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Finals > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

Describe the structure of gram-positive bacteria.

A

Gram-positive bacteria have a cell membrane (phospholipid bilayer) and a thick cell wall.

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2
Q

Describe the structure of a gram-negative bacteria.

A

Gram-negative bacteria have a cell membrane (phospholipid bilayer), thin cell wall and another phospholipid bilayer (containing lipopolysaccharides).

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3
Q

What is the primary stain used in gram-staining?

A

Crystal violet stain.

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4
Q

Explain why some bacteria are gram-positive and others are gram-negative.

A

Bacteria with thick peptidoglycan cell wall retain the crystal violet stain.
Bacteria with a thinner cell wall allow the stain to be washed out on the addition of ethanol.

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5
Q

Gram-negative bacteria: What is endotoxin?

A

The lipid component of the lipopolysaccharide cell membrane in Gram-negative bacteria is released during replication and after bacterial death… can cause septic shock.

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6
Q

Describe the structure of mycoplasma bacteria.

A

Lack a cell wall around their cell membranes.

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7
Q

How does the lack of a cell wall in mycoplasma bacteria determine antibiotic resistance?

A

Mycoplasma are resistant to antibiotics which target cell wall synthesis (cephalosporins and penicillins).

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8
Q

Which antibiotics target cell wall synthesis?

A

Cephalosporins.

Penicillins.

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9
Q

What shape are cocci bacteria?

A

Round.

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10
Q

Give three examples of Gram-positive cocci.

A

Staphylococci.
Streptococci.
Enterococci.

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11
Q

Give two examples of Gram-negative cocci.

A

Neisseria meningitidis.

Neisseria gonorrhoea.

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12
Q

Give examples of Gram-positive rods.

A 
Actinomyces. 
Bacillus anthracis. 
Clostridium. 
Diphtheria. 
Listeria monocytogenes. 
Remember: ABCD L
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13
Q

Define sepsis.

A

Life-threatening organ dysfunction caused by dysregulated host response to infection.

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14
Q

Describe the pathophysiology of sepsis.

A

Macrophages, lymphocytes and mast cells release vast amounts of cytokines, interleukins and tumour necrosis factor.
Cytokines cause vessel endothelium to become more permeable.
Fluid leaks out of the blood and into the extracellular space.
Oedema develops and loss of intravascular volume.
Oedema reduces gass exchange between blood and tissues (low oxygen).

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15
Q

What blood marker is most useful in assessing sepsis (and why)?

A

Lactate (produced in anaerobic respiration due to hypoperfusion of tissues).

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16
Q

Describe pathophysiology of sepsis (coagulation).

A

Activation of coagulation system leads to fibrin deposition throughout the circulation.
Platelets and clotting factors are consumed during clot formation.
Leads to thrombocytopenia, haemorrhages and an inability to clot / stop bleeding.

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17
Q

What factors increase the risk of sepsis?

A 
Extremes of age. 
Frail with multiple comorbidities. 
Pregnant. 
Trauma or surgery. 
Reduced immunity. 
Indwelling lines / catheters. 
Intravenous drug use. 
Skin infections/burns/cuts.
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18
Q

What scoring system can be used in sepsis assessment?

A

NEWS2.

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19
Q

At what NEWS2 score should you consider beginning the sepsis six protocol?

A

≥ 5

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20
Q

What are the sepsis six?

A 
Administer oxygen (> 94% or 88-92% if COPD). 
Take blood cultures. 
Give broad spectrum antibiotics. 
Give intravenous fluid challenges. 
Measure serum lactate. 
Measure hourly urine output.
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21
Q

What is the management of sepsis?

A

If lactate > 2 or SBP < 90mmHg give 500ml intravenous fluid over 15 minutes.
Give intravenous co-amoxiclav if not penicillin-allergic.

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22
Q

Sepsis management: How much fluid should you give before seeking senior help?

A

~ 2 litres (this is a guide and you should obviously escalate sooner if needed).

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23
Q

What is septic shock?

A

Sepsis characterised by circulatory, cellular and metabolic abnormalities that substantially increase mortality.
SBP < 90mmHg.
Lactate > 4mmol/L.

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24
Q

What is the presentation of initial HIV infection?

A

Seroconversion illness 3-12 weeks after infection… short flu-like illness, sore throat, maculopapular rash, malaise, diarrhoea, mouth ulcers.

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25
Q

What is the presentation of established HIV infection?

A

Weight loss and recurrent infections.

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26
Q

Give examples of possible transmission routes for HIV.

A

Unprotected anal, vaginal or oral sexual activity.
Mother to child at any stage of pregnancy, birth or breastfeeding.
Mucous membrane, blood or open wound exposure to infected blood/bodily fluids.

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27
Q

AIDS: When do AIDS-defining illnesses occur?

A

When CD4 count has dropped to a level that allows for unusual opportunistic infections and malignancies to appear.

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28
Q

HIV: Give six examples of AIDS-defining illnesses.

A 
Kaposi's sarcoma. 
Pneumocystis jirovecii pneumonia
Cytomegalovirus infection
Candidiasis (oesophageal or bronchial)
Lymphomas 
Tuberculosis
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29
Q

What is Kaposi’s sarcoma?

A

Type of cancer that can form masses in the skin, lymph nodes, mouth or other organs.
Typically: painless, purple skin malignancies.

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30
Q

How is diagnosis of HIV performed?

A

Combination test of HIV p24 antigen and HIV antibody.

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31
Q

When do antibodies develop in HIV infection?

A

Four to six weeks following initial infection.

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32
Q

HIV: Other than viral load, how is the extent of disease // disease severity monitored?

A

CD4 count (CD4 cells are destroyed by the HIV virus and < 200 cells is considered AIDS - high risk).

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33
Q

HIV: Individuals with AIDS (CD4 count < 200) should receive what prophylactic therapy?

A

Co-trimoxazole for protection against pneumocystis jirovecii pneumonia.

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34
Q

What is the management of HIV?

A

Antiretroviral therapy.

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35
Q

What is MRSA?

A

Methicillin resistant staphylococcus aureus.

Staph. aureus resistant to beta-lactam antibiotics such as penicillins, cephalosporins and carbapenems.

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36
Q

How is MRSA treated?

A

Skin and respiratory tract are often colonised:
Antibacterial nasal creams.
Chlorhexidine body wash.

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37
Q

What is cellulitis?

A

Infection of the skin and soft tissues underneath.

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38
Q

Cellulitis: What should you look for on examination to find cause?

A

Look for skin breaches (point of entry for bacteria).

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39
Q

Give examples of causes of cellulitis.

A

Skin trauma.
Eczematous skin.
Fungal nail infections.
Ulcers.

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40
Q

What are the clinical features of cellulitis?

A 
Erythema. 
Warm/hot to touch. 
Tense. 
Thickened. 
Oedematous. 
Bullae. 
Golden-yellow crusting.
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41
Q

Cellulitis: Define bullae.

A

Fluid-filled blisters.

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42
Q

Cellulitis: What causes gold-yellow crusting?

A

Staphylococcus aureus infection.

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43
Q

What pathogens most commonly cause cellulitis?

A

Staphylococcus aureus.
Group A streptococcus.
Group C streptococcus.

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44
Q

What is the treatment of cellulitis?

A

Flucloxacillin.

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45
Q

What is the primary differential for a person presenting with five day-history of feeling generally unwell, now has sore throat, tender lymphadenopathy and splenomegaly?

A

Glandular fever (infectious mononucleosis).

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46
Q

Infectious mononucleosis (glandular fever) is usually caused by what pathogen?

A

Epstein-Barr virus.

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47
Q

Glandular fever: How is EBV transmitted?

A

Oropharyngeal route in saliva (“kissing disease”)

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48
Q

What is the prodrome of glandular fever?

A

Flu-like illness (headache, low fever, chills) for three to five days.

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49
Q

What are the clinical features of glandular fever?

A

Exudative pharyngitis (sore throat), tender lymphadenopathy, splenomegaly and widespread erythematous macular rash.

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50
Q

What is the diagnostic triad for glandular fever?

A

Lymphocytosis.
> 10% atypical lymphocytes on peripheral blood film.
Positive serology for EBV.

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51
Q

Name an antibody test that can be performed in the investigation of glandular fever?

A

Monospot (mononuclear spot) test.

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52
Q

Glandular fever: The Monospot test detects the presence of which antibodies?

A

Heterophile antibodies.

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53
Q

Glandular fever: How is a Monospot test performed?

A

Patient’s blood is introduced to red blood cells from horses.

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54
Q

Glandular fever: What is the result of a positive Monospot test?

A

Reaction between heterophile antibodies and the horse red blood cells results in agglutination.

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55
Q

What is the management of glandular fever?

A

Supportive management. Advise to avoid contact sports and alcohol for one month.

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56
Q

Give five complications of glandular fever.

A 
Splenic rupture. 
Glomerulonephritis. 
Haemolytic anaemia. 
Thrombocytopenia. 
Chronic fatigue.
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57
Q

Epstein-Barr virus is associated with the development of what cancer?

A

Burkitt’s lymphoma (non-Hodgkin’s lymphoma).

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58
Q

What pathogen causes tuberculosis?

A

Mycobacterium tuberculosis.

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59
Q

How is tuberculosis transmitted?

A

Tuberculosis bacteria are mostly spread by inhaling saliva droplets from infected people.

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60
Q

Give three risk factors for tuberculosis?

A

Non-UK born (e.g. South Asia).
Immunocompromised (e.g. HIV).
Close contacts with TB.

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61
Q

What is active TB?

A

Active infection after exposure to Mycobacterium tuberculosis.

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62
Q

What is latent TB?

A

The immune system encapsulates the infection to stop its progression.

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63
Q

What is secondary TB?

A

Reactivation of latent TB… such as if the patient becomes immunocompromised.

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64
Q

What is miliary TB?

A

Uncontrolled, disseminated, severe disease.

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65
Q

Why does Mycobacterium tuberculosis most commonly cause pulmonary TB?

A

M. tuberculosis has high oxygen demands.

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66
Q

What % of cases of TB are pulmonary?

A

70%

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67
Q

How does tuberculosis present clinically?

A

A history of chronic, worsening symptoms such as lethargy, fever, night sweats, weight loss, cough +/- haemoptysis.
Extrapulmonary features include lymphadenopathy (usually in neck) and erythema nodosum.

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68
Q

TB: What type of vaccine is BCG vaccine?

A

Live attenuated vaccine.

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69
Q

TB: Describe the level of protection offered by the BCG vaccine.

A

Offers protection against severe and complicated disease but is less effective at protecting against pulmonary TB.

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70
Q

TB: What test is performed prior to receiving the BCG vaccine?

A

Mantoux test.

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71
Q

Describe how a Mantoux test is performed.

A

Tuberculin (purified tuberculosis protein derivative isolated from the bacteria) is injected intradermally. Results are read/measured 72 hours later.

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72
Q

How is a Mantoux test interpreted?

A

6-15mm of induration indicates hypersensitivity (e.g. previous TB or BCG).
> 15mm induration indicates strong hypersensitivity (e.g. TB infection).

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73
Q

What is the gold standard test for diagnosing tuberculosis?

A

Sputum smear and culture.

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74
Q

What stain is used in a sputum smear for tuberculosis?

A

Zeihl-Neelsen stain.

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75
Q

How does Mycobacterium tuberculosis appear with Zeihl-Neelsen stain?

A

Bacteria are bright red against a blue background.

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76
Q

What does CXR reveal in primary TB?

A

Patchy consolidation, pleural effusions, hilar lymphadenopathy.

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77
Q

What does CXR reveal in reactivated TB?

A

Patchy/nodular consolidation with cavitation (in upper zones).

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78
Q

What does CXR reveal in miliary TB?

A

“Millet seeds” uniformly distributed throughout the lung fields.

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79
Q

What is the treatment of latent tuberculosis?

A

Three months of isoniazid (+pyridoxine) and rifampicin. OR

Six months of isoniazid (+pyridoxine).

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80
Q

What drug is given alongside isoniazid in the treatment of TB (and why)?

A

Pyridoxine is vitamin B6.

Used to prevent peripheral neuropathy, a risk of isoniazid.

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81
Q

What is the treatment of active tuberculosis?

A

Two months of rifampicin, isoniazid (+pyridoxine), pyrazinamide, ethambutol… followed by four months of rifampicin and isoniazid (+pyridoxine).

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82
Q

TB management: What are side effects of rifampicin use?

A

Orange-red discolouration of secretions (urine and tears).

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83
Q

TB management: What are side effects of isoniazid use?

A

Peripheral neuropathy.

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84
Q

TB management: What are side effects of pyrazinamide use?

A

Hyperuricaemia and subsequent gout.

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85
Q

TB management: What are side effects of ethambutol use?

A

Colour blindness and reduced visual acuity.

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86
Q

What is septic arthritis?

A

An infection that occurs within a joint (either native or joint replacement).

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87
Q

What is the clinical presentation of septic arthritis?

A

Hot, red, swollen and painful joint (often the knee). Other features include stiffness and reduced ROM. Systemic features include fever, lethargy and sepsis.

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88
Q

Give examples of pathogens that can cause septic arthritis?

A 
Staphylococcus aureus (most common). 
Neisseria gonorrhoea. 
Group A Strep (Streptococcus pyogenes). 
Haemophilus influenzae.
Escherichia coli.
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89
Q

Neisseria gonorrhoea septic arthritis in more likely in which group of people?

A

The young and sexually active.

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90
Q

How is septic arthritis investigated?

A

Aspirate the joint prior to antibiotics and send for gram-staining, crystal microscopy, culture and antibiotic sensitivities.

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91
Q

What is the treatment of suspected septic arthritis?

A

Give broad-spectrum e.g. flucloxacillin and rifampicin until the sensitivities are known

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92
Q

What is syphilis?

A

A sexually transmitted infection.

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93
Q

What is the route of transmission of syphilis?

A

Skin or mucous membranes.

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94
Q

What is the causative organism of syphilis?

A

Treponema pallidum.

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95
Q

What is the incubation period of syphilis?

A

Around 21 days from initial infection to symptoms.

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96
Q

Give examples of opportunities for syphilis transmission.

A

Oral, vaginal, anal sex involving direct contact with infected area.
Vertical transmission from mother to baby during pregnancy.
Intravenous drug use.
Blood transfusions and other transplants.

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97
Q

What are the three stages of syphilis infection?

A

Primary syphilis.
Secondary syphilis.
Tertiary syphilis.

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98
Q

What are the clinical features of primary syphilis?

A

Chancre.

Local non-tender lymphadenopathy.

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99
Q

Syphilis: What is chancre?

A

A painless ulcer at the site of contact, usually genitals.

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100
Q

What are the clinical features of secondary syphilis?

A

Systemic features… fever, lymphadenopathy, maculopapular rash, buccal ‘snail track’ ulcers and condylomata lata.

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101
Q

Syphilis: Where does maculopapular rash typically affect?

A

Trunk, palms and soles.

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102
Q

Syphilis: What are condylomata lata?

A

Painless, wart-like lesions on genitals.

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103
Q

What are the clinical features of tertiary syphilis?

A

Gummas.
Aortic aneurysms.
Neurosyphilis.

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104
Q

Syphilis: What are gummas?

A

Granulomatous skin, organ and bone lesions.

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105
Q

What is neurosyphilis?

A

Can occur at any stage of infection if the infection reaches the CNS. Features: headache, altered behaviour, dementia, paralysis, tabes dorsalis and Argyll-Robertson pupil.

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106
Q

Neurosyphilis: What is an Argyll-Robertson pupil?

A

Accommodation reflex present, pupillary reflex absent.

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107
Q

How is diagnosis of syphilis made?

A

Serology (cardiolipin tests and treponemal-specific antibody tests).
Microscopic examination of infected tissue.

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108
Q

What is the management of syphilis?

A

Deep intramuscular benzylpenicillin. Refer to genito-urinary medicine for full screening for other STIs.

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109
Q

What is measles?

A

A highly infectious disease caused by the measles virus.

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110
Q

What are the stages of measles presentation?

A

Prodromal symptoms followed by general presentation.

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111
Q

What are the prodromal features of measles?

A

Cough, coryza and conjunctivitis.

Remember: Three Cs.

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112
Q

What are the clinical features of measles presentation?

A

High fever, maculopapular rash (starts behind ears and spreads to body) and Koplik spots.

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113
Q

Describe the pathognomic feature of measles.

A

Koplik spots - white lesions on the buccal mucosa.

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114
Q

Give three complications of measles.

A

Otitis media (most common).
Pneumonia (most common cause of death).
Diarrhoea.

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115
Q

What is the management of measles?

A

Supportive (nutrition and hydration). Paracetamol and ibuprofen can provide symptomatic relief.

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116
Q

What is the infective period of measles?

A

Lasts from prodrome until four days after the rash starts.

117
Q

What are the public health implications of measles infection?

A

Measles is a notifiable disease - notify PHE.
Children should stay away from school until four days after initial development of rash and avoid susceptible people.
Offer measles vaccine to any non-vaccinated contacts.

118
Q

When is measles immunised against?

A

Part of the MMR vaccine given at one year (first dose) and three years four months (second dose).

119
Q

Scarlet fever is caused by infection of what pathogen?

A

Group A haemolytic streptococci such as Streptococcus pyogenes.

120
Q

What age group is most commonly affected by scarlet fever?

A

2-6 years.

121
Q

How is scarlet fever spread?

A

Respiratory route (coughing, sneezing).

122
Q

What are the clinical features of scarlet fever?

A

Fever, headache, sore throat, strawberry tongue and rash.

123
Q

How does a measles rash spread (where does it start)?

A

Starts behind ears and spreads to the body.

124
Q

Describe the rash associated with scarlet fever.

A

Fine punctuate erythema with sandpaper texture.

125
Q

How does a scarlet fever rash spread (where does it start)?

A

Starts on the torso and spreads out to the arms and legs… sparing the palms and soles.

126
Q

How is scarlet fever diagnosed?

A

Clinically. Confirm with throat swab and culture (don’t delay treatment).

127
Q

How is scarlet fever treated?

A

Antibiotics - oral penicillin V for 10 days.

128
Q

What are the public health implications of scarlet fever infection?

A

Notifiable disease - inform PHE.

129
Q

What are the clinical features of rubella?

A

Pink maculopapular rash.

Suboccipital and post auricular lymphadenopathy.

130
Q

How does the rash of rubella spread (where does it start)?

A

Starts on the face and spreads to the whole body.

131
Q

When does the rash associated with rubella fade?

A

Often fades after three days.

132
Q

What is the infective period of rubella?

A

7 days before symptoms until 4 days after rash onset.

133
Q

When is rubella immunised against?

A

Part of the MMR vaccine given at one year (first dose) and three years four months (second dose).

134
Q

When is scarlet fever immunised against?

A

Scarlet fever is not a part of the immunisation programme.

135
Q

What are the risks of maternal rubella infection during pregnancy?

A

Development of congenital rubella syndrome.

136
Q

At what gestation is the greatest risk for the development of congenital rubella syndrome?

A

First twenty weeks of pregnancy (especially first ten weeks).

137
Q

What are features of congenital rubella syndrome?

A

Congenital deafness.
Congenital cataracts.
Congenital heart disease (patent ductus arteriosus, pulmonary stenosis).
Learning disability.

138
Q

How can congenital rubella syndrome be prevented?

A

MMR immunisation before pregnancy (do not give MMR during pregnancy as it is a live vaccine).

139
Q

Hand, foot and mouth disease is most commonly caused by what pathogen?

A

Coxsackie A16.

140
Q

What are clinical features of hand, foot and mouth disease?

A

Mild systemic upset (sore throat, fever), oral ulcers, vesicles on the palms and soles of the feet.

141
Q

What is the management of hand, foot and mouth disease?

A 
Supportive management (hydration, analgesia). 
Stay away from school if unwell until they feel better.
142
Q

Erythema infectiosum is also referred to as what?

A

Slapped cheek syndrome.

143
Q

What pathogen causes erythema infectiosum / slapped cheek syndrome?

A

Parvovirus B19.

144
Q

What is the presentation of erythema infectiosum?

A

Lethargy, fever, headache.

‘Slapped cheek’ (diffuse, bright red cheeks) rash.

145
Q

How does the rash in erythema infectiosum spread?

A

From the cheek to the proximal arms and extensor surfaces.

146
Q

What is the management of erythema infectiosum?

A

Supportive - left-liming condition.

147
Q

Give four potential complications of parvovirus B19 infection in pregnancy.

A

Miscarriage.
Fetal anaemia.
Hydrops fetalis.
Mirror syndrome.

148
Q

Parvovirus B19 infection in pregnancy: Describe how fetal anaemia can develop.

A

Infection of erythroid progenitor cells in bone marrow and liver leads to production of abnormal RBCs which have a shorter lifespan = anaemia.

149
Q

Parvovirus B19 infection in pregnancy: What is Hydrops Fetalis?

A

Anaemia leads to increased demand for blood causing heart failure and subsequently oedema.

150
Q

Parvovirus B19 infection in pregnancy: What is mirror syndrome?

A

A pre-eclampsia like syndrome of hydrops fetalis, placental oedema and oedema in the mother. Hypertension and proteinuria on investigation.

151
Q

Roseola infantum is caused by what pathogen?

A

Human herpes virus 6 (HHV6).

152
Q

What age group is typically affected by roseola infantum?

A

Aged 6 months to 2 years.

153
Q

What is the presentation of roseola infantum?

A

High fever that lasts a few days followed by maculopapular rash which starts on the trunk and spreads to the limbs.
Other features include Nagayama spots, diarrhoea and cough.
Febrile convulsions occur in 10-15%.

154
Q

What pathogen causes chickenpox?

A

Human herpes virus 3 (varicella zoster virus).

155
Q

What is the presentation of chickenpox?

A

Fever followed by an itchy rash (macular then papular then vesicular).

156
Q

How does the rash associated with chickenpox spread?

A

Starts on the head/trunk and spreads to the rest of the body.

157
Q

What is the management of chickenpox?

A

Supportive. Consider topical calamine lotion to provide relief from itching.

158
Q

How long should children with chickenpox be excluded from school?

A

Until all lesions have crusted over.

159
Q

Give an example of a (relatively) common complication of chickenpox?

A

Secondary bacterial infection.

160
Q

How should immunosuppressed children who develop chickenpox be managed?

A

Consider for intravenous acyclovir.

161
Q

What are the two types of necrotising fasciitis?

A

Type 1 - missed anaerobes and aerobes.

Type 2 - Streptococcus pyogenes.

162
Q

What are the clinical features of necrotising fasciitis?

A

Acute onset, pain (extremely tender), swelling, erythema. Systemic: fever, tachycardia.

163
Q

What is the most common pre-existing condition for people who develop necrotising fasciitis?

A

Diabetes mellitus.

164
Q

What are risk factors for the development of necrotising fasciitis?

A

Recent trauma, burns or soft tissue infections.
Intravenous drug use.
Immunosuppression.

165
Q

What is the management of necrotising fasciitis?

A

Urgent surgical debridement.

Intravenous antibiotics.

166
Q

What is congenital varicella syndrome?

A

A condition that might occur if a pregnant person develops chickenpox in the first 28 weeks of gestation.

167
Q

What are features of congenital varicella syndrome?

A

Fetal growth restriction, microcephaly, hydrocephalus, learning disability, limb hypoplasia and skin changes (in specific dermatomes).

168
Q

What is the management for pregnant people who are exposed to chickenpox?

A

Give intravenous varciella immunoglobulins within ten days of exposure.
If they develop rash and are > 20 weeks gestation give oral aciclovir within 24 hours.

169
Q

What is erysipelas?

A

A localised skin infection caused by Streptococcus pyogenes. It is a more superficial, limited version of cellulitis.

170
Q

What is the treatment of erysipelas?

A

Flucloxacillin.

171
Q

What is Lyme disease?

A

A disease caused by the spirochaete Borrelia burgdorferi.

172
Q

Lyme disease is spread by what mechanism?

A

Ticks (parasitic arachnids that feed on blood of mammals and birds).

173
Q

When do ‘early features’ present in Lyme disease?

A

Within 30 days.

174
Q

What are the ‘early features’ of Lyme disease?

A

Erythema migrans, headache, lethargy, fever and arthralgia.

175
Q

Lyme disease: What is erythema migrans?

A

Bulls-eye rash at the site of the tick bite that develops 1-4 weeks after initial bite.

176
Q

What are ‘late features’ of Lyme disease?

A 
Cardiovascular complications (heart block, pericarditis, myocarditis).
Neurological complications (facial nerve palsy, radicular pain, meningitis).
177
Q

How is a diagnosis of Lyme disease made?

A

Clinically if they have erythema migrans… start antibiotic treatment.

178
Q

What is the first-line investigation of Lyme disease if erythema migrans isn’t present?

A

Borrelia burgdorferi antibodies.

179
Q

What is the treatment of Lyme disease?

A

Doxycycline in early disease.

Ceftriaxone in disseminated disease.

180
Q

How is mumps spread?

A

Respiratory droplets.

181
Q

What is the presentation of mumps?

A

Initial flu-like illness followed by the development of fever, myalgia, lethargy, reduced appetite and headache. Followed by parotitis.

182
Q

What is the characteristic feature of mumps?

A

Parotitis - parotid gland inflammation/swelling that typically develops from unilaterally to bilaterally.

183
Q

How is diagnosis of mumps confirmed?

A

PCR testing on a saliva swab.

184
Q

What is the management of mumps?

A

Supportive - self-limiting condition.

Inform PHE.

185
Q

How is mumps vaccinated against?

A

MMR vaccine receive at one year (first dose) and three years four months (second dose).

186
Q

What is Kawasaki disease?

A

A systemic vasculitis.

187
Q

What age group are most commonly affected by Kawasaki disease?

A

Under two years.

188
Q

What are the diagnostic criteria for Kawasaki disease?

A

Fever (> 39º) for at least five days with four of the following:
Maculopapular rash.
Conjunctivitis.
Mucous membrane changes (e.g. strawberry tongue).
Cervical lymphadenopathy.
Extremity changes (erythema of palms/sole, desquamation of fingertips/toes).

189
Q

What is the most common complication of Kawasaki disease?

A

Coronary artery aneurysms.

190
Q

Kawasaki disease: How should potential coronary artery aneurysms be investigated?

A

Transthoracic echocardiography.

191
Q

What is first-line treatment of Kawasaki disease?

A

High dose intravenous immunoglobulin within first ten days.

192
Q

How can Kawasaki disease be treated (other than immunoglobulin therapy)?

A

Aspirin given to reduce the risk of thrombosis.

193
Q

Kawasaki: What complication may occur as a result of aspirin use?

A

Reye’s syndrome.

194
Q

What causes toxic shock syndrome?

A

Toxin secreting bacteria such as Streptococcus pyogenes or Staphylococcus aureus.

195
Q

What is the presentation of toxic shock syndrome?

A

Fever, diarrhoea and erythematous rash that occurs three days following a minor burn.

196
Q

What is leprosy?

A

A granulomatous disease primarily affecting the peripheral nerves of the skin.

197
Q

What pathogen causes leprosy?

A

Mycobacterium leprae.

198
Q

What is the presentation of leprosy?

A

Hypopigmented skin (typically buttocks, face and extensors surfaces of limbs) as well as sensory loss.

199
Q

What is the management of leprosy?

A

Rifampicin, dapsone and clofazimine.

200
Q

What pathogen causes Legionnaire’s disease?

A

Legionella pneumophilia.

201
Q

Legionnaire’s disease: Where does Legionella colonise?

A

Water tanks (including air conditioning units).

202
Q

What are the features of Legionnaire’s disease?

A

Flu-like symptoms (including fever), dry cough, relative bradycardia, confusion.

203
Q

What is found on investigation of Legionnaire’s disease?

A

Lymphopaenia.
Hyponatraemia.
Deranged LFTs.
Pleural effusions.

204
Q

How is Legionnaire’s disease diagnosed?

A

Urinary antigen.

205
Q

How do you treat Legionnaire’s disease?

A

Erythromycin or clarithromycin.

206
Q

What is Chagas’ disease?

A

A tropical disease caused by Trypanosoma cruzi.

207
Q

What are the features of Chagas’ disease?

A

Fever, swollen lymph nodes and headaches.

208
Q

What is schistosomiasis?

A

Parasitic flatworm infection.

209
Q

What are the features of schistosomiasis?

A

Swimmer’s itch, fever, urticaria/angioedema, arthralgia, myalgia, cough, diarrhoea, eosinophilia.

210
Q

Schistosomiasis: What is swimmer’s itch?

A

Dermatitis, allergic immune reaction.

211
Q

What pathogen causes malaria?

A

Plasmodium protozoa (of which there are four disease-causing species).

212
Q

What species of Plasmodium is most common and most lethal?

A

Plasmodium falciparum.

213
Q

How is malaria spread?

A

Malaria is spread by the female Anopheles mosquito.

214
Q

How does the female Anopheles mosquito spread malaria?

A

The mosquito draws infected blood from a human/animal.
Malaria reproduces in the gut of the mosquito to produce sporozoites (malaria spores).
The mosquito bites a human and injects sporozoites.
Sporozoites travel to the liver and becomes dormant (hypnozoites) or matures in the liver (merozoites).
Merozoites infect RBCs and reproduce over 48 hours.
RBCs rupture releasing more merozoites into the blood.
Haemolytic anaemia develops.

215
Q

Malaria causes what type of anaemia?

A

Haemolytic anaemia.

216
Q

What are non-specific clinical features of malaria?

A

Fever, rigors, malaise, sweats, myalgia, headache and vomiting.

217
Q

What signs on examination may be found in malaria?

A

Pallor.
Hepatosplenomegaly.
Jaundice.

218
Q

How is malaria diagnosed?

A

Malaria blood film - three samples sent over three consecutive days. Blood film will show parasites, concentration and type.

219
Q

What is the treatment of malaria?

A

Artesunate or

Quinine dihydrochloride.

220
Q

What are potential complications of falciparum malaria?

A 
Cerebral malaria. 
Seizures. 
Reduced consciousness. 
Pulmonary oedema. 
AKI. 
DIC. 
Severe haemolytic anaemia. 
Multi-organ failure.
221
Q

What prophylaxis is available for malaria?

A

Advise vigilance. Use mosquito spray, mosquito nets when sleeping and antimalarial medications such as malarone.

222
Q

Malaria: Give examples of antimalarial medications.

A

Malarone

Doxycycline.

223
Q

What is the most prevalent sexually transmitted infection in the UK?

A

Chlamydia.

224
Q

What pathogen causes chlamydia?

A

Chlamydia trachomatis.

225
Q

How is chlamydia transmitted?

A

Unprotected vaginal, anal or oral sex and by sharing unwashed sex toys.

226
Q

How do most cases of chlamydia present?

A

Most cases are asymptomatic.

227
Q

What is the symptomatic presentation of chlamydia in women?

A

Discharge, bleeding, pelvic pain, dysuria and dyspareunia.

228
Q

What are potential complications of chlamydia infection in women?

A

Pelvic inflammatory disease, endometriosis, increased risk of ectopic pregnancy, infertility.

229
Q

What is the symptomatic presentation of chlamydia infection in men?

A

Urethral discharge/discomfort and dysuria.

230
Q

What are potential complications of chlamydia infection in men?

A 
Epididymo-orchitis (testicular pain, scrotal swelling). 
Reactive arthritis (arthralgia).
231
Q

What is the investigation of choice for chlamydia in women?

A

Nuclear acid amplification test (NAAT) of endocervical swab (preferred) or vulvovaginal swab.

232
Q

What is the investigation of choice for chlamydia in men?

A

Nuclear acid amplification test (NAAT) of first-catch urine sample.

233
Q

When should tests for chlamydia be performed after potential exposure?

A

At least two weeks after potential exposure.

234
Q

What is the first-line management of chlamydia?

A

Seven-day course of 100mg doxycycline.

Contact tracing.

235
Q

What is the management of chlamydia in pregnant women?

A

Azithromycin, erythromycin or amoxicillin (doxycycline is teratogenic).
Contact tracing.

236
Q

What is gonorrhoea?

A

A sexually transmitted infection.

237
Q

What pathogen causes gonorrhoea?

A

Neisseria gonorrhoea.

238
Q

Where can gonorrhoea occur?

A

Any mucous membrane with a columnar epithelium (endocervix, urethra, rectum, conjunctiva, pharynx).

239
Q

Gonorrhoea: What is the presentation of genital infection in men?

A

Odourless, purulent urethral discharge (green/yellow), dysuria, testicular pain/swelling.

240
Q

Gonorrhoea: What is the presentation of genital infection in women?

A

Odourless, purulent discharge (green/yellow), dysuria, pelvic pain.

241
Q

How is gonorrhoea investigated?

A

Nuclear acid amplification test with endocervical swab (women) or first-catch urine (men).

242
Q

How is gonorrhoea investigated in men who have sex with men?

A

NAAT of rectal swabs and pharyngeal swabs.

243
Q

What follow-up investigation should be performed if NAAT is positive for gonorrhoea?

A

Charcoal endocervical / urethral swabs.

244
Q

Why should charcoal swabs be performed in gonorrhoea following positive NAAT?

A

NAAT tests for the presence of DNA/RNA of gonorrhoea and can’t inform antibiotic choice. Charcoal swabs are used for culture and assessment of antibiotic sensitivities.

245
Q

What is the management of gonorrhoea?

A

Follow local and national antibiotic prescribing guidelines. If no sensitivities are available give intramuscular ceftriaxone.

246
Q

What follow-up is required following gonorrhoea treatment?

A

Follow-up NAAT to ensure eradication given antibiotic resistance.

247
Q

What is a potential complication of untreated gonococcal infection?

A

Disseminated gonococcal infection (DGI) due to haematogenous spread of the mucosal infection to the skin and joints.

248
Q

Gonorrhoea: What are features of disseminated gonococcal infection?

A

Tenosynovitis, polyarthralgia, migratory polyarhtritis, dermatitis.

249
Q

What is trichomoniasis?

A

A sexually transmitted infection.

250
Q

What pathogen is responsible for causing trichomoniasis?

A

Trichomonas vaginalis.

251
Q

What is the presentation of trichomoniasis in men?

A

Usually asymptomatic. May feature balanitis.

252
Q

What is the presentation of trichomoniasis in women?

A

Offensive (‘fishy’), frothy, yellow/green vaginal discharge.
Vulvovaginitis.
Strawberry cervix.

253
Q

What does vaginal pH reveal in trichomoniasis?

A

Vaginal pH > 4.5

254
Q

How is diagnosis of trichomoniasis confirmed?

A

Charcoal swabs (low vaginal swab in females, urethral swab in males). Microscopy shows motile trophozoites.

255
Q

What is the treatment of trichomoniasis?

A

Oral metronidazole.

256
Q

Trichomoniasis increases the risk of development of what conditions?

A

HIV (by damaging mucosa).
Bacterial vaginosis.
Pelvic inflammatory disease.
Cervical cancer.

257
Q

What advice should be given to patients prescribed metronidazole?

A

Avoid alcohol (can = nausea, vomiting, flushing and in more severe cases seizures).

258
Q

What is bacterial vaginosis?

A

Overgrowth of predominantly anaerobic bacteria. It is not a sexually transmitted infection but is almost exclusively seen in sexually active women.

259
Q

What are risk factors for developing bacterial vaginosis?

A

Multiple sexual partners.
Vaginal douching / excessive cleaning.
Antibiotics.

260
Q

Describe the pathophysiology of bacterial vaginosis.

A

Occurs due to loss of lactobacilli (the main component of healthy vaginal bacterial flora). Lactobacilli produce lactic acid to keep vaginal pH low (< 4.5). Loss of lactobacilli increases pH and the more alkaline environment allows anaerobic bacteria to multiply.

261
Q

What bacteria are present in bacterial vaginosis?

A

Gardnerella vaginalis among others.

262
Q

What is the presentation of bacterial vaginosis?

A

Fishy-smelling, thin, white/grey vaginal discharge.

Pain and irritation NOT typically associated (consider other causes or co-occurring infection).

263
Q

What investigations are performed in bacterial vaginosis?

A

Vaginal pH.
Charcoal swab and microscopy.
Whiff test.

264
Q

What does vaginal pH reveal in bacterial vaginosis?

A

pH > 4.5

265
Q

What does charcoal swab and microscopy reveal in bacterial vaginosis?

A

Clue cells on microscopy.

266
Q

What is the management of bacterial vaginosis?

A

5-7 day course of oral metronidazole.

267
Q

What complications are associated with bacterial vaginosis in pregnancy?

A

Preterm labour.
Low birth weight.
Chorioamnionitis.
Late miscarriage.

268
Q

Genital warts are caused by what pathogen?

A

Human papilloma virus (most commonly types 6 and 11).

269
Q

What are the features of genital warts?

A

Small (2-5mm), slightly pigmented, fleshy protuberances.
Bleeding.
Itching.

270
Q

What is the management of genital warts?

A 
Topical podophyllum (multiple, non-keratinised warts). 
Cryotherapy (solitary, keratinised warts).
271
Q

How is herpes simplex virus transmitted?

A

Direct contact with affected mucous membranes or viral shedding in mucous secretions.

272
Q

What are the two strain of herpes simplex virus?

A

HSV-1

HSV-2

273
Q

What presentation is HSV-1 most associated with?

A

Cold sores (associated with temporal nerve ganglion).

274
Q

What presentation is HSV-2 most associated with?

A

Genital herpes (associated with sacral nerve ganglion).

275
Q

What are the clinical features of genital herpes?

A

Genital ulcers/blisters, neuropathic pain (tingling, shooting, burning), flu-like symptoms (fatigue, headaches), dysuria and inguinal lymphadenopathy.

276
Q

What is the treatment of genital herpes?

A

Oral aciclovir.

277
Q

What is the management of pregnant women with genital herpes?

A

Elective Caesarean section at term.

278
Q

What is vaginal candidiasis?

A

Thrush - an extremely common condition.

279
Q

What is the likely causative organism in vaginal candiasis?

A

Candida albicans.

280
Q

What factors increase the risk of developing vaginal candidiasis?

A

Diabetes mellitus.
Antibiotic use.
Immunosuppression.
Pregnancy.

281
Q

What is the presentation of vaginal candidiasis?

A

Thick, cottage cheese-like vaginal discharge (non-offensive) with vulval and vaginal itching/discomfort.
Other features include dysuria, dyspareunia and vulval erythema.

282
Q

What investigations are performed in vaginal candidiasis?

A

Vaginal pH (will be < 4.5 in thrush).

283
Q

What is the treatment of vaginal candidiasis?

A

Clotrimazole pessary.

Clotrimazole cream.

284
Q

What is pelvic inflammatory disease?

A

Infection of the upper genital tract (uterus and/or fallopian tubes).

285
Q

What causes pelvic inflammatory disease?

A

Usually the result of an ascending infection from the endocervix that can be caused by uterine instrumentation (insertion of IUCD).

286
Q

What pathogen most commonly causes pelvic inflammatory disease?

A

Chlamydia trachomatis.

287
Q

What is the presentation of pelvic inflammatory disease?

A

Deep pelvic pain (bilateral), abnormal vaginal discharge, abnormal bleeding, dyspareunia, fever and dysuria.

288
Q

What are risk factors for the development of pelvic inflammatory disease?

A

Young age.
Multiple sexual partners.
Recent partner change.
Non-use of condoms.

289
Q

How to manage pelvic inflammatory disease?

A 
Give intramuscular ceftriaxone (gonorrhoea cover). 
Give doxycycline (chlamydia cover). 
Give metronidazole (bacterial vaginosis cover).

Finals (11 decks)

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