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1 - Finals > ID and Micro > Flashcards

ID and Micro Flashcards

1
Q

define pathogen

A

an organism that is capable of causing disease

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2
Q

define commensal

A

organism which colonises the host but does not cause disease in normal circumstances

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3
Q

define opportunist pathogen

A

microbe that only causes disease if host defences are compromised

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4
Q

define virulence/pathogenicity

A

the degree to which a given organism is pathogenic

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5
Q

define asymptomatic carriage

A

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

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6
Q

describe the structure of a Gram negative bacterial cell envelope

A

inner cell membrane,thin peptidoglycan layer,outer cell membrane,lipopolysaccharide layer,outer capsule.

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7
Q

describe the structure of a Gram positive bacterial cell envelope

A

thick layer of peptidoglycan between the outer capsule + inner cell membrane.

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8
Q

what is a bacterial endotoxin? describe features

A

a component of the cell wall that is released when the bacteria is damaged.less specific actions than an exotoxin e.g. septic shock

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9
Q

what is a bacterial exotoxin? describe features

A

mainly excreted by Gram +ve bacteria. actively secreted toxins with specific actions.

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10
Q

how might bacterial genes be transferred between bacteria?

A

transformation e.g. via plasmid.transduction e.g. via phage.conjugation e.g. via sex pilus.

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11
Q

describe the process of Gram staining

A
  1. heat fix sample to slide2. add methyl violet (blue/purple)3. add iodine - fixes methyl violet to gram +ve samples4. add alcohol to decolorize Gram -ve samples5. counterstain with basic fuchsin (red)
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12
Q

what is the normal habitat of staphylococcus spp?

A

nose and skin

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13
Q

how is S aureus spread?

A

aerosol and touch

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14
Q

what agar is used to grow enterobacteria?

A

MacConkey - bile salts, lactose, pH indicator

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15
Q

How do you distinguish Salmonella/Shigella from E coli on a MacConkey-lactose agar?

A

E.coli = pink, as it is lactose fermentingShigella/salmonella = yellow, non-lactose fermenting

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16
Q

how would you distinguish between Salmonella and Shigella?

A

serology, as both are non-lactose fermenting so appear the same on MacConkey agar

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17
Q

what are the main infections caused by pathogenic E coli strains?

A 
wound infections (surgical).
UTIs.
gastroenteritis.
travellers' diarrhoea.
bacteraemia.
meningitis.
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18
Q

what 3 infections are caused by salmonella?

A
  1. gastroenteritis - food poisoning (localised infection)
  2. enteric fever - typhoid (systemic infection)
  3. bacteraemia - uncommon
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19
Q

what agar must H influenzae be grown on and why?

A

fastidious - requires haem and NAD - will not grow on blood agar, only chocolate agar (blood agar that has been heated so haem and NAD are released by RBCs).
non-motile.

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20
Q

describe the main features of Legionella pneumophila and Legionnaires’ disease

A

seen in immunocompromised (elderly, alcoholics, smokers).
severe.
culture on charcoal agar.
found in man-made aquatic environments (aircon, cruise ships etc) - replicates within freshwater protozoa.
can infect alveolar macrophages.
induces phagocytosis.

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21
Q

what are the clinical features of an infection with campylobacter?

A

mild to severe diarrhoea, often with blood.
self-limiting (up to 1 wk).
campylobacter shed in faeces for 3wks.

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22
Q

describe the features of bacteroides? where are they typically found as commensals?

A

non-motile rods.
strict anaerobes.
commensal flora of large intestine (also commensal in vagina/cervix).

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23
Q

what shape are bacteroides?

A

bacilli

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24
Q

what shape are spirochaetes?

A

spiral/helical

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25
Q

describe the cell wall of fungi and how it stains?

A

rigid. polysaccharides and chitin.
stain with Gomorra methenamine silver, and periodic acid-Schiff.
lack a capsule.

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26
Q

describe the features of yeasts

A

unicellular.
round/oval.
asexual - reproduce by budding.

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27
Q

what are dimorphic fungi?

A

fungi which grow as yeasts in tissue, but as moulds in-vitro.

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28
Q

describe the features of moulds

A

composed of tubular structures (hyphae).
grow by longitudinal extension and branching - interwoven mycelium.
reproduce by spore formation (sexual/asexual).

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29
Q

what type of fungi is candida albicans?

A

yeast

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30
Q

give some examples of moulds

A

aspergillus spp., fusarium spp. mucoraceous moulds. dark-walled fungi.

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31
Q

what are the 3 types of fungal infection?

A
  1. superficial mycoses2. subcutaneous mycoses3. systemic mycoses
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32
Q

name some common sites for superficial mycoses

A

skin, hair, nails, mucous membranes

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33
Q

what are the two main kinds of infection seen in superficial mycoses?

A

ringworm.yeast infections.

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34
Q

what pathogens cause ringworm (dermatophytosis, tinea - athletes foot, swimmers crotch etc)?

A

tricophyton spp. microsporum spp. epidermophyton spp.

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35
Q

describe the transmission of ringworm infections

A

direct or indirect transfer of infected keratin - e.g. communal bathing facilities.

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36
Q

describe the different types of aspergillus infection

A
  1. invasive aspergillosis - neutropaenic patients. treat with amphotericin.
  2. allergic aspergillosis - ABPA
  3. aspergilloma - fungus ball in pre-existing cavity of lung.
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37
Q

describe the basic idea behind the treatment of fungal infections, and give examples of drugs used.

A

use drugs that target sterols in their cell membranes.
topical - nystatin, ketoconazole.
systemic/oral - fluconazole

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38
Q

give some examples of mycobacteria of medical importance, and the diseases they cause

A 
M. tuberculosis = TB
M. leprae = leprosy
M. kansaii = chronic lung infection
M. marinum = fish tank granuloma
M. ulcerans = buruli ulcer
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39
Q

why will immunocompromised patients show disseminated mycobacterial disease, instead of characteristic granulomas?

A

they don’t have enough T cell function to form granulomatas

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40
Q

describe the microbiological features of mycobacteria

A

aerobic, non-spore forming, non-motile bacilli.
cell walls contain a lot of high molecular weight lipids - weakly gram-positive/colourless.
slow growing.

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41
Q

what does the thick lipid coating of mycobacteria allow them to do?

A

survive inside macrophages, even in low pH environment

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42
Q

what are the key cell wall components of mycobacteria?

A

mycolic acids. lipoarabinomannan (LAM - glycolipid)

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43
Q

describe Koch’s postulates for a disease to be defined as caused by bacteria (/mycobacteria etc)

A
  1. bacteria should be found in all people with disease
  2. bacteria should be isolated from infected lesions
  3. a pure culture inoculated into a susceptible person should produce disease symptoms
  4. same bacteria should then be isolated from that individual
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44
Q

what stain is used for mycobacteria and why?

A

Ziehl-Neelsen stain for acid fast bacilli - high lipid content in cell wall makes mycobacteria resistant to Gram stain

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45
Q

what type of granuloma is typically seen in TB?

A

caseating

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46
Q

what are the main principles of mycobacterial treatment?

A
  1. slowly replicating bacteria - so need prolonged treatment2. multiple drug combinations to combat resistance3. compliance is essential - directly observe therapy used
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47
Q

describe the standard drug regime for tuberculosis

A

RIPE - rifampicin, isoniazid, pyrazinamide and ethambutol for 2mths.
then rifampicin and isoniazid for 4 further months.

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48
Q

what makes up the primary complex of primary TB?

A

granuloma + lymphatics + lymph node

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49
Q

where in the lung are tuberculosis bacilli most likely to form a granuloma and why?

A

apex - there is more air and less blood supply, so fewer defending WBCs to fight

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50
Q

what is latent TB?

A

cell-mediated immune response from T cells manages to contain primary infection, but it persists. no clinical disease (normal CXR).

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51
Q

what is pulmonary TB?

A

follows after primary disease, or after latent reactivation.
necrosis in lesion. caseous material coughed up, leaving cavity. TB may spread in lung causing other lesions.

= TB in the lungs basically

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52
Q

where, apart from the lungs, may TB spread?

A 
GU TB
peritoneal TB
TB meningitis
widespread = miliary TB.
pleural TB
bone and joint TB
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53
Q

what are the three groups of helminths?

A
  1. nematodes (round worms)
  2. trematodes (flatworms, flukes)
  3. cestodes (tapeworms)
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54
Q

what do adult worms need before they can reproduce?

A

a period of development outside the body

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55
Q

what is the “pre-patent” period in relation to helminth disease?

A

the interval between infection and the appearance of eggs in the stool

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56
Q

how are intestinal nematodes transmitted?

A

faecal-oral route.transmitted from person to person via eggs/larvae - these are only infectious after a period of development in the soil.

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57
Q

what organism causes pinworm/threadworm? what is the pre-patent period?

A

enterobius vermicularis
40d.
v common in UK

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58
Q

describe the lifecycle of enterobius vermicularis (pinworm/threadworm)

A
  1. adult is resident in large bowel
  2. female emerges from anus at night to lay eggs on perineum
  3. eggs are infectious after 4hrs, ingested by next host
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59
Q

what are the clinical features of pinworm/threadworm?

A
  1. pruritis ani2. appendicitis3. vaginal penetration - endometriosis, salpingitis, infertility
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60
Q

how would you diagnose pinworm/threadworm?

A

microscopy of sellotape strip from perianal region

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61
Q

what is the general way to diagnose worms?

A

stool microscopy for eggs

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62
Q

what drug is used to treat a lot of worm infections? available in pharmacies for threadworm

A

Mebendazole

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63
Q

what causes schistosomiasis?

A

Schistosoma - an adult fluke. penetrates skin while swimming, matures in abdominal cavity.

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64
Q

what is schistosomiasis (katayama fever)? what are the clinical features?

A

initial immune-complex mediated illness 2-4wks after exposure.fever; urticaria; eosinophilia; diarrhoea; hepatomegaly; splenomegaly; cough and wheeze; cachexia.

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65
Q

what are protozoa?

A

single-celled eukaryotes.

consume bacteria, algae, microfungi

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66
Q

what are the two main stages in the general life cycle of protozoa?

A

proliferative TROPHOZOITE stage - feed and reproduce.

dormant CYST stage - can survive outside host.

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67
Q

what are the 5 major groups that protozoa are divided into?

A
  1. flagellates
  2. amoebae
  3. cilliates
  4. microsporidia
  5. sporozoa
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68
Q

what are the 4 species of plasmodia that cause human disease?

A

P. falciparum
P. ovale
P. vivax
P. malariae

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69
Q

how is malaria transmitted?

A

bite of female Anopheles mosquitoes

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70
Q

how does the Anopheles mosquito become affected?

A 
feeding from infected human. 
then they are infected for life (3-4wks). 
night-biting. 
bite indoors. 
lifecycle depends on water (to lay eggs)
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71
Q

describe the basic stages of the plasmodia lifecycle

A

in human host has exo-erythrotic cycle (in liver), and erythrotic cycle (in blood).
(P ovale/vivax also have hypnozoite stage - lie dormant).
matures in RBCs.
taken up from blood into female anopheles - sporogonic cycle.

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72
Q

describe the pathogenesis of falciparum malaria

A

fatal.parasite matures in RBCs - ‘knobs’ on RBC surface.
bind to receptors on endothelial cells in capillaries + venules.
sequestration in small vessels.
obstruction of microcirculation - tissue hypoxia.

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73
Q

what are the acute clinical features common to all 4 species of malaria?

A

FEVER.
chills and sweats; headache; myalgia; fatigue; nausea and vomiting; diarrhoea.anaemia; jaundice; hepatosplenomegaly; ‘black water fever’

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74
Q

describe the clinical features of P falciparum malaria in adults

A

coma; ARDS; hypoglycaemia; renal failure (hypovolaemia, microvascular blockade).SHOCK.

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75
Q

describe the clinical features of P falciparum malaria in children

A

non-specific - stop crying/playing/eating.
tachypnoea.
anaemia.
hypoglycaemia.
cerebral malaria can cause encephalopathy/coma - raised ICP, varied presentation - rule out meningitis.

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76
Q

how is malaria diagnosed?

A

thick AND thin blood films - 3 separate films at different times of day, examined under light microscopy.

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77
Q

how do you treat complicated falciparum malaria?

A

IV artesunate or IV quinine

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78
Q

how do you treat uncomplicated falciparum malaria?

A

oral riamet or oral quinine (±doxycycline)

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79
Q

how do you treat non-falciparum malaria?

A

oral chloroquine

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80
Q

describe the stages of viral replication

A
  1. attachement
  2. cell entry - only viral ‘core’ enters host cytoplasm
  3. interaction with host cells - use cell materials for their replication etc
  4. replication
  5. assembly - may occur in nucleus/cytoplasm or at cell membrane
  6. release - by lysis of cell, or by exocytosis
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81
Q

list the different ways in which viruses can cause disease

A
  1. direct destruction of host cells2. modification of host cell structure/function3. immuno-pathological damage4. damage through cell proliferation/immortalisation5. evasion of host defences
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82
Q

what determines the defence mechanism employed against bacterial infection?

A

no. organisms/virulence.
low = phagocytes active
high = immune response

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83
Q

what types of immunoglobulin are produced in response to worm infection?

A

IgG and IgE

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84
Q

what is the most widely used antiviral agent? what is it’s mode of action?

A

aciclovir

nucleoside analogue

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85
Q

how do nucleoside analogue antiviral agents work?

A

phosphorylated within cells to an active triphosphate and inhibit viral DNA synthesis

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86
Q

what are “notifiable diseases”? who should be notified?

A

diseases/infections/conditions that are specifically listed as notifiable.
local health authorities/Public Health England

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87
Q

define “anti-microbial”

A

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

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88
Q

what is the target site of beta lactams?

A

cell wall - inhibition of cell wall synthesis.

include penicillins, carbapenems and cephalosporins

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89
Q

give examples of antibiotics that work by interference with nucleic acid synthesis/function

A

metronidazole

rifampicin

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90
Q

how do metronidazole/rifampicin work?

A

interfere with nucleic acid synthesis or function

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91
Q

how do fluoroquinolones work?

A

inhibit DNA gyrase

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92
Q

what types of antibiotics work by inhibiting ribosomal activity and protein synthesis?

A

aminoglycosides.
tetracyclines.
macrolides.
chloramphenicol.

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93
Q

what is the difference between bacteriostatic and bactericidal antibiotics?

A 
bacteriostatic = prevent growth of bacteria.
bactericidal = kills the bacteria
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94
Q

what are the two major determinants of anti bacterial effect?

A

concentration and time that the antimicrobial remains on binding sites

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95
Q

what antibiotics put the patient at risk of C diff? (the 5Cs of C diff)

A

Ciprofloxacin; Clindamycin; Cephalosporins; Co-amoxiclav; Carbapenems

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96
Q

what are 4 ways a bacteria may resist an antimicrobial?

A
  1. target site mutation
  2. destruction/inactivation of antimicrobial
  3. prevent antimicrobial access
  4. remove antimicrobial from bacteria
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97
Q

what is septicaemia?

A

“blood poisoning” - when an infection is found in the circulating blood

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98
Q

give some examples of carbapenems and their uses

A

imipenem, meropenem, ertapenem.

broad spectrum - severe hospital acquired infections.

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99
Q

give some examples of cephalosporins

A

cefradine
cefuroxime
cefotaxime

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100
Q

give examples of glycopeptides, and how they are used

A

vancomycin , teicoplanin.
gram +ve agents.
IV only.
reserved for serious/resistant gram +ve, e.g. MRSA

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101
Q

how does chloramphenicol work? how is it used?

A

it’s a protein synthesis inhibitor. very broad spectrum (except pseudomonas).
toxicity - little used today.
still used in ophthamology.

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102
Q

give examples of macrolides, and what they are used for

A

erythromycin, clarithromycin.

good for staph/strep. alternatives to penicillins. no gram-ve cover.

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103
Q

what type of antibiotic is clindamycin? what is it used for?

A

lincosamides. active against staph, strep and anaerobes

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104
Q

give examples of aminoglycosides and what they are used for

A

gentamicin, tobramycin.

enterobacteriaceae, pseudomonas and staphylococci.

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105
Q

what type of antibiotic is ciprofloxacin? what is it used for?

A

quinolones.

used against enterobacteriaceae, pseudomonas and staph.

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106
Q

what types of organism is metronidazole active against?

A

anaerobic bacteria and protozoa.

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107
Q

what does the catalase test differentiate between?

A

staphylococci - catalase +ve

strep and enterococci - catalase -ve

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108
Q

what does the coagulase test differentiate between?

A

staph areus - coagulase +ve

other staph - coagulase -ve

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109
Q

is staph aureus coagulase negative or positive?

A

positive

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110
Q

what does the oxidase test aim to identify?

A

oxidase positive bacteria - pseudomonas spp. and neisseria spp.

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111
Q

what does the optochin test do?

A

differentiates Strep pneumoniae from other alpa haemolytic strep.
strep pneumoniae shows a zone of inhibition around the optochin disc

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112
Q

What types of bacteria form red/pink colonies on MacConkey agar?

A

E coli and Klebsiella - lactose fermenting

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113
Q

What types of bacteria form a clear colony on MacConkey agar?

A

Salmonella, shigella, pseudomonas - lactose non fermenting

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114
Q

what type of agar differentiates between alpha and beta haemolytic strep?

A

blood agar

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115
Q

how do you identify alpha haemolytic strep (strep viridans) on blood agar?

A

green pigment due to partial breakdown of blood

116
Q

how do you identify beta haemolytic strep on blood agar?

A

clear zones around the colonies - complete breakdown of blood

117
Q

what is Lancefield grouping?

A

differentiates between beta haemolytic Strep spp. by detecting surface antigens

118
Q

which bacteria are in Lancefield groups A, B and D

A 
A = strep pyogenes
B = strep agalactiae
D = enterococci
119
Q

what are the 6 key Gram +ve staining bacterial groups?

remember - Sexy Students Can Look Bad Come morning

A 
Streptococcus
Staphylococcus
Corynebacterium
Listeria
Bacillus
Clostridium
120
Q

are the 6 key groups of Gram +ve bacteria aerobic or anaerobic?

A

aerobic, apart from Clostridium spp which are anearobes

121
Q

describe the key features of streptococcus spp

A

chains or diplococci.
gram +ve.
catalase negative.
aerobic.

122
Q

describe the features of strep pneumoniae and what diseases it can cause

A

gram +ve diplococci. alpha haemolytic.
droplet transmission.
community-acquired pneumonia, sinusitis, bacterial meningitis.

123
Q

what antibiotics would be given to treat strep pneumoniae infection?

A

penicillin or erythromycin

124
Q

what diseases are caused by alpha haemolytic strep (strep viridans)?

A

bacterial endocarditis + dental caries.

125
Q

how would you treat an alpha haemolytic strep infection?

A

penicillin/amoxicillin (erythromycin if allergic).

bacterial endocarditis - penicillin and gentomycin.

126
Q

give the features of strep pyogenes, and the diseases it causes?

A

group A beta-haemolytic. transmission is airborne and hands.

cellulitis, necrotising fasciitis, pharyngitis (strep throat), tonsillitis etc

127
Q

what are the features of enterococcus spp and what diseases do they cause?

A

group D, non-haemolytic, MacConkey growth.
GI tract commensal.
infective endocarditis, UTIs, would infections, catheter infections.

128
Q

how would you treat an enterococcus infection?

A 
pencillin/vancomycin.
serious infection (e.g. IE) - penicillin/vancomycin + getamicin
129
Q

describe the key features of staphylococcus spp.

A

cocci in clumps, Gram +ve.
catalase positive.
coagulase used to differentiate staph aureus (+ve) from the others. aerobic.

130
Q

name two coagulase -ve staphylococcus spp.

A

staph epidermidis

staph saprophyticus

131
Q

give some diseases caused by staph aureus

A 
Impetigo, cellulitis, wound infection.
osteomyelitis, septic arthritis.
conjunctivitis
bacterial endocarditis (in IVDU)
pneumonia.
132
Q

how does beta lactamase confer resistance to penicillins and cephalosporins?

A

beta lactam ring is hydrolysed by this bacterial enzyme. antimicrobial is now unable to bind to the bacteria.

133
Q

give a disease caused by staph saprophyticus and its treatment?

A

UTI in sexually active young women. trimethoprim, flucloxacillin.

134
Q

what is the important species of Corynebacterium? how is it spread? what disease does it cause?

A

Corynebacterium diphtheriae. droplet spread. diphtheria.

135
Q

how would you treat diphtheria?

A

erythromycin. diphtheria antitoxin.

136
Q

are Clostridium spp aerobic or anaerobic?

A

anaerobic

137
Q

what bacteria causes tetanus? how is it spread? how would you treat it?

A

clostridium tetani.
spore-forming - spores enter open wounds.
human tetanus Ig + benzodiazepines.

138
Q

what disease does C difficile cause? how does it spread?

A

transmission = spores via faecal-oral route.

causes pseudomembranous colitis - diarrhoea following antibiotic therapy.

139
Q

how would you treat C diff diarrhoea?

A

vancomycin

140
Q

what are the 6 important Gram -ve bacterial groups?

A 
NeisseriaColiforms (also Enterobacteriaceae)
Parvobacteria
Helicobacter
Vibrio
Pseudomonas
141
Q

Are the key Gram -ve bacterial groups aerobic or anaerobic?

A

aerobic

142
Q

describe the features of Neisseria spp.

A

diplococci. gram -ve. oxidase positive. aerobic.

143
Q

Neisseria meningitidis - give its transmission, diseases caused and treatment

A

transmission is by droplets/direct mucosal contact.
Causes meningitis and septicaemia (with purpuric skin rash).
treatment - benzylpenicillin or cefotaxime.

144
Q

what disease does Neisseria gonorrhoea cause? transmission? treatment?

A

gonorrhoea
(opthalmia neonatorum, Reiter’s syndrome)
transmission is direct mucosal contact.
treatment = ciprofloxacin or cefixime.

145
Q

List the coliforms (/enterobacteriaceae) according to colour on MacConkey agar

A

red/pink colony = E coli and Klebsiella penumoniae.

clear colony = Salmonella typhi, paratyphi (A, B, C) and enteritidis

146
Q

E coli: transmission? diseases caused?

A

faecal-oral.
diarrhoea.
UTIs, hospital-acquired pneumonia.

147
Q

Klebsiella pneumoniae: diseases caused? treatment?

A

hospital acquired pneumonia. UTIs. cephalosporins.

148
Q

what diseases do Salmonella typhi and paratyphi cause? transmission and treatment?

A

typhoid and paratyphoid (enteric fever).
faecal-oral.
ciprofloxacin.

149
Q

what disease does Salmonella enteritidis cause? transmission? treatment?

A

gastroenteritis (food-poisoning).
transmitted in under-cooked food contaminated with infected animal faeces.
no treatment - self-limiting disease.

150
Q

what disease does Shigella dysenteriae cause? transmission and treatment?

A

bacillary dysentery. faecal-oral. ciprofloxacin.

151
Q

give some examples of parvobacteria

A

Haemophilus influenzae, Bordatella pertussis, Legionella pneumophila, Campylobacter jejuni.

152
Q

what diseases does Haemophilus influenzae cause?

A

meningitis, osteomyelitis, cellulitis, otitis media, septic arthritis, pneumonia.

153
Q

how would you treat an H influenzae infection?

A

cefotaxime or ceftriaxone

154
Q

what disease does Bordatella pertussis cause? transmission and treatment?

A

whooping cough. airborne droplets. erythromycin.

155
Q

what disease does Legionella pneumophila cause? transmission and treatment?

A

Legionnaires disease (severe pneumonia, high fever).
transmitted by aerosolised droplets - found in warm water such as air con units, water tanks.
treat with erythromcyin.

156
Q

what does Campylobacter jejuni cause? transmission? treatment?

A

gastroenteritis ± dysentery - food poisoning.
reactive arthritis.
Guillain-Barre.
transmitted in contaminated poultry or unpasteurised milk.
no treatment - self-limiting.

157
Q

what diseases does H pylori cause? how would you treat?

A 
chronic gastritis. 
duodenal and gastric ulcers. 
increased gastric cancer risk.
treat - clarithromycin and amoxicillin or metronidazole.
PPI (omeprazole).
158
Q

what disease does Vibrio cholerae cause? transmission and treatment?

A

cholera - rice water diarrhoea, 25l/day.
faecal-oral / seafood
treat - rehydration.

159
Q

what diseases does pseudomonas aeruginosa cause?

A

pneumonia (esp. in CF patients)
infections.folliculitis.
UTIs, esp. with catheters.

160
Q

how would you treat a patient with a Pseudomonas aeruginosa infection?

A

severe cases - gentamicin or ceftazidime (IV).

in CF/bronchiectasis - ciprofloxacin.

161
Q

what 8 important bacterial groups stain poorly/not at all with Gram stain?

A 
Chlamydia spp.
Coxiella spp.
Ricksettia spp.
Mycobacteria spp.
Trepnonema spp.Borrelia spp.
Leptospira spp.
Mycoplasma spp.
162
Q

What diseases are caused by Chlamydia trachomatis?

A

chlamydia.
trachoma - chronic follicular keratoconjunctivitis.
Reiter’s syndrome/PID.

163
Q

what is the route of transmission of Chlamydia trachomatis?

A

mucosal contact

164
Q

how would you treat a patient infected with Chlamydia trachomatis?

A

doxycycline or azithromycin

165
Q

what disease is caused by Chlamydia psittaci? treatment?

A

pigeon fanciers lung. tetracylcine.

166
Q

what culture medium is used for Mycobacteria? how long should the culture be grown for?

A

Lowenstein-Jensen culture medium. up to 12 weeks.

167
Q

what disease is caused by Mycobacterium leprae? transmission and treatment?

A

Leprosy. aerosol droplet spread.

Rifampicin and dapsone.

168
Q

what disease is caused by Treponema pallidum? transmission and treatment?

A

Syphillis. tramission is through broken mucosa during sexual contact, or blood transfusion.
treatment - penicillin or doxycycline.

169
Q

give some examples of spirochaete bacteria

A

Treponema spp.
Borrelia spp.
Leptospira spp.

170
Q

what type of virus is the herpes simplex virus? what diseases does it cause?

A

DNA virus.HSV1 = cold sores.HSV2 = genital herpes.

171
Q

how would you treat a herpes simplex infection?

A

aciclovir, famciclovir or valciclovir

172
Q

what type of virus is the varicella-zoster virus? what diseases does it cause?

A

DNA virus.
chicken pox.
reactivation = shingles.

173
Q

how would you treat someone infected with varicella zoster?

A

child - calamine lotion.

adolescents/adults - aciclovir.

174
Q

what type of virus is cytomegalovirus?

A

DNA virus.

175
Q

what type of virus is Epstein-Barr virus? what diseases does it cause?

A

DNA virus.
infectious mononucleosis (Glandular fever).
Burkitt’s lymphoma/Hodgkin’s disease.

176
Q

what type of virus is the influenza virus? how is it transmitted?

A

RNA virus.

droplet spread.

177
Q

what type of virus is the mumps virus? how is it transmitted?

A

RNA virus.

droplet spread.

178
Q

what are the clinical features of mumps?

A

prodrome - headache, malaise, fever.

enlarged parotid gland. orchitis.

179
Q

what type of virus is the measles virus? how is it spread?

A

RNA virus. droplet spread

180
Q

what are the clinical features of measles?

A

Prodromal illness. fever. rash - erythematous and maculopapular.

181
Q

what type of virus is the coronavirus? what does it cause? how it is spread?

A

RNA virus.
common cold.
droplet spread.

182
Q

what type of virus is the rotavirus? what does it cause? how is it spread?

A

RNA virus.
gastroenteritis.
faeco-oral + direct spread.

183
Q

name two groups of yeasts

A

candidia spp. and cryptococcus spp.

184
Q

where is Candida albicans found? how is it transmitted?

A

oropharynx, vagina, GI tract.disruption of normal bacterial flora leads to Candida overgrowth.

185
Q

what diseases does Candida albicans cause?

A

vaginal and oral candidiasis (thrush).
skin/nail infections.
UTIs.

186
Q

what type of protozoa is entamoeba histolyica? what disease does it cause?

A

an amoeba.

causes amoebic dysentry - faeco-oral transmission.

187
Q

what are the clinical features of amoebic dysentery?

A

abdo pain.
severe diarrhoea with blood and mucus.
tenesmus.
hepatomegaly.

188
Q

how would you treat amoebic dysentery?

A

metronidazole.

189
Q

what type of protozoa is giardia lamblia? what disease does it cause?

A

flagellate.

causes diarrhoea, including travellers diarrhoea.faeco-oral.

190
Q

give an example of a cestode

A

taenia solium - pork tapeworm

191
Q

give an example of a trematode

A

schistosomes

192
Q

what colour do Gram +ve bacteria stain?

A

Purple (Positive = Purple)

193
Q

what colour do Gram -ve bacteria stain?

A

red/pink

194
Q

what worm is the most common cause of iron-deficiency anaemia worldwide?

A

hookworm

195
Q

how is hepatitis A spread? what are the risk factors?

A

faecal-oral route.

poor sanitation, overcrowding, contaminated food/water. (fish in sewagey water)

196
Q

what would you find when looking at viral markers for hepatitis A? what other blood test would you perform?

A

Anti-HAV IgM (acute) and IgG (raised for life - carrier).

LFTs - AST/ALT are raised

197
Q

how would you treat hepatitis A?

A

supportive treatment - self-limiting.

198
Q

how would you prevent hepatitis A?

A

passive and active immunisation (inactivated protein) and good hygiene

199
Q

what type of virus is hep A?

A

RNA

200
Q

give 3 symptoms of hep A as well as 2 later signs

A

symptoms: fever, malaise, anorexia, nausea, arthralgia.later signs - jaundice, hepatosplenomegaly, lymphadenopathy.

201
Q

what type of virus is hep B?

A

enveloped DNA virus - hepadnaviridae family

202
Q

what are the routes of transmission for hep B?

A
  • vertical: can be v high % in countries where no preventative measures taken. these days it’s often that people have had it since birth if they’re from high prevalence places e.g. the Roma in Slovakia, some East Asia, Africa and Amazon basin countries.
  • horiztonal - sexual (v infectious), blood transfusions/procedures, needle-sharing, household transmission (tiny tiny proportion)
203
Q

what are the clinical features of hep B?

A

resembles hep A - fever, malaise etc - plus arthralgia and urticaria (hives).

204
Q

list 2 possible complications of hepatitis B

A

cirrhosis, HCC, fulminant hepatic failure, cholangiocarcinoma, cryoglobulinaemia

205
Q

what type of virus is hep C?

A

RNA flavivirus (hepacivirus)

third largest cause of end stage liver disease in UK!

206
Q

how is hep C transmitted and can the spread be prevented?

A

parenteral/blood products, mainly IVDUs
(also transfusions, tattoos, household transmission etc)
sexual transmission uncommon, higher risk in MSM (esp if also have HIV)
vertical transmission occurs in c.6%
can’t prevent spread - vaccination impossible due to rapid change of proteins.

207
Q

what haematological disorder is associated with hep C?

A

Non-Hodgkin’s lymphoma

208
Q

give 3 risk factors for progression of hepatitis C to cirrhosis

A

co-existing liver disease, HIV, African-Americans. excessive alcohol (liver damage).

pts should be counselled re alcohol use and given hep A and B vaccines if non-imune.

209
Q

how do you diagnose hepatitis C?

A

blood test - enzyme immunoassay, followed by confirmatory testing via immunoblot assay.
patients with +ve HCV antibody serology are then tested for HCV RNA by PCR, to confirm current infection

210
Q

give 3 possible complications of hepatitis C

A

glomerulonephritis, cryoglobulinaemia, thyroiditis, autoimmune hepatitis, PAN, polymyositis, porphyria cutanea tarda

211
Q

what other virus is needed for hep D to infect someone? why?

A

hep B.

hep D is an incomplete RNA that needs hep B for assembly.

212
Q

how can hepatitis D be prevented?

A

hep B vaccine

213
Q

how can you test for hepatitis D?

A

test for anti-HDV antibody

214
Q

what can hep D cause?

A

acute liver failure/cirrhosis

215
Q

how can you treat a hep D infection?

A

may need liver transplant as interferon alpha has limited success.

216
Q

what type of virus is hep E? what infection is it similar to?

A

RNA.hep A.

217
Q

how is hep E transmitted?

A

enterally - contaminated water.

218
Q

what can you detect in blood and stools to confirm a diagnosis of hep E?

A

hep E RNA

219
Q

what would you find in the blood of a patient that would indicate they have carrier status for HBV?

A

HBsAg - surface antigen.present 1-6 months after exposure.present for >6 months = carrier status.

220
Q

what would you find in the blood of a patient that has recently (last couple of months) been infected with HBV? what does this mean?

A

HBeAg (e antigen) - present 1.5-3 months after exposure.implies high infectivity.

221
Q

what might you find in the blood of a patient that indicates they have immunity to HBV through having previously been infected?

A

anti-HBc antibody

222
Q

what might you find in the blood of a patient that indicates they have immunity to HBV through having been vaccinated?

A

anti-HBs antibody

223
Q

what blood test would you do on an HBV patient to monitor progress?

A

HBV DNA PCR

224
Q

what blood test would you do on an HBV patient to monitor progress?

A

HBV PCR

225
Q

name the causative organism of TB and how it can be transmitted

A

Mycobacterium tuberculosis/bovis.

airborne - poor sanitation, overcrowding, coinfection with HIV

226
Q

how is TB tested for?

A

Ziehl-Neelsen stain - this has now been replaced by auramine-phenol (AP) staining + fluorescent microscope)
looking for alcohol and acid-fast bacilli.

samples cultured in MGIT liquid media for 2-8 weeks.

rapid in-house PCR now available - immediate confirmation of species and early idea re rifampicin sensitivity.

227
Q

describe the typical granulomatous lesions of TB

A

central areas of CASEATION surrounded by epithelioid cells and Langhan’s giant cells

228
Q

give 3 features of pulmonary TB

A

cough, sputum, malaise, weight loss, night sweats, pleurisy, haemoptysis, pleural effusion

229
Q

what is miliary TB?

A

occurs following haematogenous dissemination of primary TB

230
Q

describe the features of miliary TB

A

nonspecific, overwhelming signs.nodular opacities on CXR.retinal disease.biopsies of lung/liver/lymph nodes or marrow show AFB or granuloma.

231
Q

give 3 GU features of TB

A

dysuria, frequency, loin pain, haematuria, sterile pyuria

232
Q

give 1 bone feature of TB

A

vertebral collapse.Pott’s vertebra.

233
Q

give 2 abdominal features of TB

A

peritonitis, GI upset.

234
Q

give 3 signs of TB seen on CXR

A

consolidation, cavitation, fibrosis, calcification

235
Q

describe 3 different methods of testing for TB

A

Mantoux test - tuberculin sensitivity skin test - identifies latent TB, active TB and BCG exposure.Quantiferon TB gold (IFN gamma test).MC&S for AFB of 3+ sputum samples (also pleural fluid, urine, pus ascites etc).PCR - for identifying drug resistance.

236
Q

how would you treat TB?

A

RIPE for 2mths. then isoniazid and rifampicin for 4 further months (usually given as Rifinah combined tablet)

DOTS - directly observed therapy to ensure compliance + avoid resistance, used if non-compliance anticipated. slightly higher dose given only 3x a week.

TB meningitis/CNS TB treated for 12 months ± steroids to begin with.
MDR TB can be treated for up to 2 years.

237
Q

how would you diagnose typhoid/paratyphoid?

A

blood cultures of S typhi/paratyphi

238
Q

how would you treat typhoid infection?

A

fluid replacement + good nutrition.+ oral ciprofloxacin.

239
Q

what causes poliomyelitis?

A

highly contagious picornavirus.droplet or faecal-oral spread.

240
Q

describe the signs of poliomyelitis. how is it treated?

A

flu prodrome.
pre-paralytic stage - fever, tachycardia, headache, vomiting, neck stiffness.
paralytic stage.
no drug treatment available :(

241
Q

list 4 different ways HIV can be spread

A

sexual (vaginal and anal), blood products, vertical transmission (natural birth, breastfeeding), IVDU, needle stick injuries, organ donation

242
Q

describe the brief immunology of how HIV infects the body

A

HIV binds to CD4 glycoprotein receptors (gp120) on T helper lymphocytes, monocytes, macrophages and neural cells.CD+ve cells migrate to lymphoid tissue where the virus replicates producing countless new virions. These are released and infect more CD4 cells and as the infection progresses, the function of CD4 cells decreases and the actual number of cells depletes.

243
Q

how does the viral load affect a patient clinically? (in HIV)

A

as viral load increases, the CD4 count decreases making the disease more severe and the patient more ill.CD4 initially increases dramatically as it tries to fight off the infection, but eventually decreases as the virus takes over.

244
Q

when does HIV become AIDS?

A

CD4 count below 200.

presence of AIDS defining illness.

245
Q

explain the stages of infection with HIV.

A

1) acute infection - asymptomatic, when the virus first enters the body.
2) serocoversion illness - transient illness 2-6wks after exposure - malaise, fever, myalgia, pharyngitis, maculopapular rash or meningoencephalitis.
3) asymptomatic infection - latent stage
4) persistent generalised lymphadenopathy - enlarged nodes for 3+ months, then fever, night sweats, diarrhoea, weight loss, minor opportunistic infections (AIDS-related complex - prodrome to AIDs itself).
5) AIDS - presence of AIDS defining illness and CD4 count of less than 200.

246
Q

how would you confirm a diagnosis of AIDS?

A

serum/saliva ELISA test, must be at least 12 weeks after exposure - newest tests usually reliably accurate after only 2-3 weeks.
rapid antibody tests - immunoassays used in primary care.

any clinician can now request an HIV test with pts permission no need for complicated counselling now that we have effective treatments!! in some studies male life expectancy was longer in HIV +ve men due to frequency of healthcare interactions!

247
Q

list 2 respiratory AIDS defining illnesses

A

pneumocystis jivoreci (PCP), TB, aspergillus, EBV, reticular nodules, strep pneumoniae

248
Q

list 2 GI AIDS defining illnesses

A

oral candida, diarrhoea caused by shigella, salmonella, campylobacter, CMV, adenovirus, perianal warts and ulceration

249
Q

name an eye AIDS defining illness

A

CMV retinits

250
Q

give 3 CNS AIDS defining illnesses

A

cryptococcal meningitis, toxoplasmosis, cerebral lymphoma, encephalopathy.

251
Q

give some examples of classes of HAART drugs

A

nucleoSide reverse transcriptase inhibitors (NRTI) - zidovudine, didanosine, lamivudine.

nucleoTide reverse transcriptase inhibitors (act like NRTIs) e,g, tenofovir (CI in renal disease)

protease inhibitors (PI) - slow cell-to-cell spread, lengthening time to first clinical event e.g. atazanir. lots of drug interactions.

non-nucleoside reverse transcriptase inhibitors.

integrase inhibitors.

252
Q

give some ways that HIV can be prevented?

A

blood screening, Caesarean birth for HIV+ve mothers, bottle feeding, condoms or abstinence, fewer sexual partners, regular testing, decrease alcohol intake, circumcision

253
Q

give 3 risk factors for HIV

A 
men who have sex with men (MSM).
unsafe sex.
other STIs.
mother-to-child transmission.
multiple simultaneous partners.
IVDUs - sharing needles.
uncircumcised man.
254
Q

give 3 “other” AIDS defining illnesses

A

Kaposi’s sarcoma, Leishmaniasis, Burkitt’s lymphoma, cervical carcinoma, herpes simplex, wasting syndrome, shingles.

255
Q

what are the clinically important antigens to be aware of in hep B?

A
  • surface antigen = HBsAg = protein found in blood/serum of pts with current infection, used to Dx infection (also can be genetically produced to use as vaccine)
  • envelope antigen = HBeAG = used to assess phase of infection
  • core antigen = not used in diagnosis
256
Q

what are the clinically relevant antibodies in hep B?

A
  • surface antibody = HBsAb = indicates immunity to hep B (via immunisation or infection)
  • envelope antibody = HBeAb = seen in later phase of disease (either acute or chronic), evidence of immune response
  • core antibody = HbAb = found in most who have been exposed to HBV. tested as total IgG/IgM, doesn’t differentiate between acute/chronic/past infection, but not seen in immunised people.
257
Q

what other structure tested for with hep B is clinically important? (apart from the antigens/antibodies)

A

HBV DNA - measured by PCR and used to look at the grade of replication and activity of the virus.

258
Q

what is acute hep B?

A

much less commonly seen than chronic hep B. self-limiting, doesn’t really need treating but you might see them on ID ward.
occasionally it can lead to fulminant hepatitis and then liver failure - marker for this is rising INR - treat them to prevent this failure and need for transplant.

259
Q

how do people end up with chronic hep B infection? can we prevent this?

A

def. = infection persisting > 6/12 but it’s usually acquired at birth and present throughout life.
prevention = immunisation and immunoglobulin given post-exposure - if given to infectious mothers can reduce transmission rate to < 7% (instead of 90%).
if additional treatment to reduce viral load is given towards end of pregnancy can completely eliminate transmission!

260
Q

how is chronic HBV diagnosed? what is important to consider in managing it?

A

asymptomatic - diagnosed via serology.
want to diagnose before you get the complications - liver cirrhosis/cancer (oncogenic virus).
no curative treatment - aim to control viral replication and reduce inflammation in order to limit cirrhosis/cancer.

261
Q

how do you treat chronic hep B?

A
  • pegylated interferon alpha = weekly injectable for 48/52
  • or oral options = tonofovir or entecavir, daily long term.

tenofovir can cause proteinuria - always dipstick in clinic.
ALT used as marker of liver inflammation.
AFP monitored in combo with regular liver USS to find cancers early - ideally early enough that can treat with radiofrequency ablation.
also use fibroscan which uses sound waves to find fibrous bands in liver.

262
Q

how does the body react to infection with hep C? how does this initial reaction influence chance of clearing it?

A

most asymptomatic/symptoms so minimal they don’t seek medical attention.
15% get hepatic illness - malaise, nausea, RUQ pain then jaundice.
patients who get symptomatic primary infection are much more likely to clear the virus (around 50%) than those with minor/asymptomatic primary infection - these tend to end up with chronic HCV.

263
Q

what symptoms are experienced in chronic hep C?

A

often asymptomatic, might get malaise, fatigue, intermittent fleeting RUQ pain - but it has been shown that QOL improves following effective treatment.

(and obvs it causes end stage liver disease!!)

264
Q

list some extrahepatic effects of hep C infection

A
  • mixed cryoglobulinaemia
  • membranoproliferative glomerulonephritis
  • porphyria cutanea tarda
  • autoimmune thyroid disease (in women)

other associates (rarer) = lichen planus, Sjogren’s syndrome, B cell lymphoma, interstitial lung disease

265
Q

why can we “cure” hep C but not hep B?

A

because hep C is an RNA virus, whereas hep B is a DNA virus so can only be suppressed

can’t actually remember why this makes a difference but it did make sense at the time….

266
Q

what kind of clinical assessment/monitoring is done as part of follow-up/treatment of hep C?

A

liver fibrosis assessment (FibroScan) - assesses liver transient elastography (reduces need for liver biopsy).

if advanced fibrosis/cirrhosis then screening 6 monthly for HCC with AFP blood test + liver USS.
if evidence of portal hypertension pts also screened for varices vis OGD.

267
Q

how is “cure” defined in hepatitis C?

A

undetectable HCV RNA in blood 12 weeks after the end of treatment

aka sustained virological response (“SVR12”)

268
Q

what type of drugs are used in treating hepatitis C?

A

direct acting antiviral drugs.
high cure rates, shorter duration and less SEs than previous treatment.

they act on HCV viral enzymes to prevent replications.
3 classes:
- NS3/4A protease inhibitors (end in -previr)
- NS5A inhibitors (-asvir)
- NS5B inhibitors (-buvir)

often give fixed dose tablets with 2+ DAAs from 2+ DAA classes ± ribavirin (the old drug - teratogenic)

269
Q

list the four first line treatment regimens for hepatitis C

A
  • Harvoni: ledipasvir + sofosbuvir ±RBV
  • Epclusa: velpatasvir + sofosbuvir
  • Zepatie: Grazoprevir + Elbasvir ±RBV
  • Maviret: Glecaprevir + pibrentasvir

all given between 8-16weeks.
RBV = ribavirin, lots of SEs (anaemia, dyspnoea, fatigue, insomnia, agitation, anxiety etc)

270
Q

what options are there for patients who don’t have success with the four first line treatment regimens for hepatitis C?

A
  • Vosevi = sofosbuvir/velpatasvir/voxilaprevir tablet OD for 12 weeks.
  • Epclusa = Sofosbuvir/velpatasvir + ribavarin for 24 weeks
271
Q

define multi-drug resistant TB

A

TB resistant to at least isoniazid and rifampicin

extensive drug resistant TB (XDRTB) = MDRTB strains resistant to two other drug classes (fluoroquinolone + second line injectable)

272
Q

what’s the main SE to know for isoniazid toxicity?

A

peripheral neuropathy

273
Q

what’s the main SE to know for pyrazinamide?

A

arthralgia

also - most likely culprit for liver toxicity.

274
Q

what’s the main SE to know for rifampicin?

A

orange urine

275
Q

what’s the main SE to know for ethambutol?

A

optic neuritis

276
Q

what tests are used in contact screening for TB?

A

mantoux test or IGRA - for close contacts of index pts with pulmonary or laryngeal TB.
if +ve they get sent for CXR + further testing.
if theses are normal and pt asymptomatic = prophylaxis.

277
Q

explain how CD4 and viral load blood tests are used in monitoring HIV/HIV treatment

A

CD4 cell count - < 200 start being susceptible to PCP and toxoplasmosis, < 50 you get MAI and CMV.

viral load - quantity of virus per ml of pts serum. aiming for undetectable as U=U (undetectable = untransmittable) so no risk to partners.

278
Q

give examples of how a HAART regime might be structured

A
  • usually use at least 3 drugs with different mechanisms
  • usually NRTI backbone (2 NRTIs) + either integrase inhibitor, PI or (rarer) an NNRTI
  • once daily single tablet preparations are available, including truvade (tenofovir + emtricitabine) which is also used as PrEP or PEP (within 4 weeks)
279
Q

what prophylactic medications are offered to people with HIV plus CD4 count < 200?

A
  • co-trimoxazole for PCP and toxoplasma - but SE of rash/bone marrow suppression can limit its use
  • nebulised pentamidine protects against PCP, used in negative pressure side room as teratogenic
  • azithromycin - for MAI if CD4 <50
  • ganciclovir in pts with active CMV

usually withdraw prophylaxis once CD4 count is >200

280
Q

what are some risk factors for infective endocarditis?

A 
congenital - valve defects, VSD, PDA.
prosthetic valves.
IVDU.
poor dental hygiene.
soft tissue infections.
281
Q

name the most common causative organism in infective endocarditis?

A

Streptococcus viridans

282
Q

give 3 organisms (apart from Strep viridans) that can cause infective endocarditis

A

enterococci, staph aureus/epidermidis, diphtheroids, Haemophilus, actinobacillus, Coxiella burnetii, chlamydia.
fungi - Candida, aspergillus, histoplasma.

283
Q

what is an infective endocarditis patient at risk of?

A

stroke - vegetations.

destruction of valve - regurgitation - worsening heart failure.

284
Q

describe the clinical features of infective endocarditis

A

systemic features of infection - malaise, fever, night sweats, weight loss, anaemia.
heart failure + new murmurs.
vascular events - embolism ± metastatic abscesses.
immune complex deposition - petechial haemorrhages under skin, splinter haemorrhages under nails, Roth’s spots, arthrlagia, acute glomerulonephritis.

285
Q

what investigations should you carry out in suspected endocarditis?

A

3 sets of blood cultures, at different times and sites.
bloods - anaemia, neutrophilia, high ESR/CRP.

transthoracic echocardiography (TTE) - just standard echo.

286
Q

describe the Duke criteria for diagnosis of IE

A

2 major or 1 maj + 3 min, or 5 min.
Major criteria - persistently +ve blood culture. endocardium involvement seen on +ve echo, new murmur.
Minor criteria - fever, vascular/immunological signs, +ve blood culture/echo that doesn’t meet major.

287
Q

how would you treat infective endocarditis?

A

before results of culture - IV benzylpenicillin + gentamicin.
then tailor to cultures and sensitivity.

1 - Finals (15 decks)

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