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Immunodeficiencies HIV/AIDS. Immunodeficiencies. Due to impaired function of one or more components of the immune or inflammatory responses. Problem may be with: B cells T cells phagocytes or complement. Immunodeficiencies may be: Congenital (primary) Caused by a genetic abnormality

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  • Due to impaired function of one or more components of the immune or inflammatory responses.

  • Problem may be with:

    • B cells

    • T cells

    • phagocytes

    • or complement

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  • Immunodeficiencies may be:

  • Congenital (primary)

    • Caused by a genetic abnormality

  • Acquired (secondary) – more common

    • Normal physiologic changes – aging

    • Severe malnutrition or selective deficiency

    • Caused by another illness: Diabetes Cancer Viral infection

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Main cause is disruption of lymphocyte function

Stem cell defect :

Prevent normal lymphocyte development and total failure of immune system

Lymphoid organ dysfunction:

prevents maturation of B or T cells

or final maturation of B cells = lack of specific class of immunoglobulins

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Hallmark: Tendency to develop unusual or recurrent, severe infections.

Deficiencies in T cells suggested by recurrent infections with viruses, fungi and yeast.

Deficiencies in B cells suggested by recurrent infections with certain bacteria or viruses affected by humoral immunity

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Routine treatment infections.

  • No live vaccines

  • Be aware breaks in skin for routine blood tests can cause septicemia

  • At risk for Graft-versus-Host disease

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Acquired Immunodeficiencies infections.

Nutritional deficiencies

Iatrogenic drugs immunosuppressive therapy chemotherapy and radiation

Trauma – esp. burns


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HIV/AIDS infections.

  • Human immunodeficiency virus

  • Acquired immunodeficiency syndrome

  • Two forms : HIV1 and HIV-2

  • High mortality rate

  • Asymptomatic carriers

  • Logarithmic increase in number of patients

  • Medical community cannot control spread

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Transmission infections.

  • Sexual transmission

  • Contaminated needles – sharing

  • Blood products

  • Transplacental or nursing

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History infections.

  • Probably arose in central Africa before 1931

  • Believed to be a monkey virus mutated to affect humans

  • Found Ab’s against HIV in serum samples taken in 1960’s

  • First cases reported 1980’s in male homosexuals

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High Risk Individuals U.S.

  • Homosexual/bisexual men

  • I.V. drug abusers

  • Recipients of blood products

  • Female partners of bisexual men/ I.V. drug abusers

  • Children of infected mothers

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Pathogenesis U.S.

  • Retrovirus – RNA plus reverse transcriptase, integrase and protease

  • Attachment: Binds to CD4 receptors (TH) and chemokine receptors gp 120 or gp 41

  • Internalization – RNA enters the cell

  • Reverse transcriptase converts RNA →DNA

  • Integrase inserts viral DNA into Host DNA

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  • Viral DNA is transcribed into mRNA U.S.

  • mRNA is translated into protein – polyprotein

  • Cleavage of polyprotein into usable proteins

  • Viruses are assembled

  • Host cell is killed as viruses are released

  • BUT helper T cells are replaced and viruses are killed, but CD4 cells decrease over time.

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Helper T cells U.S.

  • Coordinate the response of both B and T cells

  • Patients susceptible to infections and malignancies

  • Normally 600 - 1200 /mm3

  • Category1: > 500 cells/ μL

  • Category 2: 200- 499 cells/ μL

  • Category 3: < 200 cells/ μL (AIDS)

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Clinical Manifestations U.S.

  • Category A: no symptoms or persistent generalized lymphadenopathy or symptoms of primary HIV infection

  • Category B: symptoms of immune deficiency not serious enough to be called AIDS

  • Category C: person has AIDS defining illness (chart 15-2)

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Clinical manifestations U.S.

  • Infection - serologically negative

  • In seven days followed by acute phase in 30-70 % of people lasts a few days - 2 weeks resembles influenza or mononucleosis sore throat, muscle aches, fever, swollen glands, rash, headache or meningitis

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  • Seroconversion U.S. occurs 3 – 17 weeks after infection – HIV proteins can be detected in the blood

  • Seropositive patients have anti-HIV Ab’s circulating

  • Following infection through blood products, in general see anti-HIV Ab’s in 4-7 weeks

  • Following infection through sexual exposure, it may take 6-14 months for detection of anti-HIV Ab’s (one case - years)

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  • Window period = time between infection, Ab detection: U.S.An infected person can infect others within 2 weeks of initial HIV exposure, at a time well before anti-HIV Ab’s can be detected.

    • Average time from initial infection to AIDS is about 10 years, though this rate of development is lengthening with new treatments available.

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  • Chronic phase U.S.– can last for years

    • Asymptomatic

    • Viral load decreases

    • Chronic lymphadenopathy

    • orofacial herpes zoster, oral candidiasis

    • B cells make antibodies, but are ineffective

    • Gradual drop in T4 cells – no symptoms until below 200/mm3

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  • Crisis phase U.S.– ARC – AIDS-related complex

    • CD4 count < 200 cells/ μL

    • Long lasting fever < 3 months

    • Malaise

    • Diarrhea

    • Weight loss and wasting syndrome

    • Multiple opportunistic infections

    • Persistent viral or fungal infections of the skin

    • Without therapy death in 2-3 years

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AIDS Related Diseases U.S.

  • AIDS: To be positive for AIDS requires positive lab test and clinical symptoms -Unusual infections or neoplasms

  • Kaposi’s sarcoma

  • Non-Hodgkins lymphoma

  • Wasting syndrome

  • AIDS dementia complex

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AIDS Related Diseases U.S.

  • Fungal:

    • Candidiasis

    • Cryptococcus

  • Viral:

    • Herpes simplex

    • Herpes zoster

    • Cytomegalovirus

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Opportunistic infections U.S.

Pneumocystis carinii pneumonia

Toxoplasmosis gondii

Mycobacterium avium intracellulare

Mycobacterium tuberculosis

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Treatment U.S.

  • Expensive: $1,200 -1,500 / month if healthy

  • Cocktail of 3 different meds

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Treatment U.S.

  • Restore immune function

    • Hasn’t been easy or successful:

      • Bone marrow transplant, immunomodulators, transfusions

  • Prevent viral replication

    • Reverse transcriptase inhibitors (AZT)

    • Protease inhibitors

    • Integrase inhibitiors

    • Maturation inhibitors

    • Fusion inhibitors - newest

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Difficulties with Vaccines U.S.

  • HIV is antigenically variable

  • Antibodies are not protective

  • Can be transmitted by cell to cell contact

  • Animal models are protected species

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Other problems U.S.

  • Viral DNA incorporated into host cell DNA

  • Virus mutates as the virus replicates