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Phase 2a Medicine > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is the difference between a pathogen and a commensal?

A

A pathogen is an organism that is capable of causing disease, a commensal colonises the host but under normal circumstances doesn’t cause disease.

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2
Q

What is an opportunist pathogen?

A

A microbe that only causes disease if host defences are compromised, e.g. E coli is normally present in the gut, but can cause a UTI if it gets into the urinary tract.

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3
Q

Which areas of the body are open to bacterial colonisation?

A

Nasal and oral passages
GI tract
Vagina
A small portion of the urethra

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4
Q

What shape are cocci?

A

Round

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5
Q

What shape are bacilli?

A

Rod-shaped

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6
Q

What are the different configurations of cocci?

A

Single
Diplococci
Chains
Clusters

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7
Q

How do flagellae help microorganisms?

A

Motility - they can help organisms ‘swim’ towards target cells

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8
Q

How do pili/fimbriae help pathogenic organisms?

A

They help the microbe to adhere to surfaces, allowing them to introduce toxins to a host cell.

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9
Q

What colour do gram positive bacteria appear following gram stain?

A

Purple

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10
Q

What colour do gram negative bacteria appear following gram stain?

A

Pink

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11
Q

What stain can be used if bacteria don’t stain with gram?

A

Ziehl-Neelsen stain

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12
Q

What type of bacteria don’t stain with gram and why?

A

Mycobacteria have a waxy cell wall, which gram stain struggles to penetrate

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13
Q

Which compound is found on the inner membrane of gram negative bacteria that the immune system is designed to recognise?

A

Lipopolysaccharide (endotoxin)

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14
Q

Some bacteria create free spores with their DNA inside, which can then be aerosolised. Name a bacterium that does this.

A

Anthrax

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15
Q

What diagnostic tool cannot be used for identifying microbes with a long doubling time?

A

Cultures - if the microbe has a long doubling time (e.g. M tuberculosis 24 hours), it would take months to become visible on culture.

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16
Q

Exotoxins are proteins secreted by which type of bacteria?

A

Both gram positive and gram negative

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17
Q

How can exotoxins be disabled?

A

They can be unfolded using heat –> disabled

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18
Q

What are the consequences of the rapid replication of bacterial DNA?

A

Frequent mutation, which can lead to antibiotic resistance

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19
Q

What are the possible structures of bacterial DNA?

A

Either a singular closed circular chromosome or a plasmid

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20
Q

How can bacteria share genetic information?

A

Via bacterial conjugation - a sex pilus is formed between the donor and recipient, which is a hollow tube through which genetic information can be passed.

Or via plasmids

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21
Q

What are the features of Staphylococci?

A

Gram positive (purple) cocci, which grow in clusters, facultative anaerobic

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22
Q

What test can be performed to categorise Staphylococci?

A

Coagulase

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23
Q

Is Staph aureus coagulase positive or negative?

A

Positive

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24
Q

Where is Staph aureus normally found?

A

In the nose and skin

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25
Q

What are the virulence factors of Staph aureus?

A
  • Some strains produce pore-forming toxins e.g. alpha haemolysin, proteases, TSS toxin and protein A (which makes antibodies bind in the wrong direction, preventing opsonisation)
  • MRSA is resistant to beta-lactams, gentamicin, erythromycin and tetracycline
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26
Q

Name two types of coagulase negative Staphylococci

A

Staphylococcus epidermis

Staphylococcus saprophyticus

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27
Q

Why does Staphylococcus epidermis cause infections in prostheses?

A

Its main virulence factor is the ability to form persistent biofilms, e.g. on artificial heart valves

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28
Q

Why does Staphylococcus saprophyticus cause acute cystitis?

A

It adheres to the bladder because of haemagglutinin

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29
Q

How do Streptococci appear in culture?

A

Gram positive (purple), growing in long chains

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30
Q

What test can be used to differentiate between different types of streptococcus?

A

Haemolysis

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31
Q

What is the difference in appearance between alpha and beta haemolysis on blood agar?

A

Alpha haemolysis - only partial clearing around the colony, greenish appearance
Beta haemolysis - complete clearing of blood around the colony

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32
Q

What does Lancefield grouping differentiate by?

A

Carbohydrate cell surface antigens

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33
Q

How can we check Lancefield group?

A

Adding antisera to see which one causes clumping (indicates recognition)

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34
Q

Streptococcus pyogenes is which Lancefield group?

A

Group A

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35
Q

What are the virulence factors of S pyogenes?

A 
Exported factors:
Enzymes e.g. hyaluronidase, streptokinase (breaks down  clots), C5a peptidase
Surface factors:
Capsule - hyaluronic acid (protection)
M protein (encourages complement degradation)
Toxins:
Streptolysins O and S (bind cholesterol)
Erythrogenic toxin SPeA
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36
Q

What infections are caused by Streptococcus pyogenes?

A 
Wound infections, e.g. cellulitis
Tonsillitis, pharyngitis
Otitis media
Impetigo
Scarlet fever
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37
Q

Strep pneumoniae is a normal commensal in the oropharynx present in ~30% of the population. What conditions can it potentially cause?

A

Pneumonia
Otitis media
Sinusitis
Meningitis (infants and elderly)

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38
Q

What are the virulence factors of Strep pneumoniae?

A

Capsule (polysaccharide, antiphagocytic)
Inflammatory wall
Cytotoxin - pneumolysin

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39
Q

What conditions can be caused by viridans group Streptococci?

A

Dental caries - often present in oral cavity

Endocarditis if it gets into the bloodstream

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40
Q

Name 4 gram positive bacilli

A
  1. Listeria monocytogenes
  2. Bacillus anthracis
  3. Corynebacterium diphtheriae
  4. Clostridia e.g. C tetani, C botulinum, C difficile
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41
Q

Why is lipopolysaccharide known as ‘endotoxin’?

A

It forms the outer leaflet of the outer membrane of gram negative bacteria and is toxic to human cells, triggering an inflammatory response

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42
Q

GI infections tend to be caused by which 3 gram negative bacteria?

A
  1. Shigella flexneri
  2. Escherichia coli
  3. Salmonella enterica
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43
Q

How can you identify which of the 3 bacteria has caused a GI infection?

A

Culture using MacConkey-lactose agar. E Coli can metabolise lactose, so will produce lactic acid, lowering the pH.
To differentiate between salmonella and shigella, use serology (shigella has no flagella, so will not show a flagella antigen)

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44
Q

What are the O, K and H antigens present on the cell surface of gram negative bacteria?

A

O antigen = LPS
K antigen = exopolysaccharide capsule
H antigen = flagella

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45
Q

What is the name given to antigenically distinct variants within species of gram negative bacteria?

A

Serovars

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46
Q

E coli is normally present in the GI tract. What are the 6 principal infections caused by pathogenic varieties of E coli?

A
  1. Wound infections
  2. UTIs
  3. Gastroenteritis
  4. Travellers’ diarrhoea
  5. Bacteraemia (can lead to sepsis)
  6. Meningitis in infants (rare in the UK)
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47
Q

Why are some strains of E coli pathogenic?

A

They can acquire blocks of genes from other bacteria, thereby acquiring pathogenic properties

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48
Q

What is the main symptom of Shigellosis?

A

Severe bloody diarrhoea

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49
Q

Why is Shigella able to cause illness?

A

Only a small amount is required to establish infection, so only a small amount needs to survive the low pH in the stomach - allows person to person spread and also via contamination of food and water

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50
Q

How does Shigella invade the colonic mucosa?

A

It is taken up by a macrophage, it then induces the macrophage to apoptose and is released on the basolateral side of the epithelium, where it can infect adjacent epithelial cells, moving through the cytoplasm using actin filaments from the host cell.
Destroys epithelium and also causes inflammation as the apoptotic macrophage releases cytokines

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51
Q

What is the major virulence determinant of Shigella?

A

Shiga toxin, which inhibits protein synthesis and causes cell death.

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52
Q

What potentially fatal condition can be caused by the Shiga toxin?

A

Haemolytic urinae syndrome, if Shiga toxin is absorbed systemically. Targets kidney, microvascular thrombosis in kidney results in kidney failure and possibly death.

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53
Q

What three conditions can be caused by Salmonella enterica?

A
  1. Gastroenteritis/enterocolitis
  2. Enteric fever (typhoid/paratyphoid fever, caused by specific serovars Typhi and Paratyphi)
  3. Bacteraemia (serovars Cholerasuis and Dublin) - uncommon
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54
Q

Why does salmonellosis require a high infected dose?

A

It does not tolerate low pH well, so a large amount is required for some to survive , infect the gut epithelium and trigger an inflammatory response.

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55
Q

How does the Typhi serovar of Salmonella cause typhoid?

A
  • S Typhi is ingested
  • Travels to the liver, spleen and bone marrow, where it multiplies
  • Much larger numbers are released into the bloodstream
  • The kidney and other organs are infected
  • Can result in ‘carrier’ state for over a year if it travels to the gall bladder
  • Travels to the small intestine, causing inflammation and ulceration, leading to diarrhoea and possible haemorrage/perforation
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56
Q

Where is Klebsiella pneumonaie infection usually contracted?

A

In hospital

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57
Q

What problems can be caused by Klebsiella pneumonaie infection?

A

UTIs
Pneumonia (via aspiration from the oropharynx)
Surgical wound infections
Bacteriaemia (and possibly sepsis)
Also difficult to treat as resistant to carbapenems

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58
Q

Vibrio cholerae is a facultative anaerobe that can result in severe diarrhoael disease. Which populations are most at risk?

A

Vibrio cholerae lives in saline environments and is commensal to planktonic crustaceans that are ingested by shellfish; therefore those living in coastal areas with poor sanitation are most at risk due to contamination of drinking water

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59
Q

Vibrio cholerae is highly infective. How is it transmitted from person to person?

A

Faecal-oral route

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60
Q

How can cholera be treated?

A

Oral replacement therapy

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61
Q

What is the major virulence determinant of vibrio cholerae?

A

Cholera toxin, which binds to a glycolipid receptor on an epithelial cell, resulting in continuous activation of G protein, which leads to uncontrolled cAMP production and modification of CFTR ion transporter, leading to a loss of Na+ and Cl- into the gut lumen, which results in massive loss of water.

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62
Q

Haemophilus influenzae is an exclusively human parasite, which causes opportunistic infections in which groups?

A

Young children and adult smokers. Can also cause pneumonia in CF, COPD and HIV patients.

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63
Q

What are the virulence determinants of Haemophilus influenzae?

A

Capsule - invasive strains are encapsulated, giving resistance to phagocytosis and the complement system.
LPS (endotoxin) - causes inflammation and confers some resistance to complement

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64
Q

Legionella pneumophila causes Legionnaire’s disease, which results in severe inflammatory pneumonia. Which groups are at risk?

A

Immunocompromised
Elderly
Alcoholics
Smokers

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65
Q

Where is Legionella pneumophila found?

A

In man-made aquatic environments, e.g. air conditioning systems, shower heads, nebulisers, humidifiers

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66
Q

Why does Legionella pneumophila cause severe inflammatory pneumonia?

A

It can survive and replicate within alveolar macrophages. Therefore, once it is phagocytosed, it can recruit ER, differentiate to its flagellated form and become motile. It also upregulates pro-inflammatory genes in the alveolar macrophages, resulting in excessive influx of neutrophils into the lungs.

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67
Q

Bordella pertussis causes which disease?

A

Whooping cough

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68
Q

Bordella pertusses contains which two toxins?

A
  1. Pertussis toxin, which locks S1 G protein in off state - this G protein would normally inhibit adenylate cyclase, so cAMP is massively increased
  2. Adenylate cyclase haemolysin toxin, which prevents adenylate cyclase from being broken down, resulting in a massive increase in cAMP

Hypersynthesis of cAMP leads to suppression of innate immune functions, particularly phagocytosis by macrophages.

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69
Q

What is Neisseria meningitidis also known as?

A

Meningococcus

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70
Q

How does Neisseria meningitidis spread from person to person?

A

It is normally present in the nasopharynx of 5-10% of the population and normally does not cause symptoms. It can be transmitted via aerosol.

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71
Q

N meningitidis can cause septicaemia and meningitis. How does this happen?

A

It crosses the nasopharyngeal epithelium and enters the blood stream, which can cause septicaemia. If the bacteria cross the blood brain barrier, they can enter the CSF of the subarachnoid space and cause meningitis.

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72
Q

What are the virulence determinants of N meningitidis?

A

Capsule - anti-phagocytic (non-capsulated version not pathogenic)
LPS - leads to cytokine cascade and sepsis

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73
Q

Gonorrhoea is the second most common STD worldwide. Which bacteria causes it?

A

Neisseria gonorrhoeae (also known as ‘gonococcus’)

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74
Q

What are the potential complications of gonorrhoea?

A

Urethritis, infection of female genitalia (can lead to salpingitis and/or PID). Can also cause proctitis, gingivitis and pharyngitis depending on type of sexual activity.

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75
Q

What is the most common cause of food poisoning in the UK and US?

A

Campylobacter (jejuni/coli), most commonly found in undercooked poultry and unpasteurised milk

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76
Q

What conditions can be linked to infection with Helicobacter pylori?

A

Gastritis
Peptic ulcer disease
Less commonly - gastric adenocarcinoma, lymphoid tissue lymphoma

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77
Q

What is the most abundant commensal in the large intestine?

A

Bacteroides

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78
Q

Why is bacteroides often present in polymicrobial infections with enterobacteria?

A

The enterobacteria are facultative anaerobes; they deplete the O2, which allows anaerobes such as bacteroides to proliferate

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79
Q

What opportunistic infections are caused by bacteroides?

A

Usually peritoneal cavity infections such as peritonitis and intra-abdominal abscesses following tissue injury

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80
Q

Chlamydia and Chlamydophila are obligate intracellular parasites. What are the two developmental stages?

A
  1. Elementary bodies are dormant enter the cell through endocytosis, prevent phagosome-lysosome fusion and differentiate to reticular bodies
  2. Reticular bodies are metabolically active, acquire nutrients from host cell, replicate and convert back to elementary bodies (causes cell lysis, elementary bodies are then free to enter another cell)
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81
Q

The genital tract biovar of chlamydia trachomatis is the most common STD. How does it infect people?

A

It infects the epithelial cells of the mucous membranes of the urethra in both sexes and the vagina, where it can ascend to the uterus and ovaries, potentially causing PID and infertility.

Can also cause conjunctivitis via hand to eye transmission

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82
Q

What disease is caused by Borrelia burgdorferi?

A

Lyme disease

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83
Q

Lyme disease can be transmitted to humans via tick nymphs. What symptoms does it cause?

A

A Bull’s eye rash, flu-like symptoms.
Can also disseminate to other parts of the body via the blood/lymphatic system and cause neurological problems and arthritis in the joints due to inflammation triggered by immune response.

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84
Q

What organism causes syphilis?

A

Treponema pallidum (spirochaete bacterium)

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85
Q

Describe the three stages of syphilis infection

A
  1. Primary stage: localised genital infection, highly transmissible
  2. Secondary stage: systemic infection resulting in skin rash, swollen lymph nodes, joint, pain, muscle aches, fever, headache. Still highly transmissible.
  3. Tertiary stage: Granulomas in soft tissue and bone, cardiovascular syphilis, neurosyphilis. Non-infectious at this stage.
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86
Q

What is the most common mycobacterial infection?

A

Tuberculosis (mycobacterium tuberculosis)

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87
Q

What is the standard therapy for tuberculosis infection?

A

Isoniazid, rifampicin, pyrazinamide and ethambutol for two months followed by isoniazid and rifampicin for a further four months

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88
Q

What are the possible side effects of tuberculosis standard therapy?

A 
Hepatotoxicity (isoniazid, rifampicin and pyrazinamide)
Peripheral neuropathy (isoniazid)
Optic neuritis (ethambutol)
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89
Q

Why is there a high likelihood of side effects with tuberculosis treatment?

A

Because treatment involves 4-9 months of combination therapy

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90
Q

Why is antibiotic resistance such a big problem in TB treatment?

A

The antibiotic treatment takes a long time, meaning that any bacteria left behind will be antibiotic resistant

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91
Q

Approximately one-third of the world’s population are infected with TB, although many of these cases are subclinical. Why are so many people infected?

A

Because of the extremely low infective dose - it only takes 1-2 bacilli to infect someone.

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92
Q

What is primary tuberculosis?

A

Initial contact is made by alveolar macrophages and bacilli are taken in lymphatic system to hilar lymph nodes

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93
Q

What is latent tuberculosis?

A

A cell mediated immune response from the T cells, which contains the primary infection but can persist for decades with no clinical signs (although would be detectable on a skin test).

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94
Q

What is pulmonary tuberculosis?

A

Pulmonary tuberculosis occurs as a result of a second infection or immuno compromise - the T cell control of the primary infection can be lost, causing TB to spread throughout the lungs. Granulomas form around the bacilli that settle in the apex of the lungs (these can be necrotic in the centre) and the patient starts coughing up caseous material.

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95
Q

Where can TB spread besides the lungs?

A

It can spread to the CNS and cause TB meningitis (big killer in the AIDS community) and can also spread to the bone and joints.

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96
Q

Why are a lot of antibiotics ineffective against TB?

A

M tuberculosis has a very long generation time, meaning that antibiotics that target cell division are not effective.

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97
Q

Why are HIV patients up to 20 times more likely to get TB?

A

HIV patients often have low CD4 counts. Effective immunity to TB requires CD4 T-cells, which generate interferon gamma and activate intracellular killing by macrophages (mycobacteria have adapted to withstand phagolysosomal killing)

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98
Q

How do T-cells contain primary TB infection?

A

Via the formation of granulomas. The alveolar macrophages take up TB and recruit other immune cells to form granulomas, which can contain the infection. However, if the Th1 response is lost (CD4 depletion, TNFa depletion), granulomas can become unstable and caseous material is released - this commonly happens in elderly individuals have had subclinical TB for a long time.

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99
Q

What test can be used to detect latent TB?

A

Tuberculin skin test (Mantoux test)

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100
Q

What are the three groups of worms?

A
  1. Nematodes (roundworms)
  2. Trematodes (flatworms, flukes)
  3. Cestodes (tapeworms)
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101
Q

Why don’t adult worms spread from human to human?

A

They can’t reproduce without a period of development outside the body

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102
Q

What is the ‘pre-patent’ period in worm infection?

A

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

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103
Q

How are intestinal nematodes passed from person to person?

A

Via faecal oral route

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104
Q

Loeffler’s syndrome causes cough, fever, wheeze and eosinophilia. What causes it?

A

Infection with Ascaris lumbricoides (large roundworm) - larval migration through the lungs causes Loeffler’s syndrome

105
Q

How is Ascaris lumbricoides diagnosed?

A

Stool microscopy to check for eggs

106
Q

What drugs can be used to treat Ascaris lumbricoides?

A

Piperazine, pyrantel, mebendazole, levasimole

107
Q

What are the clinical features of hookworm?

A

Ground itch due to papules at site of entry of the larvae
Pulmonary symptoms
Iron-deficiency anaemia due to adult worms feeding on blood

108
Q

How is hookworm diagnosed?

A

Stool microscopy for eggs

109
Q

What is the treatment for hookworm?

A

Iron supplements, pyrantel, mebendazole

110
Q

What is the only common helminth in the UK?

A

Enterobius vermicularis (pinworm/threadworm)

111
Q

Why does enterobius vermicularis (threadworm) cause pruritis ani?

A

Because the adult worms live in the large bowel and the female adult emerges from the anus at night to lay eggs on the perineum

112
Q

What are the clinical features of enterobius vermicularis?

A 
Pruritus ani
Commonly affects whole families
Appendicitis
Vaginal penetration (can lead to endometritis, salpingitis, infertility)
Occasionally seen in paranasal sinuses
113
Q

How can enterobius vermicularis be diagnosed?

A

Microscopy of a strip of sellotape applied to the perianal region

114
Q

How can enterobius vermicularis be treated?

A

Using drugs such as mebendazole, piperazine, pyrantel - the whole household should be treated simultaneously.

115
Q

What are the clinical features of whipworm (trichuris trichiura)?

A

Resident in large bowel
Often asymptomatic
Often co-exists with Ascaris lumbricoides
Trichuriasis results from heavy infestation –> bloody diarrhoea, rectal prolapse, anaemia, wasting, eosinophilia

116
Q

How is trichuris trichiura (whipworm) diagnosed?

A

Stool microscopy for eggs

117
Q

How is trichuris trichiura (whipworm) treated?

A

Mebendazole, albendazole

118
Q

Stronglyoides stercoralis causes strongloidiasis. What are the symptoms of strongloidiasis?

A

Pruritus at the site of larval entry
Pulmonary symptoms due to larval migration
Gut symptoms (malabsorption)
Autoinfection can also occur and in immunocompromised individuals can lead to disseminated strongloidiasis –> diarrhoea, weight loss, malabsorption, paralytic ileus, peritonitis, bacterial infections.

119
Q

Visceral larva migrans is caused by dog and cat roundworms and mainly seen in children. What are the clinical features?

A

Fever, hepatomegaly, eosinophilia

120
Q

What condition occurs when VLM larvae become trapped in the retina?

A

Ocular toxicariasis

121
Q

What stomach-wall invading helminth is found in raw fish/crustaceans?

A

Anisakidae

122
Q

What helminth causes elephantiasis?

A

Wuchereria bancrofti

123
Q

Blood flukes, liver flukes, lung flukes and bowel flukes all have which organism as an intermediate host?

A

Snail

124
Q

Katayama fever is present in 50% of patients with which helminth infection?

A

Schistosomiasis

125
Q

How do humans become infested with Schistosoma helminths?

A

The miracidium hatches from eggs, infects snail (intermediate host), then cercariae leave snail and penetrate the skin of a human who is in the water. The immature worm enters the bloodstream, lay eggs near the bladder and the eggs enter the intestinal tract or bladder –> passed in urine/faeces

126
Q

What are the 5 major groups of protozoa?

A
  1. Flagellates
  2. Amoebae
  3. Microsporidia
  4. Sporozoa
  5. Ciliates
127
Q

What is the more common name for African trypanosomiasis?

A

Sleeping sickness

128
Q

What causes African trypanosomiasis?

A

Tsetse fly bite

129
Q

What is the more common name for American Trypanosomiasis?

A

Chagas disease

130
Q

What organism causes American Trypanosomiasis?

A

Triatomine bug

131
Q

What are the symptoms of American Trypanosomiasis?

A

Acute - flu like symptoms

Chronic - cardiomyopathy, megaoesophagus, megacolon

132
Q

Leishmaniasis is caused by which organism?

A

Sandfly

133
Q

What are the cutaneous features of leishmaniasis?

A

Ulceration and tissue destruction

134
Q

What are the visceral features of leishmaniasis?

A

Fever, weight loss, hepatosplenomegaly, anaemia

135
Q

Trichomonas vaginalis is a sexually transmitted protozoal infection characterised by yellow frothy discharge and dysuria. How is it treated?

A

Metronidazole

136
Q

How is amoebiasis spread?

A

Faecal-oral route

137
Q

Amoebiasis can result in dysentry, colitis, and abscesses in the liver/lung. How is it diagnosed?

A

Trophozoites/cysts can be seen in the stool

138
Q

What is used to treat amoebiasis?

A

Metronidazole

139
Q

Cryptosporidiosis is caused by a waterborne protozoan. What are the symptoms?

A

Diarrhoea, vomiting, fever, weight loss, oocytes seen in stool.

140
Q

Cryptosporidiosis is usually self-limiting but can cause severe disease in immunocompromised individuals. If treatment is required, what would be used?

A

Nitazoxanide

141
Q

Toxoplasmosis is caused by toxoplasma gondii. How would a human contract it?

A

Ingestion of contaminated food and water or from feline faeces (cats are the only definitive host where full cycle occurs from ingestion to excretion)

142
Q

What severe symptoms can be caused by toxoplasmosis, usually in immunocompromised individuals?

A

Toxoplasma encephalitis
Chorioretinitis
Disseminated disease

Can also cause congenital toxoplasmosis (microcephaly, hydrocephalus, IUGR, miscarriage) if acute infection occurs during first trimester of pregnancy.

143
Q

Malaria is transmitted by what organism?

A

Female anopheles mosquito

144
Q

Describe how blood films can help diagnose malaria.

A

Blood sample taken for thick and thin films. A thick film is sensitive but has low resolution and can determine whether or not a person has malaria. A thin film can identify what species of malaria the person has.

Blood films need to be taken on consecutive days to see the whole lifecycle

145
Q

What are the clinical features of malaria?

A

Fever, chills, headache, myalgia, fatigue, diarrhoea, vomiting, abdominal pain, anaemia, jaundice hepatosplenomegaly, ‘black water fever’ (haemolysis –> haematuria)

146
Q

Why does the Plasmodium falciparum variant cause the most severe malaria symptoms?

A

Red blood cells infected with Plasmodium falciparum have proteinaceous knobs on the surface that bind to endothelial cells in the vessels and other red blood cells, which can result in obstruction of blood vessels with consequent hypoxia of tissues and microinfarcts of the brain and lung.

147
Q

Why might epistaxis, abnormal bleeding and worsening anaemia happen as a result of disseminated intravascular coagulation?

A

Lots of micro clots form, uses up clotting factors so there are less available circulating in the blood.

148
Q

How is complicated malaria treated?

A

IV artesunate (IV quinine and doxycycline), as well as other supportive measures to treat symptoms e.g. antiepileptics, oxygen, diuretics, ventilation, fluids, dialysis, broad spectrum antibiotics (sepsis), blood transfusion.

149
Q

How is uncomplicated malaria treated?

A

There are various options including riamet, quinine and doxycycline, oral chlorquine.

150
Q

Describe the humoral response to viral infection.

A

Humoral = antibody-mediated.
Antibodies can block virus-host cell fusion and may be involved in opsonisation.
IgM enhances the antibody response, activating complement.
Complement plays a role in opsonisation and lysis.

151
Q

Describe the cell-mediated response to viral infection.

A
  • Interferons from Th cells released –> signal neighbouring cells
  • (CD4+) or cytotoxic T lymphocytes can kill infected cells directly
152
Q

What causes most of the damage from viral infections?

A

Inflammation as a result of immune response

153
Q

How can influenza evade the immune response?

A

By changing its coat antigen

154
Q

How do mumps, measles, EBV, HIV and CMV evade the immune system?

A

By causing immune suppression, i.e. destroying/altering lymphocytes and/or macrophages

155
Q

What causes the variability in Influenza coat antigen?

A

Changes in haemagglutinin and neuraminidase surface proteins

156
Q

What causes flu epidemics?

A

Antigenic drift caused by spontaneous mutations, which occur gradually and result in minor changes in haemagglutinin and neuraminidase.

157
Q

What causes flu pandemics?

A

Antigenic shift - sudden emergence of new antigen subtype, which is different to that of preceding virus.

158
Q

What are the four types of adhesins that help bacteria bind to mucosal surfaces?

A
  1. Fimbriae and pili filamentous proteins
  2. Non-fimbrial proteins
  3. Lipid
  4. Glycosaminoglycans
159
Q

How do bacteria form biofilms?

A

Bacteria stick together on a surface by secreting extracellular substances formed from proteins, polysaccharides and DNA

160
Q

How do trypanosomes evade the immune response?

A

They have different VSG genes, which control surface antigens. By switching which VSG is expressed, they can change their surface antigens.

161
Q

What two diseases are caused by the varicella zoster virus?

A
  1. Chicken pox

2. Shingles

162
Q

Why does VZV remain in a human host lifelong?

A

The virus core mimics human DNA

163
Q

How does a chicken pox rash evolve?

A
  1. Macule (blob)
  2. Papule (palpable)
  3. Vesicle (blister)
  4. Pustule (pus-filled)
  5. Crust
164
Q

How is the chicken pox rash distributed?

A

Centrifugally - the peripheries are spared because the virus multiples in warm areas of the body

165
Q

How can chicken pox be differentiated from smallpox?

A
  • Smallpox lesions are larger
  • Smallpox lesions all evolve simultaneously, whereas chicken pox lesions can be seen at various different stages.
  • Smallpox virus divides in cooler areas of the body –> different distribution
  • Smallpox affects deeper layers of the skin
166
Q

What are the possible complications of chicken pox?

A 
Dehydration
Haemorrhagic change
Cerebellar ataxia
Encephalitis
Varicella pneumonia
Skin and soft tissue infection
Congenital varicella syndrome (pregnant women)
167
Q

Chickenpox pneumonitis is the most common complication in adults and affects 15% of healthy adults. How is it treated?

A

Antiviral treatment: IV acyclovir, then switch to oral valacyclovir when patient starts to improve.

168
Q

Why does shingles normally present as a unilateral rash?

A

VZV usually lies dormant in the dorsal root/cerebral ganglion. Reactivation causes it to migrate back along the sensory nerve, where it will affect that particular dermatome.

169
Q

What clinical sign indicates corneal involvement of shingles?

A

Hutchinson’s sign - lesion on the end of the nose

170
Q

What can be used to treat pain from shingles?

A

Gabapentin

171
Q

What would indicate that the immune system is not coping well with shingles?

A

Shingles lesions appearing in peripheral areas

172
Q

What virus causes hand, foot and mouth?

A

Enterovirus

173
Q

How does parvovirus cause anaemia?

A

Human parvovirus targets immature red cells in the bone marrow, attaches to the P antigen and prevents RBC maturation so as the RBCs die, they cannot be replaced.

174
Q

How can parvovirus affect a fetus?

A

The fetus becomes anaemic, the heart tries to work harder, results in high output cardiac failure and subsequent hydrops fetalis

175
Q

How can hydrops fetalis be detected and treated?

A

It can be detected by checking blood flow speed on ultrasound and treated with intrauterine transfusion

176
Q

Where are Herpes virus 1 and 2 lesions found?

A

Herpes 1 - usually the lips, can also appear on the genitals

Herpes 2 - usually only found on the genitals

177
Q

Which virus causes similar symptoms to glandular fever, is common in teens and young adults and causes swollen lymph nodes and atypical lymphocytes?

A

Primary cytomegalovirus

178
Q

What are the main symptoms of CMV reactivation?

A

Retinitis

Pneumonitis

179
Q

What is the treatment for secondary CMV?

A

Gancyclovir (or valgancyclovir, which can be taken orally)

180
Q

Describe the rash associated with measles infection

A

Dry, buttock-sparing, lesions in mucosa look like salt grains

181
Q

Besides a rash, what other symptoms are associated with measles?

A

Cough, coryza, diarrhoea and conjunctivitis

182
Q

What is an ‘enveloped’ virus?

A

One which has a lipid membrane derived from the host cell (e.g. influenza and HIV)

183
Q

What are the main differences between bacteria and viruses?

A
  • Viruses have no cell wall or organelles
  • Viruses can have either DNA or RNA, not both
  • Viruses cannot replicate outside of a host cell
184
Q

Briefly describe how viruses replicate

A
  1. Attachment to specific receptor on host cell
  2. Enter cell via endocytosis
  3. Uses host material to transcribe genome to mRNA and translate to proteins, using host ribosomes and nucleotides to either replicate itself or to produce the proteins it needs
  4. Assembles itself into a virion once it has what it needs
  5. Releases new virus particles - either bursts out of cell causing cell death or in some cases can escape cell via exocytosis, leaving host cell alive
185
Q

Name 5 ways in which viruses cause disease

A
  1. Direct destruction of host cells
  2. Modification of host cell
  3. Causing ‘over-reactivity’ of the immune system
  4. Damage through cell proliferation
  5. Evasion of host defences
186
Q

How does polio virus cause paralysis?

A

By direct destruction of host cells. It targets neurons, replicates inside them and causes cell lysis and death

187
Q

How does rotavirus cause profuse diarrhoea?

A

By modification of host cells - it atrophies villi and flattens epithelial cells, decreasing the small intestine surface area, preventing absorption of nutrients and water.

188
Q

How does hepatitis B destroy the liver?

A

By causing over-reactivity of the immune system. The infected hepatocyte presents the virus antigen, which is recognised by a CTL, which then destroys the hepatocyte.

189
Q

What does the influenza haemagglutinin surface antigen do?

A

It acts as a ‘grappling hook’, helping the virus to bind and enter cells

190
Q

What does the influenza neuraminidase surface antigen do?

A

It acts as ‘bolt cutters’, cutting the newly formed virus loose from infected cells (leaving host cells alive)

191
Q

Which H and N antigen subtypes have been detected in humans?

A

H1-3 and N1-2

192
Q

What are the three targets for antibiotics?

A
  1. Cell wall synthesis
  2. Nucleic acid synthesis
  3. Protein synthesis
193
Q

How do beta-lactams destroy bacteria?

A
  • Bind covalently and irreversibly to penicillin binding proteins
  • Disrupts peptidoglycan production
  • Disrupts the cell wall
  • Causes cell lysis
194
Q

Why are beta-lactams more effective against gram positive bacteria than gram negative?

A

Gram positive bacteria have more peptidoglycan in their cell walls.
Gram negative organisms have an additional LPS layer that decreases antibiotic penetration

195
Q

Name 3 antibiotics that inhibit nucleic acid synthesis

A

Rifampicin
Metronidazole
Ciprofloxacin

196
Q

Name 4 types of antibiotic that inhibit protein synthesis

A
  1. Aminoglycosides (gentamycin)
  2. Tetracyclines (doxycycline)
  3. Lincosamides (clindamycin)
  4. Macrolides (erythromycin, clarithromycin, azithromycin, chloramphenicol)
197
Q

Name an antibiotic that inhibits folate synthesis

A

Trimethoprim

198
Q

Bactericidal antibiotics (e.g. those that inhibit cell wall synthesis) can kill >99.9% of bacteria in 18-24 hours. In which situations are they particularly useful?

A
  • Poor penetration (difficult to get the agent to the bacteria, e.g. endocarditis)
  • Infection needs to e eradicated quickly (e.g. meningitis)
199
Q

What do bacteriostatic (i.e. those that inhibit protein synthesis/DNA replication) antibiotics do?

A

Prevent bacterial replication

200
Q

What is the minimum inhibitory concentration of an antibiotic?

A

The minimum amount required to prevent microbial growth

201
Q

Antibacterial effectiveness depends on concentration and the time that the antibiotic remains on the binding sites. What are the key parameters in time-dependent killing and concentration-dependent killing?

A

Time dependent killing - time that serum concentration remains above MCI during the dosing interval
Concentration-dependent killing - how high the concentration is above the MIC

202
Q

Give 4 ways in which bacteria resist antibiotics

A
  1. Changing antibiotic target
  2. Destroying antibiotic
  3. Preventing antibiotic access
  4. Removing antibiotic from bacteria
203
Q

Why is MRSA resistant to flucloxacillin?

A

Alteration in binding site caused by change in protein folding means that flucloxacillin can no longer bind to that particular type of Staph aureus

204
Q

Why is VRE resistant to vancomycin?

A

The cell wall components in the enterococci have been changed such that vancomycin binding is reduced

205
Q

How has penicillin resistance arisen?

A

Some bacteria started to produce beta lactamase enzyme, which hydrolyses the beta lactam ring in penicillins and cephalosporins, meaning that the beta lactams would be unable to bind to the target protein

206
Q

How can bacteria become resistant by preventing antibiotic access?

A

By modifying bacterial membrane porin channel size, numbers and selectivity

207
Q

Give two ways in which bacteria can acquire resistance to an antibiotic

A
  1. Spontaneous gene mutation

2. Horizontal gene transfer

208
Q

Why is metronidazole no use against aerobic bacteria?

A

Aerobic bacteria are unable to reduce metronidazole to its active form

209
Q

Why is vancomycin no use against gram negative bacteria?

A

It cannot penetrate the outer membrane

210
Q

Why were carbapenems invented?

A

They are resistant to degradation by beta lactamases or cephalosporinases

211
Q

What class of bacteria are resistant to carbapenems?

A

Carbapenem Resistant Enterobacteriaceae - produce ‘carbapenemases’

212
Q

How do CRE infections arise?

A

When people are concentrated with use of antibiotics (e.g. on a hospital ward) and there is a susceptible person

213
Q

What bacteria would be treated with beta lactams?

A

Susceptible gram positive bacteria

214
Q

When would you use cephalosporins instead of beta lactams?

A

If the patient has a penicillin allergy
Works against some penicillin resistant bacteria
If the antibiotic needs to reach the CNS, e.g. meningitis

215
Q

What is oral penicillin V good for?

A

Bacterial tonsillitis - group A/C/G strep. These are currently not resistant to penicillin

216
Q

What antibiotics would you use to treat a Strep pneumoniae infection?

A

Oral amoxicillin

IV benzylpenicillin

217
Q

Why would you use flucloxacillin to treat a Staph aureus infection? (not MRSA)

A

Most Staph aureus breaks down benzyl penicillin

218
Q

MRSA is resistant to flucloxacillin. What would you use to treat it?

A

Vancomycin and Teicoplanin (IV)

219
Q

When would you use macrolides such as clarithromycin and erythromycin?

A

In gram positive infections such as Staph aureus and beta haemolytic strep and atypical pneumonia pathogens
Patients with penicillin allergy
Severe pneumonia acquired in the community

220
Q

When would you use lincosamides such as clindamycin?

A

Gram positive bacteria e.g. Staph aureus, beta haemolytic strep, anaerobes
In cellulitis if the patient has a penicillin
In necrotising fasciitis - clindamycin turns off the toxins produced by gram positive bacteria

221
Q

When would you use doxycycline?

A

Can only be given orally. Broad spectrum, but mainly gram positive
Can use for cellulitis if the patient has a penicillin allergy
Can be used for pneumonia

222
Q

Gentamicin (IV only) can be used to treat gram negative bacteria, UTIs and endocarditis (synergistically). Why does it require therapeutic drug monitoring?

A

Due to possible toxic effects (nephrotoxicity and ototoxicity)

223
Q

What can ciprofloxacin be used to treat?

A

Much more effective against gram negative than gram positive bacteria.
Can be used in patients with penicillin allergies
UTIs
Intra-abdominal infections

224
Q

What is the first line treatment for lower UTIs?

A

Nitrofurantoin

225
Q

Name two antibiotic treatments with beta lactamase inhibitors

A
  1. Amoxicillin-clavulanate (Co-amoxiclav/Augmentin)

2. Piperacillin-tazobactam (Tazocin)

226
Q

What IV antibiotic is effective against both gram positive and negative bacteria and is sometimes used in surgical prophylaxis?

A

Cefuroxime

227
Q

When would you use meropenem?

A

In very sick, immunocompromised patients, particularly with HAI

228
Q

What are fungi?

A

Eukaryotic organisms with a chitinous cell wall, which exist in yeast/mould

229
Q

Why do candida sometimes cause line infections?

A

They produce a biofilm and are able to bind to plastic

230
Q

What fungal infection is a common cause of meningitis with HIV?

A

Cryptococcosis

231
Q

What is a non-specific test for fungal infection?

A

1,3 beta-D glucan - cell wall component of many fungi

232
Q

What are the possible target sites for antifungal drugs?

A

DNA/RNA synthesis
Protein synthesis
Cell wall (mannoproteins, B1,3-glucan, B1,6-glucan, chitin)
Plasma membrane (contains ergesterol instead of cholesterol)

233
Q

How do polyenes such as amphotericin and nystatin work?

A

They bind to ergosterol in the fungal cell membrane, intercalate themselves into the membrane and form pores that allow cations to leak out of the cell, causing cell death

234
Q

How do azoles, allyamines and morpholones work?

A

They inhibit ergesterol synthesis

235
Q

What are clotrimazole and fluconazole effective against?

A

Candida

Fluconazole also effective against Cryptococcus

236
Q

What is a normal CD4 count?

A

> 500

237
Q

What is a really bad CD4 count?

A

<200

238
Q

Why do STIs increase the likelihood of both acquiring and transmitting HIV?

A

Due to local inflammation

239
Q

What is TasP?

A

Treatment as Prevention - if an undetectable viral load is maintained, HIV becomes untransmittable

240
Q

What is PEP?

A

Post-exposure prophylaxis - antiretroviral treatment to be taken for a month, started within 72 hours of exposure

241
Q

What is PrEP?

A

Pre-exposure prophylaxis, reduces chance of acquiring HIV by ~86%

242
Q

What symptoms are suspicious for HIV?

A 
Generalised lymphadenopathy
Acute generalised rash
Glandular fever/flu like illnesses
Oral candida
Unexplained weight loss/night sweats
Persistent diarrhoea
Shortness of breath
Dry cough
Recurrent bacterial infections (inc pneumococcal pneumonia)
Multi-dermatomal shingles
243
Q

HIV-1 is a lentivirus and a member of the retrovirus family. What does that mean?

A

Lentivirus - long incubation period

Retrovirus - uses reverse transcriptase to make a DNA copy

244
Q

How does HIV invade CD4+ T cells?

A

HIV has a very high affinity for the CD4 glycoprotein expressed on T cells. It therefore binds to CD4 and is taken into the cell, where it can convert its viral RNA into viral DNA, which is taken up into the cell nucleus.

245
Q

1% of caucasians are homozygous for deletion of which gene which confers some resistance to HIV?

A

CCR5

246
Q

Why is HIV able to evolve rapidly?

A
  1. Error-prone replication (reverse transcriptase enzyme makes at least 1 error in every replication cycle)
  2. Rapid viral replication
  3. Large population sizes
247
Q

What are the main symptoms of acute HIV-1 infection?

A

Glandular fever-like illness (fever, lymphadenopathy, sore throat, oral ulcers, skin rash in upper trunk) - occurs in 90% of people around 3 weeks following transmission

248
Q

What is the natural history of HIV-1 infection?

A

A high viral load early in infection followed by an asymptomatic period, after which viral load increases again, CD4 level drops, AIDS develops –> death

249
Q

How can HIV evade antibodies in the blood?

A
  • By passing directly from cell to cell, becoming inaccessible to antibodies
  • By deriving its virion surface from the host cell membrane
  • Heavy glycosylation of the envelope spike makes it difficult for antibodies to bind
250
Q

Briefly explain how immune activation drives HIV pathogenesis

A

Early in HIV infection, there is a dramatic loss of CD4+ T cells in the lymphoid tissue in the gut. This makes the gut mucosa ‘leaky’, allowing passage of bacteria and things like LPS, stimulating immune cells and setting up a cycle of chronic immune activation that ultimately exhausts the immune system.

251
Q

What does the HIV-1 nef gene do?

A

Reduces cell surface expression of HLA class I molecules, which are needed for CTL recognition and also upregulates the death receptor Fas ligand, which can kill virus-specific CTLs

252
Q

What are the diagnostic criteria for AIDS?

A

When CD4 <200 or an ‘AIDS defining illness’ is present

253
Q

What is the most common AIDS defining illness?

A

Pneumocystitis pneumonia (PCP), caused by pneumocystitis jirovecii fungus

254
Q

How is PCP treated?

A

Co-trimoxazole (+/- prednisolone if the patient is hypoxic)

255
Q

Name 7 AIDS defining illnesses besides PCP

A
  1. Tuberculosis
  2. Candidiasis
  3. CMV pneumonitis
  4. HSV pneumonitis
  5. Kaposi’s sarcoma
  6. Lymphoma (esp primary CNS lymphoma)
  7. Toxoplasmosis
  8. Cryptococcus neoformans (meningitis)
256
Q

CNS toxoplasmosis is caused by reactivation of latent infection acquired from cat or contaminated meat/water. It causes inflammation at the back of the eye. How is it treated?

A

Sulphadiazine and pyrimethamine with folic acid

257
Q

Why is HIV associated with Kaposi’s sarcoma, lymphomas, cervical/anal/penile carcinoma and hepatocellular carcinoma?

A

Because these cancers are all associated with viral infections - Kaposi’s (HHV8), lymphomas (EBV), cervical/anal/penile (HPV), hepatocellular (Hep B/C)

258
Q

What is HAART and how does it work?

A

Highly Active Anti-Retroviral Therapy uses at least 3 antiretroviral drugs to target different things - they act on different points in the replication cycle to suppress viral replication.

259
Q

What are the 5 types of drugs used in HAART?

A
  1. Entry inhibitors
  2. NRTIs (nucleoside reverse transcriptase inhibitors)
  3. NNRTIs (non-nucleoside reverse transcriptase inhibitors)
  4. Integrase inhibitors -gravir
  5. Protease inhibitors (block HIV proteases to stop HIV from becoming a mature virion) -navir

Phase 2a Medicine (13 decks)

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