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Phase 2a Medicine > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What is a pathogen?

A

Organism that causes or is capable of causing disease

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2
Q

What is a commensal?

A

Organism which colonises host but causes no disease in normal circumstances

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3
Q

What is an opportunist pathogen?

A

Microbe that only causes disease if host defences are compromised

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4
Q

What is virulence?

A

Degree to which a given organism is pathogenic

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5
Q

What is asymptomatic carriage?

A

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

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6
Q

What are round bacteria called?

A

Cocci

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7
Q

What are rod shaped bacteria called?

A

Bacilli

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8
Q

What is a purple Gram stain?

A

Positive

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9
Q

What is a pink Gram stain?

A

Negative

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10
Q

What specialised stain detects mycobacterium??

A

Ziehl-Neelsen stain

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11
Q

What gives bacteria a hardened structure?

A

Spores

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12
Q

What component of a bacterial outer membrane can give rise to toxic shock?

A

Endotoxin

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13
Q

How big are typical bacterial chromosomes?

A

2-4x103 kb

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14
Q

How can bacteria be mutated?

A

Base substitution
Deletion
Insertion

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15
Q

How can genes be transferred in bacteria?

A

Transformation
Transduction
Conjugation

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16
Q

What is coagulase?

A

An enzyme produced by bacteria that clots blood plasma to protect against phagocytosis

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17
Q

What is an important coagulase positive bacteria?

A

Staphylococcus aureus

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18
Q

What is the normal habitat for staphylococcus?

A

Nose and skin

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19
Q

How is staph aureus spread?

A

Aerosol and touch

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20
Q

What is MRSA resistant to?

A

B-lactams, gentamicin, erythromycin, tetracycline

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21
Q

What are the virulence factors of Staph aureus?

A
  1. Pore-forming toxins
  2. Proteases (exfoliatin)
  3. Toxic shock syndrome toxin
  4. Protein A
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22
Q

Give 3 pyogenic conditions associated with Staph aureus

A
  1. Wound infections
  2. Septicaemia
  3. Abscesses
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23
Q

Give 2 toxin mediated conditions associated with staph aureus

A
  1. Toxic shock syndrome

2. Food poisoning

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24
Q

Give 2 coagulase negative conditions associated with Staph aureus

A
  1. Infected implants

2. Endocarditis

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25
Q

What is the main virulence factor for S. epidermidis?

A

Ability to form persistent biofilms

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26
Q

What are the 3 types of haemolysis?

A
  1. Alpha - partial lysis (greening)
  2. Beta - complete lysis
  3. Gamma (non) - no lysis
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27
Q

How can streptococci be classified?

A
  1. Haemolysis
  2. Lancefield typing
  3. Biochemical properties
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28
Q

What is Lancefield grouping?

A

Method of grouping catalase negative, coagulase negative bacteria based on bacterial carbohydrate cell surface antigens

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29
Q

Give 3 infections caused by S. pyogenes

A
  1. Cellulitis
  2. Tonsillitis
  3. Scarlet fever
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30
Q

What are the 2 complications of S. pyogenes infections?

A
  1. Rheumatic fever

2. Glomerulonephritis

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31
Q

What are the virulence factors for S. pyogenes?

A
  1. Enzymes
  2. Toxins
  3. Capsule
  4. M protein
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32
Q

What are the causes of S. pneumoniae?

A
  1. Pneumonia
  2. Otitis media
  3. Sinusitis
  4. Meningitis
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33
Q

What are the predisposing factors for S. pneumoniae infection?

A
  1. Impaired mucus trapping
  2. Hypogammaglobulinaemia
  3. Asplenia
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34
Q

Which streptococci are important in infective endocarditis?

A
  1. S. sanguinis

2. S. oralis

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35
Q

What is the most virulent group of streptococci?

A

Milleri group

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36
Q

Why are there differences in staining with Gram?

A

Morphological differences in the bacteria

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37
Q

What is endotoxin comprised of?

A

Lipid A, core antigen, somatic antigen

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38
Q

How does lipid A trigger an innate immune response?

A

TLR4 signalling

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39
Q

What are the main colonisation factors?

A
  1. Adhesins
  2. Invasins
  3. Nutrient acquisition
  4. Defence against host
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40
Q

Why might antibodies against the same species of bacteria not be recognised in different patients?

A

There is structural variability amongst different strains of the same species

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41
Q

What is a serovar?

A

Strains of bacteria with variant cell surface antigens

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42
Q

What is a serogroup?

A

A group of strains with have a surface antigen in common, but differ in one or more other surface antigens

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43
Q

Name 6 principal infections caused by E. coli

A
  1. Wound infections
  2. UTIs
  3. Gastroenteritis
  4. Traveller’s diarrhoea
  5. Bacteraemia
  6. Meningitis
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44
Q

What is the major complication of E. coli food poisoning?

A

Haemolytic ureic syndrome

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45
Q

How many patients with a EHEC infection develop haemolytic ureic syndrome?

A

10%

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46
Q

What are the 5 symptoms of a shigella infection?

A
  1. Small volume
  2. Pus and blood in stools
  3. Prostrating cramps
  4. Pain in straining
  5. Fever
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47
Q

How is shigella spread?

A

Person-to-person, contaminated food and water

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48
Q

How do shigella invade epithelial cells?

A

Through M cells

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49
Q

How does Shigella ensure survival in macrophages?

A

It rapidly induces apoptosis of macrophages

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50
Q

What are the 2 species of salmonella?

A
  1. S. enterica

2. S. bongori

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51
Q

What are the 3 conditions caused by S. enterica?

A
  1. Gastroenteritis/enterocolitis
  2. Enteric fever
  3. Bacteraemia
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52
Q

What can klebsiella pneumoniae cause?

A
  1. UTI
  2. Pneumonia
  3. Surgical wound infections
  4. Bacteraemia
  5. Sepsis
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53
Q

How is cholera transmitted?

A
  1. Shellfish ingestion

2. Contaminated drinking water

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54
Q

How much fluid a day can be lost in cholera?

A

20L/day

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55
Q

What is the mortality for untreated cholera?

A

50-60%

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56
Q

What is the leading cause of nosocomial pneumonia in ICU patients?

A

Pseudomonas aeruginosa

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57
Q

Name 5 opportunistic infections caused by haemophilus influenzae

A
  1. Meningitis
  2. Bronchopneumonia
  3. Epiglottitis
  4. Bacteraemia
  5. Pneumonia
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58
Q

What is the main cause of meningitis

A

Type b strain of H. influenzae

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59
Q

What is the mortality of Legionnaires’ disease?

A

15-20%

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60
Q

What causes Legionnaires’ disease?

A

Legionella pneumophila

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61
Q

What does Legionnaires’ disease cause?

A

Excessive influx of neutrophils into lungs causing severe inflammatory pneumonia

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62
Q

What does bordetella pertussis cause?

A

Whooping cough

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63
Q

How is B. pertussis transmitted?

A

Aerosol

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64
Q

What are the 2 clinically important species of neisseria?

A
  1. N. meningitidis

2. N. gonorrhoeae

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65
Q

In what % of the population is N. meningitidis present in the nasopharynx?

A

5-10%

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66
Q

What is the mechanism of N. meningitidis?

A

Invasion of meninges, bacteria enter CSF of subarachnoid space from blood stream after crossing BBB

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67
Q

What serious complications can gonorrhoea cause in women?

A

Salpingitis

Pelvic inflammatory disease

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68
Q

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

A

Campylobacter

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69
Q

What diseases does Helicobacter pylori play a role in?

A

Gastritis

Peptic ulcer disease

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70
Q

What do bacteroides often cause?

A

Peritoneal cavity infections

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71
Q

How is chlamydia detected?

A

Serum antibodies or PCR

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72
Q

What are the 2 developmental stages of chlamydia?

A
  1. Elementary bodies

2. Reticulate bodies

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73
Q

Describe the elementary body stage of chlamydia development

A
  1. Infectious
  2. Enter cell through endocytosis
  3. Prevent phagosome-lysosome fusion
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74
Q

Describe the reticulate body stage of chlamydia development

A
  1. Replicative
  2. Non-infectious
  3. Acquire nutrients from host cell
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75
Q

What C. trachomatis causes chlamydia in STI form?

A

Genital tract biovar

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76
Q

What are the symptoms of Weil’s disease?

A
  1. Jaundice
  2. Acute renal failure
  3. Acute hepatic failure
  4. Pulmonary distress
  5. Haemorrhage
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77
Q

What causes Weil’s disease?

A

Leptospira interrogans

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78
Q

What is the primary stage of syphilis?

A

A localised infection, days-weeks post infection usually in the form of an ulcer

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79
Q

What is the secondary stage of syphilis?

A

A systemic infection, 1-3 months post-infection affecting skin, joints and muscles

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80
Q

What is the tertiary stage of syphilis?

A

Infection of bone and soft tissue, aorta and nervous system, several years post-infection

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81
Q

What are the 4 main groups of gram negative pathogens?

A
  1. Proteobacteria
  2. Bacteroides
  3. Chlamydia
  4. Spirochaetes
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82
Q

Give 3 characteristics of fungi

A
  1. Eukaryotic
  2. Chitinous cell wall
  3. Heterotrophic
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83
Q

What forms can fungi exist in?

A

Yeast or mould

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84
Q

What are yeasts?

A

Small single celled organisms that divide by budding

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85
Q

What are moulds?

A

Fungi which form multicellular hyphae and spores

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86
Q

What are dimorphic fungi?

A

Fungi which exist as both yeasts and moulds switching between the two when conditions suit

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87
Q

Why do fungi often not cause human infection?

A
  1. Inability to grow at 37C

2. Innate and adaptive immune response

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88
Q

What genera of fungi are most often implicated in human infection?

A
  1. Ascomycota
  2. Basidiomycota
  3. Mucormycota
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89
Q

Name 3 common fungal infections

A
  1. Vulvovaginal candidiasis
  2. Otitis externa
  3. Tinea pedis
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90
Q

What life-threatening fungal infections can affect immunocompromised hosts?

A
  1. Candida spp. line infections
  2. Invasive aspergillosis
  3. Pneumocystis
  4. Cryptococcosis
  5. Mucormycosis
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91
Q

What ways are there of diagnosing fungal disease?

A
  1. Microscopy and histology
  2. Culture
  3. Molecular methods and serology
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92
Q

Name 3 fungi in the DDx of onychomycosis

A
  1. Trichophyton spp.
  2. Epidemophyton spp.
  3. Microsporum spp.
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93
Q

Name 3 non-fungal causes considered in the DDx of onychomycosis

A
  1. Psoriasis
  2. Trauma
  3. Lichen planus
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94
Q

What is the diagnosis of onychomycosis?

A

Microscopy and culture of nail clippings/scrapings

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95
Q

What are the most common treatments for onychomycosis?

A

Terbinafine or itraconazole

Topical amorolfine

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96
Q

What is thrush?

A

White adherent plaques on oral or genital mucosa

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97
Q

Name 4 things commonly associated with thrush

A
  1. Immunocompromised
  2. Diabetes
  3. Antibiotic use
  4. Pregnancy
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98
Q

How is thrush treated?

A

Topical antifungals or oral fluconazole

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99
Q

What is invasive aspergillosis treated with?

A

Voriconazole

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100
Q

Who does invasive aspergillosis often affect?

A

Immunocompromised and post-influenza disease

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101
Q

What causes invasive aspergillosis?

A

Galactomannan

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102
Q

How is pneumocystis diagnosed?

A

PCR of induced sputum or BAL

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103
Q

How is pneumocystis pneumonia treated?

A

Co-trimoxazole

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104
Q

Why are fungi harder to treat than bacteria?

A

They are eukaryotic

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105
Q

What do fungal cell membranes contain?

A

Ergosterol

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106
Q

Where do allylamines tend to distribute extensively?

A

To poorly perfused sites e.g. skin and nail beds

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107
Q

What is used to treat dermatophytes?

A

Terbinafine

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108
Q

What are azoles?

A

Dose dependent inhibitors of 14a-sterol demethylase

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109
Q

Name 3 azoles

A
  1. Fluconazole
  2. Itraconazole
  3. Voriconazole
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110
Q

What is voriconazole used to treat?

A

Invasive aspergillosis

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111
Q

Give 3 side effects of azoles

A
  1. Transaminitis
  2. Alopecia
  3. Severe hepatitis
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112
Q

What class of drugs are used for severe or resistant fungal disease?

A

Echinocandins

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113
Q

Name 2 echinocandins

A
  1. Caspofungin

2. Micafungin

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114
Q

What is the mechanism of action of echinocandins?

A

Inhib 1,3 beta glucan synthase

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115
Q

What is the most common fungal cause of onychomycosis?

A

Trichophyton tubrum

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116
Q

Who does pneumocystis pathogenesis often affect?

A

Moderate-severely immunocompromised

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117
Q

Give 3 treatments of pneumocystis pathogenesis

A
  1. Co-trimoxazole
  2. Clindamycin
  3. Atovaquone
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118
Q

What is a virus?

A

An infectious, obligate intracellular parasite comprising genetic material surrounded by a protein coat and/or a membrane

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119
Q

What do viruses exist as when not in an infected cell?

A

Virions

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120
Q

Why are viruses not classed as living?

A

They don’t feed, respire or reproduce independently

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121
Q

How do viruses replicate?

A
  1. Migration of genome to host cell nucleus
  2. Transcription to mRNA using host materials
  3. Use cell materials for their replication
  4. Translation of viral mRNA to produce structural proteins, viral genome and non-structural proteins
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122
Q

How are new virus particles released?

A
  1. Cell lysis
  2. Budding
  3. Exocytosis
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123
Q

How can viruses cause disease?

A
  1. Direct destruction of host cells
  2. Modification of host cells
  3. Over-reactivity of immune system
  4. Damage through cell proliferation
  5. Evasion of host defences
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124
Q

How does poliovirus cause disease?

A

Host cell neuron lysis and death

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125
Q

How does rotavirus cause disease?

A

Atrophies villi and flattens epithelial cells

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126
Q

What are 4 symptoms of hepatitis B?

A
  1. Jaundice
  2. Pale stool
  3. Dark urine
  4. RUQ pain
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127
Q

How does human papillomavirus cause cervical cancer?

A

Continuous expression of oncoprotein causing cellular DNA mutations

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128
Q

How can the host defence be evaded at a cellular level?

A
  1. Latency

2. Cell-cell spread

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129
Q

How can the host defence be evaded at a molecular level?

A
  1. Antigenic variability

2. Prevention of host cell apoptosis

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130
Q

What is antigenic variability?

A

Ability to change surface antigens in order to evade host’s immune system

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131
Q

What does prevention of host cell apoptosis allow?

A

Allows virus to continue replicating within the cell so more virus is produced and then released

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132
Q

Name 2 ways viruses evade host defence

A
  1. Downregulation of interferon and other intracellular host defence proteins
  2. Interference with host cell antigen processing pathways
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133
Q

What are protozoa?

A

Microscopic unicellular eukaryotes

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134
Q

What are the major groups of protozoa?

A
  1. Flagellates
  2. Amoebae
  3. Microsporidia
  4. Sporozoan
  5. Ciliates
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135
Q

What is African trypanosomiasis also called?

A

Sleeping sickness

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136
Q

What is the vector for African trypanosomiasis?

A

Tsetse fly bite

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137
Q

Where does African trypanosomiasis occur?

A

Remote areas of Africa

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138
Q

What are the symptoms of African trypanosomiasis?

A 
Personality change
Drowsiness
Flu-like symptoms
Chancre
Coma and death
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139
Q

How is African trypanosomiasis diagnosed?

A

Blood film or CSF

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140
Q

What is American trypanosomiasis also called?

A

Chagas disease

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141
Q

What is the vector for American trypanosomiasis?

A

Triatomine bug

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142
Q

Where is American trypanosomiasis found?

A

Central and South America

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143
Q

What are 3 acute symptoms of American trypanosomiasis?

A
  1. Fever
  2. Headache
  3. Romana’s sign
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144
Q

What are 3 chronic symptoms of American trypanosomiasis?

A
  1. Cardiomyopathy
  2. Megaoesophagus
  3. Megacolon
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145
Q

What causes Leishmaniasis?

A

Leishmania spp.

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146
Q

What is the vector for Leishmaniasis?

A

Female sandfly

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147
Q

Where is Leishmaniasis found?

A

Africa, Asia, South America

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148
Q

What are the 3 clinical manifestations of Leishmaniasis?

A
  1. Cutaneous
  2. Mucocutaneous
  3. Visceral Kala Azar
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149
Q

What is seen in cutaneous and mucocutaneous Leishmaniasis?

A

Ulceration and destruction, scarring

150
Q

How quickly do cutaneous and mucocutaneous Leishmaniasis usually resolve?

A

8 weeks

151
Q

Give 5 symptoms of visceral Leishmaniasis

A
  1. Fever
  2. Bone marrow suppression
  3. Weight loss
  4. Hepato-splenomegaly
  5. Anaemia
152
Q

How is trichomoniasis vaginalis spread?

A

Sexually transmitted

153
Q

How does trichomoniasis vaginalis present in men?

A
  1. Often asymptomatic
  2. Urethritis
  3. Prostatitis
154
Q

How does trichomoniasis vaginalis present in women

A
  1. Purulent discharge
  2. Abdo pain
  3. Dysuria
  4. Vulvar/cervical lesions
155
Q

How are most protozoa treated?

A

Metronidazole

156
Q

How is giardiasis spread?

A

Faeco-oral spread

157
Q

Give 4 symptoms of giardiasis

A
  1. Diarrhoea
  2. Cramps
  3. Bloating
  4. Flatulence
158
Q

What are the risk factors for giardiasis?

A
  1. Recent travel
  2. Close contacts
  3. Childcare
159
Q

How is giardiasis diagnosed?

A

Stool microscopy looking for cysts and trophozoites

160
Q

What causes amoebiasis?

A

Entaemoeba histolytica

161
Q

How is amoebiasis spread?

A

Faeco-oral spread, contaminated food and water

162
Q

What are the symptoms of amoebiasis?

A
  1. Dysentery
  2. Colitis
  3. Liver and lung abscesses
163
Q

How is cryptosporidiosis spread?

A

Contaminated food and water

164
Q

What are 4 symptoms for cryptosporidiosis?

A
  1. Diarrhoea
  2. Vomiting
  3. Fever
  4. Weight loss
165
Q

How is cryptosporidiosis diagnosed?

A

Pink in acid fast staining

166
Q

Who is cryptosporidiosis often seen in?

A

Immunocompromised patients

167
Q

How is toxoplasmosis spread?

A

Contaminated food and water, contact with feline faeces

168
Q

Give 3 conditions toxoplasmosis can cause?

A
  1. Disseminated disease
  2. Chorioretinitis
  3. Toxoplasma encephalitis
169
Q

How is toxoplasmosis diagnosed?

A

Ring enhancing lesion on brain CT

170
Q

What is the vector for malaria?

A

Female anopheles mosquito

171
Q

How is malaria diagnosed?

A

Blood film

172
Q

Give 5 symptoms of malaria

A
  1. Fever
  2. Headache
  3. Abdo pain
  4. Fatigue
  5. Vomiting
173
Q

What are 4 signs of malaria?

A
  1. Anaemia
  2. Jaundice
  3. Hepatosplenomegaly
  4. Black water fever
174
Q

What are the stages of the malaria lifecycle?

A
  1. Liver stage
  2. Blood stage
  3. Vector stage
175
Q

What happens in the liver stage of the malaria lifecycle?

A
  1. Mosquito takes a blood meal and injects sporozoites
  2. These travel to liver and infect liver cells
  3. Mature into shizonts
  4. Shizont rupture releases merozoites into blood
176
Q

In what types of malaria can a dormant stage persist in the liver?

A

P. vivax and P. ovale

177
Q

What happens in the blood stage of the malaria lifecycle?

A
  1. Merozoites enter circulation and inject RBCs
  2. Enter ring stage trophozoites which mature into schizonts
  3. Schizonts rupture releasing more merozoites
  4. Some immature trophozoites differentiate into sexual stage gametocytes
178
Q

What stage of the malarial lifecycle gives rise to symptoms?

A

Blood stage

179
Q

What happens in the vector stage of the malaria lifecycle?

A
  1. Mosquito takes a blood meal ingesting gametocytes
  2. These mature into an oocyst which ruptures releasing sporozoites
  3. Sporozoites are injected into host during next blood meal
180
Q

How long is the process of development in the malaria lifecycle?

A

9 days

181
Q

What causes the severe form of malaria?

A

P. falciparum

182
Q

Why does P. falciparum cause more severe malaria?

A
  1. Obstructed microcirculation
  2. Rosetting
  3. Cytoadherence
  4. Sequestration of parasites in major organs
183
Q

Why does haemolysis occur in malaria?

A

Infected cell lysis and immune mediated killing

184
Q

Give 3 symptoms of cerebral malaria

A
  1. Vascular occlusion
  2. Seizures
  3. Raised ICP
185
Q

Give 3 symptoms of ARDS

A
  1. Anaemia
  2. SOB
  3. Pulmonary oedema
186
Q

Give 3 symptoms of renal failure caused by malaria

A
  1. Dehydration
  2. Lowered BP
  3. Haemoglobinuria
187
Q

Give 3 symptoms of bleeding caused by malaria

A
  1. Thrombocytopenia
  2. Epistaxis
  3. Abnormal bleeding
188
Q

Give 3 symptoms of shock caused by malaria

A
  1. Bleeding
  2. Hypotension
  3. Pale
189
Q

What are the 5 types of complicated malaria?

A
  1. Cerebral
  2. ARDS
  3. Renal failure
  4. Sepsis
  5. Bleeding/anaemia
190
Q

How is malaria diagnosed?

A

Thick and thin blood films looking for black dots

191
Q

What is the emergency malaria treatment?

A

IV artesunate

192
Q

What is used to prevent relapses in P. ovale and P. vivax malaria?

A

Primaquine

193
Q

What is the microbiome?

A

The totality of microorganisms, their genetic elements and their environmental interactions in an environment

194
Q

What eliminates virus infected cells?

A

Cytotoxic C lymphocytes

195
Q

How can viruses cause cell damage?

A

Direct cell toxicity, innate and adaptive immune responses

196
Q

How can toxins be classified?

A
  1. Tissue target
  2. Molecular action
  3. Biological effect
  4. Contribution to disease process
197
Q

What do the changes in coat antigens in influenza result in?

A

Antigen shift and antigen drift

198
Q

What is antigen drift?

A

Spontaneous mutations which occur gradually giving minor changes in haemagglutinin and neuraminidase

199
Q

What is antigenic shift?

A

Sudden emergence of a new subtype different to that of preceding virus

200
Q

What is seen in epidemics?

A

Antigen drift

201
Q

What is seen in pandemics?

A

Antigen shift

202
Q

Describe influenza

A

Spherical particles surrounded by lipid bilayer acquired from infected host cell

203
Q

What determines the defence mechanism employed to a bacterial infection?

A

Number of organisms and virulence

204
Q

What response is given to extracellular bacteria?

A

Antibody response

205
Q

What response is given to intracellular bacteria?

A

Cellular response

206
Q

How do bacteria compete with host cells?

A
  1. Sequestering nutrients
  2. Using novel metabolic pathways
  3. Out-competing other micro-organisms
207
Q

What is the function of adhesins?

A

Help bacteria bind to mucosal surfaces

208
Q

How can bacteria stick together on a cell surface?

A

Secrete an extracellular polymeric substance of protein, polysaccharides and DNA

209
Q

What is the function of a biofilm?

A

Helps protect against antimicrobials

210
Q

How do macrophages kill infected cells?

A

Lytic enzyme release

211
Q

What is the function of pattern recognition receptors?

A

Recognise pathogen associated molecular patterns but also damage associated molecular patterns from host cells

212
Q

What can cause tissue damage?

A
  1. Trauma
  2. Necrosis
  3. Neoplasia
  4. Infection
213
Q

What is an antibiotic?

A

Agent produced by microorganisms that kill or inhibit the growth of other microorganisms in high dilution

214
Q

How do antibiotics work?

A

Bind to a target site on a bacteria defined as a point of the biochemical reaction crucial to the survival of the bacterium

215
Q

What determines the binding site bound?

A

Antibiotic class

216
Q

What methods do antibiotics use to kill bacteria?

A
  1. Binding to cell wall and inhibition of cell wall synthesis
  2. interference with nucleic acid synthesis or function
  3. Inhibition of DNA gyrase
  4. Inhibition of ribosomal activity and protein synthesis
  5. Inhibition of folate synthesis and carbon unit metabolism
217
Q

What class of antibiotics inhibit cell wall synthesis?

A

Penicillins

218
Q

How are bacteria pathogenic?

A

Bacterial raison d’être and damage

219
Q

What is bacterial raison d’etre?

A

Bacteria attach and enter, spread locally and multiply and evade host defences

220
Q

How do bacteria cause damage?

A
  1. Direct
  2. Exotoxin
  3. Endotoxin
  4. Inflammation
  5. Immune-pathology
  6. Diarrhoea
221
Q

What is the mechanism of action of beta lactam?

A

Disrupt peptidoglycan production by covalently and irreversibly binding to PBPs causing cell wall lysis

222
Q

What must happen for beta lactam to bind to PBPs?

A

They must diffuse through the bacterial cell wall

223
Q

What is bacteriostatic?

A

Prevents growth go bacteria - prevent them multiplying

224
Q

How is bacteriostatic defined?

A

Minimum bactericidal conc. to minimum inhibitory conc. of >4

225
Q

How to bacteriostatic antibiotics function?

A

Inhibit protein synthesis, DNA replication or metabolism

226
Q

What is bactericidal?

A

The agent kills the bacteria

227
Q

How do bactericidal antibiotics function?

A

Inhibit cell wall synthesis

228
Q

When are bactericidal antibiotics used?

A
  1. Poor tissue penetration
  2. Difficult to treat infections
  3. Need to eradicate infection quickly
229
Q

What makes a good antibiotic?

A

It remains at the binding site for a sufficient period of time in order for the metabolic processes of the bacteria to be sufficiently inhibited

230
Q

What are the 2 major determinants of antibacterial effects?

A

Concentration and time antibiotic remains on binding sites

231
Q

What determines the interval antibiotics are given at?

A

Half-life

232
Q

Why might antibiotics not work?

A
  1. Change antibiotic target
  2. Prevent antibiotic access
  3. Remove antibiotic from bacteria
  4. Destroy antibiotic
233
Q

How do bacteria acquire resistance?

A
  1. Spontaneous gene mutation

2. Horizontal gene transfer

234
Q

What types of horizontal gene transfer are there?

A
  1. Conjugation
  2. Transduction
  3. Transformation
235
Q

What is acquired resistance?

A

A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic

236
Q

What is a spontaneous gene mutation?

A

New nucleotide base pair change in amino acid sequence change to enzyme or cell structure reduced affinity or activity of antibiotic

237
Q

What is conjugation?

A

Sharing of extra-chromosomal DNA plasmids

238
Q

What is transduction?

A

Insertion of DNA by bacteriophages

239
Q

What is transformation?

A

Picking up naked DNA

240
Q

What is MRSA?

A

Methicillin resistant staphylococcus aureus

241
Q

What is MRSA resistant to?

A

All beta-lactam antibiotics and methicillin

242
Q

What are carbapenems resistant to?

A

Degradation by beta-lactamases or cephalosporinases

243
Q

How can drug resistance be tested for in bacteria?

A
  1. Minimum inhibitory concentration
  2. Antibiotic sensitivity testing
  3. Breakpoint plates
  4. Chromogenic plates
  5. Mechanism-specific tests
  6. Genotypic methods
244
Q

What is breakpoint?

A

A discriminating concentration used to define isolates as susceptible, intermediate or resistant

245
Q

What data sources set breakpoints?

A
  1. MIC distributions
  2. Phamacokinetics and pharmacodynamics
  3. Clinical and bacteriological response rates
  4. Phenotypic and genotypic resistance markers
246
Q

What is the formula for breakpoint concentration?

A

(Cmax/et) x f x s

247
Q

Give 4 factors to take into account for patient safety with antibiotics

A
  1. Side effects
  2. Age
  3. Liver and renal function
  4. Pregnancy
248
Q

What do beta lactams act on?

A

Cell wall of bacteria

249
Q

Name 4 beta lactams

A
  1. Amoxicillin
  2. Penicillin
  3. Cefuroxime
  4. Meropenem
250
Q

What are the benefits of cephalosporins?

A
  1. Good for people with penicillin allergy
  2. Better for more resistant bugs
  3. Get into different parts of body
251
Q

Name 2 glycopeptides

A
  1. Vancomycin

2. Teicoplanin

252
Q

Why are glycopeptides given with caution?

A

Can cause renal impairment

253
Q

What are the 5 functional groups of antibiotic?

A
  1. Cell wall synthesis inhibitors
  2. Protein synthesis inhibitors
  3. Nucleic acid synthesis inhibitors
  4. Anti-metabolites
  5. Membrane function inhibitors
254
Q

What can be used to treat necrotising fasciitis?

A

Clindamycin

255
Q

What are risk factors for Buruli ulcer?

A

Warm environment and barefoot

256
Q

What are mycobacteria?

A

Aerobic, non-spore forming, non-motile bacillus

257
Q

Why do mycobacteria give a slow disease development?

A

They grow slowly

258
Q

What stain is used for acid fast bacilli?

A

Ziehl-Neelsen

259
Q

What is nucleic acid detection recommended for?

A

Rapid diagnosis of TB in endemic countries

260
Q

How do hosts kill acid fast bacilli?

A

Using microbicidal molecules and acidification which aids digestion and degradation by proteases which results in generation of antigens for presentation to T cells

261
Q

What are granulomas?

A

Lesions that arise in a response that tries to contain mycobacteria

262
Q

What does the immune response to M. tuberculosis focus on?

A

Th1

263
Q

What is the lifetime risk for TB reactivation?

A

10%

264
Q

Who is at increased risk of TB reactivation?

A
  1. Age
  2. Malnutrition
  3. Intensity of exposure
  4. Immunosuppression
265
Q

How is the reactivity to M. tuberculosis measured?

A

Tuberculin skin test and interferon gamma release assays

266
Q

What is seen in a positive tuberculin skin test?

A

Skin swelling and redness

267
Q

What does interferon gamma release assay distinguish?

A

If infection is M. tuberculosis or BCG tuberculosis

268
Q

What is seen in tuberculoid leprosy?

A
  1. Tissue hypersensitivity and granulomata
  2. Paucibacillary lesions with low numbers of mycobacteria
  3. Tissue damage
  4. Th1 responses
269
Q

What is seen in lepromatous leprosy?

A
  1. Lesions full of bacilli
  2. Little or poorly formed granulomata
  3. Extensive skin lesions
  4. Th2 responses
270
Q

Why is leprosy associated with deformities?

A

Causes skin and nerve supply damage so don’t notice damage and pain occurring

271
Q

Why do mycobacterial infections need prolonged treatment?

A

It replicates slowly

272
Q

Name 3 common tuberculosis drugs

A
  1. Isoniazid
  2. Rifampicin
  3. Pyrazinamide
273
Q

Why do mycobacteria have unique staining patterns?

A

They have unique lipid rich cell walls

274
Q

What bacilli distribution is seen in primary TB?

A

Granuloma, lymphatics and lymph nodes

275
Q

What are the phases of HIV infection?

A
  1. Acute primary infection
  2. Asymptomatic phase
  3. Early symptomatic HIV
  4. AIDS
276
Q

What is the CD4 level seen in AIDS?

A

<200

277
Q

What is seen in the acute primary infection of HIV?

A
  1. Fall in CD4 levels

2. Acute rise in viral load

278
Q

What is seen in the asymptomatic phase of HIV?

A

Progressive loss of CD4 T cells resulting in poor immunity

279
Q

What are the 2 key markers of HIV infection?

A
  1. CD4 T cell count

2. HIV viral load

280
Q

Name 3 infections often seen in AIDS

A
  1. Candidiasis
  2. Mycobacterium TB
  3. Toxoplasmosis of internal organs
281
Q

Name 3 non-infectious conditions seen in AIDS

A
  1. Kaposi’s carcinoma
  2. HIV dementia
  3. Non-Hodgkin’s lymphoma
282
Q

How long do symptoms typically last in primary HIV infection?

A

2-4 weeks

283
Q

Name 3 symptoms seen in primary HIV infection

A
  1. Severe weight loss
  2. Fever
  3. Rash
284
Q

What should be done in a patient with fever, rash and non-specific features?

A
  1. Take a sexual history
  2. Think of HIV
  3. Tell lab to check for antigen
285
Q

How long does it typically take for HIV antibody to be positive?

A

4-10 weeks

286
Q

When is the viral load typically at a steady state by?

A

3-6 months post-infection

287
Q

What findings are seen in the clinically latent phase of HIV?

A

Persistent generalised lymphadenopathy

288
Q

Why are HIV+ women given annual smear tests rather than 3 yearly?

A

They are at increased risk of HPV infection and cervical intra-epithelial neoplasia

289
Q

What is the commonest opportunistic infection in HIV?

A

Pneumocystis pneumonia (PCP)

290
Q

Name 3 respiratory diseases common in HIV

A
  1. Bacterial pneumonia
  2. Tuberculosis
  3. PCP
291
Q

What is the Tx for cerebral toxoplasmosis?

A

Sulphadiazine + pyrimethamine

292
Q

Name 3 CNS conditions seen in HIV

A
  1. Tuberculoma
  2. Pneumococcal meningitis
  3. Toxoplasmosis
293
Q

What CD4 count is often seen in HIV patients with lymphoma?

A

<100/ul

294
Q

What is the Tx for Kaposi’s sarcoma?

A
  1. HAART
  2. Local radiotherapy
  3. Systemic chemotherapy
295
Q

What are the mechanisms of HIV medications?

A
  1. Reverse transcriptase inhibitors (nucleoside and non-nucleoside)
  2. Protease inhibitors
  3. Fusion inhibitors
296
Q

What is HAART?

A

Highly active anti-retroviral therapy

297
Q

What combinations can be given on HAART?

A
  1. 2 NRTI + 1 NNRTI

1. 2 NRTI + PI

298
Q

Wait is the goal of HAART?

A

Reduce viral load to <50 copies/ml and increase CD4 count

299
Q

What proportion of HIV cases are in Sub-Saharan Africa?

A

61%

300
Q

What is classed as a late HIV diagnosis?

A

CD4 <350

301
Q

How many deaths from AIDS are there annually?

A

~770,000

302
Q

What are the UNAIDS 90/90/90 goals?

A
  1. 90% of people living with HIV being diagnosed
  2. 90% diagnosed on antiretroviral therapy
  3. 90% viral suppression for those on ART by 2020
303
Q

How many people in the Uk are living with HIV?

A

~104,000

304
Q

What groups are at risk of being diagnosed late with HIV?

A
  1. Women
  2. > 65s
  3. Black African
  4. Heterosexual
  5. Outside of London
305
Q

What are the transmission routes for HIV?

A
  1. Blood
  2. Sexual
  3. Vertical
306
Q

Name 4 HIV prevention treatments

A
  1. ART
  2. PEP (within 72hr)
  3. Circumcision
  4. PreP
307
Q

What is the reduction in HIV transmission with circumcision?

A

50%

308
Q

What is PEP?

A

Post-exposure prophylaxis

309
Q

What is involved in PEP?

A

28 days Combination Antiretroviral Therapy within 72 hours

310
Q

What is the risk reduction of HIV when using pre-exposure prophylaxis?

A

86%

311
Q

Name 3 behavioural preventative measures against HIV

A
  1. Appropriate sex education
  2. Reduce frequency of partner change
  3. Consistent condom usage
312
Q

What are the guidelines for HIV testing?

A
  1. Unexplained blood dysplasia
  2. Oral candida
  3. Unexplained lymphadenopathy
  4. Ongoing diarrhoea
  5. Unexplained weight loss
313
Q

Give 4 risk factors for HIV

A
  1. PWID
  2. MSM
  3. Multiple sexual partners
  4. Rape
314
Q

Give 3 advantages to point of care testing for HIV

A
  1. Outreach into community settings
  2. Increase patient choice
  3. Earlier diagnosis
315
Q

Give 3 disadvantages of self-testing

A
  1. Anxiety
  2. Misdiagnoses
  3. Inadequate partner notification
316
Q

What are the stages of of viral replication?

A
  1. Attachment
  2. Cell entry
  3. Interaction with host cells
  4. Replication
  5. Assembly
  6. Release
317
Q

What happens in cell entry?

A

Central viral core caring nucleic acid and some associated proteins enter host cell

318
Q

Why do viruses interact with host cells?

A

To use cell materials for their replication and to subvert host cell defence mechanisms

319
Q

Where does viral assembly occur in viruses?

A
  1. Nucleus
  2. Cytoplasm
  3. Cell membrane
320
Q

What are the stages of HIV replication?

A
  1. Attachment
  2. Entry
  3. Uncoating
  4. Reverse transcription
  5. Genome integration
  6. Transcription of viral RNA
  7. Splicing of mRNA and translation into proteins
  8. Assembly of new virions
  9. Budding
321
Q

What does HIV release to chop up the host genome?

A

Reverse transcriptase and integrase

322
Q

What is the function of viral protease?

A

Helps chop up amino acid chains to restructure proteins into new capsid so it can be infective again

323
Q

How do HIV get genomic variability?

A

Reverse transcription step of replication is error prone

324
Q

The interaction between what is conserved in all primate lentiviruses?

A

CD4 and gp120

325
Q

What is the antigen against which we raise antibodies when doing a HIV test?

A

Glycoprotein 120 (gp120)

326
Q

What is the effect of genome mutations in HIV infection?

A

It makes it hard to respond with the immune system and makes treatment tricky

327
Q

What does Pol encode?

A

HIV enzymes

328
Q

What gene increases infectivity in HIV?

A

Nef

329
Q

What gene contributes to viral replication in HIV?

A

Tat

330
Q

What cells are often infected with HIV?

A
  1. CD4 T cells
  2. Macrophages
  3. Dendritic cells
331
Q

What is a major barrier to a vaccine against HIV-1?

A

Lack of identification of protective immune responses

332
Q

What is seen in long-term non-progressors?

A

No symptoms of infection or signs of AIDS after at least 7 years infection with CD4 count >600 cells/ml in the absence of treatment

333
Q

What immune system consequences characterises HIV?

A

Progressive decline in number and function of CD4 T-lymphocytes

334
Q

What are the mechanisms of CD4 depletion?

A
  1. Direct cytotoxicity of infected cells
  2. Activation induced death
  3. Decreased production
  4. Redistribution
  5. Bystander cell killing
335
Q

What is the primary infection of varicella zoster virus (VZV)?

A

Varicella chickenpox

336
Q

What is the secondary reactivation of VZV?

A

Herpes zoster shingles

337
Q

What is the incubation period for chickenpox?

A

7 to 21 days

338
Q

How long do the symptoms usually last in chickenpox?

A

10 days

339
Q

When is the period of highest infectivity seen in chickenpox?

A

2 days before rash to 2 days after rash

340
Q

What groups is chickenpox serious in?

A
  1. Immunocompromised
  2. Adults
  3. Pregnant women
  4. Smokers
  5. Infants
341
Q

What are the stages of rash evolution in chickenpox?

A
  1. Macule (red blotch, flat)
  2. Papule (lumpy)
  3. Vesicle (viral replication, blisters)
  4. Pustule (inflammatory response)
  5. Crust
342
Q

What is the hallmark feature of chickenpox?

A

Centrifugal distribution of rash

343
Q

How is a chickenpox infection diagnosed?

A

VZV/HSV PCR

344
Q

Give 3 complications of chickenpox

A
  1. Dehydration
  2. Cerebellar ataxia
  3. Chickenpox pneumonitis
345
Q

What is the mortality for chickenpox pneumonitis?

A

6% with treatment, 30% without

346
Q

What is the prevalence of foetal varicella syndrome?

A

10-15%

347
Q

What happens in foetal varicella syndrome?

A

Shingles in first year of life

348
Q

How many people in the UK get shingles each year?

A

250,000

349
Q

Where is shingles reactivation most often localised to?

A

Thoracic region

350
Q

What is a complication of shingles?

A

Post-herpetic neuralgia

351
Q

What are the 3 types of worm?

A
  1. Nematodes
  2. Trematodes
  3. Cestodes
352
Q

What do adult worms require to replicate?

A

A period of development outside the body

353
Q

What is the pre-patient period?

A

Interval between acquiring infection and appearance of eggs in stool/urine

354
Q

What is ascariasis lumbricoides?

A

Large roundworm

355
Q

What are the treatments for roundworm?

A

Peperazine, pyrantel, mebendazole, levamisole

356
Q

What is the diagnosis for worms?

A

Stool microscopy

357
Q

What worm is very common in the UK?

A

Enteriobius vermicularis (pinworm or threadworm)

358
Q

How is pinworm ingested?

A

Contaminated hands

359
Q

What is the pre-patient period for pinworm?

A

40 days

360
Q

Give 3 effects of pinworm

A
  1. Appendicitis
  2. Endometritis
  3. Pruritis ani
361
Q

What is the treatment for pinworm?

A
  1. Mebendazole
  2. Piperazine
  3. Pyrantel
362
Q

What are 3 symptoms of trichuriasis?

A
  1. Anaemia
  2. Bloody diarrhoea
  3. Rectal prolapse
363
Q

Wha causes heated disease?

A

Taenia sodium (pork tapeworm)

364
Q

What is the effect of pork tapeworm on the brain?

A

Fills it up, makes it look soapy

365
Q

What is the intermediate host for flukes?

A

Snail

366
Q

What causes schistosomiasis?

A

Schistosoma haematobium

367
Q

How many Schistosoma haematobium infected patients present with Katayama fever?

A

50%

368
Q

Give 3 clinical features of Katayama fever?

A
  1. Fever
  2. Eosinophilia
  3. Diarrhoea
369
Q

Give 3 clinical features of S. haematobium

A
  1. Granulomatous lesions
  2. Uropathy
  3. Calcified bladder
370
Q

How is schistosomiasis diagnosed?

A
  1. Serology
  2. Urine
  3. Stool sample
  4. Rectal biopsy
  5. USS
371
Q

Give 3 ways of treating schistosomiasis

A
  1. Praziquantel
  2. Isoquinoline
  3. Metriphonate

Phase 2a Medicine (15 decks)

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