Lymphadenopathy and HIV infection Flashcards Preview

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Flashcards in Lymphadenopathy and HIV infection Deck (19):

causes of lymphadenopathy

Proliferation of lymphocytes in response to a local infection
Proliferation of malignant cells that have metastasised to the node by lymphatic spread
Proliferation of malignant lymphocytes
Inflammation within nodes resulting from killing of lymphocytes infected by a virus


Investigation of lympatdenopathy

Look for adjacent infection e.g. boils, cellulitis
look for adjacent cancer e.g. breast, lung, skin
Look at features of cells in lymph node
Look for evidence of infection that targets lymphoid cells


common types of bacteria that infect lymph nodes

Staphylococcus aureus
Mycobacterium tuberculosis


Common viruses that infect lymph nodes

Cytomegalovirus (CMV)


common causes of illness with generalised lymphadenopathy

EBV --> glandular fever
CMV --> less severe glandular fever like illness


Herpes viruses

DNA virus
Acute infection, followed by:
Latent infection (asymptotic) with reactivation
Chronic infection (asymptomatic)


Acute EBV infection

glandular fever / infectious mononucleosis/ kissing disease
Minor illness when acquired as a child
More severe illness when acquired as adolescent / adult
virus transmitted in saliva
Incubation period of 4-6 weeks illness for 1-2 weeks (usually)
Fever, sore throat, cervical adenopathy, malaise, fatigue

Recovery but persistent salivary excretion of EBV


Laboratory diagnosis of acute EBV infection

Lymphocytosis (>50% of WBC's)
Atypical lymphocytes (>10% of lymphocytes)
Abnormal liver function tests
- mono spot test, detects hetrophile antibodies which bind to guniea pig, sheep and horse RBC's but not to EBV

- Specific EBV serology: detects antibodies that bind to EBV and EBV antigens


Laboratory diagnosis of acute CMV infection

Lymphocytosis (>50% of all WBC's)
Atypical lymphocytes (>10% of all lymphocytes)
abnormal liver function tests
Detection of antibodies (IgM or IgG) to CMV
Detection of CMV in the blood


Checklist for HIV infection

Epidimiologic risk for HIV infection
Recent (3-6 weeks previously) exposure
Glandular fever like illness
Persistant viraemia and virus in genital secretions
Presence of antibodies to HIV in the blood


Cause of the rapid evolution of HIV during infection

continuous production of HIV (10^9 HIV/day)
Highly error prone copying of HIV RNA by reverse transcriptase
No "proof reading" for errors
Generation of a very wide range of mutant viruses everyday


HIV pathogenesis

1. HIV infects T helper cell
2. New HIV is produced, these viruses differ from the infecting viruses
3. Cytotoxic lymphocytes kill those cells they recognise as infected
4. Some virus producing cells are not recognised as infected and produce more virus
5. Other cytotoxic lymphocyte clones recognise these infected cells and kill them
There is continuous selection pressure exerted by the immune system selecting HIV that is less well recognised by cytotoxic lymphocytes


Time course of untreated HIV infection

1. Infection
2. Level of HIV in tissues and blood rises
3. Cytotoxic T lymphocytes kill many HIV producing cells
4. Number of T helper lymphocytes in blood falls
5. Level of HIV in blood falls
6. Killing of infected lymphocytes causes a brief glandular fever like illness
7. B lymphocytes start producing antibodies the HIV
8. Level of HIV remains stable for many years
9. T helper lymphocyte number continues to fall
10. T helper lymphocyte depletion is severe
11. AIDS illness
12. Level of HIV in blood rises further


Diagnosis of HIV infection

1. Detect antibodies to HIV in blood
a) screening test = ELISA
b) confirmatory test = western blot
2. Detect HIV genome in blood by PCR


Describe ELISA

Enzyme linked immunosorbent assay
1. HIV antigen stuck to base of ELISA wells
2. Serum sample added - antibody in serum attaches to HIV antigen
3. anti human antibody with adherent enzyme added - attaches to serum antibody
4. reagent added - cleaved by enzyme on antihuman antibody - results in colour change


Western blot test

1. HIV proteins separated (by molecular weight and charge) by gel electrophoresis
2. Proteins transferred from gel to a membrane
3. membrane strips incubated with serum from patients - antibodies in serum attach to separated HIV protein bands
4. Human antibodies stained with silver dye


AIDS defining illnesses

Toxoplasmosis gondii = brain abscess
candida albicans = osteophagitis
mycobacterium tuberculosis
Kaposi's sarcoma
CNS lymphoma
cytomegalovirus retinitis


HIV replication cycle targets for drug treatment

reverse transcriptase e.g AZT, 3CT, tenofovir
Protease e.g. lopinavir, atazanavir
HIV binding e.g. maraviroc
DNA integration


Nucleoside analogue reverse transcriptase inhibitors (NRTIS)

a) reverse transcriptase enzyme
b) complementary strand of DNA (white circles)
c) nucleotides added to the complimentary strand
d) single strand of HIV RNA
e) altered nucleotide e.g. AZT blocks elongation of complementary strand