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Microbiology Flashcards

1
Q

What are the different types of helminths?

A

Nematodes (roundworms) - intestinal, larva migrans, tissue (filaria)
Trematodes (flatworms, flukes) - blood, liver, lung, intestinal
Cestodes (tapeworms) - invasive and non-invasive

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2
Q

What are the general features of helminths?

A

Rare in the UK - most cases are imported
Cannot reproduce without a period of development outside the body which involves specific environmental conditions, animal host and/or vectors.
The total worm burden cannot increase without contrast re-exposure to infection in humans.
Some cannot adapt fully to the human host so never develop into adults within the human.

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3
Q

What is the pre-patent period in relation to helminths?

A

The interval between acquiring infection and the appearance of eggs/larvae in the stool.

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4
Q

What are intestinal nematodes?

A

Soil-transmitted
All transmitted via eggs or larvae
The egg or larvae is not usually infectious when first passed and has to undergo a period of development in the soil.
Faecal-oral spread

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5
Q

What are the features of Ascaris lumbricoides?

large roundworm

A 
15-30cm long
Mainly in the tropics
Lives a year or more
Pre-patent period is 60-75 days
Children particularly prone to infection
Adult worms in the small intestine, female lays 200,000 eggs a day, eggs hatch and invade the mucosa of the small intestine, juveniles migrate to the lung, break out in alveoli, swallowed and return to SI.
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6
Q

What are the signs and symptoms of Ascaris lumbricoides? (large roundworm)

A
  • Loeffler’s syndrome: associated with larval migration through lungs, 10-14 days after infection commenced, cough, fever, CXR infiltrates, wheeze
  • Effects of adult: often asymptomatic, otherwise mainly mechanical (intestinal obstruction, biliary/pancreatic duct obstruction, appendicitis) or malnutrution
  • Odd presentations: emerging from eardrum, nose, mouth, anus
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7
Q

What is the treatment for Ascaris lumbricoides? (large roundworm)

A

Piperazine, Pyrantel, Mebendazole, Levasimole

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8
Q

What are the features of the hookworm?

A

Two species, similar in the disease they cause
Ancyclostoma duodenale - asia, mediterranean, middle east
Necator americanus - americas
Small white worm, 1cm, PPP 40-100 days

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9
Q

What is the life cycle of hookworms?

A

Adults attach the mucosa of the duodenum and jejunum (sometimes ileum). Female produces eggs which pass into the soil via faeces. Hatch after 24 hrs and develop into infectious filariform larvae after 5-10 days. They penetrate exposed skin and migrate to the lungs. They break out into alveoli, swallowed and mature in SI.

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10
Q

What are the clinical features of hookworms?

A
  • Ground itch: at sight of entry of larvae
  • Mild pulmonary symptoms due to pulmonary migration
  • Common cause of iron-deficiency anaemia
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11
Q

How do you diagnose roundworms?

A

See emergence of the worm with or without a gastroscope

Stool microscopy for eggs

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12
Q

How do you diagnose hookworms?

A

Stool microscopy for eggs

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13
Q

How do you treat hookworms?

A

Iron supplements, pyrantel, mebendzole

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14
Q

What is enterobius vernicularis? (pinworm/threadworm)

A

Very common in the UK
5-10 mm long, lives fo 56 days, PPP 40 days
Ingested eggs go straight into the duodenum where they hatch, mature adults go into caecum, gravid female migrates to anus and at night lays 20,000 eggs on perianal skin at night, eggs embroyate within 4-6 hours causing itching of bottom.
Commonly affects whole families.
Can cause appendicitis, vaginall penetration or even make it to the paranasal sinuses.

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15
Q

How can pinworm/threadworm be diagnosed?

A

Microscopy of sellotope strip applied to the perianal region

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16
Q

How can pinworm/threadworm be treated?

A

Mebendazole, Piperazine, Pyrantel

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17
Q

What are the features of whipworms?

A

Found worldwide, especially in the tropics
2-5cm long, live for about a year, PPP 70-90 days
Adult resides partly buried in the mucosa of the large bowel

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18
Q

What is the lifecycle of whipworms?

A

Found in the caecum, AC and occasionally throughout the colon.
Eggs pass into soil via faeces.
Embryonation in moist soil takes about 21 days.
Eggs ingested by a suitable host.
Immature larvae hatch from eggs when they reach the small intestine.
Larvae pass into the large intestine after 1 week of development.
Larvae embed in the mucosa via their thin anterior ends, reach sexual maturity and mate.

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19
Q

What are the clinical features of whipworm?

A

Resident in the large bowel
Often asymptomatic and co-exists with Ascaris lumbricoides
If infectation is heavy: bloody diarrhoea, rectal prolapse, anaemia, wasting, eosinphilia

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20
Q

How to diagnose whipworm?

A

Stool microscopy for eggs

Worms may be visible of sigmoidoscopy

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21
Q

What is the treatment for whipworm?

A

Mebendazole, Albendazole

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22
Q

What are the features of strongyloides stercoralis?

A

Causes strongyloidiasis
Found worldwide
Adult is 2-5mm long PPP 17-28 days
Adult is 2mm long and lies buried in the small intestine mucosa,

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23
Q

What is the life cycle of strongyloides stercoralis?

A

Small number of eggs laid by female whose head is buried in the submucosa of the SI, eggs hatch immediately and rhabiform larvae are passed into faeces, mature in soil. Penetrate skin and migrate to the lungs, then break out in alveoli, are swallowed and mature in the jejunum.

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24
Q

What are the clincal features of strongyloides stercoralis?

A

Pruritis are the site of larval entry
Pulmonary symptoms associated with larval migration
Gut symptoms: malabsorption with eosinophilia
Larva currens: skin rashes associated with autoinfection

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25
Q

What is hyperinfection syndrome?

A

Caused by strongyloides stercoralis
Associated with auto-infection and an immunocompromised state
Diarrrhoea, weight loss, malabsorption, paralytic ileus, peritonitis, bacterial problems
No eosinophils, larvae are found in stools and sputum

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26
Q

What is Larva Migrans?

A

Caused by toxocaracarius (dog roundworm) and t. cat (cat roundworm).
Eggs are ingested, develop into larvae, invade tissues for 1-2 years, organism develops no further.
Mainly a disease of children
Diagnosis: eosinophilia, serology
Treatment: Mebendazole, Albendazole

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27
Q

What is Ocular toxocariasis?

A 
Larvae become trapped in the retina
Granulomatous reaction
Retinal mass, blindness
Diagnosis: serology/antigen detection, biopsy
Treatment: Mebendazole, Albendazole
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28
Q

What is cutaneous larva migrans?

A

A creeping itchy skin eruption
Due to the dog hookworms ancyclostoma carinum/braziliense
Lesions at sites where larvae penetrate
Contact with dog faeces
Treatment: topical/systemic thiabendazole, topical cryotherapy

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29
Q

What is Anisakiasis?

A

Acquired through raw fish
Adult ascarids present in the stomach wall of large sea mammals, eggs are passed into the host faeces, hatching juveniles are eaten by marine crustaceans and mature to infective stage, crustaceans eaten by fish, squid or octopus, man becomes dead-end host.

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30
Q

What is Dracunculus medinerusis?

A

Guinea worm/Medina worm
Adult is up to 100cm long and lives for 1 year subcutaneously
Can emerge through hand, leg, arm, axillae, breast, vagina.
Man swallows cyclops sp. in contaminated wayer, infective larvae are liberated by digestive enzymes and penetrate the gut walls. Larvae develop and occupy subcutaneous tissues, after 1 year female head approaches skin and causes blister, blister bursts and rhabiform larvae discharge through skin into water.

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31
Q

What are the clinical features of Dracunculus medinerusis?

A

Localised pain and urticaria at site where worm protrudes.
Tetanus, other sepsis.
Other local problems: joint problems, peritonitis

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32
Q

What is the diagnosis and treatment for Dracunculus medinerusis?

A

Diagnosis: drop of water on ulcer promotes egg release
Treatment: local wind-out worm
Mebendazole to ease extraction of worm

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33
Q

What is Wuchereria bancroftii?

A

Main cause of elephantiasis
Endemic throughout the tropics
Insect borne
Adults live in the lymphatic system and survive for 20 years.

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34
Q

What is the life cycle of Wuchereria bancroftii?

A

Microfilariae (L1) ingested by insect vector. First stage larvae develop into infective third-stage larvae (L1 to L2 to L3). Insect vector feeds on human host, L3 moult in human host and mature into adults.

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35
Q

What is the diagnosis and treatment for Wuchereria bancroftii?

A

Diagnosis: demonstration of microfilaria in blood taken between 11pm-1am, serology.
Treatment: Diethylcanoamazine, Ivermectin

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36
Q

What is Trichinella Spiralis?

A

Cause of trichinosis: a zoonosis of rats that circulates between rats and various carnivores. Human is dead-end for organism. Larvae encyst in striateed muscle, infected meat is ingested.

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37
Q

What are the clinical features of Trichinella Spiralis?

A 
Usually asymptomatic
GI disturbance associated with worm development
Fever, headache, cough at 8 weeks
Periorbital oedema, haemorrhage
Splinter haemorrhages
Neurological signs: deafness, encephalitis, fits, focal signs
Myocarditis
Pneumonitis
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38
Q

What is Taenia saginatum?

A

Beef tapeworm. Adult is 5-10m long and lives up the 30 years.
PPP 12 weeks.
Caught by eating undercooked beef containing “cysts” encysted larvae
Usually asymptomatic
Proglottids may emerge from human anus

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39
Q

What is the diagnosis and treatment for Taenia saginatum?

A

Diagnosis: stools for eggs and proglottids
Treatment: Niclosamide, praziquantel

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40
Q

Name some other examples of tape worms (other than Taenia saginatum)?

A

Echinococcus granulosus - dog tapeworm, causes hydatid disease
Enchinococcus multilocaularis - artic fox tapeworm, mainly in the north of the Northern hemisphere
Diphyllobothrium lactum: fish tapeworm, one of the causes of sparyaresis
Vitamin B12 deficiency

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41
Q

What are flukes?

A

Blood, liver, lung, bowel fluke
All have a snail as their intermediate host
Schistosoma spp. causes schistamiasis
Adult fluke is 12cm long, lifespan is 3-5 years
Different species in different areas

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42
Q

What is the life cycle of a fluke?

A

Miracidium hatches from egg, infect first intermediate host (snail), cercariae leave snail and penetrate skin of human in water, immature worm enters bloodstream, ends up in vein near intestine or bladder, reach sexual maturity in veins of abdominal cavity, enter intestinal tract, passed through urine/faeces.

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43
Q

What is Schistosoma haematobium?

A

Adults live in the liver, eggs migrate to the bladder.
Granulomatous lesions - may cause obstructive uropathy - reversible if of short duration and treated
Calcified bladder
Squamous cell baldder cancer
Kidney stones

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44
Q

What is a pathogen?

A

Organisms that cause or are capable of causing disease

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45
Q

What is a commensal pathogen?

A

Organisms which colonise the host but don’t normally cause disease

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46
Q

What is an opportunist pathogen?

A

Microbe that only causes disease if host defences are compromised.

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47
Q

What is virulence/pathogenicity?

A

The degree to which a given organism is pathogenic

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48
Q

What is asymptomatic carriage?

A

When a pathogen is harmlessly carried at a tissue site where it causes no disease

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49
Q

What are the parts of the bacteria name?

A

First name is genus

Second name is species

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50
Q

What are the different types of bacterial morphology?

A

Coccus (round) - diplococcus, chain of cocci, cluster of cocci
Bacillus (rod) - chain of rods, curved rod, spiral
Exceptions such as spiral (spirochaetes)/combinations of both

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51
Q

What are the structural features of the bacteria?

A

Bacterial cell wall - can have one or two cell walls
One chromosome of circular double stranded DNA
Capsule protects the bacteria from the host
Flagella enables movement
Pilli help them attach and colonise the host

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52
Q

What is the Ziehl-Neelsen stain?

A

Used to identify acid-fast organisms, mainly mycobacteria. Acid-fast bacteria are composed of mycolic acid in their cell wall, they are stained pink by pink by carbol-fuchsin.

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53
Q

What’s the structure difference between gram postitive and gram negative bacteria?

A

Gram positive has a single peptidoglycan bilayer and capsule.
Gram negative has an inner memebrane, peptidoglycan layer, outer membrane, lipopolysaccaraide layer and a capsule.

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54
Q

What are spores?

A

Spores are a hardened structures that is resistant to hard chemicals and attack.
Contains all DNA.
Remain like this until the environment is satisfactory.
Only killed in autoclave.

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55
Q

What are the boundaries for bacterial environment?

A

Temperature

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56
Q

How can you study bacteria growth?

A

Can be grown on a rich broth or agar plate
Different bacteria have different doubling times
Can be followed by looking at light absorption or by counting bacteria

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57
Q

What is an endotoxin?

A

Component of the outer membrane of bacteria
e.g. lipopolysaccharide in gram-neg bacteria
Non-specific action
Stable under heat
Weak antigenicity
No convertibility to toxoid

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58
Q

What is an exotoxin?

A 
Secreted proteins of gram positive and gram negative bacteria.
e.g. stop macrophages taking over
Specific action
Labile under heat
Strong antigenicity
Convertibility to toxoid
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59
Q

What are the features of bacterial genetics?

A

Usually a single chromosome (dsDNA)
Quite promiscuous - swap DNA over a lot
RNA polymerase converts mRNA into protein
Mutations can occur - base substitution, deletion, insertion (antibiotic resistance)
Contain plasmids which can transfer from one bacteria

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60
Q

What is bacterial conjugation?

A

DNA is transferred from one bacterium to another. The donor cell pulls itself close to the recipient using its pilus, DNA is then transferred (usually as a plasmid).

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61
Q

What is bacterial transformation?

A

Bacterium takes in DNA from its environment. If DNA is in form of a plasmid, it can be copied in the receiving cell and passed on to its descendents.

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62
Q

What is bacterial transduction?

A

Viruses that infect bacteria (bacteriophage) move short pieces of chromosomal DNA from one bacterium to another.

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63
Q

What are the two ways bacteria can grow?

A

Obligate intracellular bacteria (must be grown in hosts) e.g. Rick elysia, Chlamydia, Coxiella
Bacteria that can grow on artificial media (may have a cell wall or not).

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64
Q

In which morphology will bacteria grow?

A

Bacteria with a cell wall may grow as single cells or as filaments.
Single cells - rods, cocci, spriochaetes
Filaments - actinoyces, nocardia, streptomyces

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65
Q

Which cocci are gram pos and gram neg?

A

Cocci can be gram negative: veillonella (anaerobic) or neisseria (aerobic)
Cocci can be gram positive: staphlococcus and streptococcus (aerobic) or peptreptococcus (anaerobic)

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66
Q

What are the types of Streptococcus?

A

B-hemolytic (S.pyogenes, S.agalactiae) - tonicilitis
a-hemolytic (S.pneumoniae) - endocarditis
Non-hemolytic (S.bovis)

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67
Q

Which rods are gram pos and gram neg?

A

Gram positive rods can be anaerobic like clostriduym and propionibacterium.
Gram positive rods can also be aerobic like corynebacterium, listeria and bacillus.
Gram negative rods can be anaerobic like bacteroids.
Gram negative rods can be aerobic like coliforms (escherichia, salmonella), pseudomonas (P.aeruginosa), Vibrio (cholerae, campylobacter, helicobacter), Parvobacteria (haemophilus, brucella).

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68
Q

What are the features of staphylococcus?

A

At least 40 species
Can be coagulase +ve or -ve (coagulase is an enzyme produced by bacteria that clots blood plasma, providing protection from phagocytosis)
Staph. aureus is most important (coagulase +ve)
Coagulase -ve are important opportunistic pathogens

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69
Q

What are the features of Staph. aureus?

A

Gram-positive bacteria
Spread by aerosol and touch
There are carriers and shedders
MRSA is a resistant strain transferred by MecA strain.
Resistant to B-lactams, gentamicin, erythromycin, tetracycline.

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70
Q

What are virulence factors?

A

Pore-forming toxins
Insert itself into host cell membranes, causing pores and leakage of cell contents.
e.g. Proteases - exfoliatin attacks desmosomes in skin
Toxic shock syndrome stimulates cytokine release
Protein A binds Igs in the wrong orientation

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71
Q

Name two important coagulase negative staphylococci?

A

S.epidermidis - infections in catheters/prostheses
Form persistent biofilms
S.saprophyticus - acute cystitis
Use haemagglutin for adhesion

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72
Q

What are the different types of haemolysis?

A

a-haemolysis: Partial. Release water which reacts with Hb.
B-haemolysis: Complete. Produce haemolysins O and S, bursting open RBCs.
Non or Y haemolysis: No lysis

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73
Q

How can streptococci be classified?

A

Can be classified by haemolysis, lancefield typing or by biochemical properties.

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74
Q

What is lancefield typing?

A

A method of grouping catalyse negative bacteria based on their bacterial carbohydrate cell surface antigens.
Antiserum to each group is added to a suspension of bacteria, clumping indicated recognition.

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75
Q

What are the streptococci groups in lancefield typing?

A

Carbohydrate cell surface antigens: Lancefield A-H and K-V.
Group A: S.pyogenes (very important pathogen!)
Group B: S.agalactiae (important in neonatal infections)

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76
Q

What are the illnesses caused by Strep. pyogenes?

A 
Gram-positive bacteria
Very sucessful pathogen
Cellulitis as a result of wound infections
Tonsillitis
Pharyngitis
Impetigo (skin infection)
Scarlet fever
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77
Q

What are the complications of Step. pyogenes?

A

Rheumatic fever - inflammatory disease of heart, joints, skin, brain. Often follows a Strep throat infection
Glomerulonephritis - inflammatory disease somemtimes following S. pyogenes infection

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78
Q

What is an Anti-SLO titre?

A

Anti-streptolysin O (ASO or ASLO) is the antibody made against streptolysin O, a streptococcal hemolytic exotoxin produced by most strains of group A and many strains of groups C and G Streptococcus bacteria.
Streptococcal exoenzymes are bound to biologically inert latex particles. If Streptococcal antibodies are present in the test sample, reaction occurs (agglutination).

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79
Q

What are the virulence factors of S. pyogenes?

A

Exported factors - to aid with spreading
Toxins - for adherence and exaggerated immune response
Surface factors - for protection and encouraging complement degradation

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80
Q

What are the features of S. pneumoniae?

A

Gram-positive bacteria
Normal commensal in oro-pharynx in 30% of population
Causes pneumonia, otitis media, sinusitis, meningitis
Predisposing factors:
- Impaired mucus trapping (viral infection)
- Hypogammaglobulinaemia (immunocompromised)
- Asplenia (removal of spleen)

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81
Q

What are the virulence factors of S.pneumoniae?

A

Capsule - antiphagocytic
Inflammatory wall constituents like teichoic acid and peptidoglycan
Cytotoxin - inserts into the host cell membrane

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82
Q

What are viridans streptococci?

A 
Gram positive bacteria
Collective name for oral streptococci
a or non-hemolytic
Important in infective endocarditis
Cause dental caries and deep organ abscesses e.g. brain and liver.
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83
Q

What are the features of C.diphtheriae?

A

Gram positive bacteria
Droplet spread
To isolate, use the presence of potassium tellurite
Its toxin inhibits protein synthesis
Infection prevented by vaccination (toxoid-inactivated toxin)

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84
Q

What is the lipopolysaccaride of a gram neg bacteria made up of?

A

Lipid A - toxin portion that is anchored in the outer leaflet of the outer membrane
Core (R) antigen - short chain of sugars, some are unique to LPS
Somatic (O) antigen - highly antigenic repeating chain of oligosaccharides

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85
Q

What are the virulence factors of gram-negative bacteria?

A

Any product or strategy that contributes to pathogenicity.
Colonisation factors - adhesins, invasins, nutrient acquisition, defence against the host
Toxins - ‘effectors’ usually secreted proteins that cause damage and subversion

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86
Q

What are the features of proteobacteria?

A

AKA enterobacteria
Gram negative bacteria
Rods
Most are mobile
Facultatively anaerobic (an aerobe that can switch to work in anaerobic conditions)
Some species colonise the intestinal tract

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87
Q

What are the cell surface antigens of Gram negative bacteria?

A 
H antigen (flagellum)
K antigen (exopolysaccharide 'capsule')
O (somatic) antigen
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88
Q

What is serotyping?

A

Serotypes refer to separate groups within a species of a microorganism that all share a similar characteristic but have different antigens.
You can mix the sample with blood containing antibodies (antiserum) leading to agglutination.

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89
Q

What are the features of E.coli?

A 
Gram negative bacteria
Commensals - most abundant facultative anaerobe
Peritrichous flagella (all over!)
Causes...
Wound infections
UTIs
Gastroenteritis
Travellers' diarrhoea
Bacteraemia
Meningitis
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90
Q

Why are some strains of E.coli pathogenic?

A

There are several different pathovars with distinct pathogenic strategies.
Common ‘core genome’ with additional acquisition of pathogenicitity genes ‘en bloc’ through lateral gene transfer.

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91
Q

What is ETEC?

A

Enterotoxigenic Escherichia coli
Gram neg bacteria
Leading cause of diarrhoea
Have pilli which allow for attachment in the intestines
Diarrhoea symptoms caused by disruption of tight junctions and effects on ion secretion.

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92
Q

What are the features of Shigella?

A

Gram neg bacteria
Four species
Produce shigatoxin
Cause severe bloody diarrhoea (>30/d), cramps, pain and fever
Person-to-person, or contaminated water or food
Entry through colic M cells
Invasion of the colonic mucosa
Takes over cell’s actin to move through more tight junctions.

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93
Q

What are the virulence factors of Shigella?

A 
Catalytic subunit (glucosidase) - cleaves N-glycosidic bone of adenosine residues in rRNA
Receptor binding subunits
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94
Q

What are the complications of Shigella?

A

Systemic absorption of shigatoxin targets the kidney.

Causes microvascular thrombosis leading to kidney failure.

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95
Q

What are the two main species of salmonella?

A

S. enterica - responsible for salmonellosis

S. bongori - rare (contact with reptiles)

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96
Q

What are some of the infections caused by Salmonella enterica?

A

Gastroenteritis/enterocolitis - frequent cause of food poisoning, localised infection, usually resolves within 7 days
Enteric fever - typhoid, systemic disease
Bacteraemia - uncommon

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97
Q

What is the pathogenesis of salmonella?

A

Ingestion of contaminated food/water
High infective dose
Invasion of gut epithelium in small intestine
Intestinal secretory and inflammatory response
Does not produce toxins
Transcytosed to basolateral membrane, enters submucosa
Intracellular survival/replication

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98
Q

What is the pathogenesis of enteric (typhoid) fever?

A

Ingestion
Incubation period (1-3 weeks)
Asymptomatic
Once titre has increased enough in the bloodstream, you begin to get symptoms.
Multiplication occurs in liver, spleen and bone marrow.

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99
Q

What is Proteus mirabilis?

A 
Gram neg bacteria
Enterobacteria
Opportunistic
Causes UTIs, pyelonephritis, septicaemia
Virulence factors: urease (increased pH), can lead to kidney stores
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100
Q

What is Klebsiella pneumoniae?

A

Gram neg bacteria
Enterobacteria
Opportunistic
Infections in neonates, elderly, immunocompromised.
Benign colonisation of GIT and oropharynx
Can lead to UTIs, pneumonia, surgical wound infections, sepsis.

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101
Q

What is vibrio cholerae?

A

Gram negative
Facultative anaerobic
Lives in saline environments
Spread through ingestion by shellfish or contamination of drinking water due to the flooding of coastal areas or poor sanitation.

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102
Q

What is cholera?

A 
Most severe diarrhoeal disease
Characterised by pandemics
Faecal-oral route (not person-to-person)
High infective dose required
Spread through faecal contaminated water or undercooked shellfish
Incubation hrs-5 days
Can lose 20 litres fluid/day plus electrolytes - dehydration and death
No blood, pus or fever
Treated with oral rehydration therapy.
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103
Q

What are the virulence factors of vibrio cholerae?

A

Toxin coregulated pili

Cholera toxin

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104
Q

What is pseudomonas aeruginosa?

A

Gram neg bacteria
Ubiquitous, free-living aerobe
Opportunistic (serious cause of nosocomial infections)
Multiple antibiotic resistance (and disinfectants) making it difficult to treat.

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105
Q

What infections does pseudomonas aeruginosa cause?

A 
Localised:
Burn/surgical wounds
UTIs
Keratitis
Systemic:
Sepsis in neutropenic patients (leukaemia, chemotherapy, AIDs)
Chronic:
Cystic fibrosis patients
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106
Q

What are the virulence factors of pseudomonas aeruginosa?

A

Multiple toxins but the main ones are…
Exoenzyme S and Exoenzyme O - inteferes with cell signalling
Exotoxin A, LasB elastase, PlcH phosphatase - involved cell death/damage.

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107
Q

What is Haemophilus influenzae?

A

Gram negative bacteria
Exclusively a human parasite
Carried in nasopharyngeal carriage in 25-80%
Opportunistic infections seen mainly in young children and adult smokers.
Can cause meningitis, bronchopneumonia, epiglottitis, sinusitis, otitis media, bacteraemia, pneumonia in CF, COPD and HIV patients.
Will not grow on blood agar but will grow on chocolate agar.

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108
Q

What are the virulence factors of Haemophilus influenzae?

A

Capsule - the invasive ones are encapsulated (6 serotypes) but the commensal ones are not
Allow for penetration of nasopharyngeal epithelium
LPS ‘endotoxin’ - inflammation and complement resistance

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109
Q

What is Legionnaire’s disease?

A

Severe inflammatory pneumonia
Caused by legionella pneumophilia
Found in man-made aquatic environments - air-conditioning, shower heads, nebulisers, humidifers)
Occurs in the immunocompromised (elderly, alcoholics, smokers)

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110
Q

What is the action of legionella pneumophilia?

A

Infected by flagellated form
Modulates trafficking of the phagosome
Differentiate to the non-flagellated form
Upregulates pro-inflammatory genes in alveoli

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111
Q

What is Bordetella pertussis?

A 
Gram negative
Causes pertussis (whooping cough)
Short rods
Non-invasive
Highly contagious, aerosol transmission
Non-specific flu-like symptoms followed by paroxysmal coughin
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112
Q

What are the toxins produced by Bordetella pertussis?c

A

Pertussis toxin - increased cAMP

Adenylate cyclase-haemolysin toxin - suppression of innate immune functions

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113
Q

What are Neisseria bacteria?

A 
Gram negative bacteria
Non-flagellated diplococci
Two species:
- N. meningitidis
- N.gonorrhoeae
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114
Q

What is Neisseia meningitidis?

A

Gram negative bacteria
AKA meningococcus
Present in nasopharynx of 6-10% population
Rises to 20-90% in outbreaks
Aerosol transmission
Cross nasopharyngeal epithelium and enters blood
Can cause low level bacteraemia or septicaemia
Meningitis - bacteria enter the CSF of subarachnoid space

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115
Q

What are the virulence factors of Neisseia meningitidis?

A

Capsule - anti-phagocytic

LPS (membrane ‘blebs’) - cytokine cascade and sepsis

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116
Q

What is Neisseia gonorrhoeae?

A

Gram negative bacteria
AKA gonococcus
Person to person transmission
Can be asymptomatic
Can cause urethritis with additional infection of proctitis, gingivitis, pharyngitis.
Complications: salpingitis (fallopian tubes) or PID

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117
Q

What are the virulence factors of Neisseia gonorrhoeae?

A

Twitching motility - grabbing hook model

LPS - inflammatory response

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118
Q

What are campylobacter?

A

Gram negative bacteria
C.jejuni and C.coli
Spiral rods
Unipolar or bipolar flagella
Most common cause of food poisoning from poultry and cattle
Mild to sever diarrhoea, often with blood
Usually self-limiting (<1 week).

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119
Q

What is helicobacter pylori?

A

Microaerophilic (requires CO2)
Spiral
Present in 50% of population
Major role in gastritis and peptic ulcer disease (80-90% ulcers)
Implicated in 10% of gastric adenocarcinoma and muscosa-associated lymphoid tissue lymphoma

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120
Q

What are bacteroidetes?

A

Gram negative bacteria
Non-motile rods
Strict anaerobes
Commensal flora
Opportunitistic - in tissue injury from surgery, perforated appendix or ulcer
Predominantly peritoneal cavity infections

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121
Q

What are chlamydiae?

A 
Gram negative bacteria
Chlamydia and chlamydophila
Very small, non-motile
Obligate intracellular parasites
Many are asymptomatic
Cannot culture in bacteriological media
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122
Q

What are the two major types of chlamydiae?

A

C. pneumoniae - respiratory tract

C. psittaci - mainly birds, psittacosis and severe pneumonia

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123
Q

What are the 3 main strains of chlamydiae?

A

Trachoma biovar - infectious blindness
Genital tract biovar - infects epithelial cells of urethra and vagina, can ascend to uterus and ovaries
Lymphogranuloma venereum - invasive urogenital or anorectal infection

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124
Q

What are Spirochaetae?

A

Gram negative bacteria
Helical and highly flexible
Most are free-living and non-pathogenic
Pathogenic varieties are difficult to culture
Modified outer sheath - replaced by a different glycolipid

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125
Q

What is an endoflagella?

A

Type of flagella that the spriochaete have
Propels bacteria in a corkscrew motion
Swim faster in high viscosity medium
Hides antigenic flagellum

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126
Q

What is Borrelia burgdorferi?

A

Gram negative bacteria
Causes lyme diseasse
Bacterium infects small mammals
Acquired by tick larvae and transmitted by nymphs
Causes flu-like symptoms and bulls-eye rash
Dissemination via lymphatics/blood to other organs

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127
Q

What is Leptospira interrogans?

A

Gram negative bacteria
Causes leptospirosis
Contact of mucous membrane or abraded skin with animal urine
Flu-like symptoms
Severe form (Weil’s disease) - jaundice, acute renal and hepatic failure, pulmonary distress, haemorrhage

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128
Q

What bacteria causes syphilis?

A

Treponema pallidum

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129
Q

What are the 3 stages of syphilis?

A

1) Localised infecction - ulcer, highly transmissable
2) Systemic (skin, lymph nodes, joints, muscles) 1-3 months post infection, highly transmissable
3) Granulomas in bone and soft tissue, cardiovascular symphilis in aorta, neurosyphilis in brain and spinal cord. Occurs several years post-infection. Non-infectious.

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130
Q

What does it mean to infect someone?

A

Affect a person with a disease-causing organism

Requires harm to be done to host - invasion, toxin, host response

131
Q

What are the principles of infection prevention control?

A

Identification of risks
Routes and modes of transmission
Virulence of organisms - ease of spread, likehood of causing infections, consequences of infections
Remediable factors

132
Q

What are CPE?

A

Carbapenemase producing enterobacteriaeae
AKA coliforms
Include E.coli, Klebsiella, Serratia, Enterobacter
Colonisers of large bowel, skin below the waist and moist sites
Have increased resistance to antibiotics

133
Q

What are the types of Carbapenemase?

A

Class A serine beta-lactamases
Class B metallo-beta-lactamases
Class D (OXA variants)

134
Q

How can we stop spread of infection from one person to another in a hospital?

A

Isolation - barrier or protective measures

Ward design - distance between beds, how many people per toilet, number of side-rooms

135
Q

Why is MRSA strain dangerous?

A

Staph. aureus is a common skin and nasal commensal. Most strains are susceptible to flucloxacillin (and other beta-lactams).
Altered penicillin binding proteins means that it can no longer be bound by beta-lactams.
Increased cases in 1990s and 2000s.

136
Q

What is norovirus?

A

Causes vomiting and diarrhoea, usually in winter, in children.
Problems in enclosed environments - schools, nuseries, cruise ships.
Resistant to alcohol gel.

137
Q

What are endogenous infections?

A

Some infections are caused by the patient’s own flora rather than being acquired.

138
Q

How to prevent endogenous infections?

A

Good nutrition and hydration
Antispesis/skin prep where indicated
Control underlying disease
Remove lines and catheters as soon as clinically possible
Reduce antibiotic pressure as much as clinically possible

139
Q

What are the top causes of death globally?

A

Number 1 is respiratory tract infections caused by bacteria and viral infections.
Number 2 is diarrhoeal diseas

140
Q

What is a virus?

A

Infectious, obligate intracellular parasite comprising genetic material (DNA or RNA) surrounded by a protein coat and/or membrane.

141
Q

How does a virus replicate?

A

1) Attachment to specific receptor
2) Cell entry - uncoating of virion within the cell
3) Translation of viral mRNA to produce structural proteins, viral genome, non-structural proteins
4) Assembly of virion
5) Release of new virus particles either by bursting out (cell death) or by budding/exocytosis

142
Q

How do viruses cause disease?

A 
Direct destruction of the host cells
Modification of the host cells
'Over-reactivity' of immune system
Damage through cell proliferation
Evasion of host defence on a cellular or molecular level
143
Q

Why do viruses vary so much?

A

Viruses vary wildly in the range of clinical symptoms they can cause. This is due to different host cells and tissues that they can infect.
Different interactions within the host cell.

144
Q

What are fungi?

A

Huge range of organisms
Can be microscopic or huge
Have a chitinous cell wall
Require carbon from an outside source (heterotrophic)
Move by generation of spore through air or water

145
Q

What are the different forms of fungi?

A

Mould or yeast
Yeast - small single celled organisms that divide by budding
Moulds form multicellular hyphae and spores

146
Q

What are dimorphic fungi?

A

Some fungi exist as both yeasts and moulds, switching between the two when conditions suit.

147
Q

How do fungi affect humans?

A

Only a few cause human infection, this is due to an inability to grow at 37C and the work of the innate and adaptive immune system.

148
Q

Which fungi can infect humans?

A

Ascomycota - aspergillus, pneumocystis, candida, fusarium, scedosporium
Basidomycota - cryptococcus, trichosporon
Mucoromycota (rare)

149
Q

How common is fungal infection?

A

Fungal infections like athlete’s foot, nappy rash, fungal nail infection and fungal asthma are common.
Life-threatening fungal infection is rare in healthy hosts.

150
Q

Who normally gets fungal infections?

A

Immunocompromised hosts
Post-surgical patients
Healthy hosts

151
Q

What are the features of the fungal cell?

A

DNA/RNA synthesis and protein synthesis is similar to Mammalian
Cell wall - mannoproteins, B1, 3 glucan, B1, 6 glucan, chitin
Plasma membrane - ergostrerol rather than cholesterol

152
Q

What drugs are used to attack fungi?

A

Flucytosine affects DNA/RNA synthesis/protein synthesis
Echinocandins affect cell walll
Amphotericin, Azoles and Terbinagine affect the plasma membrane

153
Q

How do polyenes attack fungi?

A

Form a pore in the fungal cell membrane, disrupting osmolarity.
10 times lower affinity for the cholesterol in the mammalian membranes, although some damage can occur (renal failure).

154
Q

How do azoles attack fungi?

A

Azoles are dose dependent inhibitors of 14a sterol demethylase. They also have other secondary targets in the synthetic pathway.
Newer azoles have increased spectrum of activity (and cost).

155
Q

What are the adverse effects of azoles?

A

Relatively safe
Associated with transaminitis and severe hepatitis (rare)
Alopecia with long term flulonazole
Voriconazole is associate with reversible visual disturbance, photosensitivity, skin malignancy

156
Q

Why do you need to be careful of drug-drug interactions with azoles?

A

Drug-drug interactions are largely a result of cytochrome P450 isoforms.
Their effects are variable depending on relative affinity of drugs for individual enzymes.

157
Q

What is the action of echinocandins?

A

Inhibit 1,3 B glucan synthase

Genera without large amounts of 1,3 B glucan in the cell wall are intrinsically resistant.

158
Q

What are the advantages and disadvantages of echinocandins?

A

Poor oral bioavailability
Few drug interactions
Limited drug toxicity

159
Q

What investigations can be used to diagnose fungal infections?

A

PCR and antigen testing can be used to diagnose fungal infections.
Biggest challenge is initial recognition.

160
Q

Why is underdignosis of fungal infections common?

A

Blood cultures are probably only about half as sensitive for fungi as for bacteria.
Better pick-up from tissues and fluids.

161
Q

What is 1,3 B-D-glucan?

A

Cell wall component of many fungi including common ascomycetes pathogens and pneumocystis.
Released into serum during invasive infection
Non-specific for individual fungi

162
Q

What is onychomycosis?

A

Fungal nail infection
Very common
Cuased by dermatophyte moulds - grow best at about 30C
Have evolved ability to hydrolyse keratinous debris in soil. Trichophyton rubrum is most common, some non-dermatophytes.
Broad differential diagnosis.
Microscropy is the most specific test but 30% culture negative.

163
Q

How should you obtain a sample in onychomycosis?

A

Proximal clippings
Material from underside of plate
Surface scrape of loose material
Scape away normal nail plate then obtain proximal tissue

164
Q

How long does onychomycosis last?

A

6 weeks-2 months (fingernails)
3 months (toenails)
High failure rates

165
Q

What are the treatment options for onychomycosis?

A

Topical amorolfine

Systemic (traconazole or tebinafine)

166
Q

What is the pathogenesis of pneumocystis?

A

Infection/colonisation of healthy people is frequent and occurs early in life
Disease develops only with moderate-severe immunocompromise, especially HIV, transplant, steroids.

167
Q

What is the treatment for pneumocystis?

A

Has a cholesterol rich cell wall
Azoles are not effective
Co-trimoxazole is 1st line therapy

168
Q

What are protozoa?

A

Over 50,000 species
Can be free living or parasitic
Classified based on locomotion: ameobiods (pseudopodia), ciliates (cilia), sporozoa (non-motile), flagellates (flagella)

169
Q

What are ameobiods?

A

Type of protozoa
Common in topical areas with poor sanitation
Entamoeba histolytica causes a severe dysenteric illness
Faecal-oral transmission

170
Q

What is the pathogenesis of ameoboids?

A

Ingestion of mature cysts which travel to SI
Rlease of trophocoites which travel to LI and invade the intestinal wall
Can spread through the blood to liver, brain and lungs

171
Q

What is the treatment of ameoboids?

A

Metroniadazole

172
Q

What are the flagellates?

A

Type of protozoa
Trypanosomiasis separated into African and American
Causes fever, headaches, extreme fatigue, lymphadenopathy, joint pains, splenomegaly, chancre, CNS symptoms.
Diagnosed with a blood film or CSF sample

173
Q

What is a chancre?

A

Nodular itching area at site of bite

174
Q

What is chagas disease?

A

Carried by triatomine bug
Protozoa is Trypanosoma Cruzi
Causes headache, fevers, lumphadenopathy, chagoma, Romana’s signs (periorbital swelling)
Later… cardiac manifestations, megaoesophagus, megacolon

175
Q

What is the treatment for chagas disease?

A

Benznidazole

176
Q

What is Leishmaniasis?

A 
Disease of poverty
Protozoa carried by female sandfly
3 TYPES
Cutaneous leishmaniasis (skin)
Mucocutaneous (oral mucosa)
Visceral leishmaniasis (internal organs)
177
Q

What are the effects of mucocutaneous or cutaneous leishmaniasis?

A

Very disfiguring

May resolve over 8 weeks or may need treatment under the skin

178
Q

What are the effects of visceral leishmaniasis?

A

Much more severe
Fever, bone marrow suppression, lymphadenopathy, hepato-splenomegaly, weight loss
Associated with high fatality

179
Q

What does Giardia Lambia cause?

A

Giardiasis
Causes diarrhoea, cramps, bloating
Faecal-oral spread, can live outside the body for long periods of time.

180
Q

How would you treatment Giardia Lambia?

A

Metronidazole

181
Q

What does Trichomonas vaginalis cause?

A

Sexually transmitted infection

Trichomoniasis

182
Q

What symptoms does Trichomoniasis cause for women?

A

Purulent discharge, abdominal pain, dysuria, vulvar/cervical lesions and dyspareunia

183
Q

What symptoms does Trichomoniasis cause for men?

A

Asymptomatic, urethritis, epididymitis, prostatitis

184
Q

How would you treat Trichomoniasis?

A

Metronidazole

185
Q

What is cryptosporidosis?

A

Cryptosporidium transmission via contamined food/water
Causes watery diarrhoea, vomiting, fever and fatigue
Acid-fast staining shows oocytes in stool
Usually self-limiting 2-3 weeks

186
Q

What is toxoplasmosis?

A

Caused by toxoplasma gondii
Cats are a big carrier
Transmission: ingestion of undercooked meat/shellfish, contact with feline faeces, vertical transmission
Can cause toxoplasma encephalitis, retinochoroiditis, ring enhanced lesion on brain CT
Severe consequences in pregnancy and immunodeficiency.

187
Q

Why aren’t antimalarials 100% protective?

A

Resistance to the drugs

Patients may be taking them wrong

188
Q

What are the 5 types of malaria?

A 
P. Falciparum
P. Malariae
P. Ovale
P. Vivax
P. Knowlesi
189
Q

What is the vector for malaria?

A

Female Anopheles Mosquito

190
Q

What is the lifecycle of the malaria vector?

A

LIVER STAGE
Mosquito takes a blood meal and injects sporozcites
Sporozcites travel to the liver and infect liver cells where they mature into schizonts
Schizonts rupture releases merozoites into in blood
BLOOD STAGE
Merozoites enter the circulation and infect RBCs
Enter ring-stage trophozoites which mature into schizonts.
Schizonts rupture releasing more merozoites
Some immature trophozoites differentiate into sexual stage gametocytes
VECTOR STAGE
Another mosquito takes a blood meal ingesting gameotocytes
These mature into an oocyst which ruptures release sporozoites
Sporozoites are ingected into the host during the next blood meal

191
Q

Which stage of the malaria vector lifecycle gives the clinical symptoms of malaria?

A

The blood stage

192
Q

What are the symptoms of malaria?

A 
Fever and chills
Flu-like illness
Headache
Muscle aches
Fatigue
Nausea
Vomiting
Diarrhoea
Splenomegaly
Hepatomegaly
193
Q

What causes the symptoms of malaria?

A

Parasite develops in RBCs creating waste products and toxic features
Infected cells lyse releasing meroites, surface protein and hemozoin into the blood
Stimulates macrophages to produce proinflammatory cytokines and other inflammatory mediators
Headache, nausea, vomiting, fevers, rigors, decreased platelet coagulopathy

194
Q

What protozoa causes severe malaria?

A

P. Falciparum
Replicates rapidly and responsible for most malaria deaths
Cytoadherence - infected RBCs display specific membrane proteins on their surface which adhere to microvascular endothelium
Rosetting - also adhere to other non-infected RBCs rosettes, sequestration of parasites in the major organs where they hide from immune system

195
Q

What are the haematological changes in malaria?

A

Haemolysis due to infectedd, cell lysis and immune mediated killing - anaemia, jaundice, haemoglobinuria
Monocytosis and lymphopenia
Thrombocytopenia

196
Q

What are the complications of malaria?

A 
Cerebral malaria (vascular occlusion and hypoglycaemia) - drowsy, raised ICP, seizures, coma
Renal failure (vascular occlusion, dehydration, hypotension, haemaglobinuria) - proteinuria, fatigue, haematuria
Acute respiratory distress syndrome (vasscular occlusion, anaemia, lactic acidosis, increased vascular permaebility) - SOB, hypoxia, pulmonary oedema
Bleeding (thrombocytopenia, activation of coagulation cascade) - worsening anaemia, bleeding, sepsis
197
Q

How is malaria diagnosed?

A

Thick and thin blood films - 3 performed over 24 hours
THICK - looking for ratios of blood cells to parasites, 2% is severe
THIN - spread blood out, looking at the type of malaria parasite

198
Q

What is the treatment for malaria?

A

Complicated - IV artesunate (quinine and doxycycline)
Uncomplicated - lots of options
Primaquine is used to eliminate P.ovale and P.vivax

199
Q

How would you treatment of the complications of malaria?

A 
Cerebral - anti-epileptics
ARDs - ventilator support, O2 and diuretics
Renal failure - hydration +/- dialysis
Sepsis - broad spectrum antibiotics
Bleeding/anemia - blood products
Exchange transfusions in extreme cases
200
Q

What determines the effect of a pathogen?

A

Disease pathogenesis during infection is the result of a host pathogen interaction in which microbial determinants and the host suceptibility and immune response determine the features of the disease that results.

201
Q

What is a pathogen’s infectivity?

A

The ability to become established in a host, can involve adherence and immune escape

202
Q

What is a pathogen’s virulence?

A

The ability to cause disease once established

203
Q

What is a pathogen’s invasiveness?

A

The capacity to penetrate mucosal surfaces to reach normally sterile sites.

204
Q

What are virulence factors?

A

Microbial factors that cause disease

205
Q

What are the key steps of pathogenicity?

A

Bacteria has to be able to stick to a surface (adhesion)
Translocation and invasion (stopped by polymorphs)
Stopped by oponisation and phagocytosis
If it invades this, it can release factors to cause itssue damage and inflammatory.

206
Q

What are commensals?

A

Microorganisms that are resistant and usually nonpathogenic.
May cause disease in a particular context
Normal flora can cause disease if overgrow or translocate

207
Q

What is the microbiome?

A

Totality of micro-organisms on someone’s body as well as their genetic elements and their environmental interactions in an environment
Mostly in the gut

208
Q

How is the microbiome linked to disease?

A

IBD - decreased gut bacterial diverisity

Increased numbers of proteobacteria , decreased numbers of firmicutes and bacteroidetes

209
Q

What is the humoral response to viruses?

A

IgA - blocks binding to cells, prevents cell entry
IgM - agglutinates particulates, preventing movement
Complement - oponisation, lysis

210
Q

What are toxins?

A

Viruses and bacteria can also produce toxins
Classified by tissue target, molecular action, biological effect, contribution to disease process.
Expression tightly regulated by regulatory system.

211
Q

Why does the flu change each season?

A

Influenza changes in coat antigens refults in antigenic drifts whereby spontaneous mutations occur gradually giving minor changes in haeemaggluttinin and neuraminidase.

212
Q

How do bacteria compete with host cells and colonising flora?

A

Sequestering nutrients
Using novel metabolic pathways
Out-competing other micro-organisms
Bacteria use ‘two component sensor-kinase’ systems to alter gene transcription, regulating virulence factors, competence to exchange genetic material, biofilm formation, production of bacteriocins to kill other bacteria.

213
Q

What do bacteria use to help bind to mucosal surfaces?

A 
Fimbriae and pili filamentous proteins
Non-fimbrial proteins
Lipii
Glycosaminoglycans
Lectins of viruses and parasites
Miscellaneous viral capsids
214
Q

What are biofilms?

A

Bacteria can stick together on a surface by secreting an extracellular polymeric substance of protein, polysaccherides and DNA.
Helps protect against antimicrobials

215
Q

What are PAMPs?

A

Pathogen-associated molecular patterns
Easily recognised by pattern recognition receptors but may be similar to that of our own healthy cells
Evolutionary highly conserved

216
Q

What are the common illnesses caused by protozoa?

A 
Ameobiasis
Chagas disease
Sleeping sickness
Malaria
Toxoplasmosis
Leishmaniasis
217
Q

What is an antibiotic?

A

Agents produced by micro-organisms that kill or inhibit the growth of other micro-organisms in high dilution.

218
Q

What are antimicrobials?

A

Most agents currently used are semi-synthetic derivatives of antibiotics so are more correctly termed ‘antimicrobials’.
Includes antifungal, antibacterial, antihelminthic, antiprotozoal and antiviral agents.

219
Q

How do antibiotics exert their action?

A

They work by binding a target site on a bacteria. Defined as points of biochemical reaction crucial to the survival of the bacterium,
The crucial binding site will vary with the antibiotic class.
e.g. beta-lactams work on the peptidoglycan layer

220
Q

What are the different ways in which antibiotics can exert their action?

A

Beta-lactams disrupt peptidoglycan production by binding covalently and irreversibly to the penicillin-binding proteins.
Others interfere with nucleic acid synthesis or function.
Others inhibits DNA gyrase.
Others inhibit ribosomal activity and protein synthesis.
Others inhibit folate synthesis and carbon unit metabolism.

221
Q

How do Beta-lactams exert their action?

A

Beta-lactam antibiotics disrupt peptidoglycan production by binding covalently and irreversibily to the penicillin-binding proteins.
Cell wall is disrupted and lysis occurs.
Results in a hypo-osmotic or iso-osmotic environment.
Active only against rapidly multiplying organisms.

222
Q

Why do gram neg and gram pos bacteria have different responses to antibiotics?

A

Gram neg organisms have an additional lipopolysaccharide layer that decrease antibiotic penetration
Gram pos are usually more susceptible to antibiotics

223
Q

What affects an beta-lactams’ effectiveness?

A

Differences in the spectrum and activity of B lactams antibiotics are due to their relative affinity for different pencillin-binding-proteins.
Because penicillins poorly penetrate mammalian cells, they are ineffective in the treatment of intracellular pathogens.
The antibiotic must also remain at the binding site for a sufficient period of time in order for the metabolic processes of the bacteria to be sufficiently inhibited.

224
Q

What is the bacterial raison d’etre?

A 
Attach and enter
Local spread
Multiply
Evade host defeences
Shed from body
225
Q

What 3 kinds of damage do bacteria cause?

A

Direct - destroy phagocytes or cells in which bacteria replicate
Toxin - endotoxin (gram neg), exotoxin (protein production)
Indirect - inflammation and immune pathology

226
Q

What are bacteriostatic antibiotics?

A

Prevents growth of bacteria ‘inhibitory to growth’
Kill >90% in 18-24 hours
Inhibit protein synthesis, DNA replication or metabolism.
Reduce toxin production, endotoxin surge less likely , reduced bacterial component release.

227
Q

What are bacteriocidal antibiotics?

A

The agent that kills the bacteria
Kill >99.9% in 18-24 hours
Generally inhibit cell wall synthesis
Useful if there is poor penetration, difficult to treat infections or need to eradicate infection quickly.

228
Q

What is the MIC?

A

Minimum inhibitory concentration (MIC) is the lowest concentration of an antimicrobial (like an antifungal, antibiotic or bacteriostatic) drug that will inhibit the visible growth of a microorganism after overnight incubation.

229
Q

What are the two types of bacterial killing?

A

Concentration-dependent killing - key parameter is how high the concentration is above the MIC
Time-dependent killing - key parameter is the time that serum concentration remain above the MIC during the dosing interval

230
Q

How do bacteria resist antibiotics?

A

Change antibiotic target - change the molecular configuration of the antibiotic binding site or masks it
Destroy antibiotic
Prevent antibiotic access - modify the bacterial membrane porin channel size, numbers and selectivity
Remove antibiotic from bacteria - proteins in bacterial membranes act as an export or efflux pump, reducing level of antibiotic

231
Q

How do bacteria develop resistance to antibiotics?

A

Intrinsic - naturally resistance

Acquired - spontaneous gene mutation or by horizontal gene transfer (conjugation, transduction, transformation)

232
Q

What is acquired resistance?

A

A bacterium which was previously susceptible obrains the ability to resist the activitiy of a particular antibiotic.
Only certain stains or subpopulations of a species will be resistant.

233
Q

What are the different types of horizontal gene transfer?

A

Transduction - bacteriophages mediate transfer of DNA by packaging DNA from bacterium into a virus particle to transfer to recipient
Transformation - some bacteria are able to take up free DNA from the environment and incorporate it into their chromosome
Conjugation - responsible for most concerning antimicrobial resistance. Sex pilar forms between two bacterial cells through which a plasmis is transferred from one to the other.

234
Q

Give 2 important gram pos resistant organisms?

A

MRSA (methicillin resistant staphylococcus aureus) - contains resistance gene mecA which confers resistance to all B-lactams
VRE (vancomyocin-resistant enterococci) - plasmid mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomyosin binding.

235
Q

Give 2 important gram neg resistant organisms?

A

ESBL - mutation at active site extended rnage of antimicrobial resistance to form extended spectrium beta lactamase inhibition
AmpC B-lactamase resistance - broad spectrum penicillin, cephalosporin and monobactam resistance.

236
Q

What are carbapem resistant enterobacteriaceae?

A

Produce carbapenemases
Treatment options are very few and very toxic
Important to control their spread

237
Q

What factors should you consider when choosing an antibiotic?

A 
Intolerance, allergy, anaphylaxis
Side effects
Age
Renal and liver function
Pregnancy and breast feeding
Drug interactions
Risk of resistance
238
Q

How do macrolides exert their effect on bacteria?

A

Act on protein synthesis
Act on gram positives
Used in penicillin allergy or severe pneumonia

239
Q

How do lincosamides exert their effect on bacteria?

A

Act on protein synthesis
Act on gram positives
Used in cellulitis (if pen allergy) and necrotising fascilltis

240
Q

How do tetracyclines exert their effect on bacteria?

A

Act on protein synthesis
Broad spectrum but mainly gram positives
Used in cellulitis (if pen allergy) and pneumonia

241
Q

How do aminoglycosides exert their effect on bacteria?

A

Act on protein synthesis
Acts on gram negatives and stapah
Used in UTIs and infective endocarditis

242
Q

How do quinolones exert their effect on bacteria?

A

Act on DNA synthesis
Acts on gram negatives more than gram positive
Used in pen allergy, UTIs, intra-abdominal infections

243
Q

How would you treat a UTI?

A

Nitrofurantoin for 3 days

Consider urine culture if questioning resistance

244
Q

What is cellulitis?

A

Red, hot, painful, tender skin
Systemic symptoms
Caused by S. aureus and B haemolytic strep
Diagnosed by bacterial swab and blood culutures
Treated with PO or IV flucloxacillin
Or Clarithromycin or Clindamycin if pen allergy

245
Q

What is fish tank granuloma?

A

Caused by M. marinum
Slowly developing lesion
Present on fingers/legs
Requires 2-6 months of antimicrobials

246
Q

What is a buruli ulcer?

A

Caused by M.ulcerans
Can be treated with antibiotics for 8 weeks
Begins as a nodule, small ulcer, large ulcer, deforming damage

247
Q

What is leprosy?

A

Associated with loss of limbs and deformities

Caused by M. leprae

248
Q

What are mycobacteria?

A

Aerobic, non-spore forming, non-motile bacillus
Cell wall contains high molecular weight lipids and mycolic acids
Weakly gram-positive
Ziehl-Neelsen stain for acid fast bacilli
Fluorochrome stains
Slightly curved, beaded bacilli
Slowly growing and slow response to treatment

249
Q

How to culture mycobacteria?

A

Decontamination to kill off other rapid growing bacteria
Solid culture (egg or agar based) 2-4 weeks
Liquid culture 1-3 weeks

250
Q

How to detect nucleic acid in mycobacteria?

A

Nucleic acid amplification test using PCR

Purifies and concentrates M. TB, sonicates to release genomic material, then PCR

251
Q

What is the immunological response of mycobacterial disease?

A

Mycobacteria are phagocytosed by macrophages
They have adapted to withstand phagosomal killing and escape to cytosol
Host tries to kill mycobacteria using microbicidal molecules and acidification and degradation by proteases.
Results in antigens to present to T cells.
CD4 wells generate IFN-y to activate intracellular killing

252
Q

How do granulomas form in the present of mycobacteria?

A

Highly stimulated macrophages become epitheloid cells
Some macrophages fuse with each other to form giant multinucleated cells ‘langhans giant cells’
T-cells infiltrate the mycobacterial lesion
Fibroblasts laid down around granuloma
Central tissue may necrose and form a caseating granuloma

253
Q

What increases your risk of TB?

A

Age (infants, young adults, elderly)
Malnutrition
Intensity of exposure
Immunosuppression

254
Q

What is the tuberculin skin test?

A

Mantoux test

Intradermal injection of purified protein derivative of tuberculin induces skin swelling and redness which is measured.

255
Q

What are the two types of leprosy?

A

Tuberculoid leprosy - associated with hypersentivity and granulomata, paucibaccillary lesions with low number of mycobacteria
Lepromatous leprosy - lesions full of bacilli but little or poorly formed granulomata, extensive skin lesions

256
Q

What are the two types of TB?

A

Latent TB - cell-mediated immune response from T cells, primary infection contained but persists.
No clinical disease
Detectable on tuberculin skin test

Pulmonary TB - granuloma forms around bacilli that settle in apex of lung. Necrosis in this area results in abscess of bacilli and caseous material coughed up. Can occur immediately following primary infection or after later reactivation.

257
Q

What is the treatment for TB?

A

Isoniazid, Rifampicin, Pyrazinade and Ethambutol for 2 months.
Followed by Isoniazid and Rifampicin for 4 months.
If resistance, use fluroquinolones, injectable agents and prothionamide.
Side effects: hepatotoxicity, peripheral neuropathy, optic neuritis

258
Q

Why does HIV lead to so many difficulties?

A

Sexually transmitted
Dormancy period
Attacks immune system
High ability to mutate

259
Q

What are the different stages in HIV?

A

Acute primary infection - transient immunosuppression and fall in CD4 count, acute rise in ‘viral load’ and then fall to ‘set point’
Asymptomatic phase - progressive loss of CD4 T cells resulting in poor immunity. Clinical latency with or without progressive generalised lymphadenopathy
Early symptomatic HIV (AIDS related complex)
AIDS: symptoms of immunodeficiency

260
Q

What two markers are used to monitor HIV infection?

A

CD4 T cell count

HIV viral load (RNA copies/ml)

261
Q

When does HIV develop into AIDS?

A

Variable time from infection to AIDS (typically 5-10 years)
Different for different people: long term non-progressors (HIV-2) or rapid progressors (elderly, children, high viral load).

262
Q

What are some AIDS-defining conditions?

A

Infections e.g. toxoplasmosis, candidiasis, pneumonia
Neoplasms e.g. invasive cervical carcinoma, lymphoma
Direct HIV effects e.g. dementia, encephalopathy, wastin

263
Q

How does acute HIV syndrome manifest itself?

A 
Exposure to symptoms 2-4 weels
Abrupt onset of non-specific symptoms
Symptoms can be severe
Significant weight loss can occur
Lethargy/depression can last months
Window for opportunistic diseases
Other manifestations - aseptic meningitis, PCP, thrush
264
Q

What is persistant generalised lumphadenopathy?

A

Enlarged lymph nodes involving at least 2 non-contiguous sites other than inguinal nodes

265
Q

What is oral candidasis?

A

Fungal infections that occurs in the mucosa of the mouth

266
Q

What is oral hairy leukoplakia?

A

White patch on the side of the tongue with a mitigated or hairy appearance
Caused by Epstein-barr virus

267
Q

What is characteristic of early symptomatic HIV?

A 
Occur in association with many conditions:
Oral/vaginal candida
Oral hairy leukoplania
VZV involving 2 episodes or dermatomes
Cervical dysplasia or carcinoma
Peripheral neuropathy
Bacillary angiomatosis
Pelvic inflammatory disease
Listerosis
Constitutional symptoms
268
Q

What respiratory disease can occur in HIV patients?

A

Bacterial (often pneumococcal) pneumonia
Tuberculosis
Pneumocystis jiroveci pneumonia

269
Q

What is cerebral toxoplasmosis?

A

An opportunistic infection caused by the parasite Toxoplasma gondii. It typically affects patients with HIV/AIDS and is the most common cause of cerebral abscess in these patients
Treatment: sulphadiazine and Pyrimethamine (and folinic acid)

270
Q

What are some neurological conditions that may occur in HIV positive patients?

A

CNS mass lesions: cerebral toxoplasmosis, CNS lymphoma
Meningitis: cryptococcal, tuberculosis, pneumococcal
Ophthalmic lesions: cytomegalovirus retinitis, choroidal tuberculoma

271
Q

What are the HIV-induced neoplasms?

A

Lymphoma - often high grade diffuse large B cell variant
Kaposi’s sarcoma - low grade vascular tumour, skin characteristically involved
Molluscum contagiosum - chronic herpes simplex virus

272
Q

Where do HIV drugs act?

A

Reverse transcriptase inhibitors - nucleoside and non-nucleoside
Protease inhibitors
Fusion inhibitors

273
Q

What is HAART?

A

Highly Active Anti-Retroviral Therapy
3 drugs commonly:
2 Nucleoside reverse transcriptase inhibitors and 1 Non-nucleoside reverse transcriptase inhibitor OR
2 Nucleoside reverse transcriptase inhibitors and 1 protease inhibitors
Aim to reduce viral load and increase CD4 count
Significant impact on mortality and morbidity
Good adherence is necessary
Emergence of resistance can be a problem

274
Q

What CD4 level leaves you open to opportunistic infections?

A

<200

Normal is >500

275
Q

What two blood tests are done in HIV positive patients?

A

CD4 count - measure of immunity

Viral load - amount of virus in blood

276
Q

Who gets HIV?

A

A diverse group
Assumptions need to be challenged
Both heterosexual and homosexual people

277
Q

Why is time an issue in HIV diagnosis?

A

Number diagnosed late remain high

Late diagnosis means a x10 increased risk of death in the first year

278
Q

Who usually has a late diagnosis?

A 
Women more than men
Those in their 50s or over
Black people
Heterosexual men
Outside London
279
Q

How can HIV be transmitted?

A

Blood
Sexual
Vertical

280
Q

What are the different aspects of HIV prevention?

A 
Antiretroviral treatment
PreP
Circumcision
PEP
STI control
Vaccines
Microbicides
281
Q

What does U=U mean?

A

Undetectable = Untransmittable
When a person is living with HIV and is on effective treatment, it lowers the level of HIV (the viral load) in the blood. When the levels are low (below 200 copies/ml of blood measured) it is referred to as an undetectable viral load. This is also medically known as virally suppressed. At this stage, HIV cannot be passed on sexually.

282
Q

What is PrEP?

A

Pre-exposure Prophylaxis
A course of HIV drugs taken by HIV-negative people to prevent infection.
Truvada is currently the only drug approved for use as PrEP. Truvada is a single pill that is a combination of two anti-HIV drugs, tenofovir and emtricitabine.
Highly effective - 86% reduction in risk

283
Q

What is PEP?

A

Post-exposure Prophylaxis
Taking antiretroviral medicines (ART) after being potentially exposed to HIV to prevent becoming infected.
PEP should be used only in emergency situations and must be started within 72 hours after a recent possible exposure to HIV.
28 days of combination antiretroviral therapy

284
Q

What are the benefits in patients knowing their HIV status?

A 
Access to appropriate treatment and care
Reduction in morbidity and mortality
Reduction in mother-to-child transmission
Reduction in sexual transmission
Public health
Cost-effective
285
Q

Why might you offer a HIV test?

A

Patient may have an unacknowledged but identifiable risk or have symptoms or signs of an HIV infection.

286
Q

Why don’t doctors test for HIV?

A

Underestimate the risk of HIV in their patients
Failure to recognise HIV as a modifiable prognostic indicator
Misconception that patient must have detailed pre-test counselling
Misunderstanding of the implications for insure
Anxieties about false positives

287
Q

When conditions may increase your suspicion of HIV?

A 
Generalised lymphadenopathy
Acute generalised rash
Glandular fever
Prolonged episodes of herpes simplex
Persistent frequently recurrent candidiasis
Oral candida
Indicators of immune dysfunction
Recently developed or worsening skin conditions
Odd looking mouth lesions
Unexplained weight loss or night sweats
Persistent diarrhoea
Increasing SOB and dry cough
Recurrent bacterial infections incuding pneumococcal pneumonia
288
Q

What’s the screening test for HIV?

A

Venous blood sample is preferred
p24 antigen
Will detect the majority of infections at 4 weeks
High sensitivity and specificity
Salivary antibody or finger prick screening tests also available

289
Q

What are the advantages of a finger prick HIV test?

A 
Outreach in the community
Increase patient choice
Increased access to testing and case detection
Earlier diagnosis
Reduced risk of complications
Reduce transmission
290
Q

How to manage the results of HIV test?

A

Negative result - repeat within the window period

Positive or unclear - appointment within 48 hours

291
Q

What are retroviruses?

A

Enveloped viruses
Viral genetic material is RNA which is copied into DNA by reverse transcription and incorporated into the host cell to allow for gene transcription

292
Q

What are lentiviruses?

A

Represent a genus of slow viruses with long incubation period
Within the Primate lentivirus group made up of HIV-1, HIV-2 and SIV (Simian Immunodeficiency Virus)

293
Q

How did HIV-1 arise?

A

HIV-1 arose from transmission of SIVcpz from chimpanzees to humans e.g. contaminated meat or bites
HIV-2 arose from SIVsm

294
Q

What are the different types of HIV?

A 
Main (M)
Outlying (O)
New (N)
Main group is separated into classes A-D, F-H, J-K
A is commonly found in Africa
B is commonly found in Europe and USA
295
Q

Which cells does HIV infect?

A

CD4 cells which coordinate the immune response

Glycoproteins of on the HIV allow for entry and binding to the host cell

296
Q

What is the lifecycle of HIV?

A

HIV free in plasma
Recognises CD4 cells and fuses to CD4 receptor
Passes its content into the CD4 cell
Viral RNA to viral DNA by reverse transcription
Viral DNA integrated into the nucleus
Production of new viral content
New HIV budding from CD4 cell

297
Q

Other than CD4 cells, what other cells can be infected by HIV?

A 
Dendritic cells
Occasionally...
Brain microvascular endothelial cells
CD34 bone marrow progenitors
Astrocytes
Renal epithelial cells
298
Q

How does the viral load for HIV change?

A

Within a week it is detectable in the blood
3 weeks in high viral loads - immune response partially controls virus (CD4 cells decreased)
Infected cells spread throughout the body (increased CD4 cells)
Latency period 7 years (but different for different people)

299
Q

What is the immune response to HIV?

A

Humoral immunity - neutralising antibodies, poor/slow to develop effectively because gp130 is poorly immunogenic and has a high geneteic diversity
Cell-mediated immunity - CD8 cause early decline in virus but virus escapes due to mutations
Failure of CD4 T cell proliferation
No protective immune response - major barrier for vaccine!

300
Q

What are long-term non-progressors?

A

Heterogenous group of individuals that don’t progress to AIDS.
No symptoms of infection or signs of AIDS after at least 7 years infection wiwth CD4 count >600 cells/ml in the absence of treatment.
Based on genetic features, host immune responses, differences in MHC I HLAs.

301
Q

How does HIV deplete CD4 T cells?

A

Direct cytotoxicity of directly infected cells
Activation-induced death
Decreased production - disruption in bone marrow
Redistribution to lymphoid tissue
Bystander cell killing (apoptosis)

302
Q

Where might there be a reservoir of HIV?

A

Despite effective suppression of HIV with treatment, most individuals have ongoing replication.
Sanctuary sites: genital tract, CNS, gastrointestinal system, bone marrow
Particular cells act as a reservoir too - macrophages and microglia

303
Q

Who is at risk of HIV?

A 
Men who have sex with men
Heterosexual women
Injecting drug users
Commercial sex workers
Heterosexual men
Truck drivers
Migrant workers
304
Q

How can circumcision reduce the risk of HIV transmission?

A

Safe when provided by well-trained healthcare professionals in a properly equipped setting
Removing foreskin reduces a prime target for HIV to penetrate

305
Q

How does microbicidal gel reduce the risk of HIV transmission?

A

Decreases risk by 39%

If it is used it’s effective but the groups most at risk are the ones who are least likely to use it.

306
Q

How to stop mother to child transmission of HIV?

A

Comprehensive antenatal HIV screening

Life-long antiretrovirral treatment for mother, regardless of CD4 count of clinical stage

307
Q

What are the problems with delivering ART to developing countries?

A 
Awareness
Delivery
Clinical services
Cost of drugs
Adherence
Efficacy
Co-morbidities
308
Q

What is Atripla?

A

HIV combination anti-retroviral medicines
Tenofovir disoproxil fumarate
Efavirenz
Emtricitabine

309
Q

What is the variecella zoster virus?

A

One virus, two diseases
Varicella ‘chicken pox’ - primary infection
Herpes zoster shingles - secondary reactivation

310
Q

What are the features of chicken pox?

A

2 days of early symptoms
10 days of rash until lesions have crusted off
High infectivity 1-2 days before rash appears
Common in children
Highly contagious
Can be serious in immunocompromised, patients with transplants, adults, pregnant women, smokers, infants.

311
Q

What are the stages of a chicken pox lesion?

A 
Macule
Papule (raised)
Vesicle (fluid-filled)
Pustule (inflammatory response)
Crust (fall off)
312
Q

How can you differentiate between chicken pox and small pox rash?

A

Small pox - bigger, evolve all at the same time, present on the peripheries
Chicken pox - lesions at different stages of progression, appear concurrently, centrifugal distribution

313
Q

How to confirm a diagnosis of chicken pox?

A

Pop the lesion with a sterile needle
Absorbe the vesicle contents onto swab
Replace swab in cassette and send for VSV/HSV PCR to look for the sequence of the virus

314
Q

What are the possible complications of chicken pox?

A 
Dehydration - if present on the mouth, difficulty swallowing
Haemorrhagic change
Cerebellar ataxia (common)
Encephalitis
Varicella pneumonia
Skin and soft tissue infection typically with group A Strep
Bone and joint infections - deep sepsis
Congeital (foetal) varicella syndrome
315
Q

What is the most common chicken pox complication in adults?

A

Chicken pox pneumonitis

Risk doubles if underlying lung disease or if a smoker

316
Q

What is foetal varicella syndrome?

A

Foetal infection occurs in 10-15% of cases of chicken pox in pregnancy.
Usually transient and asymptomatic.
May have shingles in first year of life.
Complications - cicatrical skin scarring, lumb hypoplasia, visceral and ocular lesions, microcephaly and growth retardation

317
Q

How does chicken pox display viral dormancy?

A 
Chicken pox lesions on the skins
Sensory neurons
Virus held dormant at the dorsal root ganglion
Reactivation
Rash in the associated dermatome
318
Q

What are the features of Shingles?

A

Most common in the elderly
Thoracic region is most commonly involved (50-70%)
Cervical, lumbar, sacral dematomes less involved
10-20% are ophthalmic
Hugely painful
Tissue fluid in vesicles burst leaving exposed areas - most at risk of post herpetic neuralgia
Can have spread beyond the dermatomes
Can become keratinised if there are areas of non-intact skin

319
Q

What are the features of Parovirus?

A

Rash across the whole body
Joint or bone pain
Virus can attach to immature RBCs, preventing maturation, profoundly anemia
Can be fatal in babies due to overworking heart (hydrops fetalis)
Can perform an intrauterine transfusion

320
Q

What are vesicular rashes?

A

Develop on the vermillion border

Can give antivirals like Acyclia to prevent maturation of vesicles

321
Q

What are the features of primary Cytomegalovirus?

A 
Macular rash
Enlarged lymph glands
Atypical sticky lymphocytes
Febrile
Decreased liver function
(Presents similar to glandular fever)
Can lie dormant and then be reactivated (pneumonitis)
322
Q

What are the features of Measles?

A

Measles is a highly contagious infectious disease caused by measles virus. Symptoms usually develop 10–12 days after exposure to an infected person and last 7–10 days. Initial symptoms typically include fever, often greater than 40 °C (104 °F), cough, runny nose, and inflamed eyes.

323
Q

What are the features of Dengue fever?

A

Fine maculopapular rash on trunk between day 3 and day 5 of illness
Spreads to face and extemities
Marked blanching
Torniquet test - looking for burst vesicles and bruises
underneath - positive if there are more than 10 to 20 petechiae per square inch
Dengue shock syndrome

Lectures (17 decks)

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