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The document provides an outline on paediatric HIV/AIDS covering epidemiology, biology, pathogenesis, natural history, clinical manifestations, and treatment. It notes that children account for 5-10% of global HIV cases, with over 90% in sub-Saharan Africa. HIV targets and destroys CD4+ cells, causing progressive immunosuppression and increased risk of opportunistic infections. Clinical stages range from asymptomatic to severe disease and death, with faster progression in children than adults.

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PAEDIATRIC HIV/AIDS
OUTLINE • INTRODUCTION • EPIDEMIOLOGY • BIOLOGICAL STRUCTURE • MOLECULAR EPIDEMIL0GY • PATHOGENESIS • NATURAL HISTORY • RISK OF PROGRESSION • TRANSMISSION • CLINICAL MANIFESTATIONS • STAGING OF DISEASE • LABORATORY DIAGNOSIS • THERAPY • CLASSES OF DRUGS USED • PREVENTION • FOLLOW UP
INTRODUCTION • HIV and AIDS is a major cause of infant and childhood morbidity and mortality in Africa • In children <5 years it accounts for 7.7% of mortality worldwide • In 2007, AIDS accounted for a rise of >19% of infant and a 36% rise in under 5 mortality rates • The high burden of paediatric HIV disease in Africa is due to: – high birth rate – high rates of mother-to-child transmission • The fast rate of progression of HIV infection in children is partly responsible for high morbidity and mortality
EPIDEMIOLOGY • HIV infection, first identified in 1981 and first case in Nigeria was in 1986 • According to UNAIDS, in 2017, 1.8million children <15years were living with HIV globally • Children less than 15years account for: – 5% of Persons Living with HIV/AIDS (PLWHA) – 10% of new infections and 9% of AIDS related death. – With introduction of ARVs, survival of paediatric patients has largely increased. • In 2017, up to 940,000 children < 15years received ART showing an increase from 640,000 in 2012.
EPIDEMIOLOGY • The World Health organisation (WHO) estimation in 2013 stated that –32million children younger than 15yrs of age worldwide were living with HIV-1 infection, –90% were from sub-Saharan Africa. In the same year, about 199,000 children were newly infected
EPIDEMIOLOGY • In Africa, almost 90 • the prevalence of HIV infection in children aged 0-14years ranges from • 500 children in Tunisia, • 220,000 children in Nigeria • to 280,000 children in South Africa. • Newly infected children ranges from 100 children in Egypt, Algeria, Morocco and Mauritania to 36,000 children in Nigeria
EPIDEMIOLOGY National HIV prevalence has increased exponentially from 1.8% in 1991 peaking at 5.8% in 2001 and progressively declining since then to the current figure of 3.1% in 2014 (ANC Survey Report). • Nigeria has the second highest burden of HIV globally with 3.4 million PLHIV as at 2014. • Over 2 million Nigerian children are AIDS ORPHANS • In 2019, The state to state variation in HIV prevalence in the country ranged from 0.3% in Katsina State to 5.5% in Akwa Ibom state • Based on geopolitical zone: • SS 3.1% NC 2.1% • SE 1.9% SW 1.2% • NE 1.1% NW 0.6%
HIV infection is acquired in children through: • Mother-to-child (or vertical) route – Accounts for >90% of transmission in children – Can occur in-utero(5-10%), at delivery(5-20%) or during breastfeeding – Prolonged breastfeeding and mixed feeding are key factors responsible for higher transmission rates in Africa – Without intervention overall transmission rate is 15-45%. • Sexual contact – forced or consensual • Blood and blood product transfusion • Use of contaminated sharps for scarification, tattoos, and surgical procedures Modes of HIV Transmission
In Nigeria, it was estimated that ONE SERO-EXPOSED INFANT is born every 5 minutes but this is declining with universal ARVs for pregnant women
• The Lenti-virus group of Retroviruses • Retroviruses contain reverse transcriptase enzyme used for synthesis of pro-viral DNA from viral RNA • The mature genome of HIV is diploid with 2 identical positive sense single-stranded RNA copies • The envelope is made of 2 glycoproteins: – Gp120 and Gp41 for HIV-1 – Gp105 and Gp36 for HIV-2. • Antibodies to these 2 sets of proteins do not usually cross react – this differentiates serologic responses of HIV-1 and HIV-2. Biology and Structure of HIV
Biology and Structure of HIV cont… • Has an outer double lipid membrane (envelope) lined by matrix protein (p17) • Surface glycoprotein gp120 and trans-membrane gp41 • The gp spikes surround the cone-shaped protein core (p24) • Core protein contains genetic material (RNA) and enzymes.
Viral enzymes • Reverse Transcriptase (RT), converts viral RNA into a double stranded (DNA) • Integrase cause integration of double stranded DNA into host’s DNA • Protease splits generated macro-proteins into smaller viral proteins which get incorporated into new viral particles. Biology and Structure of HIV cont…
There are two types of HIV: • HIV-1 – Main cause of the worldwide pandemic • HIV-2 – Mainly found in West Africa, Mozambique and Angola – Causes a similar but less severe illness to HIV-1 – Less efficient transmission, rarely cause MTCT – Less aggressive with slower disease progression. Molecular Epidemiology of HIV
• HIV-1 Subtype A is commonly found in Central, West and East Africa • HIV-1 Subtype B: – Prevalent in Western Europe and North America – Most knowledge about HIV-1 was from studies of subtype B. • All HIV-1 subtypes have been found in Africa • Recombinant forms of HIV exist • A/G recombinant is most predominant in West Africa. Molecular Epidemiology of HIV….cont….
HIV is a retrovirus with a simple cellular structure made of: Two important membrane glycoproteins responsible for its antigenic identity: − HIV-1 (Gp 120 and Gp 41) − HIV-2 (Gp 105 and Gp36). − Three important enzymes responsible for entry into host cell, incorporation of its RNA into host DNA, replication and assembly of new viral particles − Reverse transcriptase − Integrase − Protease. SUMMARY OF MOLECULAR EPIDEMIOLOGY OF HIV
• HIV-1 primarily targets CD4+ molecule on T-helper • Other target cells include macrophages and glial cells • The virus uses its gp120 and gp41 to bind to CD4+ receptors and chemokine co-receptors (CCR5 & CXCR4)on the host cell membrane • This permits entry of contents of the viral particle into host cell cytoplasm • The viral enzymes and RNA are then released to begin the process of replication while the viral envelope is shed. PATHOGENESIS
• HIV RNA is transcribed by reverse transcriptase to a double stranded DNA • It is then integrated into host DNA by integrase and continues to reside there indefinitely as a provirus • On activation, the proviral DNA is transcribed into mRNA by host enzyme RNA polymerase to begin replication • The mRNA is then translated into viral proteins which assemble and “bud-off” from the host cell membrane. PATHOGENESIS cont….
PATHOGENESIS cont…. • CD4+ cells play vital roles in humoral and cell-mediated immunity such as: – Maturation of B-cells to plasma cells to make antibodies – Induction of natural killer (NK) cells to destroy tumour cells – Activation of macrophages for efficient phagocytosis – Suppression of other T and B-cells by CD8+ suppressor T-cells – Lysis of infected cells by cytotoxic CD8+ T-cells. • Continuous CD4+ loss lead to progressive immunosuppression and increase the incidence of opportunistic infections(Ois).
PATHOGENESIS cont…. • Reduced activity of NK cells leads to increased incidence of tumours • Continuous viral replication leads to progressive CD4+ cell destruction which in turn results in: – More CD4+ cell production – Continuous infection of surviving CD4+ cells • CD4+ cells become eventually overwhelmed and the immune system fails to cope with opportunistic infections, leading to progression to AIDS.
KEY POINTS OF PATHOLOGY • HIV-1 targets CD4+ receptor and chemokine co- receptors on T-helper lymphocytes to gain entry into human host cells • Destruction of CD4+ cells causes progressive immunosuppression and increased incidence of OIs • The CD4+ cells are eventually overwhelmed and the immune system fails, leading to disease progression to AIDS.
NATURAL HISTORY OF HIV Adults and Children older than 5 years • A typical HIV infection can be divided into three stages: primary infection, asymptomatic infection, and symptomatic infection including AIDS. • Following primary HIV infection, the CD4+ cell count decreases and the HIV RNA rises significantly. • With sufficient exposure to viral antigens, cytotoxic T-lymphocyte responses are generated and the HIV viral load typically declines to an equilibrium known as a virologic “set-point,” within 6 to 12 months of infection. • Once this viral set-point is reached, the CD4+ cell count may rebound again marginally, although it does not often return to baseline values. • Concurrent with these events are clinical manifestations of acute HIV infection in 30% to 60% of individuals.
NATURAL HISTORY OF HIV contd • Absolute CD4+ count varies with age and is generally higher in healthy younger children • CD4+ counts slowly decline to adult levels by 6 years • CD4+% does not change with age; thus it is the preferred parameter for monitoring disease progression in children ≤5 years • Risk of AIDS or death rises as CD4+% falls to <25 in infants, to <20 from 1-3 years and to <15 thereafter • Disease progression is faster and prognosis is poorer in infants than in older children.
Natural History of HIV cont ….. • Viral Load(VL) trends in perinatally infected infants differs from that in adults and children >5 years: • In Infants: – VL levels are low at birth – Increases to levels >100,000 to millions of copies/ml by 2 months of age – Remain at same level throughout first year of life – Decline slowly over the next few years to a “set point”.
Viral Load and T-lymphocytes Dynamics in HIV Infected Adults and Children
There are 3 categories of disease progression: Category 1 (25 – 30%): • Disease acquired in-utero or perinatally • Rapid disease progression and death within 1st year of life. Category 2 (50 – 60%): • Develop symptoms early in life • Deteriorate and die by 3 to 5 years. Category 3 (5 – 25%): • Long-term survivors: may live beyond 8 years of age. HIV Disease Progression in African Children
• Infant factors: – Infecting viral dose (maternal VL) – Infection before 4 months of life – Infant peak viraemia – Rapid decline in CD4+ – Clinical AIDS – p24 antigenaemia. • Maternal factors: – VL at time of delivery – CD4+ count (<200) – Rapidly progressive disease – Maternal death. Factors Predicting Disease Progression
MATERNAL RISK FACORS • High VL • STI • New infection in pregnancy • Advanced disease • APH • PROM • Prolonged labour • Invasive delivery procedures • Instrumental deliveries eg forceps, vacuum • Episiotomies/genital lacerations • Breast conditions
Fetal risk factors • Oral lesions in breast feeding infant • Mixed infant feeding • Prematurity • First of twins delivered per vaginam
CLINICAL MANIFESTATIONS
• Although clinical features are used to make diagnosis of HIV infection, very often they overlap with features of other diseases. • The clinical manifestations of HIV disease in children include: • Fever • Persistent generalized lymphadenopathy • Respiratory illnesses: pneumonias, pharyngo- tonsillitis, otitis media, mastoiditis • Malnutrition • Gastrointestinal conditions: diarrhoea, vomiting, parotid enlargement.
• SOME CLINICAL MANIFESTATIONS ARE VERY SPECIFIC TO HIV INFECTION EG:
• Pneumocystis pneumonia • Oesophageal candidiasis • Extra-pulmonary cryptococcosis • Invasive salmonella infection (especially non-typhoidal) • Herpes Zoster (shingles) dermatomal • Kaposi’s Sarcoma • Lymphoma • Progressive multifocal leuco-encephalopathy. • Lymphoid interstitial pneumonitis
MANIFESTATIONS COMMON IN HIV INFECTED CHILDREN BUT NOT COMMON IN UN-INFECTED CHILDREN
• Severe/recurrent bacterial infections • Persistent or recurrent oral thrush • Bilateral painless parotid enlargement • Persistent generalized lymphadenopathy - PGL (non- inguinal) • Hepato-splenomegaly (in non-malaria area) • Persistent &/or recurrent fever • Neuro-developmental dysfunction • Herpes Zoster, single dermatome • Persistent generalized dermatitis unresponsive to treatment.
• FEATURES COMMON IN BOTH INFECTED AND UN-INFECTED CHILDREN
• Chronic recurrent otitis media with ear discharge • Persistent or recurrent diarrhoea • Severe pneumonia • Tuberculosis • Bronchiectasis • Failure to thrive • Marasmus. National Paediatric ART Training Slides Unit 3 14
Classification of HIV-associated Clinical Disease WHO Clinical Stage Asymptomatic 1 Mild 2 Advanced 3 Severe 4 WHO staging for HIV infection and disease in infants, children and adolescents
IMMUNUNOLOGICAL CLASSIFICATION FOR HIV INFECTED CHILDREN Immunological category CD4 count (cells/μL) No evidence of Immunosuppression ≥500 Evidence of Immunosuppression 200-499 Severe Immunosuppression <200
WHO CLINICAL stage 1 • Asymptomatic • Persistent generalized lymphadenopathy.
WHO CLINICAL stage 11(Mild disease) • Unexplained persistent hepatosplenomegaly • Papular pruritic eruptions • Extensive wart virus infection • Extensive molluscum contagiosum • Recurrent oral ulcerations • Unexplained persistent parotid enlargement • Linear gingival erythema • Herpes zoster • Recurrent/chronic upper respiratory infection (otitis media, sinusitis, tonsillitis) • Fungal nail infections.
WHO CLINICAL stage 111(Advanced Disease) • Moderate malnutrition unresponsive to standard therapy • Persistent diarrhoea (≥14 days) • Persistent fever (>37.5 oC, intermittent or constant, exceeding 1 month • Persistent oral candidiasis (after 6 weeks of age) • Oral hairy leukoplakia • Necrotizing ulcerative gingivitis/peri-odontitis.
WHO CLINICAL stage 111(Advanced Disease) contd • Lymph node TB • Pulmonary TB • Severe recurrent bacterial pneumonia • Lymphoid interstitial pneumonia • Chronic HIV-associated lung disease e.g. bronchiectasis • Hb level of <8g/dl • Neutrophil count of <0.5 x 109/L • Platelets count of <50 x 109/L.
WHO CLINICAL stage 1V( Very Severe Disease) • Severe malnutrition not responsive to therapy • Pneumocystis pneumonia • Recurrent/severe bacterial infection (excluding pneumonia) e.g. – Empyema – Pyomyositis – Bone/joint infections – Meningitis. • Chronic herpes simplex infection (for >1 month) • Extra-pulmonary TB.
WHO CLINICAL stage 1V(Severe Disease) contd… • Kaposi sarcoma • Candidiasis (oesophageal, tracheo-bronchial or pulmonary • CNS Toxoplasmosis after neonatal age • HIV encephalopathy • CMV retinitis or infection of other organs after neonatal age • Extra-pulmonary cryptococcosis.
WHO CLINICAL stage 1V(Severe Disease) contd… • Disseminated fungal infections – Histoplasmosis – Coccidiodomycosis. • Chronic cryptococcosis • Disseminated atypical mycobacterial infection • Cerebral B cell Non-Hodgkins lymphoma • Progressive multifocal leukoencephalopathy • HIV-associated cardiomyopathy.
DIAGNOSIS • Diagnosis may be: – Clinical - based on signs and symptoms, or – Clinical supported by laboratory findings. • HIV and AIDS should be suspected in children with suggestive clinical features or HIV-associated conditions.
• All HIV-exposed infants, the sexually assaulted and those exposed to potentially infectious body fluids should be evaluated • PITC • If infection is confirmed, clinical disease staging should be determined using the WHO staging system.
LABORATORY DIAGNOSIS • There are 2 broad categories of tests: Antibody and virology • ANTIBODY detection (reliable in children above 18 months of age) − HIV Rapid test: (DRT) simple and easy to perform − ELISA: needs more equipment, time, technical skills. − Western blot: gold standard but expensive and produce indeterminate results.
VIROLOGY TESTS • Most useful in children − DNA PCR DBS sample − RNA PCR (plasma viral load): monitors disease progression and response to treatment − P24 Ag: Very specific for detection of core Ag during early stage of infection (window period); negative result does not rule out infection − Viral cultures: highly sensitive, very specific but time consuming, expensive. Only used for research purposes
• Antibody tests are unreliable for HIV diagnosis in children <18 months, but DNA-PCR is diagnostic • All exposed babies who are breastfeeding should get 2 DNA PCR tests − If initial DNA-PCR is negative, testing should be repeated 12 weeks after cessation of breastfeeding
• irrespective of method of feeding • Antibody tests are reliable for children >18 months except during window period, thus repeat test after 3 months • DNA/RNA PCR could be used to resolve doubtful results
THERAPY • ANTI RETROVIRAL THERAPY(ART) IS LIFE-LONG • The major goals of ART in children are to: − Stop and reverse progression of disease − Improve quality of life − Promote or restore normal growth and development − Achieve optimal response with minimal toxicity
ELIGIBILITY FOR ART • All confirmed cases should be initiated on ART but preference is given to those: • Aged ≤ two years • CLINICAL STAGING---stages 3 and 4 • IMMUNOLOGICAL STAGING---depending on age and clinical staging
• ART should be initiated in all children with HIV, regardless of WHO clinical stage, or at any CD4 +cell count. • As a priority, ART should be initiated in the following situations – All children < 2 years of age – All children younger than 5 years of age with WHO clinical stage 3 or 4 disease or CD4+ cell count <750 cells/mm3 or CD4+ percentage <25% – All children 5 years and older with WHO HIV clinical stage 3 or 4 disease or CD4+ cell count <350 cells/mm3 – ART should be initiated in all adolescents with severe or advanced HIV clinical disease (WHO clinical stage 3 or 4) and a CD4 + cell count of 350 cells/mm3.
• YET TO BE CONFIRMED, <18 MONTHS, ANTIBODY POSITIVE, CLINICAL STAGE 3 or 4, commence therapy while awaiting confirmation
PRE ART(HAART) • Detailed history • Clinical examination • CD4/CD4% • TB SCREENING • BASELINE TESTS
HAART • NOT LESS THAN 3 DRUGS FROM AT LEAST 2 CLASSES
ANTI-RETROVIRAL DRUG CLASSES APPROVED ARV DRUGS Nucleoside Reverse Transcriptase Inhibitors (NRTIs)  Zidovudine (ZDV, AZT)*  Lamivudine (3TC)*  Stavudine (d4T)*  Abacavir (ABC)*  Didanosine (ddI) *  Zalcitabine (ddC)  Emtricitabine (FTC)* Nucleotide Reverse Transcriptase Inhibitors (NRTIs) Tenofovir (Disoproxil Fumarate {TDF}) Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)  Nevirapine (NVP)*  Efavirenz (EFV)*  Delavirdine (DLV)  Etravirine (ETV) * Fusion inhibitors  Enfuvirtide (T-20)* Protease inhibitors (PIs)  Lopinavir-ritonavir (LPV/r)*  Ritonavir (RTV) {as pharmaco-enhancer}*  Nelfinavir (NFV)*  Saquinavir (SQV)  Amprenavir (APV)*  Indinavir (IDV)  Atazanavir (AZV)*  Tipranavir (TPV)  Darunavir* (DRV)  Fos-amprenavir* (FPV) CCR5 inhibitor  Maraviroc Integrase Inhibitors  Raltegravir (RAL), Dolutegravir (DTG), Elvitegravir(EVG)
THE WHO RECOMMENDATION Age Group Preferred 1st line regimen Alternative 1st line regimens Special situations Neonates AZT + 3TC + RAL  AZT + 3TC + NVP  AZT + 3TC + LPV/r Children ABC + 3TC+ DTG  ABC + 3TC +LPV  ABC + 3TC +RAL  ABC + 3TC + EFV (or NVP)  AZT + 3TC + EFV (or NVP)  AZT + 3TC + LPV/r (or RAL) Adolescent  TDF + 3TC (or FTC) + DTG  TDF + 3TC (or FTC) + EFV 600mg  TDF + 3TC (or FTC) + EFV 600mg  TDF + 3TC (or FTC) + EFV 400mg  TDF + 3TC(or FTC) + EFV 400mg  TDF + 3TC (or FTC) + ATV/rb  AZT + 3TC + EFV 600mg  TDF + 3TC (or FTC) + PI/r  AZT + 3TC + EFV 600mg  TDF + 3TC (or FTC) + RAL
• Effective ART results in – recovery of the immune functions with a progressive increase in CD4+ cell count at a rate of 50 to 100 cells/μl /year. – Reduced occurrence of morbid conditions – Reduced opportunistic infections – Improved quality of life – Promotion and restoration of normal growth and development. – Reduction of HIV transmission in communities
• NNRTIs Stop viral replication by binding to reverse transcriptase preventing the transcription of HIV RNA to DNA • NRTIs Incorporate into viral DNA to stop replication and form incomplete viral DNA – cannot create a new virus • NtRTIs Act at the same stage of HIV life cycle as NRTIs, but do not require phosphorylation for anti-HIV activity. Classes and modes of action of ARVs
• Protease inhibitors (PIs) act at the last stage of HIV cycle – Prevent assembly and release of HIV particles from infected CD4 cells • Entry (fusion) inhibitors prevent HIV from infecting CD4 T cells • Integrase inhibitors prevent insertion of HIV DNA template into host DNA – Prevents viral replication • Chemokine receptor inhibitors prevent attachment of HIV surface antigens to CCR5 or CCX4 receptors. Classes and modes of action of ARVs cont…
HIV Integrase Inhibitors • HIV Integrase Inhibitors: Also known as Integrase Strand Transfer Inhibitors (INSTI). These inhibit DNA strand transfer into host- cell genome and thus prevent viral integration. Integrase Inhibitors do not confer resistance to other ART classes. Examples include: Dolutegravir (DTG), Elvitegravir(EVG), Raltegravir (RAL).
HIV LIFE-CYCLE/MODE OF ACTION OF ARVs
FIXED DOSE COMBINATIONS(FDC) • AZT+3TC±NPV • ABC+3TC • LPV/r • TDF/3TC/DTG • TDF/3TC/EFV
AZT/3TC 60/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150 1 1 AZT/3TC/NVP 60/30/50 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150/200 1 1 ABC/AZT/3TC 60/50/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/300/150 1 1 ABC/3TC 60/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150 1 1 d4T/3TC 6/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 30/150 1 1 d4T/3TC/NVP 6/30/50 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150/200 1 1 d4T/3TC 12/60 0.5 0.5 1 0.5 1 1 1.5 1 1.5 1.5 60/150 1 1 d4T/3TC/NVP 12/60/100 0.5 0.5 1 0.5 1 1 1.5 1 1.5 1.5 60/150/200 1 1 LPV/rb 100/25 NR NR 2 1 2 2 2 2 2 2 100/25 3 3 Drug Strength of Paediatric tab (mg) Children 6 weeks and above Strength of Adult tab (mg) No. of tabs by weight band No. of tabs by Kg weight-band b. d. 3-5.9 6-9.9 10-13.9 14-19.9 20-24.9 25-34.5 Kg am Pm am pm am pm Am pm am pm am pm
• Adverse events may vary from mild to severe or life- threatening • Mild toxicities • Moderate • Severe toxicities may require substitution with a drug in the same class but with different toxicity profile • Life-threatening toxicity requires discontinuation of all ARVs and the initiation of supportive therapy. ART toxicity profile cont….. National Paediatric ART Training Slides Unit 6
ADR • AZT anaemia PCV must not be <27% • NPV Hypersensitivity reaction, Stevens- Johnson syndrome • EFV nightmares, psychosis • ABC Severe hypersensitivity reaction. Should carry notification card • TDF Drug rash, potential renal toxicity, potential decrease in bone density. Not for children less than 8 years or with existing renal damage. • ABC Hypersensitivity reactions • Read up others
Special considerations • Substitution DTG for LPV/r for children with wt of 20kg+ ABC for TDF in children younger than 8 years • Switch to 2nd line drugs • Salvage ---5 ARVs, 2 must be protease inhibitors(PIs) • Suspension • stop
Routine monitoring on ART: – Every 2 weeks for the first month after starting therapy – Monthly for 6 months, then every 3 months thereafter. Follow-up visit activities: – Anthropometry (plot chart) and developmental check – Physical exam (pallor, jaundice, mouth, skin, lymph nodes, chest, abdomen) – Check immunizations, assess nutrition and conduct psychosocial assessment – Checking for adverse ARV effects – Review dosages for every 10% change in body weight. Follow-up/Monitoring schedule
Pre- Treatment (Baseline) Wk 2 Monthly x 6 Every 3 mo. thereafter Every 6 mo. thereafter 1 2 3 4 5 6 Physical Exam X X X X X X X X X Adherence Counselling X X X X X X X X X Confirm HIV status X HIV-1 RNA (VL) * X X X CD4+ X X X X FBC X X X X E & U, Cr* X X LFT X X** X X X Random BS* X Serum lipids* X Amylase* X Urinalysis X X X X X X X X Chest X-ray* X *As clinically indicated, thereafter ** To be done for children starting on NVP Monitoring schedule for children on ARV therapy
PREVENTION
The 4-pronged approach to PMTCT ! "#$ % & ' () *+#, $ - ' ' () - . "$ /) $ 01 ! 2! $ $ N IC A L R EP O R T artment of Public Health AIDS/STI Control Programme onal HIV Sero-prevalence Sentinel Survey MINISTRY OF HEALTH CAL REPORT 2010 National HIV Sero-prevalence Sentinel Survey Among Pregnant Women Attending Antenatal Clinics in Nigeria T EC H N IC A L R E Department of Public Hea National AIDS/STI Control Pro 2010 National HIV Sero-pre Sentinel Survey FEDERAL MINISTRY OF 1 Pr imar y HIV Prevention $ 2 Prevention of Unintended Pregnancies in HIV +ve Women 3 Prevention of Mother-To- Child Transmission 4 Provision of Care and Suppor t for HIV infected Children, their Mothers and Families
Care for the HIV exposed neonate • Have their mouths and nostrils wiped with gauze after delivery of the head. • Be handled with latex gloves until maternal blood and secretions are washed off. • Have the cord clamped immediately after baby is delivered and avoid milking the cord. • Have the cord cut under cover of a lightly wrapped gauze swab to avoid blood spurting. • Be kept warm.
• Be suctioned if indicated using a mechanical/electrical suction unit at a pressure below 100mmhg or bulb suction. Mouth operated suction is contraindicated. • Be cleaned with warm chlorhexidine solution or wiped dry with a towel or surgical cloth to remove maternal body fluids. • Place the baby on the mother’s chest for skin to skin contact soon after delivery. • In this position the baby will latch on to one of the mother’s breast to initiate feeding unless the mother opted for alternative feeding method. • Have vitamin k administered, ensuring injection safety
Package of services for HIV exposed children • ARV prophylaxis • Routine immunization and growth monitoring and support • Cotrimoxazole prophylaxis starting at 6 weeks • HIV diagnostic testing using DBS for DNA PCR at 6 to 8 weeks of age and 12 weeks after breastfeeding has ended. • Ongoing infant feeding counselling and support
• Screening and management of tuberculosis • Prevention and treatment of malaria • Nutritional care and support • Psychosocial care and support • Antiretroviral therapy for all HIV infected children • Symptom management and palliative care if needed
ARV Prophylaxis in neonate • All HIV exposed infants should receive ARV prophylaxis. Infants born to mothers with HIV who are at high risk of acquiring HIV should receive dual prophylaxis with AZT (twice daily) and NVP (once daily) for the first 6 weeks of life, whether they are breastfed or formula fed. • It is recommended that infants delivered to HIV positive mothers who are stable on ART should receive Nevirapine prophylaxis. Nevirapine prophylaxis is administered daily. These infants irrespective of the type of feeding should receive daily NVP from within 72 hours of birth to 6 weeks of age. • If infants are receiving replacement feeding, they should be given 4 to 6 weeks of infant prophylaxis with daily NVP (or twice-daily AZT).
• For babies with weight <2,500g (0-6weeks) – NVP 10mg or 1ml once daily – AZT 10mg or 1ml twice daily • For babies with weight ≥2, 500g(0-6weeks) – NVP 15mg or 1.5ml once daily – AZT 15mg or 1.5ml twice daily • 6 – 12weeks – NVP 20mg(2mls) once daily – AZT 20mg (2mls) twice daily • Breastfed infants who are at high risk of acquiring HIV should continue infant prophylaxis for an additional 6 weeks (total of 12 weeks of infant prophylaxis) using AZT (twice daily) and NVP (once daily).
Infant feeding in the context of HIV • It is recommended that mothers of HIV exposed infants breastfeed their babies exclusively for the first six (6) months of life. • Complementary feeds should be introduced at 6 months in addition to breast milk • Breastfeeding complemented by household foods should be continued till 12 months, after which child should be weaned off breast milk.
Immunizations for HIV Exposed Children • All HIV exposed children should be immunized as early as possible to protect them against vaccine- preventable diseases. • Children who have, or are suspected to have HIV infection but are not yet symptomatic should be given all appropriate vaccines. • Children with advanced and symptomatic HIV infection (CD4 < 200 or < 14%, or Stage 3 or 4 disease), should not be given live vaccines (BCG, varicella-zoster, OPV, measles and yellow fever vaccine). • HIV infected children should therefore be given the inactivated polio vaccine (intramuscular).
• Pre exposure Prophylaxis (PrEP) is the pre- emptive use of antiretroviral (ARV) drugs to reduce the probability of HIV negative individuals acquiring HIV infection especially persons who engage in high-risk activity. • It is recommended that PrEP should be offered only to the category of individuals listed below – 1. Serodiscordant couples – 2. Commercial sex workers – 3. Injecting drug users – 4. Individuals who engage in anal sex on a prolonged and regular basis
• Preferred daily oral dose regimen for PrEP is the combination of TDF+ FTC (Truvada) • The alternate regimen for PrEP is a daily dose of TDF. • These drugs are to be taken indefinitely until the individual no longer qualifies as high risk
• Post Exposure Prophylaxis (PEP) is the short- term use of ARV drugs to prevent HIV infection in persons accidentally exposed to a potential risk of acquiring HIV infection. • This applies usually to accidental exposure as seen in health workers or sexual assault victims especially in cases where the HIV status of the perpetrator cannot be readily determined.
In case of a needle stick injury • Do not squeeze or rub the injury site • Allow blood or secretion to flow freely • Wash exposed area immediately with soap and running water or antiseptic solutions • After a splash to the eye or any other mucous surface, irrigate/rinse the exposed area immediately with water (preferably running water) or normal saline • Report the exposure to a senior member of staff, supervisor or the PEP officer • If eligible, give antiretroviral drugs recommended for post exposure prophylaxis immediately possibly within 1 hour and at the latest within 72 hours of the exposure (persons presenting after 72 hours of the exposure should also be considered for PEP).
• PEP is continued for 28days or the source patient is known to be negative. • TDF + 3TC (or FTC) is recommended as the preferred backbone regimen for HIV post- exposure prophylaxis for adults and adolescents. • EFV is recommended as the preferred third drug for HIV post-exposure prophylaxis for adults and adolescents. However, where available, LPV/r, RAL, or DRV/r, can be considered as alternative options.
• In children <10 years AZT + 3TC is recommended as the preferred backbone regimen for HIV post exposure prophylaxis. • Alternative backbone regimen for this age category will include ABC + 3TC or TDF + 3TC (or FTC). EFV is recommended as the preferred third drug for HIV post-exposure prophylaxis for children younger than 10. • An age-appropriate alternative regimen can be identified among LPV/r ATV/r, RAL, DRV,.
Recommended Schedules of Investigations following HIV Exposure Period Recommended Investigations Baseline HIV, HBV, HCV screening, FBC , LFT, Renal function test 2 weeks Full blood count, Liver function test, Renal function test 6 weeks HIV screening 3 months HIV screening 6 months HIV screening
• As with all cases of sexual assault, it is important to arrange for continuous counselling and support for the victim. • Emergency contraception should also be considered.
Cotrimoxazole preventive therapy (CPT) • Cotrimoxazole preventive therapy (CPT) is a fixed-dose combination of two antimicrobial agents (sulfamethoxazole and trimethoprim) used for the prevention of some AIDS- associated opportunistic diseases (Pneumocystis jirovecii pneumonia [PCP] and toxoplasmosis) and the reduction of HIV- associated mortality in people with low CD4+ cell counts.
• Cotrimoxazole prophylaxis is recommended for infants, children and adolescents with HIV, irrespective of clinical and immune conditions. • Due to high prevalence of malaria and severe bacterial infections in Nigeria, cotrimoxazole prophylaxis should be continued until adulthood, irrespective of whether ART is provided. • Cotrimoxazole prophylaxis is recommended for HIV-exposed infants 6 weeks of age and should be continued until HIV infection has been excluded by an age-appropriate HIV test to establish final diagnosis after complete cessation of breastfeeding.
• In HIV positive individuals who have adverse drug reactions to cotrimoxazole, options for prophylaxis of PCP include dapsone, dapsone plus pyrimethamine plus leucovorin and atovaquone. • For those who will be started on dapsone, do a G6PD deficiency test. Dapsone should be avoided in individuals with G6PD deficiency.
DOSING OF CPT • For infants below 6 months or < 5 kg (Cotrimoxazole 120mg daily) • For children 6 months–5 years or 5-15 kg (Cotrimoxazole 240 mg daily) • For children 6–14 years old or 15–30 kg (Cotrimoxazole 480 mg daily) • For anyone over 14 years or >30 kgs (Cotrimoxazole 960 mg)
ISONIAZID PREVENTIVE TREATMENT OF TB Isoniazid Preventive Therapy (IPT) is the use of isoniazid to prevent the development of active TB disease in HIV positive individuals. • Paediatric recommendations: – Children living with HIV who have poor weight gain, fever or current cough contact history with a TB case may have TB and should be evaluated for TB and other conditions. If the evaluation shows no TB, they should be offered IPT regardless of their age .
• As part of a comprehensive package of HIV prevention and care Children living with HIV who are ≥ 12 months of age and who are unlikely to have active TB on symptom-based screening and have no contact with a TB case should receive six months of IPT (10 mg/kg/day) but not more than 300mg/day. • In children living with HIV who are < 12 months of age, only those who have contact with a TB case and who are evaluated for TB (using standard lab investigations) should receive six (6) months of IPT if the evaluation shows no TB disease. • All children living with HIV, after successful completion of treatment for TB, should receive IPT for an additional six months.

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MSL PAEDIATRIC HIV(2) COPY.pptx

  • 1.
  • 2.
    OUTLINE • INTRODUCTION • EPIDEMIOLOGY •BIOLOGICAL STRUCTURE • MOLECULAR EPIDEMIL0GY • PATHOGENESIS • NATURAL HISTORY • RISK OF PROGRESSION • TRANSMISSION • CLINICAL MANIFESTATIONS • STAGING OF DISEASE • LABORATORY DIAGNOSIS • THERAPY • CLASSES OF DRUGS USED • PREVENTION • FOLLOW UP
  • 3.
    INTRODUCTION • HIV andAIDS is a major cause of infant and childhood morbidity and mortality in Africa • In children <5 years it accounts for 7.7% of mortality worldwide • In 2007, AIDS accounted for a rise of >19% of infant and a 36% rise in under 5 mortality rates • The high burden of paediatric HIV disease in Africa is due to: – high birth rate – high rates of mother-to-child transmission • The fast rate of progression of HIV infection in children is partly responsible for high morbidity and mortality
  • 4.
    EPIDEMIOLOGY • HIV infection,first identified in 1981 and first case in Nigeria was in 1986 • According to UNAIDS, in 2017, 1.8million children <15years were living with HIV globally • Children less than 15years account for: – 5% of Persons Living with HIV/AIDS (PLWHA) – 10% of new infections and 9% of AIDS related death. – With introduction of ARVs, survival of paediatric patients has largely increased. • In 2017, up to 940,000 children < 15years received ART showing an increase from 640,000 in 2012.
  • 5.
    EPIDEMIOLOGY • The WorldHealth organisation (WHO) estimation in 2013 stated that –32million children younger than 15yrs of age worldwide were living with HIV-1 infection, –90% were from sub-Saharan Africa. In the same year, about 199,000 children were newly infected
  • 6.
    EPIDEMIOLOGY • In Africa,almost 90 • the prevalence of HIV infection in children aged 0-14years ranges from • 500 children in Tunisia, • 220,000 children in Nigeria • to 280,000 children in South Africa. • Newly infected children ranges from 100 children in Egypt, Algeria, Morocco and Mauritania to 36,000 children in Nigeria
  • 7.
    EPIDEMIOLOGY National HIV prevalencehas increased exponentially from 1.8% in 1991 peaking at 5.8% in 2001 and progressively declining since then to the current figure of 3.1% in 2014 (ANC Survey Report). • Nigeria has the second highest burden of HIV globally with 3.4 million PLHIV as at 2014. • Over 2 million Nigerian children are AIDS ORPHANS • In 2019, The state to state variation in HIV prevalence in the country ranged from 0.3% in Katsina State to 5.5% in Akwa Ibom state • Based on geopolitical zone: • SS 3.1% NC 2.1% • SE 1.9% SW 1.2% • NE 1.1% NW 0.6%
  • 8.
    HIV infection isacquired in children through: • Mother-to-child (or vertical) route – Accounts for >90% of transmission in children – Can occur in-utero(5-10%), at delivery(5-20%) or during breastfeeding – Prolonged breastfeeding and mixed feeding are key factors responsible for higher transmission rates in Africa – Without intervention overall transmission rate is 15-45%. • Sexual contact – forced or consensual • Blood and blood product transfusion • Use of contaminated sharps for scarification, tattoos, and surgical procedures Modes of HIV Transmission
  • 9.
    In Nigeria, itwas estimated that ONE SERO-EXPOSED INFANT is born every 5 minutes but this is declining with universal ARVs for pregnant women
  • 10.
    • The Lenti-virusgroup of Retroviruses • Retroviruses contain reverse transcriptase enzyme used for synthesis of pro-viral DNA from viral RNA • The mature genome of HIV is diploid with 2 identical positive sense single-stranded RNA copies • The envelope is made of 2 glycoproteins: – Gp120 and Gp41 for HIV-1 – Gp105 and Gp36 for HIV-2. • Antibodies to these 2 sets of proteins do not usually cross react – this differentiates serologic responses of HIV-1 and HIV-2. Biology and Structure of HIV
  • 11.
    Biology and Structureof HIV cont… • Has an outer double lipid membrane (envelope) lined by matrix protein (p17) • Surface glycoprotein gp120 and trans-membrane gp41 • The gp spikes surround the cone-shaped protein core (p24) • Core protein contains genetic material (RNA) and enzymes.
  • 12.
    Viral enzymes • ReverseTranscriptase (RT), converts viral RNA into a double stranded (DNA) • Integrase cause integration of double stranded DNA into host’s DNA • Protease splits generated macro-proteins into smaller viral proteins which get incorporated into new viral particles. Biology and Structure of HIV cont…
  • 13.
    There are twotypes of HIV: • HIV-1 – Main cause of the worldwide pandemic • HIV-2 – Mainly found in West Africa, Mozambique and Angola – Causes a similar but less severe illness to HIV-1 – Less efficient transmission, rarely cause MTCT – Less aggressive with slower disease progression. Molecular Epidemiology of HIV
  • 14.
    • HIV-1 SubtypeA is commonly found in Central, West and East Africa • HIV-1 Subtype B: – Prevalent in Western Europe and North America – Most knowledge about HIV-1 was from studies of subtype B. • All HIV-1 subtypes have been found in Africa • Recombinant forms of HIV exist • A/G recombinant is most predominant in West Africa. Molecular Epidemiology of HIV….cont….
  • 15.
    HIV is aretrovirus with a simple cellular structure made of: Two important membrane glycoproteins responsible for its antigenic identity: − HIV-1 (Gp 120 and Gp 41) − HIV-2 (Gp 105 and Gp36). − Three important enzymes responsible for entry into host cell, incorporation of its RNA into host DNA, replication and assembly of new viral particles − Reverse transcriptase − Integrase − Protease. SUMMARY OF MOLECULAR EPIDEMIOLOGY OF HIV
  • 16.
    • HIV-1 primarilytargets CD4+ molecule on T-helper • Other target cells include macrophages and glial cells • The virus uses its gp120 and gp41 to bind to CD4+ receptors and chemokine co-receptors (CCR5 & CXCR4)on the host cell membrane • This permits entry of contents of the viral particle into host cell cytoplasm • The viral enzymes and RNA are then released to begin the process of replication while the viral envelope is shed. PATHOGENESIS
  • 17.
    • HIV RNAis transcribed by reverse transcriptase to a double stranded DNA • It is then integrated into host DNA by integrase and continues to reside there indefinitely as a provirus • On activation, the proviral DNA is transcribed into mRNA by host enzyme RNA polymerase to begin replication • The mRNA is then translated into viral proteins which assemble and “bud-off” from the host cell membrane. PATHOGENESIS cont….
  • 18.
    PATHOGENESIS cont…. • CD4+cells play vital roles in humoral and cell-mediated immunity such as: – Maturation of B-cells to plasma cells to make antibodies – Induction of natural killer (NK) cells to destroy tumour cells – Activation of macrophages for efficient phagocytosis – Suppression of other T and B-cells by CD8+ suppressor T-cells – Lysis of infected cells by cytotoxic CD8+ T-cells. • Continuous CD4+ loss lead to progressive immunosuppression and increase the incidence of opportunistic infections(Ois).
  • 19.
    PATHOGENESIS cont…. • Reducedactivity of NK cells leads to increased incidence of tumours • Continuous viral replication leads to progressive CD4+ cell destruction which in turn results in: – More CD4+ cell production – Continuous infection of surviving CD4+ cells • CD4+ cells become eventually overwhelmed and the immune system fails to cope with opportunistic infections, leading to progression to AIDS.
  • 20.
    KEY POINTS OFPATHOLOGY • HIV-1 targets CD4+ receptor and chemokine co- receptors on T-helper lymphocytes to gain entry into human host cells • Destruction of CD4+ cells causes progressive immunosuppression and increased incidence of OIs • The CD4+ cells are eventually overwhelmed and the immune system fails, leading to disease progression to AIDS.
  • 21.
    NATURAL HISTORY OFHIV Adults and Children older than 5 years • A typical HIV infection can be divided into three stages: primary infection, asymptomatic infection, and symptomatic infection including AIDS. • Following primary HIV infection, the CD4+ cell count decreases and the HIV RNA rises significantly. • With sufficient exposure to viral antigens, cytotoxic T-lymphocyte responses are generated and the HIV viral load typically declines to an equilibrium known as a virologic “set-point,” within 6 to 12 months of infection. • Once this viral set-point is reached, the CD4+ cell count may rebound again marginally, although it does not often return to baseline values. • Concurrent with these events are clinical manifestations of acute HIV infection in 30% to 60% of individuals.
  • 22.
    NATURAL HISTORY OFHIV contd • Absolute CD4+ count varies with age and is generally higher in healthy younger children • CD4+ counts slowly decline to adult levels by 6 years • CD4+% does not change with age; thus it is the preferred parameter for monitoring disease progression in children ≤5 years • Risk of AIDS or death rises as CD4+% falls to <25 in infants, to <20 from 1-3 years and to <15 thereafter • Disease progression is faster and prognosis is poorer in infants than in older children.
  • 23.
    Natural History ofHIV cont ….. • Viral Load(VL) trends in perinatally infected infants differs from that in adults and children >5 years: • In Infants: – VL levels are low at birth – Increases to levels >100,000 to millions of copies/ml by 2 months of age – Remain at same level throughout first year of life – Decline slowly over the next few years to a “set point”.
  • 24.
    Viral Load andT-lymphocytes Dynamics in HIV Infected Adults and Children
  • 25.
    There are 3categories of disease progression: Category 1 (25 – 30%): • Disease acquired in-utero or perinatally • Rapid disease progression and death within 1st year of life. Category 2 (50 – 60%): • Develop symptoms early in life • Deteriorate and die by 3 to 5 years. Category 3 (5 – 25%): • Long-term survivors: may live beyond 8 years of age. HIV Disease Progression in African Children
  • 26.
    • Infant factors: –Infecting viral dose (maternal VL) – Infection before 4 months of life – Infant peak viraemia – Rapid decline in CD4+ – Clinical AIDS – p24 antigenaemia. • Maternal factors: – VL at time of delivery – CD4+ count (<200) – Rapidly progressive disease – Maternal death. Factors Predicting Disease Progression
  • 27.
    MATERNAL RISK FACORS •High VL • STI • New infection in pregnancy • Advanced disease • APH • PROM • Prolonged labour • Invasive delivery procedures • Instrumental deliveries eg forceps, vacuum • Episiotomies/genital lacerations • Breast conditions
  • 28.
    Fetal risk factors •Oral lesions in breast feeding infant • Mixed infant feeding • Prematurity • First of twins delivered per vaginam
  • 29.
  • 30.
    • Although clinicalfeatures are used to make diagnosis of HIV infection, very often they overlap with features of other diseases. • The clinical manifestations of HIV disease in children include: • Fever • Persistent generalized lymphadenopathy • Respiratory illnesses: pneumonias, pharyngo- tonsillitis, otitis media, mastoiditis • Malnutrition • Gastrointestinal conditions: diarrhoea, vomiting, parotid enlargement.
  • 31.
    • SOME CLINICALMANIFESTATIONS ARE VERY SPECIFIC TO HIV INFECTION EG:
  • 32.
    • Pneumocystis pneumonia •Oesophageal candidiasis • Extra-pulmonary cryptococcosis • Invasive salmonella infection (especially non-typhoidal) • Herpes Zoster (shingles) dermatomal • Kaposi’s Sarcoma • Lymphoma • Progressive multifocal leuco-encephalopathy. • Lymphoid interstitial pneumonitis
  • 33.
    MANIFESTATIONS COMMON INHIV INFECTED CHILDREN BUT NOT COMMON IN UN-INFECTED CHILDREN
  • 34.
    • Severe/recurrent bacterialinfections • Persistent or recurrent oral thrush • Bilateral painless parotid enlargement • Persistent generalized lymphadenopathy - PGL (non- inguinal) • Hepato-splenomegaly (in non-malaria area) • Persistent &/or recurrent fever • Neuro-developmental dysfunction • Herpes Zoster, single dermatome • Persistent generalized dermatitis unresponsive to treatment.
  • 35.
    • FEATURES COMMONIN BOTH INFECTED AND UN-INFECTED CHILDREN
  • 36.
    • Chronic recurrentotitis media with ear discharge • Persistent or recurrent diarrhoea • Severe pneumonia • Tuberculosis • Bronchiectasis • Failure to thrive • Marasmus. National Paediatric ART Training Slides Unit 3 14
  • 37.
    Classification of HIV-associated ClinicalDisease WHO Clinical Stage Asymptomatic 1 Mild 2 Advanced 3 Severe 4 WHO staging for HIV infection and disease in infants, children and adolescents
  • 38.
    IMMUNUNOLOGICAL CLASSIFICATION FORHIV INFECTED CHILDREN Immunological category CD4 count (cells/μL) No evidence of Immunosuppression ≥500 Evidence of Immunosuppression 200-499 Severe Immunosuppression <200
  • 39.
    WHO CLINICAL stage1 • Asymptomatic • Persistent generalized lymphadenopathy.
  • 40.
    WHO CLINICAL stage11(Mild disease) • Unexplained persistent hepatosplenomegaly • Papular pruritic eruptions • Extensive wart virus infection • Extensive molluscum contagiosum • Recurrent oral ulcerations • Unexplained persistent parotid enlargement • Linear gingival erythema • Herpes zoster • Recurrent/chronic upper respiratory infection (otitis media, sinusitis, tonsillitis) • Fungal nail infections.
  • 41.
    WHO CLINICAL stage111(Advanced Disease) • Moderate malnutrition unresponsive to standard therapy • Persistent diarrhoea (≥14 days) • Persistent fever (>37.5 oC, intermittent or constant, exceeding 1 month • Persistent oral candidiasis (after 6 weeks of age) • Oral hairy leukoplakia • Necrotizing ulcerative gingivitis/peri-odontitis.
  • 42.
    WHO CLINICAL stage111(Advanced Disease) contd • Lymph node TB • Pulmonary TB • Severe recurrent bacterial pneumonia • Lymphoid interstitial pneumonia • Chronic HIV-associated lung disease e.g. bronchiectasis • Hb level of <8g/dl • Neutrophil count of <0.5 x 109/L • Platelets count of <50 x 109/L.
  • 43.
    WHO CLINICAL stage1V( Very Severe Disease) • Severe malnutrition not responsive to therapy • Pneumocystis pneumonia • Recurrent/severe bacterial infection (excluding pneumonia) e.g. – Empyema – Pyomyositis – Bone/joint infections – Meningitis. • Chronic herpes simplex infection (for >1 month) • Extra-pulmonary TB.
  • 44.
    WHO CLINICAL stage1V(Severe Disease) contd… • Kaposi sarcoma • Candidiasis (oesophageal, tracheo-bronchial or pulmonary • CNS Toxoplasmosis after neonatal age • HIV encephalopathy • CMV retinitis or infection of other organs after neonatal age • Extra-pulmonary cryptococcosis.
  • 46.
    WHO CLINICAL stage1V(Severe Disease) contd… • Disseminated fungal infections – Histoplasmosis – Coccidiodomycosis. • Chronic cryptococcosis • Disseminated atypical mycobacterial infection • Cerebral B cell Non-Hodgkins lymphoma • Progressive multifocal leukoencephalopathy • HIV-associated cardiomyopathy.
  • 48.
    DIAGNOSIS • Diagnosis maybe: – Clinical - based on signs and symptoms, or – Clinical supported by laboratory findings. • HIV and AIDS should be suspected in children with suggestive clinical features or HIV-associated conditions.
  • 49.
    • All HIV-exposedinfants, the sexually assaulted and those exposed to potentially infectious body fluids should be evaluated • PITC • If infection is confirmed, clinical disease staging should be determined using the WHO staging system.
  • 50.
    LABORATORY DIAGNOSIS • Thereare 2 broad categories of tests: Antibody and virology • ANTIBODY detection (reliable in children above 18 months of age) − HIV Rapid test: (DRT) simple and easy to perform − ELISA: needs more equipment, time, technical skills. − Western blot: gold standard but expensive and produce indeterminate results.
  • 51.
    VIROLOGY TESTS • Mostuseful in children − DNA PCR DBS sample − RNA PCR (plasma viral load): monitors disease progression and response to treatment − P24 Ag: Very specific for detection of core Ag during early stage of infection (window period); negative result does not rule out infection − Viral cultures: highly sensitive, very specific but time consuming, expensive. Only used for research purposes
  • 54.
    • Antibody testsare unreliable for HIV diagnosis in children <18 months, but DNA-PCR is diagnostic • All exposed babies who are breastfeeding should get 2 DNA PCR tests − If initial DNA-PCR is negative, testing should be repeated 12 weeks after cessation of breastfeeding
  • 55.
    • irrespective ofmethod of feeding • Antibody tests are reliable for children >18 months except during window period, thus repeat test after 3 months • DNA/RNA PCR could be used to resolve doubtful results
  • 56.
    THERAPY • ANTI RETROVIRALTHERAPY(ART) IS LIFE-LONG • The major goals of ART in children are to: − Stop and reverse progression of disease − Improve quality of life − Promote or restore normal growth and development − Achieve optimal response with minimal toxicity
  • 57.
    ELIGIBILITY FOR ART •All confirmed cases should be initiated on ART but preference is given to those: • Aged ≤ two years • CLINICAL STAGING---stages 3 and 4 • IMMUNOLOGICAL STAGING---depending on age and clinical staging
  • 58.
    • ART shouldbe initiated in all children with HIV, regardless of WHO clinical stage, or at any CD4 +cell count. • As a priority, ART should be initiated in the following situations – All children < 2 years of age – All children younger than 5 years of age with WHO clinical stage 3 or 4 disease or CD4+ cell count <750 cells/mm3 or CD4+ percentage <25% – All children 5 years and older with WHO HIV clinical stage 3 or 4 disease or CD4+ cell count <350 cells/mm3 – ART should be initiated in all adolescents with severe or advanced HIV clinical disease (WHO clinical stage 3 or 4) and a CD4 + cell count of 350 cells/mm3.
  • 59.
    • YET TOBE CONFIRMED, <18 MONTHS, ANTIBODY POSITIVE, CLINICAL STAGE 3 or 4, commence therapy while awaiting confirmation
  • 60.
    PRE ART(HAART) • Detailedhistory • Clinical examination • CD4/CD4% • TB SCREENING • BASELINE TESTS
  • 61.
    HAART • NOT LESSTHAN 3 DRUGS FROM AT LEAST 2 CLASSES
  • 62.
    ANTI-RETROVIRAL DRUG CLASSES APPROVED ARVDRUGS Nucleoside Reverse Transcriptase Inhibitors (NRTIs)  Zidovudine (ZDV, AZT)*  Lamivudine (3TC)*  Stavudine (d4T)*  Abacavir (ABC)*  Didanosine (ddI) *  Zalcitabine (ddC)  Emtricitabine (FTC)* Nucleotide Reverse Transcriptase Inhibitors (NRTIs) Tenofovir (Disoproxil Fumarate {TDF}) Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)  Nevirapine (NVP)*  Efavirenz (EFV)*  Delavirdine (DLV)  Etravirine (ETV) * Fusion inhibitors  Enfuvirtide (T-20)* Protease inhibitors (PIs)  Lopinavir-ritonavir (LPV/r)*  Ritonavir (RTV) {as pharmaco-enhancer}*  Nelfinavir (NFV)*  Saquinavir (SQV)  Amprenavir (APV)*  Indinavir (IDV)  Atazanavir (AZV)*  Tipranavir (TPV)  Darunavir* (DRV)  Fos-amprenavir* (FPV) CCR5 inhibitor  Maraviroc Integrase Inhibitors  Raltegravir (RAL), Dolutegravir (DTG), Elvitegravir(EVG)
  • 63.
    THE WHO RECOMMENDATION AgeGroup Preferred 1st line regimen Alternative 1st line regimens Special situations Neonates AZT + 3TC + RAL  AZT + 3TC + NVP  AZT + 3TC + LPV/r Children ABC + 3TC+ DTG  ABC + 3TC +LPV  ABC + 3TC +RAL  ABC + 3TC + EFV (or NVP)  AZT + 3TC + EFV (or NVP)  AZT + 3TC + LPV/r (or RAL) Adolescent  TDF + 3TC (or FTC) + DTG  TDF + 3TC (or FTC) + EFV 600mg  TDF + 3TC (or FTC) + EFV 600mg  TDF + 3TC (or FTC) + EFV 400mg  TDF + 3TC(or FTC) + EFV 400mg  TDF + 3TC (or FTC) + ATV/rb  AZT + 3TC + EFV 600mg  TDF + 3TC (or FTC) + PI/r  AZT + 3TC + EFV 600mg  TDF + 3TC (or FTC) + RAL
  • 64.
    • Effective ARTresults in – recovery of the immune functions with a progressive increase in CD4+ cell count at a rate of 50 to 100 cells/μl /year. – Reduced occurrence of morbid conditions – Reduced opportunistic infections – Improved quality of life – Promotion and restoration of normal growth and development. – Reduction of HIV transmission in communities
  • 65.
    • NNRTIs Stopviral replication by binding to reverse transcriptase preventing the transcription of HIV RNA to DNA • NRTIs Incorporate into viral DNA to stop replication and form incomplete viral DNA – cannot create a new virus • NtRTIs Act at the same stage of HIV life cycle as NRTIs, but do not require phosphorylation for anti-HIV activity. Classes and modes of action of ARVs
  • 66.
    • Protease inhibitors(PIs) act at the last stage of HIV cycle – Prevent assembly and release of HIV particles from infected CD4 cells • Entry (fusion) inhibitors prevent HIV from infecting CD4 T cells • Integrase inhibitors prevent insertion of HIV DNA template into host DNA – Prevents viral replication • Chemokine receptor inhibitors prevent attachment of HIV surface antigens to CCR5 or CCX4 receptors. Classes and modes of action of ARVs cont…
  • 67.
    HIV Integrase Inhibitors •HIV Integrase Inhibitors: Also known as Integrase Strand Transfer Inhibitors (INSTI). These inhibit DNA strand transfer into host- cell genome and thus prevent viral integration. Integrase Inhibitors do not confer resistance to other ART classes. Examples include: Dolutegravir (DTG), Elvitegravir(EVG), Raltegravir (RAL).
  • 68.
    HIV LIFE-CYCLE/MODE OFACTION OF ARVs
  • 70.
    FIXED DOSE COMBINATIONS(FDC) •AZT+3TC±NPV • ABC+3TC • LPV/r • TDF/3TC/DTG • TDF/3TC/EFV
  • 71.
    AZT/3TC 60/30 11 1.5 1.5 2 2 2.5 2.5 3 3 300/150 1 1 AZT/3TC/NVP 60/30/50 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150/200 1 1 ABC/AZT/3TC 60/50/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/300/150 1 1 ABC/3TC 60/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150 1 1 d4T/3TC 6/30 1 1 1.5 1.5 2 2 2.5 2.5 3 3 30/150 1 1 d4T/3TC/NVP 6/30/50 1 1 1.5 1.5 2 2 2.5 2.5 3 3 300/150/200 1 1 d4T/3TC 12/60 0.5 0.5 1 0.5 1 1 1.5 1 1.5 1.5 60/150 1 1 d4T/3TC/NVP 12/60/100 0.5 0.5 1 0.5 1 1 1.5 1 1.5 1.5 60/150/200 1 1 LPV/rb 100/25 NR NR 2 1 2 2 2 2 2 2 100/25 3 3 Drug Strength of Paediatric tab (mg) Children 6 weeks and above Strength of Adult tab (mg) No. of tabs by weight band No. of tabs by Kg weight-band b. d. 3-5.9 6-9.9 10-13.9 14-19.9 20-24.9 25-34.5 Kg am Pm am pm am pm Am pm am pm am pm
  • 72.
    • Adverse eventsmay vary from mild to severe or life- threatening • Mild toxicities • Moderate • Severe toxicities may require substitution with a drug in the same class but with different toxicity profile • Life-threatening toxicity requires discontinuation of all ARVs and the initiation of supportive therapy. ART toxicity profile cont….. National Paediatric ART Training Slides Unit 6
  • 73.
    ADR • AZT anaemiaPCV must not be <27% • NPV Hypersensitivity reaction, Stevens- Johnson syndrome • EFV nightmares, psychosis • ABC Severe hypersensitivity reaction. Should carry notification card • TDF Drug rash, potential renal toxicity, potential decrease in bone density. Not for children less than 8 years or with existing renal damage. • ABC Hypersensitivity reactions • Read up others
  • 74.
    Special considerations • SubstitutionDTG for LPV/r for children with wt of 20kg+ ABC for TDF in children younger than 8 years • Switch to 2nd line drugs • Salvage ---5 ARVs, 2 must be protease inhibitors(PIs) • Suspension • stop
  • 75.
    Routine monitoring onART: – Every 2 weeks for the first month after starting therapy – Monthly for 6 months, then every 3 months thereafter. Follow-up visit activities: – Anthropometry (plot chart) and developmental check – Physical exam (pallor, jaundice, mouth, skin, lymph nodes, chest, abdomen) – Check immunizations, assess nutrition and conduct psychosocial assessment – Checking for adverse ARV effects – Review dosages for every 10% change in body weight. Follow-up/Monitoring schedule
  • 76.
    Pre- Treatment (Baseline) Wk 2 Monthly x 6Every 3 mo. thereafter Every 6 mo. thereafter 1 2 3 4 5 6 Physical Exam X X X X X X X X X Adherence Counselling X X X X X X X X X Confirm HIV status X HIV-1 RNA (VL) * X X X CD4+ X X X X FBC X X X X E & U, Cr* X X LFT X X** X X X Random BS* X Serum lipids* X Amylase* X Urinalysis X X X X X X X X Chest X-ray* X *As clinically indicated, thereafter ** To be done for children starting on NVP Monitoring schedule for children on ARV therapy
  • 77.
  • 78.
    The 4-pronged approachto PMTCT ! "#$ % & ' () *+#, $ - ' ' () - . "$ /) $ 01 ! 2! $ $ N IC A L R EP O R T artment of Public Health AIDS/STI Control Programme onal HIV Sero-prevalence Sentinel Survey MINISTRY OF HEALTH CAL REPORT 2010 National HIV Sero-prevalence Sentinel Survey Among Pregnant Women Attending Antenatal Clinics in Nigeria T EC H N IC A L R E Department of Public Hea National AIDS/STI Control Pro 2010 National HIV Sero-pre Sentinel Survey FEDERAL MINISTRY OF 1 Pr imar y HIV Prevention $ 2 Prevention of Unintended Pregnancies in HIV +ve Women 3 Prevention of Mother-To- Child Transmission 4 Provision of Care and Suppor t for HIV infected Children, their Mothers and Families
  • 79.
    Care for theHIV exposed neonate • Have their mouths and nostrils wiped with gauze after delivery of the head. • Be handled with latex gloves until maternal blood and secretions are washed off. • Have the cord clamped immediately after baby is delivered and avoid milking the cord. • Have the cord cut under cover of a lightly wrapped gauze swab to avoid blood spurting. • Be kept warm.
  • 80.
    • Be suctionedif indicated using a mechanical/electrical suction unit at a pressure below 100mmhg or bulb suction. Mouth operated suction is contraindicated. • Be cleaned with warm chlorhexidine solution or wiped dry with a towel or surgical cloth to remove maternal body fluids. • Place the baby on the mother’s chest for skin to skin contact soon after delivery. • In this position the baby will latch on to one of the mother’s breast to initiate feeding unless the mother opted for alternative feeding method. • Have vitamin k administered, ensuring injection safety
  • 81.
    Package of servicesfor HIV exposed children • ARV prophylaxis • Routine immunization and growth monitoring and support • Cotrimoxazole prophylaxis starting at 6 weeks • HIV diagnostic testing using DBS for DNA PCR at 6 to 8 weeks of age and 12 weeks after breastfeeding has ended. • Ongoing infant feeding counselling and support
  • 82.
    • Screening andmanagement of tuberculosis • Prevention and treatment of malaria • Nutritional care and support • Psychosocial care and support • Antiretroviral therapy for all HIV infected children • Symptom management and palliative care if needed
  • 83.
    ARV Prophylaxis inneonate • All HIV exposed infants should receive ARV prophylaxis. Infants born to mothers with HIV who are at high risk of acquiring HIV should receive dual prophylaxis with AZT (twice daily) and NVP (once daily) for the first 6 weeks of life, whether they are breastfed or formula fed. • It is recommended that infants delivered to HIV positive mothers who are stable on ART should receive Nevirapine prophylaxis. Nevirapine prophylaxis is administered daily. These infants irrespective of the type of feeding should receive daily NVP from within 72 hours of birth to 6 weeks of age. • If infants are receiving replacement feeding, they should be given 4 to 6 weeks of infant prophylaxis with daily NVP (or twice-daily AZT).
  • 84.
    • For babieswith weight <2,500g (0-6weeks) – NVP 10mg or 1ml once daily – AZT 10mg or 1ml twice daily • For babies with weight ≥2, 500g(0-6weeks) – NVP 15mg or 1.5ml once daily – AZT 15mg or 1.5ml twice daily • 6 – 12weeks – NVP 20mg(2mls) once daily – AZT 20mg (2mls) twice daily • Breastfed infants who are at high risk of acquiring HIV should continue infant prophylaxis for an additional 6 weeks (total of 12 weeks of infant prophylaxis) using AZT (twice daily) and NVP (once daily).
  • 85.
    Infant feeding inthe context of HIV • It is recommended that mothers of HIV exposed infants breastfeed their babies exclusively for the first six (6) months of life. • Complementary feeds should be introduced at 6 months in addition to breast milk • Breastfeeding complemented by household foods should be continued till 12 months, after which child should be weaned off breast milk.
  • 86.
    Immunizations for HIVExposed Children • All HIV exposed children should be immunized as early as possible to protect them against vaccine- preventable diseases. • Children who have, or are suspected to have HIV infection but are not yet symptomatic should be given all appropriate vaccines. • Children with advanced and symptomatic HIV infection (CD4 < 200 or < 14%, or Stage 3 or 4 disease), should not be given live vaccines (BCG, varicella-zoster, OPV, measles and yellow fever vaccine). • HIV infected children should therefore be given the inactivated polio vaccine (intramuscular).
  • 87.
    • Pre exposureProphylaxis (PrEP) is the pre- emptive use of antiretroviral (ARV) drugs to reduce the probability of HIV negative individuals acquiring HIV infection especially persons who engage in high-risk activity. • It is recommended that PrEP should be offered only to the category of individuals listed below – 1. Serodiscordant couples – 2. Commercial sex workers – 3. Injecting drug users – 4. Individuals who engage in anal sex on a prolonged and regular basis
  • 88.
    • Preferred dailyoral dose regimen for PrEP is the combination of TDF+ FTC (Truvada) • The alternate regimen for PrEP is a daily dose of TDF. • These drugs are to be taken indefinitely until the individual no longer qualifies as high risk
  • 89.
    • Post ExposureProphylaxis (PEP) is the short- term use of ARV drugs to prevent HIV infection in persons accidentally exposed to a potential risk of acquiring HIV infection. • This applies usually to accidental exposure as seen in health workers or sexual assault victims especially in cases where the HIV status of the perpetrator cannot be readily determined.
  • 90.
    In case ofa needle stick injury • Do not squeeze or rub the injury site • Allow blood or secretion to flow freely • Wash exposed area immediately with soap and running water or antiseptic solutions • After a splash to the eye or any other mucous surface, irrigate/rinse the exposed area immediately with water (preferably running water) or normal saline • Report the exposure to a senior member of staff, supervisor or the PEP officer • If eligible, give antiretroviral drugs recommended for post exposure prophylaxis immediately possibly within 1 hour and at the latest within 72 hours of the exposure (persons presenting after 72 hours of the exposure should also be considered for PEP).
  • 91.
    • PEP iscontinued for 28days or the source patient is known to be negative. • TDF + 3TC (or FTC) is recommended as the preferred backbone regimen for HIV post- exposure prophylaxis for adults and adolescents. • EFV is recommended as the preferred third drug for HIV post-exposure prophylaxis for adults and adolescents. However, where available, LPV/r, RAL, or DRV/r, can be considered as alternative options.
  • 92.
    • In children<10 years AZT + 3TC is recommended as the preferred backbone regimen for HIV post exposure prophylaxis. • Alternative backbone regimen for this age category will include ABC + 3TC or TDF + 3TC (or FTC). EFV is recommended as the preferred third drug for HIV post-exposure prophylaxis for children younger than 10. • An age-appropriate alternative regimen can be identified among LPV/r ATV/r, RAL, DRV,.
  • 93.
    Recommended Schedules of Investigationsfollowing HIV Exposure Period Recommended Investigations Baseline HIV, HBV, HCV screening, FBC , LFT, Renal function test 2 weeks Full blood count, Liver function test, Renal function test 6 weeks HIV screening 3 months HIV screening 6 months HIV screening
  • 94.
    • As withall cases of sexual assault, it is important to arrange for continuous counselling and support for the victim. • Emergency contraception should also be considered.
  • 95.
    Cotrimoxazole preventive therapy (CPT) •Cotrimoxazole preventive therapy (CPT) is a fixed-dose combination of two antimicrobial agents (sulfamethoxazole and trimethoprim) used for the prevention of some AIDS- associated opportunistic diseases (Pneumocystis jirovecii pneumonia [PCP] and toxoplasmosis) and the reduction of HIV- associated mortality in people with low CD4+ cell counts.
  • 96.
    • Cotrimoxazole prophylaxisis recommended for infants, children and adolescents with HIV, irrespective of clinical and immune conditions. • Due to high prevalence of malaria and severe bacterial infections in Nigeria, cotrimoxazole prophylaxis should be continued until adulthood, irrespective of whether ART is provided. • Cotrimoxazole prophylaxis is recommended for HIV-exposed infants 6 weeks of age and should be continued until HIV infection has been excluded by an age-appropriate HIV test to establish final diagnosis after complete cessation of breastfeeding.
  • 97.
    • In HIVpositive individuals who have adverse drug reactions to cotrimoxazole, options for prophylaxis of PCP include dapsone, dapsone plus pyrimethamine plus leucovorin and atovaquone. • For those who will be started on dapsone, do a G6PD deficiency test. Dapsone should be avoided in individuals with G6PD deficiency.
  • 98.
    DOSING OF CPT •For infants below 6 months or < 5 kg (Cotrimoxazole 120mg daily) • For children 6 months–5 years or 5-15 kg (Cotrimoxazole 240 mg daily) • For children 6–14 years old or 15–30 kg (Cotrimoxazole 480 mg daily) • For anyone over 14 years or >30 kgs (Cotrimoxazole 960 mg)
  • 99.
    ISONIAZID PREVENTIVE TREATMENT OFTB Isoniazid Preventive Therapy (IPT) is the use of isoniazid to prevent the development of active TB disease in HIV positive individuals. • Paediatric recommendations: – Children living with HIV who have poor weight gain, fever or current cough contact history with a TB case may have TB and should be evaluated for TB and other conditions. If the evaluation shows no TB, they should be offered IPT regardless of their age .
  • 100.
    • As partof a comprehensive package of HIV prevention and care Children living with HIV who are ≥ 12 months of age and who are unlikely to have active TB on symptom-based screening and have no contact with a TB case should receive six months of IPT (10 mg/kg/day) but not more than 300mg/day. • In children living with HIV who are < 12 months of age, only those who have contact with a TB case and who are evaluated for TB (using standard lab investigations) should receive six (6) months of IPT if the evaluation shows no TB disease. • All children living with HIV, after successful completion of treatment for TB, should receive IPT for an additional six months.