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Brief Reports

Indian Pediatrics 2000;37: 982-986

Pediatric HIV Infection in a Tertiary Care Center in North India: Early Impressions


Rakesh Lodha
Tanu Singhal
Yogesh Jain
Sushil K. Kabra
P. Seth*
Vimlesh Seth

From the Departments of Pediatrics and Microbiology*, All India Institute of Medical Sciences, Ansari Nagar, New Delhi 110 029, India.

Reprint requests: Dr. Sushil K. Kabra, Associate Professor, Department of Pediatrics, All India Institue of Medical Sciences, Ansari Nagar, New Delhi 110 029, India.

Manuscript received: November 8, 1999;
Initial review completed: December 7, 1999;
Revision accepted: March 7, 2000

There is scant information about clinical presentation and modes of transmission of pediatric human immunodeficiency virus (HIV) infection in India. Most published case-series from India are based on investigation of multiply transfused thalassemic children(1-3). There is no epidemiological information on the modes of transmission(4) and scant information about the clinical features of pediatric HIV infection in India(5). At the All India Institute of Medical Sciences (AIIMS), a referral center in North India, we have looked at all the cases of pediatric HIV infection over the last 4 years. We wish to share our early impressions on the clinical presen-tation, modes of transmission and management of these children. Specifically, we wish to highlight the presumed modes of transmission that are at variance with the published literature.

  Subjects and Methods

We reviewed case records of all children diagnosed as pediatric HIV infection in the last 4 years at the Department of Pediatrics, AIIMS. In children over 18 months of age, the diagnosis of HIV infection was confirmed by three positive ELISA (enzyme linked immunosorbent assay) tests according to the WHO strategy III(6). The three different ELISA kits used were provided by National AIDS Control Organization (NACO): HIV-SPOT (Genelabs Diagnostics, Singapore), HIV EIA (Labsystems OY, Helsinki) and Detect-HIVMC (Biochem Immunosystems Inc., Montreal). Polymerase chain reaction (PCR) was used to diagnose HIV infection in children younger than 18 months age. PCR for ‘gag’ and ‘env’ regions was performed on peripheral blood mononuclear cells. The test was repeated to confirm the diagnosis.

Demographic details, clinical features at presentation, diagnostic information, manage-ment and follow-up status were recorded. The presumed mode of transmission was arrived at after a confidential interview with the parents regarding sexual behavior, history of blood transfusion in parents and child and the HIV serology status of parents. The transmission was attributed to blood transfusion in those children who had history of transfusion more than 3 months ago and whose parents were seronegative.

Results of investigations, which included complete blood counts, serum chemistry, chest radiograph and tuberculin test (considered positive if the induration was ³ 5 mm), were reviewed. CD4/CD8 counts, estimated by flow cytometry, were available in 15 children.

All patients meriting hospitalization were admitted in the general pediatric ward and were subsequently followed up in a specialty clinic. The acute infections in the children were managed as per standard guidelines for children with HIV infection(7,8). Children with tuber-culosis were treated with two months of inten-sive therapy (isoniazid, rifampicin, pyrazina-mide, ethambutol) followed by seven months of daily isoniazid and rifampicin. Antiretroviral therapy was recommended for HIV-infected children with clinical symptoms of HIV infec-tion or evidence of immune suppression(7,8). Zidovudine was administered in dose of 160 mg/m2 6 hourly and lamivudine 4 mg/kg 12 hourly. Immunizations, antitubercular prophy-laxis with isoniazid, Pneumocystis carinii pneumonia (PCP) prophylaxis with cotrimoxa-zole were advised according to the available guidelines(9,10). Nutritional rehabilitation was also instituted.

  Results

Twenty-seven children (20 boys, 7 girls) were diagnosed to have HIV infection over the last 4 years. The numbers of cases seen were 2 in 1996, 3 in 1997, 10 in 1998 and 11 in 1999 (till September). The median (range) age at presentation was 4.5 years (1 months - 15 years). Six children were less than 18 months age while 12 were aged 5 years or more at presentation. Twelve of these children were residents of Delhi, 5 from Uttar Pradesh and the rest from other neighboring states.

Vertical mode of transmission was presumed in 19 (70.4%) children on the basis of mother having a positive HIV serology; while blood transfusion was the possible mode of trans-mission in 8 (29.6%). All these 8 children had received a single transfusion at least 3 months before diagnosis in various hospitals. On the review of past prescriptions and history, the indications for these transfusions included ‘weakness’, ‘sepsis’ and ‘moderate anemia’. Of the 19 children with presumed vertical trans-mission, mothers of 4 were possibly infected by transfusion either during a surgical procedure or delivery; in all these cases, the fathers of the children were seronegative and history of high-risk behavior in the mothers was absent. In the rest, history of high-risk sexual behavior was forthcoming from the father. Therefore, in 12 of 27 (44.4%) children, contaminated blood trans-fusion seems to have been the source of infection.

Twenty children were diagnosed to have HIV infection on basis of clinical suspicion. Seven children were diagnosed after either parent had tested positive; of these 5 children were asymptomatic. Most of the symptomatic children had significant failure to thrive, fever and recurrent or persistent lower respiratory tract infections [LRTI] (Table I); recurrent LRTI were defined as 2 episodes of LRTI in 1 year or 3 episodes over any period of time, while persistent LRTI was defined as persistence of radiographic abnormality for more than 3 months(11). Thirteen children had tuberculosis, 6 of them had miliary/disseminated disease. Three children developed features of encephalopathy. Of the 15 children in whom CD4 counts were done, 11 had evidence of severe immunosupression, in one child the counts were as low as 2/ml. Table II shows the classification of these children into categories based on CDC guidelines(12).

Antiretroviral therapy could be instituted in only 11 children. Of these only 4 received a combination of lamivudine and zidovudine, the rest were treated with zidovudine only, based on the recommended guidelines at the time of starting treatment(7). All children received supportive care including nutritional rehabili-tation and anti infection prophylaxis to prevent occurrence of opportunistic infections(9,10).

Table I - Clinical Features of HIV Infected Symptomatic Children (n=22)

Clinical sign/symptom No. (%) positive
Failure to thrive 22 (100)
Fever 21 (95.4)
Recurrent LRTI 12 (54.5)
Persistent LRTI 7 (31.8)
Recurrent/Persistent LRTI 19 (86.4)
Recurrent diarrhea 10 (45.5)
Lymphadenopathy 9 (40.9)
Hepatomegaly 18 (81.8)
Oral Candidiasis 8 (36.4)
Splenomegaly 14 (63.6 )
Disseminated TB 6 (27.3)
CNS involvement 3 (13.6)
Bronchiectasis 2 (9.1)

 

  Discussion

This study reveals a progressive increase in the number of children diagnosed to have HIV infection over the last 4 years. We have found prior blood transfusion as an important mode of transmission in children even in those who do not have a primary hematological disorder.

The increase in number of cases diagnosed could be due to increasing prevalence of the infection or increased awareness of the disease. As increasing numbers of adults are diagnosed to have HIV infection, referral of their children could also contribute to the increase. Since these are early observations, no conclusions regarding trends can be made.

Nearly thirty per cent of children possibly acquired infection by blood transfusion; it is unfortunate that all the transfusions were given for poorly defined indications. If transfusion to the mother is also taken into account, 44.4% of all infections can be linked to use of contami-nated blood. Blood transfusion was an important source of infection in Nigerian children, even in under-fives(13). However, these findings are different from those in the developed countries, where blood transfusions account for less than 10% of pediatric HIV infection(14,15).

Screening of all donated blood has been mandatory for more than 6 years now(16). Despite such legislation, HIV infection in children due to blood transfusion seems to be a significant problem. As even adequate screening may not prevent transmission from a donor in the ‘window period’(17), blood products should be used only when absolutely indicated.

The clinical features are similar to those reported earlier from developing and developed nations(13,18-21). Since it was not possible to document the etiologic agents of pneumonia including P. carinii in the majority of our patients, most children received empirical anti-bacterial and anti-PCP therapy. Lymphoid interstitial pneumonitis (LIP), a common feature of pediatric AIDS, was not seen in any of our children. Most of the children in our series had advanced disease, as indicated by clinical features and profound immunosupression, which indicated delayed diagnosis. This was despite numerous previous contacts with the health care system. Therefore, a high index of suspicion is necessary for early diagnosis.

It seems that at present nutritional rehabilita-tion, managing and preventing infections are the only therapeutic interventions feasible in our setup, as most of the patients are unable to afford expensive antiretoviral therapy.

In countries like India, childhood problems such as malnutrition, recurrent/persistent pneumonia, recurrent diarrhea and hepato-splenomegaly are common. As these are also commonly encountered in HIV infected children, it raises the question whether all such children should be screened. While these were common presentations in our case-series, all the children had additional features, such as a history of prior transfusion or high risk behavior in the parents, which suggested HIV infection. However, in a small study from Bombay, 18% and 24% of children with disseminated tuberculosis (n = 50) and chronic diarrhea (n = 50) respectively were seropositive(22). Therefore, more information on pediatric HIV/AIDS is required to answer this question.

Our study highlights the need to restrict the use of blood products for only genuine indications, and also to have a high index of clinical suspicion to diagnose HIV infection in children.

Contributors: SKK coordinated the study, and was involved in collection of the data, clinical management and the drafting of the paper. He will act as the guarantor for the paper. RL, TS and YJ were involved in collection of the data, clinical management and the drafting of the paper. PS provided the virologic laboratory support. VS was involved in the preparation of the manuscript.

Funding: None.
Competing interests:
None stated.

Table II - Classificaton of Children with HIV Infection

Clinical category Immune category
(n = 27) CD4 count (n = 15)
N 5 > 25% 3
A 2 15-25% 1
B 0 <15% 11
C 20    

 

Key Messages

  • There is scant epidemiologic and clinical information about pediatric HIV infection in India.

  • Blood transfusion appears to be an important mode of transmission of HIV infection 
    even in children without a primary hematological disorder, emphasizing the need for 
    judicious use of blood products.

  • Most children had advanced disease, indicating the delay in diagnosis. Respiratory 
    infections and failure to thrive were the commonest clinical features. A high index of suspicion is required to diagnose HIV infection.

  • Antiretroviral therapy could be instituted in only a small proportion of children because 
    of the high cost of therapy. In our scenario, the supportive therapy assumes great importance.


  References
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  2. Giri TK, Pande I, Misra NM, Kailash HS, Uppal SS, Kumar A. Spectrum of clinical and laboratory characteristics of HIV infection in Northern India. J Com Dis 1995; 27: 131-141.

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  10. 1997 USPHS/IDSA Report on Prevention of Opportunistic Infections in Patients Infected with Human Immunodeficiency Virus. Pediatrics 1998; 102: 1064-1086.

  11. Wald ER. Recurrent and non-resolving pneumonia in children. Semin Respir Infect 1993; 8: 46-58.

  12. Centers for Disease Control and Prevention. 1994 Revised classification system for human immunodeficiency virus infection in children less than 13 years of age. MMWR 1994; 43 (No. RR-12).

  13. Emodi IJ, Okafor GO. Clinical manifestations of HIV infection in children at Enugu, Nigeria. J Trop Pediatr 1998, 44: 73-76.

  14. Centers for Disease Control and Prevention. HIV/AIDS Surveillance Report. 1997; 9: 8.

  15. World Health Organization/EC Collaborating Center on AIDS. AIDS Surveillance in Europe. Paris, WHO Quarterly Report No 39, 1993.

  16. The Gazzette of India: Extraordinary. Part IJ, Sec 3(i), Drugs and Cosmetics Act, 22nd January, 1993, p 13.

  17. Ward JW, Holmerg SD, Allen JR, Cohn DL, Critchley SE, Kleinman SH, et al. Transmission of human immunodeficiency virus (HIV) by blood transfusion, screened as negative for HIV antibody. N Engl J Med 1988; 318: 973-978.

  18. European Collaborative study. Children born to women with HIV-1 infection: Natural history and risk of transmission. Lancet 1991; 337: 253-260.

  19. Tovo PA, Martino M, Gabiano C, Capello N, D’Elia R, Loy A, et al. Prognostic factors and survival in children with perinatal HIV-1 infection. Lancet 1992; 339: 1249-1252.

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  21. Lambert HJ, Friesen H. Clinical features of pediatric AIDS in Uganda. Ann Trop Paediatr 1989; 9: 1-5.

  22. Merchant RH, Shroff RC. HIV seroprevalence in disseminated tuberculosis and chronic diarrhea. Indian Pediatr 1998; 35: 883-887.

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