Infection and Immunology Flashcards

1
Q

what is the most common cause of candidiasis?

A

candida albicans

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2
Q

Risk factors for candidiasis infection?

A

Broad-spectrum antibiotics
immunocompromise - HIV, steroids (oral or inhaled)
DM

cushing’s
GI tract surgery
central line

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3
Q

What are the features of oral candidiasis?

A

common in neonates
a curd-like white patches on the mouth which can be REMOVED EASILY showing a red base

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4
Q

what are the features of oesophageal candidiasis?

A

dysphagia +/- pain on swallowing
white patches on OGD

it is an AIDS DEFINING ILLNESS

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5
Q

what does candidiasis of the skin look like?

A

sore + itchy
red, moist skin with ragged peeling edge
might have papules and pustules

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6
Q

Name an anti-fungal which might be used to treat candidiasis?

A

fluconazole

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7
Q

what is cellulitis?

A

it is an acute non-purulent spreading infection of the sub-cutaneous tissue

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8
Q

what are the most common causative organisms of cellulitis?

A
Streptococcus pyogenes 
staphylococcus aureus (beware of MRSA)
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9
Q

what is the cause of orbital cellulitis?

A

haemophilia influenzae

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10
Q

what are the RF for cellulitis?

A

skin break
poor hygiene
poor vascularisation of tissue

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11
Q

what is the cause of HSV encephalitis?

A

HSV 1 usually

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12
Q

What are the symptoms of HSV 1?

A

primary = usually asymptomatic. gingivostomatitis, pharyngitis, herpetic whitlow (finger lesion)
lymphadenopathy (tender)

secondary = perioral tingle -> vesicles -> ulcer + crust -> healed 8-10 days alter

may cause herpetic encephalitis

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13
Q

what are the symptoms of HSV 2?

A

painful blister/rash in genital, peri-genital or anal area
MACULOPAPULAR RASH

dysuria
fever
malaise
inguinal lymphadenopathy

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14
Q

how is HIV transmitted?

A

through exchange of bodily fluids

sexual intercourse, mother-to-child, needle sharing/stick injuries, blood transfusions, organ transplantations

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15
Q

what is the pathophysiology of HIV?

A

HIV enters CD4+ lymphocytes via GP120 receptors -> reverse transcriptase enables HIV genetic material to be added to host genome

cells produce more HIV -> dissemination -> cell death and eventual T cell depletion.

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16
Q

what are the three phases of HIV?

A
  1. seroconversion
  2. early/asymptomatic
  3. AIDS
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17
Q

what are the features of stage 1 of HIV?

A

self-limiting stage

fever, night sweats, general lymphadenopathy, sore throat

other: oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea

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18
Q

what are the features of stage 2 of HIV?

A

early/asymptomatic

usually appear well, may have persistent lymphadenopathy, progressive minor symptoms (rash, weight loss, oral thrush)

19
Q

what are the features of stage 3 of HIV?

A

AIDS

secondary diseases due to immunodeficiency

20
Q

what are some of the secondary effects arising from the immunodeficiency caused by HIV?

A

bacterial infections, viral infections (CMV, HSV, VZV, HPV, EBV)

fungal infection - pneuomocystic jirovecii pneumonia, cryptococcus, candidiasis, aspergillosis

protozoal - toxoplasmosis

tumour - kaposi sarcoma, SCC, both lymphomas

21
Q

what kind of a virus is EBV?

A

a gamma-herpes virus (dsDNA)

22
Q

how is EBV transmitted?

A

it is found in pharyngeal secretions of an infected individual

close contact leads to spread (e.g. kissing, sharing eating utensils)

23
Q

what is the pathophysiology of EBV?

A

infection of epithelial cells in oropharynx -> infects B cells -> they disseminate the disease -> humoral and cellular immune response across the body -> primary infection ends but virus is latent in B cells

reactivation of latent virus in B cells after stress of immunosuppression

atypical lymphocytes can be detected on blood film

24
Q

what happens if patients with EBV are given ampicillin or amoxicillin?

A

develop a widespread maculopapular rash

25
Q

what is the investigation to test for EBV?

A

heterophile antibody test

26
Q

what would you expect from your investigations to confirm EBV?

A

+ve heterophile antibody test
leucocytosis
raised AST/ALT
peripheral blood film showing abnormal leucocytes

27
Q

what are the signs of EBV?

A

pyrexia
cervical/generalised lymphadenopathy
splenomegaly
hepatomegaly
erythematous + oedematous pharynx, exudate on tonsils
jaundice in 5-10%

28
Q

how do you manage EBV?

A

nsaids + paracetamol, bed rest
avoid contact sport for 2/52 due to splenic rupture risk
steroids for severe cases

29
Q

what is the most severe form of malaria?

A

infection with plasmodium falciparum

30
Q

briefly describe the life cycle of plasmodium

A
  1. injection of sporozoites from FEMALE mosquite into blood
  2. invasion + replicate in hepatocytes
  3. re-enter blood and infect RBC
  4. replicate in RBC developing ring forms
  5. RBC rupture, release merozoites -> infect more RBC
  6. new mosquite bites and takes up gametocytes
  7. gametocytes -> sporozoites in mosquite gut -> move to saliva ready to reinfect
31
Q

what populations have a degree of innate immunity to malaria?

A

sickle cell trait
G6PD Deficiency
pyruvate kinase deficiency
thalassaemia

32
Q

What is the maximum incubation period for malaria?

A

up to a year

need to establish patient travel history a year prior to presenting to healthcare professionals if suspecting malaria

33
Q

what investigations are performed if you suspect malaria?

A

thick and thin blood film (thick for quantifying, thin to identify plasmodium species)

bloods: FBC (haemolytic picture), LFTs, U&Es, ABG
urinalysis for haematuria or proteinuria

34
Q

what are the signs of malaria?

A

pyrexia
anaemia (haemolytic)
hepatosplenomegaly

35
Q

what are the symptoms of malaria?

A

cyclical

high fevers, flu-like symptoms (fatigue, muscle ache, abdo/back pain), sweating, shivering cold/rigors, nausea + vomiting, headache

36
Q

how is VZV transmitted?

A

aerosol inhalation or direct contact with vesicular secretions

37
Q

where is the dormant VZV found?

A

dorsal root ganglion

38
Q

what are the features of primary VZV infection?

A

CHICKENPOX

prodromal malaise, mild fever, intense itchy rash spreading affecting mainly face and trunk, vesicles weep + crust

infections from 48 hrs before rash till vesicles have crusted (7-10 days)

MACULOPAPULAR RASH, skin excoriation, mild fever

39
Q

what are the features of secondary VZV infection?

A

tingling/hyperaesthesia in dermatomal distribution
painful skin lesions + rash in dermatomal distribution

vesicular maculopapular rash over a dermatome

recovery 10-14 days

40
Q

What is Ramsey-hunt syndrome?

A

VZV secondary infection in the geniculate ganglion

causes zoster in ear and facial nerve palsy (LMN). vesicles may be visible behind the pinna of ear canal

41
Q

what is the definition of sepsis?

A

Sepsis is life-threatening organ dysfunction caused by dysregulated host response to an infection.

42
Q

what are the components of SIRS? (not needed for sepsis)

A
  • 2 or more of:
    • Temperature < 36 or > 28
    • Heart rate > 90 bpm
    • RR > 20 or PaCO2 < 4.5 kPa or mechanically ventilated
    • WBC < 4 or > 11 or > 10% immature forms
43
Q

describe qSOFA

A

quick screening, > 2 associated with high risk of mortality and requirement for ICU

  • RR > 22
  • altered mentation (GCS < 15)
  • systolic BP < 100mmHg