Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Path > Micro > Flashcards

Micro Flashcards

1
Q

What is the name of the primary granulomatous lesion of TB (often subpleural)?

A

Ghon focus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Presentation of TB, including 3 more serious complications

A
  • Fever
  • Night sweats
  • Weight loss
  • Haemoptysis

Subacute meningitis - confusion, personality change, meningism

Spinal (Pott’s disease) - back pain, discitis, iliopsoas abscess

Miliary TB - disseminated haemotgenous spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Investigations for TB

A
  • CXR - upper lobe cavitation (post-primary)
  • Sputum sample - microscopy on Ziehl-Neelson stain, culture on Lowenstein-Jensen medium for 6 weeks (gold standard) => acid fast bacilli (red rods) seen.
  • Tuberculin skin test - shows exposure (including BCG)
  • IGRA - shows exposure (not BCG)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a more affordable and sensitive stain to Ziehl-Neelson?

A

Auramine-rhodamine

but less specific - more false positives. Specific = healthy patients getting correct diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

First line treatment for TB

A

RIPE

  • Rifampicin - 6 months
  • Isoniazid - 6 months
  • Pyrazinamide - 2 months
  • Ethambutol - 2 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Side effects of first line TB treatment

A
  • Rifampicin - orange secretions
  • Isoniazid - peripheral neuropathy
  • Pyrazinamide - hepatotoxic
  • Ethambutol - optic neuritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

2nd line TB treatment and prophylaxis

A

2nd line
• Injectables (amikacin), quinolones, linezolid
(Resistance problem)

Prophylaxis
• Isoniazid monotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical features of Leprosy (Mycobacterium leprae)

A
  • Skin depigmentation
  • Nodules
  • Trophic ulcers
  • Nerve thickening (irreversible)

Slow growing, lifelong illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Who does Mycobacterium Avium-Intracellular complex affect and what infection does it resemble?

A
  • Disseminated infection in immunocompromised

* Resembles TB if underlying lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Who does Mycobacterium Marinarum (fish tank granuloma) affect and how does it present?

A

Aquarium owners

Papules/plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is Mycobacterium ulcerans (Buruli ulcer) common and how does it present?

A

Tropics / Australia

Painless nodules => ulceration, scarring and contractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is inflamed in pneumonia?

A

Alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Score system name for pneumonia

A

CURB-65

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 common bacterial microorganisms that cause hospital-acquired pneumonia

A
  • S. aureus
  • Klebsiella
  • Pseudomonas haemophilus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the definition of hospital-acquried pneumonia?

A

Pneumonia after >48 hours of hospital admission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is atypical pneumonia different to typical?

A

Atypical
• No classic signs and symptoms
• Not in-keeping with CXR
• Don’t respond to penicillin ABx (no cell wall)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

3 common bacterial microorganisms that cause bronchitis

A
  • S. pneumoniae
  • H. influenzae
  • Moraxella catarrhalis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is bronchitis?

A
  • Inflammation of medium sized airways

* Cough with sputum for most days for 3 months, for 2 or more consecutive years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which pathogen causing penumonia typically causes rusty-coloured sputum and is usually lobar on CXR

A

S. pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which pathogen causing pneumonia is associated with recent viral infection (e.g. influenza) and shows cavitation on CXR?

A

S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which pathogen causing pneumonia is associated with alcoholism and haemoptysis?

A

Klebsiella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q 
What is seen on microscopy of 
• S. pneumonia
• H. influenza
• M. catarrhalis
• S. aureus
• K. pneumonia
A
  • S. pneumonia: +ve diplococci
  • H. influenza: -ve cocco-bacilli
  • M. catarrhalis: -ve coccus
  • S. aureus: +ve cocci “grape-bunch clusters”
  • K. pneumonia: “-ve rod, enterobacter”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How should you treat atypical pneumonia?

A

Macrolides (clarithromycin) + tetracyclines (doxycline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name 4 causes of atypical pneumonia

A
  • Legionella pneumophilia
  • Mycoplasma pneumonia
  • Chlamydia pneumonia
  • Chlamydia psittaci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What can Legionella be grown on?

A

Buffered charcoal yeast extract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cause of hyponatraemia in Legionella?

A

Diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Risk population, presentation and test for Mycoplasma pneumonia?

A

Univeristy / boarding school students

• Dry cough
• Athralgia
• Erythema multiforme
(Risk SJS, AIHA)

Cold agglutinin test +ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What can cause Chlamydia psittaci?

A

Birds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are common causes of respiratory tract infections in HIV patients?

A
  • P. jiroveci - fungus causing Pneumocystis pneumonia (desats on exercise)
  • TB
  • Cryptococcus neoformans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is a common fungal cause of respiratory tract infection and its treatment in neutropenic patients?

A

Aspergillus spp.

Amphotericin B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are common causes of respiratory tract infection in BM transplant patients?

A

Aspergillus + CMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What type of organisms commonly cause respiratory tract infection in splenectomy patients?

A

Encapsulated organisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are common causes of respiratory tract infection in CF patients?

A
  • Pseudomonas aeruginosa

* Burkholderia cepacia (high mortality)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How can S. pneumoniae and Legionella be diagnosed in severe CAP?

A

Urine antigen tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which diagnostic tests are useful in difficult-to-culture causes of pneumonia such as Chlamydia?

A

Paired serum samples

At presentation, then 10-14 days - rise in Ab level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Boat-shaped organisms seen. What is the diagnosis and the stain that was used?

A

PCP

Silver stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

ABx treatment for mild / moderate classical CAP

A

Amoxicillin

OR

Clarithromycin / doxycycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ABx treatment for severe classical CAP

A

Co-amoxiclav + Clarithromycin

OR

Erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Outline CURB-65

A
  • Confusion
  • Urea > 7
  • RR ≥ 30
  • SBP < 90, DBP ≤ 60
  • ≥ 65 yo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ABx treatment for HAP

A
  1. Ciprofloxacin +/- vancomycin
  2. ITU: piptazobactam + vancomycin

Aspiration pneumonia - cefuroxime + metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Legionella and Chlamydia psittaci ABx

A

Macrolides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

S. aureus pneumonia ABx

A

Flucloxacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

MRSA pneumonia treatment

A

Vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is infective endocarditis and the symptoms?

A

Infection of innermost layer of heart - usually valves

  • Fever
  • Anorexia
  • Weight loss
  • Night sweats

Acute - SOB, chest tightness, embolic complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Why is it important to ask about dental history if infective endocarditis is suspected?

A

Important route of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

2 risk factors for infective endocarditis

A
  • Right heart failure

* Valve replacement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What can be seen on examination in infective endocarditis?

A
  • Changing heart murmurs
  • Clubbing
  • Splinter haemorrhages
  • Osler’s nodes (tender)
  • Janeway lesions (non-tender)
  • Roth spots (fundoscopy)
  • Splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why is tricuspid valve endocarditis more common in intravenous drug abusers?

A

IV reaches right heart first

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

2 infective agents of subacute bacterial endocarditis

A
  • Low virulence strep (S. viridians)

* Staph. epidermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What type of endocarditis do the following pathogens cause:
• S. aureus - IVDA
• S. pyogenes
• Coagulase negative staphylococci - prosthetics

A

Acute bacterial endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Empirical treatment of infective endocarditis

A

Native valve
• Acute: flucloxacillin
• Indolent: penicillin + gentamycin

Prosthetic valve
• Vancomycin + gentamycin + rifampicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which valves are most commonly involved in infective endocarditis?

A

Mitral + aortic valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Outline Dukes criteria for infective endocarditis

A

2 major
1 major + 3 minor
5 minor

Major
• Positive blood cultures
• Echo findings - vegetations

Minor
• Predisposing heart condition or IVDA
• Fever >38 or high CRP
• Immunologic phenomena e.g. splinter haemorrages, haematuria
• Vascular phenomena
• Positive blood culture not typical of IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Treatment for MSSA endocarditis

A

Flucloxacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is important to note about taking blood cultures in infective endocarditis?

A

Take at least 3 from different sites (new guidelines suggest 6)

(Investigations are x3 BC and echo)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Why is 6 weeks of ABx treatment needed for infective endocarditis?

A

Valves have poor vascular supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the 3 mechanisms of GI disease

A
  • Secretory diarrhoea with no fever or white cells in stool
  • Inflammatory diarrhoea with fever and white cells in stool
  • Enteric fever with little stool change
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Give an example of secretory diarrhoea and its mechanism

A

Cholera toxin
• cAMP normally opens chloride channels in apical membrane of enterocytes
• Toxin opens chloride channels - efflux into lumen - loss of water and electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe the mechanism where systemic toxicity occurs in secretory diarrhoea, with reference to superantigens

A
  • Superantigens bind to T cell receptors outside the binding site
  • Cytokine release by CD4+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How can Staph aureus food poisoning spread?

A

Unwashed hands or skin lesions on food handlers touching food

1/3 are chronic carriers, 1/3 are transient carriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How do you diagnose staph aureus food poisoning?

A
  • Catalase and coagulase positive gram positive coccus - tetrads or clusters
  • Gold-yellow colonies with beta haemolysis on blood agar
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Mechanism and effect of staph aureus food poisoning

A
  • Produces enterotoxin (exotoxin)
  • Superantigen in GIT
  • Release of IL1 and IL2
  • Vomiting & watery diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Where can Bacillus cereus come from, how does it cause food poisoning, and how does it present?

A
  • Spores germinate in reheated fried rice
  • Heat stable emetic toxin not destroyed by reheating
  • Heat labile diarrhoeal toxin if not heated high enough
  • Watery, non-bloody diarrhoea
  • Sudden vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Food cause, mechanism and effects in clostridium botulinum (Gram positive anaerobe)

A

Gram positive anaerobe

  • Canned / vaccum packed food, honey
  • Blocks ACh release from peripheral nerves
  • Descending paralysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Food cause, mechanism and effects in clostridium perfringens (Gram positive anaerobe)

A

Gram positive anaerobe

  • Reheated meat
  • Superantigen in small intestine
  • Watery diarrhoea and gas-gangrene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Causes and name of disease caused by clostridium difficile (Gram positive anaerobe)

A
  • HAI from ABx therapy (cephalosporins, cipofloxacin, clindamycin)
  • Pseudomembranous colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Who does Listeria monocytogenes affect, what causes it, how does it present and how is it treated?

A
  • Pregnant women
  • Refridgerated food, particularly unpasteurised dairy
  • Presents with watery diarrhoea, fever (little vomiting)
  • Tx ampicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Common name for E. coli effect and where is it found?

A
  • Traveller’s diarrhoea

* Food and water contaminated with human faeces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

2 types of enterotoxins in E. coli and what do they do?

A
  • Heat labile - stimulates adenyl cylase and cAMP

* Head stable - stimulates guanylyl cylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Which parts of the GIT do E. coli toxins act?

A

Jejunum and ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the 4 types of E. coli? What do they do?

A

Enterotoxigenic (ETEC) - main cause of travellers diarrhoea

Enteropathogenic (EPEC) - infantile diarrhoea

Enteroinvasive (EIEC) - dysentery

Enterohaemorrhagic (EHEC) - caused by verotoxin producing 0157:H7 E. coli => HUS (anaemia, thrombocytopaenia, renal failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

E. coli treatment

A

No specific treatment - self-limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Outline identification of Salmonella inc. antigens

A

TSI agar - red colonies with black centres (also produce hydrogen sulphide on XLD agar)
Non-lactose fermenting

Antigens:
• Cell wall - O
• Flagellar - H
• Capsular - Vi (virulence, anti-phagocytic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Patient presents with slow onset fever, constipation and rose spots. What is the diagnosis, how is it transmitted, where does it multiply in the body and how is it treated?

A

Salmonella typhi / paratyphi
• Transmitted via water and food contaminated by human faeces
• Multiplies in Peyers patches
• Treatment with iv fluids, iv ceftriaxone, then PO azithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Patient falls ill after eating undercooked poultry and eggs. What is the pathogen responsible, how do you expect them to present, which tissue is invaded and how is it treated?

A

Salmonella enteritidis

  • No fever
  • Diarrhoea
  • Invasion of epithelial and subepithelial tissue of bowels
  • Self-limiting, no tx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Is shigella lactose fermenting and does it produce hydrogen sulphide? Furthermore, what are the cell wall and polysaccharide antigens?

A
  • Non-lactose fermenting
  • Doesn’t produce hydrogen sulphide

Antigens:
• Cell wall- O
• Polysaccharide - A-D, indentifies species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Which part of the GIT does shigella invade, how does it present, what treatment should be avoided, and which group of people are at higher risk of contracting the infection?

A

Invasion of mucosa of distal ileum and colon
Fever and severe bloody diarrhoea
Avoid abx
Increased MSM risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Patient has rice water stool with no inflammatory cells. What is the pathogen responsible, how it transmitted, what leads to the watery stool, how it treated, and what is the epidemic subset?

A

Vibrio cholerae
• Food and water contaminated with human faeces e.g. shellfish
• A + B subunits - increased cAMP opens Cl- channel at apical membrane, efflux of Cl- to lumen
• Supportive tx

O1 group - epidemic subset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Patient in Japan presents with diarrhoea. He has been eating raw seafood (oysters) recently. Treated successfully with doxycycline. What is the pathogen responsible?

A

Vibrio parahaemolyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

A HIV-positive shellfish handler was eating shellfish for dinner. He cut himself by accident at dinner, cleaned it up and went for a swim in the sea. He presented with cellulitis, diarrhoea, and vomiting, and has become septic. What is the responsible pathogen and what abx could be considered?

A

Vibrio vulnificus

• Treatment with doxycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Which genus of gram-negative bacteria are comma shaped and late lactose fermenters? Are they oxidase positive?

A

Vibriosis

• Oxidase positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Which genus of gram-negative bacteria are comma or S shaped? Are they oxidase positive?

A

Campylobacter

• Oxidase positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Patient presents with a headache and fever, followed by abdominal cramps and bloody, foul-smelling diarrhoea. He admits to drinking unpasteurised milk and having a BBQ with chicken the other day. The BBQ from the garden may not have been cleaned either. What is the responsible pathogen and how should this be treated?

A

Campylobacter jejuni

• If immunocompromised or >5 days: macrolides e.g. erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How is Yersinia enterolitica transmitted, what temperature does it prefer, how does it present, and what other manifestations is it associated with?

A
  • Food contaminated with domestic animals faeces
  • Prefers 4 degrees (cold enrichment)
  • Enterocolitis, mesenteric adenitis with necrotising granulomas
  • Associated with reactive arthritis and erythema nodosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Patient (MSM) has returned from camping where he cooked food over a fire and drank water from the stream. He has no fever, but foul-smelling non-bloody diarrhoea. He also has RUQ pain. What is the pathogen responsible, what is the cause of the RUQ pain, and how would this be treated? How could aquiring this infection through the contaminated water be prevented?

A 
Entamoeba histolytica
• Foul-smelling non-bloody diarrhoea (motile trophozoite in diarrhoeal, non-motile cyst in non-diarrhoeal)
•  RUQ pain - liver abscess
• Treat with metronidazole
• Boiling water and water filters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Flask-shaped ulcer seen on histology. Pathogen also detected in ELISA string test, stool microbiology and serology (invasive disease).

What is the pathogen responsible?

A

Entamoeba histolytica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Which part of GIT does Cryptosporidium parvum infect, how does it present, and how is it treated in aduts/kids?

A
  • Infects jejunum
  • Severe diarrhoea in immunocompromised
  • Treat with paromomycin, or nitazoxanide in kids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Oocysts seen in stool by modified Kinyoun acid fast stain. Pathogen responsible?

A

Cryptosporidium parvum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Pear shaped trophozoite seen in traveller/hiker/mental hospital. Pathogen responsible and infection it is similar to.

A

Giardia lamblia, similar to Entamoeba histolytica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How does rotavirus present and how much exposure is needed for lifelong immunity

A
  • Watery diarrhoea

* 2x exposure - immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How are UTI symptoms in children <2 years different to >2 years?

A

Non-specific i.e. failure to thrive, vomiting, fever

rather than frequency, dysuria, flank pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Diagnosis of UTI

Differentiate between coliforms / non-coliform UTI

A

• Urine dipstick - positive nitrites = coliform, -ve nitrites +ve leucotyes = non-coliform

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Why are urine samples often contaminated?

A

Urethral areas aren’t sterile, even though bladder urine is sterile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Which cells seen on microscopy are indicative of contamination of urine sample? And which are indicative of infection?

A

Contamination - squamous epithelial cells

Infection - white cells (sterile pyuria) - consider STI, TB, bladder neoplasm, prior abx treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Treatment for UTI in women andn men

A

Women

Nitrfurantoin

or Trimethoprim if low risk of resistance and EGFR >45

Men

Levofloxacin or ciprofloxacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Treatment for pyelonephritis

A

Co-amoxiclav +/- gentamicin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Treatment for candida UTI (caused by indwelling catheter)

A

No benefit of treating asymptomatic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

3 pathogens causing surgical site infections and presentation

A
  • S. aureus
  • E. coli
  • P. aeruginosa

• Failure to heal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Which layers does a deep incisional surgical site infection reach?

A

Fascial and muscle layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What number of microorganisms increases risk of surgical site infection?

A

> 10^5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Most common microorganism in osteomyelitis

A

S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

General treatment for osteomyelitis

A
  1. IV ABx for at least 6 weeks

2. Debridement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Pathophysiology of septic arthritis

A
  • Bacterial proliferation in synovial fluid
  • Inflammatory response
  • Joint damage - exposure of fibronectin
  • Bacteria (most common S. aureus) adhere to fibronectin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Diagnosis and treatment for septic arthritis

A
  • Synovial fluid aspiration (WBC >50,000)
  • Blood culture
  • ESR and CRP
  • ABx: 2 weeks IV, 4 weeks oral
  • Joint drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

3 features of prosthetic joint infection

A
  • Joint never right after operation
  • Early failure
  • Sinus tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Common microorganism in prosthetic join infection

A

Coagulase negative staphylococci (more common than S. aureus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Diagnosis and treatment for prosthetic joint infection

A
  • X-ray - loosening (bone loss)
  • Joint aspiration - higher WCC in hip vs knee
  • Intraoperative 5x tissue specimens - >3 identical organisms = PJI
  • Remove prosthesis and dead bone
  • Re-implant with antibiotic impregnated cement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Treatment for MRSA surgical site infection

A

IV linezolid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Cause of C. diff

A

Gut flora disturbed by Abx, particularly
• Clindamycin
• Cephalosporins
• Ciprofloxacin

Spore ingestion

-> pseudomembranous colitis etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Treatment for C. diff

A

ORAL metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

3 main causative organisms of acute meningitis (hours-days)

A
  • N. meningitis
  • Strep pneumoniae
  • H. influenzae B
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

3 causative organisms of meningitis in neonates

A
  • Group B Strep
  • Listeria
  • E. coli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

2 causes of chronic meningitis. What does CT show?

A

TB or Cryptococcus

Leptomeningeal enhancement on CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

2 risk factors of meningitis (N. men and S. pneu)

A
  • Complement deficiency

* Hyposplenism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Treatment for bacterial meningitis. What would you consider if consciousness was reduced?

A

Resus

Ceftriaxone and corticosteroids
Cover listeria with ampicillin
Don’t use corticosteroids under 3 months

Consider IV acyclovir if consciousness affected to cover encephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Cause of bacterial and amoebic encephalitis

A

Bacterial - Listeria

Amoebic - Naegleria fowleri (lives in warm water)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Imaginging of spinal infections

A

MRI > CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What’s the most common infection of the CNS, organisms implicated and age group affected?

A

Aseptic meningitis

Cocksackie group B and echovirus

< 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What conditions should you consider if there are painless/painful genital ulcers?

A

Painless - Syphilis

Painful - herpes

120
Q

What can develop in a neonate if gonorrhoea is untreated and transferred to the child from the birth canal?

A

Opthalmia neonatorum (neonatal conjunctivitis)

121
Q

Diagnosis and treatment of gonorrhoea

A

Urethral smear (most sensitive) and culture from this (gold standard)

Ceftriaxone or cefixime, single dose

122
Q

How does chlamydia present in most people

A

Asymptomatic

123
Q

What can the different serovars of Chlamydia cause?

A

A, B, C - trachoma -> infection of eyes -> blindness

D-K - genital chlamydia, ophthalmia neonatorum

124
Q

Diagnosis and treatment of chlamydia

A

NAAT

Azithromycin stat or doxycyline 7/7

125
Q

What are the side effects of doxycycline and when is it contraindicated?

A

N&V, photosensitivity

C/I pregnancy

126
Q

What is lympho-granuloma venereum caused by?

A

Lymphatic infection with Chlamydia trachomatis

Serovars L1, L2, L3

127
Q

Outline the stages of lympho-granuloma venereum

A

Early, primary (3-12 days): painless gentical ulcer, balanitis, proctitis, cervicitis

Early, secondary (2-25 weeks) - painful inguinal buboes, may rupture, fever

Late - abscess formation, genital elephantiasis

128
Q

How is lympho-granuloma venereum currently commonly presenting in patients?

A

MSM

Rectal pain, tenesmus, bleeding, mucous discharge

129
Q

Diagnosis and treatment for lympho-granuloma venereum

A

NAAT

Doxycycline 3 weeks

130
Q

What is syphilis caused by and what does the organism look like?

A

Treponema pallidum - obligate gram-negative spirochaete

131
Q

What type of micoscopy can treponemes be seen under in primary lesions?

A

Dark-ground microscopy

132
Q

What is the VDRL and RPR test?

A

Useful for primary syphilis
Non-treponemal test (detects non-specific antigens)

VDRL - detects lipoidal antibody on host and treponemal cells
RPR - modified VDRL

Titre falls in response to treatment - can be used to monitor response

133
Q

What do treponemal tests do, and which can be used for syphilis diagnosis? How long do they remain positive for?

A

Detect antibodies against specific antigens from T. pallidum

EIA, T. pallidum particle agglutination test (TP-PA) etc.

More specific than non-treponemal but remains positive for years

134
Q

In which stages of syphillis is a ‘snail track’ oral ulcer, condyloma acuminate (genital warts), and Argyll-Robertson pupil (not very responsive to light) seen? What is the most common tertiary sign in HIV+ve patients? When is early and late syphilis? And how does latent syphilis present?

A

Secondary (1-6 months) - ‘snail track’ oral ulcer, condyloma acuminate (genital warts)

Tertiary (2-40 years) - neurosyphilis (most common in HIV +ve), Argyll-Robertson pupil (not very responsive to light but accomodates)

Early = <12 months
Late = >12 months

Latent - asymptomatic, serological infection

135
Q

Treatment for primary syphilis

A

Single IM benzathine penicillin

136
Q

What is the Jarisch-Heimer reaction?

A

Common reaction to syphilis treatment
Fever, headache, syphilis symptom exacerbation

Develops within hours and clears within 24 hours.

137
Q

What does Haemophilus ducreyi (gram-negative) cause, where in the world it is found, presentation and diagnosis

A

Chancroid

Tropical disease mainly in Africa, rare in UK

Multiple, painful ulcers

Culture chocolate agar, PCR

138
Q

Patient from PNG presents with expanding ulcers from papule, which break down and are beefy red. Klebsiella granulomatis, gram-negative detected. What is the name of the condition and what stain is used?

A

Donovanosis

Giema stain, Donovan bodies

139
Q

Trichomoniasis pathogen type, presentation, diagnosis and treatment

A

Flagellated protozoan

Asymptmatic/urethritis in men, abnormal discharge in women

Wet prep microscopy, PCR

Metronidazole

140
Q

Microscopy shows clue cells, pH is raised, and whiff test is positive. What is the condition and its cause?

A

Bacterial vaginosis

Abnormal vaginal flora, polymicrobial, low lactobacilli, sexually associated not transmitted, hygiene practices

141
Q

Candidiasis (candida albicans) presentation and treatment

A

White thick discharge, itching, soreness, redness, vulvovaginitis (women), balanitis (men)

Not sexually transmitted

Oral antifungals e.g. clotrimazole, fluconazole

142
Q

Molluscum contagiosum cause, presentation in children, adults, PWHIV, and generally immunocompromised. Treatment.

A

Pox virus

Hands + face in children
Genital lesions in adults
Facial - adults with HIV (until proven otherwise)
Giant lesions - immunocompromised

Cryotherapy if required

143
Q

Genital warts cause and treatment

A

HPV: visible genital warts - 6 or 11

Home - podophyllotoxin solution/cream
Clinic - 1. cryotherapy 2. imiquimod

Oncogenic (16, 18) associated with cervial, anal etc. cancers

144
Q

Which abx classes inhibit cell wall synthesis (give examples)?

A

Beta lactams e.g. penicillins (benzylpenicillin), cephalosporins (ceftriaxone), carbapenems (meropenem)

145
Q

How do beta lactams work, are they bactericidal or bacteriostatic, and when are they ineffective?

A

Inactivate transpeptidases involved in terminal stages of cell wall synthesis - weaken cell wall

Bactericidal

Ineffective if in stationary phase of cell cycle or don’t have peptidoglycan wall e.g. mycoplasma and chlamydia

146
Q

Penicillin vs amoxicillin targets

A

Penicillin - gram +ve

Amoxicillin - more broad-spectrum

147
Q

How do cephalosporins change in activity with increasing generation?

A

Increased activity against gram -ve and decreased against gram +ve

148
Q

Do beta lactams cross the BBB?

A

Not if intact

Yes if inflamed meninges e.g. meningitis

149
Q

How do glycopeptides work?

A

Inhibit cell wall synthesis: instead of binding to enzymes like beta lactams, they bind to binding sites of enzymes on cell wall component precursors

Bactericidal

Large molecules so can’t pass gram -ve outer membrane

Active against gram +ve

150
Q

Which classes of abx inhibit protein synthesis (and give examples)?

A

Aminoglycosides e.g. gentamicin

Tetracyclines e.g. doxycycline

Macrolides e.g. erythromycin

Chloramphenicol

Oxazolidinones e.g. linezolid

151
Q

How do aminoglycosides work?

A

Bind to amino-acyl site of 30S ribosomal subunit

Misreading of codons along mRNA

Prevent elongation of polypeptide chain

Bactericidal

152
Q

What toxicity do aminoglycosides have?

A

Ototoxic and nephrotoxic

153
Q

Why are aminoglycosides not effective in abscesses?

A

Inhibited by low pH

154
Q

What are aminoglycosides useful in treating?

A

Gram -ve sepsis

155
Q

How do tetracyclines work and what do they target?

A

Broad-spectrum but most gram -ve are resistant

Bind to ribosomal 30S subunit, preventing binding of tRNA to acceptor site

Bacteriostatic

Activity against intracellular pathogens

156
Q

Where can tetracyclines deposit in the body?

A

Bone, causing discolouration of growing teeth

157
Q

How do macrolides work?

A

Gram +ve

Bind to ribosomal 50S subunit, interfering with translation

Bacteriostatic

158
Q

How does chloramphenicol work?

A

Binds to peptidyl transferase of 50S ribosomal subunit

Bacteriostatic

Broad spectrum

159
Q

What risks are there with taking chloramphenicol?

A

Aplastic anaemia

Grey Baby Syndrome in neonates - reduced ability to metabolise

160
Q

How do oxazolidinones work?

A

Bind to 23S of 50S to prevent 70S formation, for translation

Gram +ve e.g. MRSA and vanc. resistant E

161
Q

What are the problems with oxazolidinones?

A

Expensive

May cause thrombocytopaenia and optic neuritis

162
Q

Which abx classes inhibit DNA synthesis (give examples)?

A

Fluoroquinolones e.g. ciprofloxacin

Nitroimidazoles e.g. metronidazole

163
Q

How do fluoroquinolones work?

A

Act on DNA gyrase

Bactericidal

Better with gram negative

164
Q

How do nitroimidazoles work and which abx are related?

A

Active intermediated formed under anaerobic conditions - DNA strand breakage

Bactericidal

Nitrofurans are related compounds - concentrate in the bladder

165
Q

Which abx classes inhibit RNA synthesis (give examples)?

A

Rifamycin e.g. rifampicin

166
Q

How does rifampicin work?

A

Binds to DNA-dependent RNA polymerase, inhibiting initiation

Bactericidal

167
Q

What should and shouldn’t rifampicin be used to treat?

A

Active against Mycobacteria and Chlamydiae

Not used for short-term prophylaxis due to rapid chromosomal mutation resistance in beta-subunit of RNA polymerase
- exception is meningococcal infection

168
Q

What is important to monitor whilst taking rifampicin?

A

LFTs

Beware of interactions with other drugs metabolised by the liver

169
Q

Which abx are cell membrane toxins (give examples)?

A

Polymyxin e.g. colistin

Cyclic lipopeptide e.g. daptomycin

170
Q

What do the cell membrane toxins treat?

A

Polymyxin - gram -ve (P. aeruginosa etc.)

Cyclic lipopeptide - gram +ve (MRSA, VRE)

171
Q

Which abx inhibit folate metabolism (give examples)?

A

Sulfonamides e.g. sulphamethoxazole

Diaminopyrimidines e.g. trimethoprim

172
Q

When can combination of different folate metabolism inhibitors be useful?

A

PCP - sulphonamide resistance is common

173
Q

What stranded type of virus is influenza?

A

Negative-sense RNA

174
Q

What 3 characteristics do pandemic viruses need?

A
  • Novel antigenicity
  • Replicate efficiently in human airway
  • Transmit efficiently between people
175
Q

Which 3 flus tend to affect humans each year and when?

A
  • Influenza A (H1) - beginning of January
  • Influenza A (H1N1) - end of December
  • Influenza B - March
176
Q

What is the natural animal reservoir of Influenza A?

A

Ducks

177
Q

How do influenza viruses enter a cell?

A

1) Influenza HA (haemagglutinin) binds to exterior cell surface sialic acid receptors
2) Influenza NA (neuraminidase/sialidase) cleaves sialic acid (also needed for virus release)
3) Virus enters cell

178
Q

What is the difference between antigenic drift and antigenic shift?

A

Antigenic drift - mutation to HA/NA, new strains

Antigenic shift - complete change of HA/NA, random reassortment, only influenza A

179
Q

Where is tryptase found and what is it responsible for in influenza?

A
  • Found in bronchiolar cells
  • Cleave HA of influenza A
  • Activates the virus
180
Q

Antivirals for influenza

A

Amantadine
• Influenza A
• Targets M2 ion channel

Neuraminidase inhibitors e.g. oseltamivir (tamiflu)
• Stops virion exit
• Effective <48 hours after infection

181
Q

What strand type of viruses are coronaviruses?

A

Positive-sense single-stranded RNA

182
Q

Treatment for COVID-19

A
  • Dexamethasone

* Remdesivir (RNA polymerase inhibitor)

183
Q

HSV in immunocompromised effects

A
  • Cutaneous dissemination
  • Oesophagitis
  • Hepatitis
184
Q

How does acyclovir work?

A
  • Activated by thymidine kinase
  • Aciclovir triphophate incorporated into DNA, instead of deoxyguanosine triphosphate (dGTP)
  • Chain termination
  • No 3’ hydroxyl group - additional nucleosides prevented from attaching
185
Q

Effects of congenital HSV infection

A
  • Microcephaly
  • Scarring
  • Microphthalmia
186
Q

Effects of congenital VZV infection

A
  • Microcephaly
  • Scarring
  • Limb hypoplasia
  • Chorioretinitis, cataracts - no red reflex
187
Q

• Purpura fulminans
• Visceral infection
• Pneumonitis
Neonatal effects of which virus?

A

VZV

188
Q

Scrapings of a rash shows multinucleated giant cells (Tzanck cells). Which pathogen is responsible?

A

VZV

189
Q

Where does CMV lie latent?

A

Monocytes and dendritic cells

190
Q 
• Encephalitis
• Retinitis
• Pneumonitis
• Colitis
• Marrow suppression
Effects in immunocompromised patients infected with which pathogen?
A

CMV

191
Q

How can CMV infected cells be described to look like?

A

Owl’s eye inclusions

192
Q

CMV main congenital effect

A

Sensorineural deafness - primary cause

193
Q

CMV treatment

A

1) Ganciclovir
(IV) / valganciclovir (oral) - guanosine analogue chain terminator
2) Foscarnet (IV) - pyrophosphate analogue DNA polymerase inhibitor. Nephrotoxic.
3) Cidofovir (IV) - nucleotide analogue chain terminator

194
Q

EBV immunocompromised effects

A

Post-transplant lymphoproliferative disease - predisposes to lymphoma. Treat with rituximab

195
Q

EBV treatment

A

Supportive

Penicillin causes wide-spread maculopapular rash

196
Q

Most common cause of febrile convulsions

A

HHV6 => Roseola

197
Q

Where does HHV6 lie latent?

A

Monocytes / lymphocytes

198
Q

HHV8 immunocompromised effects

A
  • Kaposi’s sarcoma (HIV assoc)
  • Primary effusion lymphoma (EBV assoc)
  • Castleman’s disease
199
Q

Immunocompromised patient has progressive multifocal leukoencephalopathy and rapidly demyelinating disease, and so is treated with ART. What is the diagnosis?

A

JC virus

200
Q

Immunocompromised patient has haemorrhagic cystitis and nephropathy. What is the cause and treatment?

A

BK virus

Cidofovir
IVIG for nephropathy

201
Q

Who does BK virus commonly affect?

A

Patients post HSCT or kidney transplant

202
Q

Adenovirus treatment

A

Supportive

Cidofovir, IVIG if multi-organ involvement

203
Q

Hep A transmission, incubation time

A

Faeco-oral transmission

2-6 weeks incubation

204
Q

Hep A treatment

A

Supportive

Havrix vaccine

205
Q

What does high IgG and moderate IgM in hep A suggest?

A

Past infection

206
Q

Can hepatitis B be cleared?

A

90% clearance >5 y.o.

207
Q

Hep B treatment

A

Acute - supportive

  1. Inferferon alpha (don’t use in liver transplant)
    2-4. Nucleoside analogues (lamivudine, entecavir, telbivudine)
  2. Nucleotide analogue (tenofovir)
208
Q

Hep B antibodies seen in:

  1. Current infection
  2. Past infection
  3. Vaccinated
A
  1. HB surface antigen, HB core antibody
  2. HB surface antibody, HB core antibody
  3. HB surface antibody

Acute infection will have IgM anti-HBc, which chronic won’t

209
Q

Can hepatitis C be cleared?

A

60-80% chronicity

210
Q

How is hepatitis C spread?

A

Blood products

211
Q

Hep C treatment

A
  1. Vaccine
  2. Interferon
  3. NS3/4 protease inhibitors -previrs
  4. NS5A inhibitors, -asvirs
  5. Direct polymerase inhibitors, -buvirs
212
Q

When can someone only be infected with hep D?

A

With Hep B

Superinfection (catching hep D after hep B) more common than coinfection (catching both at the same time)

213
Q

Hep D treatment

A

Peginterferon-alpha

214
Q

How is hep E transmitted?

A

Faeco-oral

Shellfish, uncooked pork

215
Q

Hep E incubation range

A

2-10 weeks (6-8 week avg)

216
Q

When is the Hep E vaccine, which is being trialled, dangerous?

A

3rd trimester of pregnancy

217
Q

Patient has postauricular, occipital, and posterior cervical lymphadenopathy, maculopapular rash, fever, and red lesions on soft palate (Forchheimer sign). What is the diagnosis?

A

Rubella

218
Q

Rubella potential complications if infected between 13-18 weeks

A

Hearing defects and retinopathy

219
Q

Human parvovirus B19 signs/complications and alternative name

A

Slapped cheek syndrome (fifth disease)
• Erythema infectiosum
• Transient aplastic crisis
• Arthralgia

Viral myocarditis

220
Q

Human parvovirus B19 congenital infection complications

A

Hydrops foetalis

221
Q

Morbillivirus (measles) 2 specific signs

A
  • Koplik’s spots (white, buccal mucosa)

* Maculopapular rash - starts behind ears

222
Q

Zika virus congenital complications

A
  • Microcephaly
  • Talipes (feet turned in like club foot)
  • Hypertonia
223
Q

What does Hepatitis B e-antigen suggest?

A

Very infectious

224
Q

What are the common congenital infections?

A 
TORCH
• Toxoplasmosis
• Other (HIV, HBV)
• Rubella
• CMV
• HSV
225
Q

Diagnosis of congenital infection?

A

Maternal blood serology

Amniocentesis

226
Q

Cause of late-onset sepsis (>48 hrs)

A

Coagulase negative staph + GBS

227
Q

1st line treatment for late-onset sepsis

A

Benzylpenicillin + gent

228
Q

Late-onset sepsis from community treatment

A

Amoxicillin + cefotaxime

e.g. for listeria + community meningitis

Benzylpenicllin given in GP

229
Q

How is pyrexia of unknown origin (PUO) defined?

A
  • > 38.3°C on several occasions
  • > 3 weeks
  • Despite 1 week of intesive investigation
230
Q 
Outline the following different types of PUO:
• Classical
• Healthcare-associated
• Neutropaenic 
• HIV-associated
A

Classical
• >3 days in hospital or >3 O/P visits
• e.g. infections, neoplasms, connective tisseue diseases

Healthcare-associated
• Develops following >24 hours in hospital
• Surgery, drugs (e.g. serotonergics), medical devices

Neutropaenic (<500)
• Medical emergency
• Chemotherapy
• Haem malignancies
• Conditions that require neutrophils e.g. fungal, bacterial sepsis

HIV-associated
• Seroconversion
• TB
• Kaposi’s sarcoma

231
Q

Dengue platelet levels and diagnostic test

A

Low platelets

PCR blood

232
Q
  • Blancing maculopapular rash
  • Severe myalgia
  • Retroorbital headache

Disease?

A

Dengue

233
Q

What is sphygmo thermal dissociation and where is it seen?

A

aka Faget sign

High temperature with bradycardia

Typhoid, yellow fever, brucellosis

234
Q

P. falciparum blood film

A
  • Young trophozoites in abscence of mature trophozoites
  • Crescent-shaped gametocytes
  • Double dotted ring
  • Maurer’s clefts
235
Q

P. falciparum treatment

A
  1. Artemether/lumefantrine. IV artesunate if severe.

2. Quinine and doxycycline

236
Q

Outline approach to severe falciparum malaria

A
  • ABC
  • Correct hypoglycaemia
  • Cautious rehydration
  • Organ support
  • IV artesunate
237
Q

Seen on blood film:
Schüffner’s dots
>20 merozoites/schizonts

What is the diagnosis, where is this species common and what is the treatment?

A

P. vivax

Central America / India

Chloroquine then primaquine (check G6PD deficiency first)

238
Q

Where is P. ovale common, what is seen on blood film, what is the treatment?

A

Africa

Schüffner’s dots

Chloroquine then primaquine (check G6PD deficiency first)

239
Q

P. malariae treatment

A

Chloroquine

240
Q

Which parasite stage can lie dormant in the liver in malaria?

A

Hypnozoites

241
Q

What do schizonts look like and what do they release?

A

Daisy head

Release merzoites, which rupture from infected cell

242
Q

Difference between use of thick and thin film

A

Thick - find parasitaemia

Thin - distinguish species

243
Q

Common blood test findigns in malaria

A

WCC rarely raised
Low platelets
Deranged LFTs
Anaemia

244
Q

Features of severe malaria

A
  • Impaired consciousness or seizures (vaso-occlusive crisis)
  • Acidosis
  • Hypoglycaemia
  • Pulmonary oedema
  • Parasitaemia >2
245
Q

Which infection results after a cat scratch and how is it treated?

A

Bartonellosis

Most resolve without treatment but erythromycin can be used

246
Q

What complication is characterised by neovascular proliferation of bartonella in the skin or the internal organs?

A

Bacilliary angiomatosis

247
Q

Infection is detected with sabin feldman dye and treated with pyrimethamine + sulfadiazine + calcium folinate. What is the diagnosis and what treatment would be used in pregnant patients?

A

Toxoplasmosis

Spiramycin

248
Q

Outline bacterial infection associated with water-sports, acute form, and treatment

A

Leptospirosis

Excreted in dog/rat urine
Penetrates broken skin

Weil’s disease (acute form) - jaundice, kidney failure, bleeding

Tx - amoxicillin

249
Q

Complications of brucellosis

A

Endocarditis, osteomyelitis

250
Q

Investigation and treatment for brucellosis

A

Serology: anti-O-polysaccharide antibody

Tetracycline or doxycycline + streptomycin

251
Q

What is the histopathological feature found in the cytoplasm of nerve cells containing rabies virus (rhabdovirus) called?

A

Negri bodies

252
Q

Treatment for rabies

A

Post-exposure rabies IgG

253
Q

Patient working with cattle and small ruminants has painless round black lesions with a rim of oedema, lymphadenopathy, and mediastinal haemorrhage. What is the diagnosis, and what is is the name of the pulmonary manifestations?

A

Anthrax

Woolsorters disease

254
Q

Lyme disease transmission, signs, diagnosis and treatment

A

Tick bite

Cyclical fever, erythema chronicum migrans (ECM) - bullseye rash
Late persistent - arthritis, neuropsychiatric disturbance

Ix - Biopsy edge of ECM + ELISA for antibodies

Tx - Doxycycline

255
Q

Patient has inhaled barn dust contaminated by infected sheep, goats, cattle, and presented with signs of atypical pneumonia. What is the diagnosis?

A

Q fever

256
Q

How is Leishmaniasis transmitted?

A

Bite of sandfly

257
Q

Outline the 4 typs of leishmania

A

Cutaenous - ulcer, 1 year heal, scar, type IV

Diffuse cutaneous - nodules, immunodeficient

Muco-cutaenous - ulcers in nose/mouth/skin, months-years

Visceral = Kala Azar - young malonourished child, skin pigmentation, abdo discomfort, Leishmania donovani - invasion of reticuloendothelial system -> hepatosplenomegaly

258
Q

Outline trypanosomiasis infection
• T. brucei
• T. rhodesiense
• T. cruzi

A

Bite of tsetse fly generally in sub-Saharan Africa

  • T. brucei - most common, gradual infection
  • T. rhodesiense - rapid infection
  • T. cruzi (Chagas disease) - transmitted by Reduviidae insects only in Americas (Brazil). Initially purple eyelids. Later achalasia (difficulty for food to pass down oesophagus)
259
Q

What can be used to examine superficial fungal infections?

A

Wood’s lamp

260
Q

2 types of superficial fungal infections

A

Tinea (dermatophyte)

Pityriasis

261
Q

• Periodic acid-Schiff stain
• Sabouraud agar
• Beta-d-glucan assay
These are all used to diagnose what disease?

A

Candida (deep seated fungal infection)

262
Q

Treatment of Candida and invasive disease

A

Fluconazole for C. albicans

Amphotericin-B for invasive disease

263
Q

How does Aspergillus (deep seated fungal infection) present?

A

Pneumonia

264
Q

B-Glucan test
Grows on Czapek dox agar
Galactomannan antigen for invasive disease
Diagnosis for which diseases?

A

Aspergillus

265
Q

Treatment for Aspergillus

A

Voriconazole

266
Q

How does Cryptococcus (deep seated fungal infection) present?

A

Meningitis with insidious onset in immunocompromised

Hydrocephalus

267
Q

Which animal is Cryptococcus associated with?

A

Birds (pigeons)

268
Q

Serum is positive for the antigen of this microorganism and CSF india ink stain shows black staining for it except the capsule of the microorganism. What is the diagnosis?

A

Cryptococcus

269
Q

Cryptococcus treatment

A

Amphotericin B +/- flucytosine

270
Q

Stain for PCP

A

Methenamine Silver

271
Q

Outline mucormycosis

A

aka Black Fungus

  • Immunocompromised
  • Infects sinuses and brain
  • DM is a risk factor
  • Tx - amphotericin B and surgical debridement
272
Q

What is Sporotothrix schenckii also known as and how does it infect?

A

Rose Gardener’s disease

Present in live and decomposing plant material

Infects through cut or puncture wound in skin

273
Q

Which chromosome is prion protein gene on and what is the codon polymorphism?

A

Chr20 - predominantly expressed in CNS

Codon 129 polymorphism

274
Q

In prion disease:
What configuration does abnormal PrP(sc) fold?
What is it resistant to?
What does promote the coversion of?

A 
Abnormal PrP(sc) folds a beta-sheet configuration
...which is protease/radiation resistant

PrP(sc) acts as a template - promotes irreversible conversion of PrP to insoluble PrP(sc)

275
Q

Symptomatic and delaying prion ‘conversion’ treatment

A

For myoclonus - clonazepam

Delaying conversion - quinacrine, pentosan, tetracycline

276
Q

EEG in sporadic CJD (Creutzfeldt-Jakob disease) and variant CJD

A

Sporadic - periodic triphasic changes

Variant - non-specific slow waves

277
Q

CSF analysis in sporadic and variant CJD

A

14-3-3, marker of neurodegeneration

can be normal in variant

278
Q

Western blot PrP(sc) types in sporadic, variant, and iatrogenic CJD

A

Sporadic - types 1-3
Variant - type 4t (from tonsillar biopsy)
Iatrogenic - types 1-3

279
Q

CJD type if MRI shows basal ganglia highlighted or posterior thalamus highlighted on MRI-T2 (pulvinar sign)

A

Sporadic - normal / basal ganglia highlighted
Variant - posterior thalamus highlighted on MRI-T2 (pulvinar sign)
Inherited prion disease - sometimes basal ganglia highlighted

280
Q

Post-mortem findings in sporadic and variant CJD

A

Sporadic - spongiform vacuolation, PrP amyloid plaques

Variant - PrP(sc)4t detectable in CNS + lymphoreticular tissue, florid plaques

281
Q

Cause and presentation of sporadic CJD (sCJD)

A

Cause - somatic PRNP mutation or spontaneous conversion

Presentation - rapid, progressive demention with myoclonus, cortical blindness, akinetic mutism and LMN signs

282
Q

Mean onset age and survival time of sporadic CJD

A

Onset - 25-75 years

Survival - <6 months of symptom onset

283
Q

Variant CJD (acquired) cause and presentation

A

Cause - exposure to bovine spongiform encephalopathy (BSE)

Presentation
• Psychiatric symptoms (anxiety, paranoia, hallucinations)
• Followed by development of neurological symptoms
• Late - chorea, ataxia, dementia

284
Q

Mean onset age and survival time of vCJD

A

Onset - 30 years

Survival - 14 months

285
Q

Iatrogenic CJD (acquired) cause and presentation

A

Cause - inoculation with human prions, most commonly from surgery

Presentation - progressive ataxia, then dementia and myoclonus. Faster if CNS inoculation.

286
Q

Kuru CJD (acquired) cause and presentation

A

Cause - cannibalism

Presentation - progressive cerebellar syndrome (2 year survival) following 45 year incubation. Late or absent dementia.

287
Q

What type of prion disease is Gerstmann-Straussler-Scheinker syndrome?

A

Inherited

PRNP mutations

Autosomal dominant

288
Q

How does fatal familial insomnia present

A

Prion disease
Insomnia and paranoia

Progresses to hallucinations and weight loss, then a mute period

289
Q

How long is survival in fatal familial insomnia?

A

1-18 months following symptom onset

290
Q

Cheat sheet examples of gram positive cocci (3)

A

Staph
Strep
Enterococcus

291
Q

Cheat sheet examples of gram positive rods (5)

A

ABCDL

  • Actinomyces
  • Bacillus
  • Clostridium
  • Diphtheria
  • Listeria

(in the gut)

292
Q

Cheat sheet examples of gram negative cocci (2)

A

Neisseria

Moraxella

293
Q

Cheat sheet examples of gram negative rods (6)

A 
Enterobacteriaceae
E. coli
Salmonella
Shigella
Klebsiella
Yersinia
294
Q

Cheat sheet examples of gram negative coccobacilli (4)

A

H. influenzae
B. pertussis
P. aeruginosa
C. trachomatis

295
Q

Cheat sheet examples of gram negative spriochaetes (2)

A

Treponema pallidum e.g. syphilis

Leptospirosis borrelia e.g. Lyme disease

296
Q

Leading cause of adult onset seizures

A

Tapeworm

Path (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions