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Human Diseases Yr3 > Infections > Flashcards

Infections Flashcards

1
Q

What are Koch’s Postulates?

A

1) Microorganism must be found in abundance in all organisms with the disease and not in healthy organisms
2) Microorganism must be isolated from a diseased organism and grown in pure culture
3) Cultured microorganism should cause disease when introduced to healthy organism
4) Microorganism must be re-isolated from diseased host and be identical to original causative microorganism

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2
Q

How can opportunistic pathogens take hold in a damaged host?

A
  • Immunosupressed
  • Tissue damage
  • Catheter infections
  • Genetic defects
  • Change in host bacteria e.g. antibiotics
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3
Q

In a biofilm, what is it called when one bacteria is under stress and sends signals to other bacteria to produce a protein film for protection?

A

Quorom Sensing

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4
Q

Give examples of toxin production that is a) plasmid encoded and b) phage encoded

A

a) TSST, tetanus neurotoxin

b) Cholera toxin, diptheria toxin

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5
Q

What 3 proteins are critical for replication of a virus?

A

Reverse transcriptase, integrase, protease

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6
Q

What virus is more likely to have latency, RNA viruses or DNA viruses? Why?

A

DNA viruses as this in nucleus of cell whereas RNA in cytoplasm and has to keep replicating

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7
Q

How do yeasts replicate and how do moulds replicate?

A

Yeast = mitosis, moulds = meiosis

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8
Q

What commensal bacteria has colonised the skin as part of host defence to infections?

A

Coagulase negative staphylococci

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9
Q

What is hairy oral leukoplakia

a) Caused by?
b) Look like?
c) An indication of?

A

a) Ebstein Barr Virus (EBV)
b) White striations on lateral surface of tongue
c) HIV

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10
Q

What virus looks like a fried egg under the microscope?

A

Herpes simplex virus - yolk= spherical capsid, outside= lipid envelope

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11
Q

What is the structure of the measles virus?

A

Helical RNA coated in capsid. Lipid envelope

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12
Q

What is the structure of influenza virus?

A

REMEMBER - Spiky!!

Antigens and proetins stick out of cell wall (haemogluttanin and neuroamnidase). Lipid envelope. Capsid coating RNA.

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13
Q

What is the structure of adenovirus?

A

Capsid is icosahedral. No lipid envelope. Surface proteins

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14
Q

Give 3 examples of double stranded DNA viruses

A
  • Herpes viruses
  • Hep B
  • Adenovirus
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15
Q

Give 5 examples of single stranded RNA viruses

A
  • Measles
  • Mumps
  • Influenza
  • Rhinovirus
  • Hep C
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16
Q

What is different about retrovirus replication e.g. HIV?

A

Have reverse transcriptase stage: RNA to DNA which is integrated into host DNA to then make mRNA

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17
Q

Give 1 example of a single stranded DNA virus

A

Parvovirus

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18
Q

Give 1 example of a double stranded RNA virus

A

Rotovirus

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19
Q

In serology testing what antibodies do they look for?

A

IgM for acute infection, IgG for past exposure

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20
Q

For Herpes Simplex 1 & 2:

a) Where do they attach and release the capsid?
b) When the new virus is made in the DNA and released, where do they travel?

A

a) Epithelial cells

b) Sensory neurons to the spinal ganglia - become dormant

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21
Q

What can primary oral herpes present as if not asymptomatic?

A

Gingivostomatitis

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22
Q

Which type of herpes simplex has oral reactivation presenting as cold sores?

A

HSV1

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23
Q

Which type of herpes simplex has genital disease reactivation?

A

HSV2 (primary infection with both HSV1 & 2)

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24
Q

What is Herpetic Whitlow?

A

Herpes Simplex entering skin around fingernails - children who suck thumbs or healthcare workers with no PPE

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25
Q

How can neonatal herpes simplex infection occur (life-threatening)?

A

Mother secreting herpes simplex in vaginal secretions, or kissing baby and shedding virus

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26
Q

What complication of herpes simplex can cause lifethreatening brain damage?

A

Herpes simplex encephalitis (usually HSV1)

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27
Q

What are the treatments (drugs) for Herpes Simplex 1 and 2?

A

Aciclovir (activated by thymidine kinase from virus), Valaciclovie (better oral bioavailability)

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28
Q

Where does the Varicella Zoster Virus

a) Infect?
b) Replicate to cause primary viraemia?
c) Replicate to cause secondary viraemia?
d) Lie dormant/ latency?

A

a) Respiratory mucosa and conjunctiva
b) Lymph nodes
c) Spleen and liver
d) Dorsal route ganglion

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29
Q

What does primary and secondary infection of VZV respectively cause?

A 
Primary = chickenpox 
Secondary = shingles
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30
Q

What nerve does opthalmic zoster affect?

A

Trigeminal nerve

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31
Q

What family of viruses does Cytomegalovirus (CMV) belong and how is it shed?

A

Herpes family

Shed via respiratory and genital secretions

32
Q

What symptoms does EBV cause in young children and adolescents?

A

Young = sore throat, Adolescents = glandular fever/infectious mononucleosis

33
Q

What family of viruses does EBV belong? Where is it latent?

A

Herpes

Latent in B lymphocytes

34
Q

What is Human Herpes Virus 8 also called? Clinical features?

A

Karposi’s sarcoma associated virus - HIV or skin malignancies. Clinical feature = dark blotches

35
Q

For the lab, what colour bottle top should
a) viral swabs
b) clotted blood for serology
have?

A

a) green top

b) yellow top

36
Q

What is a normal CD4 count? Where are they most commonly found?

A

800-1500 and in lymph nodes, GI tract

37
Q

What oral presentations can be seen in Clinical Stage II HIV?

A

Angular chelitis
Oral ulcerations
Herpes Zoster

38
Q

What oral presentations can be see in Clinical Stage III HIV?

A 
Oral candidiasis (thrush)
Oral hairy leukoplakia
39
Q

What oral presentations can be seen in Clinical Stage IV HIV?

A

Karposi’s sarcoma on hard palate

40
Q

What is the treatment for HIV?

A

2 x Nucleotide reverse transcriptase inhibitors (NRTIs)
1 x NNRTI/ protease inhibitor / integrase inhibitor
HAART target = enzyme inhibition and cell entry

41
Q

What signs of hepatitis can be seen on examination?

A
  • Jaundice
  • Spider nevii
  • Sialosis (enlargement of salivary glands)
  • Scratch marks (deposition of bile salts under skin)
  • Bruising (effects clotting factors)
  • Dupuytrens contracture
  • Liver flap/asterixis (brain irritated by ammonia compounds and hand flaps)
  • Gynaecomastia (breast tissue in males, oestrogen not metabolised)
  • Palmer erythema
42
Q

What are the common viral causes and drug causes of hepatitis? What is a very rare cause?

A

Hep A, B, C and EBV and paracetamol (25g is fatal)

Wilsons Disease

43
Q

How does acute liver damage occur?

A

Infection of the hepatocytes with direct killing of hepatocytes by effector lymphocytes.
Self limiting and damage is from the immune response not viral particles

44
Q

How does chronic liver damage occur?

A

Long-term infection and long-term low level immune response.
Fibrotic response to repair damaged tissue forms scars, liver tries to regenerate scarred tissue leading to cirrhosis.
6 month +

45
Q

What is Hepatitis A?

A

Form of foodpoisoning, never chronic or in carrier state as become unwell then immune system overcomes infection

46
Q

When can Hepatitis A be fatal?

A

In pregnancy - severe immune response. In chronic liver disease pts - always vaccinated now.

47
Q

What is Hepatitis E?

A

Food poisoning (origin from pork). Acute, chronic only in immunosuppressed or liver disease.

48
Q

How does a carrier state exist in Hepatitis B and what are the symptoms?

A

Vertical transmission (mother to baby) - no immune response so no damage to liver but have a high viral load

  • High infectivity
  • High risk of hepato-cellular carcinoma (cancer) as high viral integration
49
Q

Why does Hep B cause primary liver cancer?

A

DNA virus so integrates into genome, especially risky if near oncogene

50
Q

What is the incubation period for Hep B?

A

6 weeks acute symptoms start

51
Q

What test results allow for diagnosis of Hepatitis B?

A

ALT high - released by damaged liver blood cells
Bilirubin high - liver cant clear it
Alkaline phosphatase high
Albumin low
Prothrombin time low - less clotting factors

52
Q

What does HepBsAg show?

A

Surface antigen - marker of viral presence

53
Q

What does HepBeAg show?

A

Virus core - marker of degree of viral load and replication, shows severity

54
Q

What does HepBsAb show?

A

Surface antibody - Marker of immunity (vaccination or previous infection

55
Q

What does HepBeAb show?

A

Marker of low risk in hepatitis pts - +ve = low level of viral infection

56
Q

What does HepBcAb show?

A

Core antibody - useful if have mutant virus with no surface antigen

57
Q

Chronic hepatitis patients with eAg+, eAb-, cAb- are…. risk?

A

High risk

58
Q

Chronic hepatitis patients with eAg-, eAb+, cAb+ are… risk?

A

Low risk - have the infection but also have immunity

59
Q

What drugs can be given to Hepatitis B patients to help control (but not clear) the virus?

A

Interferon, Lamivudine, Adefovir

60
Q

What is Hepatitis C?

A

An RNA virus that causes chronic disease. Does not integrate into the genome but can still cause cancer from high degree on inflammation

61
Q

What are the 3 risk groups for Hepatitis C?

A
  • IV drug abusers
  • Receivers of blood products (link to haemophilia)
  • Factor X - ie the unknown

Remember: Not sexual contact

62
Q

Why is there no vaccination for Hep C?

A

Mutates in situ

63
Q

If a patient has severe jaundice/liver problems and is undergoing GA, what are they at risk of?

A

Hepato-renal syndrome (renal failure)

64
Q

If you are giving LA to a patient with liver problems what would you give and why?

A

Lidocaine limited to 2 cartridges
Articaine and prilocaine may be better as metabolised in lungs
(LA undergoes amide biotransformation in liver)

65
Q

Why is sedation best avoided in patients with cirrhosis?

A

Benzodiazepine not metabolised

66
Q

What are contraindicated in patients with hepatitis/liver problems?

a) Antifungal agents
b) Antibiotics
c) Painkillers

A

a) Miconazole, fluconazole
b) Erythromycin, Tetracycline, Metronidazole
c) NSAIDs (risk of GI bleed), parecetamol

67
Q

In the Lancefield grouping of streptococci, what colour are:

a) a-haemolytic
b) b-haemolytic
c) y-haemolytic

A

a) green
b) clear
c) none (red)

68
Q

What are the 4 aetiological agents of pharyngitis?

A
  • Viral causes
  • Beta-haemolytic streptococci group A,C,G
  • Corynebacteria diphtheriae and ulcerans
  • Arcanobacterium haemolyticum
69
Q

What tests can you do to identify Group A streptococcus e.g. S. pyogenes as the cause of pharyngitis?

A
  • Culture on blood agar to see haemolysis
  • 16s PCR
  • Serology (late stage) i.e. antibodies present
70
Q

What are the complications of pharyngitis?

A
  • Peritonsillar abscess/quinsy
  • Scarlet fever
  • Systemic sepsis
  • Rheumatic fever
  • Acute glomerulonephritis (renal failure)
71
Q

What does the diphtheria toxin

a) inhibit?
b) symptoms?

A

a) Protein synthesis
b) Initially pharyngitis, then psuedomembranes form risking airway obstruction, then toxin absorbed and causes myocarditis, paralytic symptoms and nephritis

72
Q

What is the difference between arcanobacterium haemolyticum and beta-haem strep?

A

Arcanobacterium is a gram positive bacillus even though it makes blood agar clear

73
Q

What is gonorrhoea as a bacteria?

A

Fastidious (hard to culture) gram-negative diplococci

74
Q

What is syphilis caused by?

A

Treponema pallidum, a spirochete

75
Q

What is mycobacterium tuberculosis?

A

Acid-alcohol fast bacilli

76
Q

What presents secondary to pulmonary infection with TB?

A

Oral mucosal lesions - painful ulcerations in posterior part of mouth
Cervical lymphadenopathy - may develop absesses and sinuses

77
Q

What does primary syphilis present as?

A

Single, painless, indurated genital ulcer (chancre)

Human Diseases Yr3 (6 decks)

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