Flu in the slums

Australia's severe flu season reminds us, in dramatic fashion, that "regular" (seasonal) influenza can still be a severe disease. It's not just the elderly, but children, too. What about children in the developing world? What would you find if you went into one of Bangladesh's urban slums? We now have some information, presented as a Letter to the Editor in CDC's journal, Emerging Infectious Diseases. Children under the age of 13 with fever and symptoms of an influenza-like illness (dengue fever was excluded) in 2001 were tested for acute infection via antibodies to H1N1 or H3N2 influenza, influenza B, respiratory syncytial virus, parainfluenza virus types 1,2 and 3, or human metapneumovirus (HMPV). The site was the Kamalapur surveillance and intervention site in a slum section in Dhaka, Bangladesh. which was divided into seven areas, each subdivided into geographic clusters of 50 - 100 houseeholds. Eighty-six cllusters were randomaly selected and 5000 househlds wh=ithin them enrolled. What did they find?

Acute infections coincided with warm pre-monsoon and monsoon periods. Of 128 children in which there was sufficient serum for influenza testing (out of a total of 198 with febrile illness during the year in these households), one in six had acute influenza infections, 10 influenza A (80% H1N1), 13 with influenza B (2 children had both A and B infections). The influenza cases were older than the non-influenza cases, but the only symptom which separated them from other viral causes of febrile respiratory illness was a greater frequency of joint and muscle aches. Only three of the influenza cases had pneumonia on clinical exam. Thus most of the cases discovered in this survey would not have come to a hospital or clinic.

What we learn is that infection with influenza virus (A and B) is the cause of a significant portion (16%) of respiratory disease in an urban slum, but that most influenza-like illness is from other agents. This is not different than elsewhere. In the event of a pandemic the proportion of influenza infections will rise dramatically but even if it goes up by a factor of five, over half of the febrile illnesses in children would still be from non flu viruses. This is something to keep in mind.

Something else to remember is that even carefully done studies like this are difficult to do and come with many caveats:

First, the surveillance system was not originally designed to identify influenza and relied on fever for specimen collection. Our retrospective selection criteria reflected the classic initial manifestations of influenza, and thus could have missed nonfebrile cases. Second, the study was not designed to reflect age distribution of children with respiratory infection, but rather those with fever and who had adequate amounts of available sera. This feature potentially biases toward older children. Third, data describe only 1 year, and patterns of illness may differ in other years. Fourth, acute infection was determined by serologic analysis. Previous studies in Bangladesh reported nutrition-related impaired immune responsiveness. Thus, some influenza-infected children who showed a nondetectable immune response may not have been included. (Brooks et al., Emerging Infectious Diseases [Epub ahead of print], cites omitted)

It's another little piece of the puzzle. Where it goes in the big pattern, where we have so many missing pieces, we don't know yet.