Infection and Immunology Flashcards
what is the most common cause of candidiasis?
candida albicans
Risk factors for candidiasis infection?
Broad-spectrum antibiotics
immunocompromise - HIV, steroids (oral or inhaled)
DM
cushing’s
GI tract surgery
central line
What are the features of oral candidiasis?
common in neonates
a curd-like white patches on the mouth which can be REMOVED EASILY showing a red base
what are the features of oesophageal candidiasis?
dysphagia +/- pain on swallowing
white patches on OGD
it is an AIDS DEFINING ILLNESS
what does candidiasis of the skin look like?
sore + itchy
red, moist skin with ragged peeling edge
might have papules and pustules
Name an anti-fungal which might be used to treat candidiasis?
fluconazole
what is cellulitis?
it is an acute non-purulent spreading infection of the sub-cutaneous tissue
what are the most common causative organisms of cellulitis?
Streptococcus pyogenes staphylococcus aureus (beware of MRSA)
what is the cause of orbital cellulitis?
haemophilia influenzae
what are the RF for cellulitis?
skin break
poor hygiene
poor vascularisation of tissue
what is the cause of HSV encephalitis?
HSV 1 usually
What are the symptoms of HSV 1?
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
what are the symptoms of HSV 2?
painful blister/rash in genital, peri-genital or anal area
MACULOPAPULAR RASH
dysuria
fever
malaise
inguinal lymphadenopathy
how is HIV transmitted?
through exchange of bodily fluids
sexual intercourse, mother-to-child, needle sharing/stick injuries, blood transfusions, organ transplantations
what is the pathophysiology of HIV?
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.
what are the three phases of HIV?
- seroconversion
- early/asymptomatic
- AIDS
what are the features of stage 1 of HIV?
self-limiting stage
fever, night sweats, general lymphadenopathy, sore throat
other: oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea
what are the features of stage 2 of HIV?
early/asymptomatic
usually appear well, may have persistent lymphadenopathy, progressive minor symptoms (rash, weight loss, oral thrush)
what are the features of stage 3 of HIV?
AIDS
secondary diseases due to immunodeficiency
what are some of the secondary effects arising from the immunodeficiency caused by HIV?
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
what kind of a virus is EBV?
a gamma-herpes virus (dsDNA)
how is EBV transmitted?
it is found in pharyngeal secretions of an infected individual
close contact leads to spread (e.g. kissing, sharing eating utensils)
what is the pathophysiology of EBV?
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
what happens if patients with EBV are given ampicillin or amoxicillin?
develop a widespread maculopapular rash
what is the investigation to test for EBV?
heterophile antibody test
what would you expect from your investigations to confirm EBV?
+ve heterophile antibody test
leucocytosis
raised AST/ALT
peripheral blood film showing abnormal leucocytes
what are the signs of EBV?
pyrexia
cervical/generalised lymphadenopathy
splenomegaly
hepatomegaly
erythematous + oedematous pharynx, exudate on tonsils
jaundice in 5-10%
how do you manage EBV?
nsaids + paracetamol, bed rest
avoid contact sport for 2/52 due to splenic rupture risk
steroids for severe cases
what is the most severe form of malaria?
infection with plasmodium falciparum
briefly describe the life cycle of plasmodium
- injection of sporozoites from FEMALE mosquite into blood
- invasion + replicate in hepatocytes
- re-enter blood and infect RBC
- replicate in RBC developing ring forms
- RBC rupture, release merozoites -> infect more RBC
- new mosquite bites and takes up gametocytes
- gametocytes -> sporozoites in mosquite gut -> move to saliva ready to reinfect
what populations have a degree of innate immunity to malaria?
sickle cell trait
G6PD Deficiency
pyruvate kinase deficiency
thalassaemia
What is the maximum incubation period for malaria?
up to a year
need to establish patient travel history a year prior to presenting to healthcare professionals if suspecting malaria
what investigations are performed if you suspect malaria?
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
what are the signs of malaria?
pyrexia
anaemia (haemolytic)
hepatosplenomegaly
what are the symptoms of malaria?
cyclical
high fevers, flu-like symptoms (fatigue, muscle ache, abdo/back pain), sweating, shivering cold/rigors, nausea + vomiting, headache
how is VZV transmitted?
aerosol inhalation or direct contact with vesicular secretions
where is the dormant VZV found?
dorsal root ganglion
what are the features of primary VZV infection?
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
what are the features of secondary VZV infection?
tingling/hyperaesthesia in dermatomal distribution
painful skin lesions + rash in dermatomal distribution
vesicular maculopapular rash over a dermatome
recovery 10-14 days
What is Ramsey-hunt syndrome?
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
what is the definition of sepsis?
Sepsis is life-threatening organ dysfunction caused by dysregulated host response to an infection.
what are the components of SIRS? (not needed for sepsis)
- 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
describe qSOFA
quick screening, > 2 associated with high risk of mortality and requirement for ICU
- RR > 22
- altered mentation (GCS < 15)
- systolic BP < 100mmHg
