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Parasitology International
j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p a r i n t

Dynamic changes in white blood cell counts in uncomplicated Plasmodium falciparum

and P. vivax malaria
Noppadon Tangpukdee a,, Haur-Sen Yew b, Srivicha Krudsood c, Nataya Punyapradit d,
Waraporn Somwong d, Sornchai Looareesuwan a,1, Shigeyuki Kano e, Polrat Wilairatana a
a

Department of Clinical Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand
The Bangkok School of Tropical Medicine, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand
Department of Tropical Hygiene, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand
d
Hospital for Tropical Diseases, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand
e
Department of Appropriate Technology Development and Transfer, Research Institute, International Medical Center of Japan, Ministry of Health, Labour and Welfare of Japan, Tokyo, Japan
b
c

A R T I C L E

I N F O

Article history:
Received 15 January 2008
Received in revised form 18 June 2008
Accepted 21 June 2008
Available online xxxx
Keywords:
White blood cell counts
Uncomplicated malaria
Plasmodium falciparum
Plasmodium vivax

A B S T R A C T
Total and differential white blood cell (WBC) counts are basic and essential indicators in any type of illness
resulting from infection. In malaria, WBC counts are generally characterized as low to normal during
treatment. WBC-counts data, before and during treatment with artemisinin derivatives, was gathered for
patients with either Plasmodium falciparum or Plasmodium vivax infection (at 28-day follow-up), to
investigate dynamic changes in WBC count. We analyzed and compared the WBC counts of 1310 inpatients
presenting with uncomplicated P. falciparum and P. vivax malaria at the Hospital for Tropical Diseases, in
Bangkok, Thailand. Before-treatment, a statistically signicant negative correlation was found between initial
WBC count and highest temperature on admission. Before and during treatment, WBC counts were
signicantly lower in P. falciparum than P. vivax infection on days 0 and 7, but the numerical difference was
small. We also found clinically signicantly low WBC counts during the acute stages of both types of malaria,
which subsequently normalized by day 28 follow-up. This nding has important clinical implications for the
conventional method of estimating parasitemia using an assumed WBC count of 8000 cells/L. The most
signicant nding in our analysis is that WBC counts in acute P. falciparum and P. vivax malaria are
signicantly lower than previously assumed for estimating malaria-parasite density. However, these
abnormalities returned to normal within several weeks after artemisinin-derivative-based treatment.
2008 Elsevier Ireland Ltd. All rights reserved.

1. Introduction
Total and differential white blood cell (WBC) counts are basic and
essential indicators in any type of illness resulting from infection. They
can help to differentiate between different types of infections and
serve as a tool in monitoring the patient's progress during illness.
Malaria infections can produce low, normal, or high WBC counts.
Plasmodium falciparum (P. falciparum) and Plasmodium vivax (P.
vivax) are the two predominant malaria species causing human
disease in Thailand and Southeast Asia, and many other parts of the
world. P. falciparum malaria is generally regarded as the more severe
of the two infections. It differs from P. vivax malaria in many respects,
including its pathophysiology, laboratory data, clinical manifestations,
treatments, and outcomes.
Corresponding author. Department of Clinical Tropical Medicine, Faculty of Tropical
Medicine, Mahidol University, 420/6 Ratchawithi Road, Ratchathewi, Bangkok, 10400
Thailand. Tel.: +66 2354 9159; fax: +66 2354 9158.
E-mail address: tmntp@mahidol.ac.th (N. Tangpukdee).
1
Deceased.

Many methods are used to quantify malaria parasites in thick blood

smears. The most common method is to count the total number of
asexual parasites per 200 WBC and multiply this by 40, to give the
number of parasites per microliter (assuming 8000 WBC/L blood) [1].
These estimates are commonly used in the eld and in epidemiological studies, and also in evaluating the effects of interventions with
individuals and communities. However, a common weakness in
estimating parasite levels by counting parasites against an arbitrary
WBC number is the assumption that all blood samples contain
8000 WBC/L. If suitable instruments are available, it is far preferable
to count the WBC/L of each blood sample under investigation, and so
obtain an accurate conversion factor for each sample.
Some studies have reported WBC counts in malaria patients in
different geographical areas [24]; however, the weekly serial WBC
counts for 28-days' follow-up for P. falciparum and P. vivax patients
have not been fully investigated. In this study, we attempted to gather
WBC counts before and during treatment with artemisinin derivatives,
from patients with either P. falciparum or P. vivax malaria (at 28-day
follow-up). The aims were (i) to investigate dynamic changes in WBC

1383-5769/$ see front matter 2008 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.parint.2008.06.005

Please cite this article as: Tangpukdee N, et al, Dynamic changes in white blood cell counts in uncomplicated Plasmodium falciparum and P.
vivax malaria, Parasitol Int (2008), doi:10.1016/j.parint.2008.06.005

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N. Tangpukdee et al. / Parasitology International xxx (2008) xxx-xxx

counts, and (ii) to compare the conventional approach (use of

8000 WBC/L blood) with use of the patients' own total WBC counts.

Table 1
Baseline patient characteristics
Characteristic

P. falciparum
(N = 718)

P. vivax
(N = 592)

p-values

Sex [Male (%)/Female (%)]

544(76%)/
174(24%)
24 (1565)
11,840
(130179,040)
4 (17)

381(64%)/
211(36%)
22 (1561)
9970
(12288,480)
4 (15)

b 0.001

38.3
(37.941.2)

37.9
(37.642.3)

b 0.001

2. Materials and methods

2.1. Study site and recruitment procedure
The medical records of 1310 adult inpatients with uncomplicated
P. falciparum or P. vivax malaria were reviewed retrospectively. Each
of these patients had: (1) been admitted to the Hospital for Tropical
Diseases, Faculty of Tropical Medicine, Mahidol University, Bangkok,
Thailand for at least 4 days, for the treatment of acute uncomplicated
P. falciparum or P. vivax malaria between January 2000 and December
2006, were either male or female, body weight 35 kg, age 15 years;
(2) positive for either P. falciparum or P. vivax parasites on admission,
before-treatment, with microscopic conrmation; (3) enrolled in
artemisinin combination therapies (ACTs) for uncomplicated P.
falciparum or P. vivax malaria infection; (4) had no history of antimalarial therapy pre-admission. The patients studied fullled the
following selection criteria:
(1) asexual forms of P. falciparum or P. vivax cleared from peripheral
blood with therapy, with no parasite reappearance during
follow-up;
(2) no blood transfusion given during the study period;
(3) no evidence of P. ovale, P. malariae, or mixed infection;
(4) no evidence of severe malaria or transition towards severe
malaria during treatment for uncomplicated malaria [5];
(5) no clinical evidence of severe malnutrition or clinically signicant
disorder;
(6) also excluded were patients who had recently received
treatment with antibiotics, corticosteroids, or immunosuppressives. In addition, only non-lactating or non-pregnant females
were included, and had to be willing to use a contraceptive
method during the study period.
Of the 1310 malaria patients that met the inclusion criteria, 718 had
uncomplicated P. falciparum malaria and 592 P. vivax infection by
microscopic conrmation. The study was reviewed and approved by
the Ethics Committee, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand.
2.2. Baseline and follow-up studies
Age, gender, history of malaria in the past year, initial highest fever
and duration of fever pre-admission, and initial parasite count, were all
recorded. Baseline and follow-up laboratory data, e.g., WBC and
differential counts, were determined by automated cell counter (Advia
120 Hematology System, Siemens Medical Solutions Diagnostics;
commercial reagent by Roche Diagnostic). Thick and thin blood lms

Fig. 1. Percentage of patients whose data were still available at each scheduled follow-up.

Age (years) Median (MinMax)

Malaria parasite density on day 0
(parasites/L) Median (MinMax)
Reported days of fever before admission
(days) Median (MinMax)
Highest temperature during admission
(C) Median (MinMax)

0.017
b 0.001
0.858

were prepared from ngerprick blood samples and stained with

Giemsa. Peripheral blood concentrations of asexual form P. falciparum
or P. vivax were routinely estimated by counting the number of asexual
forms per 200 WBC on thick smears, and multiplying by WBC count, or
by counting the number of asexual forms per 1000 erythrocytes on thin
smears and multiplying by RBC count. For the conventional method,
however, we estimated by counting the number of asexual forms per
200 WBCs on thick smears and multiplying by the assumed WBC count
(8000 cells/L). Throughout this time, WBC counts and parasite density
counts were collected for these patients every 7 days during the study
period, starting the 1st day of examination, i.e. on days 0, 7, 14, 21, and
28. A physical examination was performed and vital signs, including
blood pressure (mmHg), heart rate (beats/min), respiratory rate
(breaths/min), and body temperature (C), were measured at the rst
screening and then daily until discharge.
2.3. Treatment
Upon admission, the patients received the following treatments
with artemisinin combination therapy (ACT), as part of clinical trials
using alternative regimens of antimalarial drugs for falciparum or
vivax malaria:
P. falciparum infection: oral artesunate single dose 200 mg/day for
3 days, together with meoquine 8 mg/kg/day for 3 days [6].
P. vivax infection: oral artesunate single dose 200 mg, on day0,
followed by single daily doses of 100 mg for the next 4 days (to
complete total artesunate 600 mg in 5 days of treatment, days 04),
after which primaquine (0.6 mg/kg) was administered once daily for
14 days (i.e., days 518) [7].
2.4. Statistical analysis
All p-values reported were from 2-tailed testing, and statistical
signicance was set at 0.05. The KolmogorovSmirnov test was used

Fig. 2. Median for white blood cell (WBC) counts in patients infected with P. falciparum
and P. vivax malaria. : p-values b 0.001. : Mean of WBC count in healthy Thai volunteer is 7.5 1.7 (103/L) [21].

Please cite this article as: Tangpukdee N, et al, Dynamic changes in white blood cell counts in uncomplicated Plasmodium falciparum and P.
vivax malaria, Parasitol Int (2008), doi:10.1016/j.parint.2008.06.005

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Table 2
Relationships between white blood cell counts on day 0 (WBC0), age (age), malarial
parasite densities on admission (parasite density), highest temperature on admission
(highest temp) and days of fever preceding admission (days of fever) in patients
infected with P. falciparum
Spearman's correlation coefcient ()

Parasite density
WBC0
Age
Highest temp
a
b
c

WBC0

Age

Highest temp

Days of fever

0.03
1.00
(0.08)
(0.11)b

0.08
(0.08)
1.00
0.10

0.16a
(0.11)b
0.10
1.00

(0.14)c
(0.04)
0.03
(0.01)

p-value b 0.001.
p-value = 0.032.
p-value = 0.014.

Fig. 3. Differential WBC counts on days 0, 7, 14, 21, and 28 for patients infected with P.
falciparum and P. vivax (MOD: Median of differential).

to test for normality, but the data distributions generally did not
exhibit normality. Therefore, the data were expressed as median
(MinMax) and number of observations, with percentage (%). Three
statistical tests were performed: the Chi-square test was used to test
for any association between qualitative variables; the Mann-Whitney
U test was used to test for differences between quantitative variables;
and the Spearman's rank correlation coefcient was used to analyze
the relationships between initial WBC counts, initial parasite
densities, age, highest temperature on admission, and reported days
of fever before admission.
3. Results
3.1. Patient characteristics
The sample consisted of a total of 1 310 inpatients, 718 of whom
were infected with P. falciparum and 592 with P. vivax. Around 5%
were lost to follow-up due to social reasons unrelated to adverse
effects (Fig. 1). The data obtained for such patients, before loss to
follow-up, were included in the analysis.
The patients' characteristics are shown in Table 1. There was a
statistically signicant difference (p-value = 0.017) between the age
distributions of the two groups. Nevertheless, the median age for the
P. falciparum group was only 2 years older than the P. vivax group; the
oldest patient in the P. falciparum group was 65 years, and in the P.
vivax group 61. Clinically or biologically, these differences were
unlikely to be signicant. There were statistically signicant differences (p-value b 0.001) between the two patient groups for gender,
malaria-parasite density, and highest temperature on admission.
3.2. WBC counts
The median WBC counts (MinMax) for the two patient groups
are shown in Fig. 2. The median WBC counts for P. falciparum patients

were lower than for P. vivax patients on days 0, 7, 14, and 28. The
differences were only statistically signicant for days 0 and 7 (pvalue b 0.001). In contrast, the median WBC counts for P. falciparum
patients were statistically signicantly higher on day 21 (pvalue b 0.001). The WBC counts in each patient group on different
days were also compared. Fig. 2 shows relatively low WBC on day 0
for both patient groups (P. falciparum group median WBC count =
5.10 103 cells/L; P. vivax group = 5.70 103 cells/L). This is statistically signicantly different from other days (all p-valuesb 0.001), which
had median WBC counts of 7.50 103 cells/L to 8.00 103 cells/L, which
were closer to the assumed WBC count of 8.00 103 cells/L used in
conventional parasite-density estimation methods. To investigate
leukocyte changes during malaria infection, weekly differential WBC
counts during 28 days' follow-up are shown in both percentages and
absolute numbers (Figs. 3 and 4). The results showed that lymphopenia
(dened as absolute lymphocyte counts 1500 cells/L) was common in
acute-stage malaria infection. We also found that patients with acute
falciparum and vivax infection had low eosinophil levels. Eosinophil
levels (normal values 350 cells/L) were low in the early stage, and then
increased over the following few weeks.
3.3. Correlational relationships between WBC counts and other variables
Values for Spearman's correlation coefcient () and p-values are
shown in Table 2 (P. falciparum group) and Table 3 (P. vivax group).
Different variables were analyzed for possible correlational
relationships.
For both groups, we found statistically signicant, but weak,
negative correlations between WBC count on day 0 and highest
temperature on admission ( = (0.11), p-value = 0.03 for P. falciparum
group; = (0.16), p-value b 0.001 for P. vivax group). There were also
weak negative correlations between malarial parasite densities and
reported days of fever pre-admission ( = (0.14), p-value = 0.01 for P.
falciparum group; = (0.15), p-value b 0.001 for P. vivax group). In the

Table 3
Relationships between white blood cell counts on day 0 (WBC0), age (age), malarial
parasite densities on admission (parasite density), highest temperature on admission
(highest temp) and days of fever preceding admission (days of fever) in patients
infected with P. vivax
Spearman's correlation coefcient ()

Parasite density
WBC0
Age
Highest temp
a
b

Fig. 4. Differential (absolute number) for WBC counts on days 0, 7, 14, 21, and 28 of
patients infected with P. falciparum and P. vivax (AMD: Absolute median of differential).

c
d

WBC0

Age

Highest temp

Days of fever

0.08
1.00
(0.11)a
(0.16)c

( 0.04)
( 0.11)a
1.00
0.01

0.16b
(0.16)c
0.01
1.00

(0.15)d
(0.02)
(0.06)
(0.02)

p-value = 0.023.
p-value b 0.001.
p-value b 0.001.
p-value b 0.001.

Please cite this article as: Tangpukdee N, et al, Dynamic changes in white blood cell counts in uncomplicated Plasmodium falciparum and P.
vivax malaria, Parasitol Int (2008), doi:10.1016/j.parint.2008.06.005

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Table 4
Comparison of parasite density using actual WBC count and assumed WBC count
(8000 cells/L)
Malaria
infection

Based on actual WBC

count Median (MinMax)

Based on assumed WBC

count Median (MinMax)

P-values

P. falciparum,
n = 358
P. vivax,
n = 266
All cases,
n = 624

640 (3017920)

960 (4403 680)

b 0.001

812 (3228623)

1 040 (4403480)

b 0.001

719 (3018623)

920 (4403680)

b 0.001

Calculations only for thick blood lms.

P. vivax group, there was a weak negative correlation between WBC

count on day 0 and patient age ( = (0.11), p-value = 0.02), but not in
the P. falciparum group.
There were weak positive correlations for both groups between
malarial parasite densities on day 0 and highest temperature on
admission ( = 0.16, p-value b 0.001 for both P. falciparum and P. vivax
groups). It is noteworthy that WBC count on day 0 did not appear to
correlate with malaria-parasite density on day 0.
3.4. Initial parasite density using subject's WBC count and assumed WBC
count
Initial parasite densities, using subjects' WBC count (actual count
method) and assumed WBC counts (conventional count method) were
compared to investigate any differences in outcome between the two
methods. The results showed that parasite density for P. falciparum
infection, P. vivax infection, and for all cases, calculated using assumed
WBC count, was higher than parasite density calculated using actual
WBC counts, with statistically signicant difference, p-values b 0.001
(Table 4). Since the actual WBC counts were b8 000 cells/L in both P.
falciparum and P. vivax in the initial phase, this implies that the
conventional method of calculating parasitemia resulted in overestimation in both P. falciparum and P. vivax infections. All patients
were parasitemia-negative by day 7 follow-up, after receiving
effective drug treatment. Therefore, it was not possible to compare
actual-count and conventional-count methods for parasitemia density
at any follow-up interval.
4. Discussion
4.1. Comparison of WBC counts in uncomplicated P. falciparum and P.
vivax malaria
WBC counts may be high, normal, or low in acute malaria infections.
Low WBC counts are often seen in acute malaria; two recent studies of
adult populations have conrmed this observation [2,8].
In this study, we tried to investigate differences between WBC
counts in patients with uncomplicated P. falciparum and P. vivax
malaria. The results of this study agreed with previous ndings, that
the WBC counts of P. falciparum patients were lower than P. vivax
patients [2]. However, our study differed in that the data were derived
from inpatients admitted for the length of the study to one hospital
located in Bangkok, Thailand, whereas McKenzie and co-worker
analyzed the data of patients from outpatient malaria clinics in
Thailand and Peru. We could follow and repeat WBC counts every
7 days, up to day 28 post-treatment, and exclude reinfection as a
potential confounder [2]. Thus, to the best of our knowledge, we have
been able to conrm that the WBC counts in the P. falciparum group
were still statistically signicantly lower than the P. vivax group on
day 7 post-treatment. In contrast, Jadhav and co-worker found no
differences in mean WBC counts for patients infected with P.
falciparum and P. vivax [9]. Although this discrepancy is not easily

explained, McKenzie et al. mentioned a number of possible factors in

their excellent discussion [2].
The lower WBC counts in P. falciparum infection may reect its
greater severity than P. vivax. However, despite achieving statistical
signicance, we nd it difcult to afrm that the difference in WBC
counts between the two groups has any meaningful clinical
signicance. The numerical difference is small in clinical terms, and
can hardly be used for effectively differentiating between uncomplicated P. falciparum and P. vivax malaria infection in the clinical setting,
or for any other clinically meaningful purpose.
4.2. Implications of low WBC in acute-stage malaria
The hematological changes during acute malaria have been well
described [10]. During acute P. vivax infection, neutropenia (dened as
absolute neutrophil counts 1000 cells/L) seems attributed to the
rapid release of marrow granulocytes into the blood (creating
apparent neutropenia, due to changes in intravascular granulocyte
distribution), coupled with a shift of neutrophils from the circulating
to the marginated cell pools [11]. Lymphopenia is probably due to the
redistribution of lymphocytes, with sequestration in organs like the
spleen; moreover, atypical lymphocytes and plasmacytoid lymphocytes are present after the second day of fever [10]. In acute P.
falciparum infection, eosinophil counts are low in the early stage, and
then increase over the following few weeks; it has been suggested that
a robust eosinophilic response after completion of antimalarial
therapy is predictive of a good recovery from malaria-associated
anemia [12]. Although our data were unclear on changes in
neutrophils, lymphocyte and eosinophil changes were well illustrated
(Figs. 3 and 4).
The low WBC found during early-stage malaria infection is
clinically signicant. The clear normalizing trend of WBC counts
with time and cure (Fig. 2) means that WBC counts may be used as an
indicator for the progress of malaria infection, so providing guidance
for its management.
The other area where early low WBC has clinical implications is in
the microscopic estimation of parasitemia. The median WBC count on
day 0 was 5.1 103/L for the P. falciparum group, and 5.7 103/L for
the P. vivax group. McKenzie and co-worker found that one-sixth
(16.6%) of their Thai patients with P. falciparum malaria had WBC
counts b4.0 103/L [2]. In comparison, approximately 25% and 15% of
our patients with P. falciparum and P. vivax infection, respectively, had
WBC counts 4.0x103/L.
4.3. Immunopathogenesis of leukopenia in malaria patients
At present, the immunopathophysiological processes causing
hematological changes in malaria are complex, multiple, and incompletely understood. Recently, Wickramasinghe and Abdalla discussed
the role of lymphokines in malaria patients [10], and explained that IL12 may be involved in the pathogenesis of malarial pancytopenia.
Another study illustrated that the malarial toxin glycosylphosphatidylinositol acts directly on monocytes and macrophages and triggers
the release of pro-inammatory cytokines [13]. The explanation for
this potential mechanism may be that macrophage function is altered
by the phagocytosis of debris released during schizogony. The
phagocytosis of red blood cells and white blood cells by monocytes
and macrophages is known to increase phagocyte production of TNF-
and IL-1 [14]. Increased levels of IL-1 may in turn stimulate further
IFN- production by T-lymphocytes [15], and TNF may also cause
further macrophage activation [16]. However, as previously discussed,
high levels of TNF may cause suppression of hemopoiesis and
dyshemopoiesis [1416]. In acute malaria, the considerable ineffectiveness of hemopoiesis may be the consequence of (1) modest
increases in TNF acting on hemopoiesis over a prolonged period,
(2) cytokine imbalance with underproduction relative to TNF of IL-10

Please cite this article as: Tangpukdee N, et al, Dynamic changes in white blood cell counts in uncomplicated Plasmodium falciparum and P.
vivax malaria, Parasitol Int (2008), doi:10.1016/j.parint.2008.06.005

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and possibly IL-12 or other cytokines, and (3) macrophage dysfunction

affecting stimulatory and inhibitory hemopoietic growth factors. In
addition, the malarial toxins or phagocytosed material may alter the
pattern of secretion of hemopoietic growth factors, or stimulate
macrophages to release cytotoxic chemicals, e.g. oxygen-derived free
radicals or nitric oxide, which damage surrounding hemopoietic cells
[17]. In the current study, unfortunately, no cytokine study was
performed, so that the clinical implications and underlying mechanism
of these abnormalities were not elucidated.
4.4. Malarial parasite density by conventional calculation method
Malaria-parasitemia density can be expressed as percentage of
parasitized red blood cells (RBCs) per 1000 RBCs in a thin blood lm.
At lower densities of parasitemia, the percentage can be very difcult
to determine. Hence, another method is to estimate the number of
parasites per L of blood, by counting the number of parasitized cells
per 200 or 500 WBCs in a thick blood lm. The parasite-to-WBC ratio
is then multiplied by the number of WBCs per L of blood, which then
yields the number of parasites per L of blood. If the WBC count is not
known, it is conventionally assumed to be 8000 cells/L blood [18].
This estimation method, utilizing an assumed WBC count of 8000
cells/L blood, has previously been evaluated [19,20] and has been
found wanting, due to the variability of actual WBC counts. Given our
ndings, i.e., that the median WBC count was actually much lower
than the assumed number, parasite density estimates can be grossly
inated using this method. In our sample population, 88% of P.
falciparum patients and 86% of P. vivax patients actually had WBC
counts b8000 cells/L. While it is probably true that it is better to
overestimate parasitemia when treating an ill patient in a clinical
setting, this may not be true for research and trial settings, where
overestimation may invalidate the results [2]. However, in reality,
there are situations where WBC count is not easily available, and
estimation is necessary. We propose that it may be better to utilize a
lower number for assumed WBC count, given the results of our study
and other studies cited above. A future study should investigate
estimation of parasitemia using different assumed WBC counts,
comparing the results with other, more accurate, methods.
4.5. Leucocytosis in malaria a consideration for future investigations
A study in Africa found that children with malaria had higher WBC
counts than normal healthy children [3]. In the same study,
leucocytosis was found to be strongly associated with younger age,
deep breathing, severe anemia, thrombocytopenia, and death; this
contrasts with an earlier study [4], which found that, in African
children, a combination of hyperparasitemia and leucocytosis was not
a poor prognostic indicator in the absence of other evidence for severe
or complicated disease. Hence, this was not a reliable indicator of
severity or a poor prognosis in falciparum malaria.
For practical purposes, the sample patient population in our study
may be considered representative of an adult population, although
about 5% were aged 1518 years. The median age of the sample
population combined was 23 years. The study was not designed to
elucidate associations between leucocytosis and severity or prognosis
of malaria infection in adults, since all of the patients in our study
were uncomplicated-malaria, not severe, cases.
5. Conclusion

were different, they were not found to be sufciently clinically

signicant for practical use.
Acknowledgements
This study was partly supported by a grant from the Ministry of
Health, Labour and Welfare, Japan and a Mahidol Research Grant. We
thank the Faculty of Tropical Medicine, Mahidol University, for pagecharge support. We also thank the staff and nurses of the Hospital for
Tropical Diseases for their help. The English in the manuscript was
edited by Mr. Paul R. Adams, consultant to the Faculty of Tropical
Medicine, Mahidol University, Bangkok, Thailand.
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The most signicant nding was that WBC counts in acute P.

falciparum and P. vivax malaria were signicantly lower than previously assumed for estimations of malaria parasite density. This underlines
the importance of re-evaluating the assumptions of this method.
Although the WBC counts in acute P. falciparum and P. vivax malaria

Please cite this article as: Tangpukdee N, et al, Dynamic changes in white blood cell counts in uncomplicated Plasmodium falciparum and P.
vivax malaria, Parasitol Int (2008), doi:10.1016/j.parint.2008.06.005