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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
Who is at risk of Hep B infection?
``` Children in highly endemic areas IVDU Sexual contacts of those infected Long term household contacts HCP ```
26
What are the acute S/S of hepatitis B infection?
``` Significant proportion are asymptomatic Jaundice Fatigue Abdominal pain Anorexia Nausea Vomiting Arthralgia ```
27
What AST/ALT levels would you expect to see in a pt with acute hepatitis B infection?
In the 1000s
28
What are the sequelae of acute hepatitis B infection?
Usually cleared w/in 6 months Small proportion (more in children than adults) develop chronic infection 1% develop fulminant hepatic failure
29
In what sequence do antigens appear in the serum in Hepatitis B infection?
HBsAg --> HBeAg --> HBcAg
30
What is HBsAg?
Surface antigen seen first upon infection
31
Which serum antigen suggests host is highly infectious?
HBeAg (e antigen)
32
Which is the first antibody to appear on serology?
Core antibody (HBcAg)
33
Which antibody indicates viral clearance and recovery?
Surface antibody (HBsAB)
34
Which core antibody persists for life?
IgG
35
What is the serological definition of chronic Hep B?
Presence of HBsAg after 6 months
36
What are the outcomes of chronic Hep B infection?
25% develop cirrhosis | 5% hepatocellular carcinoma
37
How are Hep B carriers identified?
HBsAg +ve and HBeAg, HBeAb and HBV viral load assessed
38
How is hepatitis B vaccinated against?
Genetically engineered HBsAg given as 3 doses with boosters if needed
39
What surface antibody levels confer with adequate and long-term protection?
Adequate >10 | Long term >100
40
Who is at risk of Hep C infection?
IVDU/ crack or heroin smokers Blood transfusion before 1991 Children born to infected mothers HCP
41
What is the likely progression of Hep C infection?
~80% develop chronic infection --> cirrhosis/chronic liver disease --> decompensated liver disease, hepatoma, transplant, death
42
What are the S/S of Hep C infection?
80% have none | 20% have vague, e.g. fatigue, anorexia, dark urine, nausea, RUQ pain
43
What is used to cure Hep C?
Pegylated interferon and ribovirin
44
Is there a vaccine currently available for Hep C?
No
45
How is a diagnosis of necrotising fasciitis made?
Surgical exploration to assess fascial layers | Biopsy with microscopy
46
What is the causative agent in necrotising fasciitis?
Strep pyogenes
47
Which group of pathogens cause the majority of cutaneous infections?
Group A beta-haemolytic streptococci - mainly strep pyogenes but some abdominal/perineal cases
48
What virulence factors do streptococci possess?
``` 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
What is the difference in haemolysis between alpha- and beta-haemolytic streptococci?
``` Alpha = incomplete Beta = complete ```
50
Which type of haemolytic streptococci are more virulent and why?
Beta due to iron release from RBCs
51
What is the difference between an erythematous and purpuric rash?
Erythematous - RBCs in capillaries so always blanching | Purpuric - RBCs in intersticium
52
Give some examples of infections caused by beta-haemolytic streptococci.
Scarlet fever Erysipelas Impetigo Puerperal sepsis
53
Give some examples of infections cause by alpha-haemolytic streptococci.
Pneumonia Meningitis Abdominal sepsis UTI
54
What are the S/S of scarlet fever?
Erythematous rash Circumoral pallor Strawberry tongue
55
What causes the characteristic S/S of scarlet fever?
Erythrogenic toxin from strep pyogenes
56
What are the important two treatments for streptococcal infection?
Beta-lactams | Glycopeptides
57
What is the clinical empiric treatment for streptococcal infection?
Tazocin and clindamycin | Replace Tazocin with benzypenicillin if GAS identified
58
What post-streptococcal sequelae can occur?
Acute rheumatic fever | Acute glomerulonephritis
59
When will acute rheumatic fever following streptococcal infection present?
2-3 weeks later
60
What causes acute rheumatic fever following streptococcal infection?
Cross-reaction b/w heart or joint tissues and M proteins on streptococcal antigens
61
What causes acute glomerulonephritis following streptococcal infection?
Formation of antigen-antibody complexes on glomerulus basement membrane
62
How are staphylococci split into two categories?
Coagulase test
63
Why are coagulase +ve staphylococci generally more virulent than coagulase -ve?
Stimulate clotting of blood around colony which increases survival
64
What skin infections are caused by staphylococci infection?
Impetigo Furuncle/boil Carbuncle Surgical wound infection
65
Give an example of a coagulase +ve staphylococcus.
Staph aureus
66
Give an example of a coagulase -ve staphylococcus.
Staph epidermis
67
What is the treatment for staphylococcal infection?
Flucoxacillin Some cephalosporins Beta-lactamase combinations Vancomycin for flucoxacillin-resistant strains
68
What features are considered in choosing an Abx?
``` Severity of infection Site of infection Likely pathogen Route of administration Possible adverse effects ```
69
What is empirical Abx therapy?
'Best guess' Tx when causative agent is not known
70
How does pneumocystis pneumonia present differently in HIV +ve vs HIV -ve pts?
+ve: subacute, low grade fever | -ve: rapid progression, high fever

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