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Semester 3 > Infection Session 6 > Flashcards

Infection Session 6 Flashcards

1
Q

What is the causative agent in pneumocystis pneumonia?

A

Pneumocystis jirovecii

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2
Q

What is the relevance of pneumocystis pneumonia in HIV?

A

It is an AIDS defining illness

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3
Q

How does Kaposi’s sarcoma present?

A

Small, painless, flat lesions on skin and inside mouth

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4
Q

What infection are you likely to be able to see in the mouth of a HIV +ve pt?

A

Oral candidiasis

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5
Q

How is HIV most likely transmitted between genders?

A

Male –> female

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6
Q

Describe the pathogenesis of HIV infection.

A

Virus bins to CD4+ cell and empties into it
Reverse transcriptase turns RNA to DNA
Integrase combines viral and host DNA
On cellular division viral proteins are made and immature virus buds out taking some CSM
Immature virus breaks free and protease enzymes mature viral proteins allowing virus to function

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7
Q

How does Raltegravir treat HIV?

A

Inhibits integrase

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8
Q

What action do Ritonavir and Lopinavir take to treat HIV?

A

Inhibit protease so viral proteins do not mature

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9
Q

What two types of reverse transcriptase inhibitors are used to treat HIV?

A

NRTI (nucleoside)

NNRTI (non-nucleoside)

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10
Q

Why can HIV not currently be vaccinated against?

A

Conversion of RNA–>DNA allows evasion of vaccine

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11
Q

During which stage of HIV infection are pts most infectious?

A

Acute infection

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12
Q

What are the S/S of acute HIV infection?

A 
Malaise
Headache
Fever
Weightloss
Lymphadenopathy
Oral and oesophageal sores
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13
Q

What are the four stages of HIV infection?

A

Acute infection
Latent infection
Symptomatic infection
Severe infection/AIDS

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14
Q

When is viral load highest in HIV infection?

A

During acute infection but rises if individual progresses to AIDS

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15
Q

Why do some HIV pts never progress to AIDS?

A

Slow progressor - present vital viral proteins

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16
Q

What are the S/S of chronic HIV infection?

A 
Meningitis
CMV
Cold sores, ulcers and oral thrush
HCV
HIV wasting syndrome
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17
Q

How can HIV be transmitted?

A

Sexual contact
Sharing injecting equipment
Vertical
Medical procedures

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18
Q

What diagnostic tests can be used in HIV?

A

HIV antigen and antibody

Rapid blood/saliva tests

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19
Q

What problems are associated with HIV antigen and antibody testing?

A

Takes 4-6 weeks

May give false -ve

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20
Q

What is the problem with rapid HIV tests?

A

May give false +ve

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21
Q

What CD4+ level must be met to start HAART in a +ve HIV test?

A

None, it is started regardless as proven to be beneficial

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22
Q

Why are 3 drugs used in HAART?

A

Virus rapidly replicates therefore mutates frequently allowing resistance to develop in days/weeks

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23
Q

How do Hep A&E differ from B, C and D?

A

Transmitted via foecal-oral route rather than blood

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24
Q

Which hepatitis infections are self-limiting rather than chronic?

A

A&E

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25
Q

Who is at risk of Hep B infection?

A 
Children in highly endemic areas
IVDU
Sexual contacts of those infected
Long term household contacts
HCP
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26
Q

What are the acute S/S of hepatitis B infection?

A 
Significant proportion are asymptomatic
Jaundice
Fatigue
Abdominal pain
Anorexia
Nausea
Vomiting
Arthralgia
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27
Q

What AST/ALT levels would you expect to see in a pt with acute hepatitis B infection?

A

In the 1000s

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28
Q

What are the sequelae of acute hepatitis B infection?

A

Usually cleared w/in 6 months
Small proportion (more in children than adults) develop chronic infection
1% develop fulminant hepatic failure

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29
Q

In what sequence do antigens appear in the serum in Hepatitis B infection?

A

HBsAg –> HBeAg –> HBcAg

30
Q

What is HBsAg?

A

Surface antigen seen first upon infection

31
Q

Which serum antigen suggests host is highly infectious?

A

HBeAg (e antigen)

32
Q

Which is the first antibody to appear on serology?

A

Core antibody (HBcAg)

33
Q

Which antibody indicates viral clearance and recovery?

A

Surface antibody (HBsAB)

34
Q

Which core antibody persists for life?

A

IgG

35
Q

What is the serological definition of chronic Hep B?

A

Presence of HBsAg after 6 months

36
Q

What are the outcomes of chronic Hep B infection?

A

25% develop cirrhosis

5% hepatocellular carcinoma

37
Q

How are Hep B carriers identified?

A

HBsAg +ve and HBeAg, HBeAb and HBV viral load assessed

38
Q

How is hepatitis B vaccinated against?

A

Genetically engineered HBsAg given as 3 doses with boosters if needed

39
Q

What surface antibody levels confer with adequate and long-term protection?

A

Adequate >10

Long term >100

40
Q

Who is at risk of Hep C infection?

A

IVDU/ crack or heroin smokers
Blood transfusion before 1991
Children born to infected mothers
HCP

41
Q

What is the likely progression of Hep C infection?

A

~80% develop chronic infection –> cirrhosis/chronic liver disease –> decompensated liver disease, hepatoma, transplant, death

42
Q

What are the S/S of Hep C infection?

A

80% have none

20% have vague, e.g. fatigue, anorexia, dark urine, nausea, RUQ pain

43
Q

What is used to cure Hep C?

A

Pegylated interferon and ribovirin

44
Q

Is there a vaccine currently available for Hep C?

A

No

45
Q

How is a diagnosis of necrotising fasciitis made?

A

Surgical exploration to assess fascial layers

Biopsy with microscopy

46
Q

What is the causative agent in necrotising fasciitis?

A

Strep pyogenes

47
Q

Which group of pathogens cause the majority of cutaneous infections?

A

Group A beta-haemolytic streptococci - mainly strep pyogenes but some abdominal/perineal cases

48
Q

What virulence factors do streptococci possess?

A 
Antiphagocytic M proteins 
Pyrogenic exotoxins
Streptolysin O and S for cell lysis
Streptokinase for clot lysis
Streptodornase to promote spread
C5a peptidase to inactivate complement
49
Q

What is the difference in haemolysis between alpha- and beta-haemolytic streptococci?

A 
Alpha = incomplete
Beta = complete
50
Q

Which type of haemolytic streptococci are more virulent and why?

A

Beta due to iron release from RBCs

51
Q

What is the difference between an erythematous and purpuric rash?

A

Erythematous - RBCs in capillaries so always blanching

Purpuric - RBCs in intersticium

52
Q

Give some examples of infections caused by beta-haemolytic streptococci.

A

Scarlet fever
Erysipelas
Impetigo
Puerperal sepsis

53
Q

Give some examples of infections cause by alpha-haemolytic streptococci.

A

Pneumonia
Meningitis
Abdominal sepsis
UTI

54
Q

What are the S/S of scarlet fever?

A

Erythematous rash
Circumoral pallor
Strawberry tongue

55
Q

What causes the characteristic S/S of scarlet fever?

A

Erythrogenic toxin from strep pyogenes

56
Q

What are the important two treatments for streptococcal infection?

A

Beta-lactams

Glycopeptides

57
Q

What is the clinical empiric treatment for streptococcal infection?

A

Tazocin and clindamycin

Replace Tazocin with benzypenicillin if GAS identified

58
Q

What post-streptococcal sequelae can occur?

A

Acute rheumatic fever

Acute glomerulonephritis

59
Q

When will acute rheumatic fever following streptococcal infection present?

A

2-3 weeks later

60
Q

What causes acute rheumatic fever following streptococcal infection?

A

Cross-reaction b/w heart or joint tissues and M proteins on streptococcal antigens

61
Q

What causes acute glomerulonephritis following streptococcal infection?

A

Formation of antigen-antibody complexes on glomerulus basement membrane

62
Q

How are staphylococci split into two categories?

A

Coagulase test

63
Q

Why are coagulase +ve staphylococci generally more virulent than coagulase -ve?

A

Stimulate clotting of blood around colony which increases survival

64
Q

What skin infections are caused by staphylococci infection?

A

Impetigo
Furuncle/boil
Carbuncle
Surgical wound infection

65
Q

Give an example of a coagulase +ve staphylococcus.

A

Staph aureus

66
Q

Give an example of a coagulase -ve staphylococcus.

A

Staph epidermis

67
Q

What is the treatment for staphylococcal infection?

A

Flucoxacillin
Some cephalosporins
Beta-lactamase combinations
Vancomycin for flucoxacillin-resistant strains

68
Q

What features are considered in choosing an Abx?

A 
Severity of infection
Site of infection
Likely pathogen
Route of administration
Possible adverse effects
69
Q

What is empirical Abx therapy?

A

‘Best guess’ Tx when causative agent is not known

70
Q

How does pneumocystis pneumonia present differently in HIV +ve vs HIV -ve pts?

A

+ve: subacute, low grade fever

-ve: rapid progression, high fever

Semester 3 (50 decks)

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