1. Prepared by: Mae Michelle F. Aguilar RN
Advance Pathophysiology
USI-Graduate School MAN-MS

2. HYPERSENSITIVITY DISORDERS
• The excessive or
inappropriate activation of
the immune system.
• Disorders caused by the
immune responses are
collectively referred to as
hypersensitivity reactions.

4. TYPE 1 IMMEDIATE
HYPERSENSITIVITY

5. • IgE mediated, occurs rapidly within minuites
of antigen challenge.
• Referred to as allergic reactions and the
antigens causing the response as allergens.

8. •CD4+ helper
T cells of the
TH2 type and
Mast Cells or
basophils.

9. • CD4+ T cell of TH2 cells differentiate in
response to allergens and helminthes
(intestinal parasites).
• Cytokines of TH2 stimulate differentiation of
B cells into IgE producing plasma cells, acts as
growth factor for mast cells and recruit and
activate eosinophils

10. • MAST CELLS are tissue cells while BASOPHILS
are blood cells.
• Distributed throughout connective tissue,
beneath the skin and mucous membranes of
the respiratory tract, GIT, GUT and adjacent to
blood and vessles.

12. • With subsequent exposure, the sensitizing
allergen binds to the cell associated IgE
• Degranulation of sensitized mast cells occur
(Release of their performed mediators)

13. Initial or Early Response
• 5 to 30 mins of exposure to antigen and
subsides within 60 mins.
• Mediators: Histamine, Acetylcholine,
enzymes such as trypsin and chymase that
lead to generation of kinins
• Vasodilation, vascular damage, smooth muscle
spasms

14. Secondary or Late Phase
• 2 to 8 hours later and lasts for several days.
• Results from lipid mediators and cytokines
involved in the inflammatory response.
• Mast cell membrane phospholipids which
broken down to form Archidonic Acid where
leukotrienes and prostaglandins are
synthesized.

15. • Similar effects with histamine and
acetylcholine though effects are delayed and
prolonged by comparison.
• Mast cells also produce cytokines and
chemotactic factors that attract eosinophils
and leukocytes to the site of allergen contact.

16. • Responses: Mucosal edema, Mucus secretion,
Leukocyte infiltration, Epithelial damage,
bronchospasm.

17. Clinical Effects:
• Systemic anaphylactic shock occurs with the
activation of mast cells in the vascular system.
• Local or atopic reactions occur if confined to a
particular site by virtue of exposure.

18. Source:
Robbins
PATHOLOGIC BASIS
OF DISEASE 6th ed

20. ALLERGIC DISORDERS

21. ANAPHYLAXIS
• Systemic, life-threatening hypersensitivity
reaction characterized by vasodilation.
• Fall in blood pressure, airway constriction,
vascular swelling, obstruction of upper airway
ANAPHYLACTIC SHOCK

24. • MILD SYSTEMIC
REACTIONS
– Peripheral tingling
– Sensation of warmth
– Fullness of mouth and
throat
– Nasal congestion
– Periorbital swelling
– Pruritus
– Sneezing
– Tearing of the eyes

25. • MODERATE SYSTEMIC REACTIONS
– Flushing
– Warmth
– Anxiety
– Itching in addition to above symptoms
– Dyspnea, coughing, wheezing, bronchospasm, edema of
airways.

26. • SEVERE SYSTEMIC
REACTIONS
– Bronchospasm
– Laryngeal edema
– Severe dyspnea
– Cyanosis
– Hypotension
– Dysphagia
– Abdominal Cramping
– Vomiting
– Diarrhea
– Seizure
– Cardiac arrest and coma

27. Common medications that cause
anaphylaxis
• Antibiotics (Penicillin and sulfa antibiotics)
• Allopurinol
• Radio contrast agents
• Anesthetic agents (lidocaine, procaine)
• Vaccines
• Hormones
• Aspirin
• NSAIDs

28. Prevention
• Avoidance of
potential allergens
• Screening for
allergies
• Wear medical alert
bracelets
• Desensitization
• Carry an Emergency
Kit (EpiPen)

29. Medical Management
• CPR
• Oxygen
• Epinephrine
• Intravenous infusion (NSS), volume expanders
and vassopressors
• Antihistamines and corticosteroids to treat
urticaria and angioedema
• Aminophylline and corticosteroids

30. NURSING MANAGEMENT
• Assess the airway, breathing pattern and other
vital signs.
• Emergency measures ( intubation,
administration of emergency medications,
insertion of intravenous lines, fluid
administration, oxygen administration)
• Health Teaching!

31. ALLERGIC RHINITIS
• Inflammation of the nasal mucosa.
• hay fever; chronic allergic rhinitis, pollinosis
• Most common form of respiratory allergy.
• Often occurs with other conditions such as allergic
conjunctivitis, sinusitis and asthma.

32. • Induced by airborne pollen or molds.
• Histamine is the major mediator of allergic
reactions in the nasal mucosa.
• Upon inhalation or ingestion of the antigen,
nasal mucosa reacts by slowing the ciliary
action, edema formation and leukocyte
(eosinophils) infiltration.

34. • Complications may result to allergic asthma,
chronic nasal obstruction, chronic otitis media
with hearing loss, anosomia (absence of the
sense of smell)

35. Assessment and Diagnostic Findings
• Nasal smears
• Peripheral blood counts
• Total serum IgE
• Epicutaneos and intradermal screening
• RAST
• Food elimination and challenge
• Nasal provocation test

37. Medical Management
AVOIDANCE THERAPY
PHARMACOLOGIC THERAPY
GOAL: RELIEF from symptoms!

38. PHARMACOLOGIC THERAPY
• Antihistamines
– H1 receptor antagonist (H1 blockers)
– H1 blockers selectively bind to H1 receptors
preventing actions of histamines at these sites
– Oral antihistamines – limited to certain patients
with hay fever, vasomotor rhinitis, urticaria (hives)
and mild asthma
–Major side effect : SEDATION

39. • Nervousness, tremors, dizziness, dry mouth,
palpitations, anorexia, nausea and vomiting.
• Contraindicated: Third trimester of pregnancy,
nursing mothers and newborns, in children
and elderly people and in patients with
conditions that can be aggravated by
muscarinic blockage.

40. • 2nd generation or non-sedating H1 receptor
antagonists
– Does not cross the blood brain barrier and do not
bind to the cholinergic, serotonin, or alpha-
adrenergic receptors.
– Binds to the peripheral nervous system H1
receptors causing less sedation.

41. • Sedating
– Ethanolamine : Diphenhydramine (Benadryl)
•MAJOR SIDE EFFECTS NURSING IMPLICATIONS:
•drowsiness, and confusion Teach patient to avoid alcohol,
driving or engaging in hazardous
activities
•dry mouth, nausea,
vomiting
Sucking on hard candy or ice
chips for relief of dry mouth,
•Photosensitivity Encourage use of sunscreen and
hat while outdoors
•urinary retention Assess for urinary retention,
monitor urinary output

42. • Non-Sedating
–Loratadine (Claritin)
–Cetirizine (Zyrtec)

43. • ADRENERGIC
AGENTS
– Vasoconstrictors of
mucosal vessels, are
used topically (nasal
and ophthalmic) in
addition to the oral
route.
– Drops or spray has
fewer side effects,
however used for a
few days to avoid
rebound congestion.
• Xylometazoline
hydrochloride

44. • MAST CELL STABILIZERS
– Intranasal cromolyn sodium (Nasalcrom)
– A spray that acts by stabilizing the mast cell
membrane thus reducing histamine and other
mediators of the allergic response.
– Used prophilactically before exposure to allergens.
– Benefits may take a week or so to occur.

45. • CORTICOSTEROIDS
– For more severe cases that cannot be controlled
by conventional medications.
– Dexamethasone, budesonide, fluticasone,
beclomethasone.
– Anti-inflammatory
– Suppress host defenses so they must be used with
caution for patients with tuberculosis, untreated
bacterial infections of the lungs.

46. • Side Effects: Fluid retention, weight gain,
hypertension, gastric irritation, glucose
intolerance, and adrenal suppression.

47. • IMMUNOTHERAPY
– Used to treat IgE mediated diseases by injections
of allergen extracts.
– Patient is at risk for general and potentially fatal,
anaphylaxis

48. NURSING INTERVENTIONS
• Improving Breathing Pattern
• Promoting understanding of allergy control
• Coping with a chronic disorder
• Monitor and manage potential complications.

49. ATOPIC DERMATITIS
• Family history is common.
• Highest incidence in infants and children

50. • Significant elevations of
serum IgE and peripheral
eosinophilia.
• Pruritus and
hyperirritability of the skin.
• Large amounts of
histamine in the skin.
• Chronic condition with
remissions and
exacerbations.
• Tendency to recur with
remission from
adolescence to age 20

51. DERMATITIS MEDICAMENTOSA
(DRUG REACTIONS)
• Skin rashes induced by
the internal
administration of
certain medications.
• Common causes are
cephalosporins,
including ampicillin,
semi synthetic
penicillins, and
barbiturates.

52. FOOD ALLERGIES
• Primary target of food
allergy may be the skin,
the gastrointestinal
tract or the respiratory
system.
• Occur at any age but
manifests during
childhood.

53. LATEX ALLERGY
• Allergic reaction to
natural rubber proteins.

54. TYPE II ANTIBODY- MEDIATED
HYPERSENSITIVITY

55. • Type II (Cytotoxic) hypersensitivity are
mediated by IgG and IgM antibodies directed
against target antigens on the surface of cells
or other tissue components.
• Complement-mediated or antibody-mediated
cytotoxicity
• Antigens are endogenous or exogenous

56. Source: Robbins PATHOLOGIC
BASIS OF DISEASE 6th ed.

57. 1.Transfusion reactions
2.Erythroblastosis fetalis
3.Autoimmune hemolytic anemia,
agranulocytosis, thrombocytopenia – (+)
antibodies vs own blood cells
4.Pemphigus vulgaris – Ab’s vs. desmosomes
5.Drug reactions

58. BLOOD TRANSFUSION REACTION
• Cells from an
incompatible donor
react with
autochthonous
antibody of the host.

60. Nursing Interventions when complications
occurs in Blood transfusion
• If blood transfusion reaction occurs. STOP THE TRANSFUSION.
• Start IV line (0.9% NaCl)
• Place the client in fowler’s position if with SOB and administer O2
therapy.
• The nurse remains with the client, observing signs and symptoms and
monitoring vital signs as often as every 5 minutes.
• Notify the physician immediately.
• The nurse prepares to administer emergency drugs such as
antihistamines, vasopressor, fluids, and steroids as per physician’s
order or protocol.
• Obtain a urine specimen and send to the laboratory to determine
presence of hemoglobin as a result of RBC hemolysis.
• Blood container, tubing, attached label, and transfusion record are
saved and returned to the laboratory for analysis.

61. ERYTHROBLASTOSIS FETALIS
• Antigenic difference between mother and
fetus and antibodies from the mother cross
the placenta and cause destruction of fetal
blood cells.

64. Antibody-Dependent Cell-Mediated
Cytotoxicity (ADCC)
• due to NK activity  non-sensitized cells with Fc
receptors
• Ab + Ag  activation of NK cells  bind to Fc
fragment of IgG  cell lysis without
phagocytosis
• Destruction of targets too large to be
phagocytosed (parasites, tumor cells) + graft
rejection

65. Antibody-Dependent Cell-Mediated
Cytotoxicity (ADCC)
Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.

66. Antibody-Mediated Cellular
Dysfunction
1.Myasthenia gravis – acetylcholine receptors
2.Goodpasture’s syndrome – type IV collagen
3.Pernicious anemia – intrinsic factor
4.Acute rheumatic fever – antibodies vs.
Streptococcal antigens cross-react with heart

67. • Antibodies directed against cell surface
receptors  impair or deregulate function
Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.

68. MYASTHENIA GRAVIS
• a type of autoimmune
disorder, a
neuromuscular disease
that usually results to
muscle weakness and
fatigue primarily in the
face. This makes the
muscles get tired and
weakened more easily
than what is normal.

70. TYPE III
(IMMUNE COMPLEX MEDIATED)
HYPERSENSITIVITY

71. Immune Complex Mediated
• Formation of immune complexes in
circulation  deposit in various tissues 
trigger classical pathway of complement
activation
• Produce damage as they localize within
blood vessel walls or when trapped in
filtering structures (e.g. renal glomeruli)

72. Source: Robbins
PATHOLOGIC BASIS
OF DISEASE 6th ed.

73. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.

74. Source: Robbins PATHOLOGIC BASIS OF DISEASE 6th ed.

75. ANTIGEN CLINICAL MANIFESTATION
EXOGENOUS
Infectious agents:
Bacteria: Y. enterocolitica
Streptococci
T. pallidum
Viruses: Hep. B, CMV
Parasites: Plasmodium
Schistosoma
Fungi: Actinomycetes
Arthritis
GN, Infective endocarditis
Glomerulonephritis
Polyarteritis nodosa
Glomerulonephritis
Farmer’s lung
ENDOGENOUS
Nuclear antigens
Immunoglobulins
Tumor antigens
SLE
Rheumatoid arthritis
Glomerulonephritis
Antigens Associated with Immune
Complex Disorders

76. SERUM SICKNESS
• Patient forms antibodies to xenogeneic Ig
administered during passive immune therapy
regimens
ARTHUS REACTION
• Seen when boosters are administered to individuals
who already possess high antibody titers to vaccine
molecules
• Localized area to tissue necrosis  edema,
hemorrhage, ulceration
• Develop over a few hours

78. TYPE IV (CELL-MEDIATED)
HYPERSENSITIVITY

79. • Initiated by sensitized T lymphocytes
• Principal pattern of immunologic
response to intracellular microbiologic
agents (particularly Mycobacterium
tuberculosis) as well as
viruses, fungi, protozoa
& parasites

80. Delayed-type hypersensitivity
• Mediated by CD4 T cells
• 1st exposure to Ag  CD4 T cells + class
II MHC  differentiation of naïve CD4 T
cells to TH1 cells  release of IL-12, IFN-
, IL-2, TNF & lymphotoxin
• Tuberculin skin test, contact dermatitis,
granulomatous inflammation

81. Tuberculin Test

82. CONTACT DERMATITIS
• (Dermatitis venenata) Acute or Chronic skin
inflammation that results from direct skin
contact with other chemicals or allergens

83. P
o
i
s
o
n
I
v
y

84. Treatment
• Avoidance of offending material
• Burrow’s solution or cool water compress
• Systemic Corticosteroids (Prednisone)
• Topical Corticosteroids
• Oral antihistamines
• Hydrophilic cream or petrolatum
• Antibiotics for infection

85. T Cell-Mediated Cytotoxicity
• Mediated by CD8+ T cells
• Sensitized CD8+ T cells kill antigen-
bearing target cells
• Graft rejection, virus infections,
tumor immunity

86. • Two mechanisms:
a)Perforin-granzyme-dependent
killing  cause perforation of
plasma membrane
b)Fas-FasL-dependent killing 
activation of apoptosis

87. TRANSPLANT REJECTION
• One of the goals of present day
immunologic research is successful
transplantation of tissues in humans
without immunologic rejection.

90. Mechanisms in Graft Rejection
• Antigens responsible for
rejection in humans are
those of the Major
Histocompatibility
antigen (HLA) system
• T cell-Mediated
Reactions and
Antibody-mediated
reactions

91. T cell mediated Reactions
• Activation of the CD8 CTLsand delayed
hypersensitivity reactions triggered by
activated CD4 helper cells seem to be
involved.

92. Increasing Graft Survival
• Immunosuppressive Therapy
– Azathiprine, steroids, cyclosporine,
antilymphocyte globulins, monoclonal anti-T cell
antibodies
– Cyclosporine suppresses T cells mediated
immunity by inhibiting activation of cytokine
genes, in particular, the gene for IL 2.

93. AUTOIMMUNE DISEASES

94. • Caused by the breakdown in the ability of the
immune system to differentiate between self
and non self.

95. • The ability of the immune system to differentiate self
from non-self is called SELF TOLERANCE.
• Maintained through central and peripheral mechanisms
that delete auto reactive B or T cells or suppress or
inactivate immune responses that would be destructive
to host tissues.

96. • Defects on these mechanisms could impair
self-tolerance and predispose one to
autoimmune disorders.

97. Mechanisms of Autoimmune Disease
• Genetic Susceptibility
– Increase incidence and severity of autoimmune
diseases is shown in familial clustering of several
autoimmune diseases and the observation that a
certain inherited HLA genotypes occur
more frequently with a variety of autoimmune
disorders.

98. – 90% of people with Ankylosing Spondylitis carry
the HLA-B27 antigen
– Rheumatoid Arthritis (HLA-DR4)
– SLE (HLA-DR3)

99. • Environmental Factors
– Breakdown of T cell Anergy
– Release of Sequestered Antigens
– Molecular Mimicry
– Superantigens

100. RHEUMATOID ARTHRITIS
• The
autoimmune
reaction
primarily occurs
in the synovial
tissue.

101. Presentation of
antigen to T cells
T and B cell proliferation.
Angiogenesis in synovial
lining
Neutrophil accumulation
in synovial fluid. Cell
proliferation. No cartilage
invasion.
Synovitis.
Early pannus invasion.
Chondrocyte activation.
Degredation of cartilage by
proteinase
Subchondral bone erosion
Pannus invation of cartilage.
Chondrocyte proliferation.
Laxity of ligaments
Swelling of small joints,
pain, stiffness, fatigue
Warm, swollen,
effusions, pain, poss.
Rheumatoid nodules,
decreased motion
Increase in severity of
signs and symptoms Joint instability,
contractures, decreased
ROM, systemic
complications

103. Treatment
• Medications that treat pain and inflammation.
– Aspirin
– NSAIDs
– Corticosteroids
– DMARDs (disease modifying anti rheumatic drugs)

104. LUPUS
• condition characterized by chronic inflammation
of body tissues caused by autoimmune disease
• abnormal antibodies produced in blood  target
tissues within own body rather than foreign
infectious agents
• antibodies & accompanying cells of inflammation
can involve tissues anywhere in the body  has
potential to affect a variety of areas of the body

105. • can cause disease of the skin, heart, lungs,
kidneys, joints, and/or nervous system
• only the skin involved  discoid lupus
• internal organs involved  SLE

108. • shape  referred to as the "butterfly rash" of SLE
• painless, does not itch
• worsened by exposure to sunlight (photosensitivity)

110. • no permanent cure for SLE
• goal of treatment - to relieve symptoms & protect
organs by decreasing inflammation and/or the
level of autoimmune activity in the body
• mild symptoms - need no treatment or only
intermittent courses of antiinflammatory
medications
• serious illness (damage to internal organ) -
require high doses of corticosteroids with other
medications that suppress the body's immune
system

111. • NSAIDs
• Topical corticosteroid creams
• Anti-Malarials to treat joint pain, skin rashes,
mouth ulcers, fatigue and fever
• Systemic corticosteroids
• Cytotoxic therapy to treat diffuse proliferative
Glomerulonephritis
• Immunosuppressive
• Methotrexate (anti inflammatory and
immunosuppressive.)

112. IMMUNODEFICIENCY
DISORDERS

113. BITS OF HISTORY
HIV came from a similar virus found in chimpanzees - SIV.
HIV probably entered the United States around 1970
CDC in 1981 noticed unusual clusters of Kaposi’s sarcoma in
gay men in NY and San Francisco, which led to the disease
to be called GRID (Gay Related Immune Deficiency).
By 1982 the disease was apparent in heterosexuals and was
renamed AIDS (Acquired Immune Deficiency).
1984- Scientists(Dr. Luc Montagnier, Dr. Robert Gallo)
identify HIV (initially called LAV or HTLV-III) as the cause of
AIDS
1987- AZT is the first drug approved for treating AIDS

114. AIDS HIV STATISTICS
• DOH Current report

115. Who is at risk?
The following are behaviors that increase chances of getting HIV:
• Injecting drugs or steroids or shared equipment (such as needles, syringes,
works) with others
• Unprotected vaginal, anal, or oral sex, multiple partners, or anonymous
partners
• Diagnosed with or treated for hepatitis, tuberculosis (TB), or a sexually
transmitted disease (STD)
• Had unprotected sex with someone who could answer yes to any of the
criteria as listed above.

116. HIV LIFE CYCLE
• Binding- HIV searches for cells that have CD4 surface receptors. Main
target is the T4-lymphocyte. The T4-cell is responsible for warning your
immune system that there are invaders in the system.
• Reverse Transcription- Makes a DNA copy of the virus’s RNA. Can be
blocked by Nucleoside Reverse Transcriptase Inhibitors (NRTIs) and Non-
Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
• Integration-The HIV DNA is then carried to the cell’s nucleus. When the cell
makes new proteins, it accidentally makes new HIVs. Integration can be
blocked by integrase inhibitors, a new class of drugs that are in the earliest
stage of research.

117. • Transcription-Once HIV’s genetic material is inside the cell’s nucleus, it
directs the cell to produce new HIV. The strands of viral DNA nucleus
separate and special enzymes create messenger RNA (mRNA). This can
be blocked by antisense antiviral or transcription inhibitors (Tis) new classes
of drugs that are in the earliest of research.
• Translation-The mRNA carries instructions for making new viral proteins
from the nucleus.
• Viral Assembly and Maturation-The virus becomes an infection and each
infected cell can produce lots of new viruses. Viral assembly can be blocked
by Protease Inhibitors (PIs).

118. • Helper T-Cells (also called T4 or CD4)- help other cells destroy infective
organisms.
• Suppressor T-Cells (also called T8 or CD8)-suppress the activity of other
lymphocytes so they don’t destroy normal tissue.
• Killer T-Cells (also called cytotoxic T lymphocytes, or CTLs, and are
another kind of T8 or CD8 cell)- recognize and destroy abnormal or infected
cells.
CD4/T-CELLS

119. How long after exposure?
• It can take some time for the immune system to produce enough antibodies for
the antibody test to detect, and this time period can vary from person to person.
This time period is commonly referred to as the “window period.”
• Most people will develop detectable antibodies within 2 to 8 weeks (the average is
25 days). Even so, there is a chance that some individuals will take longer to
develop detectable antibodies.
• Therefore, if the initial negative HIV test was conducted within the first 3 months
after possible exposure, repeat testing should be considered >3 months after the
exposure occurred to account for the possibility of a false-negative result. Ninety-
seven percent of persons will develop antibodies in the first 3 months following the
time of their infection. In very rare cases, it can take up to 6 months to develop
antibodies to HIV.

120. TESTING FOR THE VIRUS
• EIA (enzyme immunoassay) used on blood drawn from a vein, is the most
common screening test used to look for antibodies to HIV. A positive (reactive)
EIA must be used with a follow-up (confirmatory) test such as the Western blot
to make a positive diagnosis. There are EIA tests that use other body fluids to
look for antibodies to HIV. These include:
Oral Fluid Tests – use oral fluid (not saliva) that is collected from the
mouth using a special collection device. This is an EIA antibody
test similar to the standard blood EIA test. A follow-up confirmatory
Western Blot uses the same oral fluid sample.
Urine Tests – use urine instead of blood. The sensitivity and
specificity (accuracy) are somewhat less than that of the blood and oral
fluid tests. This is also an EIA antibody test similar to blood EIA tests
and requires a follow-up confirmatory Western Blot using the same
urine sample.

121. • Rapid Tests:
A rapid test is a screening test that produces very quick results, in approximately 20
minutes. Rapid tests use blood from a vein or from a finger stick, or oral fluid to look for the
presence of antibodies to HIV. As is true for all screening tests, a reactive rapid HIV test
result must be confirmed with a follow-up confirmatory test before a final diagnosis of
infection can be made.
• Home Testing Kits
The testing procedure involves pricking a finger with a special device, placing drops of
blood on a specially treated card, and then mailing the card in to be tested at a licensed
laboratory. Customers are given an identification number to use when phoning in for the
results. All individuals receiving a positive test result are provided referrals for a follow-up
confirmatory test, as well as information and resources on treatment and support services.
• RNA Tests
RNA tests look for genetic material of the virus and can be used in screening the blood
supply and for detection of very early infection rare cases when antibody tests are unable
to detect antibodies to HIV.

122. Modes of
transmission
Sexual
contact
Homosexuals
(MSM), &
Heterosexuals
Parenteral
transmission
IVDA,
Hemophiliacs
, accidental
needle sticks
Vertical
transmission
From mother to
child during
delivery
(MTCT)

124. • HIV stands for human immunodeficiency virus. This is
the virus that causes AIDS. HIV is different from most
other viruses because it attacks the immune system. The
immune system gives our bodies the ability to fight
infections. HIV finds and destroys a type of white blood
cell (T cells or CD4 cells) that the immune system must
have to fight disease.

126. Symptoms of HIV
HIV can cause any symptoms of illness, since infections can occur
throughout the body. Special symptoms relating to HIV infection include:
• Diarrhea
• Fatigue
• Fever
• Frequent vaginal yeast infections
• Headache
• Mouth sores, including candidal infection
• Muscular stiffness or aching
• Rash of various types, including seborrheic dermatitis
• Sore throat
• Swollen lymph glands

127. AIDS
• AIDS stands for acquired immunodeficiency syndrome.
AIDS is the final stage of HIV infection. It can take years
for a person infected with HIV, even without treatment, to
reach this stage. Having AIDS means that the virus has
weakened the immune system to the point at which the
body has a difficult time fighting infections. When
someone has one or more of these infections and a low
number of T cells, he or she has AIDS.

128. Symptoms of AIDS
• The following is a list of AIDS-related infections and
cancers that people with AIDS acquire as their CD4
count decreases. Previously, having AIDS was defined
as having HIV infection and getting one of these
additional diseases. Now it is additionally defined as a
CD4 count below 200, even without an opportunistic
infection. Many other illnesses and corresponding
symptoms may develop in addition to those listed here.

130. Absolute CD4 Count
• Normal Values- in a healthy adult, a normal CD4 count can vary a great
deal but is typically 600-1200 cells per cubic millimeter of blood
• Between 600 and 350 – in an HIV+ person, this range is considered “very
good”. HIV medications are typically not indicated.
• Between 350-200-the immune system is weakened and therefore the HIV+
person may be at increased risk for infection and illness. May start taking
HIV medications.
• Less than 200 – The immune system is severely weakened and the HIV+
person is at much greater risk of opportunistic infections. HIV medications
and prophylactic antibiotics will be prescribed to help prevent illnesses and
infections. The patient be classified as having AIDS.

131. CD4 count below 200 cells/ml
• Pneumocystis carinii pneumonia, "PCP pneumonia," now called
Pneumocystic jiroveci pneumonia
• Candida esophagitis -- painful yeast infection of the esophagus
• Bacillary angiomatosis -- Skin lesions caused by a bacteria called
Bartonella, which is usually acquired from cat scratches

132. CD4 count below 100 cells/ml
• Cryptococcal meningitis -- infection of the lining of the brain by a yeast
• AIDS dementia -- worsening and slowing of mental function, caused by HIV
itself
• Toxoplasmosis encephalitis -- infection of the brain by a parasite, which is
frequently found in cat feces; causes discrete lesions in the brain
• Progressive multifocal leukoencephalopathy -- a viral disease of the brain
caused by a virus (called the JC virus) that results in a severe decline in
cognitive and motor functions
• Wasting syndrome -- extreme weight loss and loss of appetite, caused by
HIV
• Cryptosporidium diarrhea -- Extreme diarrhea caused by one of several
related parasites

140. Asymptomatic HIV
• Asymptomatic HIV infection is a phase of chronic infection with human
immunodeficiency virus (HIV) during which there are no symptoms of HIV infection.
• The length of this phase varies from person to person. It depends on how quickly
the HIV virus is copying itself and the genetic differences that affect the way the
immune system handles the virus.
• Some people can go 10 years or longer without symptoms, while others may have
symptoms and worsening immune function within a few years after the original
infection.
• People with asymptomatic infection can progress to symptomatic HIV infection and
develop opportunistic infections associated with HIV. In addition, pregnant women
with asymptomatic HIV infection can still transmit HIV to their fetus.
• People who are asymptomatic but who have CD4 lymphocyte counts of less than
200 should be on therapy.

141. HIV-Type 2
• Persons infected with HIV-2, immunodeficiency seems to develop more slowly
and to be milder. Compared with persons infected with HIV-1, those with HIV-2
are less infectious early in the course of infection.
• Both HIV-1 and HIV-2 have the same modes of transmission and are associated
with similar opportunistic infections and AIDS.
• As the disease advances, HIV-2 infectiousness seems to increase; however,
compared with HIV-1, the duration of this increased infectiousness is shorter.
HIV-1 and HIV-2 also differ in geographic patterns of infection; the United States
has few reported cases.
• HIV-2 is highly concentrated in West Africa countries such as Senegal, Nigeria,
Ghana, and the Ivory Coast. HIV-2 also spreads to other parts of the world but
predominantly to those countries having strong ties to West Africa.