Type I hypersensitivity, also known as immediate hypersensitivity, is an exaggerated immune response mediated by IgE antibodies. It causes allergic reactions and is triggered by exposure to common allergens like pollen, dust mites, animal dander, etc. Type IV hypersensitivity is a delayed cell-mediated response that occurs 48-72 hours after exposure and is characterized by induration and erythema, as seen in tuberculin skin tests. HIV attacks CD4 T cells, weakening the immune system and leaving the body vulnerable to opportunistic infections. If untreated, HIV develops into AIDS, defined by a CD4 count below 200 or the presence of AIDS-defining illnesses.
T cells are one of the important white blood cells of the immune system and play a central role in the adaptive immune response and are distinguished from other lymphocytes by the presence of a T-cell receptor (TCR) on their cell surface.
B cells, also known as B lymphocytes, are a type of white blood cell of the lymphocyte subtype. They function in the humoral immunity component of the adaptive immune system.. B cells produce antibody molecules.
In mammals, B cells mature in the bone marrow, which is at the core of most bones. In birds, B cells mature in the bursa of Fabricus.
B cells present antigens (they are also classified as professional antigen-presenting cells (APCs)) and secrete cytokines.
T cells are one of the important white blood cells of the immune system and play a central role in the adaptive immune response and are distinguished from other lymphocytes by the presence of a T-cell receptor (TCR) on their cell surface.
B cells, also known as B lymphocytes, are a type of white blood cell of the lymphocyte subtype. They function in the humoral immunity component of the adaptive immune system.. B cells produce antibody molecules.
In mammals, B cells mature in the bone marrow, which is at the core of most bones. In birds, B cells mature in the bursa of Fabricus.
B cells present antigens (they are also classified as professional antigen-presenting cells (APCs)) and secrete cytokines.
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
this slide can help you to know full details about the major type of antigen based on its activity on B or T cell. This slide consists of images to clarify your doubts
Hypersensitivity (also called hypersensitivity reaction or intolerance) refers to undesirable reactions produced by the normal immune system, including allergies and autoimmunity.
this slide can help you to know full details about the major type of antigen based on its activity on B or T cell. This slide consists of images to clarify your doubts
Introduction
Hypersensitivity is increased reactivity or increased sensitivity by the animal body to an antigen to
which it has been previously exposed.
The term is often used as a synonym for allergy, which describes a state of altered reactivity to an
antigen.
Hypersensitivity has been divided into categories based upon whether it can be passively transferred
by antibodies or by specifically immune lymphoid cells.
The most widely adopted current classification is that of Coombs and Gell that designates
immunoglobulin-mediated (immediate) hypersensitivity reactions as types I, II, and III, and
lymphoid cell-mediated (delayed-type) hypersensitivity/cell-mediated immunity as a type IV
reaction.
“Hypersensitivity” generally represents the “dark side,” signifying the undesirable aspects of an
immune reaction, whereas the term “immunity” implies a desirable effect.
A hypersensitive response (HR) is an anti-pathogen response in plants produced by avr-R system
activation that leads to alterations in Ca+ flux, MAPK activation, and NO and ROI formation.
There is rapid necrosis of plant cells in contact with the pathogen.
This process prevents spread of the pathogen and releases hydrolytic enzymes that facilitate injury to
the pathogen’s structural integrity.
Causes of Hypersensitivity
Immune responses that are the cause of hypersensitivity diseases may be specific for antigens from different
sources:
Autoimmunity: reactions against self antigens.
Reactions against microbes.
Reactions against non-microbial environmental antigens.
Mechanism of Hypersensitivity
Hypersensitivity diseases are commonly classified according to the type of immune response and the
effector mechanism responsible for cell and tissue injury. These mechanisms include some that are
predominantly dependent on antibodies and others predominantly dependent on T cells, although a role for
both humoral and cell-mediated immunity is often found in many hypersensitivity diseases.
Normally, immune responses eradicate infectious pathogens without serious injury to host tissues.
However, these responses are sometimes
inadequately controlled
inappropriately targeted to host tissues
triggered by commensal microorganisms or environmental antigens that are usually harmless.
In these situations, the normally beneficial immune response is the cause of disease.
Disorders caused by immune responses are called hypersensitivity diseases.
This term , hypersensitivity , arose from the clinical definition of immunity as sensitivity, which is based on the observation that an individual who has been exposed to an antigen exhibits a detectable reaction, or is sensitive, to subsequent encounters with that antigen.
Today, we will describe the pathogenesis of different types of hypersensitivity reactions, with an emphasis on the effector mechanisms that cause tissue injury.
A variety of human diseases are caused by immune responses to non-microbial environmental antigens, and involve the type 2 cytokines interleukin-4 (IL-4), IL-5, and IL-13 produced by Th2 cells and innate lymphoid cells (ILCs), immunoglobulin E (IgE), mast cells, and eosinophils.
The antigens that elicit immediate hypersensitivity are called allergens. Most of them are common environmental proteins, animal products, and chemicals that can modify self proteins.
In the effector phase of these responses, mast cells and eosinophils are activated to rapidly release mediators that cause
increased vascular permeability
Vasodilation
bronchial and visceral smooth muscle contraction
This vascular reaction is called immediate hypersensitivity because it begins rapidly, within minutes of antigen challenge in a previously sensitized individual (immediate), and has major pathologic consequences (hypersensitivity).
Following the immediate response, there is a more slowly developing inflammatory component called the late-phase reaction characterized by the accumulation of neutrophils, eosinophils, and macrophages.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
2. Hypersensitivity and Allergy
Hypersensitivity-An exaggerated
immune response that may cause
damage to the host. The trigger is often
an innocuous antigen
Allergy-A hypersensitive response to
an environmental antigen. Often
presents as “hay fever”, asthma,
dermatitis or anaphylaxis.
3. Four types of Hypersensitivity
Immediate-Type Hypersensitivity:
Type I (Anaphylactic/ Allergic Reactions)
IgE-mediated
e.g.most common allergies
Type II (Cytotoxic Reactions)
IgG-mediated
e.g.ABO transfusion reaction
4. Four types of Hypersensitivity
Type III (Immune Complex Reactions)
Immune-complex mediated
e.g.serum sickness
Delayed-Type Hypersensitivity:
Type IV (Cell Mediated Reaction)
T cell-mediated; delayed type
e.g.tuberculin reaction
5.
6. Type I Hypersensitivity
Allergens
Proteins
Examples: drugs, foods, house dust,
insect venom, latex, mold spores, &
pollens.
Atopy-Predisposition to type I
hypersensitivity (atopic people)
Higher levels of circulating IgE
Greater numbers of eosinophils
7. Type I Hypersensitivity
Factors in the Development of Type I
Hypersensitivity:
Nature of Antigen
Route of entry
Amount of antigen
Ability to produce IgE antibodies
Frequency of exposure
Length of exposure time
8.
9. Table 1. Pharmacologic Mediators of Immediate
Hypersensitivity
MEDIATOR
Preformed mediators in granules
histamine
bronchoconstriction, mucus secretion, vasodilatation,
vascular permeability
tryptase proteolysis
kininogenase
kinins and vasodilatation, vascular permeability,
edema
ECF-A
(tetrapeptides)
attract eosinophil and neutrophils
10. Newly formed mediators
leukotriene
B4
basophil attractant
leukotriene
C4, D4
same as histamine but 1000x more potent
prostagland
ins D2
edema and pain
PAF
platelet aggregation and heparin release:
microthrombi
11. Type I Hypersensitivity
Localized Anaphylaxis
Allergic reaction takes place in
specific part of the body.
Systemic Anaphylaxis
Allergic Reaction takes place in
different parts of the body.
13. Type I Hypersensitivity
Clinical manifestations
Allergic rhinitis
Asthma
Food allergies
Systemic anaphylaxis
14. Type II Hypersensitivity
Cell associated antigens
Transfusion reactions
Hemagglutinins
Complement mediated
Clinical symptoms include fever, chills,
nausea
15. Type II Hypersensitivity
A typical Type Hypersensitivity reaction
might follow these sequence:
1. A particular drug binds to the surface of the
cell.
2. Anti-drug antibodies then bind to the drug.
3. This initiates complement activation on the
cell surface.
4. The complement cascade leads to the lysis
of the cell.
16.
17. Type II Hypersensitivity
Erythroblastosis fetalis
Rh+ fetus born to Rh- mother
First pregnancy sensitizes
Subsequent pregnancies result in anti Rh
Ab
Mild to severe anemia in fetus
Rhogam
18.
19. Type II Hypersensitivity
Drug induced hemolytic anemia
Some antibiotics can be antigenic
Bind nonspecifically to RBC surface
proteins
Ab fixes C and lyses RBCs
20. Type III Hypersensitivity
Immune complexes consist of antigen
and antibodies bound together.
Diseases involved are Systemic Lupus
Erythematosus and rheumatoid arthritis.
21. Type IV Hypersensitivity
T cell mediated
T helper 1 cells
Effector response is through
macrophages not T cytotoxic cells
Cytokine mediated
IL3 Hematopoiesis
Interferon, TNF, IL 1 Extravasation
MCAF Attracts macrophages
MIF Retains macrophages
22. Delayed hypersensitivity reactions
Type
Reaction
time
Clinical
appearance
Histology Antigen and site
contact 48-72 hr eczema
lymphocytes, followed by
macrophages; edema of
epidermis
epidermal ( organic
chemicals, poison ivy,
heavy metals, etc.)
tuberculin 48-72 hr
local
induration
lymphocytes, monocytes,
macrophages
intradermal (tuberculin,
lepromin,etc.)
granuloma
21-28
days
hardening
macrophages, epitheloid
and giant cells, fibrosis
persistent antigen or
foreign body presence
(tuberculosis, leprosy, etc.)
23. Type IV Hypersensitivity
Positive Result for TB skin test
1. Within 2-3 hours after injection of the
PPD (Purified Protein Derivative),
there is an influx of
polymorphonuclear cells into the
site.
2. This is followed by an influx of
lymphocytes and macrophages while
PMN’s dispersed.
24. Type IV Hypersensitivity
3. Within 12-18 hours, the area become
red (erythematous) and swollen
(edematous).
4. The erythema (redness) and edema
(swell) reach maximum intensity bet.
24-48 hours.
5. With time, as the swelling and
redness disappear, the lymphocytes and
macrophages disperse.
25. Five possibilities why TB skin
test may be positive:
A person has tuberculosis.
A person has tuberculosis in the past.
A person has been infected by M.
tuberculosis, but the organism has been
killed by that person’s host defence
mechanism.
A person harvors live M. tuberculosis but
does not have TB.
A person had received BCG (Bacille de
Calmette et Guérin) vaccine.
26. Table 5 - Comparison of Different Types of hypersensitivity
Characteristics
type-I
(anaphylactic)
type-II
(cytotoxic)
type-III
(immune
complex)
type-IV
(delayed type)
antibody IgE IgG, IgM IgG, IgM None
antigen exogenous cell surface soluble
tissues &
organs
response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours
appearance weal & flare lysis and necrosis
erythema and
edema,
necrosis
erythema and
induration
histology
basophils and
eosinophil
antibody and
complement
complement
and neutrophils
monocytes and
lymphocytes
transferred with antibody antibody antibody T-cells
examples
allergic
asthma, hay
fever
erythroblastosis
fetalis,
Goodpasture's
nephritis
SLE, farmer's
lung disease
tuberculin test,
poison ivy,
granuloma
27. Autoimmune Diseases
Autoimmune Diseases result when a
person’s immune system can no
longer recognizes certain body tissues
as “self” and attempt to destroy those
tissues.
28. Immunosuppression
Acquired Immunodeficiency maybe
caused by drugs, irradiation, or
certain infectious diseases.
Inherited Immunodeficiency diseases
are inherited immune diseases.
30. WHAT IS HIV??
“Human Immunodeficiency Virus”
A unique type of virus (a retrovirus)
Invades the helper T cells (CD4 cells) in
the body of the host (defense
mechanism of a person)
Threatening a global epidemic.
Preventable, managable but not curable.
31. OTHER NAMES FOR HIV
Former names of the virus include:
Human T cell lymphotrophic virus (HTLV-
III)
Lymphadenopathy associated virus (LAV)
AIDS associated retrovirus (ARV)
32. WHAT IS AIDS ???
“Acquired Immunodeficiency Syndrome”
HIV is the virus that causes AIDS
Disease limits the body’s ability to fight
infection due to markedly reduced helper T
cells.
Patients have a very weak immune system
(defense mechanism)
Patients predisposed to multiple
opportunistic infections leading to death.
33. AIDS (definition)
Opportunistic infections and
malignancies that rarely occur in the
absence of severe immunodeficiency
(eg, Pneumocystis pneumonia, central
nervous system lymphoma).
Persons with positive HIV serology who
have ever had a CD4 lymphocyte count
below 200 cells/mcL or a CD4
lymphocyte percentage below 14% are
considered to have AIDS.
40. Stage 1 - Primary
Short, flu-like
illness - occurs
one to six weeks
after infection
Mild symptoms
Infected person
can infect other
people
41. Stage 2 - Asymptomatic
Lasts for an average of ten years
This stage is free from symptoms
There may be swollen glands
The level of HIV in the blood drops
to low levels
HIV antibodies are detectable in
the blood
42. Stage 3 - Symptomatic
The immune system deteriorates
Opportunistic infections and cancers
start to appear.
43. Stage 4 - HIV AIDS
The immune
system
weakens too
much as CD4
cells decrease in
number.