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Unit 22 Clinical laboratory

immunology
The body
against others
and itself.
Objectives, to know the
tests in
 Immune disease
 Autoimmune disease
 Infectious disease
 Allergies
 Inflammatory diseases
 Complement diseases
 Arthritis.
Immunoglobulins:
 Produced by B lymphocytes in
response to foreign or self antigens.
 Two light chains: kappa or lambda.
 Two heavy chains: alpha, gamma,
delta, epsilon or mu.
 Immunoglobulins: IgA, IgG, IgD,
IgE and IgM.
Immunoglobulins:
Form Found in Function
IgM Penta ECF,membrane 1st response.
IgG Mono ECF Toxin, activates
complement.
IgA Dimer ECF, secretions Antimicrobial.
IgE Mono ECF Anti allergic/
anti parasites.
IgD Mono ECF,membrane Unknown.
Immunoglobulin deficiency:
 Normal: IgM and IgA are low at
birth and for months after.
 Inherited agammaglobulinaemia:
the “boy in the bubble”.
 Acquired: malnutrition, malignancy,
infections, drugs, overstress.
Immunoglobulin excess
 Paraproteins in cancers –
monoclonal. Unit 13.
 Autoimmune disease –
polyclonal. Units 15, 21, 22,
24,25
 Infections –polyclonal. Unit
22.
Some autoimmune diseases
and laboratory tests:
Systemic lupus Anti nuclear antibodies
erythematosus ANA
Arthritis ANA,Rheumatoid factor
Sjogren’s,scleroderma Extractable Nuclear Ag
Vasculitis Antineutrophil
cytoplasmic antibodies
Anti self Human leukocyte Antig
Thyroiditis Antithyroid antibody
Infections, symptoms:
 Pain, heat, redness, swelling.
 Toxic reactions: rashes , muscle pains,
cardio respiratory, gastrointestinal.

 Acute: fever, chills, flushing, increased


pulse.
 Chronic: fatigue, lassitude, weight loss.
Infective organisms:
 Viruses
 Bacteriophage, plasmids, transposons.
 Bacteria
 Chlamydia, rickettsia, mycoplasma.
 Fungi,
 Protozoa
 Helminths
 Ectoparasites.
Infections, laboratory work:
 Erythrocyte sedimentation rate, ESR
 Complete blood count, CBC
 Serum C-reactive protein, CRP
 Serum IgG, IgM.
 Serology – specific tests for
organisms.
 DNA and RNA based tests.
Laboratory work in
infectious diseases:
 Most bacteria found by culture.
 Serological test for antibodies against
bacteria are used for:
3. Population studies post infection.
4. Current or recent infection where culture
is negative.
5. Fever of unknown origin > 2-3 weeks.
6. Unique applications.
Immunology issues:
 Is there an antibody?
 Can it be measured?
 Is it increasing or decreasing
in amount?
Infections, serology and
other NPLEx tests:
1. Antistreptolysin O:
streptococcus pyogenes.
Note: this is by titration.
Increases a week after infections
Peaks at 3-5 weeks.
6-12 months to normal.
NPLEx infectious serology:
2. Chlamydia.

Note: may be STD or from


parrots.
50% men 70% women have no
symptoms.
NPLEx infectious serology:
3. Cytomegalovirus IgG and
IgM.
4. Epstein Barr virus:
Monospot IgG.
5. Escherichia coli:
NPLEx infectious serology:
6. Helicobacter pylori.

IgG and IgA seen in 80-100%


with infection.
Elderly 60% positive.
NPLEx infectious serology:
7. Hepatitis viruses A, B, C, D,
E.
8. Herpes simplex: HSV1,
HSV2.
Most adults have had this.
Infectious disease testing
(continued)
9. Human Immunodeficiency virus:
HIV-IgG, HIV load, CD4, CD8.
P24 soon after infections but fades
away.
HIV-1 Ab 4-12 weeks after infection.
No Ab just before death and p24 etc
antigens increase.
CD4 and CD8 response to treatment.
NPLEx serology
10. Human papilloma virus. 16 type
causes cancer. A success!
11. Rubella. Very serious to foetus in
pregnant women.
12. Syphilis: VDRL, RPR (screening
test). Tests positive 2-3 weeks after
infection.
NPLEx infectious serology:
13. Tuberculosis: BCG,
Bovine TB given. Skin test
1-3 days later see reaction
14. Lyme disease.
Allergy testing:
1. RAST: serum IgE,
general and specific
tests.
2. Skin prick test.
Inflammation markers:
 Erythrocyte sedimentation rate (ESR).
 Plasma viscosity.
 Serum C-reactive protein- acute phase
reactant.
 Other serum acute phase reactants:
complement, ceruloplasmin,
haptoglobulin, fibrinogen, alpha-1-
antitrypsin, alpha-1-acid glycoprotein
(orosomucoid).
Acute phase reactants:
 Illness
 Infection
 Trauma
 Tissue necrosis.
Serum C-reactive protein
 Always: rheumatic fever, rheumatoid
arthritis, acute bacterial infections, viral
hepatitis, myocardial infarction – high
sensitivity version
 Frequent: active tuberculosis TB, gout,
advanced malignancy, leprosy, active
cirrhosis, burns, peritonitis.
 Sometimes: multiple sclerosis, Guillain-
Barre, scarlet fever, varicella, post
surgery, intrauterine contraception.
Serum complement
 Classical – triggered by
antigen/antibody.
 Alternate – triggered by foreign and
cell surfaces.
 Recognition: C1q, C1r, C1s,
 Activation: C2, C3, C4.
 Membrane attack: C5, C6, C7, C8,
C9.
Serum complement, clinical
 Systemic lupus erythematosus-
deficiency in serum C1q, C1r,
C1s, C2 or C4.
 Rheumatoid arthritis - some
have decreased serum C1.
 Most have decreased serum C2
and C4.
Complement, laboratory
measurements:
 Whole system: serum CH50.
 Assay of individual
components; serum C3 and
C4.
 Activation: serum C1q, C2,
C3 and C4.
7 elite Swedish orienteers
aged 25-29 years from Dala
 Sudden unexplained
deaths (really 20)
Possible explanations:
 Viral infection TWAR
 Coronary disease
 Lyme disease
 Inbreeding
 Dope: amphetamines,
cocaine, steroids.
EPO…
Official explanation
 Virus infection.

But
 Why is this not seen in parallel
sports and activities.
 The consequence of official action….
SUD, what the Swedes did
 No orienteering competition allowed
for 6 months (1992).
 National team disbanded.
 No foreign visitors for training or
competition.

 No further cases reported.

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