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Laz's Pathology - Parm > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What are the four processes that occur in septicaemia?

A

Capillary leak – albumin and other plasma proteins lead to hypovolaemia
Coagulopathy – leads to bleeding and thrombosis, endothelial injury results in platelet release reactions, the protein C pathway and plasma anticoagulants are affected
Metabolic derangement – particularly acidosis
Myocardial failure – and multi-organ failure

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2
Q

What is a typical MRI feature of TB meningitis?

A

Leptomeningeal enhancement

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3
Q

Name two types of amoeba that cause encephalitis.

A

Naegleria fowleri

Acanthamoeba species and Balamuthia mandrillaris

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4
Q

What is toxoplasmosis and how is it spread?

A

Obligate intracellular parasite
Spread via oral, transplacental or organ transplant route
From raw/undercooked meats (particularly in France) and contact with cat faeces

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5
Q

List some organisms that can cause brain abscesses.

A 
Staphylococci
Streptococci
Gram-negative organisms (mainly in neonates)
TB 
Actinomyces and Nocardia species
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6
Q

Describe the Gram-stain and microscopic appearance of:

a. S. pneumoniae
b. N. meningitidis
c. L. monocytogenes
d. TB
e. Cryptococcus

A

a. S. pneumoniae
Gram-positive alpha-haemolytic diplococci
b. N. meningitidis
Gram-negative non-haemolytic diplococci
c. L. monocytogenes
Gram-positive rods
d. TB
Stains positively with Ziehl-Neelsen (red and blue)
e. Cryptococcus
Stains positively with India ink (appears like an orbit – yeast in the middle with a capsule around the outside)

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7
Q

What is another key clinical feature of Cryptococcal meningitis?

A

High opening pressure

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8
Q

What is the generic therapy used in meningitis?

A

Ceftriaxone 2 g IV BD
If > 50 years or immunocompromised = amoxicillin 2 g IV 4 hourly
NOTE: this is because ceftriaxone does NOT cover Listeria

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9
Q

What is the generic therapy used in meningo-encephalitis?

A

Aciclovir 10 mg/kg IV TDS
Ceftriaxone 2 g IV BD
If > 50 years or immunocompromised = amoxicillin 2 g IV 4 hourly

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10
Q

Name the specific therapy for meningitis caused by:

a. S. pneumoniae
b. N. meningitidis
c. H. influenzae
d. Group B Streptococcus
e. Listeria
f. Gram-negative bacilli
g. Pseudomonas

A 
a.	S. pneumoniae
Pen G 18-24 mu/day
b.	N. meningitidis
Ceftriaxone 4 g/day
c.	H. influenzae
Cefotaxime 12 g/day
d.	Group B Streptococcus
Pen G 18-24 mu/day
e.	Listeria
Ampicillin 12 g/day
f.	Gram-negative bacilli
Cefotaxime 12 g/day
g.	Pseudomonas
Meropenem 6 g/day
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11
Q

What type of toxin is produced by Staphylococcus aureus?

A

Enterotoxin – this is an exotoxin that can act as a superantigen in the GI tract triggering the release of IL1 and IL2

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12
Q

What type of organism is Bacillus cereus?

A

Gram-positive rods that are spore-forming

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13
Q

Name three types of Clostridium infection and describe the diseases that they cause.

A

Clostridium botulinum – causes botulism
• From canned food
• Causes disease due to preformed toxin which blocks acetylcholine release at peripheral nerve synapses
- Causes descending paralysis
• Treated with antitoxin
Clostridium perfringens – food poisoning
• From reheated food
• Generates a superantigen that mainly affects the colon
• Causes watery diarrhoea and cramps that last 24 hours
Clostridium difficile – pseudomembranous colitis
• Hospital-acquired infection related to antibiotic use

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14
Q

Which antibiotics are most commonly implicated in C. difficile colitis?

A

Cephalosporins
Clindamycin
Ciprofloxacin

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15
Q

What type of organism is Listeria monocytogenes?

A

Gram-positive, rod-shaped, facultative anaerobe

Beta-haemolytic, aesculin-positive with tumbling motility

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16
Q

What type of organisms are Enterobacteriaceae?

A

Facultative anaerobes
Lactose fermenters
Oxidase-negative

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17
Q

What type of bacteria are Salmonella enteritidis?

A

Gram-negatives
Oxidase negative
Urease negative
Non-lactose fermenting
Produce hydrogen sulphide (form black colonies)
Grows on TSI agar, XLD agar and selenite F broth

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18
Q

Which antigens are found on Salmonellae?

A

Cell wall O (groups A-I)
Flagellar H
Capsular Vi (virulence, antiphagocytic)
NOTE: differences in these antigens help identify types of Salmonellae

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19
Q

Describe the presentation of Salmonella typhi.

A

Slow onset fever and constipation
May cause splenomegaly, rose spots, bradycardia, anaemia and leucopaenia
Blood cultures may be positive
Transmitted only by humans
Ingested by monocytes and multiplies in Peyer’s patches and spreads via the endoreticular system

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20
Q

How is Salmonella typhi treated?

A

Ceftriaxone

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21
Q

List some types of Shigella.

A

Shigella sonnei
Shigella dysenteriae
Shigella flexneri (MSM)

NOTE: avoid antibiotic treatment (use ciprofloxacin if necessary)

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22
Q

What are the microbiological features of Vibrio?

A

Comma-shaped
Late lactose-fermenters
Oxidase-positive
Gram-negative

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23
Q

Name and describe the key features of other types of Vibrio.

A

Vibrio parahaemolyticus – caused by ingestion of raw/undercooked seafood, causes self-limiting diarrhoea, grows on salty agar
Vibrio vulnificus – causes cellulitis in shellfish handlers, can cause fatal septicaemia with D&V in HIV patients, treated with doxycycline

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24
Q

What are the main microbiological features of Campylobacter?

A 
Comma-shaped 
Microaerophilic 
Oxidase-positive 
Gram-negative 
Motile
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25
Q

What are the key microbiological features of Entamoeba histolytica?

A

Motile trophozoite in diarrhoeal illness
Non-motile cyst in non-diarrhoeal illness
Killed by boiling
Contains four nuclei
No animal reservoir

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26
Q

Describe the pathophysiology of diarrhoeal illness caused by Entamoeba histolytica?

A

Ingestion of cysts  trophozoites move into the ileum  colonise the colon  causes flask-shaped ulcers

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27
Q

How is Entamoeba histolytica infection diagnosed and treated?

A

Diagnosis: stool microscopy, serology of invasive disease
Treatment: metronidazole + paromomycin

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28
Q

What are the key microbiological features of Giardia lamblia?

A

Pear-shaped trophozoites
Two nuclei
Four flagellae and a suction disc

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29
Q

Outline the pathophysiologiy of GI disease caused by Giardia.

A

Transmitted by ingestion of cyst from faecally contaminated water
Excystation in the duodenum leads to trophozoite attachment
Results in malabsorption of protein and fat
Presentation: foul-smelling non-bloody diarrhoea, cramps, flatulence, NO fever

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30
Q

What are the main features of Cryptosporidium parvum?

A

Causes severe diarrhoea in the immunocompromised
Oocysts can be seen in the stool using modified Kinyoun acid fast stain
Rx: paromomycin

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31
Q

Which stain is used to identify PCP?

A

Silver stain (Grocott-Gomori stain)

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32
Q

Which organisms do the following defects make you susceptible to?

a. T cell defect
b. B cell defect
c. Neutrophil defect
d. Complement defect

A 
a.	T cell defect 
Sepsis 
CMV, EBV, VZV
Candida, PCP 
Usually aggressive opportunistic infections 
b.	B cell defect
Streptococcus, Staphylococcus, Haemophilus 
Giardia
Usually recurrent sinopulmonary infections 
c.	Neutrophil defect
Staphylococcus, Pseudomonas
Candida, nocardia, aspergillus
d.	Complement defect
Neisseria
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33
Q

What is Actinomyces and what does it cause?

A

Gram-positive rod that causes lung abscesses in immunocompromised patients (particularly alcoholics)
NOTE: it’s closely associated with Nocardia

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34
Q

Describe the histological features of Actinomyces.

A

Basophilic sulfur granules

Gram-positive rods that branch as they grow

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35
Q

How is non-severe C. difficile disease treated?

A

Metronidazole 400 mg TDS for 10-14 days

If intolerant or not responding at 72 hours, change to vancomycin 125 mg QDS for 10-14 days

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36
Q

Describe the MRI appearance of sporadic CJD.

A

Increased signal in the basal ganglia

Increased intensity on DWI MRI of the cortex and basal ganglia

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37
Q

On which chromosome is the normal prion gene found?

A

20

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38
Q

On which codon are the three polymorphisms of prion proteins found? What are the three polymorphisms?

A 
Codon 129
MM (predisposes to prion diseases)
MV
VV
NOTE: M = methionine, V = valine
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39
Q

Which gene mutation is associated with prion diseases?

A

PRNP

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40
Q

Which investigation is most useful for vCJD?

A

Tonsillar biopsy – prions localise in lymphoid tissue

NOTE: this is not useful in CJD

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41
Q

Outline the clinical features of iatrogenic CJD.

A

Starts with progressive ataxia

Dementia and myoclonus occur at a later stage

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42
Q

Describe the clinical features of Gerstmann-Straussler-Sheinker syndrome.

A

Slowly progressive ataxia
Diminished reflexes
Dementia
NOTE: PRNP P102L mutation is most common

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43
Q

Describe the clinical features of fatal familial insomnia.

A 
Untreatable insomnia
Dysautonomia (blood pressure and heart rate dysregulation)
Ataxia
Thalamic degeneration 
NOTE: PRNP D178N mutation is most common
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44
Q

What number of white cells in the urine represents inflammation?

A

More than 10^4/mL

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45
Q

In which patient groups should screening of the urine for white cells before MC&S NOT be performed?

A

Immunocompromised patients, pregnant women and children

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46
Q

List some causes of sterile pyuria.

A 
STIs (e.g. chlamydia)
TB
Prior antibiotic treatment (MOST COMMON)
Calculi
Catheterisation
Bladder cancer
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47
Q

What type of agar is used for urine culture? What do the colours suggest?

A

Chromogenic agar
• Pink = E. coli
• Blue = other coliforms
• Light blue = Gram-positives

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48
Q

In which groups of patients is a short course of antibiotics not appropriate?

A

Women with a history of UTI caused by antibiotic resistant organisms
More than 7 days of symptoms
Men

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49
Q

Which part of the kidney is more susceptible to infection?

A

Renal medulla

NOTE: the kidney is a frequent site for abscesses in patients with S. aureus endocarditis

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50
Q

What is the main treatment option for pyelonephritis?

A

Co-amoxiclav with or without gentamicin

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51
Q

What is the incubation period for hepatitis A?

A

2-6 weeks

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52
Q

Describe the molecular organisation of hepatitis B virus.

A

DNA virus with four overlapping reading frames (core, X, polymerase and surface antigen)
NOTE: as they overlap, a mutation in one reading frame could affect others

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53
Q

What is a strong indicator of risk of cirrhosis in people with hepatitis B infection?

A

HBV DNA level (copies/mL)

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54
Q

What components constitute the viral RNA genome of hepatitis C?

A

Core
Envelope
Non-structural components

NOTE: most drugs used for hep C are protease inhibitors

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55
Q

What is the incubation period of HCV?

A

6-8 weeks

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56
Q

List some treatment options for chronic HBV.

A 
Interferon alpha
Lamivudine
Tenofovir
Entecavir 
Emtricitabine
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57
Q

How is HCV treated?

A

Early treatment with peginterferon alfa

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58
Q

How is the response to treatment with peginterferon-alfa assessed in HCV infection?

A

Sustained viral response (SVR12) – no HCV RNA 12 weeks after stopping treatment

NOTE: SVR 24 can also be done

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59
Q

What is the main difference in the treatment of genotype 1 and non-genotype 1 HCV?

A

Genotype 1 and 4 – less responsive to ribavirin and protease-based therapy, requires longer treatment
Genotype 2 and 3 - more responsive to protease-based therapy

NOTE: ribavirin can also be used to treat RSV

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60
Q

Outline the treatment of hepatitis E.

A

Supportive

Ribavirin

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61
Q

Name three major pathogens that cause surgical site infections.

A

Staphylococcus aureus
Escherichia coli
Pseudomonas aeruginosa

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62
Q

What are the three levels of surgical site infections?

A

Superficial incisional – skin and subcutaneous tissues
Deep incisional – fascial and muscle layers
Organ/space infection – any part of the anatomy that is not the incision

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63
Q

List some bacterial factors that enable bacteria to cause septic arthritis.

A

Staphylococcus aureus has receptors such as fibronectin-binding protein
Kingella kingae have bacterial pili which adhere to the synovium
Some strains of S. aureus produce Panton-Valentine Leukocidin which is associated with fulminant infections

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64
Q

List some host factors that increase the risk of septic arthritis.

A

Leukocyte-derived proteases and cytokines
Raised intra-articular pressure
Deletion of macrophage-derived cytokines
Absence of IL-10

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65
Q

Outline the presentation of chronic osteomyelitis.

A

Pain
Brodie’s abscess
Sinus tract

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66
Q

Name two techniques for treating chronic osteomyelitis.

A

Laubenbach technique – debridement all the way to healthy bleeding bone and removal of all prosthetic material. Double lumen irrigation used to instil antibiotics into the central lumen
Papineau technique – complete excision of infected tissue and necrotic bone followed by open cancellous bone grafting and split skin grafting to the close the wound

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67
Q

Which organism most commonly causes prosthetic joint infection?

A

Coagulase-negative staphylococcus

Others: streptococci, enterococci, enterobacteriaciae, Pseudomonas aeruginosa, anaerobes

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68
Q

How is prosthetic joint infection diagnosed?

A

Radiology – shows loosening of the prosthesis
CRP > 13.5 for prosthetic knees
CRP > 5 for prosthetic hips
Joint aspiration (>1700/mL if knee; >4200/mL if hip)

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69
Q

How should specimens be taken intraoperatively?

A

Specimens should be taken from at least 5 sites around the implant and sent for histology
NOTE: if 3 or more specimens yield identical organisms, this is suggestive of prosthetic joint infection

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70
Q

List 5 HAIs in order of prevalence.

A 
Pneumonia
Surgical site infection 
UTI
Blood stream infection 
Gastrointestinal infection
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71
Q

Define pyrexia of unknown origin.

A

A fever > 38.3 degrees lasting > 3 weeks with an uncertain diagnosis after 7 days in hospital

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72
Q

List some differentials for PUO.

A 
Infection
•	Infectious endocarditis 
•	HIV
•	TB
Inflammation
•	Polymyalgia rheumatica
•	Still’s disease 
•	Sarcoidosis 
•	ANCA-associated vasculitis 
•	Rheumatoid arthritis 
Malignancy
•	Malignant lymphoma 
•	Castleman’s disease
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73
Q

List some infectious causes of PUO.

A 
Bacteria
•	TB/NTM
•	Enteric fever (e.g. Salmonella typhi)
•	Zoonoses
Viruses
•	EBV/CMV
•	HIV
•	Hepatitis 
Fungi
•	Cryptococcosis 
•	Histoplasmosis
Parasites
•	Malaria 
•	Amoebic liver abscess
•	Schistosomiasis 
•	Toxoplasmosis 
•	Trypanosomiasis
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74
Q

What are the different components of EBV serology?

A

Viral capsid antigen (VCA) IgM – rises early in acute infection
VCA IgG – rises later in infection
EBNA-1 IgG – rises later in infection
EBNA DNA – rapidly cleared if immunocompetent so will be negative in most, may be positive if immunocompromised
NOTE: the heterophile antibody test is not recommended because of poor sensitivity and specificity

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75
Q

List two causes of very high ferritin.

A

Adult-onset Still’s disease

Macrophage activation syndrome

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76
Q

Outline the major and minor criteria for infective endocarditis.

A 
Major
•	Persistent bacteraemia (> 2 positive blood cultures)
•	Vegetations on echocardiogram
•	Positive serology for Bartonella, Coxiella or Brucella 
Minor
•	Predisposition (murmur, IVDU)
•	Raised inflammatory markers
•	Immune complexes (RBC in urine)
•	Embolic phenomena (Janeway lesions) 
•	Atypical echo 
•	1 positive blood culture 
2 major + 1 minor OR 3 minor = infective endocarditis

IMPORTANT: 3 blood cultures should be taken in suspected infective endocarditis

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77
Q

Outline the key features of Adult-onset Still’s disease.

A 
Salmon pink rash 
Arthralgia
Sore throat 
Lymphadenopathy
Fever
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78
Q

List some miscellaneous causes of PUO.

A

Subacute thyroiditis
Addison’s disease
PE
Dressler’s syndrome
Drugs – idiosyncratic or adverse drug reaction
NOTE: 25% of drug reactions will cause eosinophilia and a rash

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79
Q

Give examples of zoonoses in the UK that are transmitted by:

a. Farm/wild animals
b. Companion animals

A 
a.	Farm/wild animals
Campylobacter 
Salmonella
b.	Companion animals
Toxoplasmosis
Bartonella
Ringworm 
Psittacosis
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80
Q

For Campylobacter, describe the following:

a. Reservoir
b. Transmission
c. Clinical presentation
d. Investigations
e. Management

A 
a.	Reservoir 
Poultry 
Cattle
b.	Transmission
Contaminated food 
c.	Clinical presentation 
Bloating
Diarrhoea 
Cramps 
d.	Investigations 
Stool culture
e.	Management
Supportive
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81
Q

For Salmonella, describe the following:

a. Reservoir
b. Transmission
c. Clinical presentation
d. Investigations
e. Management

A 
a.	Reservoir 
Poultry 
Reptiles/amphibians
b.	Transmission
Contaminated food 
Poor hygiene
c.	Clinical presentation 
Diarrhoea 
Vomiting 
Fever 
d.	Investigations 
Stool culture 
e.	Management
Supportive 
Ciprofloxacin 
Azithromycin
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82
Q

For Cat Scratch Disease, describe the following:

a. Presentation
b. Investigations
c. Management

A 
a.	Presentation 
Macule at site of inoculation 
Becomes pustular 
Regional adenopathy 
Systemic symptoms (FLAWS)
b.	Investigations 
Serology 
c.	Management
Erythromycin 
Doxycycline
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83
Q

For baciliary angiomatosis, describe the following:

a. Presentation
b. Investigations
c. Management

A 
a.	Presentation 
Skin papules 
Disseminated multi-organ and vasculature involvement 
Leads to bursting of blood vessels in various organs and tissues 
Can be FATAL 
b.	Investigations 
Histopathology 
Serology 
c.	Management 
Erythromycin
Doxycycline 
Rifampicin
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84
Q

For Toxoplasmosis, describe the following:

a. Reservoir
b. Transmission
c. Clinical presentation
d. Investigations
e. Management

A 
a.	Reservoir 
Cats 
Sheep
b.	Transmission
Infected meat 
Faecal contamination 
c.	Clinical presentation 
Fever 
Adenopathy 
Stillbirth 
Infants with progressive visual, hearing, motor and cognitive issues 
Seizures 
Neuropathy 
d.	Investigations 
Serology 
e.	Management
Spiramycin
Pyrimethamine + sulfadizine
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85
Q

For Brucellosis, describe the following:

a. Reservoir
b. Transmission
c. Clinical presentation
d. Investigations
e. Management

A 
a.	Reservoir 
Cattle 
Goats 
b.	Transmission
Unpasteurised milk
Undercooked meat 
Aerosolisation
c.	Clinical presentation 
Fever (and rest of FLAWS)
Back pain/bone pain
Orchitis 
Focal abscess (psoas or liver) 
Hepatosplenomegaly
d.	Investigations
Blood/pus culture 
Serology 
NOTE: the lab should be warned that you are sending suspected Brucella (they are Gram-negative cocco-bacilli)
e.	Management
Doxycycline + gentamicin or rifampicin
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86
Q

Which two infectious agents can cause rat bite fever?

A

Streptobacillus moniliformis

Spirilum minus

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87
Q

For rat bite fever, describe the following:

a. Reservoir
b. Transmission
c. Clinical presentation
d. Investigations
e. Management

A 
a.	Reservoir 
Rats 
b.	Transmission
Bites 
Contact with infected urine or droppings 
c.	Clinical presentation 
Fevers 
Polyarthralgia 
Maculopapular progressing to purpuric rash 
Can progress to endocarditis 
d.	Investigations 
Joint fluid MC&S
Blood culture 
e.	Management
Penicillins
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88
Q

List the most prevalent pathogens causing CAP in the following age groups:

a. 0-1 months
b. 1-6 months
c. 6 months – 5 years
d. 16-30 years

A 
a.	0-1 months
Escherichia coli
Group B Streptococcus
Listeria monocytogenes
b.	1-6 months
Chlamydia trachomatis
Staphylococcus aureus
RSV
c.	6 months – 5 years 
Mycoplasma pneumoniae
Influenza
d.	16-30 years
Mycoplasma pneumoniae
Streptococcus pneumoniae
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89
Q

What medium is Legionella grown on?

A

Buffered charcoal yeast extract

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90
Q

How is PCP investigated?

A

Bronchoalveolar lavage

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91
Q

How is invasive aspergillosis treated?

A

Amphotericin B

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92
Q

Which organisms cause pneumonia in the following subgroups of patients:

a. HIV
b. Neutropaenia
c. Bone marrow transplant
d. Splenectomy

A 
a.	HIV
PCP
TB
Atypical mycobacteria
b.	Neutropaenia
Fungal (e.g. Aspergillus)
c.	Bone marrow transplant
CMV 
d.	Splenectomy 
Encapsulated organisms (e.g. Streptococcus pneumoniae, Haemophilus influenzae)
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93
Q

Which respiratory organism is investigated using immunofluorescence?

A

PCP

NOTE: PCP can also be detected using silver stain

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94
Q

What are the 1st and 2nd line treatment options for HAP?

A 
1st = ciprofloxacin +/- vancomycin
2nd = tazocin AND vancomycin
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95
Q

Which antibiotics are used to treat HAP caused by:

a. MRSA
b. Pseudomonas

A

a. MRSA
Vancomycin
b. Pseudomonas
Tazocin OR ciprofloxacin +/- gentamicin

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96
Q

What is the difference between yeasts and moulds?

A 
Yeast = unicellular 
Moulds = multicellular and has filaments (hyphae)
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97
Q

List three types of mycobacterial complex.

A 
Mycobacterium tuberculosis complex
•	Mycobacterium tuberculosis
•	Mycobacterium bovis
Mycobacterium avium complex
•	Mycobacterium avium
•	Mycobacterium intracellulare
Mycobacterium abscessus complex
•	Mycobacterium abscessus
•	Mycobacterium massiliense
•	Mycobacterium bolletii
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98
Q

Describe the morphology of mycobacteria.

A

Non-motile rod-shaped bacteria
Relatively slow-growing
Cell wall composed of mycolic acids, complex waxes and glycoproteins
Acid-alcohol fast

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99
Q

List three examples of slow-growing non-tuberculous mycobacteria and the diseases that they cause.

A

Mycobacterium avium intracellulare
• May invade bronchial tree or pre-existing bronchiectasis/cavities
• Disseminated infection in immunocompromised patients
Mycobacterium marinum
• Swimming pool granuloma
Mycobacterium ulcerans
• Skin lesions (e.g. Bairnsdale ulcer, Buruli ulcer)
• Chronic progressive painless ulcer

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100
Q

List three examples of rapid-growing non-tuberculous mycobacteria.

A

Mycobacterium abscessus
Mycobacterium chelonae
Mycobacterium fortuitum

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101
Q

What are the two types of Mycobacterium leprae infection?

A

Paucibacillary tuberculoid – few skin lesions, robust T cell response
Multibacillary lepromatous – multiple skin lesions, poor T cell response

NOTE: tends to present with paraesthesia and hairless skin plaques

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102
Q

List some types of extra-pulmonary TB.

A

Lymphadenitis (scrofula) – cervical lymph nodes most commonly
Gastrointestinal – due to swallowing of tubercle
Peritoneal – ascitic or adhesive
Genitourinary
Bone and joint – due to haematogenous spread (e.g. Pott’s disease)
Miliary TB
Tuberculous meningitis

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103
Q

What is NAAT and why is it useful for TB?

A

Nucleic acid amplification test
Allows speciation and the detection of drug resistance mutations
Rapid

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104
Q

List some side-effects of:

a. Rifampicin
b. Isoniazid
c. Pyrazinamide
d. Ethambutol

A 
a.	Rifampicin 
Raised transaminases 
CYP450 induction 
Orange secretions 
b.	Isoniazid
Peripheral neuropathy (give with pyridoxine)
Hepatotoxicity
c.	Pyrazinamide
Hepatotoxicity
Hyperuricaemia 
d.	Ethambutol
Visual disturbance
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105
Q

What is multi-drug resistant TB?

A

Resistant to rifampicin and isoniazid

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106
Q

What is extremely drug resistant TB?

A

Resistant to rifampicin, isoniazid, fluoroquinolones and at least 1 injectable (e.g. amikacin, capreomycin)

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107
Q

Which valvular defect is most common in rheumatic fever?

A

Mitral stenosis

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108
Q

What is the most common cause of hospital-acquired pneumonia?

A

Pseudomonas aeruginosa

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109
Q

Which congenital infection is associated with periventricular calcification?

A

CMV

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110
Q

Why does influenza cause respiratory disease in humans?

A

The virus has a haemagglutinin (HA) protein which must be cleaved for the virus to be able to fuse with the endosome membrane and release its genome into the host
Human airway tryptase found in the lining of the lung is capable of cleaving HA
NOTE: there are some mutated forms of influenza that do not require cleavage of HA to be able to enter host cells (these are particularly virulent)

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111
Q

Describe the influenza life cycle.

A

The virus attaches to cells via the sialic acid receptor
They enter through endosomes
The acidity of the endosome triggers a fusion event by which the virus releases its genome into the host cell
The genome travels to the nucleus and takes over host factors to drive transcription and translation
New viral products are produced, which assemble at the surface of the cell and bud off producing hundreds of copies of the virus

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112
Q

Which specific mutation is associated with enabling influenza to cross into humans from birds?

A

PB2 627K (polymerase protein)

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113
Q

What is the mechanism of action of amantadine?

A

Targets the M2 ion channel

A single amino acid mutation (S31N) renders the virus resistant

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114
Q

List three examples of neuraminidase inhibitors.

A

Oseltamivir (Tamiflu) – oral
Zanamivir (Relenza) – inhaled or IV
Peramivir – IV

NOTE: effective if given < 48 hours after infection

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115
Q

List two examples of polymerase inhibitors used to treat influenza.

A

Favipiravir

Baloxavir

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116
Q

Outline the mechanism of action of aciclovir.

A

Guanosine (nucleoside) analogue that is incorporated into growing viral DNA and blocks further elongation
Requires activation by viral thymidine kinase (which is only present in host cells that are infected by the virus)
Aciclovir has a higher affinity for viral DNA polymerase than host DNA polymerase

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117
Q

What are two 2nd line treatment options for aciclovir-resistant VZV infection?

A

Foscarnet
Cidofovir
NOTE: they inhibit viral DNA synthesis

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118
Q

HSV encephalitis is a medical emergency. How should it be treated?

A

IMMEDIATE treatment with IV aciclovir 10 mg/kg TDS without waiting for test results
If confirmed, treat for 21 days

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119
Q

What is HSV meningitis and how should it be treated?

A

Usually self-limiting
Immunocompromised patients and those who are unwell enough to require hospital admission require treatment
IV aciclovir for 2-3 days followed by oral aciclovir for 10 days

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120
Q

List some indications for treatment of VZV.

A

Chickenpox in adults (high risk of pneumonitis)
Shingles in adults > 50 years (risk of post-herpetic neuralgia)
Infection in immunocompromised patients
Neonatal chickenpox
If increased risk of complications (e.g. underlying lung disease)

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121
Q

In which cells does CMV lie dormant?

A

Monocytes and dendritic cells

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122
Q

What is a characteristic histological feature of CMV infection?

A

Owl’s eye inclusions

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123
Q

What is the 1st line treatment option for CMV infection?

A

Ganciclovir (IV)

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124
Q

How is ganciclovir activated?

A

Requires activation by viral UL97 kinase enzyme

NOTE: ganciclovir is used in conjunction with IVIG in patients with CMV pneumonitis

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125
Q

What is a major side-effect of ganciclovir?

A

Bone marrow toxicity

NOTE: therefore, its use is limited in bone marrow transplant patients

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126
Q

What is the mechanism of action of foscarnet?

A

Non-competitive inhibitors of viral DNA polymerase
NOTE: foscarnet does NOT require activation
Tends to be used in CMV infections if ganciclovir is contraindicated

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127
Q

What is the mechanism of action of cidofovir?

A

Competitive inhibitors of viral DNA synthesis (nucleotide analogue)
NOTE: does not require activation

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128
Q

What is a major side-effect of foscarnet and cidofovir?

A

Nephrotoxicity

Cidofovir requires hydration and probenecid

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129
Q

What is the mechanism of action of maribavir?

A

Inhibits viral kinase

Effective in vitro, currently undergoing clinical trials

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130
Q

What is the mechanism of action of letermovir?

A

CMV DNA terminase inhibitor

Approved in the USA for CMV prophylaxis in bone marrow transplant patients

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131
Q

What are the roles of haemagglutinin and neuraminidase in the influenza virus?

A

Haemagglutinin – mediates viral binding and entry into target cell
Neuraminidase – allows release of progeny virus particles from the host cell

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132
Q

What are the 3 indications for use of neuraminidase inhibitors in the community according to NICE?

A

National surveillance indicates that influenza is circulating
Patient is in a risk group
Within 48 hours of onset of symptoms

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133
Q

What disease states does BK virus cause?

A

Bone marrow transplant  haemorrhagic cystitis

Renal transplants  BK nephritis and ureteric stenosis

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134
Q

Outline the treatment of BK haemorrhagic cystitis.

A

Bladder washouts
Reduce immunosuppression
Cidofovir IV (may consider intravesical)

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135
Q

Outline the treatment of BK nephropathy.

A

Reduce immunosuppression
IVIG
NOTE: cidofovir cannot be used because it is nephrotoxic

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136
Q

Outline the treatment of adenovirus infection in transplant patients.

A 
Cidofovir IV 
IVIG 
Brincidofovir (prodrug of cidofovir currently undergoing clinical trials)
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137
Q

What are most cases of HSV drug resistance caused by?

A

Mutations in viral thymidine kinase

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138
Q

What are most cases of CMV drug resistance caused by?

A

Mutations in protein kinase gene UL97

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139
Q

What are the main treatment options for drug resistant HSV and CMV infection?

A

Foscarnet and cidofovir

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140
Q

What is the herd immunity threshold?

A

Threshold = 1 – 1/R0

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141
Q

Describe the following types of vaccines:

a. Inactivated
b. Live attenuated
c. Toxoid
d. Subunit
e. Conjugate
f. Heterotypic

A

a. Inactivated
Whole microorganism is destroyed (using heat, radiation or antibiotics)
NO risk of causing infection in the host
Immune response may not be particularly strong or long-lasting
b. Live attenuated
Live organisms are modified to be less virulent
Risk of acquiring virulence
Should be avoided in pregnant women and immunocompromised patients
c. Toxoid
Inactivated toxin components
d. Subunit
Protein components of the microorganism or synthetic virus-like particles
Lack genetic material and are unable to replicate
e. Conjugate
Poorly immunogenic antigens are paired with a protein that is highly immunogenic (adjuvant)
f. Heterotypic
Using pathogens that infect other animals but do NOT cause disease in humans

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142
Q

List examples of the following types of vaccine:

a. Inactivated
b. Live attenuated
c. Toxoid
d. Subunit
e. Conjugate
f. Heterotypic

A 
a.	Inactivated 
Influenza
Polio
Cholera
b.	Live attenuated 
MMR 
Yellow fever 
c.	Toxoid
Diphtheria 
Tetanus
d.	Subunit
Hepatitis B 
HPV  
e.	Conjugate
Haemophilus influenzae type B
f.	Heterotypic 
BCG
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143
Q

List some contraindications for vaccines.

A

Previous anaphylactic reactions
Anaphylactic reaction to egg is contraindicated with the influenza vaccine
Immunocompromised and pregnant women should not receive live attenuated vaccines
If acutely unwell on the day of vaccination
DTP is contraindicated if evidence of neurological abnormality

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144
Q

List some examples of serious reactions associated with the following vaccines:

a. DTP
b. Poliovirus
c. Measles
d. Rubella
e. T/DT/Td
f. Hepatitis B

A 
a.	DTP 
Encephalopathy 
Shock 
Anaphylaxis
b.	Poliovirus
Guillain-Barre syndrome 
Polio
c.	Measles 
Anaphylaxis 
Thrombocytopaenia
d.	Rubella 
Acute arthritis 
e.	T/DT/Td
Guillain-Barre syndrome 
Brachial neuritis 
Anaphylaxis
f.	Hepatitis B
Anaphylaxis
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145
Q

Which type of genome do all herpes viruses have?

A

DNA

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146
Q

What is the most common cause of UTI in young, sexually active women?

A

Staphylococcus saprophyticus

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147
Q

List some antibiotics that have anti-Pseudomonas activity.

A

Gentamicin
Ciprofloxacin
Tazocin

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148
Q

What is the most common viral cause of rapidly progressive glomerulonephritis?

A

Hepatitis B

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149
Q

Which organisms most commonly cause non-bloody diarrhoea and vomiting soon after eating contaminated food?

A

Bacillus cereus

Staphylococcus aureus

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150
Q

What are the two types of paralysis caused by clostridia?

A

Botulinum –> flaccid paralysis

Tetani –> spastic paralysis

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151
Q

What are the possible outcomes for neonates with congenital toxoplasmosis?

A 
Asymptomatic (60%) at birth but go on to develop long-term sequelae such as deafness, low IQ and microcephaly 
Symptomatic (40%) at birth 
•	Choroidoretinitis
•	Microcephaly/hydrocephalus
•	Intracranial calcifications 
•	Seizures 
•	Hepatosplenomegaly/jaundice
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152
Q

What is the triad of features in congenital rubella syndrome?

A

Cataracts
Congenital heart disease (PDA is most common)
Deafness
Other features: microphthalmia, glaucoma, retinopathy, ASD/VSD, microcephaly, meningoencephalopathy, developmental delay

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153
Q

How if Chlamydia trachomatis transmitted to the neonate and what disease does it cause in the neonate?

A

During delivery
Causes neonatal conjunctivitis (ophthalmia neonatorum) or pneumonia
NOTE: it is treated with erythromycin

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154
Q

Which mycoplasma species can cause neonatal infection?

A

Mycoplasma hominis

Ureaplasma urealyticum

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155
Q

What are the three main organisms that cause early-onset infection?

A

Group B Streptococcus
E. coli
Listeria monocytogenes

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156
Q

What type of bacterium is Group B Streptococcus?

A

Gram-positive coccus
Catalase negative
Beta haemolytic

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157
Q

What type of organism is Listeria monocytogenes and what disease can it cause?

A

Gram-positive rods

Causes sepsis in the mother and the newborn

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158
Q

Which antibiotics are commonly used to treat early-onset sepsis?

A

Benzylpenicillin + gentamicin

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159
Q

What are the main causes of late-onset sepsis?

A

Coagulase negative staphylococci (e.g. S. epidermidis)
GBS
E. coli
Listeria monocytogenes
S. aureus
Enterococcus sp.
Gram-negatives (e.g. Klebsiella, Enterobacter, Pseudomonas)

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160
Q

Outline the treatment of late-onset sepsis.

A

Treat early with antibiotics
Guidelines differ
Example antibiotic regimen: 1st line = cefotaxime + vancomycin; 2nd line = meropenem

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161
Q

What is the main bacterial cause of meningitis at the moment?

A

Meningitis B

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162
Q

What type of organism is Streptococcus pneumoniae?

A

Gram-positive diplococcus

Alpha haemolytic

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163
Q

What type of organism is Haemophilus influenzae?

A

Gram-negative cocco-bacilli

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164
Q

What is the most common cause of death in:

a. Postnatal children (1-59 months)
b. Neonates

A 
a.	Postnatal children (1-59 months)
Pneumonia
Followed by congenital anomalies
b.	Neonates 
Prematurity 
Followed by intra-partum complications
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165
Q

Which children are mainly affected by Mycoplasma pneumoniae?

A

Older children (> 4 years)

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166
Q

List some extra-pulmonary manifestations of Mycoplasma pneumoniae.

A

Haemolysis – IgM antibodies to I antigen on erythrocytes, cold agglutinins
Neurological – encephalitis, aseptic meningitis, peripheral neuropathy, transverse myelitis
Polyarthralgia
Otitis media
Bullous myringitis (vesicles on the tympanic membrane – pathognomonic of Mycoplasma)
Erythema multiforme

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167
Q

List three examples of:

a. Yeast
b. Moulds

A 
a.	Yeast
Candida
Cryptococcus
Histoplasma (dimorphic)
b.	Moulds
Aspergillus
Dermatophytes
Agents of mucormycosis
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168
Q

List some patient groups that are at risk of invasive Candida infection.

A

VLBW infants
Immunocompromised
Patients on ITU (especially if they have lines in)
Patients receiving TPN
Immunocompetent patients who have had antibiotic treatment

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169
Q

List some agents that can cause candidiasis.

A

Candida albicans (MOST COMMON)
Candida glabrata
Candida krusei
Candida tropicalis

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170
Q

Describe a screening test for candidiasis.

A

Candida albicans forms a germ tube

Can be identified by microscopy

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171
Q

What does generalised candidiasis in babies usually occur secondary to?

A

Seborrhoeic dermatitis

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172
Q

What type of agar is needed for culturing Candida?

A

Sabouraud agar – impregnated with antibiotics to prevent bacteria from outcompeting the fungi

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173
Q

Outline the management of candidiasis.

A

At least 2 weeks of antifungals after the last negative culture
Echo and fundoscopy to look for endocarditis/endophthalmitis
Echinocandins – empirical for non-albicans infections
Fluconazole – empirical for Candida albicans

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174
Q

What is the treatment of choice for Cryptococcus infection?

A

Ambisome (amphotericin B)

NOTE: it is inherently resistant to echinocandins

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175
Q

Describe the appearance of Cryptococcus under the microscope.

A

Distinct capsule around the yeast
India ink can be used to stain
NOTE: the capsule is not always present

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176
Q

Why might a lumbar puncture be negative in cryptococcal meningitis?

A

Cryptococcal meningitis can cause hydrocephalus which prevents the circulation of CSF meaning that the sample taken at LP may not have been exposed to CSF within other parts of the ventricular system

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177
Q

Outline the treatment options for Cryptococcus infection.

A

3 weeks amphotericin B (ambisome) +/- flucytosine
Repeat LP for pressure measurement
Secondary suppression – fluconazole

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178
Q

List the aetiological agents that can cause Aspergillus infection.

A 
Aspergillus fumigatus 
Aspergillus flavus
Aspergillus niger
Aspergillus niduland
Aspergillus terreus
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179
Q

List some investigations used in the diagnosis of Aspergillus infection.

A 
Blood test 
Serology (check IgE for allergic response (e.g. ABPA))
•	Antigen detection (galactomannan) 
•	Also detected in BAL 
PCR 
Histology 
Culture
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180
Q

What is the mainstay of treatment for aspergillosis?

A

Amphotericin for at least 6 weeks

Other options: voriconazole, caspofungin, itraconazole

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181
Q

What is tinea pedis caused by?

A 
Tricophyton rubrum (MOST COMMON) 
Tricophyton interdigitale
Epidermophyton floccosum (can also cause tinea cruris)
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182
Q

What is pityriasis versicolor caused by?

A

Malassezia furfur

NOTE: it has a spaghetti and meatballs appearance on microscopy

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183
Q

Which groups of patients are affected by mucormycosis?

A

Immunocompromised patients

Patients with poorly controlled diabetes

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184
Q

What is the characteristic clinical manifestation of mucormycosis?

A

Cellulitis of the orbit and face which progresses with discharge and black pus from the palate and nose
NOTE: black eschars may be seen as the fungus destroys tissues

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185
Q

What is the term used to describe invasion of the brain by mucormycosis?

A

Rhinocerebral mucormycosis

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186
Q

List three aetiological agents that can cause mucormycosis.

A

Rhizopum spp.
Rhizomucor spp.
Mucor spp.

187
Q

List antifungals that target:

a. Cell membrane
b. DNA/RNA synthesis
c. Cell wall

A 
a.	Cell membrane 
Polyene – amphotericin B, nystatin
Azole – ketoconazole, itraconazole, fluconazole, clotrimazole
b.	DNA/RNA synthesis
Flucytosine (pyrimidine analogue)
c.	Cell wall
Echinocandins – caspofungin acetate
188
Q

What is the mechanism of action of azoles?

A

Inhibit ergosterol production by inhibiting CYP450 enzyme lanosterol 14-demethylase
This inhibition leads to the accumulation of toxic steroids in the cell membrane which cause cell death

189
Q

List examples of the following types of azoles along with their usual indications:

a. Water-soluble triazoles
b. Lipophilic triazoles

A

a. Water-soluble triazoles
Fluconazole – active against Candida and Cryptococcus
Voriconazole – similar to fluconazole but better activity against Aspergillus
b. Lipophilic triazoles
Itraconazole – useful against dermatophytes
Posaconazole – activity against mucor

190
Q

List some examples of echinocandins.

A

Caspofungin
Micafungin
Anidulafungin

191
Q

What is the mechanism of action of echinocandins?

A

Cyclic lipopeptide antibiotic that inhibits beta-(1,3) D-glucan synthase
This enzyme is responsible for the production of beta D-glucan which is a component of the fungal cell wall
This inhibition results in osmotic fragility of the cell

192
Q

Which fungi are echinocandins active against?

A

Candida species
Aspergillus species (NOT other moulds)
IMPORTANT: it has NO coverage for Cryptococcus

193
Q

How is amphotericin B produced?

A

Fermentation product of Streptomyces nodusus

194
Q

Describe the mechanism of action of amphotericin B.

A

Binds to ergosterol in the fungal cell membrane and creates transmembrane channels leading to electrolyte leakage
This leads to fungal cell death

195
Q

Amphotericin B is active against most fungi except…

A

Aspergillus terreus

Scedosporium spp.

196
Q

What is the main side-effect of amphotericin B? Describe the mechanism of this toxicity.

A

Nephrotoxicity
Renovascular – decrease in renal blood flow leads to reduced GFR (azotaemia)
Tubular – distal tubular ischaemia, wasting of sodium, potassium and magnesium

197
Q

Describe the mechanism of action of flucytosine.

A

Inhibits DNA synthesis (pyrimidine analogue)

198
Q

What are some mechanisms of resistance to flucytosine?

A 
Decreased uptake (permease activity)
Altered 5-FC metabolism
199
Q

Which fungi are flucytosine active against?

A

Candidiasis

Cryptococcosis

200
Q

Which fungi are flucytosine active against?

A

Candidiasis

Cryptococcosis

201
Q

Describe the mechanisms of teratogenicity of rubella.

A

Decrease in rate of cell division (leading to structural malformation)
Decrease in overall number of cells (small babies)
Interference with the development of key organs
Tissue necrosis due to viral replication

202
Q

Describe some tests that are used in the diagnosis of rubella.

A

Rubella IgG
• Seroconversion – if woman initially has negative IgG but then has a positive IgG result after possible exposure, it suggests that they have been exposed to rubella
• Avidity – high avidity means that exposure occurred > 3 months ago
• This is part of routine antenatal screening
Rubella IgM
Detection of virus (PCR) – blood, urine, tissues

203
Q

What is the role of pre-natal diagnosis of rubella?

A

All cases of symptomatic rubella infection in the 1st trimester should be considered for termination of pregnancy without prenatal diagnosis

204
Q

What is the definition of congenital CMV infection?

A

Detection of CMV from bodily fluids (normally urine and saliva) or tissues within the first 3 weeks of life
NOTE: it is the MOST COMMON congenital viral infection

205
Q

What is the term used to describe congenital changes that occur as a result of CMV infection? List some features.

A

Cytomegalic inclusion disease
• CNS: microcephaly, mental retardation, epilepsy
• Eye: chorioretinitis
• Ear: sensorineural deafness
• Liver: hepatosplenomegaly, jaundice
• Lung: pneumonitis
• Hear: myocarditis
• Thrombocytopaenic purpura
• Haemolytic anaemia
NOTE: late sequelae include hearing defects and reduced intelligence
RCHEP: retinitis, colitis, hepatitis, encephalitis, pneumonitis

206
Q

Outline some tests used in the diagnosis of CMV infection.

A

Virus detection – cell culture, detection of early antigen fluorescent foci (DEAFF), CMV DNA (PCR)
Serology – IgG seroconversion, IgG avidity, IgM

207
Q

How is congenital CMV infection treated?

A

There is NO vaccine
Congenital CMV with significant organ disease
• Valganciclovir or ganciclovir for 6 months
• Audiology follow-up until age 6 years
• Ophthalmology review

208
Q

Outline the manifestations of neonatal HSV disease.

A

Skin, eyes and mouth (SEM) disease
CNS disease with or without SEM
Disseminated infection involving multiple organs (high mortality)

209
Q

Describe the clinical presentation of intrauterine HSV infection.

A

Neurological – microcephaly, encephalomalacia, intracranial calcification
Cutaneous – scarring, active lesions
Ophthlamologic – microophthalmia, optic atrophy, chorioretinitis

210
Q

Describe the treatment of neonatal HSV infection.

A

High-dose IV aciclovir (60 mg/kg/day) in three divided doses
For 21 days minimum in disseminated disease (repeat LP and CSF PCR until PCR-negative)
For 14 days minimum in SEM disease
Monitor neutrophil count

211
Q

List the main features of congenital varicella syndrome.

A 
LBW 
Cutaneous scarring 
Limb hypoplasia
Microcephaly 
Chorioretinitis 
Cataracts 
NOTE: risk is highest at 13-20 weeks
212
Q

Describe the manifestations of neonatal varicella infection.

A

Mild course
Disseminated skin lesions
Visceral infection
Pneumonia

213
Q

List some complications of measles.

A

Opportunistic bacterial infection (otitis media, pneumonia, bronchitis)
Encephalitis
Subacute sclerosing panencephalitis
• Tends to occur 6-15 years after measles infection
• Present with delays motor skills and behavioural problems

214
Q

What are the risks of measles in pregnancy?

A

Foetal loss (miscarriage, intrauterine death)
Preterm delivery
Increased maternal morbidity
IMPORTANT: NO congenital abnormalities to the foetus

215
Q

How should pregnant women who have been in contact with suspected/confirmed measles be treated?

A

Measles immunoglobulin attenuates the illness if given within 6 days of exposure

216
Q

What type of virus is parvovirus B19?

A

DNA virus
Parvoviridae family
NOTE: MMR are all RNA viruses

217
Q

What does the virus require in order to infect red cell precursors?

A

P blood antigen receptor (globoside)

218
Q

Describe the pathophysiology of congenital parvovirus B19 infection.

A

Virus crosses the placenta and destroys foetal red blood cell precursors causing foetal anaemia  high-output congestive cardiac failure  hydrops fetalis
Virus can also directly damage myocardial cells

219
Q

Describe how maternal parvovirus B19 infection can be diagnosed.

A

PCR – DNA amplification
Serology – parvovirus IgG seroconversion and IgM
Foetal infection – same tests

220
Q

What are some consequences of Zika virus infection in pregnancy.

A 
Miscarriage
Stillbirth
Congenital zika syndrome
•	Severe microcephaly 
•	Decreased brain tissue 
•	Seizures
•	Retinopathy/deafness
•	Talipes 
•	Hypertonia
221
Q

Give two examples of glycopeptides.

A

Vancomycin

Tiecoplanin

222
Q

Outline the mechanism of action of beta-lactam antibiotics.

A

Inactivate enzymes that are involved in the terminal stages of cell wall synthesis
Inhibits transpeptidases (aka penicillin-binding protein)
This means that there are no peptide crosslinks between peptidoglycan chains so the cell wall is weak
Beta-lactam is a structural analogue of the enzyme substrate
NOTE: they are ineffective against bacteria with no cell wall (e.g. mycoplasma, chlamydia)

223
Q

For each of the following antibiotics, describe their coverage and mechanisms of resistance:

a. Penicillin
b. Amoxicillin
c. Flucloxacillin
d. Piperacillin

A

a. Penicillin
Active against Gram-positives (e.g. Streptococci, Clostridia)
Broken down by beta-lactamases (mainly produced by S. aureus)
NOTE: penicillin is the MOST ACTIVE beta-lactam antibiotic
b. Amoxicillin
Broad-spectrum penicillin
Extends coverage to Enterococci and Gram-negative organisms
Broken down by beta-lactamase produced by S. aureus and many Gram-negatives
c. Flucloxacillin
Similar to penicillin but less active
Does NOT get broken down by beta-lactamase produced by S. aureus
d. Piperacillin
Similar to amoxicillin
Extends coverage to Pseudomonas and other non-enteric Gram-negative organisms
Broken down by beta-lactamase produced by S. aureus and many Gram-negatives

224
Q

What is a disadvantageous association of ceftriaxone?

A

Associated with C. difficile infection

225
Q

What is a benefit of ceftazidime?

A

Good anti-Pseudomonas cover

226
Q

List examples of bacteria that have shown carbapenem resistance.

A

Acinetobacter

Klebsiella

227
Q

Outline the key features of beta-lactam antibiotics.

A

Relatively non-toxic
Renally excreted (reduced dose in renal impairment)
Short half-life
Will not cross an intact blood-brain barrier (may cross inflamed meninges in meningitis)
Cross allergenic (penicillins have 5-10% cross-reactivity with cephalosporins and carbapenems)

228
Q

What are glycopeptides often used to treat?

A

Serious MRSA infections

C. difficile infections (oral vancomycin)

229
Q

What is a major side-effect of glycopeptides?

A

Nephrotoxic

Monitor blood levels to prevent accumulation

230
Q

Outline the mechanism of action of glycopeptides.

A

Glycopeptides bind to amino acid chains at the end of peptidoglycan precursors and prevent glycosidic bonds being formed (via transglycosidase) and prevent peptide crosslinks being formed (via transpeptidase)
NOTE: they are similar to beta-lactams but instead of binding to the enzymes, they bind to substrates (cell wall component precursors)

231
Q

List some classes of antibiotics that work by inhibiting protein synthesis.

A 
Aminoglycosides
Tetracyclines
Macrolides 
Lincosamides (e.g. clindamycin)
Streptogramins (e.g. Synercid)
Chloramphenicol
Oxazolidinones (e.g. linezolid)
232
Q

Outline the mechanism of action of aminoglycosides.

A

Binds to amino-acyl site of the 30S ribosomal subunit and prevents elongation of the polypeptide chain
It also causes misreading of the codons along the mRNA

233
Q

What are some major side-effects of aminoglycosides?

A

Ototoxic and nephrotoxic

234
Q

Which aminoglycosides are particularly active against Pseudomonas aeruginosa?

A

Gentamicin

Tobramycin

235
Q

Which type of bacteria do aminoglycosides have no activity against?

A

Anaerobes

236
Q

List some examples of aminoglycosides.

A 
Gentamicin 
Tobramycin
Amikacin
Neomycin 
Paromomycin
237
Q

Which environmental feature will inhibit the activity of aminoglycosides?

A

Inhibited by low pH so are not very effective in abscesses

238
Q

Which class of antibiotics are particularly effective against intracellular bacteria (e.g. chlamydia, rickettsia, mycoplasma)?

A

Tetracyclines

Newer quinolones are also effective

239
Q

List some examples of tetracyclines.

A

Tetracycline
Doxycycline
Oxytetracycline

240
Q

Which new tetracycline has extended the spectrum of tetracyclines?

A

Tigacycline

Before this, there was widespread resistance amongst Gram-negatives

241
Q

Which groups of patients should not receive tetracyclines?

A

Children and pregnant women
Because it can deposit in bone and cause discoloration of growing teeth

NOTE: a well known side-effect is a light-sensitive rash

242
Q

Outline the mechanism of action of tetracyclines.

A

Binds to the ribosomal 30S subunit and prevents the binding of aminoacyl-tRNA to the ribosomal acceptor site, thereby inhibiting protein synthesis

243
Q

What are macrolides mainly used for?

A

Mild staphylococcal and streptococcal infections in penicillin-allergic patients
Also active against Campylobacter, Legionella and Pneumophila

244
Q

Outline the mechanism of action of macrolides.

A

Binds to the 50S ribosomal subunit and interferes with translation
Also stimulates the dissociation of peptidyl-tRNA

245
Q

What are two major risks of taking chloramphenicol?

A

Aplastic anaemia

Grey baby syndrome – neonates have reduced ability to metabolise the drug

246
Q

Outline the mechanism of action of chloramphenicol.

A

Binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation

247
Q

Outline the mechanism of action of oxazolidinones.

A

Binds to the 23S components of the 50S subunit to prevent the formation of a functional 70S initiation complex (needed for translation)

248
Q

Which organisms are oxazolidinones active against?

A

Gram-positives (including MRSA and VRE)

Not active against Gram-negatives

249
Q

What are some disadvantages of oxazolidinones?

A

Expensive

May cause thrombocytopaenia and optic neuritis

250
Q

List two groups of antibiotics that inhibit DNA synthesis.

A

Quinolones

Nitroimidazoles

251
Q

List 3 examples of quinolones.

A

Ciprofloxacin
Moxifloxacin
Levofloxacin

252
Q

List 2 examples of nitroimidazoles.

A

Metronidazole

Tinidazole

253
Q

Outline the mechanism of action of quinolones.

A

Acts on the alpha-subunit of DNA gyrase predominantly with other actions

254
Q

Describe the activity of quinolones.

A

Broad antibacterial activity, especially against Gram-negatives, including Pseudomonas aeruginosa
NOTE: newer agents increased activity against Gram-negatives and intracellular organisms

255
Q

Outline the mechanism of action of nitroimidazoles.

A

Under anaerobic conditions, an active intermediate is formed, which causes DNA strand breakage

256
Q

Describe the activity of nitroimidazoles.

A

Active against anaerobic bacteria and protozoa (e.g. Giardia)

257
Q

Outline the mechanism of action of rifampicin.

A

Inhibits RNA synthesis by binding to DNA-dependent RNA polymerase thereby inhibiting initiation

258
Q

Describe the activity of rifampicin.

A

Mainly Mycobacteria and Chlamydiae

259
Q

Why should rifampicin never be used alone?

A

Resistance develops rapidly due to chromosomal mutation (single amino acid change in beta-subunit of RNA polymerase)

260
Q

Name two cell membrane toxins.

A

Daptomycin

Colistin

261
Q

Describe the activity of daptomycin.

A

Gram-positives
Likely to be used in treating MRSA and VRE
NOTE: it is a cyclic lipopeptide

262
Q

Describe the activity of colistin.

A

Active against Gram-negatives including Pseudomonas aeruginosa, Acinetobacter baumanii and Klebsiella pneumoniae
NOTE: it is a polymyxin

263
Q

Name two families of antibiotics that work by inhibiting folate metabolism.

A

Sulphonamides (sulfamethoxazole)

Diaminopyrimidines (trimethoprim)

264
Q

List some mechanisms of antibiotic resistance.

A

Chemical modification or inactivation of the drug
Modification or replacement of the target
Reduced antibiotic accumulation (impaired uptake or enhanced efflux)
Bypass antibiotic-sensitive step in cell division

265
Q

Which bacteria produce beta-lactamases?

A

S. aureus and Gram-negative bacilli (coliforms)

NOTE: this is not the mechanism of resistance in pneumococcus and MRSA

266
Q

Describe how MRSA uses ‘altered targets’ as a mechanism of resistance.

A

MRSA has a mecA gene which encodes novel PBP2a

This has a low affinity for binding beta-lactams therefore is not inactivated by beta-lactams

267
Q

Describe the mechanism of resistance in Streptococcus pyogenes.

A

Results from acquisition of a series of stepwise mutations in PBP genes
Lower level resistance can be overcome by increasing the dose

268
Q

What are AmpC beta-lactamases?

A

Breakdown penicillins and cephalosporins but are not inhibited by clavulanic acid

269
Q

Describe the mechanism of resistance to macrolides.

A

Adenine-N6 methyltransferase modifies the 23S RNA
This reduces the binding of macrolides thereby resulting in resistance
Encoded by erm (erythromycin ribosome methylation) genes
NOTE: caution when using clindamycin in Staphylococcus and Streptococcus which is resistant to macrolides because lincosamides can induce this mechanism of resistance

270
Q

Name two methods of rapid antigen detection.

A

PCR

Immunofluorescence

271
Q

Describe the type I pattern of antibiotic activity. Give an example of an antibiotic of this type.

A

Concentration-dependent killing
Peak above the MIC (Cmax) is the most important parameter
Example: aminoglycosides
These drugs tend to be given as one big dose
The benefits of achieving a higher Cmax must be balanced with the increased toxicity
Trough concentration should also be measured to ensure that the drug is being eliminated (this determines the frequency of drug administration)

272
Q

Describe the type II pattern of antibiotic activity. Give an example of an antibiotic of this type.

A

Time-dependent killing
Time spent above the MIC is the most important factor
Example: penicillins
Therefore, penicillins need to be given frequently

273
Q

Describe the type III pattern of antibiotic activity. Give an example of an antibiotic of this type.

A

Concentration and time-dependent
AUC above the MIC is the most important factor
Example: vancomycin
NOTE: infusions may be used to maintain an AUC above the MIC

274
Q

How should invasive group A streptococcal infection be treated?

A

Aggressive and early debridement
Early use of antibiotics (e.g. clindamycin)
Use of IVIG

275
Q

How is meningitis in babies < 3 months treated?

A

Cefotaxime + amoxicillin

NOTE: ceftriaxone is NOT used in neonates because it displaces bilirubin from albumin and causes biliary sludging

276
Q

List some primary causes of immune compromise.

A

UNC93B deficiency and TLR deficiency (associated with predisposition to herpes simplex encephalitis)
Epidermodysplasia verruciformis
SCID
Haemophagocytic lymphohistiocytosis in perforin deficiency
HHV8 is associated with STIM1 mutation
NOTE: perforin deficiency is also associated with increased incidence of EBV

277
Q

List some iatrogenic causes of immunosuppression in order of increasing risk of opportunistic viral infection.

A 
DMARDs and steroids (LOWEST RISK)
Cytotoxic chemotherapy
Monoclonal antibodies 
Solid organ transplant 
Advanced HIV 
Allogeneic stem cell transplant (HIGHEST RISK)
278
Q

List some diseases that it is important to monitor for in post-transplant patients.

A

CMV monitoring and prophylaxis
EBV monitoring
Adenovirus monitoring (in paediatric BMT)
HSV prophylaxis if indicated

279
Q

List the sites of latent infection of:

a. VZV
b. CMV
c. EBV

A 
a.	VZV 
Dorsal root ganglion
b.	CMV 
Monocytes 
c.	EBV 
B cells
280
Q

In bone marrow transplant patients, describe the timescale in which the herpes infections tend to occur.

A

HSV, HHV6 and HHV7 tend to occur < 1 month after transplant

CMV, VZV and EBV tend to reactivate later

281
Q

List some manifestations of VZV infection.

A 
Skin lesions 
Pneumonitis 
Encephalitis 
Hepatitis 
Purpura fulminans (neonates) 
Acute retinal necrosis 
VZV-associated vasculopathy
282
Q

What is the pathological hallmark of CMV infection?

A

Owl’s eye appearance of lung pneumocytes due to the presence of inclusion bodies

283
Q

How is the risk of reactivation of CMV different in solid organ transplantation compared to bone marrow transplantation?

A

Solid organ: greatest risk is if the donor has had past CMV but the recipient is naïve
Bone marrow transplant: greatest risk is if the donor is naïve and the recipient has had past CMV infection
NOTE: CMV is a destructive virus that directly threatens the graft and damaged endothelial cells

284
Q

Which other diseases is HHV8 associated with?

A

Primary effusion lymphoma

Multicentric Castleman’s disease

285
Q

What deadly condition is JC virus associated with?

A

Progressive multifocal leukoencephalopathy (PML)
This is a dementing process characterised by loss of higher functions (personality change, motor deficits, focal neurological signs)
Characterised by demyelination of white matter

NOTE: diagnosed by MRI or PCR of CSF

286
Q

Which specific medication is associated with an increased risk of PML?

A

Natalizumab – monoclonal antibody used in the treatment of multiple sclerosis

287
Q

What can BK virus cause?

A 
BK cystitis (post-stem cell transplant)
BK nephropathy (post-renal transplant) 
NOTE: can be treated by reducing immunosuppression
288
Q

List some manifestations of adenovirus infection in bone marrow transplant patients.

A

Fever
Encephalitis
Pneumonitis
Colitis

289
Q

How is parvovirus B19 infection in the immunocompromised treated?

A

IVIG

Blood transfusion may be required to correct the anaemia

290
Q

Which treatments particularly increase the risk of hepatitis B infection?

A

B-cell depleting therapies (e.g. rituximab)

This can be prevented by using nucleoside analogue (e.g. tenofovir) prophylaxis

291
Q

What are the three main types of worms? List some examples of each.

A 
Cestodes (tape worms) 
•	Pork/beef/fish tapeworms
•	Hydatid disease 
Trematodes (flukes)
•	Schistosomiasis
Nematodes (roundworms)
•	Hookworms 
•	Ascarids 
•	Strongyloides
292
Q

What are the two types of pork and beef tapeworms?

A

Taenia solium – pork (can invade human tissues causing cysticercosis)
Taenia saginata – beef

293
Q

Outline the lifecycle of schistosomiasis.

A

Cercariae invade human skin when in contact with contaminated water
Worms develop in the venous plexus
Eggs are excreted into the urine and faeces
They hatch into miracidia, which parasitise snails
Snails release cercariae

294
Q

How is schistosomiasis diagnosed?

A 
Microscopy
•	Urine: S. haematobium
•	Stools: S. mansoni, S. japonicum
Serology 
Biopsy 
Response to treatment
295
Q

What are the five main soil-transmitted helminths?

A 
Ascaris lumbricoides
Strongyloides stercoralis
Trichuris trichiura
Enterobius vermicularis
Hookworm
NOTE: they are very well adapted to humans so cause little disease
296
Q

Outline the lifecycle of Strongyloides.

A

Larvae invade skin
Mature into adult pinworms in the small bowel
Eggs are produced which hatch to release rhabtidiform larvae
They mature into filariform larvae (infectious)
These can autoinfect via perianal skin
NOTE: in the stool microscopy of someone with Strongyloides, you will see motile larvae rather than eggs

297
Q

How is Strongyloides treated?

A

Ivermectin

298
Q

How are the nematode infections that cause filariasis spread?

A

Blackflies and mosquitoes

299
Q

Outline the classification of filariasis.

A 
Based on location 
Lymphatic filariasis
•	Wucheria
•	Brugia
Subcutaneous filariasis 
•	Onchocerciasis 
•	Mansonella 
•	Loa Loa 
Serous cavity filariasis 
•	Mansonella 
•	Dirofilaria
NOTE: adult worms are only found in humans
300
Q

What causes damage in filariasis?

A

Adults: lymphatic filariasis (scrotal swellings, elephantiasis) and oncho nodules
Microfilariae: onchocerciasis (depigmentation, river blindness)

301
Q

What is myiasis?

A

Parasitisation of human flesh by fly larvae

302
Q

Outline the components of a reasonable parasite screen.

A

Serology: Strongyloides, Schistosoma, filaria

Stool microscopy

303
Q

How is the acquisition of pig tapeworm different from the acquisition of cysticercosis?

A

Ingesting cysts from undercooked pork will lead to the development of adult tapeworms in the human GI tract
Ingesting tapeworm eggs will lead to cysticercosis
NOTE: humans and pigs are immunologically very similar

304
Q

Outline the management of cysticercosis.

A

Anticonvulsants
Advice not to drive
Ventriculo-peritoneal shunt if hydrocephalus
Cestocidal drugs (e.g. praziquantel, albendazole)
This MUST be given with steroids to reduce inflammation around dying cysts

305
Q

How long does TB take to divide?

A

18-24 hours

306
Q

List some risk factors for TB.

A 
Malnutrition (most common)
HIV (very serious risk factor)
Poverty 
Underweight 
Past TB
307
Q

List some clinical features of severe malaria.

A 
High parasitaemia
Altered consciousness 
ARDS 
Circulatory collapse 
Metabolic acidosis 
Renal failure 
Hepatic failure 
Coagulopathy 
Severe anaemia 
Hypoglycaema
308
Q

Which stains are used for malaria?

A

Giemsa

Field’s

309
Q

Outline the treatment options for non-falciparum malaria.

A

Chloroquine – 3 days

Primaquine – 30 mg for 14 days

310
Q

What must you do before giving someone primaquine?

A

Screen for G6PD deficiency as primaquine can cause extensive haemolysis

311
Q

Outline the treatment options for mild falciparum malaria.

A 
Oral malarone (atovaquone and proguanil)
Artemisinin combination therapy (ACT) 
Oral quinine (RARELY used)
312
Q

Outline the treatment of severe falciparum malaria.

A 
ABCDE approach 
Correct hypoglycaemia 
Cautious hydration 
Organ support if necessary 
IV artesunate 
Daily parasitaemia monitoring 
Follow on with oral antimalarials
313
Q

Why is quinine not used in this situation?

A

Extensive side effects:
• Cinchonism: tinnitus, dizziness, nausea and vomiting
• Arrhythmias
• Hyperinsulinaemia

314
Q

Outline the clinical features of dengue.

A 
Fever 
Headache (retro-orbital pain) 
Myalgia 
Erythrodermic rash 
Bleeding 
Hepatitis 
Severe: encephalitis, myocarditis
315
Q

Which tropical virus is similar to dengue? What is a key difference?

A

Chikungunya

Arthralgia is more severe

316
Q

What is the term used to describe a high temperature with a relatively normal heart rate? List some causes.

A

Sphygmothermic dissociation

Causes: typhoid, yellow fever, brucellosis, tularaemia

317
Q

What type of organism is Salmonella typhi?

A

Gram-negative rod

318
Q

Outline the clinical features of typhoid.

A 
High prolonged fever 
Headache 
Rose spots 
Constipation 
Dry cough
Hepatosplenomegaly
319
Q

What is the incubation period of typhoid?

A

7-18 days

320
Q

Outline the treatment of typhoid.

A

1st line: ciprofloxacin
Ceftriaxone 2 g IV OD
Azithromycin PO 500 mg BD 7 days

321
Q

List some investigations for mononucleosis.

A

Monospot
IgM EBV/CMV
NOTE: always consider HIV

322
Q

Which antibiotic should be given as prophylaxis in close contacts of a patient with meningococcal meningitis?

A

Ciprofloxacin (or rifampicin)

323
Q

Which organism can cause bacterial endocarditis after a colonoscopy?

A

Streptococcus bovis

324
Q

How is latent TB treated?

A

Isoniazid for 6 months

NOTE: TB meningitis and spinal TB chas the same treatment as pulmonary TB but R + I are taken for 8-10 months

325
Q

What type of bacterium is Moraxella catarrhalis?

A

Gram-negative coccus

Associated with smoking

326
Q

What type of bacterium is Klebsiella pneumoniae?

A

Gram-negative rod (enterobacter)

NOTE: more common in alcoholics and the elderly

327
Q

Which bacteria tend to cause respiratory infection in cystic fibrosis patients?

A

Pseudomonas aeruginosa

Burkholderia cepacia

328
Q

List some causes of painful genital ulcers.

A

Herpes

Chancroid

329
Q

List some causes of painless genital ulcers.

A

Syphilis (also causes snail track ulcer in the mouth)
Lymphogranuloma venereum (LGV)
Granuloma inguinale

330
Q

How is gonorrhoea treated?

A

IM Ceftriaxone 250 mg single dose

NOTE: if resistant - IM spectinomycin 2 g single dose

331
Q

Which serovars of chlamydia cause genital chlamydia?

A

D-K

NOTE: A, B and C cause trachoma (infection of the eyes that can lead to blindness)

332
Q

How is chlamydia diagnosed?

A

NAAT

NOTE: chlamydia cannot be grown on agar, it needs to be grown on cell culture (as it is an obligate intracellular bacterium)

333
Q

How is chlamydia treated?

A

Azithromycin 1 g stat

Doxycycline 100 mg BD for 7 days

334
Q

What causes lymphogranuloma venereum?

A

Chlamydia trachomatis serovars L1, L2 and L3

NOTE: starts with a painless genital ulcer and progresses to cause systemic upset, inguinal buboes and rectal symptoms (affects the lymphatics)

335
Q

Which investigations are used for syphilis?

A

Dark ground microscopy
Non-Treponemal Tests (VDRL, RPR) - detects non-specific antigens and used as a screening test
Treponemal Tests (EIA, TPHA, TPPA) - detects antibodies against specific antigens for T. pallidum. More specific

336
Q

Outline the stages of syphilis.

A

Primary - painless genital ulcer (may persist for weeks)
Secondary - systemic bacteraemia, low grade fever, non-pruritic, maculopapular rash, condylomata lata
Tertiary - neurosyphilis, cardiovascular complications, gumma

NOTE: tabes dorsalis is a demyelinating condition caused by advanced syphilis

337
Q

How is syphilis treated?

A

IM benzathine penicillin (doxycycline if allergic)

338
Q

What causes chancroid?

A 
Haemophilus ducreyi (Gram-negative coccobacillus)
Grows on chocolate agar
339
Q

What causes granuloma inguinale?

A

Donovanosis - Klebsiella granulomatis (Gram-negative bacillus)

Causes large expanding ulcers with a beefy red appearance

340
Q

What might be seen on microscopy of bacterial vaginosis?

A

Clue cells

341
Q

What is herpangina?

A

Painful mouth ulcers caused by Coxsackie A virus

342
Q

What feature may be seen on blood film analysis of P. vivax and P. ovale?

A

Shuffner’s dots

NOTE: these types of malaria tend to predominate in the hypnozoite (liver) stage
NOTE: in falciparum malaria you would see Maurer’s clefts on blood film

343
Q

What is Mollaret’s meningitis?

A

Benign recurrent aseptic meningitis usually due to HSV-2

NOTE: unlike most herpes simplex encephalitis which is caused by HSV-1

344
Q

What is Herpes gladiatorum?

A

Scrum pox - painful blisters, inguinal lymphadenopathy, rugby players

345
Q

Which cell type can be seen in cytological analysis of scrapings from herpes viruses?

A

Tzanck cells - acanthocytic cells found in HSV, VZV and CMV

346
Q

What are the different types of GI disease that can be caused by E. coli?

A

ETEC - toxigenic, travellers’ diarrhoea, heat labile toxin stimulated adenyl cyclase and cAMP, heat stable toxin stimulates guanylate cyclase
EIEC - invasive dysentery
EHEC - haemorrhagic, caused by verotoxin
HUS - anaemia, thrombocytopaenia, renal failure (O157:H7 toxin)
EPEC - infantile diarrhoea

347
Q

What does Yersinia enterocolitis cause?

A

Enterocolitis, mesenteric adenitis with necrotising granulomas associated with reactive arthritis and erythema nodosum

348
Q

What is leptospirosis?

A

Disease caused by Leptospira interrogans
This is excreted in dog/cat urine, penetrates broken skin from contaminated water
Causes high spiking temperature, headache, jaundice, meningism, carditis, renal failure and haemolytic anaemia
Ix: microscopic agglutination test

349
Q

How does anthrax manifest?

A

Caused by Bacillus anthracis
Cutaneous - painless round black lesions with a rim of oedema
Pulmonary (Woolsorters disease) - massive lymphadenopathy, mediastinal haemorrhage, pleural effusion

350
Q

What is Q fever?

A

Caused by Coxiella burnetii
From cattle/sheep
Fever, dry cough, fatigue, diarrhoea (like atypical pneumonia)

351
Q

What are the different types of Leishmania?

A

Cutaneous - transmitted through bite of sandly, causes skin ulcer at bite site, local lymphadenopathy
Diffuse cutaneous - in patients with immunodeficiency, nodular skin lesions
Mucocutaneous - dermal ulcer, affects mucous membranes, disfiguring facial features
Visceral (Kala-Azar) - caued by L. donovani, young malnourished children, abdominal discomfort and distension, hepatosplenomegaly, dermal disease

352
Q

What is the preferred first line treatment choice for Hepatitis B?

A

Entecavir + peginterferon alpha 2a + tenofovir

NOTE: treatment usually initiated if HBV DNA > 2000 iU/mL, moderate-severe histology or raised aminotransferases

353
Q

What are the risks of influenza in pregnancy?

A 
Stillbirth 
Preterm delivery 
Severe influenza 
NO congenital abnormalities 
Pregnant women should receive the vaccine
354
Q

What are the most common causative organisms in aseptic meningitis?

A

Coxsackie group B viruses
Echoviruses

NOTE: babies < 1 year are susceptible for aseptic meningitis

355
Q

Which bacterium is particularly associated with causing encephalitis?

A

Listeria monocytogenes

356
Q

List some reportable GI infections.

A 
Campylobacter 
Salmonella
Shigella 
Escherichia coli O157
Listeria
357
Q

Describe the mechanism by which Vibrio cholerae causes secretory diarrhoea.

A

The cholera toxin has subunits A and B which stimulate adenylate cyclase
This leads to the production of cAMP which opens chloride channels on the membranes of enterocytes
Chloride efflux into the lumen is accompanied by water and electrolyte loss

358
Q

What type of toxins does B. cereus produce?

A

Heat stable emetic toxin

Heat labile diarrhoeal toxin

359
Q

List three species of Salmonella.

A

Salmonella typhi (and paratyphi)
Salmonella enteritidis
Salmonella choleraesuis

360
Q

Which subset of patients are at increased risk of Salmonella bacteraemia?

A

Sickle cell patients

361
Q

How does Shigella infection manifest?

A

Dysentery – severe diarrhoea with blood and mucus in the faeces
NOTE: Shigella produces shiga toxin
NOTE: avoid antibiotics when treating Shigella

362
Q

How is Campylobacter infection treated?

A

Only treated if immunocompromised

Erythromycin/clarithromycin or ciprofloxacin

363
Q

What are some complications of Campylobacter infection?

A

Guillain-Barre syndrome

Reactive arthritis

364
Q

How is Giardia infection diagnosed and treated?

A

Stool microscopy
ELISA
String test
Treatment: metronidazole

365
Q

Which bacteria are all stool samples tested for?

A

Salmonella
Shigella
E. coli O157

If > 65 years, C. difficile is also checked

366
Q

Which C. difficile ribotype caused a severe outbreak in June 2005?

A

Ribotype 027

367
Q

What are the actions of the two toxins produced by C. difficile?

A

One damages the epithelial cells (cytotoxin) resulting in neutrophilic infiltration of the tissues
The other disrupts tight junctions leading to loss of fluid into the bowel
NOTE: high WCC and low CRP is a common feature in C. difficile colitis

368
Q

Describe the clinical features of sporadic CJD.

A 
Rapid dementia
Myoclonus
Cortical blindness
Akinetic mutism 
LMN signs 
NOTE: usually in older people (> 65)
369
Q

Describe the clinical features of vCJD.

A

Younger age of onset (20s)
Psychiatric onset (dysphoria, anxiety, delusions, hallucinations)
Followed by neurological symptoms (peripheral sensory symptoms, ataxia, myoclonus, chorea, dementia)

NOTE: characteristic MRI feature is pulvinar sign (high intensity in the putamen)

370
Q

What are some alternative diagnoses for someone presenting with features suggestive of prion disease?

A

Spinocerebellar ataxia

Huntington’s disease

371
Q

Which virulence factor allows S. saprophyticus to stick to the urinary tract epithelium?

A

P-fimbriae

NOTE: S. saprophyticus causes infection in young women

372
Q

In which patients do Candida UTIs tend to occur?

A

Patients with indwelling catheters

Treated by removal of catheter only (unless renal transplant)

373
Q

Which bacterium is associated with causing infection on prosthetic heart valves?

A

Staphylococcus epidermidis

374
Q

Which antiviral can be used to prevent RSV infection in at risk infants?

A

Ribavirin

NOTE: ribavirin is a guanosine nucleoside analogue

375
Q

What is the mechanism of action of zidovudine?

A

Nucleoside reverse transcriptase inhibitor (NRTI)

376
Q

Which virus is associated with causing acute necrotising encephalitis?

A

HSV1

This is the MOST COMMON cause of encephalitis

377
Q

What are the three classes of herpes viruses?

A

Alpha: neurotropic
Beta: epitheliotropic
Gamma: lymphotropic

378
Q

What causes oral hairy leukoplakia and which patient subgroup is associated with this condition?

A

EBV

Immunocompromised (e.g. HIV or IVDU)

379
Q

Which naturally occurring cytokine can inhibit HIV fusion with CD4 cells?

A

MIP-1-alpha

380
Q

Describe the main clinical features of giardiasis.

A

Severe flatulence
Bloating
Explosive diarrhoea

381
Q

Where does cryptococcus neoformans come from?

A

Pigeon droppings and pigeon nests

NOTE: histoplasmosis also comes from bird droppings

382
Q

What are the typical symptoms of rubella?

A

Macular rash beginning behind the ears
Lymphadenopathy
Joint pain
Fever

383
Q

List some causes of ring-enhancing brain lesions.

A

Abscess
Tuberculoma
Toxoplasmosis
CNS lymphoma

384
Q

What is the most common cause of UTI in catheterised men?

A

E. coli

385
Q

Describe the typical presentation of bacterial prostatitis.

A

Fever and rigors
Lower back pain
Dysuria

386
Q

Describe the microbiological appearance of Enterococcus.

A

Gram-positive cocci in chains (or pairs)

387
Q

Describe the microbiological appearance of Pseudomonas.

A

Gram-negative bacilli
Produce green pigment
Oxidase positive

388
Q

List some examples of Gram-positive bacilli.

A 
Bacillus cereus, bacillus anthracis
Clostridia
Corynebacterium diphtheriae
Listeria
Actinomyces
389
Q

List some examples of Gram-negative bacilli.

A 
E. coli
Klebsiella
Proteus
Salmonella
Shigella
Yersinia
Pseudomonas
Bordatella pertussis
Haemophilus influenzae
Legionella
390
Q

List some examples of Gram-negative comma-shaped or curved bacteria.

A

Vibrio
Campylobacter
Helicobacter

391
Q

List some examples of spiral-shaped bacteria (spirochete).

A

Treponema pallidum
Borrelia burgdorferi
Leptospira interrogans

392
Q

What CXR feature might be seen in invasive aspergillosis?

A

Halo sign

393
Q

How is a surgical site infection caused by MRSA treated?

A

IV linezolid

394
Q

Which investigation should be requested if the initial tests for PUO fail to establish a diagnosis?

A

PET-CT

395
Q

List some organisms that cause HAP.

A 
Enterobacteriaciae (MOST COMMON – e.g. E. coli, K. pneumoniae)
Staphylococcus aureus
Pseudomonas
Haemophilus influenzae
Acinetobacter baumanii
Fungi (e.g. Candida)
396
Q

What counts as a positive result on the Mantoux Test?

A

> 15 mm: if no risk factors for TB
10 mm: from high-prevalence country, employees in high-risk settings, comorbidities that increase risk (e.g. DM)
5 mm: HIV positive, recent contact with TB patient, immunosuppressed, CXR changes

397
Q

How is post-transplant lymphoproliferative disease treated?

A

Reduce immunosuppression

Rituximab (anti-CD20)

398
Q

Which score is used to determine if a patient has sepsis?

A

Q-SOFA
Altered Mental Status (GCS < 15)
Tachypnoea (22 or more)
Hypotension (< 100 mm Hg)

Score of 2 or more is high risk

399
Q

What are Amsel’s criteria for diagnosing BV?

A

Thin, white homogenous discharge
Clue cells on microscopy: stippled vaginal epithelial cells
Vaginal pH > 4.5
Positive whiff test (addition of potassium hydroxide results in fishy odour)

Needs 3 out of 4

400
Q

Which antibiotic should be given in a case of human or animal bite?

A

Co-amoxiclav

401
Q

Which antibiotics are used to treat the following GI infections:
Campylobacter
Salmonella
Shigella

A

Campylobacter = clarithromycin or erythromycin

Salmonella or Shigella = ciprofloxacin

402
Q 
Give one example of each of the following types of HIV drugs:
NRTI
NNRTI
Protease Inhibitor 
Integrase Inhibitor
A

NRTI: zidovudine
NNRTI: nevirapine
Protease Inhibitor: saquinavir
Integrase Inhibitor: raltegravir

403
Q

State the antibiotic regimens used to treat subacute and acute bacterial endocarditis.

A

Subacute: Benzylpenicillin + gentamicin; or vancomycin for 4 weeks
Acute: Flucloxacillin for MSSA, rifampicin + vancomycin + gentamicin for MRSA.

404
Q

Name three types of brucella.

A 
Brucella abortus (cows)
Brucella melitensis (goats)
Brucella suis (pigs)
405
Q

Which respiratory pathogen commonly causes pneumonia in smokers with COPD?

A

Haemophilus influenzae

NOTE: Moraxella catarrhalis is also associated with smoking

406
Q

When does pneumonia caused by S. aureus tend to occur?

A

After a recent viral infection (influenza)

407
Q

Outline the management of an infective exacerbation of COPD.

A

Mild: doxycycline/amoxicillin/clarithromycin + inhalers + prednisolone
Mod/Severe: IV antibiotics + nebulisers + hydrocortisone

408
Q 
List diarrhoeal diseases that have the following incubation periods:
< 6 hours 
12-48 hours 
48-72 hours 
> 1 week
A

< 6 hours: Bacillus cereus, Staphylococcus aureus
12-48 hours: Salmonella enteritidis, E. coli
48-72 hours: Shigella, Campylobacter, V. cholerae
> 1 week: Listeria, typhoid, Giardia, amoebiasis

409
Q

Which emerging fungal infection causes invasive hospital-acquired infections?

A

Candida auris

Particularly in immunocompromised patients with indwelling catheters

410
Q

How can Aspergillus flavus cause hepatocellular cancer?

A

Aflatoxin A1

411
Q

What is a fungal cell wall made up of?

A

Glucan

Chitin

412
Q

List some investigations used for PUO.

A 
Urine (dipstick, antigen, microscopy)
Bloods (FBC, eosinophils, ESR, 3 x blood culture, thick and thin blood films)
HIV test 
Autoantibody screen
CXR
CT-TAP
413
Q

How is infective endocarditis treated?

A

S. viridans: benzylpenicillin + gentamicin
S. aureus: flucloxacillin
MRSA: vancomycin + gentamicin
May require removal of the valve

414
Q

What is the most common cause of fever in the returning traveller?

A

Malaria

415
Q

Describe the clinical presentation of lyme disease.

A

Localised: flu-like illness, erythema migrans
Early disseminated: heart block, pericarditis, aseptic meningitis, bilateral facial palsy
Late: chronic arthritis, short-term memory loss and confusion
Treatment: doxycycline

416
Q

Which medications are used to treat hepatitis C?

A

Protease inhibitor (e.g. sofosbuvir + daclatasvir) with or without ribavirin is the mainstay

NOTE: interferon-based treatments are no longer used

417
Q

What is the technical term for dog tapeworm?

A

Echinococcus granulosus

418
Q

List the bacteria that fall under alpha, beta and gamma haemolytic streptococci.

A

Alpha: S. pneumoniae, S. viridans
Beta: S. pyogenes, S. epidermidis
Gamma: Enterococcus (faecalis, faecum)

NOTE: beta haemolytic streptococci are further divided into Lancefield groups

419
Q

Which bacteria is optochin sensitivity useful to differentiate between?

A

Optochin Sensitive: S. pneumoniae

Optochin Resistant: S. viridans (and other alpha haemolytic streptococci)

420
Q

List the organisms that are oxidase-positive.

A 
Pseudomonas
Neisseria
Campylobacter 
Helicobacter 
Moraxella 
Vibrio
Legionella

Mnemonic: PuNCH Me Very Lightly

421
Q

Which organisms cause the following types of leishmaniasis:
Visceral
Cutaneous
Mucocutaneous

A

Visceral: L. donovani, L. infantu, L. chagasi
Cutaneous (most common): L. major, L. tropica
Mucocutaneous: L. braziliensis

422
Q

What are the main clinical features of trypanosomiasis and what are the two main forms?

A

Subcutaneous chancre at the site of Tsetse fly bite
Fevers, weakness, arthralgia and headache
Later: disturbance of sleep cycle, ataxia
T. brucei gambiense (95%) - chronic course, West and Central Africa
T. brucei rhodesiense (5%) - rapid infection (over weeks/months), Southern Africa
T. cruzi - Chagas disease

423
Q

Briefly describe the lifecycle of plasmodium.

A

Injected into the blood as sporozoites from the female Anopheles mosquito
Moves to liver
Become merozoites which escape the liver and infect blood cells (erythrocytic phase)
Multiply in erythrocytes and are released at intervals
Some merozoites become gametocytes
NOTE: in the liver, sporozoites can sometimes lie latent as hypnozoites

424
Q

What is the best diagnostic test for hepatitis C?

A

HCV RNA

NOTE: chronic infection is defined as the persistence of HCV RNA after 6 months

425
Q

How long is the HIV incubation period?

A

3-12 weeks

Therefore, an HIV test should only be performed 3 months after exposure

426
Q

What are the first and second line treatment options for PCP?

A

1st line: co-trimoxazole

2nd line: clindamycin and primaquine

427
Q

Which viral and fungal/parasite infections are T and B cell deficiencies associated with?

A 
T cells 
- Viruses: CMV, EBV, VZV
- Fungi/Parasites: Candida, PCP
B cells
- Viruses: enteroviral encephalitis
- Fungi/Parasites: Giardia
428
Q

What is a ‘complicated’ UTI?

A 
Infection in a UTI with structural or functional abnormalities (including indwelling catheters and calculi)
Includes any UTI in:
- Men
- Pregnant Women
- Children
- Hospitalised patients
429
Q

How would you manage a patient with leucocyte positive, nitrite negative urine?

A

Treat if severe symptoms and send urine culture

430
Q

When should patients with a UTI have urine sent for microscopy, culture and sensitivities?

A

Pregnancy, children or men
Suspected pyelonephritis
Catheterised patients
Failed antibiotic treatment (resistance)
Abnormalities of the genitourinary tract
Renal impairment

431
Q

What is the antibiotic regimen of choice for an uncomplicated UTI in a woman?

A

Nitrofurantoin or Cephalexin

432
Q

What is the antibiotic regimen of choice for a UTI in a pregnant woman?

A

1st line: nitrofurantoin (avoid at term)

2nd line: cefalexin or co-amoxiclav

433
Q

What is the antibiotic regimen of choice for a UTI in a man?

A

Cefalexin or ciprofloxacin

Chronic prostatitis: ciprofloxacin 500 mg BD PO for 4-6 weeks

434
Q

What is the antibiotic regimen of choice for pyelonephritis or urosepsis?

A

IV co-amoxiclav
Consider adding IV amikacin or gentamicin
Penicillin allergy: ciprofloxacin 400 mg IV BD

If frail, elderly and high-risk of C. difficile: IV gentamicin or IV amikacin

435
Q

How is catheter-associated UTI treated?

A 
Remove catheter (but give stat doses before removal of infected catheter)
Gentamicin or Amikacin (stat 30-60 mins before the procedure)
436
Q

What eye condition can be caused by candida?

A

Endophthalmitis

437
Q

How is cryptococcus diagnosed?

A

EIA looking for antigen components

438
Q

Which organisms cause tinea capitis and onychomycosis?

A

Tinea capitis: Tricophyton rubrum, Trichophyton tonsurans

Onychomycosis: Tricophyton spp., Epidermophyton spp. and Microsporum spp.

439
Q

List the classes of beta-lactam containing antimicrobials.

A

Penicillins
Cephalosporins
Carbapenems
Monobactams

440
Q

Outline the different generations of cephalosporins.

A

1st: Cephalexin
2nd: Cefuroxime
3rd: Ceftriaxone, Cefotaxime, Ceftazidime

441
Q

Which classes of antibiotic have bacteriostatic action?

A

Tetracyclines
Macrolides
Chloramphenicol

442
Q

Which classes of antibiotic have bactericidal action?

A 
Beta lactams 
Glycopeptides 
Aminoglycosides
Quinolones
Rifampicin 
Nitroimidazoles
443
Q

For each of the three types of antibiotic pharmacokinetics, list the classes of antibiotics that fall into that category.

A 
Type 1 (concentration-dependent): aminoglycosides, daptomycin, quinolones
Type 2 (time-dependent): all beta-lactams, erythromycin, linezolid 
Type 3 (mixed): tetracyclines, oxazolidinones, vancomycin, clindamycin, azithromycin
444
Q

How are mild and severe community-acquired pneumonias treated?

A

Mild: amoxicillin
Severe: co-amoxiclav + clarithromycin

445
Q

How are hospital-acquired UTIs treated?

A

Cephalexin or co-amoxiclav

446
Q

How is aspiration pneumonia treated?

A

Cefuroxime + metronidazole

447
Q

Name an antibiotic that has good cover against pseudomonas but poor anaerobe cover.

A

Ciprofloxacin

448
Q

Name two Gram-negative lactose-fermenting rods.

A

E. coli
Klebsiella

NOTE: lactose fermentation status is based on growth on MacConkey agar

449
Q

Which drug is red man syndrome associated with?

A

Vancomycin

Characterised by pain and thrombophlebitis

450
Q

Describe the mechanism of HIV entry into CD4 cells.

A
  1. Initial interaction between gp120 and CD4.
  2. Conformational change in gp120 allows for secondary interaction with CCR5.
  3. The distal tips of gp41 are inserted into the cellular membrane.
  4. gp41 undergoes significant conformational change; folding in half and forming coiled-coils. This process pulls the viral and cellular membranes together, fusing them.
451
Q

Describe the appearance of erysipelas and state which organism is most commonly implicated.

A

Red, well demarcated, oedematous rash on the face

Usually caused by S. pyogenes

452
Q

What is the most common cause of acute viral haemorrhagic cystitis in children?

A

Adenovirus

453
Q

Which organism causes gas gangrene? Describe its presentation.

A

Clostridium perfringens
Oedema and discoloration with necrotic bullae
Soil-transmitted through breaks in the skin

454
Q

For which conditions is post-exposure prophylaxis available?

A

Rabies
HIV
Tetanus

455
Q

List some examples of anaerobic bacteria.

A 
Actinomyces
Bacteroides
Clostridium
Porphyromonas
Propionibacterium
456
Q

Which types of bacteria are chocolate agar used to grow?

A

Fastidious bacteria
Haemophilus influenza
Neisseria meningitidis (usually requires a variant of chocolate agar which contains antibiotics called Thayer-Martin agar)

NOTE: Mueller-Hinton agar is an alternative

457
Q

What is sporotrichosis?

A

Rose gardener’s disease (caused by Sporothrix schenckii)
Fungus found in plants and soil
Prick by thorn leads to nodular lesions to appear on the skin
They are initially small and painless but will become ulcerated
Infection can spread to joints, bone and muscle

458
Q

What are the HACEK organisms?

A 
Fastidious Gram-negative bacteria that are an unusual cause of infective endocarditis 
Haemophilus 
Aggregatibacter
Cardiobacterium
Eikenella
Kingella
459
Q

What is the mechanism of action of tenofovir?

A

NucleoTide reverse transcriptase inhibitor (NtRTI)

460
Q

What is the mechanism of action of lamivudine and entecavir?

A

Nucleoside reverse transcriptase inhibitor (NRTI)

461
Q

List some examples of obligate intracellular bacteria and protozoa.

A

Bacteria: Chlamydia, Rickettsia, Coxiella, Mycobacteria
Protozoa: toxoplasma, cryptosporidium, leishmania

462
Q

Which organisms can be identified with wet slide microscopy?

A

BV
TV
Candida

463
Q 
For each of each of the following types of GI infection, state a likely source:
B. cereus
C. botulinum
Campylobacter
C. perfringens
E. coli
Hep A
Listeria
Salmonella
Shigella
Staphylococcua
Vibrio
A

B. cereus - rice
C. botulinum - canned food
Campylobacter - milk, chicken, shellfish
C. perfringens - beef, poultry (reheated)
E. coli - leafy greens, beef, milk
Hep A - shellfish, water
Listeria - dairy, pate
Salmonella - vegetables, chicken, pork, eggs
Staphylococcus - sliced meat, pastry, sandwiches
Vibrio - shellfish

Laz's Pathology - Parm (5 decks)

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