Q1

What causes Hepatitis C infection?

  • Flaviviridae family RNA Virus

Describe the clinical course of Hepatitis C infection.

  • Incubation period 2-26 wks (mean 6-12 wks)
  • Acute infection usually mild or asymptomatic (1-3 weeks)
  • Persistent and Chronic hepatitis with exacerbations in 80%
  • Cirrhosis in 20-30%
  • Fulminant hepatic failure rare

Pass criteria:

  • 3 out of 5

What are the risk factors for acquiring Hepatitis C?

  • IVDU (54%)
  • Multiple sex partners (36%)
  • Needle stick (10%) ( risk of HCV is 1.8% v 0.3% for HIV)
  • HCW (1.5%)
  • Blood Transfusion (in the 1980’s),
  • Vertical,
  • Unknown (32%)

Pass criteria:

  • 3 out of 7

What features of the Hepatitis C virus make vaccine development difficult?

  • Highly stable core, extremely variable envelope ( E protein)
  • RNA polymerase inherently unstable; frequent mutations, multiple quasispeciesfound in any one pt
  • Genomic and Antigenic variability
  • Actively inhibits interferon mediated cellular response at many levels

Q2

Describe the pathogenesis of tuberculosis in a previously unexposed immunocompetent person.

  • Infection by M. tuberculosis airborne
    • M. tuberculosis usually person to person airborne droplet  spread
  • M tuberculosis enters alveolar macrophages and replicates
    • Enters alveolar macrophages and replicates by blocking phagosome/lysosome fusion leading to bacteraemia (person generally asymptomatic or mild flu like illness
  • Immunity through T cell mediated delayed type hypersensitivity  reaction that also causes hypersensitivity and tissue destruction- in particular granuloma formation and caseation
    • About 3 weeks later T cell activation via MHC antigens on macrophages and IL-2 leading to macrophage becoming bactericidal (thru IFN-gamma)
    • This macrophage response also causes tuberculin positivity and formation of granuloma and caseation by recruiting monocytes (“epithelioid histiocytes”)
  • Re- exposure or reactivation causes  heightened immune reaction as well as tissue destruction
    • Infection may be contained  or may progress and may reactivate with immunosuppression from any cause

Pass criteria:

  • Bold to pass

Q3

What micro-organisms cause malaria?

  • Parasitic protozoa
  • Plasmodium falciparum, vivax, ovale, malarie

Pass criteria:

  • Falciparum PLUS 1

How does Plasmodium falciparum infection differ from other forms of malaria?
Prompt: How does it compare clinically? By what mechanism?

  • All do: sporozoite -> liver -> merozoites formed  ->  release & bind to RBC ->  Hb hydrolysed  -> trophozoite -> schizont -> merozoite/gametocyte
  • P. falciparum: infects RBCs of any age, causing clumping/rosetting so ischemia, high cytokine production, high level parasitemia, severe anemia, cerebral symps, renal failure, pul oedema, death
  • Others: infect only new or old RBCs, P vivax & ovale form latent hynpnozoites (relapses), low parasitemia, mild anemia, rarely splenic rupture, nephrotic synd

Pass Criteria:

  • 2/3 Highlighted and 1 clinical feature

What factors can make people less susceptible to malaria?

  • Inherited alterations in RBCs: HbS trait, HbC, Duffy Ag neg
  • Repeated exposure stimulates immune response: Ab and T lymphocytes (P falc avoids this), HLAB53

Pass criteria:

  • Bold to pass

Q4

What is the clinical spectrum of candida infection?

  • Benign commensal
  • Superficial mucosal infn – mouth, vagina, oesophagus
  • Superficial cutaneous  infn – intertrigo, nappy rash, balanitis, folliculitis, paronychia, onychomycosis
  • Chronic mucocutaneous (T-cell defects, endocrinopathy)
  • Invasive (disseminated) – myocardial/ abscess/endocarditis, cerebral abscess/meningitis, renal/hepatic abscess, endophthalmitis, pneumonia

Pass criteria:

  • Bold to pass

What mechanisms enable candida to cause disease?
Prompt: What are the virulence factors?

  • Phenotypic switching to adapt rapidly to changes in host environment
  • Adhesion to host cells –  imp. determ. of virulence –via adhesins (several types)
  • Production of enzymes (aspartyl proteases and catalases) degrade extracellular matrix proteins and may aid intracellular survival
  • secretion of adenosine – blocks neutrophil degranulation

Pass Criteria:

  • Pass – 1 out of 3 bold

Q5

Describe the clinical course of Hepatitis A infection.

  • Oral faecal transmission.
  • Incubation period: 2-6 weeks.
  • No carrier state or chronic hep or cause hepatocellular Ca.
  • Rarely causes fulminant hepatitis, and so the fatality rate is about 0.1%.

Pass criteria:

  • 3 out of 4

How do the serological markers change with time in Hep A infection?

  • IgM anti HAV appears at the onset of symptoms.
  • Faecal shedding of the virus ends as IgM titre rises (2-12 weeks).
  • IgM Ab (months)
  • Replace by IgG anti HAV (years) .
  • Encourage graph

infectious 1

 


Q6

Describe the potential outcomes of acute hepatitis C infections in adults.

  • Acute fulminant rare
  • 15% resolve
  • 85% chronic  – >80% stable/20% cirrhosis (50% mortality) hepatocellular Ca

Pass criteria:

  • 3 major points with most > chronic fulminant) and potential for cirrhosis/Ca

How does the serology for Hepatitis C infection change in case of resolution?

  • Incubation period (2-26 weeks)
  • HCV-RNA (detectable for 1-3 weeks co-incident with transaminitis)
  • Anti HCV antibodies emerge. Only about 50% detectable during symptomatic acute infection.  Remainder after 3-6 weeks.  IgG/IgM. IgG persists

infectious 2

Pass Criteria:

  • All major points & ‘window’ when both virus & Ab may be –ve
  • Diagram encouraged.

Q7

Name some clostridial diseases and causative organisms?

  • Tetanus (lockjaw) – Clostridium tetani
  • Botulism (paralytic food poisoning) – Clostridium botulinum
  • Gas gangrene, necrotizing cellulitis – Clostridium perfringens, C. septicum
  • Pseudomembranous colitis – Clostridium difficile

Pass criteria:

  • 2 out of 4

What is the pathogenesis of gas gangrene (C. perfringens, C. septicum)?

  • Release enzymes – hyaluronidase; collagenase
  • Virulence factors – TOXINS
  • alpha-toxin
    • multiple actions
    • phospholipase C: degrades membranes; muscle; RBC
    • release phospholipid derivatives: ITP; prostaglandins
    • these cause derangement in cell metabolism and cell death

Pass Criteria:

  • Bold PLUS 2 others

Q8

Please give some examples of clinical Herpes Simplex Infection?

  • Cold sores, Gingivostomatitis, Encephalitis, Genital herpes, Keratitis (epithelial & stromal)
  • Disseminated visceral herpes (esophagitis, bronchopneumonia, hepatitis, Kaposi varicelliform eruption, eczema herpeticum)

Pass criteria:

  • At least 3

After primary herpes simplex infection, how does reactivation occur?

  • Viral nucleocapsids travel from the skin/ oropharynx/genitalia to the nucleus in the sensory neurone.
  • During latent period, only viral mRNA is produced, no viral proteins are made to escape immune recognition.
  • Reactivation from latency occurs by avoiding immune recognition, inhibiting the MHC class I recognition pathway, and elude humoral immune defences by producing receptors for the Fc domain of immunoglobulin and inhibitors of complement.  Antidromically along sensory nerve

Pass Criteria:

  • 2 out of 3 to pass

Q9

What is the mode of transmission of the measles virus?

  • Respiratory droplets
  • Upper respiratory epithelial cells

Describe some of the systemic features of measles virus infection.
Prompt: One feature is croup or pneumonia. Tell me others?

  • Rash–blotchy, red/brown. Skin hypersensitivity reaction
  • Oral mucosal ulceration – Koplik’s spots
  • Croup, or interstitial pneumonia
  • Keratitis, with scarring and visual loss
  • Encephalitis; – plus SSPE,  measles inclusion-body encephalitis    (immunocompromised)
  • Diarrhoea with protein-losing enteropathy
  • Secondary bacterial infection

Pass Criteria:

  • Rash and 3 others

What are the cell-surface receptors for the measles virus?
Prompt: One example is CD46. Tell me about this

  • CD 46 ( complement regulatory protein): inactivates C3 convertases; present on all nucleated cells; binds viral haemagglutinin protein
  • SLAM (Signalling Lymphocytic Activation Molecule): involved in T cell activation; only present on cells of the immune system; binds viral haemagglutinin protein

Q10

What are the different types of meningitis?

  • Infectious:
    • Bacterial, aseptic/viral, chronic (TB, spiro, crypto)
  • Chemical: nonbacterial irritant
  • Ca, lymphoma

Pass criteria:

  • Bold PLUS 1 other point

What organisms commonly cause bacterial meningitis?

  • Neonates: E coli, grp B strep
  • Children: Strep pneu, H flu reducing with vaccines
  • Young adults: Neisseria meningitidis,
  • Elderly: Strep pneum, Listeria
  • Immunosuppressed: Klebsiella, anaerobes

Pass Criteria:

  • Bold PLUS 1 other

How do the cerebrospinal fluid findings typically differ between acute bacterial and viral meningitis?

  • Bacterial:
    • Cloudy, higher pressure, *more neutrophilsraised protein, *reduced glucose
  • Viral:
    • *lymphocytes, moderately raised protein, *normal glucose

Pass criteria:

  • 3 to pass

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