Basic Immunology
Basic Immunology
Basic Immunology
IMMUNOLOGY
INTRODUCTION
Immunology is the study of host
defence mechanisms.
Immunity is the ability of the host to
protect itself against foreign
organisms.
The immune system comprises the
tissues, cells & molecules which
mount the immune response.
Coagulation
Cascade
Plasma Fibrinogen
XIIa
Fibrinolytic
Cascade
Thrombin
Complement
Cascade
Fibrin
Plasmin
Bradykinin
PCV
Kinin
Cascade
Kallikrein
Cellular mediators
MAC
Immunology
Natural (innate) immune system
Skin, tears, saliva, mucus, acids
Property of all living creatures
INTRODUCTION
Immunogenicity is the capacity
to induce an immune response by
foreign, complex, high molecular
weight compounds
Antigenicity is the ability to bind
to Ig or immune cells; an immune
response need not result
Haptens
INTRODUCTION
Epitopes
aka antigenic determinants
Immunological cross-reactivity
the sharing of epitopes by different
substances
toxoids & immunisation
physicochemical barriers
molecules normally present in body
fluids e.g. lysozyme, complement,
antiproteases
phagocytic & cytotoxic cells such as
neutrophils, macrophages, natural
killer cells
superoxide radicals
hyperchlorous acid
H2O2
chloramines
T-LYMPHOCYTES
Cell-mediated immunity especially
intracellular organisms, protozoa &
fungi
Graft rejection
Immune surveillance of neoplasia
70-80% of total lymphocytes
Long-lived memory cells
Activity is by cytokine production
T-LYMPHOCYTES
Th - CD4+: Respond to antigen in
association with MHC Class II
Tc - CD8+: Respond to antigen
presented via MHC Class I
Antigen MUST be peptide
Tdth
Ts
T-LYMPHOCYTES
CD4+ cells recognize antigens that
have been taken up by antigen
presenting cells which present
antigen fragments on the cell surface
CD8+ cells recognise cells infected
with virus, which they then kill
T-LYMPHOCYTES
CD4 (Th) cells interact directly with
other cells by releasing cytokines to
control development of the immune
response
Two types of Th cell
Th-1 cells activate macrophages to
destroy material phagocytosed
Th-2 cells help B-cells make antibody
B-LYMPHOCYTES
Specialised for the production of
immunoglobulins after differentiation
into plasma cells
Controls pyogenic bacteria
Prevents blood-borne infections
Neutralise toxins
12% of total lymphocytes
B-LYMPHOCYTES
Can respond to peptide,
carbohydrate & glycolipids
Usually require T-cell help to respond
to antigen (interleukins) but can also
recognise antigen directly through
surface Ig
B cells mature & proliferate in lymph
nodes
B-LYMPHOCYTES
B-cells process & present antigen via
surface MHC class II
Responses are antigen-specific but
effects are not specific - mainly via
complement
IMMUNOGLOBULINS
The 5 classes of Ig are:
IgM
IgA
IgD
IgG
IgE
IMMUNOGLOBULINS
4-chain structure
2 light chains
2 heavy chains
IMMUNOGLOBULINS
Terminal regions of H & L chains are
the variable regions
The variable region is the site where
Ig combines with antigen
This regions variability is responsible
for wide range of antigen specificity
IMMUNOGLOBULINS
The other domains are the constant
regions which are similar within
isotypes of Ig
Using enzymes, a number of Ig
fragments have been identified.
Important ones are:
Fab
Fc
IMMUNOGLOBULINS
Fc regions formed from H chains &
determine isotype & so biological
function
Hinge region also has effect on
function
These functions are distinct from
antigen binding
IMMUNOGLOBULINS
IgG
neutralises toxins
activates complement
opsonisation
able to cross placenta (only Ig that can)
IMMUNOGLOBULINS
IgA
monomeric & dimeric forms
dimeric = secretory IgA - found in
secretions
important antiviral Ig
IMMUNOGLOBULINS
IgM
pentameric
good agglutinator
good at activating complement
IMMUNOGLOBULINS
IgD
true function unknown
appears to be involved in B-cell
differentiation
IMMUNOGLOBULINS
IgE
parasitic infections
Fc portion binds to mast cells
triggers mast cell degranulation
T- & B-LYMPHOCYTES
T- & B-cells recognise the antigen,
proliferate in response to it, &
migrate back to the site of injury
There they release cytokines that
attract effector cells (cytotoxic Tcells, activated macrophages,
committed B-cells)
ANTIGEN PRESENTING
CELLS
Examples of APCs are:
macrophages
B-cells
dendritic cells
ANTIGEN PRESENTING
CELLS
COMPLEMENT
The complement system
comprises at least 9 plasma proteins &
some regulatory factors, that mediate
several functions of the inflammatory
process
synthesised by macrophages or
hepatocytes
usually circulate as inactive proenzymes
heat labile (c.f. Ig is heat stable)
COMPLEMENT
Complement pathways
Cascade of sequential activation
converts each proenzyme into its active
state & amplifies the response.
Two main pathways:
Classical pathway - bound IgG, IgM
Alternative pathway - certain
antigens (LPS, endotoxin, IC)
COMPLEMENT
Functions
opsonisation, chemotaxis, immune
adherence (MAC)
acceleration of acute inflammation
immune cytolysis
virus neutralisation
IMMUNOLOGICAL
DISORDERS
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Hypersensitivity (allergy)
Definition:
Itisanabnormal,heightenedreactiontoanytypeofstimuli.
(Smeltzer,etal,2004)
Immuneresponsethatresultsintissueinjuryorother
physiologicalchangesarecalledhypersensitivity(allergic)
reactions.
(Mellors,1999).
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Typesofhypersensitivityreactions
Hypersensitivity reactions are classified into four types:
TypeI:anaphylactichypersensitivity
TypeII:cytotoxichypersensitivity
TypeIII:immunecomplexhypersensitivity
TypeIV:cellmediatedhypersensitivity
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Types of hypersensitivity
reactions
Type I: Anaphylactic hypersensitivity:
Itisanimmediatereactionbeginningwithinminutesof
exposuretoanantigen.
ItismediatedbyI.e.antibodies.
Itrequirespreviousexposuretospecificantigen.
Itusuallyaffectsonskin,lungsandgastrointestinaltract.
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Anaphylactic (type I)
Hypersensitivity
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Anaphylactic (type I)
Hypersensitivity
Examples:
Asthma
Allergicrhinitis
Systemicanaphylaxis.
Atopicdermatitis
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Types of hypersensitivity
reactions
Type II: cytotoxic hypersensitivity
Itoccurswhenthesystemmistakenlyidentifiesa
normalconstituentofthebodyasforeign.
Thisreactionmaybearesultofcross-reacting
antibody,possiblyleadingtocellandtissuedamage
ItinvolvesactivationofcomplementbyIgGorIgM
antibodybindingtoanantigeniccell.
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Cytotoxic(typeII)Hypersensitivity
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Cytotoxic(typeII)Hypersensitivity
Examples:
Myastheniagravis
BloodTransfusionreaction
Thrombocytopenia
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Types of hypersensitivity
reactions
Type III: Immune complex hypersensitivity
Itinvolvesintheformationofimmunecomplexes
whenantigenbindstoantibodies.
ThesetypeIIIcomplexesdepositintissuesor
vascularendotheliumandleadstoinjurywiththe
helpofvasoactiveaminesandtheincreasenumberof
circulatingcomplexes.
Thejointsandkidneysareparticularlysusceptible.
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Types of hypersensitivity
reactions
Type IV: Cell mediated hypersensitivity
Alsoknownascellularhypersensitivity
Itoccurs24-72hrsafterexposuretoanallergen
ThereactionismediatedbysensitizedTcellsand
macrophages.
ThereactionresultsIntissuedamagebyreleasing
lymphokines,macrophagesandlysozymes.
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Allergic Rhinitis
ItisalsocalledasHay Fever
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ALLERGIC RHINITIS
Definition:
Itisaninflammationofthenasalmucosabyan
allergen.
(Smeltzer,2004).
Incidence:
Itaffectsabout8-10%ofU.S.population.
(Smeltzer,2004).
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Perennial
Year-roundwithallergic
triggers
Sneezing,itching,
waterydischargefrom
noseandeyes
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Seasonal
Earlyspring,earlyfall,
earlysummer
Intensesymptoms
triggeredbyair-borne
pollens,housedustand
animalfeather.
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Pathophysiology:
ALLERGIC
RHINITIS
Inhalationofanantigen(sensitization)
Re-exposure
Nasalmucosareacts(histamineismediator)
Slowingofciliaryaction,edemaformationand
leukocyteinfiltration
Tissueedemaandincreasecapillarypermeability
(vasodilatation).
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Allergic rhinitis
Diagnostic tests:
Nasalsmears(nasaleosinophilia)
TotalserumIgE
Medical management:
Oralantihistamines(blockstheactionofhistamine)
Adrenergicnasaldecongestant
Mastcellstabilizers.
Analgesicsandantipyretics.
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Allergic rhinitis
Nursing management:
Assessment
Examination(Assesssymptoms)
Historyofpatient(Allergyassessment)
Diagnosis
Ineffectivebreathingpatternrelatedtoallergic
reactions
Knowledgedeficitrelatedtoallergyandthe
recommendedmodificationsinlifestyleandself-care
practices
Ineffectiveindividualcopingwithconditionandneed
forenvironmentalmodification.
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Allergic rhinitis
Nursing interventions:
1. Patientisinstructedtomodifytheenvironmentto
reducetheseverity.
2. Encouragefordeepbreathingandcoughfrequently
foradequategasexchange.
3. Encourageforsteaminhalation
4.Promoterest.
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Pathophysiology: Atopic
dermatitis
Allergen/Sensitizingantigen
Effecttheskin(changesinlipidcontent,sebaceousglandactivityand
sweating)
Skinreducedwater-bindingcapacityintheskin
Highertransepidermalwaterlossanddecreasedwatercontent
Dryskin
Itching,rubbingleadstoinfection
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Medical Management:
Atopic dermatitis
Moisturizers
Topicaland
systemicsteroids
Antibiotics
Antihistamines
Performallergen
test
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Anaphylaxis
Definition:
Itisanimmediatelifethreateningsystemicreactionthatcan
occuronexposuretoparticularsubstances
Itisanimmediate(typeIhypersensitivity)immunologic
reaction,resultsfromIgEantibody
Thisreactionaffectsmanytissuesandorgans.
Deathmayoccurduetorespiratorytractspasmandconstriction
orcollapse.
.
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Causes: Anaphylaxis
Food(peanuts,fish,milk,eggs,wheatandchocolate).
Medications(penicillin,NSAIDs)
Insectsstings(bees,ants)
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Pathophysiology: Anaphylaxis
InteractionofforeignantigenwithIgEantibodies
Releaseofhistamine
Activationofplatelets,eosinophilsandneutrophils
smoothmusclespasm,bronchospasm,mucosaledemaand
inflammation.
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Moderate
Same
Severe
Same
Peripheraltingling Flushing
Sensationof
Itching
warmth
Broncospasm
Laryngealedema
Fullnessinmouth
andthroat
bronchospasm
SevereDyspnea,
cyanosis
Nasalcongestion
Edemaoflarynx
Hypotension
Periorbital
swelling
Dyspnea
Cardiacarrestand
comamayfollow.
Pruiritis
Sneezing
Cough
wheezing
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Assessforsignsofanaphylaxis.
Restoreeffectivebreathing
Reduceanxietybyreassuringthepatient
Provideoxygen,andmaintainairway
Monitorvitalsigns.
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Serum sickness
ItisatypeIIIhypersensitivityreaction.
ThereactionresultfromadministrationoftherapeuticAntiSeratakenfromanimalsourceforthetreatmentand
preventionofinfectiousdiseasesliketetanus,rabies,
diphtheria
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Clinical manifestations
Serum sickness
Localized:
Inflammatoryreactionatthesiteofinjection.
Generalized:
Skinrashes
Tendernessandswellingofjoints
vasculitismostlyinkidneysresultsinproteinuria
Glomerulonephritis
Peripheralneuritisleadstotemporaryparalysis
Fever
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Serumsickness
Medical management:
Antihistamines
Corticosteroids
Nursing management:
EncourageforROMexercises,provideDVTstockings
(adeepveinthrombosisandpulmonaryembolismare
treatstothesepatients.
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Disorders of
the immune
system
An overactive immune
system/hypersensitivity
If you are born with certain genes, your
immune system may react to substances
inthe environment that are normally
harmless.
Asthma
The response in your lungs can cause
coughing, wheezing, and trouble
breathing. Asthma can be triggered
by a common allergen like dust or
pollenor by an irritant like tobacco
smoke.
Allergic rhinitis
Sneezing, a runny nose, sniffling, and
swelling of your nasal passages from
indoor allergens like dust and pets or
outdoor allergens like pollens or molds.
Eczema
An allergen causes an itchy rash known as
atopic dermatitis
Skin testing
Type II (Cytotoxic)
Clinical symptoms occur 5-12 hours
Antigen causes formation of IgM and IgG
antibodies that bind to target cell , when
combined with action of complement,
destroys target cell
-Examples: Transfusion reactions, Rh
Incompatibility, HDNB
Drug-Induced Cytotoxic
Reactions
Thrombocytopenic purpura
Agranulocytosis
-immune-caused destruction of
agranulocytic white cells and it affects the
body's phagocytic defenses.
Hemolytic anemia
-when RBCs are destroyed
Glomerulonephritis is an immune
complex condition, usually resulting from
an infection, that causes inflammatory
damage to the kidney glomeruli.
ALLERGIC CONTACT
DERMATITIS
Autoimmune
disease
Inautoimmune diseases, the body
attacks normal, healthy tissues. The
cause is unknown. It is probably a
combination of a person's genes and
something in the environmentthat
triggers those genes.
Cytotoxic
Autoimmune
Graves' disease
Reactions
The immune system
produces antibodies
that stimulate the thyroid gland to release
excess amounts of thyroid hormone into
the blood (hyperthyroidism).
Symptoms: bulging eyes weight loss,
nervousness, irritability, rapid heart rate,
weakness, and brittle hair.
Treatment:Destruction or removal of the
thyroid gland
Graves disease
Myasthenia gravis
Antibodies bind to nerves and make them
unable to stimulate muscles properly.
Weakness that gets worse with activity is
the main symptom of myasthenia gravis.
Mestinon (pyridostigmine) is the main
medicine used to treat myasthenia gravis.
Myasthenia gravis
Immune Complex
Autoimmune Reactions
Systemic lupus erythematosus
(lupus)
People with lupus develop autoimmune
antibodies that can attach to tissues
throughout the body.
The joints, lungs, blood cells, nerves, and
kidneys are commonly affected in lupus.
Treatment often requires daily oral
prednisone.
Systemic lupus
erythematosus
Rheumatoid arthritis
The immune system produces antibodies
that attach to the linings of joints.
Immune system cells then attack the
joints, causing inflammation, swelling, and
pain
Treatments for rheumatoid arthritis can
include various oral or injectable
medications that reduce immune system
over activity.
Rheumatoid arthritis
Cell-Mediated Autoimmune
Type 1 diabetes
Reactions
In this type of diabetes,the immune
systemattacksthe cells inthe pancreas
that make insulin.
Psoriasis
In psoriasis, overactive immune system
blood cells called T-cells collect in the skin.
The immune system activity stimulates
skin cells to reproduce rapidly, producing
silvery, scaly plaques on the skin.
psoriasis
HLA typing
Tissue typing
-Lymphocytes from the person being tested
are incubated with laboratory test stocks of
anti -HLA antibodies specific for a particular
HLA. If the antibodies react with the
antigens on a lymphocyte then complement
damages the lymphocyte and they can
enter the cell.
5 times
Rheumatic fever
4- 5 times
Endocrine Diseases
Addison's disease
4- 10 times
Graves' disease
10- 12 times
Malignant Disease
Hodgkin's disease
Rheumatic fever
Adissons disease
hodgkinss disease
Reactions to transplantation
Transplants recognized as non self are
rejected- attacked by T
cells that directly lyse the grafted cells.
types of transplants
bone marrow
lungs
heart
liver
cornea
Privileged tissue
An example is replacing a person's
damaged heart valve with a valve
from a pig's heart.
Stem Cells
Embryonic Stem Cells (ESCs)
These cells can be isolated from the very
earliest stage of an embryo, usually from
discarded embryos created for attempts at
in vitro fertilization.
ESCs are capable of generating many
different types of tissue cells and cell lines
such as muscle, nerve, or blood cells
Grafts
AUTOGRAFT
-when one's own tissue is grafted to
another part of the body.
ISOGRAFT
Identical twins have the same genetic
makeup; therefore, skin or organs
such as kidneys may be transplanted
between them without provoking an
immune response.
ALLOGRAFTS
Grafts between people who are not
identical twins.
XENOTRANSPLANTATION
Tissues or organs that have been
transplanted from animals.
Graft-Versus-Host(GVH) Disease
the transplanted bone marrow contains
immunocompetent cells that mount primarily
a cell-mediated immune response against the
tissue into which they have been transplanted
.
immunosupression
-to suppress cell-mediated immunity, the
most important factor in transplant
rejection.
Sirolimus(Rapamune)
-are among those that inhibit both cellmediated and humoral immunity.
Mycophenolate Mofetil
-inhibit the proliferation of T cells and
B cells.
Some biological agents such as the
chimeric monoclonal antibodies
basiliximab and daclizumab also block
IL-2 and are useful
immunosuppressives.
cancer
cancer
New growth of abnormal cells.
Benign tumor -self contained mass within
an organ that does not spread into
adjacent tissues.
Malignant tumor -uncontrolled growth of
abnormal cells within normal tissues.
Immunotherapy for
Cancer
Herceptin
consists of monoclonal antibodies against
a breast cancer growth factor.
Immunotoxins
are chemical poisons linked to a
monoclonal antibody ; the antibody
selectively locates the cancer cell for
release of the poison.
Immunotherapy for
cancer
Immunodeficiencies
The absence of a sufficient immune
which can be
either congenital or acquired.
Congenital Immunodeficiency
defects in, or the absence of a
number of inherited genes.
Severe combined
immunodeficiency
(SCID).This is an example of an
immune deficiency that is present
at birth. Children with SCID are
missing important white blood
cells.
Acquired
Immunodeficiency
a variety
of drugs, cancers, or
infectious agents
Selective IgA
immunodeficiency
B, T cells
Affects about 1 in 700, causing
frequent mucosal infections
specific cause uncertain
Mucosal Infections
Common variable
hypogammaglobulinemia
B, T cells (decreased
immunoglobulins)
Frequent viral and bacterial infections
second most common immune
deficiency, affecting about 1 in 70,000
inherited
hypogammaglobulinemia
Reticular dysgenesis
B, T. and stem cells (a combined
immunodeficiency: deficiencies in
Band T cells and neutrophils)
Usually fatal in early infancy:
inherited
Reticular dysgenesis
Severe combined
immunodeficiency
B. T. and stem cells(deficiency of
both Band T cells)
Affects about 1 in 100,000: allows
severe infections:
Inherited
Thymic aplasia
(DiGeorge syndrome)
T cells (defective thymus causes
deficiency of T cells)
Absence of cell-mediated immunity;
usually fatal in infancy
from Pneumocyslis pneumonia or viral
or fungal infections: due to failure of the
thymus to develop in embryo
DiGeorge syndrome
Wiskott-Aldrich syndrome
B, T cells (few platelets in blood,
abnormal T cel ls)
Frequent infections by viruses, fungi,
protozoa: eczema,
defective blood clotting; usually causes
death in childhood:
inherited on X chromosome
Wiskott-Aldrich
syndrome
HIV (Human
Immunodeficiency
Virus) Infection
HIV(human immunodeficiency
virus) is a virus that attacks the
immune system.
HIV infects and destroys certain
whitebloodcells called CD4+ cells.
AIDS(acquired
immunodeficiency
syndrome)
The last stage of HIV infection .
People with AIDS have a low number of
CD4+ cells and get infections or cancers
that rarely occur in healthy people. These
can be deadly.
aids
Risk factors
contact with infected blood, semen, or
vaginal fluids.
unprotectedsexwith someone who has HIV.
sharing drug needles with someone who is
infected with HIV.
duringpregnancy, birth, orbreast-feeding.
casual contact like kissing or sharing
drinking glasses with an infected person.
Diagnostic examination
A doctor may suspect HIV if symptoms last and
no other cause can be found.
If you have been exposed to HIV, your immune
system will make antibodies to try to destroy
the virus. Doctors use tests to find these
antibodies in urine,saliva or blood.
Viral load which shows the amount of virus in
your blood.
CD4+ cell count,which shows how well your
immune system is working.
treatment
prevention
HIV is often spread by people who don't know they
have it. So it's always important to protect yourself
and others by taking these steps:
Practice safersex.Use acondomevery time you
have sex (including oral sex) until you are sure that
you and your partner aren't infected with HIV or
other sexually transmitted infection (STI).
Don't have more than one sex partnerat a
time. The safest sex is with one partner who has
sex only with you.
Talk to your partnerbefore you have sex the first
time. Find out if he or she is at risk for HIV. Get
tested together. Getting tested again at 6, 12, and
24 weeks after the first test can be done to be sure
neither of you is infected. Use condoms in the
meantime.
Phase I
The number of viral RNA molecules per
milliliter of
blood plasma may reach more than 10
million in the first week. Billions of CD4 + T
cells may be infected within a couple of
weeks.
Phase 2
The numbers of CD4 + T cells decline steadily.
HIV replication continues but at a relatively low
level, probably controlled by CDS+ T cells
mainly in lymphatic tissue.
Other early HIV symptoms include slight fever,
headaches, fatigue, and muscle aches. These
symptoms may last for only a few weeks. Then
there are usually no HIV symptoms for many
years. That is why it can be hard to know if you
have HIV.
Phase 3
-Clinical AIDS emerges, usually within 10 years of
infection.
CD4 + T cell counts are below 350 cells/f.ll (200
cells/f.ll
defines AIDS).
Important AIDS indicator conditions appear,such as
C. albicaus infections of bronchi, trachea, or lungs;
cytomegalovirus eye infections; tuberculosis;
Puel/moeys/is
pneumonia; toxoplasmosis of the brain; and Kaposi's
sarcoma.