Biol 123- Infection and Immunity Flashcards

Question

a little less than 1 million people in 2019 died from diarrhoea (morbidity was 74%), due to what?

Answer 1

WASH- water, sanitation and hygiene

Answer 2

disability adjusted life year- the measure used to give an indication of overall burden of disease. measures the consequences of ill health. measures 'life years' lost due to premature mortality + equivalent years lost due to lower quality of life. allows comparisons to be made across range of health problems- quantitative basis for deciding health policies + evaluating cost-effectiveness of control programmes.

Answer 3

mortality doesn't give the complete picture of the burden of disease borne by individuals in different populations

Answer 4

adding 'years of life lost (YLL) due to premature mortality' and 'years of healthy life lost due to disability (YLD)' for people living with health condition or its consequences. DALY = YLL + YLD

Answer 5

DALYs only measure direct health loss + don't consider economic + social impacts e.g. 1. agriculture 2. school attendance 3. child development 4. if they can work or not 5. direct treatment costs + surveillance 6. prevention measures 7. stigma associated with disease 8. loss of tourism 9. general overload on health system e.g. blindness

Answer 6

pandemics e.g. covid, flu natural/ social disasters, poverty, deprivation movement of refugees drug-resistant pathogens + vectors e.g. malaria rapid + widespread air travel: ( ~ 3 bill passengers/ year) increase in immune-suppressed people: organ transplants lifestyle: urbanisation, drugs, sex environment: global warming, climate change, deforestation, irrigation, antimicrobials

Answer 7

Thucydides 430 BC: Athens Plague, only recovered people nurse the sick 15th Century: China/ Aztecs- Inhaled crusts of smallpox to provide protection Jenner 18th C: infected this child who had cowpox with smallpox, and they survived (not a nice experiment). It was discovered that if you’re infected with a pathogen, it can give protection to a more virulent strain= VACCINE DISCOVERED. Pasteur 19th C: attenunated rabies virus used as a vaccine- VACCINE IMPROVED 1980: smallpox eradicated by vaccine 2011: Nobel Prize for discovering dendritic cells 2018: did research on checkpoint inhibitory receptors on T cells, that could basically turn T cells on/off depending on whether a ligand was bound or not

Answer 8

systems: lymphatic, blood organs: bone marrow, thymus, lymph nodes, spleen cells: innate + adpative molecules: antibodies, cytokines, complements

Answer 9

skin: 1.dead cells + bacteria. 2. sebaceous gland- fatty acids, lactic acid= low pH due to these, the skin is dry as fuck + unappealing, preventing bacterial growth.

Answer 10

they stop ingested antigens passing into the body + blood circulation, in the intestinal tract with epithelial cells.

Answer 11

mucosal surfaces are literally just slippery, loads of mucus-secreting cells that make it hard for the pathogen to get into the cell if it’s slippery + cilia help as well- flushes out intestinal worms + pathogens. the mucus also traps microorganisms which are then shed from the body e.g. respiratory mucous membrane

Answer 12

1. stomach- low pH, kills pathogenic microorganisms 2. normal commensal microbiota- out compete pathogenic strains for nutrients

Answer 13

1. anti-microbial peptides: defensives damage pathogens 2. anti-microbial proteins: lysozyme in tears + saliva 3. cytokines: interferons induce anti-viral state in cells (signal to other cells there’s an issue) 4. complement: membrane attack complex lyses bacteria

Answer 14

1. they're just really big- they can burrow through the skin + just evade mechanical and physiological barriers in place. 2. they can hook themselves onto the intestinal wall or anchor themselves so they can’t be flushed out easily. Some transit into your feet which isn’t good.

Answer 15

neutrophils, eosinophils, mast cells, basophils

Answer 16

neutrophils, macrophages, dendritic cell

Answer 17

innate lymphoid cells (ILCs), natural killer cells (NKs)

Answer 18

Neutrophils can unravel their nuclear DNA, uncondense it and spit it out, which can trap bacteria. instead of individually eating bacteria, they can just gobble a huge clump of them

Answer 19

when a pathogen has broken through our innate barriers

Answer 20

heat (calor) redness (rubor) swelling (tumour) pain (dolor) cool latin words

Answer 21

1. tissue damage + bacteria cause resident sentinel cells (dendritic) to release chemoattractants + vasoactive factors that trigger vasodilation + higher capillary permeability. 2. permeable capillaries allow an influx of fluid (exudate) + cells. 3. neutrophils + other phagocytes migrate to site of inflammation (chemotaxis) 4. phagocytes + antibacterial substances destroy bacteria.

Answer 22

1. chemokine release: CXCL8/ IL-8 release from damaged endothelial cells + TNF-a release from macrophages= recruits neutrophils + allows migration from blood. 2. Histamine release from mast cells- vasodilation + increases blood vessel permeability. 3. Activation of clotting + complement cascades 4. Neutrophils secret chemokine to recruit monocytes from blood. 5. Phagocytosis of pathogens 6. Macrophages migrate to tissue + secrete IL-1 and TNF-a to recruit lymphocytes, monocytes + neutrophils.

Answer 23

1. fever (speeds up phagocytosis + body reactions but is costly) 2. leukocytosis (white cell production increase) 3. liver produces acute phase proteins: C-reactive protein which binds to microbes + activates complement proteins to aid phagocytosis. also, Type-1 interferons, IL-6, CXCL8

Answer 24

they're a group of serum proteins in the blood that performs a critical defence against pathogens, especially extracellular ones

Answer 25

little over 35

Answer 26

mostly made in the liver, + some are produced in large quantities during that acute-phase response stimulated by the pro-inflammatory cytokines IL-6 + TNF-a

Answer 27

both- links to the innate one (e.g. phagocytosis) + adaptive (e.g. antibodies)

Answer 28

1. initiators- bind to pathogen's components or antibodies e.g. C1q, MBL 2. enzymes- convertases e.g. C1r, C1s, C4b, C2a, also enzyme mediators like C3 convertase 3. opsonins- promote phagocytosis e.g. C3b 4. anaphylatoxins- cause inflammation e.g. C5a 5. membrane attack proteins- lyse pathogens 6. complement receptors- on phagocytes or neutrophils e.g. CR1, CR3 7. regulatory proteins- limit complement activation e.g. factor 1

Answer 29

1. pathogen associated molecular proteins (PAMPs)- innate immune system detects molecules from pathogens USING pattern recognition receptors (PRRs)

Answer 30

1. bacteria have pathogens associated molecular patterns 'PAMPS' 2. phagocytes have pattern recognition receptors 'PRRS' 3. bacterium becomes attached to pseudopodia 4. bacterium is ingested forming phagosome 5. phagosome fuses with lysosome 6. bacterium is killed + digested by lysosomal enzymes + reactive oxygen species 7. digestion products are released from cells

Answer 31

1. oxygen-dependent killing: oxidative burst, superoxide + other toxic oxidants are generated, acts as an anti-microbial 2. oxygen-independent killing: lysozyme (hydrolytic enzyme), defensives (peptides kill many bacteria)

Answer 32

1. innate is non-specific, adaptive is specific for certain antigens + requires a specific receptor on B and T-lymphocyte cells to detect a specific antigen on the surface of a cell. 2. innate has elements present at birth, adaptive is gained after exposure to foreign material 3. innate is effective against loads of pathogens, adaptive has a delay before effect (usually like 5-6 days) as it needs the innate immune system to activate it first. 4. innate is lifelong, adaptive is kinda but not as much 5. innate is present in all animals, adaptive is only in vertebrates. 6. innate doesn't have memory, adaptive does

Answer 33

innate lymphoid cells (ILCs) natural killer cells (NK) mast cells eosinophils neutrophils macrophages dendritic cells kinda????? they're innate but are relevant in adaptive as well

Answer 34

CD4+- T-Helper cell CD8+- cytotoxic T cell B cell dendritic cell not really but is relevant here so

Answer 35

they don’t have the surface markers that we usually require to know a cell exists.

Answer 36

Adaptive cells can detect antigens from foreign pathogens without them being presented to them

Answer 37

6 micrometers diameter, short life-span (3 days- 8 weeks)

Answer 38

bone marrow of flat bones, mostly sternum or hip or something. more specifically, a hematopoietic stem cell in bone marrow

Answer 39

blood + lymph

Answer 40

neutrophils- 50-70% lymphocytes- 20-30%

Answer 41

Bone marrow of flat bones again xxxx

Answer 42

thymus (primary lymphoid organ), after they leave the bone marrow

Answer 43

Myeloid- usually produce innate cells. Lymphoid- usually lymphocytes.

Answer 44

1. interstitial fluid bathes tissue + along with blood cells enters lymphatic vessels 2. lymph flows through lymphatic vessels throughout body 3. within LNs, pathogens and particles in the lymph encounter + activate antigen-presenting cells 4. lymphatic vessels return lymph to the blood via 2 large ducts that drain into veins.

Answer 45

lymph nodes: lymph flows in through the afferent, where it's filtered. also, dendritic cells + macrophages function there with phagocytosis, and lymphocytes do their cool immune responses. Antibodies can be produced by B cells, as they can be activated by antigens in there.

Answer 46

spleen: it is a blood filter about 12 cm long behind the stomach, which has white pulp containing B + T cells, and macrophages which can hold antigens on their surface to be detected. also a germinal centre, where B-lymphocytes proliferate. the red pulp is where old/ dead RBC are removed.

Answer 47

dendritic cells, macrophages, B cells

Answer 48

humoral: B-cell/antibody mediated. defends against pathogens + toxins in extracellular fluid. Deals with stuff that isn’t within our cells. cell-mediated: mostly about cytotoxic T cells. defends against infected cells, cancer cells + transplanted cells

Answer 49

T helper cells are required in both, as B cells + cytotoxic lymphocytes need the T-cell help.

Answer 50

any foreign molecule which is specifically recognised by lymphocytes + elicits a response from them

Answer 51

B + T cell receptors they have receptors embedded in their plasma membrane. each B or T cell is specific for 1 antigen epitope (the structure on the antigen recognised by the immune system).

Answer 52

Antigens bind to the variable regions of B + T-cell receptors. The constant regions help cellular signalling- signals from outside the cell can be integrated into the cell.

Answer 53

1. developing B cells undergo a selection process in bone marrow: self-reactive cells are destroyed. 2. receptor interacts directly with pathogen 3. mature B cells are released from bone marrow 4. becomes either plasma B-cell which releases antibodies, or memory B-cell (affinity maturation- where antibodies gain increased affinity).

Answer 54

IgM antibodies are cool, looks more like a flower than the classic Y shape. IgD doesn’t get secreted into the blood. IgE responds to helminths. IgA forms a dimer, present in secretion in breast milk, present in the mucosal lining. IgG produced the most in the body.

Answer 55

which is why we have booster vaccinations xxxx faster, greater, longer immune response

Answer 56

T-helper cells e.g. Th1= type-1 immune responses. Th2= type 2, helminths + asthma. Th17- inflammatory skin conditions e.g. psoriasis. Cytokines produced by these Th’s direct the immune response that happens after.

Answer 57

developing T cells undergo 2 selection processes. Initially known as double-negative, haven’t decided whether to become a helper or cytotoxic. Goes through positive selection first, and becomes double positive, expressing both CD4 + CD8. cells die if they don't recognise their MHC. then, those that recognise our cells too strongly go through apoptosis, as we don’t want to go through autoimmunity, and don’t want cell death of cells that are required. Then mature + express only CD4 (T-helper) OR CD8 (cytotoxic).

Answer 58

BY RECOGNITION OF ANTIGEN PRESENTED ON MHC MOLECULES CTL (cytotoxic T lymphocyte) activated by presented antigen from infected cell----- becomes either active cytotoxic T cell or memory cytotoxic T cell (both CTLs) T helper cell activated by antigen on APC------- becomes either active T helper cell (help B cells) or memory T helper cell

Answer 59

All cells with a nucleus express MHC-1, allows cells to call for help if in trouble basically . they all need to be able to alert the immune system of stuff like viral infections in the cell.

Answer 60

CTL (cytotoxic T lymphocyte) is activated by presented antigen from infected cell, with the help of MHC-1 binding to the antigen, which binds to a TCR. a T-helper cell is activated by APC, with MHC-2.

Answer 61

specialised APCs e.g. dendritic cells, macrophages + B-cells. It’s important for B cells to express MHC-2, so it can get help from CD4+ T-helper cells.

Answer 62

CD8+ cytotoxic T lymphocytes, resulting in antigens being presented on infected cells

Answer 63

CD4+ T-helper cells, resulting in antigen on the APCs.

Answer 64

Dendritic cells can activate naïve t cell that have never been exposed to the antigen before- hence, professional.

Answer 65

1, phagocytes 2. migrate from site of infection to lymphoid tissues 3. display processed antigen to naive t-helper cell 4. important in triggering a PRIMARY immune response

Answer 66

secondary!!!!

Answer 67

1. B-cells bind to antigens via B cell receptors. 2. receptor + antigen endocytosed 3. B cells present antigens via MHC-2 to helper T cells with same epitope recognition 4. activated helper T cell secretes cytokines 5. cytokines activate B cell to produce memory B cells + plasma cells

Answer 68

B-cell mediated

Answer 69

phagocytosis-mediated + complement- mediated killing

Answer 70

antibody-antigen mediated

Answer 71

1. macrophage/ dendritic cell phagocytoses pathogen (usually dendritic because they’re professional) 2. antigen processed in macrophage/ DC + presented on surface via MHC-2. 3. specific T-helper cell (CD4+) recognises processed antigen + binds (aided via CD4 binding to MHC-2) 4. SHTC activated 5. B-cell phagocytoses BCR + antigen, presents it on MHC-2 6. SHTC recognises antigen presented by B-cell 7. cytokines from activated SHTC fully activate B cell 8. B cell activated to produce clones of plasma cells + memory B cells 9. antibody production from plasma cells 10. pathogen elimination

Answer 72

1. neutralisation- blocks viral binding sites; coats bacteria and/or opsonisation 2. agglutination of antigen-bearing particles, such as microbes 3. precipitation of soluble antigens 4. complement fixation (activation of complement), which leads immediately to CELL LYSIS

Answer 73

improves the ability of a phagocyte to phagocytose. Neutralisation, agglutination + precipitation all enhance phagocytosis.

Answer 74

a pathway composed of around 35 or so different soluble proteins in the blood

Answer 75

basic lore- The classical pathway is mediated by an antibody binding to an antigen. It requires C1- a complex of C1q which is a hexomeric molecule, + C1s and C1r. 1. Complement binds to antigen-antibody complexes on cell surface. 2. Complement cascade is activated by antibodies- several complement proteins form MAC- a hole in the foreign cells, which forms membrane lesions where the MAC has inserted itself.

Answer 76

basically a corkscrew thing of loads of C9 complement proteins, ending with other ones like C5b, C6, C7 and so on tailing off.

Answer 77

basically directly lyses pathogens by activating signalling pathways with the pores it forms on pathogenic cells.

Answer 78

T-cell mediated CTL for cell-mediated response, aided by T-helper cells

Answer 79

MHC-1 antigen T-cell receptor xxxxx

Answer 80

cytotoxic T cells mediated killing + humoral response activation by SHTC

Answer 81

1. cell infected with pathogen presents antigens on surface to CTL, helped by MHC-1. 2. the CD8 on T-cell surface binds MHC-1 + TCR on the CTL binds the presented antigen with this cool cognate interaction (recognises specific epitope). 3. CTL (which is CD8+) becomes activated. Releases perforin + granzyme from the cell. 4. the perforin insert themselves into the membrane of the target cell membrane + makes these pores. 5. granzymes are key enzymes: they enter through the pores + initiate apoptosis in the target cell.

Answer 82

1. macrophage or something phagocytoses bacterium, becomes APC 2. T-helper cell binds antigen, with help of MHC-2 on the APC + TCR on itself (also CD4 as well !!!) 3. interleukin-2 + other cytokines tells cells to proliferate, divide + survive 4. they become either cytotoxic lymphocyte (cell-mediated immunity so they just attack on infected cells) 5. OR become B cell (humoral immunity, just secrete antibodies by plasma cells)

Answer 83

1. upon 1st exposure of antigen, dendritic cell phagocytoses + presents it to T-helper cell, which become memory cells + proliferates to produce clones. 2. T-helper cell helper B cell, after it has been exposed to same antigen and is activated. B cell gives rise to clones of plasma cells which produce antibodies to defend. (HUMORAL) 3. some of B cells will become memory ones, helping with re-exposure. (HUMORAL) 4. at same time, after the APC thing, cytotoxic T cells are activated via recognition of antigens from infected cells. (CELL-MEDIATED) 5. memory helper T-cells can stimulate + support both the memory B cells + memory cytotoxic T cells upon 2nd exposure (CELL-MEDIATED)

Answer 84

Yersinia pestis, rod shaped, gram-negative

Answer 85

they are capable of surviving in both aerobic and anaerobic environments

Answer 86

Xenopsylla cheopis

Answer 87

(i) the gut of a flea, at ambient temperature (ii) blood or tissues of a mammalian host, at body temperature

Answer 88

Sylvatic cycle= wild, Urban cycle= the main stuff that caused the plague that we all know and love. 1. Sylvatic: goes from wild rodent to infected flea to another wild rodent then either to another infected flea to continue cycle or to a human. 2. Urban: goes from domestic rodent to infective flea to domestic rodent to infective flea to human or to another domestic rodent to continue the cycle.

Answer 89

If the rodent bites a human, or just coming into direct contact, they can become infected.

Answer 90

Mongolia: marmots Africa: gerbils North America: ground squirrels, chipmunks and prairie dogs South America: wild guinea pigs

Answer 91

Some wild rodents are relatively resistant to plague and so form permanent foci of infection

Answer 92

When wild rodents form foci of infection, the immune system can’t get rid of the pathogen + the rodent just lives with the pathogen in its body, doesn’t really cause any harm.

Answer 93

brown rat (Rattus norvegicus)

Answer 94

The black rat (Rattus rattus), is usually the source of human infection, it is very susceptible to plague

Answer 95

Estimated 2,500 species and subspecies of fleas - constituting 220 genera and 15 families in insect order Siphonaptera

Answer 96

Approximately 80 species

Answer 97

1.insect immunity - e.g. antimicrobial peptides 2. midgut digestive enzymes - pathogen must evade these 3. frequency of feeding and defecation – pathogen must avoid being removed from the vector 4. flea life span after infection - pathogen must not kill vector (too quickly!)

Answer 98

1. Vectors become infected following uptake of a blood meal 2. then the pathogen replicates and disseminates in the vector, where it goes depends on the pathogen-vector pair 3. Y. pestis remains confined to the flea digestive tract and is transmitted by regurgitation during its 2nd blood meal.

Answer 99

Y. pestis does not adhere to, or invade, the midgut epithelium

Answer 100

(i) formation of multicellular aggregates (too large to be passed in faeces) AND (ii) their ability to form a biofilm and which creates a blockage in the proventriculus (PV) – a valve that connects the oesophagus (E) and midgut (MG).

Answer 101

As the biofilm grows, it fills the lumen and when the flea tries to feed it impedes blood flow into midgut Blocking the proventricular valve enhances regurgitative transmission of the bacterium Those biofilms and aggregations disrupt the normal feeding of the flea, which it needs to clear.

Answer 102

it can overcome host defences and multiply within the body - (mainly) extracellularly.

Answer 103

Following inoculation, Y. pestis induces a local lesion and inflammation - followed by rapid spread and multiplication. it is the toxins produced by Yersinia that causes most of the harm - endothelial damage and necrosis - leading to vascular destruction and local haemorrhaging

Answer 104

1. Early in infection Y. pestis may be killed by neutrophils (N), however as it is surrounded by the F1 capsule protein, phagocytosis by N is prevented. 2. Later in infection Yp injects effector proteins (Yops) into N killing/disabling them.

Answer 105

Macrophages can phagocytose Y. pestis but cannot kill it so it just kind of chills inside the vesicle once it’s trapped. Its ability to survive in the gut is like one of the main reasons it’s such an issue. bacterial toxins can destroy macrophages and other phagocytic cells

Answer 106

destruction of tissue and effects of endotoxins - peripheral vascular collapse and disseminated intravascular coagulation (DIC)

Answer 107

(named after Byzantine emperor Justinian I) was followed by frequent outbreaks over the next two hundred years – estimated to have killed over 25 million people around the Mediterranean basin. In 540, 26M people in ME reduced to 17M by 610.

Answer 108

originated in China in 133, spread along great trade routes to Constantinople (now Istanbul) which was the centre of the Byzantium Empire and then on to Europe – estimated to have killed 30-50% of the European population. Led to large and long-lasting increases in the purchasing power of wages and higher levels of consumption and standards of living for those that survived.

Answer 109

began in China in the 1860s and appeared in Hong Kong by 1894. Over the next 20 years, it spread to port cities around the world – estimated to have caused approximately 10 million deaths

Answer 110

With that famous doctor beak mask thing picture, the beak was filled with cool herbs and spices as they believed that it was transmitted by air, so they believed they should be protected. Also, used to hit people with the stick they were holding to appease God xxxx

Answer 111

Ancient Yersinia pestis genomes from across Western Europe reveal early diversification during the First Pandemic’. The disease would appear to have split from Y. pseudotuberculosis around seven thousand years ago e.g. a case of bubonic plague was reported in Oregon last year

Answer 112

1. worldwide availability 2. capacity for mass production + aerosol dissemination 3. high fatality rate of pneumonic plague 4. potential for rapid secondary spread 5. In 1970, WHO published a report that estimated the deliberate release of 50 kg of Yersinia pestis in an aerosolised form over a city of 5 million could result in pneumonic plague in up to 150,000 people and 36,000 deaths. also this kind of thing did happen in the 14th century so not new

Answer 113

Incubation period 2-4 days - but may be as long as 10 days

Answer 114

patients often develop 'flu-like' symptoms- fever, chills, head ache, body ache, vomiting, nausea - prodromal period

Answer 115

bubonic, septicemic, pneumonic

Answer 116

usually initiated by infected flea bite. Bacteria enter body and multiply at site of entry in skin – then spreads via the lymphatic system to lymph nodes, which become painful and enlarged - forming BUBOES with haemorrhagic inflammation 2-6 days after flea bite (reallyyyyyy painful) Usually get FEVER + CHILLS, also DELIRIUM + CONFUSION. later in infection buboes can burst to form open sores.

Answer 117

50-60% if untreated, but if you recover you're immune

Answer 118

Septicaemia (blood poisoning) occurs when infection spreads to bloodstream. comes from flea bites + also from direct contact with infective stuff e.g. skinned animals (primary septicaemic plague). bloodstream infection- MENINGITIS, ENDOTOXIC SHOCK (comes form all the bacteria releasing the toxins) , DISSEMINATED INTRAVASCULAR COAGULATION (DIC).

Answer 119

systemic activation of blood coagulation leads to gangrene of the extremities (Black Death) and multi-organ failure

Answer 120

100% if untreated

Answer 121

yeah- Bubonic plague can develop into secondary septicaemic plague

Answer 122

like a really really severe localised inflammatory response

Answer 123

caused by infection spreading to lungs in advanced bubonic plague, but can result from human-human transmission- infected people can form aerosolised infective droplets. In lungs - causes ACUTE PULMONARY INSUFFICIENCY (when pulmonary valve won't fully close + some blood gets back in the heart), SEPSIS and TOXIC SHOCK

Answer 124

Death usually ensues if treatment is not begun within 18-24h of disease onset - even then the mortality rate remains extremely high usually 100% if untreated

Answer 125

flea bites: most often this -may result in primary bubonic or septicaemic contact with contaminated fluid/ tissue: most commonly results in bubonic or septicaemic infectious droplets: a person with pneumonic can cough droplets containing bacteria in the air, and if breathed in by another person can cause pneumonic. Usually requires direct and close contact with a person with pneumonic plague environmental: Y. pestis is very sensitive to sunlight and heat, so doesn't survive long outside a host. WHO estimates plague aerosols remain effective and infectious for ~1 hour. Although it's been reported that Y. pestis can survive for several months in soil – no evidence this poses an environmental risk to humans

Answer 126

patients can still die from the toxins the bacteria released before they were killed (toxaemia).

Answer 127

lymph nodes: bubo containing Y. pestis- direct microscopy/ culturing blood: if septicaemic, bacteria in blood (smears taken early in infection may be negative by microscopy but positive by culture) sputum: culture is possible from sputum of very ill pneumonic patients; however, blood is usually culture-positive at this time bronchial/ tracheal washing: throat specimens are not ideal, since they contain other bacteria that can mask presence of Y. pestis. (you can also diagnose post mortem with antigen detection methods/ PCR)

Answer 128

If given early, and in large doses, treatment with antibiotics such as streptomycin, tetracycline and chloramphenicol are effective (drugs disrupt protein synthesis). Until recently, Y. pestis was considered uniformly susceptible to the recommended antibiotics, however multidrug-resistant strains have now emerged in Madagascar .

Answer 129

However, therapy must start as soon as plague is suspected – duration of treatment usually 10-14 days. Early diagnosis essential as plague can be rapidly fatal - pneumonic plague can kill within 18-24 hours of disease onset

Answer 130

derives from the practice of isolating ships and people for 40 days before they were allowed to enter the city of Venice

Answer 131

Based on formaldehyde inactivated whole-cells. The vaccine only gives partial protection and is only recommended for laboratory and field personnel working with Y. pestis. New efforts to develop a sub-unit vaccine e.g. based on the F1 capsular protein.

Answer 132

1. avoid direct contact with infected body fluids + tissues 2. rodent control- especially at ports + airports 3. inform people when zoonotic plague is present in environment 4. advise people to take precautions against flea bites + avoid handing animal carcasses

Answer 133

causes relatively mild, self-limiting disease (Yersiniosis) and is transmitted by faecal-oral route

Answer 134

just a few genetic changes were sufficient to give rise to flea borne transmission Gene gain and gene loss are the major drivers of bacterial evolution

Answer 135

add: horizontal gene transfer between different bacterial species stir: intra-genomic changes reduce: gene deletions + accumulation of pseudogenes

Answer 136

DNA from human skeletons dating from early Bronze Age reveals ancestral Y. pestis was NOT flea transmitted (possibly transmitted by blood or saliva?) Evolved into a flea-borne pathogen at the beginning of the 1st millennium BC.

Answer 137

1. sample collection 2. recovery + sequencing of DNA/RNA from pathogen 3. phylogenetic analysis + comparative genomics you can find out virulence + transmission, origins + geographic spread, vectors + host reservoirs, and evolutionary rates + genetic diversity

Answer 138

Yersinia murine toxin (ymt) gene encodes a protein called phospholipase D - this protects Y. pestis within the flea gut. it enabled a bacterium previously found in the gut to use an arthropod vector (survives insect gut). Mutants lacking functional ymt are cleared from fleas within 24 hours of infection. Conversely, transfer of the Y. pestis ymt gene into Y. pseudotuberculosis (or even E. coli) greatly increases their ability to infect flea mid gut

Answer 139

Homologues of >200 Y. pseudotuberculosis genes are present as non-functional pseudogenes in Y. pestis. Selective loss of gene function enabled Y. pestis to form a biofilm in flea gut e.g. rcsA - negative regulator of biofilms rcsA is functional in Y. pseudotuberculosis but not in Y. pestis.

Answer 140

disease associated with ‘evil-smelling’ vapours from swamps

Answer 141

'ague or marsh fever’

Answer 142

Genus Plasmodium – approx. 175 species currently recognised – 5 or 6 species infect humans

Answer 143

Italy was only declared malaria free in 1970. Marshlands of Kent and Essex had exceptionally high levels of mortality from the sixteenth to the nineteenth century. Five indigenous species of Anopheles mosquito are capable of transmitting malaria in England. Malaria was eradicated in England ages ago, primarily by draining marshlands.

Answer 144

they can be environmentally toxic (still ok to use according to the WHO, but not nearly used as much as it used to be).

Answer 145

Burden is heaviest in WHO African Region; estimated 90% of all malaria deaths occur in this region

Answer 146

less effective immune system

Answer 147

3 different life cycles: the SPOROGONIC cycle (basically when it’s inside the insect), the EXO-ERYTHROCYTIC cycle (inside the human + outside of red blood cells in the liver) and the ERYTHROCYTIC cycle (inside red blood cells).

Answer 148

1. plasmodium way more complex (3 life cycles) 2. plasmodium has cycles in the insect + human, plague one doesn't 3. plasmodium one doesn't have an intermediate host (e.g. rats in the plague) so not a zoonosis

Answer 149

P. malariae, P. ovale (Two distinct species? P. ovale curtisi and P. ovale wallikeri, maybe lol) + P. knowlesi

Answer 150

caused when developmental stages in the red blood cells erupt in a synchronised way due to merozoites on the surface. e.g. P. falciparum- this species needs immediate treatment.

Answer 151

shows signs of fever

Answer 152

links to their periodicity of fever e.g. differences in erythrocytic cycle Peaks coincide with the synchronized release of parasites from rupturing erythrocytes brings on the fever.

Answer 153

female Anopheles mosquito – blood meal needed for egg development When female mosquitoes feed, they inject infected stages of malaria into the person

Answer 154

this is between latitudes 60oN and 40oS and below 2000 metres. also temperature is important

Answer 155

INTRODUCED malaria - local mosquitoes become infected by biting people who acquired malaria in endemic areas and transmit malaria to locaLS - 63 outbreaks of locally transmitted mosquito-borne malaria in US (1957-2009) AIRPORT Malaria - infected mosquitoes transported by aircraft from malaria endemic country to non-endemic country - local residents can acquire malaria without ever having travelled abroad TRANSFUSION malaria - acquired via blood transfusion – between 1963-2009 96 cases of transfusion-transmitted malaria reported in US MAINLINE malaria - acquired via shared needles and syringes CONGENITAL malaria - infected mothers transmit Plasmodium to child during pregnancy, before or during delivery

Answer 156

1.Sporozoites inoculated into skin by mosquito – penetrate blood vessel and enter circulation. 2.Circulate in bloodstream for up to 30 minutes – but must penetrate hepatocytes (liver cells) to initiate an infection. 3. Within a liver cell Plasmodium undergoes schizogony – a form of asexual reproduction in which nucleus divides many times before the cytoplasm divides to form ~30,000-40,000 merozoites.

Answer 157

happens after an infected female mosquito bites a human host xxx 1. she will have an infected stage of malaria in her salivary gland called sporozoites, which invade liver cells + nucleus divides loads, producing schizonts. 2. schizont ruptures when mature, releasing merozoites which are inside, which enter blood circulation + infect RBCs 3. the merozoites go through another developmental stage, producing different stages, some of which circulate in the blood, infecting other RBCs, producing more schizonts but in RBCs instead of liver cells. 4. Again the RBCs will rupture + release stuff, and the cycle goes on xxxxx

Answer 158

Hypnozoites are dormant forms of things that can sometimes be formed. they are less sensitive to antimalarial drugs and can reactivate many years after initial infection – problems with mis-diagnosis.

Answer 159

erythrocytic cycle is an incubation stage – no symptoms. 1. Merozoite infects RBCs, which multiply asexually 2. trophozoites grow in RBCs, forming more schizonts (asexual reproduction) or gametocytes (sexual reproduction). 3. schizont ruptures, releasing more merozoites which infect more RBCs. 4. OR or mosquitoes take gametocytes in next blood meal

Answer 160

must invade RBCs to continue infection. Multiply by asexual reproduction – this results in the erythrocytic part of the parasite life cycle. This is the “disease” causing stage. they also have Apical organelles (rhoptries and micronemes) which contain proteins required for parasite invasion are visible in the piccy.

Answer 161

This is a single-celled nucleated mass of protoplasm – highly metabolically active. The growing parasite needs to acquire nutrients from the host and modifies the RBC to meet its nutritional demands. Trophozoites ingest haemoglobin - this is broken down to give an iron haem pigment called haemozoin - which accumulates in the food vacuole.

Answer 162

After several hours of growth within the RBC, schizogony occurs (timing depends upon the Plasmodium species). The trophozoite divides to give 8-16 merozoites – these are released when the RBC ruptures. Note the irregular appearance of the red blood cell surface – note the presence of ‘knobs’ which are merozoites.

Answer 163

Occurs inside the mosquito gut. 1. some trophozoites from 2nd cycle will develop into sexual forms called gametocytes (usually takes like 4 days to mature), which are taken up in a blood meal 2. within minutes of ingestion by the mosquito, the male and female gametocytes burst out of the RBC. 3. male one produces 8 microgametes – (a flagellum with an attached nuclear mass). The micro and female macrogamete fuse to form a zygote. 4. over like 5-10 hours, the zygote differentiates into a cigar-shaped INVASIVE ookinete, which penetrates the intestinal wall of the mosquito. 5. ookinete then differentiates to become an oocyst – this attaches to the external side of the midgut wall of the mosquito. 6. oocysts grow rapidly and divide internally into up to 1000 sporozoites (takes days +goes quicker with higher temp). 7. oocyst bursts - sporozoites are released into the body cavity, which migrate + accumulate in the mosquito salivary glands. 8. The cycle is completed when the mosquito bites a susceptible host and injects saliva along with the sporozoites.

Answer 164

Toxins released when schizonts burst stimulate T-cells to produce cytokines such as TNFa

Answer 165

anaemia (deficiency of red cells or haemoglobin in the blood)

Answer 166

Hypoglycaemia (low blood sugar)

Answer 167

septicaemia

Answer 168

enlargement of liver and spleen

Answer 169

haemoglobin in blood plasma + urine (Blackwater fever) respectively.

Answer 170

haemorrhage + anoxia (oxygen deficiency). especially happens with P. falciparum

Answer 171

1. Happens when RBCs infected with malaria become more sticky than normal, and stick to endothelial cells lining capillary venules in brain, heart, liver, kidney, muscles and placenta. 2. Parasite proteins transported to surface of iRBC. 3. Parasite proteins bind to host receptors on endothelial cells. 4. this blocks blood flow, so oxygen-carrying RBCs can’t get through, not good.

Answer 172

1. Blood smears - stained with Giemsa to detect and identify Plasmodium species. 2. Rapid diagnostic tests (RDTs) detect Plasmodium proteins - > some detect single species, others multiple species or distinguish between P. falciparum and non-P. falciparum infection. Finger-prick sample - results ~15-30 minutes. 3. Nucleic acid amplification-based diagnostics - sensitive detection of low density malaria infections (approx. limit of detection <1 parasite/µl).

Answer 173

Quinine - originally extracted from the bark of the cinchona tree – found in rain forest on the eastern slopes of the Andes. For 300 years quinine was the only effective treatment for malaria. After World War II quinine was replaced by synthetic drugs such as chloroquine.

Answer 174

1. Safer 2. More effective (against all Plasmodium species) 3. Easier to make 4. Few side effects - low cost

Answer 175

1. Intracellular parasite (trophozoite) digests haemoglobin - generates free haem which is toxic. 2. Digestion takes place inside Plasmodium food vacuole – contains lipid bodies that take up haem which is polymerised into a black non-toxic pigment (haemozoin). 3. Uncharged chloroquine diffuses through parasite plasma membrane and food vacuole (FV) membrane 4. FV is acidified- CQ becomes charged and concentrates up to several 1000-fold within the FV. 5. This interferes with haemozoin formation – haem remains, is highly toxic and kills the parasite.

Answer 176

1. caused by transporter protein (PfCRT) exporting CQ from the food vacuole reinforced by: 1. Exposure of parasites to sub-therapeutic dose of drug 2. Incomplete compliance - sharing drugs 3. Parasites not killed - opportunity to become resistant.

Answer 177

bed nets + long-lasting insecticide stuff BUT it is estimated that 43% of the population of sub-Saharan Africa are not protected by nets (WHO). reduces child deaths dramatically

Answer 178

1. since Oct 2021, WHO recommended RTS,S/AS01 malaria vaccine among children living in regions with moderate to high P. falciparum malaria transmission. it has been shown to significantly reduce malaria, and deadly severe malaria, among young children. 2. in Oct 2023, WHO recommended a second safe and effective malaria vaccine, R21/Matrix-M. 3. Vaccines are now being rolled out in routine childhood immunisation programmes across Africa. 4. Malaria vaccines in Africa are expected to save tens of thousands of young lives every year. 5. The highest impact will be achieved, however, when the vaccines are introduced alongside a mix of other WHO-recommended malaria interventions such as bed nets and chemoprophylaxis.

Answer 179

many are free-living but some are parasites of humans, animals + plants= of major medical, veterinary and agricultural importance.

Answer 180

‘a tube within a tube’ – alimentary canal extends from mouth at anterior (head) to anus at posterior (tail)

Answer 181

Smallest are simply scaled down versions of largest e.g. Dioctophyme renale (Kidney worm 1m) vs Enterobius vermicularis (pinworm 10mm)

Answer 182

Parasitic nematodes exhibit a high degree of preadaptation (an adaptation that serves a different purpose from the one for which it evolved)

Answer 183

1. survive wide range of conditions e.g. osmotic pressure, temperature and pH 2. survive under both aerobic and anaerobic conditions 3. utilise wide range of food sources 4. tough outer cuticle can withstand environmental insults – e.g. host immune responses

Answer 184

there are always four larval stages and four moults (kind of like shedding) Life cycles can be complex - does NOT represent an evolutionary sequence.

Answer 185

Nematodes do NOT undergo asexual reproduction (parthenogenesis has been reported – i.e. development of gametes without fertilisation – but this is rare in parasitic nematodes of animals).

Answer 186

e.g. Ascaris 200,000 eggs/day

Answer 187

at least 9

Answer 188

many people harbour many different species of parasites (GI nematodes and other parasites as well).

Answer 189

concerns incidence, distribution + possible control of diseases

Answer 190

number of infected adult worms in a host is due to number of infection events (L3 larvae) - DEGREE OF EXPOSURE btw: INTENSITY of infection is important – not prevalence.

Answer 191

over 70% of the worms are found in less than 15% of hosts. Most heavily infected hosts are at greatest risk of morbidity and are the major source of infective stages.

Answer 192

there may be an underlying physiological defect to explain this overdispersion. means that you can treat the highly infected individuals - but they may be more susceptible to reinfection.

Answer 193

Ascariasis (note the difference between the name of the parasite and the name of the disease)

Answer 194

they're transmitted by human faeces, which contaminate the soil in areas with poor sanitation. Access to host is easily achieved through ingestion.

Answer 195

Vertebrate intestine (gastrointestinal tract). Parasite survival favoured by availability of nutrients in gut.

Answer 196

by the ease of exit to outside world

Answer 197

1. Widespread distribution of nematodes 2. Resilience of eggs to harsh environmental conditions 3. High number of eggs produced per parasite 4. Poor socioeconomic conditions 5. Lack of education

Answer 198

males 10-30cm, females 20-35cm

Answer 199

warm, moist soil

Answer 200

1. Adult worms live in the small intestine. 2. A female may produce 200,000 eggs per day, which are passed with the faeces. Unfertilized eggs can be ingested but aren't infective. 3. Larvae develop to infectivity within fertile eggs after 18 days to several weeks, depending on the environmental conditions (optimum: moist, warm, shaded soil). 4. After infective, eggs are swallowed the larvae hatch, invade the intestinal mucosa + are carried via the portal, then systemic circulation to the lungs. 5. The larvae mature in the lungs (10 - 14 d), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. 6. Upon reaching the small intestine, develop into adult worms. Between 2 - 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 - 2 years.

Answer 201

Highest prevalence in tropical and subtropical regions and areas with inadequate sanitation.

Answer 202

1. Associated with the ingestion and migration of larvae 2. Associated with adult parasites in the intestine 3. Due to “wandering” adults outside of the intestine

Answer 203

severe haemorrhagic pneumonia – can lead to life-threatening respiratory failure.

Answer 204

this may still lead to breathing difficulties, pneumonia and/or fever

Answer 205

eosinophilia and can cause allergic hypersensitivity reactions such as asthma

Answer 206

parasite burden - severe cases can consist of many hundreds of worms

Answer 207

mass of worms physically block intestine and need to be surgically removed 85% of obstructions occur in children aged 1-5 years

Answer 208

1. Bile duct - becomes blocked causing jaundice and a general interference in fat metabolism. 2. break through Appendix or intestinal wall - may cause fatal peritonitis 3. Up the intestinal tract - vomited up or emerge through the nose 4. If adult worms enter the trachea they may cause suffocation

Answer 209

1. coprological- detection of eggs in faeces 2. Serological - detection of antibodies or antigens – but presently no point-of-care test available for STHs 3. Molecular - PCR detection of parasite DNA from eggs passed in faeces. (multiplex PCR can detect multiple parasite species in single reaction qPCR enables quantification of infection intensity in children) 4. Image-based diagnostics

Answer 210

Radiological examination of the small bowel after a barium meal reveals worms as elongated filling defects. High resolution ultrasound showing intestinal ascariasis

Answer 211

Filariasis family: Filarioidea (all nematodes from this family cause this infection)

Answer 212

Lymphatic filariasis – worms occupy the lymphatic system (e.g. Wuchereria bancrofti - responsible for 90% of cases) we will focus on this Subcutaneous filariasis - worms occupy subcutaneous layer of skin (e.g. Loa loa and Onchocerca volvulus - river blindness) Serous cavity filariasis – worms occupy peritoneal, pleural or pericardial cavity (e.g. Mansonella perstans & Dirofilaria immitis - dog heartworm).

Answer 213

mosquitoes and black flies

Answer 214

Africa, South America, South Asia Currently, 856 million people in 52 countries live in areas that require preventive chemotherapy to stop the spread of infection. Status of mass drug administration in 2018 shown.

Answer 215

Elephantiasis

Answer 216

Females 80-100 mm (length) 0.24 to 0.30 mm (diameter) Males 40 mm (length) and 0.1 mm (diameter)

Answer 217

1. during a blood meal, an infected mosquito introduces L3 larvae onto the skin of the human host, where they penetrate into the bite wound. 2. they develop into adults (living in the lymphatics) + produce sheathed nocturnal microfilariae that migrate actively into lymph + blood channels. 3. a mosquito ingests the microfilariae during a blood meal. 4. after this, the microfilariae lose their sheaths + some penetrate the mosquito's midgut, reaching thoracic muscles. 5. microfilariae develop into L1 larvae + then to L3 infective ones. 6. these migrate into the hemocoeal + prosbocis and can infect another person when the mosquito takes a blood meal

Answer 218

~300 μm (length) ~10 μm (diameter)

Answer 219

circulate in the blood at night + migrate to skin at night

Answer 220

improper functioning of lymph system - results in swelling caused by fluid collection - mostly affects legs but also arms, breasts and genitalia - ~25 million men affected by hydrocele (swelling in the scrotum).

Answer 221

Swelling and decreased lymph system function also make it difficult to fight infection - bacterial infections cause hardening and thickening of skin – called elephantiasis.

Answer 222

cough, shortness of breath and wheezing.

Answer 223

1. Social stigma and sub-optimal mental health 2. Loss of income-earning opportunities 3. Increased medical expenses for patients (and their carers)

Answer 224

simple hygiene measures, skin care, exercises and elevation of affected limbs

Answer 225

1. Sleep under a mosquito net, or in air-conditioned room 2. Wear long sleeves and trousers 3. Use mosquito repellent on exposed skin

Answer 226

reduces microfilariae in the blood of infected people and diminishes transmission

Answer 227

1. Binds to β-tubulin and inhibits microtubule assembly 2. Impaired uptake of glucose by larval and adult stages 3. Reduced energy production - parasite is immobilised and eventually dies

Answer 228

Poorly absorbed (5-10%) from gut – good for treating GI nematode infections as drug concentration remains high - but treating tissue dwelling nematodes is more difficult. the worm only needs to be paralysed for expulsion of GI nematodes because you can just poo them out.

Answer 229

1. Periodic administration of anti-helminthic drugs to eliminate infecting worms (i.e. de-worming) (WHO only recommends for high prevalence areas) 2. Health and hygiene education to prevent re-infection by encouraging ‘healthy’ behaviour 3. Improved sanitation to reduce soil contamination with infective eggs (This is not always possible in resource-poor countries or communities).

Answer 230

1. Ivermectin binds with high affinity to glutamate-gated chloride channels in invertebrate nerve and muscle cells. 2. Binding causes increased permeability of cell membrane to chloride ions and hyperpolarization of nerve or muscle cell 3. Hyperpolarization results in paralysis and death - either directly or by causing the worms to starve

Answer 231

reduce microfilariae in bloodstream

Answer 232

14 countries have achieved elimination of lymphatic filariasis as a public health problem, but preventive chemotherapy still required in 52 countries

Answer 233

6.7 billion treatments delivered to >850 million people

Answer 234

Dorso-ventrally flattened (flat), ribbon like bodies – cestodes can be very long (but not always).

Answer 235

Taenia saginata (beef tw): 4-12 m Taenia solium (pork tw): 4 - 8 m Echinococcus granulosus (dog tw): 3-6 mm

Answer 236

scolex (anterior attachment organ with hooks/ suckers to attach to host tissue) strobila (the segmented part of the body of a tapeworm that consists of a long chain of proglottids).

Answer 237

sensory systems, muscles and locomotory systems are reduced and there is no gut. no body plan- unlike nematodes

Answer 238

a metabolically active layer through which nutrients are absorbed AND secretions and waste materials exported.

Answer 239

bud sequentially + grow continuously from the neck behind the scolex, going from immature-mature-gravid (pregnant). (new proglottids replace old)

Answer 240

700-1000 proglottids – 10 shed per day (1 million eggs)

Answer 241

help in grabbing hold of your gut lining- attachment

Answer 242

contains both male and female sex organs - testes and ovaries

Answer 243

Fertilisation can occur between proglottids of the same or a different tapeworm. After fertilisation, proglottids fill with eggs and gravid proglottids break off the chain and pass out in faeces OR can crawl ‘caterpillar like” through the anal sphincter.

Answer 244

Visualisation of primary lateral branches (carmine staining) of the uterus allows differentiation between species and so can be used for diagnosis.

Answer 245

Cestodes absorb nutrients from the host intestine directly through the tegument. This is not a passive process and specialised membrane transport systems exist within the tegument to allow active transport. Act in a similar manner to brush border on mammalian mucosal cells but may also serve attachment function.

Answer 246

Microvillous projections (microtriches) Increased tegument surface area (3-6 fold)

Answer 247

Protonephridium/ flame cells (due to beating cilia looking like a flame) which extend into a fine tubule

Answer 248

Cilia generate current in the protonephridium– excess water containing nitrogenous waste forced into tubule and eventually out of tapeworm body via excretory pores. Allows tapeworm to conserve water and eliminate salts - essential for survival in the host intestine.

Answer 249

an organism which supports the adult or sexually reproductive form of a parasite

Answer 250

cows/ pigs

Answer 251

1. gravid proglottids produce eggs, which are ingested by intermediate host containing a larval stage called the oncosphere. 2. cattle (T.saginata) + pigs (T.solium) become infected by ingesting vegetation contaminated by eggs/ gravid proglottids. 3. oncosphere penetrates through the gut wall through the mucosa of duodenum due to acidic environment, passes into blood + encysts within tissues 4. thick membrane (embryophore) forms protection around oncosphere, called a cysticercus. 5. humans ingest infected meat, the cysticerci excyst within the human intestine- scolex evaginates (activated by bile) + attaches to intestinal wall and develops into adult tapeworm.

Answer 252

immediately viable and can remain in the environment for several weeks = enormous reproductive potential

Answer 253

infective within 7-10 weeks and remain viable for several months

Answer 254

the infected parts are condemned and remaining meat is frozen (for at least 21 days; <-7oC) and declared safe for human consumption.

Answer 255

Freezing lethal to cysticerci

Answer 256

at least 56°C (133°F)

Answer 257

worldwide distribution - common in Africa, some parts of Eastern Europe, Philippines and Latin America – very rare in India as Hindus do not eat beef

Answer 258

Partially cooked, smoked, or pickled beef can be infective, although raw beef (steak tartare) is commonest cause of infection

Answer 259

worldwide- More prevalent in regions where humans live in close contact with pigs and eat undercooked pork - very rare in Muslim countries as they do not eat pork

Answer 260

Adult worms can (rarely) cause intestinal blockage (segments lodged in the appendix, bile or pancreatic ducts) or penetrate gut wall but pathology is usually inconsequential.

Answer 261

passing motile segments lol

Answer 262

T. saginata is larger (maximum 12 vs 8 metres)

Answer 263

digestive disturbances, abdominal pain, nausea and weight loss

Answer 264

several years

Answer 265

praziquantel

Answer 266

The body has adapted quite well to tapeworms and stuff because they’ve been around for ages, unlike the plague and such, which are fairly recent.

Answer 267

Greater difficulty in detecting animals that are lightly infected Global tendency to consume raw or semi-cooked beef.

Answer 268

so humans are the normal definitive host for T. solium; cysticercosis results from humans acting as accidental intermediate hosts for the parasite (this role is normally fulfilled by pigs).

Answer 269

Humans infected with EGGS either by ingestion of food contaminated with faeces, or by autoinfection. Not by eating undercooked pork. Embryonated eggs are ingested by the human host and those oncospheres which are developing in the gut of the pig actually develop in the gut of the human, and they penetrate the intestinal wall + jump into your muscles.

Answer 270

autoinfection- infection by an organism that is already present in the body. here, humans can have proglottids being carried back into the stomach by reverse peristalsis.

Answer 271

major cause of neurological effects + adult onset seizures in most low-income countries. wayyyyy worse than tapeworm infection

Answer 272

yeah if diagnosed early enough

Answer 273

50 million

Answer 274

outbreak in Orthodox Jewish community in New York City blamed on domestic employees from Latin America (where T. solium infection is highly endemic)

Answer 275

Muscles generally no symptoms – may feel lumps under the skin Eyes - rare but can cause disturbed vision or detached retina

Answer 276

seizures and headaches but also confusion, difficulty with balance, swelling of the brain. Death can occur suddenly with heavy infections

Answer 277

acquired epilepsy

Answer 278

‘emergency room’ visits for seizures

Answer 279

inflammation around dying cysts causes brain to swell

Answer 280

in the tissue

Answer 281

seizure control with anti-epilepsy drugs and treatment of increased intracranial pressure

Answer 282

As praziquantel kills viable cysts it can provoke an inflammatory response and so can actually make symptoms worse – co-administration with corticosteroids to manage inflammation.

Answer 283

definitive: dog intermediate: sheep, goats, swine, etc

Answer 284

1. the adult tapeworm exists in the dogs small intestine 2. gravid proglottids produce eggs, which become embryonated + exist in the faeces (either infects humans or sheep or cycle keeps going) 3. oncosphere hatches + penetrates intestinal wall 4. hydatid cysts in liver, lungs, etc 5. protoscolex from cyst 6. scolex attaches to intestine

Answer 285

Northern Africa, South America, some parts of Asia

Answer 286

hydatid cysts

Answer 287

Cysts can be 1–20 cm - larger cysts can contain litres of fluid

Answer 288

1. Germinal layer (GL) (20µm thick) is a living, syncytial tissue, within which developing (D) and mature brood capsules (MBC) form. These produce protoscoleces (P, 100µm), (equivalent to cysitcerci). 2. Protoscoleces can either be retained in BCs or burst into cyst fluid (CF) – each protoscolex has potential to differentiate into another hydatid cyst. 3. Laminated layer (LL) is a thick (several mm), non-living, carbohydrate-rich matrix, secreted by the GL.

Answer 289

As they get larger, they exert pressure on surrounding organs

Answer 290

95% of cysts develop in lungs or liver but as shown in this MRI scan can also form in the brain.

Answer 291

1. Sheep farmers – from contact with sheep dogs 2. Dog breeders and dog handlers 3. Street cleaners and waste disposal workers 4. Veterinary surgeons

Answer 292

as infection is often asymptomatic, so during surgery or when imaging is being used for other reasons.

Answer 293

1. PAIR (Puncture, Aspiration, Injection (colicide = hypertonic saline to kill protoscoleses), Re-aspiration) technique 2. Surgery - if the lesion is confined, radical surgery can be curative 3. Drug treatment – albendazole (inhibitory effect on tubulin polymerization) 4. ‘Watch and wait’

Answer 294

Decision based on location of cyst and both the medical infrastructure and human resources available – but frequent relapses often occur due to late diagnosis.

Answer 295

they are parasitic flukes (trematodes) they're the 2nd most devastating parasitic disease in terms of socio-economic importance + public health impact. Endemic > 70 tropical and sub-tropical countries. 200 million people infected - 600 million people at risk Also known as Bilharzia or Snail Fever

Answer 296

Neglected Tropical Disease

Answer 297

85% of cases occur in Africa, especially the mid region. also Brazil

Answer 298

Schistosoma mansoni (Africa) S. haematobium (Africa and Middle East) S. japonicum (S.E. Asia and China)

Answer 299

1. humans 2. fresh water snails

Answer 300

Snails act as an intermediate host for the parasites, allows asexual reproduction to occur in the alternative host

Answer 301

infecting more than one host species allows parasites to survive periods when one host is scarce. e.g. the parasites can go into water, maintain their viability here and infect a snail if there haven’t been humans there for a while.

Answer 302

intermediate host releases parasites into host environment or is part of the definitive host's food chain. e.g. when humans wash their clothes or something in the water, the snail can infect host.

Answer 303

1. Pollution of water with excreta containing eggs 2. Presence of suitable snail hosts 3. Human contact with water infected with cercariae

Answer 304

1. cercariae (motile, free living) are released from the infected cell and use water turbulence + skin-derived fatty acids to locate a human host- they migrate towards light where humans probs will be as they're phototropic. 2. they attach to skin + use proteases to break through the epidermis within like 10 minutes. they shed their tail + glycocalyx (sugar coat) to become schistosomula. 3. they migrate from skin-liver via lungs in the lymphatics + progress through 3 developmental stages: skin, lung + liver schistosomula. 4. they mature into adult worms in the liver, where they pair up for life + migrate to their final egg-laying site. 5. paired female worms release eggs, which have a spine, throughout adult life (300-3000 eggs per day). Period of time between infection to egg laying~ 25 to 30 days.

Answer 305

the female and male schistosomes have different bodies + different sexual organs

Answer 306

inside male's gynaecophoric canal

Answer 307

Female 7-20 mm, males slightly shorter but broader up to 5 years depending on species

Answer 308

the venous system

Answer 309

You can only get transmission of the infection if there are both a male and female schistosome present

Answer 310

1. eggs reach suitable freshwater conditions and hatch to become motile (miracidia- ciliated larval stage) + infect a snail 2. remain infective in snails for 6-8 hours after hatching 3. in the snail tissue, miracidium transforms into a non-motile primary sporocyst, producing generations of secondary ones, which produce lots of cercariae (1000s per week) 4. cercariae released from snail can infect human host

Answer 311

using external stimuli such as light and snail derived chemicals

Answer 312

caused by cercariae burrowing through the skin and causing allergic reaction. symptoms: 1. Occurs on secondary exposure to infection 2. Present < 15 minutes after exposure 3. Continues to develop for 2-3 days 4. Resolves within 5 days also happens when cercariae from a species that can't develop further in humans penetrates human skin.

Answer 313

Begins 2-8 weeks post infection - resolves after several days or weeks. Usually mild and transient but can be severe/life threatening. Symptoms: 1. Dry cough 2. Mild to moderate hepatosplenomegaly 3. Pyrexia (fever) 4. Weight loss Giant urticaria (hives) – transient, slightly elevated patches of skin redder or paler than surrounding skin - often accompanied by intense itching – caused by release of vasoactive mediators, predominantly histamine, from mast cells.

Answer 314

S. haematobium: Haematuria – blood in urine Dysuria - painful or difficult urination Abdominal pain Bladder inflammation Other species (S. mansoni etc.) Abdominal pain Diarrhoea – may be bloody Hepatomegaly – with or without splenomegaly

Answer 315

1. S. japonicum: Intestinal schistosomiasis 2. S. mansoni: Hepatosplenic schistosomiasis, Pulmonary schistosomiasis, CNS schistosomiasis 3. S. haematobium: Urogenital schistosomiasis

Answer 316

ureteric obstruction and renal failure, bladder cancer, genital lesions, infertility, ectopic pregnancies (female genital schistosomiasis)

Answer 317

You don’t really get cercarial dermatitis or acute schistosomiasis if you live in one of the countries where schistosomiasis is endemic, but if you’re visiting + it’s upon secondary exposure (like if you go swimming one day then go swimming the next day), then you can develop it.

Answer 318

1. Egg deposition 2. Inflammation 3. Granuloma formation 4. Obstruction of urinary tract or portal circulation 5. Fibrosis

Answer 319

1. immune cells accumulate around egg (trapped eggs can become miracidia) 2. antigens are released by egg/ miracidia (like 4-8 days after egg deposition) 3. miracidia die + the granuloma protects the host from effects of toxins from dying miracidia 4. egg-induced granulomas result in pathological change in liver-leading to disease

Answer 320

Pipe-stem fibrosis causes portal vein branches to resemble sections of clay pipe stems. Blockage of portal vein branches and development of anastomoses (cross-connections between adjacent channels). (you can get fibrotic regions in the tissue that don’t allow the function of blood filtering to happen properly)

Answer 321

Hepatosplenomegaly (enlarged liver and spleen). Portal hypertension i.e. a build-up of pressure in the vein connecting intestines and liver due to: cirrhosis of liver (scarring of the liver) ascites (fluid within the abdominal cavity)

Answer 322

1. playing in water/not collecting water for the household. 2. Some evidence for immunity also as people age, probs have host defences against it as only 30-50% of cercariae can mature. 3. Schistosomes are able to evade the host immune response – they coat themselves in host proteins to hide within the host. Evidenced by transplantation experiments between schisotsomes from different species.

Answer 323

Presence of eggs in either stool or urine samples Presence of worm antigen circulating cathodic antigen (CCA) in urine

Answer 324

1. Ultrasound - also evaluates the disease severity and complications in target organs 2. Bladder or rectal biopsy – eggs passing across intestinal or bladder wall 3. Serological testing – antibodies against adult worms

Answer 325

mass drug administration of chemotherapy to school age children WHO set ambitious goals of control of schistosomiasis by 2020 and its elimination as a public health problem by 2025

Answer 326

Well absorbed from gastrointestinal tract - but serum half-life of only 0.8-1.5 hours Few side effects and few contra-indications Distributed primarily to school age children (highest infection burden)

Answer 327

1. Increased cell membrane permeability 2. An imbalance in ion transport 3. Loss of intracellular calcium 4. Massive contraction and paralysis of musculature 5. Disintegration of the schistosome tegument

Answer 328

The tegument covering trematodes and cestodes - metabolically active surface Damage to the tegument exposes the worm to immune mediated damage

Answer 329

S. mansoni

Answer 330

1. re-infection is common due to the presence of the snail host 2. praziquantel is less active against immature worms 3. chemo doesn't always kill adult worms, but can just suppress egg production 4. limited availability of praziquantel- in 2021, only 29.9% of people requiring treatment received it 5. disease control via preventative chemo unlikely to interrupt transmission

Answer 331

1. chemo 2. snail control 3. improved sanitation 4. provision of safe water 5. health education 6. avoiding swimming in freshwater in disease-endemic countries 7. drink 'safe water'

Answer 332

headaches, fever, tiredness, joint aches, runny nose, sore throat, coughing, vomiting

Answer 333

a simple, tiny, infectious parasite

Answer 334

only reproduce within living cell

Answer 335

genetic material (DNA or RNA), surrounded by a protein coat and/or envelope (derived from a host cell membrane)

Answer 336

limited range of animals which can be infected- differs differs between all pathogens e.g. SARS-CoV-2 has a very broad range, whereas measles has a very limited host range.

Answer 337

it can’t be translated on its own and needs to be a + one before that can happen.

Answer 338

8 segments of genome. This increases the coding capacity to produce more proteins.

Answer 339

Binds sialic acid receptors -> viral entry Agglutinates RBCs Antigenic (neutralizing)

Answer 340

Cleaves sialic acid to release virus Degrades mucin, allowing virus to get very close to cell + stuff Antigenic (non-neutralizing)

Answer 341

Forms proton channel that facilitates uncoating and assembly Stabilizes the virus budding Antigenic (neutralizing)

Answer 342

Lipid bilayer from plasma membrane of infected host cell Supported by the M1 protein, which play role in virion assembly

Answer 343

Each of eight different single stranded RNA + nucleoprotein (NP) + RNA polymerase (PB1, PB2 and PA)* basically just RNA with 4 different proteins combined.

Answer 344

A: very wide host range- human, swine, birds, horses, bats, dogs B: not too serious- human, seals C: basically not there- human, swine, dogs D: literally no info on it- swine cattle

Answer 345

A: severe clinical diseases B: generally mild but could be severe C: only mild or asymptomatic D: no information available

Answer 346

A: most capable of unleashing epidemics + pandemic B: generally cause only milder epidemics C: doesn't cause epidemics or pandemics D: no information available

Answer 347

Epidemic: rapid spread of infection in a city, state or entire country over a short period of time Pandemic: an epidemic that spreads across boarders, even worldwide, affecting large numbers

Answer 348

Viruses are named like H3N2 for example, meaning the 3rd type of HA and the 2nd type of N2. some cool ones includes H1N1 + H3N2

Answer 349

birds bless them

Answer 350

Spanish flu: 1918- H1N1, 50 million deaths Asian flu: 1957-58- H2N2, 2 million deaths Hong Kong flu: 1968-69- H3N2, 1 million deaths Swine flu: 2009- H1N1, 18200 deaths

Answer 351

people develop immunity to strains

Answer 352

1. attachment: HA-sialic acid on host cell. virus endocatosed, vessel membrane transferred to endosome 2. uncoating: endosome application- M2 increases H+ -> uncoating 3. transcription: nucleocapsid goes to the nucleus + transcribed mRNA are translated into proteins in the cyotplasm 4. replication: the vRNP (-s) converts to cRNP (+s), then through replication generates vRNP (-s) -> cytoplasm 5. assembly: HA/NA transported to cell surface with M1 + genome segments 6. budding: virus buds off by NA

Answer 353

The Receptor Binding site - confers host-specificity The Cleavage site where the single chain is cut into two chains. At the N-terminus it is fusion peptide which is critical for infectivity

Answer 354

Pathogenicity: how severe the illness is. Specificity: like how many different hosts and stuff can be infected.

Answer 355

N-acetylneuraminic acid- α2,6 linked galactose

Answer 356

N-acetylneuraminic acid- α2,3 linked galactose

Answer 357

Biochemically, the sialic acid receptor is split into 2 parts. Birds and humans are decorated with different conformations of sialic acid receptors, while pigs have both so any virus that comes out of birds or humans can infect the poor pigs :(

Answer 358

antigenic drift entails minor changes in the antigenic sites of the HA and NA, which makes different strains of subtypes, which causes he epidemics. this is because of: error prone replication + no proofreading. Provides a selective advantage: seasonal flu (epidemics) Influenza A, B, and C

Answer 359

antigenic shift is major changes due to a re-assortment of genes that occurs when 2 different influenza viruses infect the same host. also when segments from influenza A and B, for example, can combine, forming a new strain that we haven’t seen before so we don't have immunity. this occurs due to: Segmented genome. Wide host ranges. causes complete change in HA, NA or both, but only in influenza A. usually, requires on-human intermediate

Answer 360

H1 + H3 are the most prevalent ones.

Answer 361

The WHO investigates the strain that could most likely cause a pandemic in the next year, which gets sent to a vaccine production centre, and they manufacture + assemble it for dissemination.

Answer 362

Treatment or Prophylaxis- Influenza A only CNS + anticholinergic effect, teratogenic The gene for M2 is susceptible to mutations, so strains are developing resistance (90 % viruses are now resistant to this category).

Answer 363

Influenza A+B Generally well-tolerated, some nausea/vomit- most effective within 48h of onset Relief from symptoms for ~1-2 days or less Treatment or prophylaxis (oseltamivir) Oral or inhaled (zanamavir)

Answer 364

1. 2002 2. 2012 3. 2019

Answer 365

Coronaviridae

Answer 366

All the conventional ones we’ve seen that are infectious to humans belong to the genus Betacoronavirus, in the subfamily Coronavirinae.

Answer 367

Gamma + delta-coronaviruses don’t really have potential to cause infections in humans, but the other ones do. The alpha- + beta-coronaviruses are the ones that pose concern to public health.

Answer 368

SARS + MERS have different receptors in the body, hence why they have different intermediate hosts and stuff.

Answer 369

SARS: 8098 cases, 774 total deaths (epidemic ended) (~1% case fatality) MERS: 2521 cases, 866 total deaths (infections still occurring) (35% case fatality rate)

Answer 370

1. with 1, we knew the reservoir (civet cats), we don't really know what it is with 2 2. with 1, most transmission occurred in hospitals, but with 2, there was widespread community transmission 3. there was no transmission until 24-36h after symptoms with 1 + it had like no asymptomatic cases because it was a bit ore pathogenic. 2 had loads xxx

Answer 371

1. a cluster of pneumonia cases appeared in Wuhan wet market 2. sequencing of nasal samples identified a coronavirus in all patients 3. phylogenetic + genetic analysis highlighted that the coronavirus is closely related to SARS-CoV-1 + a previously isolated bat-CoV called RaTG13. 4. due to closer association with SARS-CoV-1, the new coronavirus was called SARS-CoV-2

Answer 372

Single-stranded, non-segmented, positive sense, ~30 kb long genome influenza is segmented + +ve sense

Answer 373

S,E,M,N constitute the virion

Answer 374

Include NSP1, NSP2, NSP3, NSP14 etc

Answer 375

Produced only in infected cells- non-essential to the virion but needed for replication by antagonising the immune systems when the virus infects the cell. Includes ORF3b, ORF6, ORF7a etc

Answer 376

Host tropism Protective immune responses (vaccines) Virulence – severity of the disease

Answer 377

Component of nucleocapsid Virus transcription efficiency Protective immune responses (vaccines)

Answer 378

Most abundant amongst structural proteins Assembly of virus particles

Answer 379

Smallest amongst all the structural proteins Virus assembly, and release

Answer 380

SARS-COV-2 undergo discontinuous transcription

Answer 381

non-structural ones xxxx

Answer 382

polyproteins xxx

Answer 383

ACE2-TMPRSS2 Route (Delta variant) Endocytosis Route (Omicron variant) The enzyme TMPRSS2 basically chops the S1/S2 site so the virus becomes infectious + fuses with the plasma membrane, or it can just endocytose. Cleavage of S protein is marker of disease severity.

Answer 384

Spike protein interacts with cell surface protein ACE2 to enter the cells

Answer 385

1. Once the virus enters the cytoplasm, the genome comes out (REMEMBER it’s positive so the ribosome immediately comes over + starts translating those proteins e.g. pp1a). 2. the viral genomic RNA acts like mRNA- it can directly make proteins. 3. genomic RNA produces proteins + RNA necessary for viral reproduction by hijacking host cell machinery. 4. pp1a + pp1b are cleaved by PL proteinase and 3CL proteinase (smaller non-structural proteins), which interact with the genome and become part of it. 5. NSPs and RdRp make replication-transcription complex (RTC) 6. The genome then becomes converted into sub-genomic RNA, which are translated into proteins which are released into protein-maturing bodies e.g. Golgi.

Answer 386

1. protein synthesis happens in double membrane vesicles budding off from ER 2. structural proteins + newly-formed RNA are modified, packaged + assembled before release. 3. loads of viruses are assembled at the same time, until the cell must burst.

Answer 387

cytokine storm xxx

Answer 388

it uses the TMPRESS thing. Omicron only infects the upper respiratory tract as it doesn’t require TMPRESS, so the lungs are spared. They will still have loads of coughing and sneezing though, allowing way more spread.

Answer 389

1. Important in almost all currently licensed human COVID vaccines- people usually judge how good a vaccine is based on how many antibodies it produces, as this correlates with disease severity. 2. Most COVID recovered patients have antibodies within 1-3 weeks 3. Severe disease correlates with higher level of antibodies

Answer 390

1. Critical for antibodies responses 2. Protection independent of antibodies in SARS 3. Cross reactive immunity against pan-coronaviruses

Answer 391

1. Important in many viral infections 2. May prevent re-infection

Answer 392

1. droplets 2. aerosols (like breathing, speaking, singing etc) 3. smear infection (like infected surface I think)

Answer 393

Droplets are bigger + heavier, and normally don’t go over like 1 meter. Aerosols go about 2 meters, hence why the social distancing thing was 2 meters.

Answer 394

11% drop !!!!!

Answer 395

live attenuated, whole inactivated, RNA, DNA, recombinant subunits, recombinant viral vectors

Answer 396

1. mAB/ convalescent plasma for ACE-2: prevents virus entering host cell 2,. camostat mesylate: prevent virus entering cell by acting TMPRSS2 3. Lopinanvir-Ritonavir (HIV): inhibition of protease activity 4. Ribavirin (HCV): may inhibit mRNA capping 5. RNA synthesis inhibitors (Remdesivir): inhibits the viral RNA 6. chloroquine group: interfere with the release of progeny from infected host cells

Answer 397

public health, living standards (e.g. nutrition and sanitation), medical science and technology, and clinical practice.

Answer 398

Vaccination – refers to having received the vaccine i.e. getting the injection. Immunisation - means both receiving a vaccine and becoming immune to a disease, as a result of being vaccinated.

Answer 399

Induces active immunity – induces immunity and immunologic memory similar to that acquired by exposure to natural infection but without the risk of disease Immunological memory – allows rapid recognition and response to infection; prevents or modifies effects of disease.

Answer 400

Safety- shouldn’t cause illness/ should be able to be delivered to a wide range of people e.g. elderly, pregnant, etc. Stability- doesn’t require being stored cold (faster, cheaper, better distribution). Cost- link between economics + infectious disease- LICs are more prone to infectious disease- vaccines need to be cheaper + work globally. Ease of administration- oral vs inject. ideally doesn’t need to be administered by a healthcare professional. Also, needle phobia could be dealt with with intranasal stuff. Interrupt spread- instead of limiting the impact on the person, should be able to be killed + stop spread. Doesn't cause disease- elicit a response that gives same immune protection that usually follows natural infection without disease xxx

Answer 401

whole pathogen (bacteria or viruses) for which virulence has been artificially reduced = attenuation

Answer 402

whole “killed” organisms

Answer 403

certain components of pathogens; can be purified; now often generated using recombinant DNA technology. toxoid vaccines, surface protein vaccines, viral vector vaccines, DNA + RNA vaccines

Answer 404

Where you take antibodies present in one body/ host + transfer them to someone else. Can be used with the movement of antibodies from a horse or something to a person, provides protection in warzones. Can be complications with the antibodies as they can form complexes in the human host and stuff.

Answer 405

1 in 200 infections result in irreversible paralysis - 5-10% of those affected by paralysis die

Answer 406

Afghanistan, Nigeria and Pakistan

Answer 407

US$ 40–50 billion

Answer 408

people encased in a chamber with a seal around their neck. The air pressure in the container can be changed, forcing the body to inhale without using the lungs. Used as muscles which aid breathing become paralysed with polio.

Answer 409

1. Polio is transmissible by the faecal/oral route (contaminated food), enters the intestine + gets taken into the gut. 2. The virus passes by GALT (gut-associated lymphoid tissues) in the lymphatics where it can enter the blood in the liver/ spleen. 3. It can replicate in the tissues, so you get a high concentration of it in the blood, and it can transmit into the blood-brain barrier, which can cause meningitis. 4. It can also interact with neurones using the blood-brain barrier, causing paralysis.

Answer 410

antibodies produced against one serotype do not provide protection against other serotypes. The vaccine has the strains from all 3 serial types but doesn’t cause a paralytic response.

Answer 411

by allowing polio virus to grow in non-optimal conditions and selecting randomly occurring mutants that had lost neuro-virulence

Answer 412

Inexpensive and easily administered - supplied as a single oral dose (costs less than US$0.15 per dose). Induces both systemic and mucosal immunity (because it's oral) - antibodies in blood prevent spread of polio to CNS. Mucosal immune response activates the immune system in the GALT, limiting viral replication, which can block transmission. Also, blocks spread to the CNS by blocking route to the blood-brain barrier. Potent response resembles optimal naturally acquired immune response - immunity is probably life long Short-term shedding of OPV in faeces can result in passive immunisation of persons in close contact.

Answer 413

May reproduce features of the disease as subclinical or mild form of the infection. Contraindicative - cannot be given to pregnant patients or immunosuppressed patients (people with a medication that suppresses the immune response/ organ transplant/ etc) - side effects likely to be stronger. Unstable - 12 months: 4oC, 6 weeks: 25oC, 1 week: 37oC- will probably need cold-chain storage which is annoying. May revert to virulent form (e.g. neuro-virulence) - serotype 1 required 57 base substitutions to stop it reverting. 2 + 3 needed 2 base substitutions.

Answer 414

Consists of 3 serotypes – chemically inactivated. BECAUSE OF THIS, cannot cause circulating Vaccine Derived Polio Virus. Antibodies - prevent spread of poliovirus to CNS

Answer 415

Administered as a sub-cutaneous injection (higher cost, starting at US$1 per dose for low-income countries). because it’s not delivered orally, it doesn’t produce the mucosal immune response- protects the individual but doesn’t stop spread. No effect on viral replication in the gut or viral transmission in stool - protects the individual but as wild polio virus can replicate in gut wild virus can be spread to infect others.

Answer 416

Advantages - Cannot cause infection - Can be given to immunosuppressed and pregnant individuals Disadvantages - Less immunogenic and require addition of adjuvants and booster doses to keep up the memory.

Answer 417

To enhance immune response to the antigens included in the vaccine. Mode of actions not precisely defined: To carry the vaccine antigen and slow its release To provoke a local inflammatory response. an adjuvant is aluminium hydroxide (Alum)

Answer 418

1. Poliovirus cannot survive for long periods outside of the human body 2. Type 2 eradicated (1999) and Type 3 eradicated (2019)- required collaborations between the public and large health organisations, as well as funding. 3. Cheap and effective vaccines are available 4. OPV can be administered by anyone - even volunteers.

Answer 419

e.g. in Pakistan and Afghanistan - Taliban targetred workers carrying out polio vaccination programme - children were not being immunised (2018- Nov 2021) and polio cases rose

Answer 420

Clostridium tetani - spores of this bacterium are widespread in the environment

Answer 421

Tetanus is caused by a neurotoxin produced when C. tetani grows in anaerobic conditions e.g. dirty wounds. Tetanus is characterised by muscle spasms - initially in the jaw muscles (lock-jaw). As disease progresses mild stimuli trigger tetanic seizures – prolonged contraction of skeletal muscles - serious complications and eventually death.

Answer 422

diseases that are caused solely through production of toxins by bacteria or something - possible to vaccinate against a ‘detoxified’ version of the toxin.

Answer 423

chemical inactivation to remove toxicity but it is essential that it retains antigenicity

Answer 424

diptheria, tetanus, pertussis (causes whooping cough), these are all bacterial infections.

Answer 425

Purified and inactivated – 95% protective in trials Derived from human blood – risk of viral transmission Extremely expensive to produce - because it’s required for the surface protein to be filtered out of people’s blood.

Answer 426

safer and cheaper to produce (and in this case equally effective in generating immunity)

Answer 427

1. Adenovirus from a chimpanzee is modified to be non-pathogenic and contain the gene for the SARS-CoV-2 spike protein + the DNA is inserted into the vaccine. 2. The vector delivers the vaccine into the patient’s body via sub-cutaneous vaccine. 3. Cells take up the gene expressed + produce the spike protein, stimulating an immune response + making antibodies that provide protection.

Answer 428

Adenoviruses

Answer 429

injecting nucleic acids encoding antigens, uptake by host cells resulting in the expression in situ and stimulation of an immune response

Answer 430

DNA is usually delivered in a plasmid vector, so it can go to the nucleus produce mRNA and be expressed.

Answer 431

1. absence of any infectious agent 2. improved vaccine stability 3. relative ease of large-scale manufacture 4. stimulation of both B- and T-cell responses 5. insertion multiple variants of antigens into single vaccine

Answer 432

possible genomic incorporation of immunising DNA might activate oncogenes. gene integration in the nucleus could disrupt normal gene functions + activate oncogenes, telling genes to over-proliferate= oncogenesis. So, not licensed for human use. RNA vaccines avoid this concern but are less stable.

Answer 433

mRNA is usually encapsulated in a lipid vesicle to protect it and facilitate direct uptake into the host cell cytoplasm where is it expressed (produces viral spike protein). Moderna & Pfizer Covid19 vaccines were the first mRNA vaccines to be deployed for mass immunisation of humans.

Answer 434

requires careful long term cold storage – Pfizer vaccine at -70°C and Moderna vaccine at -20°C.

Answer 435

Primary failure - an individual fails to make an adequate immune response to initial vaccination and so infection is possible any time post vaccination. Secondary failure - an individual makes an adequate immune response initially, but then immunity wanes over time (this is a feature of most inactivated vaccines, hence the need for booster vaccinations).

Answer 436

1. HIV has an really high mutation rate, with variants arising within a single infected individual – which has frustrated efforts to make an effective HIV vaccine despite significant investment. 2. Parasites are “master immunologists” – because of the chronic nature of their infections they each have various ways to evade the immune response: antigenic polymorphisms and/or variation, drifts and shifts etc. 3. Also most of the people that are affected by these diseases live in poorer countries so there has not been sufficient financial incentive or investment to develop vaccines. usually herd immunity thresholds of diseases are at least like 75-85%

Answer 437

1. More immune individuals in a population - less likely it is that a susceptible person will come into contact with person with infectious disease. 2. Herd immunity - prevents spread of disease and protects groups who cannot be vaccinated e.g. infants and immunocompromised individuals. 3. These people get some protection because spread of contagious disease is contained.

Answer 438

VACCINE HESITANCY Vaccination has proven to be very good, but vaccine hesitancy – ‘the reluctance or refusal to vaccinate despite the availability of vaccines’ (WHO) threatens to reverse the significant progress made in tackling vaccine-preventable diseases. Vaccine hesitancy reported in more than 90% of countries in the world and has been identified by WHO as one of its Top Ten Priorities.

Answer 439

this neek Dr Andrew Wakefield claimed to show a link between the MMR vaccine and autism and bowel disease – this work has been completely discredited because he's stupid. Measles cases rising right now is probably due to people not getting their MMR vaccines as children because idiots still believe this man.