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Passmedicine - Infection Flashcards

1
Q

What kind of bacteria is staph aureus?

A

Facultative anaerobe
Gram positive cocci
Catalase +ve

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2
Q

How do most staph aureus strains have resistance to penicillin?

A

Beta-lactamase production

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3
Q

How is resistance to methiillin usually mediated by?

A

Mec operon (penicillin binding protein is altered to be resistant to methicillin)

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4
Q

What kind of bacteria is strep pyogenes?

A

Gram positive
Chain forming
Lancefield group A (produces beta-haemolysis on blood agar)
Catalase negative

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5
Q

What superantigens can strep pyogenes release? What can this superantigen result in?

A

Pyogenic exotoxin A which –> scarlet fever

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6
Q

What kind of antibiotic is used for strep pyogenes infections?

A

Penicillin/macrolides

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7
Q

What kind of bacteria is E. coli?

A

Gram negative rod

Facultative anaerobe, non-sporing

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8
Q

What is the mechanism of action of enterotoxigenic E. coli?

A

Produces enterotoxin that results in a large volume fluid secretion into the gut (via cAMP activation)

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9
Q

What is the mechanism of action of enteropathogenic E. coli?

A

Binds to intestinal cells + causes structural damage –> large volume diarrhoea and fever

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10
Q

What kind of bacteria is c. jejuni?

A

Gram negative, non-sporulating

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11
Q

What kind of symptoms does c. jejuni infection cause?

A

Diffuse diarrhoea

RIF pain

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12
Q

What antibiotic should be given for c. jejuni infection?

A

Usually self-limiting so does not require antibiotics

Quinolones often rapidly effective

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13
Q

What kind of bacteria is H. pylori?

A

Gram negative, helix shaped rod, microaerophilic

Flagellated

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14
Q

What enzyme do h. pylori produce?

A

Hydrogenase which derives energy from hydrogen released by intestinal bacteria

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15
Q

How can h. pylori cause ulcers?

A

Secretes urase which breaks down gastric urea –> CO2 and ammonia –> bicarbonate which neuralises gastric acid (so stomach produces more acid)

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16
Q

Where does h. pylori most commonly colonate?

A

Gastric antrum

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17
Q

What patients get gastric ulcers + which patients get duodenal ulcers with h. pylori infections?

A

If colonises antrum - irritation leads to increased gastrin release + higher levels of gastric acid –> duodenal ulcers

More diffuse infection –> gastric acid levels lower and ulcers develop by local tissue damage from h. pylori –> gastric ulcers

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18
Q

How is h. pylori infection diagnosed?

A

Serology

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19
Q

What is the standard active TB therapy?

A

First 2 months:
rifampicin, isoniazid, pyrazinamide, ethambutol

Next 4 months:
rifampicin, isoniazid

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20
Q

What is the treatment of latent TB?

A

3 months isoniazid (with pyridoxine) + rifampicin OR 6 months of isoniazid (with pyridoxine)

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21
Q

What is the treatment of meningeal TB?

A

Treat for 12 months with steroids

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22
Q

Who may have to undergo directly observed therapy (with 3x weekly dosing regimen) for TB?

A

Homeless with active TB
Patients who are likely to have poor concordance
All prisoners with active/latent TB

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23
Q

Visual acuity should be checked before starting what TB drug?

A

Ethambutol

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24
Q

What are features of genital herpes?

A

Painful genital ulceration

Urinary retention may occur

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25
Q

How is genital herpes managed?

A

Oral aciclovir

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26
Q

What is the management of primary attack of herpes during pregnant?

A

Elective c-section >28 weeks

Supressive oral aciclovir until delivery

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27
Q

How is transmission of herpes to a baby in a women with recurrent herpes minimised?

A

Treatment with suppressive therapy until delivery

NB risk of transmission to baby is low

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28
Q

What is EBV aka?

A

Herpesvirus 4

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29
Q

What is the most common cause of infectious mononucleosis?

A

EBV

Less common causes include CMV, HHV-6

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30
Q

What classic triad of symptoms is seen in 98% of IM patients?

A

Sore throat
Pyrexia
Lympadenopathy

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31
Q

What other features can be seen in IM?

A

Malaise, anorexia, headache
Palatal petechiae
Splenomegaly (may predipose to splenic rupture)
Hepatitis
Lymphocytosis
Haemolytic anaemia secondary to cold agglutins
Maculopapular, pruritic rash develops in 99% of IM patients who take ampicillin/amoxicillin

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32
Q

How long do symptoms of IM typically take to resolve?

A

2-4 weeks

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33
Q

How is IM diagnosed?

A

Heterophil antibody test (monospot)

NICE recommend this + FBC in 2nd week of illness to confirm diagnosis

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34
Q

How is IM managed?

A

Supportive - rests, avoid alcohol, simple analgesia, hydration

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35
Q

What must those with IM avoid?

A

Contact sports for 8 weeks after having glandular fever to reduce risk of splenic rupture

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36
Q

List the live attenuated vaccines

A 
BCG
measles, mumps, rubella (MMR)
influenza (intranasal)
oral rotavirus
oral polio
yellow fever
oral typhoid
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37
Q

List the inactivated vaccines

A

rabies
hepatitis A
influenza (intramuscular)

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38
Q

List the toxoid vaccines (inactivated toxins)

A

tetanus
diphtheria
pertussis

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39
Q

What is a subunit vaccine?

A

Only part of the pathogen is used to generate an immunogenic response

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40
Q

What is a conjugate vaccine?

A

A vaccine that links the immunogenic bacterial polysaccharide outer coats to the proteins to make them more immunogenic

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41
Q

List some conjugate vaccines

A

Pneumococcus
Haemophilus
Meningococcus

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42
Q

List some subunit vaccines

A

Hep B

HPV

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43
Q

What does the Hep B vaccine contain?

A

HbsAg adsorbed onto aluminium hydroxide adjuvant

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44
Q

What groups are at risk from HIV?

A

IVDAs

Those who received a blood transfusion prior to 1991

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45
Q

What kind of virus is hep C?

A

RNA flavivirus

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46
Q

What is the risk of transmission of hep C during a needlestick injury?

A

2%

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47
Q

What is the risk of vertical transmission of hep C?

A

6%

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48
Q

Is breastfeeding CI in hep C positive mothers?

A

No

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49
Q

What are the features of hep C infection?

A

Usually asymptomatic

May experience: rise in aminotransferases/jaundice, fatigue, arthalgia

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50
Q

What is the investigation of choice to diagnose acute hep C infection?

A

HCV RNA

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51
Q

What is the outcome of a hep C infection?

A

15-45% clear it after an acute infection

55-85% go on to develop a chronic infection

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52
Q

Define chronic hepatitis C

A

Persistence of HCV RNA in the blood for 6 months

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53
Q

What are potential complications of chronic hep C?

A 
Arthalgia, arthritis
Sjogren's
Cirrhosis
Heptocellular cancer
Cryoglobulinaemia (usually type II)
Porphyria cutanae tarda
Membranoproliferative GN
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54
Q

How is chronic hep C infection treated?

A

Depends on viral genotype (test prior)

Combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin

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55
Q

What are SEs of ribavirin?

A

Haemolytic anaemia
Cough
Teratogenic (do not become pregnant <6m after use)

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56
Q

What is the best way to assess response to treatment of hep C infection?

A

Viral load

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57
Q

What types of HPV generally cause genital warts?

A

6 and 11

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58
Q

How are genital warts treated?

A

First line
Topical podophyllum - multiple/non-keratinised
Cryotherapy - solitary/keratinised

Second line
Imiquimod (topical cream)

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59
Q

What is the most common cause of oesophagitis in HIV patients?

A

Oesophageal candidiasis

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60
Q

What CD4 count is oesophagal candidiasis typically seen in?

A

<100

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61
Q

What are typical symptoms of oesophageal candidiasis?

A

Dysphagia

Odynophagia

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62
Q

How is oesophageal candidiasis treated?

A

Fluconazole, itraconazole

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63
Q

What kinds of infections can E. coli cause?

A

Diarrhoea
UTI
Neonatal meningitis

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64
Q

What are the different E. coli antigens
A - O
B - K
C - H?

A

A - O = lipopolysaccharide layer
B - K = capsule (usually what causes neonatal meningitis)
C - H = flagellin

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65
Q

What does mycoplasma pneumoniae tend to cause?

A

An atypical pneumonia in younger patients

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66
Q

What are characteristic complications associated with mycoplasma pneumonia?

A 
Erythema multiforme 
Cold autoimmune haemolytic anaemia
Meningoencephalitis, GBS
Bullous myringitis
Pericarditis/myocarditis
GI - hepatitis/pancreatitis
Acute GN
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67
Q

What are features typical of a mycoplasma pneumonia?

A

Prolonged + gradual onset

Flu like symptoms preceding a dry cough

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68
Q

What do you see on CXR in mycoplasma pneumonia?

A

Bilateral consolidation

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69
Q

What is bullous myringitis?

A

Painful vesicles on the tympanic membrane

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70
Q

How is mycoplasma pneumonia generally diagnosed?

A

Mycoplasma serology

also have a positive cold agglutination test

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71
Q

How is mycoplasma pneumonia managed?

A

Doxycycline or macrolide

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72
Q

What kind of bacteria are salmonella spp?

A

Aerobic, gram negative robs

Remember - these are not normally gut commensals

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73
Q

What bacteria causes typhoid?

A

Salmonella typhi

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74
Q

What bacteria causes paratyphoid?

A

Salmonella paratyphi

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75
Q

How is typhoid transmitted?

A

Faecal-oral

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76
Q

What are the clinical features of typhoid/paratyphoid?

A

Systemic upset (headache, fever, arthalgia)
Relative bradycardia
Ab pain, distension
Constipation (more common in typhoid) or diarrhoea
Rose spots on the trunk (more common in paratyphoid)

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77
Q

What are complications of typhoid/paratyphoid?

A 
Osteomyelitis (esp. in sickle cell disease) 
GI bleed/perforation 
Meningitis
Cholecystitis
Chronic carriage
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78
Q

What antibiotic can be used to treat typhoid/paratyphoid?

A

Ciprofloxacin

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79
Q

What is the first line treatment of syphillis?

A

IM benzylpen

Alt: doxycycline

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80
Q

What reaction is sometimes seen after treatment of syphillis?

A

Jarisch-Herxheimer
(fever, tachycardia, rash after first dose)
Thought to be due to release of endotoxins following bacterial death (occurs few hours after treatment)

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81
Q

How is Jarisch-Herxheimer treated?

A

Antipyretics

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82
Q

Following splenectomy, what infections are patients particularly at risk of?

A

Pneumococcus
Haemophilus
Meningococcus

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83
Q

When should patients due to undergo splenectomy receive their vaccinations?

A

2 weeks prior to the operation

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84
Q

What vaccinations should those undergoing splenectomy receive?

A

Hib, meningitis A and C
Annual flu jab
Pneumococcal every 5 years

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85
Q

What antibiotic prophylaxis should those who have undergone splenectomy receive?

A

Penicillin V

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86
Q

What are indications for splenectomy?

A

Trauma
Spontaneous rupture, e.g. EBV
Hypersplenism - hereditary spherocytosis, elliptocytosis etc..
Malignancy - lymphoma/leukaemia
Splenic cysts, hydatid cysts, splenic abscesses

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87
Q

What are complications of splenectomy?

A

Haemorrhage
Pancreatic fistula (due to damage to pancreatic tail)
Thrombocytosis
Encapsulated bacteria infection (e.g. strep pneumoniae, Hib, Neisseria meningitidis)

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88
Q

What changes will occur in the body post-splenectomy?

A

Platelets rise
Howell-jolly bodies appear
Target cells, Pappenheimer bodies

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89
Q

Post-splenectomy sepsis typically occurs with what organisms?

A

Encapsulated organisms

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90
Q

What pathogen causes bronchiolitis?

A

RSV

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91
Q

What pathogen causes croup?

A

Parainfluenza virus

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92
Q

What pathogen causes the common cold?

A

Rhinovirus

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93
Q

What pathogen causes flu?

A

Influenza

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94
Q

What pathogen most commonly causes community acquired pneumonia?

A

Strep pneumoniae

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95
Q

What pathogen most commonly causes bronchiectasis exacerbations?

A

Hib

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96
Q

What pathogen causes acute epiglottitis?

A

Hib

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97
Q

What pathogen causes pneumonia, especially following flu?

A

Staph aureus

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98
Q

What organisms most commonly cause an atypical pneumonia?

A

Mycoplasma pneumoniae - flu symptoms –> dry cough

Legionella pneumoniae - causes dry cough, lymphopenia, deranged LFTs, hyponatraemia

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99
Q

What classically spreads legionella?

A

Air conditioning systems

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100
Q

What is a common cause of pneumonia in HIV patients?

A

PJP

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101
Q

What are typical features of a PJP pneumonia?

A

Few chest signs, exertional SoB

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102
Q

What are typical features of pulmonary TB?

A

Cough
Night sweats
Weight loss

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103
Q

What is meant by a ‘notifiable disease’?

A

Disease that the proper officer at the local health protection team needs to be notified about

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104
Q

What are notable exceptions to notifiable diseases?

A

HIV

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105
Q

List 5 notifiable diseases

A 
Acute encephalitis
Acute infectious hepatitis
Acute meningitis
Acute poliomyelitis
Anthrax
Botulism
Brucellosis
Cholera
Diphtheria
Enteric fever (typhoid or paratyphoid fever)
Food poisoning
Haemolytic uraemic syndrome (HUS)
Infectious bloody diarrhoea
Invasive group A streptococcal disease
Legionnaires Disease
Leprosy
Malaria
Measles
Meningococcal septicaemia
Mumps
Plague
Rabies
Rubella
SARS
Scarlet fever
Smallpox
Tetanus
Tuberculosis
Typhus
Viral haemorrhagic fever (VHF)
Whooping cough
Yellow fever
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106
Q

What kind of virus is CMV?

A

Herpes virus

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107
Q

It is thought that ___% of people have been exposed to CMV virus, but it only causes disease in those who are…

A

50%

Immunocompromised, e.g. HIV/following organ transplant

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108
Q

What do cells infected with CMV look like?

A

Owl’s eye appearance due to intranuclear inclusion bodies

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109
Q

What are features of congenital CMV infection?

A 
Growth retardation 
Pinpoint petechial blueberry muffin skin lesions
Microencephaly
Sensorineural deafness
Encephalitis (seizures)
Hepatosplenomegaly
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110
Q

Who does CMV retinitis tend to develop in?

A

HIV patients with a low CD4 (<50)

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111
Q

How does CMV retinitis present?

A

Visual impairment, e.g. b blurred vision

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112
Q

What do you see on fundoscopy in CMV retinitis?

A

Multiple retinal haemorrhages and necrosis - pizza retina

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113
Q

What is the treatment of choice for CMV retinitis?

A

IV ganciclovir

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114
Q

What organism causes chancroid?

A

Haemophilus ducreyi

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115
Q

What are features of chancroid?

A

Painful genital ulcers (with sharply defined, ragged, undetermined border)
Unilateral, painful inguinal LN enlargement

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116
Q

What causes lymphogranuloma venereum?

A

Chlamydia trachomatis

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117
Q

What are the three stages of lymphogranuloma venereum?

A

1 - small painless pustule which later forms an ulcer
2 - painful inguinal lympadenopathy
3 - proctocolitis

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118
Q

How is LVG treated?

A

Doxycycline

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119
Q

What organisms typically cause cellulitis?

A

Strep pyogenes

Staph aureus

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120
Q

What are features of cellulitis?

A

Erythema, pain, swelling
Systemic upset, e.g. fever

Commonly occurs on shins

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121
Q

What classification is used to guide how we manage patients with cellulitis?

A

Eron

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122
Q

Eron I

A

No signs of systemic toxicity

No uncontrolled co-morbs

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123
Q

Eron II

A

Systemically unwell

Systemically well with co-morb

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124
Q

Eron III

A

Significant systemic upset, e.g. acute confusion, tachycardia, tachynoea, hypotension or unstable co-morbs

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125
Q

Eron IV

A

Sepsis or severe life-threatening infection, e.g. necrotizing fasciitis

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126
Q

What patients with cellulitis should be admitted for IV antibiotics?

A

Eron III or IV
Severe/rapidly deteriorating cellulitis, e.g. large areas of skin
Very young (<1y) or frail
Immunocompromised
Has significant lymphoedema
Has facial cellulitis/periorbital cellulitis

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127
Q

How are Eron II patients managed?

A

Can be treated with IV antibiotics in the community

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128
Q

How are all other patients (Eron I) with cellulitis managed?

A

Oral antibiotics

Flucloxacillin 1st line (clarithromycin, erythromycin (in pregnancy), doxcycline if penicillin allergic)

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129
Q

What antibiotic should be given to those with severe cellulitis?

A

Co-amoxiclav, cefuroxime, clindamycin, ceftriaxone

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130
Q

When is trimethoprim a risk for teratogenicity?

A

First trimester

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131
Q

What patients should be screened for MRSA?

A

All patients awaiting elective admissions

Emergency admission

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132
Q

How should a patient be screened for MRSA?

A

Nasal swab and skin lesions/wounds

Wipe inside rim of nose for 5 seconds

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133
Q

How is MRSA supressed from a carrier once identified?

A

Nose - mupirocin 2% in white soft paraffin tds for 5 days

Skin - chlorhexidine gluconate od 5 days (apply all over)

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134
Q

What antibiotics can be used to treat MRSA infections?

A

Vancomycin
Teicoplanin
Linezolid (reserve for resistant cases)

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135
Q

What organisms can cause community acquired pneumonia?

A

Strep pneumoniae
H. influenzae
Staph aureus
Viruses

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136
Q

What organism classically causes pneumonia in alcoholics?

A

Klebsiella pneumoniae

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137
Q

What are the characteristic features of a pneumococcal pneumoniae?

A

Rapid onset
High fever
Pleuritic chest pain
Herpes labialis

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138
Q

What causes kaposi’s sarcoma?

A

HHV-8

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139
Q

How does kaposi sarcoma present?

A

Purple papules/plaques on skin or mucosa which may ulcerate

Respiratory involvement may –> massive haemoptysis + pleural effusion

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140
Q

How is kaposi sarcoma treated?

A

Radiotherapy + resection

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141
Q

What causes amoebiasis?

A

Entamoeba histolytica

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142
Q

What kinds of syndromes can amoebiasis lead to?

A

Amoebic dysentry

Amoebic liver abscess

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143
Q

How is amoebic dysentry treated?

A

Metronidazole

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144
Q

What is an amoebic liver abscess classically like?

A

Single mass in right lobe filled with ‘anchovy sauce’

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145
Q

What are clinical features of an amoebic liver abscess?

A

Fever

RUQ pain

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146
Q

Give examples of tetracyclines

A

Doxycyline

Tetracycline

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147
Q

What is the mechanism of action of tetracyclines?

A

Protein synthesis inhibitors

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148
Q

What is the commonest mechanisms of resistance against tetracyclines?

A

Increased efflux of the bacteria by plasmid-encoded transport pumps, ribosomal protection

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149
Q

What are indications for tetracycline use?

A

Acne vulgaris
Lyme disease
Chlamydia
Mycoplasma pneumoniae

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150
Q

What are notable AEs associated with tetracyclines?

A

Discolouration of teeth - do not use before age 12
Photosensitivity
Anigioedema
Black hairy tongue

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151
Q

What are important CIs to the use of tetracyclines?

A

Pregnancy + breastfeeding due to discolouration of the neonates teeth

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152
Q

What malignancies are associated with EBV?

A

Burkitt’s lymphoma
Hodgkin’s lymphoma
Nasopharyngeal carcinoma
HIV-associated central nervous system lymphomas

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153
Q

What non-malignant condition is EBV associted with?

A

Hairy leukoplakia

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154
Q

What is leprosy?

A

Granulomatous disease primarily affecting the peripheral nerves and skin

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155
Q

What causes leprosy?

A

Mycobacterium leprae

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156
Q

What are the clinical features of leprosy?

A

Patches of hypopigmented skin typically affecting the buttocks, face, extensor surfaces of limbs
Sensory loss

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157
Q

What determines the type of leprosy a patient gets?

A

Low degree of cell mediated immunity –> lepromatous leprosy = extensive skin involvement, symmetrical nerve involvement

High degree of cell mediated immunity –> tuberculoid leprosy = limited skin disease, asymmetric nerve involvement

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158
Q

How is leprosy managed?

A

Triple therapy - rifampicin, dapsone, clofazimine

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159
Q

Gram positive cocci =

A

Staph, strep

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160
Q

Gram negative cocci =

A

Neisseria meningitis/gonorrhoeae

Moraxella catarrhalis

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161
Q

Gram positive bacilli =

A 
ABCD L
Actinomyces
Bacillus anthracis 
Clostridium
Diphtheria
Listeria monocytogenes
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162
Q

Gram negative rods =

A 
E. coli
H. influenzae
Pseudomonas aeruginosa
Salmonella spp.
Shigella spp.
C. jejuni
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163
Q

What diseases does parovirus B19 cause?

A

Erythema infectiosum (slapped cheek syndrome)

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164
Q

How does slapped cheek syndrome present?

A

Mild feverish illness +/- bright, red rash over the cheeks

Child feels better as rash appears

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165
Q

How long does the rash in slapped cheek syndrome tend to take to go away?

A

Usually peaks after a week and then fades

BUT for some months after, a warm bath, sunlight, heat/fever may trigger its recurrence

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166
Q

How is slapped cheek managed?

A

Usually self-limiting

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167
Q

Is school exclusion with slapped cheeky req?

A

No as once the rash appears the child is no longer infectious

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168
Q

In adults what can parovirus B19 cause?

A

An acute arthritis

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169
Q

What is the most important thing to remember about parovirus B19?

A

Can affect unborn baby in first 20 weeks

If women exposed before 20 weeks must have IgM and IgG checked

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170
Q

When is someone with parovirus B19 infectious?

A

3-5 days before the rash appears

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171
Q

How might parovirus B19 infection present in immunocompromised patients?

A

Pancytopenia

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172
Q

How might parovirus B19 infection present in sickle cell patients?

A

Aplastic crises (parovirus B19 supresses erythropoiesis for about a week)

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173
Q

What are the two types of necrotizing fasciitis?

A

1 - caused by mixed anaerobes + aerobes (often occurs post-surgery in DM) - most common

2 - strep pyogenes most common cause

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174
Q

What are the clinical features of necrotizing fasciitis?

A

Acute onset
Painful, erythematous lesion develops
Often presents as rapidly worsening cellulitis with pain out of keeping with physical features
Extremely tender over underlying tissue

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175
Q

How is necrotizing fasciitis managed?

A

Urgent surgical referral for debridement

IV antibiotics

176
Q

What is a spinal epidural abscess (SEA)?

A

Collection of pus superficial to the dura mater of the spinal cord

177
Q

Why is SEA an emergency?

A

Requires urgent treatment to avoid progressive spinal cord damage

178
Q

Define abscess

A

Collection of pus encapsulated by a pyogenic membrane

179
Q

How can bacteria enter the epidural space to cause SEA?

A

Contiguous spread from adjacent structures, e.g. discitis
Haematological spread, e.g. from bacteraemia from IVDU
Direct infection, e.g. post-spinal surgery

180
Q

What is a major risk factor for SEA?

A

Immunosupression, e.g. HIV, DM, alcoholism, chemotherapy, steroids etc.

181
Q

What organism most commonly is responsible for SEA?

A

Staph aureus

182
Q

How do patients with SEA typically present?

A

Fever
Back pain
Focal neurological deficits according to the segment of cord affected

183
Q

What investigations should be done in suspected SEA?

A

Bloods - inflammatory markers, HIV, Hep B, Hep C, coagulation, group and save
Blood cultures
Infection screen (incl. CXR and urine culture)
MRI whole spine

184
Q

Why do you need to MRI the whole spine in SEA?

A

Skip lesions may be present

185
Q

If the primary source of infection in SEA is not clear what further investigations may be required?

A

Dental x-rays, ECG etc.

186
Q

What is the management of SEA?

A

Long term broad spectrum antibiotics, later refined based on cultured results

Large/compressive abscess or significant neurological deficits/not responding to antibiotics alone –> surgery

187
Q

What are potential complications of chlamydia?

A 
Epididymitis
PID
Endometritis
Increased risk of ectopic
Infertility
Reactive arthritis
Perihepatitis (Fitz-Hugh-Curtis syndrome)
188
Q

When should chlamydia testing be carried out?

A

2 weeks after a possible exposure

189
Q

How is chlamydia managed?

A

7d doxycycline or azithromycin (single dose) 1g

190
Q

What is the main technique used to test for latent TB?

A

Mantoux test

191
Q

In which people would you use interferon gamma blood test to test for latent TB?

A

Then the mantoux test is positive/equivocal

In those where the tuberculin test may be falsely negative

192
Q

What does the mantoux test involve?

A

0.1ml of 1:1, 000 purified protein dervative injected intradermally

Result read 2-3d later

193
Q

How do you interpret a mantoux test?

A

Diam <6mm - negative (no significant hypersensitivity to tuberculin protein - never been exposed to TB/BCG)

Diam 6-15mm - positive (hypersensitive to tuberculin protein - do not need BCG as have had it before/had TB before)

Diam >15mm - strongly positive (strongly hypersensitive to tuberculin - suggests TB infection)

194
Q

What things may cause a false negative mantoux test?

A 
Miliary TB
Sarcoidosis
HIV 
Lymphoma
Very young age (<6m)
195
Q

What test for TB is no longer used in the UK?

196
Q

When should someone receive their tetanus vaccinations?

A 
2 months
3 months
4 months
3-5 years
13-18 years

This gives long term protection against tetanus

197
Q

What wounds are considered to be at high risk of leading to tetanus?

A 
Compound fractures
Delayed surgical intervention (>6h)
Significant degree of devitalised tissue
Wounds contaminated with soil
Wounds containing FBs
Wounds/burns in people with sepsis
198
Q

How should wounds at high risk of tetanus be managed?

A

IM human tetanus Ig regardless of whether they have been vaccinated

If vaccination history incomplete/unknown give dose of tetanus vaccine as well

199
Q 
What are the following CSF characteristics:
A. appearance
B. glucose
C. protein 
D. white cells
In bacterial meningitis?
A

A. appearance: cloudy
B. glucose: low (<1/2 plasma)
C. protein: high
D. white cells: 10-5, 000 polymorphs

200
Q 
What are the following CSF characteristics:
A. appearance
B. glucose
C. protein 
D. white cells
In viral meningitis?
A

A. appearance: clear/cloudy
B. glucose: 60-80% plasma
C. protein: normal/raised
D. white cells: 15-1, 000 lymphocytes

Exceptions - mumps and herpes encephalitis –> low glucose

201
Q 
What are the following CSF characteristics:
A. appearance
B. glucose
C. protein 
D. white cells
In tuberculous meningitis?
A

A. appearance: slight cloudy, fibrin web
B. glucose: low (<1/2 plasma)
C. protein (high)
D. white cells: 10-1, 000 lymphocytes

202
Q

What else can you do to the CSF if you suspect tuberculous meningitis?

A

ZN stain (but only sensitive in 20%) so PCR sometimes used

203
Q

What causes cholera?

A

Gram negative vibro cholerae

204
Q

What are features of cholera?

A

Rice water diarrhoea (profuse)
Dehydration
Hypoglycaemia

205
Q

How is cholera managed?

A

Oral dehydration therapy

Doxycyline, ciprofloxacin

206
Q

Where is chancroid usually acquired?

A

In the tropics

207
Q

In post-splenectomy patients what organism does penicillin V prophylaxis not protect against?

A

H. influenzae (due to production of beta-lactamases)

208
Q

What vaccines should not be given to immunocompromised patients?

A

Live attenuated ones - e.g. BCG

209
Q

What causes tetanus?

A

Tetanospasmin exotoxin released from clostridium tetani

210
Q

Where are tetanus spores found?

211
Q

How does tetanospasmin cause tetanus?

A

Prevents release of GABA

212
Q

What are features of tetanus?

A 
Prodrome fever, lethargy, headache
Trismus
Risus sardonicus
Opishtotonus (arched back, hyperextended neck)
Spasms, e.g. dysphagia
213
Q

How is tetanus manaed?

A

Supportive, e.g. muscle relaxants, ventilatory support
IM human tetanus Ig for high risk wounds
Metronidazole is first line antibiotic

214
Q

What is the pathophysiology of mycobacterium tuberculosis?

A

Macrophages migrate to regional LNs (lung lesion + affected LNs = Ghon complex)
Leads to formation of granuloma (collection of epitheloid histiocytes)
Caseous necrosis in centre
Inflammatory response mediated by T4HS
In healthy people, disease may be contained, in immunocomp patients disseminated (miliary TB) may occur

215
Q

Why can’t you use normal stains to view mycobacterium tuberculosis?

A

It membrane is waxy and prevents binding with normal stains

216
Q

What stain is typically used to see TB?

A

Ziehl Neelsen stain

217
Q

What is the recommended antibiotic therapy for exacerbations of COPD?

A

Amoxicillin

Tetracycline or clarithromycin

218
Q

What is the recommended antibiotic therapy for uncomplicated CAP?

A

Amoxicillin
(doxycyline/clarithromycin if penicillin allergic)
Add in fluclox if staph suspected e.g. flu

219
Q

What is the recommended antibiotic therapy for pneumonia caused by atypical pathogens?

A

Clarithromycin

220
Q

What is the recommended antibiotic therapy for hospital acquired pneumonia?

A

Within 5d of admission - co-amoxiclav or cefuroxime
>5d after admission - piperacillin with tazobactam or broad spectrum cephalosporin (e.g. ceftazidime) or a quinolone (e.g. ciprofloxacin)

221
Q

What is the recommended antibiotic therapy for a lower UTI?

A

Trimethoprim or nitrofuratoin

Alt: amoxicillin

222
Q

What is the recommended antibiotic therapy for acute pyelonephritis?

A

Broad spectrum cephalosporin or quinolone

223
Q

What is the recommended antibiotic therapy for acute prostatitis?

A

Quinolone or trimethoprim

224
Q

What is the recommended antibiotic therapy for impetigo?

A

Topical fusidic acid

Oral fluclox or erythromycin if widespread

225
Q

What is the recommended antibiotic therapy for celullitis?

A

Flucloxacillin (clarithromycin, erythromycin or doxy if penicillin allergic)

226
Q

What is the recommended antibiotic therapy for cellulitis near nose or eyes?

A

Co-amoxiclav (clarithromycin, + metronidazole if penicillin-allergic)

227
Q

What is the recommended antibiotic therapy for erysipelas?

A

Flucloxacillin (clarithromycin, erythromycin or doxycycline if penicillin-allergic)

228
Q

What is the recommended antibiotic therapy for animal/human bite?

A

Co-amoxiclav (doxycycline + metronidazole if penicillin-allergic)

229
Q

What is the recommended antibiotic therapy for mastitis whilst breast feeding?

A

Flucloxacillin

230
Q

What is the recommended antibiotic therapy for throat infections?

A

Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)

231
Q

What is the recommended antibiotic therapy for sinusitis?

A

Amoxicillin or doxycycline or erythromycin

232
Q

What is the recommended antibiotic therapy for otitis media?

A

Amoxicillin (erythromycin if penicillin-allergic)

233
Q

What is the recommended antibiotic therapy for otitis externa?

A

Flucloxacillin (erythromycin if penicillin-allergic)

234
Q

What is the recommended antibiotic therapy for periapical/periodontal absces?

A

Amoxicillin

235
Q

What is the recommended antibiotic therapy for gingivitis (acute necrotizing ulcerative)?

A

Metronidazole

236
Q

What is the recommended antibiotic therapy for gonorrhoea?

A

Intramuscular ceftriaxone

237
Q

What is the recommended antibiotic therapy for chlamydia?

A

Doxycycline or azithromycin

238
Q

What is the recommended antibiotic therapy for PID?

A

Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole

239
Q

What is the recommended antibiotic therapy for syphillis?

A

Benzathine benzylpenicillin or doxycycline or erythromycin

240
Q

What is the recommended antibiotic therapy for BV?

A

Oral or topical metronidazole or topical clindamycin

241
Q

What is the recommended antibiotic therapy for c. diff infections?

A

First episode: metronidazole

Second or subsequent episode of infection: vancomycin

242
Q

What is the recommended antibiotic therapy for campylobacter enteritis?

A

Clarithromycin

243
Q

What is the recommended antibiotic therapy for salmonella?

A

Ciprofloxacin

244
Q

What is the recommended antibiotic therapy for shigellosis?

A

Ciprofloxacin

245
Q

What baseline tests are required before someone starts anti-TB therapy?

A

LFTs as all drugs are hepatotoxic
UE
Baseline visual assessment (ethambutol)
FBC for platelet count

246
Q

What are the features of primary syphillis?

A

Chancre - painless ulcer at site of sexual contact

Local non-tender lymphadenopathy

247
Q

What are features of secondary syphillis?

A

6-10w post primary infection
Systemic symptoms -fever, lymphadenopathy
Rash on trunk, palsm and soles
Buccal snail track ulcers
Condylomata lata (painless, warty lesions on genitalia)

248
Q

What are features of tertiary syphillis?

A 
Gumma (granulomatous lesions of skin and bones) 
Ascending aorta aneurysm
General paralysis of the insane
Tabes dorsalis
Argyll-Robertson pupil
249
Q

What are features of congenital syphillis?

A

Blunted upper incisor teeth (Hutchison’s teeth), mulberry molars
Rhagades (linear scars at angle of mouth)
Keratitis
Saber shins
Saddle nose
Deafness

250
Q

What causes legionnaire’s disease?

A

Intracellular bacterium Legionella pneumophilia

251
Q

Why does legionella typically spread?

A

Colonizes water tanks or can spread through AC systems

252
Q

What are features of legionnaire’s disease?

A 
Flu like symptoms + fever
Dry cough
Relative bradycardia
Confusion 
Lymphopaenia
Hyponatraemia
Derranged LFTs
Pleural effusion 30%
253
Q

How is legionnaire’s disease diagnosed?

A

Urinary antigen

254
Q

How is legionnaire’s disease treated?

A

Erythromycin/clarithromycin

255
Q

What is the most common cause of viral encephalitis in the adult population?

256
Q

What features are suggestive of a viral encephalitis?

A

Sudden change in behaviour
Fever
Seizures

257
Q

What kind of bacteria is pseudomonas aeruginosa?

A

Aerobic gram negative rod

258
Q

What kind of infections does pseudomonas cause?

A

Chest infections (esp. in CF)
Skin - burns, chronic wound infections
Otitis externa (esp in DM)
UTIs

259
Q

What is the most common organism found in central line infections?

A

Staph epidermidis

260
Q

What are the main differences between staph aureus and staph epidermidis?

A

Aureus - coagulase +ve, skin infections, asbcesses, OM, toxic shock syndrome

Epidermidis - coagulase -ve, central line infections, IE

261
Q

How is BV treated in pregnancy?

A

Oral metronidazole still

262
Q

What PEP is used for hep A?

A

Human normal immunoglobulin or hep A vaccine

263
Q

What PEP is used for Hep B?

A

Vaccinated (HBsAg positive) - booster dose of HBV vaccine

Non-vaccinated/non-responder - hepatitis B Ig and vaccine

In process of being vaccinated - accelerated course of HBV

264
Q

What PEP is used for hep C?

A

Monthly PCR - if seroconversion then inferferon +/i ribavirin

265
Q

What PEP is used for HIV?

A

Low risk incidents, e.g. human bites don’t req. PEP

Combination of ARTs ASAP (within 72h) for 4 weeks
Serological testing 12 weeks after completion of PEP

266
Q

What PEP is used for VZV?

A

VZIg for Ig negative pregnant women/immunosupressed

267
Q

What is the risk of transmission of Hep B from a needlestick injury?

268
Q

What is the risk of transmission of Hep C from a needlestick injury?

269
Q

What is the risk of transmission of HIV from a needlestick injury?

270
Q

What herpes virus mostly causes oral lesions?

271
Q

What herpes virus mostly causes genital herpes?

272
Q

How is herpes gingivostomatitis managed?

A

Oral aciclovir

Chlorhexidine mouthwash

273
Q

How are cold sores managed?

A

Topical aciclovir

274
Q

How is genital herpes managed?

A

Oral aciclovir (if frequent exacervations may require long term aciclovir)

275
Q

What is classical of the fever in malaria?

A

It comes on alternating days

Nb other symptoms of malaria include headache, myalgia, hepatomegaly

276
Q

What investigations are recommended by NICE in suspected meningitis?

A 
FBC
CRP
Coagulation screen
Blood culture
Whole blood PCR
Blood glucose
Blood gas
LP if no signs of raised ICP
277
Q

How is suspected meningitis managed?

A

Admit to hospital

If in GP + meningococcal disease suspected –> IM benzylpenicillin + transfer to hospital

278
Q

What initial empirical therapy is given for meningitis in those aged <3 months?

A

IV cefotaxime + amoxicillin

279
Q

What initial empirical therapy is given for meningitis in those aged 3 months - 50 years?

A

IV cefotaxime

280
Q

What initial empirical therapy is given for meningitis in those aged >50 years?

A

IV cefotaxime + amoxicillin

281
Q

What therapy is given for meningococcal meningitis?

A

IV benzylpenicillin or cefotaxime

282
Q

What therapy is given for meningitis for those with pneumococcal meningitis?

A

IV cefotaxime

283
Q

What therapy is given for meningitis due to H. influenzae?

A

IV cefotaxime

284
Q

What therapy is given for meningitis due to listeria?

A

IV amoxicillin + gentamicin

285
Q

What drug (aside from antimicrobials) should be given in meningitis management and why?

A

IV dexamethasone to reduce risk of neurological sequelae

286
Q

What drug should be used to treat meningitis if the patient is allergic to penicillin or cephalosporins?

A

Chloramphenicol

287
Q

For what kind of meningitis must you offer household/close contacts prophylaxis? What is this prophylaxis?

A

Meningococcal
(If been in contact within 7 days of onset)
Oral ciprofloxacin (1st line) or rifampicin
Offer meningococcal vaccine to close contacts when serotype results are available

288
Q

What are the most common causes of meningitis in those aged 0-3 months?

A

Group B Streptococcus (most common cause in neonates)
E. coli
Listeria monocytogenes

289
Q

What are the most common causes of meningitis in those aged 3 months - 6 years?

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae

290
Q

What are the most common causes of meningitis in those aged 6 years - 60 years?

A

Neisseria meningitidis

Streptococcus pneumoniae

291
Q

What are the most common causes of meningitis in those aged >60 years?

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

292
Q

What is a common cause of bacterial meningitis in those who are immunosupressed?

A

Listeria monocytogenes

293
Q

Which STI is a ‘strawberry cervix’ associated with?

A

Trichomonas vaginalis

294
Q

How is uncomplicated falciparum malaria treated?

A

1st line - Artemisinin based combination therapies

295
Q

How is complicated falciparum malaria treated?

A 
IV artesunate
(parasite >10% - consider exchange transfusion)
296
Q

What is rabies?

A

Viral disease that causes an acute encephalitis

297
Q

What kind of virus causes rabies?

A

Lyssavirus

298
Q

What kinds of bites can spread rabies?

A

Usually dog

Others - bat, racoon, skunk

299
Q

Following a bite how does the rabies virus spread in the body?

A

Up nerve axons towards the central nervous system

300
Q

What are the clinical features of rabies?

A

Prodrome - headache, fever, agitation
Hydrophobia - water provoking muscle spasms
Hypersalivation

301
Q

What kind of bodies are seen in neurons infected with rabies?

A

Negri bodies (cytoplasmic inclusion bodies)

302
Q

How should animal bites in at risk countries (of rabies) be managed?

A

Wash wound
Vaccinated - give further 2 doses of vaccine
Not vaccinated - human rabies Ig + full vaccination course (administer locally around wound)

303
Q

What is the prognosis of rabies?

A

Untreated disease is nearly always fatal

304
Q

What is the first line treatment of animal bites?

A

Co-amoxiclav

305
Q

What individuals are offered a BCG?

A

All infants (0-12m) living in areas where annual incidence of TB 40/100, 000+ or with a grandparent/parent who was born in a country where the incidence of TB is that
Previously unvaccinated tuberculin -ve contacts of cases of respiratory TB
Previously unvaccinated tuberculin negative new entrants under 16 who were born/lived (>3m) in a country with annual TB incidence 40/100, 000+
Healthcare workers
Prison staff
Staff of care home for the elderly
Those working with the homeless

306
Q

What does the BCG vaccine contain?

A

Live attenuated mycobacterium bovis

307
Q

What must you have prior to having a BCG?

A

Tuberculin skin tests (unless younger than 6 and no contact with TB)

308
Q

What can BCG not be given at the same time as?

A

Other live vaccines (leave 4 week interval)

309
Q

What are contraindications to getting a BCG?

A 
Prev. BCG
Hx of TB
HIV
Pregnancy
>35 years (no evidence of efficiacy)
Positive tuberculin test
310
Q

What are the two tuberculin tests?

A

Heaf and mantoux

311
Q

When is it appropriate to perform stool microbiological investigations for a child with diarrhoea?

A
  1. Suspected septicaemia
  2. Blood/mucous in stool
  3. Child is immunocompromised
312
Q

Define PUO

A

Fever >3 weeks with resists diagnosis after 1 week in hospital

313
Q

What are causes of PUO

A

Neoplasia - lymphoma, hypernephroma, preleukaemia, atrial myxoma
Infections - TB, abscess
Connective tissue disorders

314
Q

What is the quickest way to determine lactate levels?

A

ABG or VBG

315
Q

What is co-trimaxazole a mix of?

A

Trimethoprim and sulfamethoxazole

316
Q

Drugs that end in -navir are from what class of drugs?

A

Protease inhibitors

317
Q

Drugs that end in -gravir are from what class of drugs?

A

Integrase inhibitors

318
Q

How is legionella pneumophilia best diagnosed?

A

Urinary antigen test

319
Q

What is the single most effective single measure to reduce the incidence of MRSA?

A

Hand hygiene

320
Q

What organism is responsible for causing toxoplasmosis?

A

Toxoplasma gondii

321
Q

How does toxoplasmosis spread?

A

Protozoa infects via GIT, lungs or broken skin

Its oocytes release trophozoites which migrate around the body, including to the muscle, eyes and brain

322
Q

What is the usual reservoir for toxoplasma gondii?

323
Q

What is a common presentation of toxoplasmosis?

A

IM type illness (fever, malaise, lymphadenopathy)

Less common manifestations include meningioencephalitis + myocarditis

324
Q

How do you test for toxoplasmosis?

A

Ab test

Sabin Feldman dye test

325
Q

Who is treated for toxoplasmosis?

A

Those with severe infections/immunosupressed

326
Q

What is the treatment of toxoplasmosis?

A

Pyrimethamine + sulphadiazine for 6 weeks (at least)

327
Q

What causes congenital toxoplasmosis?

A

Transplacental spread from mother

328
Q

What are features of congenital toxoplasmosis?

A

Microcephaly, hydrocephalus, cerebral calcification + choriodoretinitis

329
Q

What family is the ebola virus from?

A

Filoviridae virus family

330
Q

How does ebola spread?

A

Human to human transmission through broken skin or mucous membranes with blood, secretions, organs or other bodily fluids of infected people and surfaces contaminated with these fluids

331
Q

What is the incubation period of ebola?

A

2-21 days

Only infectious once symptoms develop

332
Q

What are the first symptoms of ebola?

A

Sudden onset fever, fatigue, muscle pain, headache, sore throat

333
Q

What follows the initial symptoms of ebola?

A 
Vomiting
Diarrhoea
Rash
Impaired kidney and liver function 
Internal + external bleeding
334
Q

In which patients should you consider a diagnosis of ebola?

A

Fever 37.5C+ or have hx of fever in past 24h AND have recently visited any of the affected areas in the last 21 days/cared for/come in contact with bodily fluids of someone strongly suspected/known to have VHF

335
Q

How should ebola be managed?

A

Advise not to visit surgery

Contact PHE

336
Q

What is this history typical of?:

Bilateral conjunctivitis, bilateral calf pains, high fever in a sewage worker

A

Mild leptospirosis

337
Q

What fluid therapy should be given to someone as part of the sepsis 6 bundle?

A

If >16y IV fluid resus with crystalloids 500ml STAT (over 15 min)

338
Q

What causes giardiasis?

A

Flagellated protozoan giardia lamblia

339
Q

How is giardia lamblia spread?

A

Faecal oral

340
Q

What are the clinical features of giardiasis?

A 
Often asymptomatic
Bloating, lethargy, ab pain
Flatulence
Non-bloody diarrhoea
Chronic diarrhoea, malabsorption, lactose intolerance
341
Q

How is giardiasis treated?

A

Metronidazole

342
Q

What happens if you take metronidazole with alcohol?

A

Disulfiram like reaction (flushing, nausea, vomiting, sweatiness, headache, palpitations)

343
Q

How does metronidazole work?

A

Forms reactive cytotoxic metabolites inside bacteria

344
Q

What is an aspergilloma?

A

Mass like fungus ball (mycetoma) which often colonises an existing lung cavity (e.g. secondary to TB, lung cancer etc.)

345
Q

What are clinical features of an aspergilloma?

A

Usually asymptomatic

Cough, haemoptysis

346
Q

What does an aspergilloma appear like on CXR?

A

Rounded opacity

Crescent sign may be present

347
Q

Flu like symptoms, a dry cough, relative bradycardia and confusion. Blood tests show a hyponatraemia.

What is this a typical history of?

A

Legionnaire’s disease

348
Q

List antifungal agents

A 
Azoles
Amphotericin B 
Terbinafine
Griseofulvin
Flucytosine
Caspofungin
Nystatin
349
Q

What is the mechanism of action of azoles?

A

Inhibits 14α-demethylase which produces ergosterol

350
Q

What is the mechanism of action of amphotericin B?

A

Binds with ergosterol forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl) leakage

351
Q

What is the mechanism of action of terbinafine?

A

Inhibits squalene epoxidase

352
Q

What is the mechanism of action of griseofulvin?

A

Interacts with microtubules to disrupt mitotic spindle

353
Q

What is the mechanism of action of flucytosine?

A

Converted by cytosine deaminase to 5-fluorouracil, which inhibits thymidylate synthase and disrupts fungal protein synthesis

354
Q

What is the mechanism of action of capsofungin?

A

Inhibits synthesis of beta-glucan, a major fungal cell wall component

355
Q

What is the mechanism of action of nystatin?

A

Binds with ergosterol forming a transmembrane channel that leads to monovalent ion (K+, Na+, H+ and Cl) leakage

356
Q

How is nystatin normally administered?

A

Usually topical, e.g. for oral thrush as it is very toxic

357
Q

What is a SE of caspofungin?

358
Q

What is an SE of flucytosine?

359
Q

What AE are associated with griseofulvin?

A

Induces P450 system

Teratogenic

360
Q

What drug is commonly used in the oral form to treat fungal nail infections?

A

Terbinafine

361
Q

What drug is mostly used to treat systemic fungal infections?

A

Amphotericin B

362
Q

What SEs are associated with amphotericin B?

A

Nephrotoxicity
Flu like symptoms
Hypokalaemia
Hypomagnesaemia

363
Q

What AEs are associated with azoles?

A

P450 inhibition

Liver toxicity

364
Q

What investigation is required before starting a patient on terbinafine?

A

LFTs (before treatment and 4-6 weeks into treatment)

365
Q

How re streptococci divided?

A 
Alpha haemolytic (partial haemolysis)
Beta haemolytic (complete haemolysis)
366
Q

What is the most important alpha haemolytic strep?

A

Strep pneumoniae

Other e.g. is strep viridians

367
Q

How are beta haemolytic streptococci divided?

A

A-H

A, B and D are the most important ones

368
Q

What is the most important group A beta haemolytic strep?

A

Strep pyogenes

369
Q

What kinds of infections does strep pyogenes cause?

A

Erysipelas, impetigo, cellulitis, type 2 necrotizing fasciitis, pharyngitis/tonsillitis
Erythrogenic toxins –> scarlet fever
Can cause rheumatic fever, post-strep GN

370
Q

What a group B beta haemolytic strep?

A

Strep agalactiae (can cause neonatal meningitis/septicaemia)

371
Q

What are group D beta haemolytic streps?

A

Enterococcus

372
Q

What is the most common way hepatitis E is spread?

A

Undercooked pork

373
Q

What is the most common cause of short term hepatitis in the UK?

374
Q

What causes leishmaniasis?

A

Intracellular protozoa leishmania

375
Q

How is leishmania spread?

A

Sand flies

376
Q

What are the types of leishmaniasis?

A

Cutaneous leishmaniasis
Mucocutaneous leishmaniasis
Visceral leishmaniasis (kala-azar)

377
Q

What causes cutaneous leishmaniasis?

A

Leishmania tropica or Leishmania mexicana

378
Q

What are features of cutaneous leishmaniasis?

A

Crusted lesion at site of bite

May be underlying ulcer

379
Q

What causes mucocutaneous leishmaniasis?

A

Leishmania braziliensis

380
Q

What are features of mucocutaneous leishmaniasis?

A

Skin lesions spread to involve mucosae of nose, pharynx etc.

381
Q

What most commonly causes visceral leishmaniasis?

A

Leishmania donovani

382
Q

What are features of visceral leishmaniasis?

A 
Fever, sweats, rigors
Massive splenomegaly, hepatomegaly
Poor appetite, wt loss
Grey skin (kala-azar = black sickness)
Pancytopenia secondary to hypersplenism
383
Q

What is the gold standard for diagnosing visceral leishmaniasis?

A

Bone marrow/splenic aspirate

384
Q

Do you require consent to test for HIV?

385
Q

What is red man nsyndrome?

A

Vancomycin related activation of mast cells with release of histamine due to rapid IV infusion of vancomycin

386
Q

What are typical symptoms of redman syndrome?

A

Redness
Pruritus
Burning sensation in upper body

Severe cases can cause hypotension + chest pain

387
Q

How is red man syndrome managed?

A

Cessation of infusion

After symptoms have resolved, recommence at slower infusion rate

388
Q

What AEs are associated with vancomycin?

A

Nephrotoxicity
Ototoxicity
Thrombophlebitis
Red man syndrome

389
Q

What is vancomycin used to treat?

A

Gram positive infections, esp MRSA

390
Q

BV is primarily due to the overgrowth of what bacteria?

A

Gardnerella vaginalis

which leads to a fall in lactic acid producing lactobacilli –> pH to increase

391
Q

What kind of virus is mumps?

A

RNA paramyxovirus

392
Q

How is mumps spread?

A

By droplet

393
Q

Where does mumps tend to spread?

A

Respiratory tract epithelial cells –> parotids –> other tissues

394
Q

What are clinical features of mumps?

A

Fever
Malaise, muscular pain
Parotitis (earache, pain on eating), unilateral initially and then usually becomes bilateral

395
Q

How is mumps managed?

A

Rest
Paracetamol
Notifiable disease

396
Q

What are complications of mumps?

A

Orchitis (4-5 days after parotitis)
Hearing loss (usually unilateral and transient)
Meningoencephalitis
Pancreatitis

397
Q

What should all HIV patients with CD4 <200 be given?

A

Prophylaxis against PJP (co-trimoxazole)

398
Q

If an asymptomatic contact of a chlamydia patient comes in should you still treat?

A

Yes - treat straight away without waiting for results of test

399
Q

How are animal bites managed?

A

Cleans wound
Co-amoxiclav
(if penicillin allergic - doxycyline + metronidazole)

400
Q

What organisms commonly infect human bites?

A 
Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella
401
Q

What antibiotic is recommended for human bites?

A

Co-amoxiclav

402
Q

What cancers is HPV linked to?

A 
Cervical 
Anal 
Vulval and vaginal 
Penile
Mouth and throat
403
Q

Apart from boys and girls aged 12-13, who else should be offered the HPV vaccination?

A

MSM under the age of 45 (due to risk of anal, throat and penile cancers)

404
Q

What kind of bacteria is clostridium botulinum?

A

Gram positive anaerobic bacillus

405
Q

What toxin does clostridium botulinum produce?

A

Botulinum toxin (neurotoxin which irreversibly blocks release of ACh)

406
Q

How might someone get botulism?

A

From eating contaminated foods (e.g. tinned) or IVDA

407
Q

What nerves does the botulinum toxin often affect?

A

Bulbar muscles and ANS

408
Q

What are features of botulism?

A 
No sensory disturbance
Descending flaccid paralysis
Diplopia
Ataxia
Bulbar palsy
409
Q

How is botulism managed?

A

Botulism antitoxin (only effective if given early) + supportive care

410
Q

What are the main two forms of trypanosomiasis?

A

African trypanosomiasis - sleeping sickness

American trypanosomiasis - Chagas disease

411
Q

How is trypanosomiasis spread?

A

Tsetse fly

412
Q

What are clinical features of African trypanosomiasis?

A

Trypanosoma chancre - painless s/c nodule at site of infection
Intermittent fever
Enlargement of posterior cervical LNs
Later => CNS involvement, e.g. somnolence, headaches, mood changes, meningoencephalitis

413
Q

How is early African trypanosomiasis managed?

A

IV pentamidine or suramin

414
Q

How is late African trypanosomiasis or African trypanosomiasis with CNS involvement managed ?

A

IV melarsoprol

415
Q

How does acute Chaga’s disease present?

A

Chagoma (an erythematous nodule at site of infection) + periorbital oedema

416
Q

What are features of chronic Chaga’s disease?

A

Myocarditis ==> dilated cardiomyopathy + arrhythmias

GI features - megaoesophagus + megacolon –> dysphagia and constipation

417
Q

What is the management of Chaga’s disease?

A

Acute phase - azole/nitroderivates (benznidazole)

Chronic - treat complications

418
Q

Should asymptomatic bacteruria in catheterised patients be treated?

419
Q

What is the most frequent and severe manifestation of chronic Chaga’s disease?

A

Cardiomyopathy

420
Q

What is the mode of action of rifampicin?

A

Inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA

421
Q

What AEs are associated with rifampicin?

A

Potent CYP450 liver inducer
Hepatitis
Orange secretions
Flu like symptoms

422
Q

What AEs are associated with isoniazid?

A

Hepatitis
Peripheral neuropathy
Agranulocytosis

423
Q

What AEs are associated with pyrazinamide?

A

Myalgia
Arthalgia
Hepatitis
Hyperuricaemia

424
Q

Why should nitrofuratoin not be given to pregnant women in the third trimester?

A

Can cause haemolytic anaemia in newborn

425
Q

What AEs are associated with trimethoprim?

A

Myelosupression
Transient rise in cr
Hyperkalaemia
(due to tubular dysfunction by blocking the ENaC channel)

426
Q

How quickly do symptoms of norovirus develop after becoming infected?

A

15-50 hours

427
Q

What are symptoms of norovirus?

A

Nausea, vomiting, diarrhoea

Headaches, low grade fevers, myalgia

428
Q

How is norovirus spread?

A 
Faecal oral (when virus aerosolized by vomiting/toilet flushing)
Can be transmitted by cross contamination from surfaces
429
Q

Once the norovirus enters the body what does it do?

A

Enters cell via host receptor mediated endocytosis and replicates in small intestine

430
Q

How is transmission of norovirus limited?

A

Isolation of infected individuals
Hand hygiene with soap and water
Hand gels not effective enough

431
Q

How is norovirus diagnosed?

A

Hx and stool culture viral PCR

432
Q

What are neurological sequalae of meningitis?

A

Sensorineural hearing loss (most common)
Epilepsy, paralysis
Sepsis, intracranial abscess
Brain herniation, hydrocephalus

433
Q

What are CIs to LP for meningitis?

A 
Any signs of raised ICP - 
Focal neurological signs
Papilloedema
Significant bulging of fontanelles
DIC
Signs of cerebral herniation

For patients with menigococcal septicaemia an LP is CI - blood cultures and PCR for meningococcus should be obtained

434
Q

How should meningitis in children be managed?

A
  1. Antibiotics
  2. IV dexamethasone if >3 months and any of:
    a. frankly purulent CSF
    b. CSF WCC >1000/microlitre
    c. raised CSF WCC with protein conc >1g/l
    d. bacteria on gram stain
  3. Fluid
  4. Cerebral monitoring
  5. PH notification and prophylaxis of contacts
435
Q

What are symptoms of meningococcal sepsis/meningitis?

A 
Headache
Fever
NV
Photophobia
Drowsiness
Seizures
436
Q

What are signs of meningococcal sepsis/meningitis?

A

Neck stiffness

Purpuric rash

Infection (22 decks)

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