Since the end of last winter's influenza season in the Northern
Hemisphere, low levels of activity of influenza
A/Taiwan/1/86(H1N1)-like strains (the predominant strain last
winter)
have been reported in Asia and Oceania. Similar strains have been
reported from outbreaks in South Africa (Table 1). An isolated
infection with influenza A(H1N1) was confirmed in the United
Kingdom.
In the Americas, A/Taiwan/1/86-like viruses have been reported from
Uruguay and Chile -- the first reported spread of the 1986 A(H1N1)
variant to South America following its circulation in North
America.
Influenza B has been the most frequently isolated virus. In
Oceania, localized outbreaks were reported in Australia and
epidemic
activity in New Zealand. In the Americas, influenza B was isolated
from children in Guatemala during May, and localized influenza B
activity was reported in Brazil during July and August. Influenza B
infections were documented in the United States during summer and
early fall. A child in Wisconsin became ill during June upon
returning
from the Philippines, where the infection was most likely acquired.
Four cases were reported from Tucson, Arizona: one in July and
three
in October. In October, influenza B virus was also isolated from a
14-year-old in Hawaii.
Influenza A(H3N2) occurred sporadically in Australia and New
Zealand, but no major outbreaks were reported. However, from April
through September, an increasing number of Asian and Pacific
countries
including Hong Kong, Singapore, the People's Republic of China,
Guam,
and Taiwan reported A(H3N2) isolates. Brazil reported a localized
outbreak of influenza A(H3N2) in Rio de Janeiro during May and
June.
In the United States, one patient, a Vermont resident, has had a
serologically confirmed case of influenza A(H3N2). The patient was
among a group of tourists who developed respiratory illness while
on a
ship off Alaska in late August (1).
Reported by: National Influenza Centers, Microbiology and
Immunology
Svcs, World Health Organization, Geneva. Contractors of the Acute
Respiratory Diseases Program of the National Research Council Board
on
Science and Technology in Developing Nations, Washington, DC. Naval
Medical Research Unit 2, Indonesia. US Air Force School of
Aerospace
Medicine, San Antonio, Texas. G Ray, MD, Arizona Health Svcs
Center,
Tucson, Arizona. Participating State Epidemiologists and State
Laboratory Directors. Div of Field Svcs, Epidemiology Program
Office;
WHO Collaborating Center for Influenza, Influenza Br, Div of Viral
Diseases, Center for Infectious Diseases, CDC.
Editorial Note
Editorial Note: International surveillance data confirm the
continuing circulation of three antigenically distinct influenza
viruses: type A(H3N2), type A(H1N1), and type B. Influenza A(H1N1)
and
A(H3N2) viruses are antigenically related through internal
proteins,
rather than through the surface glycoproteins, hemagglutinin (H)
and
neuraminidase (N). Whereas antibodies that recognize the outer
proteins (particularly the hemagglutinin) can neutralize virus
infectivity or reduce spread of virus, antibodies to the internal,
cross-reactive proteins do not appear to prevent infection.
However,
immunity to these shared proteins may be important in terminating
infection through the actions of cytotoxic T-cells and might
contribute to early recovery (4). H3-containing viruses were
responsible for the Hong Kong influenza pandemic of 1968, which
spread
among all age groups, and have evolved antigenic variants
responsible
for epidemics with associated excess mortality in the United States
during seven seasons since then.
H1-containing viruses reappeared in 1977 after a 20-year
absence
and caused epidemics with low or no mortality during the 1978-79,
1983-84, and 1986-87 influenza seasons. Many persons born before
about
1955 are sufficiently immune to H1N1 viruses evolving since 1977
that
they are resistant to infection or have mild illnesses.
Consequently,
in recent years, early recognition of H1N1 virus has always
occurred
in children or young adults. However, the first recognized A(H3N2)
infections in the United States usually involve adults, as they
apparently did this year with the tourists in Alaska (1).
Influenza B viruses, which are antigenically distinct from type
A
viruses, were first recognized in the 1930s. Although variation
occurs
in the hemagglutinin of type B viruses, the strains represent a
continuum, with no distinct subtypes. Despite this, from the
mid-1930s
until 1970, nine probable epidemics of influenza B (2) were
associated
with excess mortality. However, from 1970 to 1979, when influenza B
epidemics occurred several times, infections appeared to be mainly
confined to children or young adults, and no excess mortality
occurred. With the appearance of the B/Singapore/79 strain in 1979,
the pattern of excess mortality reemerged, and many B virus
infections
and associated deaths occurred among the elderly (3). Influenza B
viruses were also responsible for major outbreaks or epidemics in
the
United States in 1983-84 (the B/USSR/83 variant) and in 1985-86
(the
B/Ann Arbor/86 variant).
Because the degree of spread of current influenza strains is
unpredictable and because it is likely from current observations
that
both type A(H3N2) and type B viruses will circulate this winter,
high-risk persons and those providing their care at home or in
medical
facilities should be encouraged, in advance of any outbreaks in
their
area, to receive the trivalent vaccine licensed for this year. The
available antiviral agent, amantadine, is effective against all
known
subtypes of influenza A viruses but is ineffective against
influenza B
viruses. Laboratories providing support for physicians with
patients
requiring urgent care (e.g., hospitalized patients) should at this
time be evaluating their capabilities to perform rapid viral
diagnosis
so as to differentiate between influenza A and B infections.
Information about reagents and procedures for such diagnosis may be
obtained from state health department laboratories or from CDC.
References:
CDC. Outbreak of influenza-like illness in a tour
group--Alaska.
MMWR 1987;36:697-8, 704.
Noble GR. Epidemiological and clinical aspects of influenza.
In:
Beare AS, ed. Basic and applied influenza research. Boca Raton,
Florida: CRC Press, 1982:11-50.
Nolan TF, Goodman RA, Hinman AR, Noble GR, Kendal AP, Thacker
SB.
Morbidity and mortality associated with influenza B in the
United
States, 1979-1980. A report from the Center for Disease
Control. J
Infect Dis 1980;142:360-2.
McMichael AJ, Gotch FM, Noble GR, Beare AS. Cytotoxic T-cell
immunity to influenza. N Engl J Med 1983;309:13-7.
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