1. Microbiology
Introduction to Microbiology
1. What are the 4 basic groups of pathogens?1
2. What is the purpose of a flagella and which basic sub group has them? 2
3. What is the purpose of pilli?3
4. Why is penicillin effective only against foreign organisms (not host cells)? 4
5. What are the rough diameters/lengths of: an erythrocyte, E.coli, staphylococcus,
viruses, parasites5
6. What is a nucleocapsid?6
7. What are rods and cocci?7
8. What do gram positive and gram negative signify?
9. What other differences are there between gram negative and gram positive? 8
10.TB bacteria do not have a positive or negative gram stain, so how are they
identified?9
1 Bacteria, Fungi, Viruses, Parasites
2 Movement or sensitivity (to temperature and chemical changes), some bacterial have flagella
3Pilli are hair like organelles found on many bacteria, they are used to attach to host cells (in the case of
pathogenic bacteria) and are also the targets for B cells to latch onto during immune response
4 Because it attacks the bacterial cell wall which host cells donʼt have
5Erythrocytes (Red blood cells) are 8 micro metres, E coli 2-3 micrometres, Staphylococcus Aureus 1 micro
metre, Viruses 20-300nano metres, parasites can be metres long in the case of worms
6A nucleocapsid is the basic unit of a virus, it is the capsule within which the viral DNA is carried and many
can be released from a host cell to replicate the virus.
7 These are used to signify whether a bacteria is long and thin (rod) or round like an ʻeyeʼ (cocci).
8Gram positive survive drying, some produce spores and have teichoic acid in their cell walls. Gram
negative do not survive drying and have endotoxin in their cell walls, they do not produce spores.
9 ZN stain

2. 11.What causes peritonitis?10
12.List the primary and secondary lymphoid organs11
13.Roughly how many are there of the following cell types in the body per ml of
blood: white blood cells overall, neutrophils, lymphocytes, monocytes12
Collagen Synthesis and Disorders
1. What defines something as a collagen? 13
2. What are collagens type 1, type III, type IV and type VIII? Which are fibrillar and
which are non-fibrillar? 14
3. How does the collagen helix differ structurally from the DNA helix?15
4. What needs to happen to proline for it to support the collagen structure? 16
5. What chemical structural difference exists between alpha 1 and alpha 2 chains?17
6. What causes collagen to have tensile strength?18
7. Is a mutation in collagen more dangerous if it is close to the ribosome, or away
from it? and why?19
10 A ruptured spleen or appendix allows harmful gut bacteria to get into the organ, causing infection.
11 Primary: Bone marrow, thymus (T-lymphocytes must pass through here). Secondary: 50-200 lymph nodes
throughout the body, spleen, Peyerʼs patches in the gut
white blood cells overall (4-7 million/ml), neutrophils (2-4 million/ml), lymphocytes (1-2 million/ml),
12
monocytes (0.2-0.5 million/ml)
13Anything with the amino acid sequence glycine-x-y (with x usually being proline and y hydroxyproline),
collagens are fibrous and insoluble
14Type 1 = most abundant (90%) found in bone, Type 2 = cartilage, Type 3 = found in extensible tissue such
as lung, foetal skin, vascular system, Type 4 = basal lamina of epithelium, structurally kinked so partially
permeable (Types 1-3 are fibrillar, 4 is non fibrillar)
15 Unit of collagen is a loose helix because it has 3 amino acids per turn of the helix whereas DNA has 4, this
is because glycene is the smallest amino acid. The basic unit of collagen is tropocollagen (2 alpha 1 and 1
alpha 2 chains). Collagen gets its tensile strength because the helix cannot be undone in a single movement.
16 Proline and lysine must be hydrolysed to provide structural support for collagen, doing this requires vitamin
C
17Alpha 1 contain glycoproteins and disulphide bridges at the outward ends of the structure, Alpha 2 lack
these
18Collagen gets its tensile strength because the helix cannot be undone in a single movement. Individual
helixes must be left handed whereas triple helix right handed.
19 Mutation nearest the ribosome is most dangerous since the collagen chain is synthesised from the
ribosome outwards and therefore a mutation here will affect the whole chain from that point onwards

3. 8. Lysyl hydroxylase is also required for the formation and support of collagen, how
is it activated?20
9. What structural modification makes the basic unit of tropocollagen into collagen
type 1?21
10.In which type of collagen are the ends not trimmed? 22
11.Give examples of a heritable collagen disease and an environmental one23
12.What are the symptoms and cause of osteogenesis imperfecta?24
13.What are the types and effects of Ehlers’ Danlos Syndrome? 25
14.Which collagen disease is a competitive inhibitor to lysine oxidase?26
15.What is Cu2+ needed for in collagen synthesis?27
16.What does scurvy do in terms of collagen?28
17.Which collagen diseases affect collagen types II, X and XI and therefore cartilage?
29
Bacterial Pathology
20Lysyl hydroxylase is responsible for the hydroxylation of lysine to lysine hydroxylase and is activated by
the reduction of Fe3+ to Fe2+, which requires vitamin C
21The loose ends are trimmed (COO- at the ribosome and +H3N at the outward end) leaving the central
helical chain
22 Collagen type 4 since it needs the ends to provide gaps in its looser structure
23 Heritable (genetic): Osteogenesis imperfecta, Environmental (source): Vitamin C/Copper deficiency
24An autosomal dominant heritable condition (50% chance if parent sufferer) which causes brittle bones,
caused by substitution of glycine in collagen with another amino acid
25
ED type 4 affects collagen type 3 which is used in extensible smooth muscle, can lead to aortic rupture.
ED type 3 affects collagen in joints (type 2) and leads to hyper-mobility of joints and later arthritis.
26 Lathyrism
27 Needed in activation process of lysine oxidase along with vitamin C
28Scurvy is Vitamin C deficiency, vitamin C is crucial in the activation of lysyl hydroxylase because it reduces
Fe3+ to Fe2+, without lysyl hydroxylase collagen cannot be synthesised or stabilized.
29 Chondrodystrophies

4. 1. What are the three classes of bacteria in relation to how infective they are and
what characterizes them?30
2. What is the name of the bacteria found commonly on everyone’s skin?31
3. Which bacteria are the most commonly found in gut flora?32
4. What is a subclinical infection? 33
5. What is a localised infection (give examples)?34
6. What are the most dangerous toxins produced by Staphylococcus Aureus and
what do they do?35
7. What is the toxic mechanism of septicemia?36
8. What happens in toxic shock syndrome?37
9. What sort of ‘host responses’ can be signs of infection? 38
10.Why would giving antibiotics to a meningitis patient worsen the condition initially
before ultimately curing it? 39
30 Commensal = normal generally harmless colonies & flora, Opportunist = mostly harmless flora but can
cause infection if they get into the wrong places, Pathogenic = primarily cause diseases (e.g. TB), nobody is
a ʻnormalʼ carrier
31 Staphylococcus Epidermis
32 E. Coli
33An infection which does not cause severe/noticeable symptoms e.g. being a carrier of the common cold or
chickenpox (can have this as a symptomless infection as a child)
34An infection which is self limiting and can only affect a particular area of the body, e.g. sore throat,
diarrhea, rarely progress to systemic infection
35Coagulase enzyme (converts fibrinogen into fibrin and results in the clotting of blood) and PVL (kills white
blood cells and allows infection to take hold further)
36 Produces endotoxin which damages cell walls, toxin invades blood and has 1/3 mortality rate
37 Bacterial toxins produced by S. aureus or S. pyogenes called superantigens allows the nonspecific binding
of MHC with T cell receptors resulting in up to 20% of the bodyʼs T cells being activated against host tissues
causing multiple system failure.
38Cytokines produced, antigens presented to T cells, histamine release, neutrophils excreted to area and
increased blood vessel permeability.
39They increase the level of ʻbacterial productsʼ in the system. Immune symptoms increase against
antibiotic. Sometimes steroids are given in conjunction with the antibiotic to lessen this effect.

5. 11.What is the biological mechanism of fever?40
Viral Infection
1. What is ‘tropism’?41
2. What is the difference between active and passive immunity? 42
3. What defines an ‘obligate intracellular parasite’? 43
4. What is the size range for viruses?44
5. What are the basic structural features of a virus? 45
6. How are viruses detected in the lab? 46
7. What categories might viruses be classified by? 47
8. What needs to happen to -ve sense stranded viral RNA to replicate? 48
9. Give 2 examples of DNA based viruses and say whether they are enveloped or
non-enveloped49
40Increased cytokine production, effect on hypothalamus (thermoregulation) and prostaglandin E2
production in hypothalamus
41Tropism refers to what types of cell the virus can get into. In terms of invasiveness, can they break down
barriers/membranes to get into cells.
42 Active is developing your own immunity in response to pathogen exposure. Passive is inherited immunity
i.e. fetus inheriting maternal antibodies or by antibody transfusion in immunodeficiency
43 An obligate intracellular parasite is a virus. They can only grow inside ʻhost cellsʼ and invade cells via
either DNA or RNA based mechanism and express receptor binding proteins for antibodies as well as
potential cells to invade.
44 20-300nm
45 All viruses contain a DNA or RNA core which is surrounded by a capsule forming a nucleocapsid. Many
viruses also have a virus envelope studded with glycoproteins. The viral envelope usually originates from an
invaded host cell. Non-enveloped viruses are better at surviving in harsh environments such as the GI tract,
as the envelope makes them more susceptible to chemical attack a lipid bilayer also means the virus may
dry up.
46 Either serological techniques (identification of virus specific antibody in the plasma.
47Enveloped or non-enveloped, RNA or DNA based, number of strands (one genome or segments), +ve or -
ve sense strand.
48Needs to be changed to +ve sense stranded. Many -ve stranded DNA contain ssRNA dependent RNA
polymerase to make +ve stranded. Double stranded viruses contain double stranded RNA dependent RNA
polymerase. Retroviruses (HIV) contain reverse transcriptase.
49Parvoviridae (non-enveloped), papovaviridae (non-enveloped), hepandnaviridae (Hepatitis, enveloped),
adenanridae ((non-enveloped), herpesviridae (enveloped)

6. 10.Give 2 examples of DNA based viruses and say whether they are enveloped or
non-enveloped50
11.Which cells/molecules does the Influenza virus affect? 51
12.Which cells/molecules does Rabies affect?52
13.Which cells/molecules does HIV invade?53
14.Which cells/molecules does Epstein Barr virus invade? 54
15.Which cells/molecules does Reovirus (not rhinovirus) attack? 55
16.Describe the 6 main stages in a cycle of lytic viral infection/replication56
17.What is latent infection?57
18.What is the acute phase of infection? 58
19.What defines chronic infection? 59
50Picorna viridae (non-enveloped), thomyxoviridae (enveloped), paramyxoviridae (enveloped), retroviridae
(enveloped)
51 Salic acid on glycoproteins
52 Acetylcholine A
53 T cells, causing failure of immune response
54 B cells, causing failure of immune response
55 B-adrenergic hormone receptor
56 1/ Replication (synthesis of DNA), 2/Assembly of capsids containing nucleic acid, 3/Release of capsids
from cell, 4/Binding of capsids to receptors on new cell, 5/Penetration of new host cell by membrane fusion/
phagosome uptake, 6/Uncoating, capsids release RNA/DNA
57 Virus persistence after initial clearance at which point the infection may become asymptomatic
58The acute phase describes rapid replication of the virus after initial infection when symptoms are most
obvious
59Chronic infection is when a virus may stay in the system in large numbers for an extended period without
causing a symptom/disease episode