Problems with diagnosis are related to the fact that flu-like illnesses may not be caused by influenza viruses. If the clinical syndrome alone is considered indicative of influenza, the apparent efficacy of vaccine will decline; infection by other agents, unaffected by the vaccine, will be counted against it. Laboratory identification of the influenza virus would solve that, but isolation of the virus is too inconsistent among cases to be useful in assessing vaccine effectiveness. Clinicians often rely on a four-fold rise in antibody level, from before to after illness, to show infection by a particular agent. But the usual antibody rise in response to infection may be stifled by recent vaccination. Hence, persons genuinely ill from flu soon after getting shots might not be counted as cases of influenza; apparent vaccine efficacy then would rise higher than it was in fact.
Finally, observed vaccine effectiveness in one population may not apply to others. Findings in the military may not apply to civilian populations; findings in nursing homes may not apply to the elderly living on their own; and findings in one age group may not apply to another.
Taken together, the foregoing comments elaborate, selectively, the five features of influenza we set forth in Chapter XII: first, a capricious virus; second, short-lived (and partial) protection against it; third, attribution to it of assorted other ailments; fourth, a mimicking by others of its symptoms; and as a consequence, the fifth, entanglement of influenza-the-virus with influenza-the-disease, causing confusion in the measurement of impact. These are the features that, taken together, give influenza standing in our eyes as an extremely slippery phenomenon.
Regarding swine flu, one question remains to be asked. In 1918, something extraordinary happened: Why? What accounts for the most devastating influenza pandemic history records? Why were young, healthy adults carried off as surely as the elderly and infirm? Epidemiologists have debated for sixty years. Theories abound, but nobody knows. Perhaps concomitant bacterial or other infection played a major role, perhaps the stress of war or other environmental factors made a difference. If so, well and good, for the times have changed and today we have potent antibiotics. But conceivably a large part of that pandemic mortality was due to some intrinsic feature of the virus, a characteristic that may be harbored even today on a gene fragment somewhere in the animal kingdom, a gene that could just possibly combine with human virus.
Despite impressions left by the swine flu affair, this remains a possibility. Ford could not accurately predict the killer and was thus severely limited in seeking to guard everyone against it. Mathews, Cooper and Sencer could not do so either. Neither could their scientific advisers. Nor can anyone in 1978. Only research, perhaps, someday will manage that.