Assessment and management for the patient

with HIV/AIDS

By: abdinar. A (MSc in AH)

Address: narulah09@gmail.com

1 03/25/2023
 Chapter objectives

Describe pathogenesis of HIV/AIDS

List mode of transmissions of HIV and body fluid

that contain HIV in higher rate

Describe HIV/AIDS staging and clinical

manifestations
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 HIV
HIV stands for human immunodeficiency virus

It reproduces itself inside a living cell, infects

HUMANS and weakens the IMMUNE system

HIV infection leads to a weakened immune system,

making a person with HIV vulnerable to a group of

3 illnesses called opportunistic infections /OIs/ 03/25/2023

 What is AIDS?

A: Acquired, to come into possession of something new

I: Immunodeficiency, decrease or weakness in the

body’s ability to fight infections and illnesses

S: Syndrome, a group of signs and symptoms that

occur together and characterize a particular abnormality

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 HIV/AIDs

HIV disease is a chronic infectious disease caused by

the Human Immune Deficiency Virus

characterized by:
Starting from primary infection,

 with or without the acute syndrome, followed by

long period of asymptomatic stage

progress mostly to advanced and life threatening

5 disease (AIDS) 03/25/2023

 Trends:
Prevalence =stabilized
Incidence=somewhat decreasing
Deaths =decreased with introduction of
ART

Reservoir: human

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 Mode of Transmission

HIV enters the bloodstream through:

Open Cuts

Breaks in the skin

Mucous membranes

Direct injection
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 Mode of Transmission
a) Sexual Transmission:
Is the major mode of transmission worldwide ( 90 % )
The virus is found in high quantities in the sexual
fluids (seminal and vaginal fluid) of people with HIV
infection
The presence of other STDs increase the risk of

acquiring or transmitting HIV infection by several fold

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 Mode of Transmission
b) Through blood and blood products
IV drug abusers who share needles and syringes

Blood or blood products transfusion(90-100%)

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 Mode of Transmission

c) Mother to Child Transmission

Pregnancy: 10 %
Delivery: 70 %
Breast Feeding : 10-15 %

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 Factors Influencing MTCT
i- Maternal Factors

Maternal viral Load

Severe immune deficiency

Use of ART during pregnancy and postpartum to mother

and newborn

Nutritional status, particularly vitamin A

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 Factors Influencing MTCT
ii- Labor and Delivery
Prolonged rupture of membranes (> 4 hours)
Invasive delivery technique
Mixing of maternal and fetal body fluids
Episiotomy
iii- Fetal Conditions
Premature delivery
Immature immune status

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 Factors Influencing MTCT
iv- Infant Feeding Practices/Breastfeeding
Mother becomes infected with HIV while breastfeeding
(risk increases up to 20%)
Breast pathologies (lésions, infections)
Advanced disease in the mother
Poor maternal nutritional status
Breastfeeding during the first 4–6 months
The longer mother breastfeeds, the greater the risk

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 The following fluids of infected person
contain HIV
Blood
semen
vaginal secretion
Breast Milk
CSF
peritoneal fluid
synovial fluid
Pericardial fluid
pleural fluid
amniotic fluid
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 HIV in Body Fluids

Blood
Semen
18,000 Vaginal
11,000
Fluid Amniotic
7,000 Fluid
4,000 Saliva
1

18 Average number of HIV particles in 1 ml of these body fluids

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 Morphology of the Virus
The external envelope (lipid membrane)

The lipid membrane has two major proteins gp120

and gp41
This lipid bi-layer helps to:

Mediate recognition of CD4+ cells

Enabling the HIV virus to attach to and invade the

CD4+ cells.

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 Morphology of the Virus
An internal core contains
 two single stranded copies of the genomic material
(RNA)
Multiple proteins and enzymes necessary in the
process of HIV replication and maturation:
P24
P17
Reverse transcriptase
Integrase
Protease
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 Life Cycle of HIV: Replication

Attachment /binding and fusion of the virus to the host

cells

Uncoatting of the viral capsid and release of Viral RNA

into the cytoplasm of the host cell

Reverse transcription

Translocation

Integration of proviral DNA to host-cell DNA

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 Life Cycle of HIV: Replication

Cellular activation causes transcription (copying) of

HIV DNA back to RNA

Maturation : viral Proteases enzymes cleave longer

proteins in to important viral proteins and help to
convert immature viral particle into and infectious HIV

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 HIV-Infected T-Cell

HIV HIV Infected New HIV

T-Cell
Virus T-Cell Virus

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 Diagnostic tests

1. ELISA

2. Western Blot

3. Rapid tests

4. PCR test

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 Clinical Manifestations of HIV infection

Primary HIV Infection : Acute HIV syndrome and

Seroconversion

Asymptomatic stage – Clinical latency

Early Symptomatic Diseases – mild immunodeficiency

AIDS defining illnesses : Advanced immunodeficiency

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 a) Primary HIV Infection
The period immediately after infection

characterized by high level of viremia (>1 million)

Associated with a transient fall in CD4

Nearly half of patients experience some symptoms

(fever, rash, swollen lymph glands)

Primary infection resolves as body mounts HIV-specific

adaptive immune response
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 b) Asymptomatic stage

In most ( 90% ) of patients

Viral replication continues during this period of clinical

latency

The CD4 cell count fall progressively with an average rate

of 50-100 cells/μl/year

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 c) Early Symptomatic Diseases
CD4 cell count < 500/μl,
Patients begin to develop sign and symptoms of clinical
illness
Most of the manifestations are due to minor
opportunistic infections
The clinical findings include:
 Generalized lymphadenopathy, Oral lesions, Herpes

zoster , Thrombocytopenia, Genital herpes simplex.

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 d) AIDS defining illnesses
Viral load is high,
CD4+ count < 50 cells/mm3, and Death is imminent
Pt continue to develop new OI
The following illnesses can occur as Ois
Pulmonary TB, meningitis
Toxoplasmosis, Kaposi’s sarcoma
Cytomegalovirus , Candidiasis
Extra-pulmonary TB , Infective dermatoses
Bacterial pneumonia

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 CD4 LEVELS IN RELATION TO THE
SEVERITY OF IMMUNOSUPPRESSION
Not signinficant immuno- >500/mm3
suppression

Mild immuno suppression 350−499/mm3

Moderate immuno suppression 200−349/mm3

Severe immunosuppression <200/mm

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 WHO Clinical Staging of HIV/AIDS

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 WHO staging system for HIV infection and
Diseases
Clinical Stage I
Asymptomatic

Persistent Generalized L/Adenopathy (PGA)

Performance scale 1- Asymptomatic normal activity

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 WHO staging cont’d
Clinical stage 2:
Wt. loss <10% of body weight

Minor mucocutaneous manifestation (seborrhoeic

dermatitis, fungal nail infection, recurrent oral ulceration,

angular chilitis)
HZ with in last 5 years

Recurrent URTI i.e. bacterial sinusitis

Performance scale 2 –symptomatic, normal activity

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 WHO staging cont’d
Clinical stage 3:
Wt. Loss, <10% body wt
Un explained chronic diarrhoea > 1 month
Oral Candidiasis (thrush)
Oral hairy leukoplakia
Pulmonary TBC with in the past year
Sever bacterial infection (i.e. Pneumonia)
Performance scale 3: bed ridden <50% of the day during
last month

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 WHO staging cont’d
Clinical stage 4:
HIV wasting syndrome (wt loss >10%, Plus either
unexplained Chronic diarrhoea >1month, or chronic
weakness and unexplained fever >1month.
Toxoplasmosis of the brain
Cryptosporidiosis with diarrhoea > 1 month
Cryptococcosis,
EPTB
HSV, KS,
HIV encephalopathy
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> 50% bed ridden for more than a month 03/25/2023
 WHO clinical criteria for HIV Diagnosis

Major sign/disease
oWt loss of 10% or more
oChronic diarrhoea
oProlonged fever for more than one month

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 WHO clinical criteria for HIV Diagnosis
Minor signs/disease
Oropharyngeal Candidiasis
Persistent cough for more than 1 month
Body weakness ,Night sweating
Loss of appetites ,KS, Pneumonia
Generalized skin infection
Generalized lymph adenopathy
HZ, Chronic Herpes simplex infection

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 Antiretroviral Therapy
1. Nucleoside reverse transcriptase inhibitor (NRTIS)

2. NNRTIS

3. PIs (protease inhibitors)

4. Fusion Inhibitors (not available in Ethiopia and not

widely used in westerns

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 Antiretroviral Drugs (ARTs)

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 Classes of Antiretroviral Drugs
1) Nucleoside reverse transcriptase inhibitors ( NRTIs)
Lamivudine (3TC) Stavudine ( d4t )
Zidovudine (AZT) Abacavir ( ABC)
Didanosine (DDI ) Zalcitabin ( DDC )
Emtricitabine (FTC) Tenofovir (TDF )

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2) Non-nucleoside reverse transcriptase inhibitors (
NNRTIs)

• Nevirapine (NVP, Nevipan®)

• Efavirenz (EFV, Stocrin®)

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 3) Protease Inhibitors
Lipinavir /ritonavir/ LPV/R

Nelfinavir (NFV)

Saguinavir (SQV/ritonavir

PIs are mainly used as second line drugs in resource

limited settings as these drugs are expensive and most
formulations need refrigeration.

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 Goals of ART: (HAART )

1. Improve the length and quality of the patient’s life

2. Increase total lymphocyte count (TLC) and CD4 cell

count

3. HIV RNA < 400 copies/ml or “undetectable” within 4-6

months of ART initiation

4. Reduce HIV-related morbidity and mortality

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 What does HAART require to be effective?
Strict adherence to this regimen

Proper monitoring of side effects and disease

progression
Recognition and treatment of co-morbidities

Recognition of drug interactions

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 WHO Criteria to Initiate ART in Adults and adolescents

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 Recommended HAART Regimens in infected
Adult & Adolescent

First line
AZT/3TC/NVP or

TDF/3TC/EFV

Replace NVP for EFZ in pregnancy

Second Line drugs
ABC or TDF or ZDV (if not taken)/+ Didanosin or
NFV
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 The indications for changing from First line to Second
line regime is when there is evidence of treatment
Clinical failure

Immunological failure

Virological failure

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 Prevention and control
Reduce sexual transmission
Awareness and life skill education
Condom promotion
STI control
Mother to child transmission
Prevent HIV among young women
Preventing pregnancy among HIV positive (FP)
Preventing transmission of HIV from infected
mother to the infant-prophylaxis, feeding, safe
delivery
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 Blood safety
Testing all transfused bloods
Avoiding non-essential blood transfusion
Recruiting safe blood donor pool
Universal precautions
Physical protection-vulnerable groups
Protecting health care workers-PEP,VCCT, reduce
nosocomial infection

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