B. D. Schoub, M.D., D.Sc., F.R.C.Path.,72 B. N. Archer, B.Med., M.P.H.,73 C. Cohen, M.Sc., M.B.B.Ch., F.C.Path.,73 D. Naidoo, M.Sc.,74 J. Thomas, M.B.B.Ch., F.C.Path.,74 C. Makunga, B.Sc.Hons., M.B.B.Ch.,74 M. Venter, Ph.D.,74 G. Timothy, M.B.B.Ch.,75 A. Puren, Ph.D., M.B.B.Ch.,73 J. McAnerney, R.N.,74 A. Cengimbo, M.B.B.Ch.,74 and L. Blumberg, M.B.B.Ch., M.Med.73
The 2009-H1N1 influenza A pandemic took many by surprise. Unexpectedly arising in North America and spreading rapidly throughout the northern hemisphere summer, it encircled the globe within a couple of months. This event has again highlighted the crucial need for a more comprehensive global surveillance system for influenza (Lipsitch et al., 2009; Ortiz et al., 2009).
The World Health Organization (WHO) Influenza Programme has provided valuable information on circulating influenza viruses globally through its network of 128 national influenza centers in 99 countries, supported by five WHO collaborative centers (WHO, 2002, 2008, 2009a). Virus isolates from the majority of these laboratories provide the basis for the annual recommendation by WHO of the strains to be incorporated into the influenza vaccines for the Northern and Southern Hemispheres in February and September, respectively, of each year (WHO, 2009b,c).
However, the African continent is poorly capacitated for influenza surveillance (Schoub et al., 2002). Of the 46 countries constituting the WHO AFRO region, only 18 possess national influenza centers and only 10 are able to perform diagnostic PCR (WHO, 2009d,e). As of September 30, 2009, 12,382 cases of 2009-H1N1 influenza A were reported from this region; the great majority (93 percent) were reported from South Africa (WHO, 2009f).
Systematic surveillance for influenza in South Africa dates back to 1984, when the first surveillance network of sentinel medical practitioners, the “Viral
Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 283
283
APPENDIX A
A10
PRELIMINARY OBSERVATION OF THE
EPIDEMIOLOGY OF SEASONAL AND PANDEMIC
INFLUENZA A (H1N1) IN SOUTH AFRICA, 2009
B. D. Schoub, M.D., D.Sc., F.R.C.Path.,72 B. N. Archer, B.Med., M.P.H.,73
C. Cohen, M.Sc., M.B.B.Ch., F.C.Path.,73 D. Naidoo, M.Sc.,74 J. Thomas,
M.B.B.Ch., F.C.Path.,74 C. Makunga, B.Sc.Hons., M.B.B.Ch.,74 M. Venter,
Ph.D.,74 G. Timothy, M.B.B.Ch.,75 A. Puren, Ph.D., M.B.B.Ch.,73 J. McAnerney,
R.N.,74 A. Cengimbo, M.B.B.Ch.,74 and L. Blumberg, M.B.B.Ch., M.Med.73
Introduction
The 2009-H1N1 influenza A pandemic took many by surprise. Unexpectedly
arising in North America and spreading rapidly throughout the northern hemi-
sphere summer, it encircled the globe within a couple of months. This event has
again highlighted the crucial need for a more comprehensive global surveillance
system for influenza (Lipsitch et al., 2009; Ortiz et al., 2009).
The World Health Organization (WHO) Influenza Programme has provided
valuable information on circulating influenza viruses globally through its network
of 128 national influenza centers in 99 countries, supported by five WHO col-
laborative centers (WHO, 2002, 2008, 2009a). Virus isolates from the majority
of these laboratories provide the basis for the annual recommendation by WHO
of the strains to be incorporated into the influenza vaccines for the Northern and
Southern Hemispheres in February and September, respectively, of each year
(WHO, 2009b,c).
However, the African continent is poorly capacitated for influenza surveil-
lance (Schoub et al., 2002). Of the 46 countries constituting the WHO AFRO
region, only 18 possess national influenza centers and only 10 are able to per-
form diagnostic PCR (WHO, 2009d,e). As of September 30, 2009, 12,382 cases
of 2009-H1N1 influenza A were reported from this region; the great majority
(93 percent) were reported from South Africa (WHO, 2009f).
Influenza Surveillance in South Africa
Systematic surveillance for influenza in South Africa dates back to 1984,
when the first surveillance network of sentinel medical practitioners, the “Viral
72National Institute for Communicable Diseases and University of the Witwatersrand, South Africa.
73 National Institute for Communicable Diseases, South Africa.
74 National Institute for Communicable Diseases and University of Pretoria, South Africa.
75 School of Public Health, University of the Witwatersrand, South Africa.
OCR for page 283
284 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
Watch,” was established in Johannesburg (Besselaar et al., 2001; McAnerney et
al., 1994; Schoub et al., 1986, 1994). Currently, the Viral Watch network consists
of 243 sentinel sites, which provide clinical and epidemiological data on influenza
in the community, as well as material for isolation and antigenic and molecular
characterization of viruses, for input to WHO for decision making as to annual
vaccine composition recommendations. In response to the 2009-H1N1 influenza
A pandemic, the Viral Watch program was supplemented with an additional
10 hospital-based sites situated in all 9 provinces. Additional surveillance was
provided by a Severe Acute Respiratory Infection (SARI) surveillance program,
also established in 2009 in four large hospitals in three provinces. In addition, a
large number of diagnostic specimens were received by the laboratory following
widespread concern around the pandemic. Finally, active surveillance was intro-
duced to collect information on all laboratory-confirmed cases due to 2009-H1N1
influenza A nationally, from both private and public laboratories.
Up until 2009, the pattern of influenza isolations, as identified through the
Viral Watch program, universally showed a typical unimodal distribution, as
shown in Figure A10-1, with a median onset at week 23 (range 15-28), a median
peak at week 27 (range 20-32) and a median duration of 10 weeks (range 7-17)
(Figure A10-2). This pattern is consistent with other temperate Southern Hemi-
sphere countries. The distribution of influenza subtypes is shown in Figure A10-3.
Over the past 25 years, H3N2 was the dominant subtype in 13 of the years, H1N1
in 7, and influenza B in 2 of the years, with an equal distribution of all three in
2 years and an equal combination of H3N2 and B in one of the years.
The 2009-H1N1 Influenza A Pandemic in South Africa
The epidemic curve of the 2009-H1N1 influenza A pandemic as determined
through active surveillance for all laboratory-confirmed cases nationally in South
Africa, as of September 29th, is shown in Figure A10-4. The first case of 2009-
H1N1 influenza A was confirmed in South Africa on June 13, some 2 months after
that of the United States and a month or more after other Southern Hemisphere
countries (Table A10-1). The reason for this inordinate delay in importation
into South Africa is probably related to the relatively low volume of air traffic
between it and North America (Chen and Wilson, 2008; Khan et al., 2009).
The first confirmed South African case was in a healthy 16-year-old boy who
had visited family in Texas and returned to South Africa on June 10th presenting
with clinical signs and symptoms of influenza-like-illness (ILI). A positive diag-
nosis of 2009-H1N1 influenza A infection was made at the National Institute for
Communicable Diseases (NICD) using the CDC real-time (RT-) PCR protocol
for the detection and characterization of swine influenza. He was treated with
oseltamivir on day 3 after onset of symptoms and made an uneventful recovery; no
secondary contacts were identified. During the following 2 weeks, NICD contin-
ued to detect sporadic (H1N1) among individuals returning from North America,
OCR for page 283
2005 2006
120 70
120 70
60
60 100
100
50
50 80
80
40
40
60
60
30
30
40
Isolation rate (%)
40
Isolation rate (%)
20
Number of isolates
Number of isolates
20
20
20 10
10
0 0
0 0
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 48
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 48
Week Week
A H1N1 A H3N2 B Isolation rate A H1N1 A H3N2 B Isolation rate
2008
2007
75 140 70 40
120 60
30
100 50
50
80 40
20
60 30
25
40
**Isolation rate (%)
Number of isolates
Number of isolates
Number Specimens
20
10
20 10
0 0 0 0
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51 1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51
Week Week
A H1N1 A H3N2 B Isolation rate
A H1N1 A H3N2 Influenza B Specimens
285
FIGURE A10-1 Influenza results by type and subtype: South Africa 2005-2008.
OCR for page 283
R01627
vector editable
landscape above, scaled for portrait below
286 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
2007
2006
• Median onset: 2005
2004
– Week 23 2003
2002
2001
– Range 15-28 2000
1999
• Median peak: 1998
1997
1996
– Week 27 1995
1994
– Range 20-32 1993
1992
• Median 1991
1990
1989
duration: 1988
1987
– 10 weeks 1986
1985
– Range 7-17
15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40
Apr May Jun Jul Aug Sep
Epidemiological week
Mean onset
FIGURE A10-2 Onset and duration of influenza season, South Africa, 1985-2007.
100
80
60
Percentage
40
20
0
1985 1987 1989 1991 1993 1995 1997 1999 2001 2003 2005 2007
1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 2006 2008
B A H3N2 A H1N1
FIGURE A10-3 Influenza strains detected, South Africa, 1984-2008.
Figure A10-3
OCR for page 283
287
APPENDIX A
2,500 25
Confirmed deaths
Confirmed cases
Number of Deaths
Number of Cases
2,000 20
1,500 15
1,000 10
500 5
0 0
May 25-31
Jun 08-14
Jun 22-28
Jul 06-12
Jul 20-26
Aug 03-09
Aug 17-23
Aug 31-Sep 06
Sep 14-20
Sep 28-Oct 04
Oct 12-18
Oct 26-Nov 01
Nov 09-15
Nov 23-29
Dec 07-13
Week
FIGURE A10-4 Epidemic curve of laboratory-confirmed pandemic 2009-H1N1 influenza
A cases and deaths by week, South Africa, as of December 15, 2009 (n[cases] = 12,683).
Figure A10-4
R01627
TABLE A10-1 Firstuneditable bitmapped image
Confirmed Cases of 2009-H1N1 Influenza A
type replaced
Argentina May 16
Australia May 7
Chile May 17
New Zealand April 28
Uruguay May 27
USA April 17
South Africa June 13
South America, and Europe, with documented cases of local transmission resulting
to a close household contact. A week later, on June 27th, an outbreak of H1N1
occurred at a sports event in Johannesburg, where 20 young athletes with ILI were
confirmed at NICD as pandemic H1N1. The index case of this cluster was proba-
bly an 18-year-old male attending from Zimbabwe, believed to have been infected
while in transit (possibly through contact with other travellers). Over the next
2 weeks the number of confirmed cases rose steeply and, on July 13th, a month
after the first case was diagnosed, over 100 cases had been confirmed in South
Africa. At that stage the majority of cases were identified in the Gauteng province,
the province with the largest population (incorporating both Johannesburg and
Pretoria) and with the highest international exposure through OR Tambo Interna-
tional Airport in Johannesburg. In conformance with the WHO recommendations
OCR for page 283
288 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
to cease universal laboratory testing of all suspected cases once the 100-case mark
had been reached, the NICD and other academic centers reverted to testing only
selected cases. Of the first 100 cases, 42 gave a travel history consistent with hav-
ing acquired the infection abroad (Table A10-2).
Epidemiological Characteristics
As of September 29, 2009, a total of 11,729 cases had been confirmed
nationally (Figure A10-4). The first death was confirmed on July 28th; a 22-year-
old male student with no apparent comorbid condition. As of September 28th,
83 deaths had been laboratory-confirmed; the details are described below.
The 2009 influenza season, as reflected through the Viral Watch program
(community influenza surveillance), showed, for the first time, a bimodal curve
(Figure A10-5). A similar bimodal distribution of 2009-H1N1 influenza A cases
was also seen from the SARI program (Figure A10-6). Using mid-year population
estimates (STATSSA, 2009), incidence data of laboratory-confirmed cases per
100,000 population were calculated for each of the nine provinces of South Africa
(Table A10-3). The highest incidence was, not unexpectedly, seen in the Gauteng
province, the commercial hub of the country, which is the smallest province geo-
TABLE A10-2 Travel History of 42 Cases Within the First 100 Investigated
North America 6 14%
USA 6
South America 5 12%
Argentina 2
Brazil 2
Chile 1
Europe 15 36%
Other European Countries 5
Germany 1
Greece 1
Netherlands 1
Sweden 1
Turkey 1
UK 5
Asia 8 19%
China 2
Singapore 4
Dubai 1
Bali 1
Other African Countries 3 7%
Mauritius 2
Zimbabwe 1
Australia 5 12%
OCR for page 283
289
APPENDIX A
300 80
250
60
% Detection rate
200
Number
150 40
100
20
50
0 0
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51
Week
A awaiting typing Seasonal A (H1N1) A H3N2
B Pandemic A (H1N1) Detection rate
FIGURE A10-5 Positive samples by influenza types and subtype: Viral Watch South
Africa 2009.
Figure A10-5
R01627
uneditable bitmapped image 50
50
45
45
40
40
35
35
Number of samples
Detection rate (%)
30
30
25
25
20
20
15
15
10
10
5
5
0
0
1 3 5 7 9 11 13 15 17 19 21 23 25 27 29 31 33 35 37 39 41 43 45 47 49 51 53
Weeks
Detection rate
A (Unsubtyped) A H1N1 (Seasonal) A H1N1 (Novel) A H3N2 B
FIGURE A10-6 Severe acute respiratory illness (SARI) surveillance: respiratory virus
Figure A10-6
report.
R01627
uneditable bitmapped image
type replaced
OCR for page 283
290 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
TABLE A10-3 Laboratory-Confirmed Pandemic 2009-H1N1 Influenza A
Cases by Province, South Africa, as of December 15, 2009
Laboratory-Confirmed Cases
Incidence Rate
Province Cumulative Total (per 100,000 population)
Eastern Cape 682 10.26
Free State 314 10.82
Gauteng 5,579 52.98
KwaZulu-Natal 2,258 21.61
Limpopo 545 10.43
Mpumalanga 500 13.86
Northern Cape 134 11.68
North West 465 13.48
Western Cape 2,113 39.44
Unknown 42 —
South Africa Total 12,632 25.61
graphically but has the largest population, the highest population density, and the
greatest contact internationally. This was followed by Western Cape (including
Cape Town) and KwaZulu-Natal (including Durban). These provinces are also
more urbanized and individuals there would be more likely to seek care and
diagnostic testing for influenza than persons in more rural provinces. The age
distribution of cases showed a predominance in children and young adults as also
seen in countries throughout the world (CDC, 2009; Gilsdorf and Poggensee,
2009; Levy-Bruhl and Vaux, 2009; Lytras et al., 2009; Munayco et al., 2009;
WHO, 2009g)—Figure A10-7, Table A10-4. The ages ranged from newborn to 90
years with a median age of 16 years. The age distribution curves for the different
influenza subtypes as they presented in the Viral Watch program were compared.
The pandemic 2009-H1N1 influenza A pattern was distinct from both the H3N2
of 2009 and the seasonal H1N1 of 2008 (Figures A10-8 and A10-9) and more
closely resembled that of influenza B in 2009 (Figure A10-10).
Preliminary Investigation of the First 100 Cases
A more detailed follow-up investigation was carried out on the first 100 cases
in South Africa. These cases, however, represented a more affluent, upper socio-
economic section of the population and were also not representative of the racial
composition of the South African population (Table A10-5). International travel
within 7 days of onset of symptoms was reported in 42 cases and no travel or
any contact with international travelers in the remainder. Only a minority of
cases had recognized comorbid conditions—asthma (7), heart disease (5), preg-
OCR for page 283
291
APPENDIX A
3000
2412
2500
2188
2082
Number of cases
2000
1500 1281
991
1000
775
597
558
450
500 359 316
238
130 58 62
0
<1 1-4 5-9 10-14 15-19 20-24 25-29 30-34 35-39 40-44 45-49 50-54 55-59 60-64 65+
Age group (years)
Figure A10-7
FIGURE A10-7 Number of laboratory confirmed pandemic 2009-H1N1 influenza A
cases by age group, as of December 15, 2009 (n = 11,729).
R01627
uneditable bitmapped image
type replaced
TABLE A10-4 Pandemic 2009-H1N1 Influenza A Cases by Age Group, South
Africa, as of December 15, 2009
Incidence per 100,000a
Age (years) Number Percentage of total
1-4 1,229 243 10
5-9 2,082 402 18
10-14 2,412 460 21
15-19 2,188 420 19
20-24 1,281 260 11
25-29 775 175 7
30-34 558 144 5
35-39 597 182 5
40-44 450 184 4
45-49 359 159 3
50-54 316 155 3
55-59 130 79 1
60-64 58 45 0.5
>65 62 26 0.5
aPopulation figures based on mid-year population estimates 2009 (STATSSA, 2009).
OCR for page 283
292 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
50
40
30
Percentage
20
10
0
=60yr
Age group
A H3N2 Pandemic H1N1
FIGURE A10-8 Age distribution of patients with seasonal A H3N2 and pandemic 2009-
H1N1 influenza A.
50
Figure A10-8
40
R01627
vector editable
30
Percentage
20
10
0
=60yr
Age group
Seasonal H1N1(2008) Pandemic H1N1
FIGURE A10-9 Age distribution of patients with seasonal A H1N1 (2008) and pandemic
2009-H1N1 influenza A.
Figure A10-9
R01627
editable vectors
OCR for page 283
293
APPENDIX A
50
40
30
Percentage
20
10
0
=60yr
Age groups
Infuenza B Pandemic H1N1
FIGURE A10-10 Age distribution of patients with influenza B and pandemic 2009-H1N1
influenza A.
TABLE A10-5 Breakdown of First 100 Cases by Race
Figure A10-10 Total South African Populationa
H1N1 Cases
R01627
Race N / Percentage N / Percentage
editable vectors
Asian 12 2.6
African 6 79.3
Mixed race 5 9.0
White 74 9.1
Unknown 3 —
Total 100 100.0
aBased on 2009 mid-year population estimates (STATSSA, 2009).
nancy (3), and obesity (2) (BMI > 30). The distribution of reported symptoms in
these cases followed that seen generally throughout the world (Eurosurveillance,
2009b-e)—Figure A10-11.
The mean time from onset of symptoms to presentation at a health facility
was 2.0 days (SD 1.5 days, range 0-7 days) and symptom onset to recovery was
7.9 days (SD 1.5 days, range 0-7 days). Eleven cases were hospitalized, some
as a precaution to isolate the patient and 6 developed complications including
pneumonia (3), otitis media (1), myocarditis (1), and other (1).
OCR for page 283
294 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
100 88
75 74
80 68 65 64
% of cases
55
60
47
40 32
25
18
20 13
7
0
Cough
Sore throat
Feeling
feverish
Nasal
congestion
Muscle pain
Headache
Fever >38
Sneezing
Shortness
of breath
Diarrhea
Vomiting
Conjunctivitis
Nausea
FIGURE A10-11 Reported symptoms in first 100 confirmed cases, South Africa.
Symptoms reported
Preliminary Investigation of Deaths
Figure A10-11
As of December 17, 2009, 92 laboratory-confirmed deaths were recorded
R01627
in South Africa. The ages range from 3 days to 70 years, with a median age of
33 years—significantly higher than bitmapped image of 15 years. Deaths
uneditable the overall median age
were more common in females (60 percent) whereas the gender ratio was approx-
type replaced
imately equal in nonfatal cases. This was due, to a large extent, to the unusually
large proportion of deaths in pregnant woman: 26 of the 91 cases (28 percent)
with known clinical history. All but three of the deaths in pregnancy occurred in
the third trimester (one in the second trimester and two in the puerperium). Of
the 14 pregnancy-related fatal cases with known HIV status, 10 (71 percent) were
HIV-positive; the national HIV seroprevalence in women attending public-sector
antenatal clinics is 29 percent (Department of Health, 2009). Other comorbid con-
ditions in this group were tuberculosis (TB) in 9 (11 percent) and pre eclampsia
in 2 (8 percent).
Of the 66 nonpregnant deaths, most (61 percent) were male. HIV was
recorded in 6 of 17 patients (35 percent) as compared to the overall HIV preva-
lence of 17 to 19 percent for South Africa (Department of Health, 2009). Active
TB was found in 2 of 46 cases (4 percent) and other comorbid conditions included
obesity (12 of 46; 26 percent), diabetes (11 of 45; 24 percent), and cardiac disease
(8 of 44; 18 percent).
Conclusion
In many respects the 2009-H1N1 influenza A pandemic has behaved simi-
larly to both developed and developing countries throughout the world. These
OCR for page 283
295
APPENDIX A
include age distribution, epidemiology, clinical features and overall relative mild-
ness. The late introduction into South Africa appeared, to some extent, to be due
to relatively lower air traffic levels and provided a window to observe any further
genetic movement in the virus. Phenotypic changes in the virus were certainly
not apparent from the clinical and epidemiological observations. Virological
characterization is presently under way to determine antigenic drift, resistance,
and presence of any virulence markers. Two particular risk groups in South
Africa do perhaps need to be highlighted—those involving pregnancy and HIV.
Although pregnancy is a well-recognized risk factor in H1N1 (Jamieson et al.,
2009; Mangtani et al., 2009), South Africa experienced an unusually high number
of women in late pregnancy who succumbed to H1N1. Second, the high rate of
HIV positivity in both pregnant and nonpregnant individuals who died (consid-
erably higher than the background HIV positivity in these two groups) needs
special attention. In both groups the HIV prevalence was nearly double that of
the respective national prevalence rates (Department of Health, 2009). These are,
however, preliminary observations and are subject to potentially significant bias.
For example, pregnancy may well be a factor that could increase the likelihood
of a death being reported because of relatively greater access to a health facility.
Also HIV may be artificially high as patients with more advanced disease and the
stigma of HIV infection may be more likely to be treated and also more likely to
succumb to H1N1. Whether persons living with HIV constitute a risk group for
more severe influenza infection in the absence of secondary infection remains to
be established (Kunisaki and Janoff, 2009). A study in an HIV-infected pediatric
population in South Africa, also failed to demonstrate differences in outcome of
influenza infection (Madhi et al., 2002). An understanding of these risk factors
is of urgent importance, particularly in countries with a high prevalence of HIV
and limited vaccine resources.
References
Besselaar, T. G., B. D. Schoub, and J. M. McAnerney. 2001. Phylogenetic studies of South African
influenza A viruses: 1997-1999. In Options for the Control of Influenza IV, edited by A. D. M. E.
Osterhaus, N. Cox, and A. W. Hampson. Proceedings of the Fourth International Conference on the
Control of Influenza IV, Crete, Greece, September 23-28, 2000. Excerpta Medica 1219:139-145.
CDC (Centers for Disease Control and Prevention). 2009. Update: Novel influenza A (H1N1)
virus infections—worldwide, May 6, 2009. Morbidity and Mortality Weekly Report
58(RR17):453-457.
Chen, L. H., and M. E. Wilson. 2008. The role of the traveler in emerging infections and magnitude
of travel. Medical Clinics of North America 92(6):1409-1432.
Department of Health. 2009. 2008 National Antenatal Sentinel HIV and Syphilis Prevalence Survey,
South Africa.
ECDC Working Group on Influenza A(H1N1)v. 2009. Preliminary analysis of influenza A(H1N1)v
individual and aggregated case reports from EU and EFTA countries. Eurosurveillance 14(23),
http://www.eurosurveillance.org/images/dynamic/EE/V14N23/art19238.pdf (accessed Octo-
ber 22, 2009).
OCR for page 283
296 IMPACTS OF THE 2009-H1N1 INFLUENZA A PANDEMIC
Gilsdorf, A., and G. Poggensee. 2009. Influenza A(H1N1)v in Germany: the first 10,000 cases.
Eurosurveillance 14(34), http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19318
(accessed October 22, 2009).
Jamieson, D. J., M. A. Honein, S. A. Rasmussen, J. L. Williams, D. L. Swerdlow, M. S. Biggerstaff,
S. Lindstrom, J. K. Louie, C. M. Christ, S. R. Bohm, V. P. Fonseca, K. A. Ritger, D. J. Kuhles,
P. Eggers, H. Bruce, H. A. Davidson, E. Lutterloh, M. L. Harris, C. Burke, N. Cocoros, L.
Finelli, K. F. MacFarlane, B. Shu, S. J. Olsen. 2009. H1N1 2009 influenza virus infection during
pregnancy in the USA. Lancet 374(9688):451-458.
Khan, K, J. Arino, W. Hu, P. Raposo, J. Sears, F. Calderon, C. Heidebrecht, M. Macdonald, J. Liauw,
A. Chan, and M. Gardam. 2009. Spread of a novel influenza A (H1N1) virus via global airline
transportation. New England Journal of Medicine 361(2):212-214.
Kunisaki, K. M., and E. N. Janoff. 2009. Influenza in immunosuppressed populations: a review of
infection frequency, morbidity, mortality, and vaccine responses. Lancet Infectious Disease
9(8):493-504.
Levy-Bruhl, D., and S. Vaux. 2009. Influenza A(H1N1)v investigation teams. Modified surveil-
lance of influenza A(H1N1)v virus infections in France. Eurosurveillance 14(29), http://www.
eurosurveillance.org/images/dynamic/EE/V14N29/art19276.pdf (accessed October 22, 2009).
Lipsitch, M., S. Riley, S. Cauchemez, A. C. Ghani, and N. M. Ferguson. 2009. Managing and
reducing uncertainty in an emerging influenza pandemic. New England Journal of Medicine
361(2):112-115.
Lytras, T., G. Theocharopoulos, S. Tsiodras, A. Mentis, T. Panagiotopoulos, and S. Bonovas. 2009.
Enhanced surveillance of influenza A(H1N1)v in Greece during the containment phase.
Eurosurveillance 14(29), http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19275
(accessed October 22, 2009).
Madhi, S. A., N. Ramasamy, T. G. Bessellar, H. Saloojee, and K. P. Klugman. 2002. Lower respira-
tory tract infections associated with influenza A and B viruses in an area with a high prevalence
of pediatric human immunodeficiency type 1 infection. Pediatric Infectious Disease Journal
21(4):291-297.
Mangtani, P., T. K. Mak, and D. Pfeifer. 2009. Pandemic H1N1 infection in pregnant women in the
USA. Lancet 374(9688):429-430.
McAnerney, J. M., S. Johnson, and B. D. Schoub. 1994. Surveillance of respiratory viruses—a 10 year
laboratory based study. South African Medical Journal 84(8 Pt. 1):473-477.
Munayco, C. V., J. Gomez, V. A. Laguna-Torres, J. Arrasco, T. J. Kochel, V. Fiestas, J. Garcia, J. Perez,
I. Torres, F. Condori, H. Nishiura, and H. Chowell. 2009. Epidemiological and transmissibil-
ity analysis of influenza A(H1N1)v in a southern hemisphere setting: Peru. Eurosurveillance
14(32), http://www.eurosurveillance.org/images/dynamic/EE/V14N32/art19299.pdf (accessed
October 22, 2009).
Ortiz, J. R., V. Sotomayor, O. C. Uez, O. Oliva, D. Bettels, M. McCarron, J. S. Bresee, and A. W.
Mounts. 2009. Strategy to enhance influenza surveillance worldwide. Emerging Infectious
Diseases 15(8):1271-1278.
Schoub, B. D., S. Johnson, J. M. McAnerney, E. Martin, and I. L. Dos Santos. 1986. Laboratory
studies of the 1984 influenza epidemic on the Witwatersrand. South African Medical Journal
70(13):815-818.
Schoub, B. D., S. Johnson, and J. M. McAnerney. 1994. Benefits and limitations of the Witwatersrand
influenza and acute respiratory infections surveillance programme. South African Medical
Journal 84(10):674-678.
Schoub, B. D., J. M. McAnerney, and T. G. Besselaar. 2002. Regional perspectives on influenza
surveillance in Africa. Vaccine 20(2):S45-S46.
STATSSA (Statistics South Africa). 2009. Mid-year population estimates 2009, www.statssa.gov.za
(accessed November 17, 2009).