methods for qualitatively and quantitatively assessing antibiotic resistance in clinical isolates. He also highlights the differences in standards set by professional groups across the world, in particular variation between recommendations from the European Committee on Antimicrobial Susceptibility Testing (EUCAST) and the Clinical and Laboratory Standards Institute (CLSI) from the USA. The last part of the video describes some new methodology for automatic testing, which is likely to become more widely available over the next few years. Video 9.6 Conventional and automated methods of antimicrobial susceptibility testing. (A transcript of this video is available from the 'Study resources' section of the module website.) Make notes on this mini-lecture (using, if you wish, the printable slide handout sheet in the 'Study resources' section of the module website) and ensure that you can answer the following questions: (1) Explain how antibiotic concentration is related to growth patterns in disc and strip tests. (2) Explain what breakpoints, are and how they are used clinically. (3) Describe how diagnostic processes can be automated.
Answer Question 1 Slides 7 and 8 (02:14-03:17) demonstrate the appearance of bacterial plates when using antibiotic disc tests, while Slide 25 (11:35) demonstrates the appearance of bacterial plates when using strip tests. Question 2 See 13:00-22:27. Breakpoints are specific MIC values or zone of inhibition diameters that define bacteria that are 'susceptible', 'intermediate' or 'resistant' to a specified antibiotic. Clinical breakpoints (15:00) are used to determine whether a given antibiotic concentration is likely to successfully treat a bacterial infection. The question of whether that concentration can be realistically achieved in the patient forms part of the decision about which antibiotic to use. Question 3 See 22:27-29:15. By using computerised optical plate readers to measure the diameters of zones of inhibition, or machine-readable plastic cards containing multi wells for growing bacteria in different concentrations and types of antibiotics (e.g. Vitek system).
Block 1 Unit 5 Bacteria Question 5.1 (This question relates to unit learning objectives 1 and 2.) Complete Table 5.6 by using the rules of nomenclature to write the plural forms of the genera shown. The first one is done for you. Table 5.6 Plural forms of the genus of some common bacteria Genus________________________________ Plural form Bordetella__________________________ bordetellae Borrelia Clostridium Corynebacterium Neisseria Salmonella Shigella Yersinia
Answer Table 5.7 is a completed version of Table 5.6. Table 5.7 Completed version of Table 5.6 Genus ___________________________Plural form Bordetella----------------- bordetellae Borrelia ------------------- borreliae Clostridium---------------- clostridia Corynebacterium--------- corynebacteria Neisseria------------------- neisseriae Salmonella----------------- salmonellae Shigella--------------------- shigellae Yersinia---------------------- yersiniae
Block 1 Unit 8 Parasitic Invertebrates Question 8.3 (This question relates to unit learning objectives 1 and 3.) Briefly explain the difference between the terms 'definitive host' and 'intermediate host' in the life cycle of parasitic worms
Answer The definitive host harbours the sexually mature stage of the parasite. The intermediate host harbours a series of different larval stages, which often undergo asexual reproduction, so increasing the chance of transmission to the definitive host.
Block 1 Case Study - Tuberculosis Question 1.1 Study Figure 1.2. What does it show? Can you explain these results in three or four sentences using your general knowledge?
Answer The figure shows that the mortality rate from TB in the USA decreased from at least 1930, until 1949. When streptomycin was introduced in 1944, the decrease in the mortality rate became sharper. The decrease in the TB deaths that occurred before the introduction of antibiotics may have been due to better standards of living, especially in cities.
Block 1 Case Study - Cholera Question 1.3 (This question relates to case study learning objective 5.) Describe in fewer than 75 words the body's response to infection with V. cholerae.
Answer The gut lymphoid tissue (Peyer's patches) recognises the vibrios and cholera toxin as foreign and initiates an immune response. Antibodies IgA and IgM are released into the mucus secretions of the gut to bind and inactivate the cholera bacteria and the toxin. IgG is produced in the bloodstream and some of this leaks into the gut in areas of damage to further combat the cholera infection. (66 words)
Block 1 Unit 7 Fungi Question 7.1 (This question relates to unit learning objectives 1 and 3.) A farm worker goes to a doctor with a mycosis on his foot. Suggest three possible routes by which he could have acquired this infection.
Answer The infection might be one of the following: (1) tinea pedis, acquired from another person (2) a ringworm acquired from a farm animal (3) a subcutaneous mycosis acquired from fungal spores in the soil.
Block 1 Unit 8 Parasitic Invertebrates Question 8.4 (This question relates to unit learning objectives 1 and 2.) In the city of Rio de Janeiro, a hypothetical common invertebrate parasite, whose definitive host is human, has an intermediate host that lives in freshwater ponds. Investigations show that poor people living at the bottom of the nearby Sugarloaf Mountain are ten times more likely to be infested with the worm than wealthy people living 500 m up the mountain. Suggest two reasons why this might be so.
Answer The reasons could be biological or social. The prevalence of the secondary host may be lower at a higher altitude because of factors such as temperature, rainfall or rate of water evaporation. In Rio, people with more money tend to live further up Sugarloaf Mountain than the poor, who live at the bottom. With more money comes better sanitation, cleaner water and living conditions, and better general health. Both groups of factors could explain the observation.
Block 1 Unit 5 Bacteria Question 5.4 (This question relates to unit learning objectives 1 and 6.) Give one example of each class of microbial toxin, and explain briefly its mode of action.
Answer The two classes of microbial toxin are endotoxins and exotoxins. Endotoxins are components of the bacterial surface, and the most wellknown is lipopolysaccharide, LPS. This works by stimulating the host's immune system to produce fever and endotoxic shock. Exotoxins are (usually) proteins secreted by pathogens that can cause symptoms even in the absence of the pathogen itself. They have a variety of actions: they may bind to host cell surface receptors, thereby initiating signalling pathways (cholera toxin affects ion channels); they may disrupt host cell membranes (pertussis cytotoxin kills ciliated epithelial cells); or they may target intracellular components (diptheria toxin interferes with protein synthesis). You may have used different examples.
Block 1 Unit 5 Bacteria Question 5.2 (This question relates to unit learning objectives 1-4.) Make a list of molecules found in acid-fast bacteria that might be used as targets for selective toxicity.
Answer There are three main substances that are found only in the cell walls of acid-fast mycobacteria and so could be targets for selective toxicity: (1) Arabinogalactan, the branched polymer made of alternating arabinose and galactose residues, which is just outside the peptidoglycan layer. (2) Mycolic acid, the long-chain fatty acid that gives the bacteria a waxy coating and is covalently attached to the arabinogalactan. (3) Lipo-arabinomannan and the other glycolipids that form the outermost layer of the mycobacterial cell. Any of these three mycobacterial cell wall components could be targets for antimycobacterial drugs.
Block 1 Case Study - Malaria Question 1.1 (This question relates to learning objectives 1 and 2) What are the relative merits of thin and thick blood smears for diagnosing malaria?
Answer Thick films allow quantitation of the density of parasites in the patient's blood and are quite sensitive (as few as five parasites per microlitre can be detected). Thin films provide a much clearer view than thick films and allow the species of Plasmodium parasite and the various stages of the erythrocytic lifecycle to be identified. However, thin films take much longer to analyse than thick films.
Block 1 Case Study - Tuberculosis Question 1.3 (This question relates to case study learning objectives 4 and 8.) A 32-year-old male patient was diagnosed with HIV three months ago; he was started on antiviral therapy ten weeks ago. He has since presented with cough that produces whitish sputum, and a low-grade fever of one month's duration. State what could be the cause of these most-recent symptoms, and briefly explain what procedures would need to take place to test your initial diagnosis. What advice should also be given to the patient and his family?
Answer This HIV patient should be suspected of having tuberculosis or other infections that occur at the late stage of HIV. You should refer the patient for possible TB diagnosis, including clinical evaluation, sputum examination (Ziehl-Neelsen stain, followed by microscopy) and a chest X-ray. As well as initiating these further tests you should advise the patient not to stop taking his antiviral drugs. You should also advise screening for TB of family members, as well as tests for HIV.
Block 1 Unit 4 Prions Question 4.1 (This question relates to unit learning objectives 1-3.) Suppose that a hypothetical condition, 'mad dog disease' (MDD), is starting to appear among domestic pet dogs. Describe in a few paragraphs the kinds of evidence that might lead you to believe that MDD is a TSE caused by a prion.
Answer To determine whether MDD is a TSE, you would need to examine the brains of affected dogs microscopically to see whether changes consistent with a TSE were occurring. Next, you would need to rule out the involvement of more conventional pathogens. You would probably look for non-canine nucleic acid in the affected animals. It is likely that you would find plenty; the crucial test is whether you find nucleic acid from the same pathogen in all the affected dogs (remember Koch's postulates). If this failed, you would begin a search for a protein molecule closely resembling a canine neuron membrane glycoprotein, that was insoluble in mild detergents and resistant to Proteinase K. If you found such a molecule, you would test your hypothesis by injecting it into healthy dogs and seeing if they developed MDD. If they did, this would be strong evidence that MDD is a TSE caused by a prion.
Block 1 Unit 5 Bacteria Question 5.5 (This question relates to unit learning objectives 1 and 6.) Explain what is meant by a virulence factor, and give an example of each group of virulence factors.
Answer Virulence factors are factors that assist pathogens in the infective process. They are generally encoded in pathogenicity islands. They act in mediating attachment of pathogen to host (adhesins, pili or fimbriae, capsules), in aiding pathogen nutrition (siderophores), or in facilitating pathogen spread (flagella, toxins, degradative enzymes).
Block 1 Case Study - Malaria Question 1.2 (This question relates to learning objectives 1 and 4) What is similar about the mechanism of action of quinoline and artemisinin antimalarial drugs?
Answer Within the erythrocyte, Plasmodium digests haemoglobin as a food source, forming toxic heme as a byproduct. The parasite counteracts this toxicity by converting heme to non-toxic crystals of hemozoin. Quinoline and artemisinin drugs are transported to the food vacuole and inhibit this conversion, thereby poisoning the parasite with its own waste products.
Block 1 Unit 5 Bacteria Question 5.6 (This question relates to unit learning objectives 1 and 7.) Host organisms have a number of structures and processes that protect them against infection. List and briefly describe five barriers, and for each one explain how the barrier can be overcome.
Answer You could have chosen any five of the following: (1) Negative charge: bacteria and host cells are both negatively charged, so there is a repulsion between them. This can be overcome by 'anchors' such as bacterial adhesins. (2) Impermeable skin: skin is dry and impenetrable, and can usually only be breached through a wound or burn. Pseudomonas aeruginosa infects in this way. (3) Impermeable epithelia: many bacteria get no further than epithelial surfaces, although they can colonise these and cause a localised infection. Bordetella pertussis causes respiratory infections in this way. (4) Mucociliary escalator: this generally acts to remove bacteria from the airways, but some toxins, such as those produced by Bordetella pertussis, can inhibit its action and allow infection to establish. (5) Antibodies in secretions such as saliva, sweat or tears: this can be overcome if there are more bacteria than antibodies that recognise them, either because the bacteria have not been encountered before, or because there are so many of them that they outnumber the specific antibodies. (6) Lysozyme in tears: lysozyme causes bacteria to lyse, but a heavy inoculum will mean that some bacteria survive for long enough to establish an infection. (7) Flushing by urine, tears, etc. Some bacteria resist the flushing action by strong adhesion to host surfaces via adhesins such as flagella (Vibrio cholera) or haemagglutinins (Helicobacter pylori or Bordetella pertussis). (8) Bindingtofibronectin to aid elimination of bacteria: note, however, that bacteria such as Treponema pallidum pallidum and Staphylococcus aureus can specifically bind to fibronectin, using it as a receptor to access the tissues below.
Block 1 Unit 8 Parasitic Invertebrates Question 8.2 Examine Slides 19-21 and note any features that you observe that are atypical of nematodes.
Answer You should observe the presence of the stichosome - a column of secretory cells associated with the oesophagus. It is characteristic of the trichocephalida order of roundworms, which includes trichina worms (Trichinella spp.) and whipworms (Trichuris spp.). Other features include a viviparous female and an intracellular larval stage. The stichosome of Trichuris can be seen on Slide 19 in several locations, including the following X, Y coordinates: 3692, 7646 (at ×10 magnification). The larvae of Trichinella are visible in the uterus of the parasite in Slide 20 at coordinates 1654, 3678 (at ×20 magnification). The intracellular larval stage is visible inside the 'nurse cell'.
Block 1 Case Study - Cholera Question 1.1 (This question relates to case study learning objectives 1 and 2.) What key pieces of evidence suggest that: (a) cholera is a water-borne (rather than an air-borne) disease; and (b) V. cholerae is the causative agent?
Answer (a) John Snow's realisation, in 1854, that many cases of cholera in Golden Square centred on the use of one communal water pump played a major role in demonstrating that cholera is a water-borne disease. When he disabled this pump, the local cholera cases subsided. (b) Robert Koch demonstrated in 1884 that a distinctive comma-shaped bacterium (Vibrio cholerae) was present in the gut of cholera patients, and could be spread via dirty water.
Block 1 Unit 6 Protists Activity 6.1 Human African trypanosomiasis (HAT) Allow 1 hour Watch the mini-lecture (Video 6.1) on human African trypanosomiasis by Ken Hudson. The lecture cover the life cycle and epidemiology of trypanosomes, and the genetic basis for how they frequently change their surface proteins in order to evade the host's immune defences. You should be able to answer the following questions after watching the minilecture: 1 HowareAfricantrypanosomesabletoproduceprolongedinfectionsin vertebrate hosts? 2 HowcantheAfricantrypanosomeachievethiscomparedwiththe situation in the Influenza virus? 3 Outlinethegeneticmechanismbywhichvariantsurfaceglycoprotein (VSG) antigen change is achieved. (Note: some researchers prefer the term 'variant specific glycoprotein'. The two terms are interchangeable.) 4 ThetrypanosomegenomecontainsmanyVSGpseudogenes- do these pseudogenes play any role? 5 WhyaretherenovaccinesagainstAfricantrypanosomes?
Answer Question 1 The prime means of producing prolonged infections relates to the trypanosome's ability to vary a major surface antigen (the variant surface antigen, VSG) within a single infection, thus progressively evading the immune response of the host. Question 2 The African trypanosomes have an extensive repertoire of genes (perhaps up to 1700) for these VSGs in their genome, of which, in any individual trypanosome, just a single gene is expressed at any one time, whereas the influenza virus depends on mutation and also recombination between the genome of different viruses. Question 3 The expression of a VSG gene is primarily dependent on a recombination process called gene conversion. Here non-expressed versions of a VSG gene are copied from an internal chromosome site into one of a number of sub-telomeric expression sites. Question 4 Early in infection, gene conversion via recombination appears to involve complete VSG genes. However at later stages of infection parts of nonexpressed VSG pseudogenes appear able to recombine with VSG genes already in an expression site and produce novel complete genes. Question 5 The ability to vary their surface antigens is so extensive that it has, so far, completely frustrated any attempt to produce vaccines.
Block 1 Unit 6 Protists After viewing the 'Parasites I' slides, you should be able to use the Digital Microscope to answer the following questions. Question 6.1 Trypanosomes are able to sense their own concentration within the blood, and above a critical threshold density they will differentiate from the dividing long slender form to the short stumpy non-dividing form. It has been speculated that this is an adaptation to prevent the parasitemia from killing the host - a necessity when tsetse bites are infrequent (Vassella et al., 1997). Accordingly, a study by Nolan et al. (2001) showed that mice infected with T. brucei brucei initially show mostly long, slender forms of the parasite within the blood two days after infection, which are gradually replaced by stumpy forms by the eighth days post infection (see Figure 1 in that paper). Long slender forms of T. brucei brucei are typically 23-30 μm in length, while short stumpy forms have lost their flagellum and are typically 17-22 μm long (Uilenberg, 1998, Chapter 1 Figure 6). Use the Digital Microscope to examine Slide 8 from the 'Parasites I' slide set. This shows T. brucei brucei in a mouse blood sample. Switch on the graticule and calibrate it using the 'Calibration' slide (Slide 12) with the ×20 objective. Then measure the lengths of a random selection of T. brucei brucei parasites in Slide 8 and make a note of this average value (measurements of about ten parasites should be sufficient). Using the information already given to you in this question, determine whether this is an early or a late stage infection with T. brucei brucei.
Answer With the calibration slide at a magnification of ×20, the distance from the start of one calibration black line to the start of the next calibration black line is 20 μm, and this corresponds to two major units of the red graticule (which is the same as four minor red graticule units). Thus, each major unit is 20 ÷ 2 = 10 μm. Each parasite measures around 2 or 3 of the major graticule units (i.e. 4-6 minor units) in length. The length of each parasite is therefore approximately 20-30 μm. Because all of the parasites are of the long slender type (around 23- 30 μm long) this sample has been taken at an early stage of infection, before the parasite density has become high enough to trigger differentiation to the non-dividing stumpy form.
Block 1 Unit 3 Viruses. Question 3.6 (This question relates to unit learning objectives 1 and 6.) Several viral infections give rise to skin rashes, and the exact appearance of the rash is often important for diagnosis. Match the list of skin disorders (A-E) with infections by either (a) the measles virus or (b) the smallpox virus. A: Koplick's spots B: pustules C: papules D: macules E: vesicles
Answer. (a) Disorders A, C and D are symptoms of measles. (b) Disorders B and E are symptoms of smallpox.
Block 1 Unit 3 Viruses. Question 3.5 (This question relates to unit learning objectives 1 and 5.) (a) What are the possible cytopathic effects of viral infection? (b) Are any of these changes seen following infection with cytocidal viruses?
Answer. (a) The main cytopathic effects are: changes in appearance, such as rounding up or syncytium formation; the formation of inclusion bodies; membrane damage; triggering of apoptosis; and transformation. (b) Membrane damage and triggering of apoptosis are commonly seen with cytocidal viral infections.
Block 1 Unit 1 Infectious Diseases: an Introduction. Question 1.5 (This question relates to learning objective 5.) The population of Scotland has been stable at just over 5 million people since the 1950s and is predicted to remain so for at least the next 20 years. However, the age structure has been shifting towards an older profile and this trend is expected to accelerate in the future. Between 1991 and 2000 there was a fall of 2% in the proportion aged under 14 years, and a further fall of 16% in this age group is projected to occur by 2021. (a) Why must the change in age structure be taken into account when evaluating trends in childhood infectious diseases in Scotland? (b) Explain why children are the principal 'population at risk' from infections such as measles.
Answer. (a). In estimating trends in the impact of childhood infections in a population over time, account must be taken of changes in the size of the population 'at risk'. In Scotland (as in other high-income nations) the proportion of children is predicted to fall so rapidly over the next 20 years that the number of cases of childhood infections is also likely to fall since there are fewer children at risk of contracting them. However, this apparent decline could disguise a rising trend in the rate of an infection, that is, an increasing proportion of the dwindling child population could be affected. For example, concerns about the safety of vaccines in the 1990s resulted in falling vaccination take-up for some childhood infections in the UK, followed by rising infection rates of measles in some areas. (b). Some infectious diseases primarily affect children because babies (once breast feeding is over) are 'susceptibles' without the immunity to infectious agents that older people have developed after exposure to the pathogen or a vaccine. Thus, children are the principal population 'at risk' from infections such as measles
Block 1 Unit 1 Infectious Diseases: an Introduction Question 1.1 (This question relates to learning objective 1.) (a) Which of the following infectious diseases are due to zoonoses, according to the WHO definition given in this unit, and (b) which are transmitted by insect vectors? ◦ malaria ◦ TB ◦ sleeping sickness ◦ plague.
Answer. (a). TB, sleeping sickness and plague are zoonoses, which can be transmitted to humans under naturally occurring circumstances from other vertebrates, e.g. cattle, large 'game' animals such as antelope and buffalo, and rodents, including rats, gerbils and ground squirrels. However, TB transmission to humans from cattle herds and milk production is now extremely rare in high-income countries, and even in the less wealthy countries the main reservoir of TB infection is in humans. The bacteria are now most commonly passed directly from person to person, so although technically defined as a zoonosis since it can still be transmitted from cattle to humans, TB is on the borderline of the WHO definition. Malaria does not have a reservoir of infection in non-human vertebrates and thus is not a zoonosis. (b). Malaria, sleeping sickness and plague are all vector-borne diseases transmitted from mammals to humans by insects, e.g. mosquitoes, tsetse flies and the fleas of rodents. However, during epidemics, plague can also be passed directly between infected people when the bacteria proliferate in the lungs (pneumonic plague).
Block 1 Unit 3 Viruses. Question 3.8 (This question relates to unit learning objectives 1 and 8.) In a short paragraph, explain what bacteriophages are and how they may be used therapeutically.
Answer. A bacteriophage is a virus that infects bacteria. There are cytocidal and non-cytocidal phages, and the cytocidal ones could be used therapeutically. The idea is that phages could be used to destroy bacteria that are resistant to antibiotics. The phages would be introduced into the patient by topical application, injection, inhalation or by mouth, as appropriate, and would seek out and destroy the pathogenic bacteria without affecting the host (selective toxicity). There has been only limited success so far with this approach.
Block 1 Unit 3 Viruses. Question 3.7 (This question relates to unit learning objectives 1 and 7.) What is a haemorrhagic fever, and how does it kill a patient? Give one example of a recently emerged viral haemorrhagic fever.
Answer. A haemorrhagic fever is a usually fatal fever that starts with headache and muscle pain, then progresses to local and systemic haemorrhage. This haemorrhaging leads to circulatory shock (massive loss of blood volume), and this is what kills the patient. The Ebola virus is a recently emerged virus that causes haemorrhagic fever.
Block 1 Unit 3 Viruses. Question 3.3 (This question relates to unit learning objectives 1 and 3.) Give one advantage and one disadvantage of the Baltimore viral classification system.
Answer. Advantage: all known viruses fall clearly into a discrete class. Disadvantage: a virus cannot be classified merely by observation (e.g. by capsid shape); it must be studied to ascertain its replication strategy.
Block 1 Case Study - Influenza. Question 1.3 (This question relates to case study learning objectives 2, 4, and 5.) It is very uncommon for a strain of influenza that infects other animals to infect people; nevertheless such strains are very important for human disease. Why is this?
Answer. Animal strains of influenza act as a reservoir of genes that may recombine with human influenza viruses to produce new strains that can spread rapidly in humans. Such pandemic strains frequently produce serious diseases with high mortality
Block 1 Unit 2 Pathogenic Organisms. Question 2.3 (This question relates to unit learning objectives 1, 3 and 5.) Compare the adaptations shown by some bacteria and some helminths to a lifestyle inside a host's gut.
Answer. Both bacteria and helminths gain access to the gut by contaminated food or water. Both must be able to survive exposure to stomach acid. Bacteria are adapted to acidic conditions, and some, like Helicobacter, cannot live at higher pH levels. Helminths are able to pass through the stomach into the intestine as resistant cysts. Once in the intestine, both types of pathogen must anchor themselves to the gut mucosa to avoid being swept away. Bacteria do this by adherent molecules and filamentous structures such as pili. Helminths attach via hooks or suckers.
Block 1 Unit 3 Viruses. Question 3.4 (This question relates to unit learning objectives 1 and 4.) In a few short paragraphs compare and contrast the replication strategies of variola major and adenovirus
Answer. Both variola major and adenovirus are DNA viruses. Variola major replicates and is assembled entirely in the cytoplasm. It carries its own DNA-dependent RNA polymerase in the nucleosome. New virions acquire an envelope from the host cell membrane, and may be released without lysing the cell. On the other hand, adenovirus is replicated and assembled entirely in the nucleus. New virions lie in clusters forming paracrystalline arrays. These arrays may become so big as to cause damage to host chromosomes.
Block 1 Case Study - Influenza. Question 1.4 (This question relates to case study learning objectives 2 and 3.) Which immune defences are able to recognise and destroy virallyinfected host cells?
Answer. Cytotoxic T cells and NK cells are able to recognise and destroy virallyinfected host cells.
Block 1 Unit 3 Viruses. Question 3.1 Explain (in approximately 100 words) the different reasons for the emergence of the five viral diseases examined in Sections 9.1-9.5.
Answer. Ebola virus occurred when humans exploited new environments, disturbing the balance of natural host-virus relationships. Pulmonary hantavirus was brought about by an increasing deer mouse population and the subsequent infiltration of homes, and finally hepatitis C and HPV types 16 and 18 remained undetected until the technology was available to find it in the blood or to differentiate between viral types in tumour cells, respectively. In the case of HIV, the exact mechanisms of transmission from non-human apes to humans remain unknown. (83 words)
Block 1 Case Study - Influenza. Question 1.1 (This question relates to case study learning objective 2.) Why would Robert Koch have been unable to demonstrate that influenza viruses cause the disease influenza, according to his own postulates?
Answer. Koch's second postulate states that the pathogen can be isolated in pure culture on artificial media. Viruses can only multiply within host cells, so Koch would have been unable to isolate the virus using artificial media. (Much later, eggs and live cells in tissue culture came to be used for growing flu virus, but this was long after Koch's death, and they do not strictly conform to the original postulate.)
Block 1 Unit 2 Pathogenic Organisms. Question 2.1 (This question relates to unit learning objectives 1 and 2.) Make a list of the main groups of pathogen that you have met so far in the module and for each one give an example of a disease caused by this type of agent.
Answer. Table 2.3 gives several examples of diseases caused by different types of pathogens discussed so far, but the list is not exhaustive and you may have come up with others. View Table 2.3 Examples of diseases spread by different groups of pathogen
Block 1 Unit 1 Infectious Diseases: an Introduction. Question 1.4 (This question relates to learning objectives 2 and 4.) What consequence for human infectious disease is believed to have followed the adoption of pastoralism around 10 000 years ago, and how might pastoralism still be exerting an influence in the present on certain categories of emerging infectious diseases?
Answer. The domestication of livestock and poultry brought their pathogens and parasites into close and prolonged contact with humans; over several thousand years, some of these infectious agents adapted to survive in humans and became the source of important zoonotic diseases (e.g. TB), or adapted still further to become exclusive to human hosts (e.g. smallpox, influenza). In the present day, intensive farming of livestock and poultry is believed to have contributed to the increase in certain food-borne infections (e.g. Salmonella and Escherichia coli bacteria); the extensive routine administration of antibiotics to food-producing animals may also have contributed to the emergence of antibiotic-resistant bacterial strains.
Block 1 Unit 1 Infectious Diseases: an Introduction. Question 1.2 (This question relates to learning objective 2.) In 1817, the East India Company deployed its substantial army against the troops loyal to various local princes and tribal leaders in the region then known as Bengal, in fierce campaigns to acquire territory for commercial exploitation. According to European historians, before that date cholera was endemic in Bengal but occurred only rarely elsewhere in the Indian sub-continent. How did this military action influence the subsequent history of cholera as a force in human history?
Answer. The military campaigns in Bengal, and the subsequent dislocation of population, spread the bacteria that cause cholera beyond the water courses of regions in which the disease was endemic, to the rest of India and beyond. Although cholera was known in Europe before this time, it reached epidemic levels after it was imported from India along trade routes, arriving in ports such as London where 7000 people died in one outbreak in 1832. From Europe it was transported to other colonial territories, reaching North America in 1832 and subsequently spreading into Central and South America. This example illustrates the speed with which an endemic disease in one location can 'globalise' as a consequence of human actions.
Block 1 Unit 3 Viruses. Question 3.2 (This question relates to unit learning objectives 1 and 2.) Historically, what were the two most important pieces of equipment used to identify viruses?
Answer. The porcelain bacterial filter and the electron microscope
Block 1 Case Study - Influenza. Question 1.5 (This question relates to case study learning objectives 4-6.) Why do most people suffer from influenza several times in their lives?
Answer. The virus mutates regularly (antigenic drift); also new strains are occasionally generated by recombination (antigenic shift). Since the immune response is generally specific for a particular strain of virus, new strains are not susceptible to immune defences which have developed against earlier strains.
Block 1 Unit 1 Infectious Diseases: an Introduction. Question 1.3 (This question relates to learning objective 3.) Identify at least one similarity and one significant difference between the infectious disease patterns in low- and middle-income countries (LMICs) at the end of the twentieth century and those of Western Europe in the pre-industrial period (i.e. before about 1850).
Answer. There are many similarities and differences, but here are a few of the most important. . Infectious diseases are still currently the major cause of death in LMICs, as they were in pre-industrial Western Europe (indeed until the 1940s). . Several infectious diseases of current importance in LMICs were also common in pre-industrial Europe, including plague, TB, cholera, measles and malaria. However, infection has declined in poorer countries below the death rates experienced in pre-industrial Europe. For example, even the HIV/AIDS pandemic has not (yet) reached the mortality levels seen during the medieval plagues, when 25% of Europe's population died; smallpox, which caused millions of deaths in the past, has been eradicated worldwide; infant mortality rates in LMICs currently average 65 per 1000 live births - roughly half the rate seen in Scotland as recently as 1900.
Block 1 Case Study - Influenza. Question 1.2 (This question relates to case study learning objective 2.) List the various structural components of an influenza A virus and note where each of these elements is synthesised within an infected cell.
Answer. Viral RNA is synthesised in the nucleus of the infected cell. The Mprotein and other internal proteins are synthesised on ribosomes in the cytoplasm. The capsid is then assembled in the nucleus. The haemagglutinin and neuraminidase are synthesised on ribosomes on the endoplasmic reticulum. The envelope is derived from the host cell's own plasma membrane.
