PAEDIATRIC HIV / AIDS I & II��

Prof. Yakubu Mava. MBBS (ABU), FWACP, FIMC, LMIH (USA)

OUTLINE�

- Introduction

- Historical background

- Aetiology / Pathogenesis / Pathophysiology

- Epidemiology

- Clinical staging

- Diagnosis: clinical and laboratory

- Treatment

- Immune reconstitution syndromes

- Opportunistic infections

- Cotrimoxazole prophylaxis

- Nutrition

- Psychological support

Introduction

• HIV/AIDS is one of the leading cause of death among infants and children.
• Clinically 25% of children infected with HIV in Africa have a rapid down hill course with manifestation of AIDS within one year.
• It is estimated that 50% of infected infants die before their 2^nd birthday.
• The rate of down hill course reflects in part the level of care.
• Clinical trials in children are particularly few

To understand what HIV and AIDS are, let’s break it down:

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Causative agent:

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H – Human – This particular virus can only infect human beings.

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I – Immunodeficiency – HIV weakens your immune system by destroying important cells that

fight disease and infection. A "deficient" immune system can't protect you.

V – Virus – A virus can only reproduce itself by taking over a cell in the body of its host.

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http://aids.gov/hiv-aids-basics/hiv-aids-101/what-is-hiv-aids/

What is HIV?

Disease:

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A – Acquired – AIDS is not something you inherit from your parents like eye color.

You acquire AIDS.

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I – Immuno – Your body's immune system includes all the organs and cells that work to

fight off infection or disease.

D – Deficiency – You get AIDS when your immune system is "deficient,"

or isn't working the way it should.

S – Syndrome – A syndrome is a collection of symptoms and signs of disease. AIDS is a syndrome,

rather than a single disease. It is a complex illness with a wide range of symptoms.

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http://tcf.epfl.ch/page-20833-en.html

The HIV genome is composed of 9 genes, which encode 15 proteins.

For comparison, the E. Coli bacterium contains around 4,377 genes and the human genome encodes around 21,000 genes.

http://biology.kenyon.edu/slonc/gene-web/Lentiviral/Lentivi2.html

Where did HIV come from?

http://what-when-how.com/medical-microbiology-and-infection/zoonoses-systemic-infection/

Zoonosis = Cross-species transmission event

Phylogeny of lentiviruses.

Sharp P M , and Hahn B H Cold Spring Harb Perspect Med 2011;1:a006841

©2011 by Cold Spring Harbor Laboratory Press

©2011 by Cold Spring Harbor Laboratory Press

Sharp P M , and Hahn B H Cold Spring Harb Perspect Med 2011;1:a006841

Where did HIV come from? Cont.

HIV entered the human population from primates, which harbor a related virus known as SIV (simian immunodeficiency virus). This probably occurred during the butchering and consumption of monkey meat in Africa.

http://www.avert.org/hiv-types.htm

HIV “family tree”

HIV-1 group M, which is the most prevalent HIV strain, jumped from chimpanzees into humans.

http://www.awf.org/content/wildlife/detail/chimpanzee

HIV-2 originated in sooty mangabeys and is responsible for fewer infections than HIV-1

New viruses are still being transferred from primates to humans, and have the potential to cause new diseases and epidemics.

http://pin.primate.wisc.edu/factsheets/entry/sooty_mangabey

Origins of human AIDS viruses.

Sharp P M , and Hahn B H Cold Spring Harb Perspect Med 2011;1:a006841

©2011 by Cold Spring Harbor Laboratory Press

When did HIV first jump into humans?

The strain of HIV responsible for the majority of global infections (HIV-1 Group M) probably jumped into humans in western Africa sometime between 1884 and 1924.

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From there it then spread throughout the world.

Origin and Spread of HIV

Historical Background of HIV/AIDS

• (Kaposi’s Sarcoma and Pneumocystis pneumonia among homosexual men. (New York and California MMWR (Morb Mortal Wkly Rep) 1981; 30: 305.)
• In 1981 the disease entity called Acquired Immunodeficiency Syndrome (AIDS) was recognized by the CDC in the USA
• In 1983 Barre-Sinousi et al from Institute of Pasteur in Paris discovered the infectious agent responsible for AIDS, which they named Lymphadenopathy Associated Virus (LAV)
• Isolation of T- lymphotropic retrovirus from patient with AIDS. (Science 1983; 220: 868 – 71).

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Historical background cont.

• In 1984 Popovic et al at NIH, Bethesda Maryland USA, described a virus in AIDS patients which they called human T-cell Lymphotropic virus Type III (HTLV-III; Isolation and Continuous production of cytopathic retrovirus (HTLV-III) from patients with AIDs and pre-AIDS. Science 1986; 232: 697.
• In 1986 the term human immunodeficiency virus (HIV) was recommended for universal usage for LAV and HTLV-III by the International Committee on the Taxonomy of viruses (Coffin J, Haase A, Levy JA et al. Human Immunodeficiency Viruses (Letter) Science 1986; 232: 697.

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Aetiology and Pathogenesis�

• HIV is a retrovirus of the group Lentiviridae
• Humans are the only known reservoir of the virus
• Although related viruses, simian immunodeficiency virus (SIV) have been found in Zooty mangabey monkeys
• Two major types of HIV: HIV 1 and HIV –2, each with different serotypes have been identified.

Aetiology and Pathogenesis

• The virus possesses an enzyme reverse transcriptase, with which it converts the viral RNA into proviral DNA,
• proviral DNA is then integrated with the host DNA. In this way, replication of the infected host cell through cell division results in automatic production of multiple copies of the virus for further infection of other cells.
• Consequently the virus persists for life in infected persons.
• HIV – 2 is less pathogenic than HIV – 1 and is therefore less frequently transmitted from mother to child (Adjorlolo – Johnson et al 1994; Morgan et al 1990; Andreasson et al 1993).

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PATHOPHYSIOLOGY

• Infected cells remain in a dormant state for a variable period of time. Up to 15 yrs in adult
• proviral DNA transcribes genomic and messenger RNA = > formation of daughter cells which goes into circulation.
• The virus then start to cause depletion of the CD4 cells, directly and indirectly mechanism.
• Disruption of the architecture of lymphoid organs, qualitative function of the CD4 lymphocyte and monocyte-macrophages are affected
• CD4 lymphocytes appear to be the primary reservoir of HIV in infected persons.

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THE STRUCTURE OF HIV�

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Cellular Immune Response to HIV

= CD8 cytotoxic T Lymphocytes (CTL)

. Critical for containment of HIV

. Derived from naïve T8 cells which recognizes viral Ag in

context of MHC class 1 presentation

. Directly destroy infected cells

. Activities augmented by Th1 response

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= CD4 Helper T Lymphocytes (Th)

. plays an important role in cell mediated response

. Recognizes viral Ag by an Ag presenting cell (APC)

. Differentiated according to the ‘help’:

-Th1 activates Tc (CD8) lymphocytes promoting cell mediated

immunity

-Th2 activates B lymphocytes promoting Ab mediated immunity

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Humoral Immune Response to HIV

• Neutralization

. Ab binds to surface of virus to prevent

attachment to target cells

• Ab dependant cell mediated cytotoxicity (ADCC)

. Fc portion of the Ab binds to NK cells

. Stimulate NK cells to destroy infected cells

HIV Evasion Methods

• Makes 10 billion copies/day leading more rapid mutation of HIV Ag
• Integrates into host DNA
• Depletes DC4 lymphocytes
• Down regulates MHC 1 process
• Impair Th1 response of CD4 T lymphocytes
• Infects cells in the region of the body where Ab penetrates poorly eg CNS
• Disrupts the lymph nodes architecture

Epidemiology: Global situation

• Since the beginning of the epidemic, more than 70 million people have been infected with the HIV virus
• 35 million people have died of HIV.
• Globally, 36.9 million [31.1–43.9 million] people were living with HIV at the end of 2017.
• An estimated 0.8% [0.6-0.9%] of adults aged 15–49 years worldwide are living with HIV
• The WHO African region remains most severely affected, with nearly 1 in every 25 adults (4.1%) living with HIV and accounting for nearly two-thirds of the people living with HIV worldwide.

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HIV Epidemiology

HIV Epidemiology cont.

HIV Epidemiology

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• 5,000 new infections per day. This includes 180,000 children (<15 years).
• An estimated 1.8 million individuals worldwide were newly infected with HIV in 2017
• Most of these children live in sub-Saharan Africa and were infected by their HIV-positive mothers during pregnancy, childbirth or breastfeeding

Nigeria: HIV Epidemiology

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• National HIV prevalence in Nigeria is 1.4% among adults aged 15–49 years (Mar. 2019)
• Previous estimates had indicated a National HIV prevalence of 2.8%.
• UNAIDS and the National Agency for the Control of AIDS estimated that there are 1.9 million people living with HIV in Nigeria.

HIV Epidemiology

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• women aged 15–49 years are more than twice as likely to be living with HIV than men (1.9% versus 0.9%.)
• The difference in HIV prevalence between women and men is greatest among younger adults
• young women aged 20–24 years more than three times as likely to be living with HIV as young men in the same age group.
• Among children aged 0–14 years, HIV prevalence according to the new data is 0.2%. (2019)

HIV Epidemiology by geopolitical zones in Nig.

• The South-South zone of the country has the highest HIV prevalence, at 3.1% among adults aged 15–49 years.
• HIV prevalence is also high in the North Central zone (2.0%)
• South East zone (1.9%).
• South West zone (1.1%)
• North East zone (1.1%)
• North West zone (0.6%).

HIV Epidemiology cont.

• Nigeria has shown steady progress on increasing access to treatment for people living with HIV, with the adoption of a test and treat policy in 2016.
• This measure has further accelerated referrals to treatment facilities for people who test positive for the virus.
• 2010 to 2017, the country almost tripled the number of people living with HIV having access to antiretroviral therapy
• 360 000 people in 2010 access antiretrivirus
• >1 million people in 2018. access antiretrivirus

MODES OF TRANSMISSION�

• More than 80% of all HIV infections in Africa are acquired through heterosexual contact.
• Mother – to – child transmission is the 2^nd over 90% of infection in children worldwide (ref. UNAIDS/WHO 1998)

1. Intrauterine 25 – 40%

2. Intrapartum (during labour or delivery) 60 –75%

3. Postpartum 15% (through breastfeeding).

4. Breast-feeding thus accounts for the 15%

MODES OF TRANSMISSION Cont.

• Blood and Blood products transfusion is the 3^rd

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• contaminated needles and syringes.

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• Use of sharp objects / traditional scarification, uvelectomy, local barbers, Circumcission, FGM, etc.

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http://aids.gov

Pediatric HIV Clinical Staging -New WHO

• Clinical Stage 1
• Asymptomatic
• Generalized lymphadenopathy
• Clinical Stage 2
• Hepatosplenomegaly
• Papular pruritic eruptions
• Seborrhoeic dermatitis
• Extensive human papilloma virus infection
• Extensive molluscum contagiosum
• Fungal nail infections
• Recurrent oral ulcerations
• Lineal gingival erythema (LGE)
• Angular cheilitis
• Parotid enlargement
• Herpes zoster

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• Clinical Stage 3
• Conditions where a presumptive diagnosis can be made on the basis of clinical signs or simple investigations
• Moderate unexplained malnutrition not adequately responding to standard therapy
• Unexplained persistent diarrhoea (14 days or more )
• Unexplained persistent fever (intermittent or constant, for longer than one month)

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STAGE 3 cont.

• Oral candidiasis (outside neonatal period )
• Oral hairy leukoplakia
• Acute necrotizing ulcerative gingivitis/periodontitis
• Pulmonary TB
• Severe recurrent presumed bacterial pneumonia

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• Clinical Stage 4
• Conditions where confirmatory diagnostic testing is necessary
• CMV infection (CMV retinitis or infection of organs other than liver, spleen or lymph nodes; onset at the age one month or more)
• Extrapulmonary cryptococcosis including meningitis
• Any disseminated endemic mycosis (e.g. extrapulmonary histoplasmosis, coccidiomycosis, penicillinosis)
• Cryptosporidiosis

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STAGE 4 CONT.

• Isosporiasis
• Disseminated non-tuberculous mycobacteria infection
• Candida of trachea, bronchi or lungs
• Visceral herpes simplex infection
• Acquired HIV associated related rectal fistula
• Cerebral or B cell non-Hodgkin lymphoma
• Progressive multifocal leukoencephalopathy (PML)
• HIV-associated cardiomyopathy or HIV-associated nephropathy

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Herpes Zoster (Shingles): varicella zoster virus

Seborrheic Dermatitis: Malassezia fungus

Oral Candidiasis / Thrush (WHO stage III)

HIV wasting syndrome (WHO stage IV)

Karposi Sarcoma: HHV-8

Non-Hodgkin Lymphomas:

INVESTIGATIONS PAEDIATRICS HIV

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Basic Serologic Testing

• Rapid Tests
• Various tests that provide results in ~10 minutes
• Sensitivity approaches 100%; specificity is >99%
• Negative tests can be reported as negative, assuming proper laboratory quality assurance system in place (such as use of controls)
• Positive results should be confirmed, perhaps using a 2^nd rapid test for antibodies to another part of the virus.
• Useful in situations where immediate results are important to manage decisions

More Advanced Serologic Testing

• ELISA/EIA
• Tests for a number of antibody proteins in combination
• A very sensitive test, but not very specific
• Positive result means sample needs to be tested by western blot or different ELISA test
• Western blot test (WB)
• Used as a confirmatory test
• Very specific for HIV
• Antibodies to only a selection of viral proteins may yield an indeterminate Western blot
• Bands corresponding to p24 and p55 are detected early in seroconversion followed by glycoprotein bands

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Other HIV testing modalities

• DNA PCR
• A qualitative test used to detect intracellular virus
• Can detect 1-10 copies of HIV proviral DNA
• Primarily used for viral detection with infant infection and with indeterminate serology

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• RNA PCR
• Measures “viral load” in copies/ml
• Used more for monitoring than diagnosis
• Can have an undetectable viral load (virus levels so low that the machine can’t detect it) but still be HIV+
• Rare, but possible even when not on therapy
• May be used to diagnose infection in infants since viral load is usually very high

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WHO Testing Strategy

• HIV infection is diagnosed by a positive HIV test.
• WHO has recommended testing strategies based on a combination of rapid tests that do not require expensive Western Blot confirmation assays.
• Nigeria Ministry of Health has adopted these strategies
• HIV diagnosis based purely on clinical features is less common
• Use confirmatory assays to resolve indeterminate results for diagnostic purposes.

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• First rapid test
• If positive, repeat with a second test
• If negative, no need for 2^nd test; patient is reported as negative
• Second rapid test
• If positive, patient is reported as positive
• If negative, this is an “indeterminate” result
• need 3^rd test as tie breaker
• Third rapid test
• “Tie Breaker”

Window period

• Window period = time in which a person may be infected with HIV but test negative
• May take 6 weeks to 6 months (usually < 3 months) to develop antibodies in order to test positive

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• People who test HIV negative should be strongly counseled to return in three months for repeat testing

Pediatric HIV Diagnosis

• Laboratory Diagnosis
• Timing of PCR:
• Test at birth can distinguish in utero from peripartum or breastfeeding infection
• Positive in the first 2-3 days of life, then infection was in utero
• Negative in the first 2-3 days of life, positive later, then infection was peripartum or postpartum
• If only one PCR is done, it should be done at 1 month of age or later

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Positivity of DNA PCR in HIV-infected infants during the first month of life

Pediatric HIV Diagnosis

• Ruling out the diagnosis of HIV infection
• Two negative DNA PCR tests, the first at 1 month or older, and the second at 4 months or older, or
• One negative HIV serology test at 18 months of age or older, and
• No clinical signs of HIV infection (WHO Stage 3 or greater)

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Immune categories by CD4 count and CD4 %

Treatment Modalities

• Antiretroviral therapy.
• Treatment of acute bacterial infections
• Prophylaxis and treatment of opportunistic infections
• Maintenance of good nutrition
• Immunization.
• Management of AIDS- defining illnesses
• Psychological support for the family
• Palliative care for the terminally ill child

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Pediatric HIV Treatment Principles

• Successful treatment requires education of the mother and father

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• Successful treatment of older children may require disclosure to the child of his/her HIV status

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When to Start ARV Children Age <18 Months

• If CD4 assay available:
• Positive viral test (proven infection):
• New WHO Pediatric stage 4, regardless of CD4%
• New WHO Pediatric stage 3, use CD4 <20% to assist decision-making
• New WHO Pediatric stage 1 or 2 only if CD4 <20%
• Infants with proven antigenic test for HIV
• Now any child proven positive should be on HAART

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When to Start ARV Children Age >18 Months

• If CD4 assay available:
• HIV antibody seropositive (proven infection):
• New WHO Pediatric stage 4, regardless of CD4%
• New WHO Pediatric stage 3, consider using CD4 <15% to assist decision-making
• WHO Pediatric stage 1 or 2 only if CD4 <15%
• Now any child proven positive should be on HAART

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WHO Recommended First-line ARV Regimen for Children

First-Line Regimen

• d4T or ZDV
• Plus
• 3TC
• Plus
• NVP or EFZ

NNRTI choice:

• If age <3 yrs or wt <10 kg: NVP
• If age >3 yrs or wt >10 kg: NVP or EFV

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Special Considerations for Pediatrics

• Dosing must be adjusted as child grows
• Formulation problems:
• Some liquid formulations (ZDV, 3TC, NVP) are good, but
• d4T liquid needs refrigeration; it may also be large volume (only 1 mg/ml)
• ddI suspension may be difficult for the child to take not palatable
• LPV/r (Kaletra) liquid tastes very bad

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Special Considerations for Pediatrics cont.

• Powder (NFV) is difficult to take in large amounts Crush 250 mg tablet, suspend in warm water, give to child or mix in formula.

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• If child has TB and needs rifampicin, EFV is NNRTI of choice or consider Rifabutin

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• If <3 yrs, ZDV/3TC/ABC may be considered.

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• SQV/r can be considered for older child (>25 kg).

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Clinical Assessment of Children on ARV Therapy

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• Clinical monitoring should also include:
• Nutrition and nutritional status
• Weight and height growth
• Head circumference in younger children
• Developmental milestones
• Neurologic symptoms

Clinical Treatment Failure

• Should not be considered until the child has been on ARV’s for 4-6 months.
• Always look for another explanation
• Always MEASURE CD4+
• If percentage is not falling, another explanation is likely
• Always MEASURE viral load before switching
• If it is low, another explanation is likely
• If it is low, switching may not improve things

Definition of Clinical Treatment Failure

• WHO Criteria:
• Lack of, or decline in, growth among children with initial growth response to ARV

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• Loss of neurodevelopmental milestones or onset of encephalopathy
• New OI or malignancy

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• Recurrence of prior OI (e.g., oral candida refractory to treatment)

Clinical Treatment Failure cont.

• Other explanations rather than Treatment failure
• Failure of weight gain
• Inadequate food supply
• GI intolerance to ARV drugs, poor appetite
• Failure of linear growth
• Very common in HIV infection, even if treated adequately
• New OI
• Immune Reconstitution Syndrome
• Poor adherence to OI prophylaxis (e.g. cotrimoxazole)
• Loss of milestones or onset of “encephalopathy”
• Psychological deprivation

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Immunological Treatment Failure

• WHO Criteria:
• 1) Return of CD4 cell percentage (or for children > 6 years of age, of absolute CD4 cell count) to pretherapy baseline or below, in absence of other concurrent infection explaining transient CD4 decrease. Or

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• 2) ≥ 50% fall from peak level on therapy of CD4 cell percentage (or for children >6 years of age, of absolute CD4 cell count) in absence of other concurrent infection explaining transient CD4 decrease.

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Immune Reconstitution Syndrome (IRS)

• ...is not Treatment failure

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IRS: Definition

• Paradoxical worsening of clinical or laboratory parameters despite improved HIV markers (increased CD4 count or reduced viral load)

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IRS: Common Pathogens

• Mycobacteria:
• TB and MAC.
• BCG in children

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• Fungal: Cryptococcosis, PCP, Histoplasma

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• Viral: CMV, HZV

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IRS Management

• Avoid interruption of ARV

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• Treat with antimicrobials if new infection is suspected, continue previous therapy.

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• Anti-inflammatory medications
• Non-steroidal anti-inflammatories
• Corticosteroids: No definitive protocol though clinicians often use 1mg/kg/day of prednisolon with a taper over several weeks.

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Antiretrovirus Combinations to Avoid

• AZT + d4T

.Antagonistic and additive side effect of anaemia

• ddI + d4T

.More mitochondrial toxicity, particularly in adults

.May be permissible in children

• Tenofovir + ddI

.Reduced efficacy

• EFV + NVP

.Same action, no additional activity

.Additive toxicity

Opportunistic Infections

• The major cause of death in children with HIV infection are opportunistic infections, these include:

Pneumocystis jiroveci, Candidiasis

Mycobacteria tuberculosis

Mycobacterial avium complex

Toxoplasma gondii, Cryptosporidia

Cytomegalovirus, Herpes simplex

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Opportunistic Infections (contd)

Pneumocystis jiroveci pneumonia

• A protozoan spread by water droplet.
• Peak incidence in infants is between the age of 3 and 6 months.
• Common presentation is acute onset of tachypnoea, fever, cough and hypoxaemia

Opportunistic Infections (contd)

Candidiasis

• Punctate or diffuse white plaques on the oral or oropharyngeal mucosa.
• Occurs in healthy bottle-fed infants or children who have been on prolonged antibiotics therapy.
• In HIV- infected children, it tends to be more florid and responds poorly to usual treatment which are gentian violet or nystatin.
• Other treatment include ketoconazole and fluconazole.

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Opportunistic Infections (contd)

Tuberculosis

HIV and tuberculosis often co-exist.

• Definitive diagnosis of Tb may be difficult.
• Tuberculosis skin test may be negative.
• INH prophylaxis is recommended for TB exposed
• Treatment is by the usual combination chemotherapy
• Thiacetazone should not be used because it could cause Steven – Johnson’s Syndrome.
• Rifampicin can affect pharmacokinetics of some ARV medications eg NVP

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Pediatric Cotrimoxazole Prophylaxis

recommended for:

• All HIV-exposed infants (all infants whose mothers are known to have HIV) from 4-6 weeks of age until the child is no longer breast feeding and is determined to be uninfected.
• All HIV –infected infants <12 months.
• All HIV- infected infants and children with:

- clinical features suggestive of HIV/AIDS and/or

- prior Pneumocystis jiroveci pneumonia and/ or

- evidence of immune dysfunction including:

• CD4 percent < 15% and /or
• In children 1-5 years, total CD4 < 500 cells
• In children over 6 years, total CD4 < 200 cells

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Nutrition in HIV Children

• Adequate counseling on infant feeding to enable the mother make an informed choice as to the method of feeding.
• WHO recommends replacement feeds, if it is affordable, feasible, acceptable, sustainable and safe (AFASS Creteria) If not, exclusive breastfeeding for the first 6 months, with abrupt weaning to avoid mixed feeding.
• Now mothers to continue BF if on HAART with adequate viral suppression

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Nutrition in HIV Children cont.

• Micronutrients play critical roles in cellular differentiation, enzymatic process, immune system reactions and other body functions. Hence they are critical in the fight against infections pathogens
• Complementary food should be high calorie and rich in micronutrient.

Psychological Support

• Consists of assessment of family support and coping mechanism.
• Counseling to assist the family to cope with the social implications of the illness
• Particularly important where the mother or father is also ill with HIV/AIDS and the child faces the possibility of being orphaned

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PMTCT OF HIV

Factors increases the risk of HIV infections in women.

• Immaturity of the genital tract
• Cervical ectopy
• STIs
• Poor nutritional status.
• Others are poverty, lack of information, abuse, violence and coercion by men.

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Comprehensive Approach to Prevention of HIV Infection in Infants and Young children.� Consists of Four elements.

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1. Primary prevention

• Safe & responsible sexual behaviour & partners.
• A=>Abstinence
• B=> Be faithful to partners
• C=> Condom use
• D=> Delaying onset of sexual activity
• BCC=> Behaviour change communication = individuals modify their behaviours.
• Supports from Organizations, providing condoms. Early diagnosis & treatment of STIs.
• VCT to be widely available and assessable

2. Prevention of unintended pregnancies among HIV +ve women

• Provision of comprehensive Information and Education about HIV /AIDs, the risks associated with child bearing.
• Providing good quality and user-friendly family planning services.
• Promoting condom either alone or in combination with a more effective contraception.
• Information- protection = family planning counseling.

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3. Prevention of HIV transmission from women infected with HIV to their infants

• A= HIV counseling /testing (HCT)=> Identify women infected with HIV, if not infected, to remain uninfected.
• B= Antiretroviral treatment and prophylaxis =>Reduce maternal viral load.
• C= Safer delivery practices=> To reduce infant exposure to the virus during labour and delivery.

1.Modification of routine obstetric practices for all women => Accessibility and Affordability of ANC.

All medical persons involved in care management of pregnant women should be trained in VCT.

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2. Specific modification of obst care for HIV +ve women-Should be given optimal care for safe delivery with focus on HIV related symptoms and illnesses.

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• -Invasive procedures should be avoided.

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D. Safer Infant –feeding practices Infant-feeding counseling for safer feeding practices.

• Breast-feeding is an import. route of HIV transmission, counseling about this risk is of great importance.
• For unknown status or HIV –ve EBF best option.
• In PMTCT, challenges is to strengthen and support mothers and partners to make breast milk substitute acceptable, feasible, affordable, sustainable and safe(AFASS).
• Should be well informed about the various feeding option

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4. Provision of treatment, care, and support to women infected with HIV, their infants and their family

• HIV-related treatment, care, an support services for women,include the following:
• Prevention and treatment of opportunistic infections
• ARV treatment
• Treatment of symptoms
• Palliative care
• Nutritional support
• Reproductive health care, including family planning, cervical screening and counseling
• Psychosocial and community support

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Care and support of the infant and child who are HIV- exposed

• Nutritional support for the infant or child who is HIV-exposed, bcos, they are at risk of Malnutrition, illnesses, no protective benefits of breast-feeding( if not breast-feeding)
• Support the mother’s infant-feeding choice
• Provide education on hydration and early reporting of diarrhoea.
• Monitor for growth and development, during the 1^st 2 yrs, including immunization, HIV testing.
• Monitor for signs of infection that can alter feeding patterns.

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Thank you for listening!�