The Triangle of Doom - The Monster at Our Door: The Global Threat of Avian Flu - page 37

ited every household that might have had contact with infected birds. Since the ordinary flu season was in
progress, vaccinations were made obligatory for poultry workers and their families, although this policy
was implemented too late to prevent several worrisome cases of co-infection by H7N7 and normal H3N1.
Meanwhile, the outbreak team was stunned by the scale of infection they discovered: 553 people out of
an exposed population of approximately 4,500 reported conjunctivitis or other symptoms; subsequent ser-
ological studies demonstrated that, in fact, as many as 2,000 of the exposed group had been infected but
not always sickened. Surgical masks and goggles, for whatever reason, had afforded the poultry cullers
little or no protection against the virus. 144
Moreover, relatives and housemates of poultry workers, who had no direct contact with infected birds,
also developed conjunctivitis. Public-health officials were convinced that the virus had acquired a lim-
ited but real ability to spread via person-to-person contact, although the exact mode of transmission was
unclear. The outbreak team also found evidence that H7N7 was accumulating dangerous mutations as
it passed through the human population. The event's most frightening moment was the death of a fifty-
seven-year-old veterinarian on 19 April; soon after exposure to sick chickens, he had developed viral
pneumonia (and later ARDS) instead of relatively benign conjunctivitis. Previously in good health, he was
not immune-compromised, nor did he have any underlying disease. Alarmingly, his catastrophic decline
matched the gruesome clinical descriptions of the 1997 deaths in Hong Kong, or for that matter, the acute
cases in 1918. 145
An urgent analysis of viral samples removed from the vet's lungs revealed that the strain that killed
him was not an avian-human reassortant, as some had feared, but a variant of the original H7N7 virus
which had undergone twelve amino acid substitutions; some mutations affected its hemagglutinin, while
others modified the PB2 protein, part of the polymerase complex that helped replicate the virus. While
HA has always been influenza's celebrity protein because of its crucial role in determining host range,
and possibly, virulence, the Dutch researchers, like colleagues elsewhere, were coming around to the idea
that mutations in internal proteins—such as PB2 or the nonstructural protein NS2—might be important
co-factors in the severity of infection. They knew that previous research had shown that a mutation in
PB2 had increased the virulence of H5N1 in mice—perhaps H7N7 reacted the same way. In any event,
the Dutch outbreak, with its deadly index case, now had the WHO's attention, even if the world press was
diverted by the ongoing battle against SARS. 146
After H7N7's brief forays into Belgium and Germany, the outbreak was officially contained in August.
Dutch experts regarded it as another harrowingly close call with a potentially deadly pandemic:
Although we launched a large and costly outbreak investigation (using a combination of pandemic
and bioterrorism preparedness protocols), and despite decisions being made very quickly, a sober-
ing conclusion is that by the time full prophylactic measures were reinforced . . . more than 1000
people from all over the Netherlands and from abroad had been exposed. Therefore if a variant with
more effective spreading capabilities had arisen, containment would have been very difficult. 147
Like the earlier H9 outbreak, the Gelderland epidemic demonstrated that multiple subtypes (including H9,
H7, and possibly H4 and H6, as well as reborn H2) were racing H5 to the pandemic finish line. The rapid-
ity and scale of the Dutch outbreak also proved that south China no longer had a monopoly on deadly
influenza: there were now multiple epicenters.
The H7N7 crisis also provided an additional reason for public-health officials and human influenza
researchers to talk to their expert animal-virus counterparts. In the past, human and veterinary medicines
had been parallel sciences that only occasionally intersected during rare interspecies disease events, but
now the two viral universes, animal and human, seem to be locked together in a frenetic evolutionary