Q21

What are the routes of transmission of Hepatitis C virus?

  1. Blood inoculation with IV drug use 60%.
  2. Unknown
  3. Transmission via blood products pre1991 10%
  4. Dialysis < 5%
  5. Occupational exposure < 5%
  6. Sexual transmission infrequent
  7. Vertical transmission very low.

Pass: Bold and 2 others

What are the potential outcomes of infection?

1.            Acute Infection generally asymptomatic, rarely fulminant hepatitis

2.            85% progress to chronic persistent hepatitis

3.            15% resolve completely

4.            20% of chronic infection progress to cirrhosis

5.            Some cirrhotics develop Hepatocellular carcinoma

Pass: Bold


Q22

What are the two clinically significant Neisseria?

Meningitides, gonorrhoeae
Pass: Both

Describe the pathogenesis of a N. meningitidis infection.
Prompt: How does it spread?

1.            Respiratory spread

2.            Common coloniser of the oropharynx

3.            (10% of the population at any one time)

4.            Colonisation lasts for months

5.            Immune response leads to protection against that strain

6.            Invasive disease crosses respiratory epithelium to enter blood

7.            Capsule of Neisseria reduces opsonisation & protects against destruction by complement proteins

8.            Outbreaks in young people living in crowded quarters who encounter new strains

Bold: 5 of 8


Q23

Describe the pathogenesis of atopic asthma
Prompt: What are the major changes which occur in the airways in asthma.

1 Initial sensitisation to inhaled allergen (antigen) — favours IgE production and eosinophil recruitment
eg dusts, pollens, animal dander, foods

2 (Immediate phase — minutes) Re-exposure to antigen triggers Ag induced cross !inking of IgE bound to IgE receptors on mast cells in airways and release of chemical mediators. This results in opening of tight junctions between epithelial cells

Antigen can then enter mucosa to release further mediators (via mast cell and eosinophil activation) and cause bronchoconstriction / oedema / mucus secretion +/- hypotension

3 Mediators act directly or via neuronal reflexes to induce bronchospasm / increased vascular permeability / mucus production / recruit mediator releasing cells form blood

4 (Late phase asthma – hours ) Recruited leucocytes arrive (neutrophils, eosinophils, basophils, lymphocytes, monocytes) initiates fresh round of mediator release and epithelial damage and airway constriction

Pass: 4 of 5. Underlined mandatory


Q24

What is the causative organism of salmonella dysentery?

1.            Salmonella enteritidis, typhimurium

2.            Gram negative, flagellated

What is the pathogenesis of salmonella dysentery?

1.            Invades epithelium (low oxygen environment)

2.            Taken up by macrophages

3.            Gut wall inflammation

4.            Neural reflex pathway

Pass: 1 plus inflammation


Q25

What is the causative organism of cholera?

Vibrio cholerae

Gram -ye, flagella, water-borne comma- shaped bacterium

How does the organism cause diarrhoea?

  1. Non-invasiye in gut lumen
  2. Release of enterotoxin
  3. Secretory diarrhoea
  4. Acts on G proteins

Q26

How may Hepatitis B viral infection be transmitted?

  1. Parenteral: contaminated blood product transfusion
  2. Sexual intercourse, esp. homosexual activity
  3. IV drug use / dialysis
  4. Accidental needle stick injury with contaminated blood
  5. Vertical transmission (during delivery)
  6. Conjunctival splash of infected body fluid
  7. One third of cases unknown transmission

Pass: Bold plus 3 others

Describe the patterns of disease progression following Hepatitis B viral infection.

  1. subclinical disease (60-65%), with 100% recovery
  2. acute hepatitis (20-25%) with 99% recovery, <1% fulminant hepatitis (potentially lethal)
  3. ‘healthy carrier’ state 5-10%
  4. persistent infection 4%, with 67-90% recovery, 10-33% chronic hepatitis (20-50% develop cirrhosis—? 10% hepatocellular carcinoma or other lethal complication)

Pass: 3 of 4

What are the characteristic serological findings associated with the carrier state of HepB virus?

1.            Presence of HBsAg in the serum for > 6 months

2.            Chronic HepB viral replication has persistent HBsAg, as well as HBeAg, and MIT DNA, usually with anti-HBc and occasionally anti-HBs

Pass: Bold


Q27

Describe the features of the illness caused by Hepatitis A virus.
Prompt: How is hepatitis A transmitted?

  1. Faecal-oral transmission; consumption of raw/steamed shellfish which have concentrated the virus from sewage contaminated seawater.
  2. Incubation 2-6 weeks
  3. in childhood symptoms mild or asymptomatic
  4. adult life: febrile illness, nausea, lethargy, vomiting, possible dehydration.
  5. rare (<0.1%) progression to fulminant hepatitis
  6. acute disease more severe if superimposed on chronic hepatitis (B, C or alcoholic)
  7. does not cause chronic hepatitis, nor carrier state

Pass: 4 of 7

Describe the pattern of appearance of markers in Hepatitis A viral hepatitis. (With aid of a graph if you wish)

  1. Incubation: 15-45 days (2-6 weeks)
  2. Acute rise in Faecal HAV lasting 2-12 weeks (peaks within 1-2 weeks)
  3. 3.       IgM anti-HAV begins to appear in blood as faecal HAV peaks, rises over 2-12 weeks
  4. IgG-antiHAV begins to appear shortly after 1gM and continues to rise more slowly over many months and remains elevated for many years.

infectious 3

Pass: Bold


Q28

Outline the pathogenesis of septic shock.

Bacterial toxin (endotoxin or exotoxin) binds to LPS binding protein in serum

Complex binds  to receptors on leucocytes, and endothelial cells

Induce release and synthesis of inflammatory mediators

Induce direct cell damage

Pass: Bold plus 2 others

What chemical mediators are involved?

  1. Vasoactive amines Histamine, Serotonin
  2. Plasma proteases — complement, Kinins
  3. Arachadonic acid metabolites — prostaglandin, leucotrienes
  4. Platelet activating factor
  5. Cytokines – IL1 and TNF
  6. Lysosomal constituents — proteases, lysozymes,
  7. Oxygen free radicals, neuropeptides, Nitric oxide

Pass: At least 4


Q29

Describe the illness caused by acute varicella infection.
Prompt: How is it transmitted?

  1. Transmitted in epidemic fashion by aerosols, dissemination haematogenously
  2. Rash occurs about 2 weeks after respiratory aerosol exposure.
  3. Rash begins centrally & spreads centifugally in multiple waves. Rash initially macular with rapid progression to a vesicle
  4. After a few days the vesicle ruptures, and crusts over. Most heal with no scarring (unless bacterial superinfection)
  5. Involves skin & mucous membranes.
  6. A milder illness in childhood cf. adults

Pass: At least 3

What are the complications of acute varicella infection?
Prompt: What possible complications from the skin lesions?

  1. Secondary bacterial skin infection
  2. encephalitistcerebellitis
  3. interstitial pneumonitis
  4. transverse myelitis
  5. necrotizing visceral lesions (esp. in the immunosuppressed)

Pass: Bold plus one other

Describe the relationship between varicella infection and subsequent zoster eruption.
(Optional question) Prompt: Describe the clinical picture of zoster eruption.

  1. VZV evades immune defences & infects neurons in and around dorsal root ganglia
  2. Able to remain latent here for many years
  3. Usually a single episode of recurrence in the form of zoster
  4. Reactivation often in the elderly or immuno-compromised
  5. Vesicular eruption along dermatome of one or more sensory nerves
  6. Associated intense burning, itching and pain due to radiculoneuritis. May cause nerve dysfunction (eg Ramsay Hunt syndrome)

Q30

How is Legionella acquired?

Aerosols/artificial aquatic environments – cooling towers, water supplies etc. Also in other moist conditions

Aspiration of aerosolised organisms or aspiration of contaminated water. (L.longbeachae)

What groups of patients are at risk of Legionella infection?

Underlying co-morbidities – cardiac, renal, immune, hematologic. Transplant pts especially.

(Smokers, chronic lung and elderly)

How is Legionella diagnosed?

Urinary antigen or fluorescent Ab test on sputum. Culture is gold standard. – special medium (PCR)


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