1. HIV attacks T-cells in the immune system, leading to AIDS in advanced stages. 2. Clinical manifestations in children vary widely and can include failure to thrive, respiratory issues, gastrointestinal diseases, and neurological problems. 3. Diagnosis is made through HIV antibody testing after 18 months or virological testing before 18 months, and management includes prophylaxis, antiretroviral therapy, treating opportunistic infections, adequate nutrition, and immunization.

1. NUR HANISAH BINTI ZAINOREN
PAEDIATRIC

2. CONTENT
• Introduction
• Clinical manifestations
• Diagnosis
• Management

3. INTRODUCTION

4. • HIV is the virus which attacks the T-cells in the
immune system
• AIDS is the syndrome which appears in
advanced stages of HIV infection
• HIV is a virus
• AIDS is a medical condition

5. CLINICAL
MANIFESTATIONS

6. • Vary widely among infants, childrens and adolescents
• In most infants, physical examination at birth is normal
• Initial signs and symptoms may be subtle and non-
specific (eg: failure to thrive, lymphadenopathy,
hepatosplenomegaly, chronic/recurrent diarrhea,
interstitial pneumonia, oral thrush)

7. • In United States and Europe:
systemic and pulmonary
findings are common
• In Africa: chronic diarrhea,
wasting, malnutrition are
common

8. • Symptoms commonly found MORE in
CHILDREN than adults are:
– Recurrent bacterial infection
– Chronic parotid swelling
– Lymphocytic interstitial pneumonitis
– Early onset neurologic deterioration

9. • Paediatic HIV staged by two parameters
– Clinical status
– Degree of immunologic impairment

10. Clinical status
(WHO Clinical Staging of HIV/AIDS with Confirmed Infection)
• Clinical stage 1
• Clinical stage 2
• Clinical stage 3
• Clinical stage 4

11. Clinical status
(WHO Clinical Staging of HIV/AIDS with Confirmed Infection)
• Clinical stage 1
• Clinical stage 2
• Clinical stage 3
• Clinical stage 4
• Asymptomatic
• Persistent generalized
lymphadenopathy

12. Clinical status
(WHO Clinical Staging of HIV/AIDS with Confirmed Infection)
• Clinical stage 1
• Clinical stage 2
• Clinical stage 3
• Clinical stage 4
• Unexplained persistent hepatosplenomegaly
• Papular pruritic eruptions
• Fungal nail infection
• Angular cheilitis
• Lineal gingival erythema
• Extensive wart virus infection
• Extensive molluscum contagiosum
• Recurrent oral ulceration
• Unexplained persistent parotid enlargement
• Herpes zoster
• Recurrent/chronic URTI (otitis media,
otorrhea, sinusitis, tonsillitis)

13. Clinical status
(WHO Clinical Staging of HIV/AIDS with Confirmed Infection)
• Clinical stage 1
• Clinical stage 2
• Clinical stage 3
• Clinical stage 4
• Unexplained moderate malnutrition or wasting not
adequately responding to standard therapy
• Unexplained persistent diarrhea (14 days or more)
• Unexplained persistent fever
• Persistent oral candidiasis
• Oral hairy leukoplakia
• Acute necrotizing ulcerative gingivitis/periodontitis
• Lymph node TB
• Pulmonary TB
• Severe recurrent bacteria pneumonia
• Symptomatic lymphoid interstitial pneumonitis
• Chronic HIV-associated lung disease including
bronchiectasis
• Unexplained anemia, neutropenia or chronic
thrombocytopenia

14. Clinical status
(WHO Clinical Staging of HIV/AIDS with Confirmed Infection)
• Clinical stage 1
• Clinical stage 2
• Clinical stage 3
• Clinical stage 4
• Unexplained severe wasting, stunting or severe
malnutrition not responding to standard therapy
• Pneumocystic pneumonia
• Recurrent severe bacterial infections
• Chronic herpes simplex infection
• Esophageal candidiasis
• Extrapulmonary/disseminated TB
• Kaposi sarcoma
• CMV infection
• CNS toxoplasmosis
• Extrapulmonary cryptococcosis
• HIV encephalopathy
• Chronic cryptosprodiosis
• Chronic isosporiasis
• Cerebral or B cell non-Hodgkin lymphoma
• Progressive multifocal leukoencephalopathy
• Symptomatic HIV-associated nephropathy or HIV-
associated cardiomyopathy

15. Degree of immunologic impairment
(Severity of immmune suppression based on CD4 levels in children)
Immune Status Age
<11mo 12-35mo 36-59mo >5yr
Not significant >35% >30% >25% >500 cells/mm3
Mild 30-35% 25-30% 20-25% 350-499
cells/mm3
Advanced 25-30% 20-25% 15-20% 200-349
cells/mm3
Severe <25% or
<1500
cells/mm3
<20% or
<750 cells/mm3
<15% or
<350 cells/mm3
<15% or
<200 cells/mm3

16. Respiratory
diseases

17.  Pneumocystis pneumonia
 Recurrent bacterial infections
 Tuberculosis
 Viral infections
 Fungal infections
 Lymphoid interstitial
pneumonitis

18. Pneumocystis pneumonia
 Pneumocystis jiroveci
(previously P.carinii) pneumonia
(PCP) is the opportunistic
infection that led to the initial
description of AIDS
 Treatment: cotrimoxazole
 Untreated  FATAL

19. Recurrent bacterial infection
 90% had history of recurrent
pneumonias
 Initial episodes often occur before
the development of significant
immunosupression
 As the immunosuppression
frequency increases, the frequency
increases

20. Recurrent bacterial infection
 Community-acquired pneumonia:
 Strep. Pneumoniae
 H. influenza
 Staph. Aureus
 Hospital-acquired infection:
 Pseudomonas aeruginosa

21. Recurrent bacterial infection
 Treatment:
 Combination of a broad
spectrum cephalosporin +
aminoglycoside
 Nonsevere pneumonia: 2nd/3rd
generation cephalosporin or a
combination like amoxicillin-
clavulanic acid
 Supportive care

22. Tuberculosis
 More likely to have
extrapulmonary and
disseminated TB; course is
likely to be more rapid
 Coexistent TB + HIV
accelerate the progression
of both diseases

23. Tuberculosis
 The overall risk of active TB
in HIV-infected children is at
least 5-10 fold higher
 Should received longer
duration of antitubercular
therapy (9-12 month)

24. Viral infections
 Respiratory syncytial virus,
influenza and para influenza
viruses more often result in
symptomatic disease
 Adenovirus and measles virus
are more likely to lead to
serious sequelae

25. Fungal infections
 Primary infection is uncommon
 Pulmonary candidiasis should
be suspected in any sick HIV-
infected child with LRTI that
does not respond to the common
therapeutic modalities

26. Lymphoid Interstitial
pneumonitis (LIP)
 In absence of antiretroviral therapy,
nearly 20% of HIV-infected children
developed LIP
 Usually diagnosed in children with
perinatally acquired HIV infection
when they are older than 1yr of age

27. Lymphoid Interstitial
pneumonitis (LIP)
Characterized by nodule formation
and diffuse infiltration of the
alveolar septae by lymphocytes,
plasmacytoid lymphocytes, plasma
cells and immunoblasts

28. Lymphoid Interstitial
pneumonitis (LIP)
 Etiology and pathogenesis is not well understood
 Suggested etiologies are:
- Exagerrated immunologic
response to inhaled/circulating
antigens
- Primary infection of the lung
with HIV, EBV, or both

29. Lymphoid Interstitial
pneumonitis (LIP)
 Mostly are aymptomatic
 Severe Tachypnea, cough,
wheezing and hypoxemia
 Advanced Clubbing
 Can progress to chronic
respiratory failure/bronchiectasis

30. Lymphoid Interstitial
pneumonitis (LIP)
Diagnosis:
 Chest Xray: reticulonodular pattern,
with/without hilar lymphadenopathy
that persists =/>2 months
 Unresponsive to antimicrobial
therapy
 Histopathology (definitive diagnosis)

31. Lymphoid Interstitial
pneumonitis (LIP)
Management:
 Steroids – if children with LIP have
symptoms and signs of chronic
pulmonary disease, clubbing,
hypoxemia
 initial 4-12 week course of
prednisolone (2mg/kg/day) 
tapering dose

32. Gastrointestinal
diseases

33. Infections
 Bacteria – Salmonella,
Campylobacter, M. avium
 Protozoa* – Giardia,
Cryptosporidium, Isospora
 Fungi – Candida
 Virus – CMV, HSV, Rotavirus
* most severe

34. AIDS enteropathy
 a syndrome of malabsorption
with partial villous atrophy not
associated with a specific
pathogen
• Result of direct HIV infection of
the gut

35. Chronic liver inflammation
 Common in HIV infected children
 In some children, hepatitis caused by
CMV, hepatitis B or C viruses, or
mycobacteria may lead to liver failure
and portal hypertension.
*several of the antivirus drugs (eg: didanosine and protease inhibitors)
may also cause reversible elevation of transaminases

36. Pancreatitis
 Uncommon
 May be the result of drug therapy
(eg: didanosine, lamivudine,
nevirapine, or pentamidine)
 Rarely, opportunistic infections such
as mycobacteria or CMV may be
responsible for acute pancreatitis

37. Neurologic
diseases

38. Incidence may be >50% in
developing countries but
lower in developed countries.
With a median onset at about
one and a half year of age.

39. Progressive encephalopathy
 Loss/plateau of developmental
milestones
 Cognitive deterioration
 Impaired brain growthacquired
microcephaly
 Symmetric motor dysfunction

40. Meningitis
 Due to bacterial pathogens,
fungi (eg: Cryptococcus) and
a number of viruses may be
responsible

41. Toxoplasmosis
 Extremely rare in young
infants
 But may occur in HIV-
infected adolescents

42. Cardiovascular
diseases

43. Cardiac abnormalities is
common, persistent and often
progressive in HIV-infected
children

44. Left ventricular structure and
function progressively may
deteriorate in the first 3 years
of life  increased ventricular
mass

45. Children with encephalopathy
or other AIDS-defining
conditions have the highest
rates of adverse cardiac
outcomes

46. Resting sinus tachycardia and
marked sinus arrhythmia has
been reported in upto nearly
2/3 and in 1/5 of the HIV-
infected children

47. Congestive heart failure
clinically indicated by gallop
rhythm with tachypnea and
hepatosplenomegaly

48. Renal diseases

49. Nephrotic syndrome
with azotemia & normal
blood pressure
Renopathy
unusual
(more common
in older children)

50. • Principles of management of
gastrointestinal and neurological diseases
are similar to those in non-HIV-infected
children
• Electrocardiography and
echocardiography are helpful in assessing
cardiac function before the onset of
clinical symptoms

51. DIAGNOSIS

52. Diagnosis can be made by:
HIV antibody testing
(beyond 18 months of age)
Virological testing
(before 18 months of age)

53. HIV antibody testing
• All infants born to HIV-infected mothers are test antibody-
positive at birth (due to passive transfer of maternal HIV
antibody across placenta)
• Most uninfected children lose maternal antibody between 6-12
months of age; only small proportion continue to have up to 18
months of age
• Hence, positive IgG antibody tests in infant younger than this
age cannot be used to make definitive diagnosis

54. Methods:
 Demonstration of IgG antibody to HIV: -
- Reactive enzyme immunoassay (EIA)
 Confirmatory test
- Western blot
- Immunofluorescence assay

55. Virological testing
• Essential for young infants born to a HIV-
infected mother
• Methods:
- HIV DNA/RNA PCR
- HIV culture
- HIV p24 Ag immune dissociated p24

56. MANAGEMENT

57. • Management of HIV-infected child includes:
– Prophylaxis
– Antiretroviral therapy
– Treatment of opportunistic infection
– Adequate nutrition
– Immunization

58. Cotrimoxazole prophylaxis
• Recommended for:
1. All HIV-exposed infants, starting at 4-6 weeks of
age; continued until HIV infection can be excluded
2. HIV-exposed breastfeeding children of any age;
continued until can be excluded by HIV antibody
testing or virological testing at least 6 weeks after
complete cessation of breastfeeding

59. 3. All children <1yr of age documented to be living
with HIV
4. Symptomatic children >1yr of age
*all children who begin cotrimoxazole prophylaxis
should continue until age of 5 yr, when they can be
reassessed

60. The World Health Organization
now recommends initiation of ART
for all HIV infected children <2yr age
irrespective of clinical symptoms and
the immunologic stage
Antiretroviral therapy

61. The currently available therapy does not
eradicate the virus and cure the child;
Rather it suppresses the virus replication for
extended periods of time

62. Antiretroviral therapy
The main 3 groups of drugs:
1. Nucleoside reverse transcriptase
inhibitors (NRTI)
2. Non-nucleoside reverse transcriptase
inhibitors (NNRTI)
3. Protease inhibitors (PI)

63. NRTI
• Zidovudine (AZT)
• Lamivudine (3TC)
• Stavudine (d4T)
• Abacavir (ABC)
• Didanosine
• Zalcitabine
NNRTI
• Nevirapine (NVP)
• Efavirenz (EFV)
PI
• Lopinavir (LPV)
• Amprenavir
• Indinavir
• Nelfinavir
• Ritonavir
• Saquinavir

64. • Highly active antiretroviral therapy (HAART) is a
combination of 2 NRTIs with a PI/NNRTI
• The national program recommends a combination of
Zidovudine + Lamivudine + Nevirapine (1st line therapy)
• Alternative regimen:
Stavudine + Lamivudine + Nevirapine

65. Nutrition
• It is important to provide adequate nutrition
to HIV-infected children.
• Many of these children have failure to thrive.
• These children will need nutritional
rehabilitation.
• Micronutrients like zinc may be useful

66. Immunization
• The vaccines that are recommended in the
national schecule can be administered to HIV
infected children except that symptomatic HIV
children should not be given oral polio and
BCG vaccines

67. Prevention of Mother to Child
Transmission (PMTCT)

68. the risk of MTCT can be reduced to under 2%
Antiretroviral
prophylaxis during
pregnancy
Intrapartum
interventions
Regimens for
infants
Avoidance of
breastfeeding

69. 1. Antiretroviral drug regimens for
pregnant women
• FOR THEIR OWN HEALTH, ART
should be administered
irrespective of gestational age
and is continued throughout
pregnancy, delivery and
thereafter
(recommended for all HIV-infected pregnant
women with CD4 cell count <350cells/mm3 or
WHO clinical stage 3 or 4)

70. Recommended regimen for pregnant women
with indication of ART is combination of…
Zidovudine
(AZT)
Lamivudine
(3TC)
Nevirapine (NVP)
or Efavirenz (EFV)**EFV-based regimen should not be newly-initiated
during the first trimester of pregnancy

71. Recommended regimen for pregnant women
who are NOT ELIGIBLE for ART , BUT FOR
PREVENTING MTCT is…
To start ART as early as 14 weeks gestation OR
as soon as possible (when women present late
in pregnancy, in labor or at delivery)
*EFV-based regimen should not be newly-initiated
during the first trimester of pregnancy

72. For them, 2 options are available:
Option 1:
• Daily AZT in antepartum period
• AZT + single dose NVP at
onset of labor
• AZT + 3TC during labor
• AZT + 3TC for 7 days in
postpartum period
Option 2:
• Triple ART starting as early as 14
week of gestation until 1 week after
exposure to breastmilk has ended
• AZT + 3TC + LPV (lopinavir)
• AZT + 3TC + ABC (abacavir)
• AZT + 3TC + EFV

73. 2. Regimens for infants
• If mother only received AZT during antenatal period:
– For BF infants: daily NVP from birth until 1 week after all
exposure to breast milk has ended
– For non-BF infants: daily AZT/NVP from birth until 6 week
• If mother received triple drug ART during pregnancy
and entire breastfeeding:
– daily AZT/NVP from birth until 6 weeks irrespective of
feeding Dosage:
NVP – 10mg/day (infants<2.5kg) or
15mg/day (infants>2.5kg) PO
AZT – 4mg/kg BD, PO

74. 3. Intrapartum interventions
• Delivery by elective cesarean section at 38 weeks before
onset of labor and rupture of membrane should be
considered
• Avoid artificial rupture of membrane (ARMs) unless
medically indicated
• Avoid procedures increasing risk of exposure of child to
maternal blood and secretions like use of scalp electrodes

75. 4. Breastfeeding
• Important modality of transmission of HIV infection in
developing countries
• Risk of infection via BF highest in the early months of BF
• Increase Risks:
– Detectable levels of HIV in breast milk
– Presence of mastitis
– Low maternal CD4+ T cell count

76. 4. Breastfeeding
• Mothers known to be HIV-infected should only
give commercial infant formula milk as a
replacement feed when specific conditions are
met:
– referred earlier as affordable, feasible, acceptable,
sustainable and safe (AFASS) in 2006 WHO
recommendations on HIV and infant feeding
– Otherwise, exclusive BF during first 6 months of life
– Cessation of BF should be gradual

77. REFERENCE
Ghai Essential Paediatrics, 8th Edition, Vinod K Paul and Arvind Bagga

78. THANK YOU
NUR HANISAH ZAINOREN