immunodeficiencies hiv aids
Download
Skip this Video
Download Presentation
Immunodeficiencies HIV/AIDS

Loading in 2 Seconds...

play fullscreen
1 / 34

Immunodeficiencies HIV - PowerPoint PPT Presentation


  • 166 Views
  • Uploaded on

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

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Immunodeficiencies HIV' - taya


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
immunodeficiencies
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
slide3

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
slide4

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

slide5

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

routine treatment
Routine treatment
  • No live vaccines
  • Be aware breaks in skin for routine blood tests can cause septicemia
  • At risk for Graft-versus-Host disease
slide7

Acquired Immunodeficiencies

Nutritional deficiencies

Iatrogenic drugs immunosuppressive therapy chemotherapy and radiation

Trauma – esp. burns

Stress

hiv aids
HIV/AIDS
  • 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
transmission
Transmission
  • Sexual transmission
  • Contaminated needles – sharing
  • Blood products
  • Transplacental or nursing
history
History
  • 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
slide11
In 1995, the number 1 cause of death for ages 25 – 44 in U.S.
  • Heterosexual transmission is increasing in the U.S. and is the most common route of transmission outside of the U.S.
  • Greater than 50% of cases are women
high risk individuals
High Risk Individuals
  • Homosexual/bisexual men
  • I.V. drug abusers
  • Recipients of blood products
  • Female partners of bisexual men/ I.V. drug abusers
  • Children of infected mothers
slide13
Health care workers are at risk
    • Nurses
    • Clinical lab techs
  • Most HIV + workers infected off duty
  • TAKE PRECAUTIONS !!!
pathogenesis
Pathogenesis
  • 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
slide15

Viral DNA is transcribed into mRNA

  • 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.
helper t cells
Helper T cells
  • 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)
clinical manifestations
Clinical Manifestations
  • 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)
clinical manifestations20
Clinical manifestations
  • 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
slide21

Seroconversion 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)
slide22

Window period = time between infection, Ab detection: 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.
slide23
Chronic phase – 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
slide24
Crisis phase – 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
aids related diseases
AIDS Related Diseases
  • 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
aids related diseases27
AIDS Related Diseases
  • Fungal:
    • Candidiasis
    • Cryptococcus
  • Viral:
    • Herpes simplex
    • Herpes zoster
    • Cytomegalovirus
opportunistic infections
Opportunistic infections

Pneumocystis carinii pneumonia

Toxoplasmosis gondii

Mycobacterium avium intracellulare

Mycobacterium tuberculosis

treatment
Treatment
  • Expensive: $1,200 -1,500 / month if healthy
  • Cocktail of 3 different meds
treatment30
Treatment
  • 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
difficulties with vaccines
Difficulties with Vaccines
  • HIV is antigenically variable
  • Antibodies are not protective
  • Can be transmitted by cell to cell contact
  • Animal models are protected species
other problems
Other problems
  • Viral DNA incorporated into host cell DNA
  • Virus mutates as the virus replicates
ad