Gross Anatomy and Histology of Tongue by Dr. Rabia Inam Gandapore.pptx
GROUP HIV ASSIGNMENT.pdf
1.
2. HIV AND AIDS
PRESENTATION
1. LOICE PENDO – CLM/M/2744/09/18
2. MUNGAI PHELLISIA-CLM/M/1963/09/17
3. OKUMU SAMUEL-CLM/MG/1616/05/18
4. ABRAHAM KIPROTICH –CLM/M/0963/09/16
3. DEFINITION
• Acquired immunodeficiency syndrome (AIDS) is a collection of symptoms
and infections resulting from the specific damage to the immune system
caused by the Human immunodeficiency virus (HIV).
• H – infects Humans only
• I – immunodeficiency virus that weakens the immune system and increases
the risk of infection
• V – virus that attacks the body
• A – Acquired inherited
• I –weakens the immune system
• D – created a deficiency of CD4 cells in the immune system
• S –Syndrome, or a group of illness taking place at the same time
4. • Human immunodeficiency virus commonly known in the ward as
P24,PITC, RVD, ISS and HIV positive patients are called KP(known
positive). In different geographical areas HIV has different local names
eg;
• Kenya – kagunyo(kikuyu)- the worm.
• Uganda –slim disease.
5. HISTORY OF HIV
• HIV/AIDs case in Kenya was first detected in 1984 and it has had a
devastating impact on all sectors of the Kenyan society.
• 2022 marks 38 years since the disease was discovered in Kenya.
• The first specialists to attend to HIV patients were skin doctors, because
skin cancer is a common opportunistic infection. A dermatologist at the Aga
Khan University hospital, Dr D.M. Owili ,recalls that in 1984, he sent blood
samples of a patient with severe skin lacerations and swelling to the US. A
month later the results came back: HIV positive.
• The Ministry of Health instituted an AIDS Control Committee in 1987,
when it developed the first 5-year strategic plan for AIDS control (1987–
91).
• The second plan was for the period 1992–96. The Sessional Paper No. 4 of
1997 on AIDS in Kenya marked an important change on the political front
and outlined a new institutional framework
• .
6. • President Daniel T. Arap Moi addressed Members of Parliament on 25 November 1999, declaring AIDS a
national disaster and stating:
• "AIDS is not just a serious threat to our social and economic development, it is a real threat to our very
existence ... AIDS has reduced many families to the status of beggars…no family in Kenya remains untouched
by the suffering and death cause by AIDS... the real solution of the spread of AIDS lies with each and
everyone of us.“
• With the creation of the National AIDS Control Council, AIDS control units (ACUs) were put in place in all
the ministries where the disastrous effects of HIV/AIDS had been felt the most and where it was anticipated
that interventions would have the greatest beneficial effect.
• In 2002 ,A declaration of ‘Total War on AIDS’ was one of the first acts of President Kibaki, and bringing
together an ecumenical group of religious leaders has been an important step in this fight.
• Now Kenyans are involved in a comprehensive effort to confront all aspects of the disease’s spread and
impact. The government has put in place policies and infrastructure to help implement programmes at all
levels and has issued guidelines for conducting activities in all HIV/AIDS-related areas
7. Institutional response
• Kenya has gone through different phases of national response—
widespread denial in the late 1980s and early 1990s, adoption of a
multisectoral policy in the mid 1990s,and strong government
leadership and political commitment since the year 2000.
• The inadequate response in the 80s was partly because of the
perceived threat to the tourist industry, the country’s most important
single foreign currency earner. At the time HIV/AIDS was not
perceived as a serious problem for the country. Policy makers
described it in the press as “a disease of westerners”.
8. • In 1985 an AIDS Programme secretariat was established with technical and financial support from
WHO and Global Programme on AIDS .
• It was renamed the National AIDS and STD Control Programme (NASCOP) in 1988. All major
hospitals, both government and private, were required to report the number of HIV/AIDS cases
diagnosed in their hospitals to the NASCOP on a monthly basis.
• Responsibility for managing the HIV/AIDS response however remained with the ministry of
health. It raised the warnings about the consequences of the disease in Kenya, but since HIV/AIDS
was still not seen as a priority then, inadequate resources were allocated to address the issue.
• The ministry of health embarked on an extensive HIV/AIDS-education from 1990, centered on
educating basic health providers and community leaders. Sex and HIV/AIDS education was given
in mother tongues, alongside condom distribution. However this approach was not aggressive
enough as evidenced by continued rise of HIV/AIDS infections.
• The public did not respond by changing sexual behavior. At the same time, influential religious
leaders spoke out against the use of condoms as a mechanism for disease prevention.
9. • In 1995 Cardinal Otunga, then head of the Catholic Church in Kenya and
Imam Ali Shee then of Jamia Mosque burnt condoms and sex education
books before youth in Nairobi’s Uhuru Park. They argued that condoms
were a “western solution” that did not fit Kenya’s situation, and was likely
to encourage young people to engage in immoral sexual behavior.
• A Short Term Plan (STP) was formulated in 1986 that mainly focused on the
prevention of HIV by screening blood and promoting safer sex practices
and early diagnosis of STDs.
• Non- Governmental Organizations (NGOs), and NASCOP with support from
selected international donors began creating the required institutional
infrastructure to confront HIV/AIDs.
10. Constraints / effects.
1. Budget – inadequate funds in the Kenya health care budget to get
involved in prevention strategies.
2. Increase in the number of orphans-caused an increased burden on
the extended family, which has the traditional mandate to care for
the orphans.
3. Economically
4. Agriculture
5. Education – reduced number of students and teachers.
11.
12. International agencies and Aid
• The global strategy for the prevention and control of AIDS was initially
drawn by WHO in 1986-1987 and unanimously approved by the
World Health Assembly (1987), the Venice Summit of the Heads of
States and government (June 1987) and the United Nations General
Assembly (October 1987). It has since served as the main policy
framework for the response to the pandemic.
• The three main objectives of the strategy are; to prevent HIV
infection, to reduce personal and social impact of HIV/AIDS and to
mobilize and unify national and international efforts against AIDS.
• Later the joint United Nations Programme on HIV/AIDS (UNAIDS), an
international organization, was created specifically to address the
HIV/AIDS pandemic. It was established as an independent UN agency
13. • January 1, 1996. It brings together the efforts of five UN
organizations: UNICEF, UNDP, UNFPA, UNESCO, WHO and the World
Bank. The primary focus of UNAIDS has been to strengthen the
capacities of national governments for an expanded response to
HIV/AIDS
14. ARVS and other intervention.
• Antiretroviral drugs, or ARVs, are drugs that work against the HIV virus replicating in a person.they
administered together with drugs to treat opportunistic infections.
• First only one drug was administered, then two, and finally it was realized that it was necessary to
use three drugs to successfully suppress the virus. That slow process of scientific experiment and
accumulated learning about what drugs it takes to succesfully prevent viral mutation and
resistance was all performed in the Western developed countries.
• Thus, most HIV- positive people in these countries have a virus that is resistant, and they
therefore are not able to benefit from the new, inexpensive first-line regimen of drugs.
• In the year 2000, the cost of drugs to the patient was prohibitively high for the majority, at USD
10,000 per year
• Combination therapy with at least three anti-retroviral drugs was introduced in 1995 and became
widespread in 1996 and they include stavudine (d4T),lamivudine (3TC), nevirapine (NVP) or
efavirenz (EPZ).For women of child-bearing age nevirapine is used because efavirenz can affect
the foetus;
15. • By 2000 , two vaccines had been tested.
• The International AIDS Vaccine Initiative (IAVI)-Kenyan-Oxford
partnership was specifically designed for Africa.
• IAVI is a scientifically based non profit initiative formed by the
Rockefeller Foundation with a mission to ensure development of safe,
effective and accessible preventive HIV vaccines for use throughout.
• In December 2000 Kenyan scientists, based at the University of
Nairobi were allowed to jointly own patent rights for the HIV/AIDS
vaccine and trials were done in February 2001.
• The same trial was done in Britain in august 2001.
16. Epidemiology
• Today in Kenya, the HIV epidemic is better understood.
• Data from surveys conducted over time, such as Kenya National Population-based
HIV Impact Assessment (KENPHIA), Demographic Health surveys and ANC sites
sentinel surveys provides data for generation of the estimates used to guide HIV
programming.
• Kenya generates annual HIV estimates for key indicators such as prevalence and
incidence among others. The national estimates reports are published every two
years and mainly point out the performance of the Kenya HIV Response
• Over the years, Kenya has made tremendous strides towards alleviating the HIV
epidemic resulting in 68.5% Reduction of New HIV infections between 2013 and
2021 .
• .
• .
17.
18. • However, as the country advances towards getting to zero new HIV
infections, zero HIV-related deaths, and zero discrimination, the HIV
prevalence is yet to stabilize. (A 2011 strategy- getting to zero).
• CHANGES THAT HAVE BEEN ADOPTED;
✓HIV prevention and treatment services, including increased
antiretroviral treatment, have led to reduced incidence rates and
reduced HIV-related mortality.
✓Changes in a greater understanding of the epidemic by strengthening
its national and regional modeling initiatives during the generation
and projection of estimates using different mathematical models.
19. Estimation of prevalence
• Methods used:
1) Sentinel surveillance of HIV prevalence in pregnant women- it has been conducted every year
since 1990, provides information about the trend in the rate of infection over time. This
information can also provide an estimate of the number of children who are infected with HIV
since nearly all HIV infection in children is transmitted from mother to child.
2) The second method is through a general population survey, in which a carefully selected
sample of the population is tested for HIV.
3) Kenya has both a generalized and a concentrated epidemic. The epidemic is deeply rooted
among the general population while there is also concentration of very high prevalence among
key populations.
• Key populations identified by the Mode of Transmission study, 2008 include
✓sex workers and their clients
✓men having sex with men
✓people who inject drugs among others
20.
21. Prevalence in adults (15-49years)
• Adult HIV prevalence refers to the estimated number of adults aged
15-49 living with HIV infection, whether or not they have developed
symptoms of AIDS, expressed as percentage of the total population in
that specific age group
• There has been a decline in the overall prevalence among adults aged
15-49 from 6 per cent in 2013 to 4.5 per cent in 2019 .
24. Prevalence by gender
• The distribution of prevalence by gender shows that females (5.8%)
have approximately twice the prevalence of males (3.1%), with
approximately 942,653 females and 565,752 males living with HIV as
at December 2019.
• In 2021 the prevalence is
✓5.5% in women and 2.9% in men.
25.
26.
27. Prevalence by age
• Kenya has a predominantly young population, with 67% aged 29 years
and below. Despite the significant reduction in the number of new
HIV infections among adolescents and young people, the country did
not meet the target of 75% reduction.
• Approximately, 42% of new adult HIV infections are amongst
adolescents and young people (15-24 years). Nairobi, HomaBay, Uasin
Gishu and Meru counties had the highest number of new HIV
infections among young people
30. Prevalence across counties
• HIV incidence differed across the counties, with an incidence as high as 6.9
per 1,000 in Kisumu and Siaya counties, to 0.01 per 1,000 in Wajir and
Mandera counties.
• About 55% of counties lie in the low incidence category (below 500 cases
annually) while 25% of the counties including (Homa Bay, Siaya, Kisumu,
Migori, Kiambu, Kajiado, Mombasa, Kisii, Nairobi, Nakuru, Uasin Gishu and
Kakamega) recorded above 1,000 new infections annually hence
categorised as ‘High incidence counties).
• A further review of the sources of these infections by the Kenya Modes of
Transmission study revealed that 62% of all new infections were among the
15-29-year-olds with 15-24-year-olds contributing 42%.
• Across the age bands, new infections were mostly from the females,
especially among 15-19-year-olds.
33. NATURAL HISTORY OF HIV
• HIV infection progresses from an early acute syndrome to a prolonged asymptomatic state to advanced
disease. There are different clinical manifestations at different stages.
1. Acute HIV syndrome
Entry of HIV into the body is heralded by the following sequence of events:
I. High levels of plasma viraemia due to replication of the virus.
II. Virus-specific immune response by formation of anti-HIV antibodies (seroconversion) after 3-6 weeks of
initial exposure to HIV.
III. Initially, sudden marked reduction in CD4+ T cells (helper T cells) followed by return to normal levels.
IV. Rise in CD8+ T cells (cytotoxic T cells).
V. Appearance of self-limited non-specific acute viral illness (flu-like or infectious mononucleosis-like) in 50-
70% of adults within 3-6 weeks of initial infection. Manifestations include: sore throat, fever, myalgia, skin
rash, and sometimes, aseptic meningitis. These symptoms resolve spontaneously in 2-3 weeks.
34. 2. Middle chronic phase
The initial acute sero conversion illness is followed by a phase of competition between HIV
and the host immune response as under:
I. Viraemia due to viral replication in the lymphoid tissue continues which is initially not
as high but with passage of time viral load increases due to crumbling host defenses.
II. Chronic stage, depending upon host immune system, may continue as long as 10
years.
III. Although CD 4+ T cells continue to proliferate but net result is moderate fall in CD4+ T
cell counts.
IV. Cytotoxic CD8+ T cell count remains high.
V. Clinically, it may be a stage of latency and the patient may remain asymptomatic, or
may develop mild constitutional symptoms and persistent generalized
lymphadenopathy.
35. 3. Final crisis phase
This phase is characterized by profound immunosuppression and onset of
full-blown AIDS and has the following features:
I. Marked increase in viraemia.
II. The time period from HIV infection through chronic phase into full-
blown AIDS may last 7-10 years and culminate in death.
III. CD 4+ T cells are markedly reduced (below 200 per μl).
• The average survival after the onset of full-blown AIDS is about 2 years.
• Children often have a rapidly progressive disease and fullblown AIDS
occurring at 4 to 8 years of age.
36. CRYPTOCOCCAL MENINGITIS
• It is the inflammation of the meninges caused by a Cryptococcus
organism
• Epidemiology
• It develops in immunocompromised persons
• It is especially an important cause of meningitis in patients with AIDS
• Has an incidence of about 9%
37. ETIOLOGY
• Caused by the fungus Cryptococcus neoformans which is often
acquired through inhalation of bird droppings (specifically the pigeon
bird)
• The major risk factor is immunosuppression
38. CLINICAL FEATURES
• Onset may be insidious with nonspecific symptoms such as:
• Fever
• Nausea
• Headache
• Drowsiness and confusion
• Vomiting
• Positive Brudzinski’s
• Positive Kerning’s
• As the infection progresses, conscious levels may be impaired
• It may be fulminant and fatal in a few weeks or be indolent for months to years
39. TYPES OF MENINGITIS
• Broadly classified as acute pyogenic, acute lymphocytic (viral, aseptic) and
chronic (bacterial or fungal).
• Cryptococcal meningitis develops particularly in debilitated or
immunocompromised persons, usually as a result of hematogenous
dissemination from a pulmonary lesion.
• Cryptococcal meningitis is especially an important cause of meningitis in
patients with AIDS.
• Tuberculous meningitis occurs in children and adults through
hematogenous spread of infection from tuberculosis elsewhere in the
body, or it may simply be a manifestation of miliary tuberculosis.
• Less commonly, the spread may occur directly from tuberculosis of a
vertebral body.
40. • Tubercle bacilli may be found on microscopy of centrifuged deposits
by ZN staining in tuberculous meningitis.
• Pathognomonic capsulated cryptococci with a halo are appreciated in
India ink preparation of CSF in cases of cryptococcal meningitis, while
the capsule is better demonstrated by mucicarmine stain.
43. SCREENING
• All adult and adolescent PLHIV with a baseline CD4 count of ≤ 200 cells/mm3
should be screened for cryptococcal infection .
• This should be a reflex test performed by the laboratory as soon as the low CD4
count is noted, rather than requiring the clinician to order a special test for
screening.
• PLHIV, including children and adolescents, should receive cryptococcal screening
if clinically suspected. For patients who are symptomatic for meningitis but
screen serum CrAg negative, alternative diagnoses for sub-acute meningitis
should be explored, such as TB meningitis.
• All patients with clinical meningitis should be assessed and managed at a facility
that can perform lumbar punctures.
• Whenever performing CSF CrAg for patients with symptomatic meningitis, CSF
GeneXpert ultra for TB should be performed at the same time, as well as urine
for TB-LAM.
44.
45. INVESTIGATIONS
• CT scan before lumbar puncture to rule out space occupying pathology
• CSF exam involving Indian ink staining
• Culture of Cryptococcus from CSF or blood
• The CSF findings are;
• I. Clear or turbid CSF which may form fibrin web on standing
• ii. Raised CSF pressure (above 300 mm water).
• iii. Mononuclear leukocytosis of mostly lymphocytes and some
macrophages (100-1000 cells/μl)
• iv. Raised protein content
• v. Lowered glucose concentration
47. • Fluconazole use during first trimester of pregnancy increases the risk
of birth defects.
• All pregnant women who screen positive with serum CrAg should be
offered a lumbar puncture (irrespective of symptoms) to determine if
they have cryptococcal meningitis.
• If the CSF CrAg is positive, they should be treated with 2 weeks of
amphotericin B for induction (without fluconazole).
• Pregnant women with negative CSF CrAg should start ART
immediately (without pre-emptive fluconazole therapy) and be
monitored for symptoms of CM.
48. REFERENCE
1. Harsh Mohan Textbook OF Pathology, 7TH EDITION, JAYPEE
BROTHERS.
2. KENYA HIV PROGRESS INDICATORS 2020 WORLD AIDS DAY REPORT
3. Kenya AIDS Response Progress Report 2018
4. Kenya AIDS Response Progress Report 2014 ,Progress towards Zero.
5. The Kenya National HIV/AIDS Strategic Plan 2000 – 2005
6. KENYA WORLD AIDS DAY PROGRESS REPORT 2013 – 2021