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At least 19 recordsLinked to original sources
PubMed1997

Dose- and time-dependent relations between infective Anopheles inoculation and outcomes of Plasmodium falciparum parasitemia among children in western Kenya.

Blood-stage level Plasmodium falciparum infection (parasitemia density) is generally elevated prior to, or at the time of, clinical presentation of severe pediatric malaria episodes. Intensity of exposure to infective Anopheles mosquito bites is a suspected determinant of higher density parasitemia. Analyses of entomologic and parasitologic data collected in 1986-1987 were conducted to investigate whether the dose of infective bites predicted the incidence or degree of P. falciparum parasitemia in Kenyan children < 6 years old. At 21 consecutive 30-day intervals, a new cohort (n approximately 50 each) was enrolled, cured of malaria parasites, and monitored over 84 days for recurrent parasitemia. Outcomes included time to parasitemia, time to parasitemia > or = 5,000/microliter, and parasitemia density. Ecologic and individual-level analyses were conducted. The mean infective bite exposure experienced by each cohort was significantly associated with the incidence of parasitemia (age-adjusted r2 = 0.38, p = 0.022) and more strongly associated with the incidence of parasitemia > or = 5,000/microliter (age-adjusted r2 = 0.72, p < 0.001). The infective bite dose, analyzed as a time-dependent covariate, was associated with a 2.8 times higher rate of parasitemia > or = 5,000/microliter among children exposed to > or = 1 infective bite per day as compared with the referent (rate ratio (RR) = 2.82, 95% confidence interval (CI) 2.24-3.56). Cumulative infective bite exposure, exposure duration, and age were significant predictors of recurrent parasitemia density in multiple linear regression analyses. The results support the contention that reductions in P. falciparum transmission intensity, in the absence of complete elimination, will reduce higher level parasitemia among African children.

Animals↗
PubMed1999

Plasmodium chabaudi chabaudi: effect of low parasitemias on immunity in CB6F1 mice.

We examined the effect that low parasitemias have on the immune response of CB6F1 mice infected with Plasmodium chabaudi chabaudi AS. Ascending parasitemias were stopped by chloroquine treatment when they were between 1.6 and 9.4%. Mice that suffered low parasitemias developed good immunity to homologous reinfection but, contrary to what happened in mice that suffered full parasitemias, they did not develop immunity to heterologous reinfection with Plasmodium yoelii 17XL. Total IgG antiparasite antibody responses were similar in mice that suffered low or full parasitemia, both in primary infection and after reinfection. At the level of isotypes, IgM, IgG1, IgG2b, and IgG3 responses were similar in mice that suffered low or full parasitemias, but after reinfection, mice that suffered low parasitemias responded with higher levels of IgG2a than mice that suffered full parasitemias. Mice that suffered low parasitemias did not have splenomegaly but their immunity to homologous reinfection was diminished after splenectomy in a manner similar to that of splenectomized mice that suffered full parasitemia. CB6F1 mice can develop homologous immunity even if exposed to low parasitemias but cannot develop heterologous immunity unless exposed to high parasite loads.

Animals↗
PubMed1979

Prevalence of parasitemia and seroreactivity to Trypanosoma cruzi in a rural population of Northeast Brazil.

Age-specific prevalence rates of parasitemia and seroreactivity to Trypanosoma cruzi were determined in a rural area endemic for Chagas' disease in Northeast Brazil. Parasitemia was detected by blood cultures and xenodiagnosis, and serum antibodies to the parasite were measured by the complement fixation (CF) and indirect immunofluorescence (IFA) tests. Of the 116 persons examined, 39 (33.7%) had antibodies and 23 (19.8%) had parasitemia. Ninety-six percent of parasitemic individuals were seropositive and 56% of seropositive individuals were parasitemic. The percentage of seropositive individuals with detectable parasitemia declined with age; all seropositive children in the 1- to 4-year age group and two-thirds of seropositive persons 5-19 years old had parasitemia while only one-third of seropositive adults above 19 years had parasitemia. CF and IFA tests were equally sensitive in detecting persons with parasitemia. Xenodiagnosis was more sensitive than culture for detecting parasitemia, but the two methods together were more sensitive than either method alone. Using the age-dependent relationship of parasitemia to seropositivity determined in this study, the prevalence rate of T. cruzi parasitemia was estimated in a much larger adjacent population in which seropositivity rates and the demographic structure were already known.

Adolescent↗
PubMed1979

Antigenic analysis by agglutination of Trypanosoma brucei brucei parasitemias initiated in mice with in vitro-produced metacyclics.

Trypanosomes from 14 first-peak parasitemias initiated in mice by injection of in vitro-produced metacyclics were stabilated. Strains derived from these stabilates were analyzed for their antigenic composition by cross-agglutination with immune sera produced in rabbits against 12 of the stabilates. The antigenic composition of the 14 stabilates was compared also with two first-peak parasitemias from mice inoculated with fly-derived metacyclics, the variant-specific antigen of the strain used to initiate the cultures that ultimately became infective, and the antigenic variant that was used to infect the flies. One variant-specific, presumably basic, antigen was found, either as the predominant (nine parasitemias) or as a minor (seven parasitemias) antigen, in all first peak-parasitemia strain initiated with culture- or fly-derived metacyclics; it was absent, however, from the strains (not first-peak parasitemias) used to start the cultures or to infect the flies. Only one of the first-peak parasitemias appeared to have the basic antigen alone. The remaining parasitemia populations seemed to have from about two to six antigens, some of which were common to culture- and fly-derived infections. There was very little, if any, antigenic relationship between the foregoing populations and the strains employed for initiation of cultures or for infection of flies. It is evident from the results that much antigenic similarity exists between the culture- and tsetse fly-derived first-peak parasitemias.

Adsorption↗
PubMed1982

Genetic control of responses to Trypanosoma cruzi in mice: multiple genes influencing parasitemia and survival.

Inbred strains of mice can be divided into two groups based on the level of parasitemia which develops after injection with 10(3) trypomastigotes of Trypanosoma cruzi (Peru). Strains which developed parasitemias of greater than 10(7) trypomastigotes per ml by day 17, including C3H/HeJ, BALB/c, and CBA/N mice, were termed high parasitemia strains. Low parasitemia strains, including C57BL/6J and DBA/2J mice, developed parasitemias of less than 5 x 10(6) trypomastigotes per ml by day 17 of infection. Congenic mice from C57BL/10J, C57BL/6J, and BALB/c backgrounds which differed at the H-2 region were injected with 10(3) trypomastigotes to determine the effect of the H-2 locus on response to infection. The H-2 locus had no effect on the level of parasitemia attained during infection. However, one strain, B10.S (H-2s), was unusual in that most of the mice survived infection. The results of infection of F1 hybrid progeny with T. cruzi (Peru) suggest that the low parasitemia response in inherited in a dominant manner and that survival may be influenced by several other genes. The response to T. cruzi infection in inbred mice, as measured by parasitemia and survival time, was influenced by several genes. One or more genes, located outside the H-2 region, were involved in regulating the level of parasitemia reached during infection. Another H-2-linked gene(s) was involved in survival of the infection and appeared to be unique to the H-2s haplotype.

Animals↗
PubMed2000

Effect of Plasmodium falciparum parasitemia density on hemoglobin concentrations among full-term, normal birth weight children in western Kenya, IV. The Asembo Bay Cohort Project.

The relative importance of acute high-density versus persistent low-density Plasmodium falciparum parasitemia in contributing to the public health problem of malarial anemia remains unclear. The Asembo Bay Cohort Project in western Kenya collected monthly hemoglobin (Hb) and parasitologic measurements and biweekly assessments of antimalarial drug use among 942 singleton live births between 1992 and 1996. A mixed-model analysis appropriate for repeated measures data was used to study how time-varying parasitemia and antimalarial drug exposures influenced mean Hb profiles. Incidence of World Health Organization-defined severe malarial anemia was 28.1 per 1,000 person-years. Among children aged less than 24 months, concurrent parasitemia was significantly associated with lower mean Hb, especially when compared to children with no concurrent parasitemia. Increased densities of the 90-day history of parasitemia preceding Hb measurement was more strongly associated with mean Hb levels than concurrent parasitemia density. While the highest quartile of 90-day parasitemia history was associated with lowest mean Hb levels, children in the lowest 90-day exposure quartile still experienced significantly lower Hb levels when compared to children who remained parasitemia-free for the same 90-day period. The results highlight the importance of collecting and analyzing longitudinal Hb and parasitologic data when studying the natural history of malarial anemia.

Anemia↗
PubMedDate not supplied

[Parasitemia in chronic chagasic patients evaluated using the index of infected Triatoma in xenodiagnosis].

As part of a pre-treatment study of chronic Chagas infections, the parasitemia of 206 patients (85 men and 121 women, aged 7 to 80 y) from Virgem da Lapa, Minas Gerais State Brazil, was evaluated by three xenodiagnoses per patient during a one year period. Each time, 40 3rd or 4th instar nymphs of Triatoma infestans were applied. The parasitemia was arbitrarily classified as: not detected (when all nymphs were negative), low (when the number of infected nymphs was less than 2%), medium (when it was higher than 2% and up to 7%) and high (when higher than 7%). The parasitemia was not detected in 105 (51%) of the patients, and was considered low in 55 (26.7%), medium in 27 (13.1%) and high in 19 (9.2%). There was no significant differences in levels of parasitemia in relation to sex or age, but the high parasitemia was more frequent among the patients with chagasic cardiomyopathy. Persistent parasitemia (all three xenodiagnoses positive) was observed in 100% of the patients with high parasitemia, in 22.2% with medium and in none with low parasitemia.

Adolescent↗
PubMed1984

Behaviour of a Trypanosoma brucei brucei stock (STIB 348C) in mice. 4. Different course of primary parasitemia in trypanosome variants of different virulence.

In three types of trypanosomes with low virulence, trypanosome numbers increased by a factor of 18-21 per day on average during prepatency and by a factor of 70-219 on average from the first to second day of patency. By contrast, a very virulent trypanosome variant showed an average increase of trypanosome numbers per day by 32 and 28 during prepatency and early patency, respectively. --In detailed studies, trypanosomes of low virulence exhibited a rapidly rising parasitemia in early patency which lasted for 20-30 hours and was followed by a plateau of slowly rising and falling parasitemia. Trypanosomes of high virulence showed a constant logarithmic increase of their numbers, slowing down at concentrations above antilog 5.5 per microliters of blood. In mild trypanosomes with peak parasitemias of antilog 5-5.7 per microliters of blood, after low dose infections the primary parasitemia was abruptly terminated after 70-100 hours of patency, obviously by the action of antibody. After massive infections, the parasitemia was terminated at 109-122 hours after infection. --In trypanosomes with higher peak parasitemias, primary parasitemias were seen to last longer, in some cases for 7 to 12 days. --Mice infected with low doses of highly virulent trypanosomes died with high parasitemias after some 60-90 hours of patency, before antibodies could normally become effective. After massive infections they died at 40-60 hours after infection. There is clearly no need to invoke non-immunogenicity of these trypanosomes or immunosuppression by these trypanosomes to explain this course of the infection.

Animals↗
PubMedDate not supplied

[The evolution of chronic chagasic cardiopathy. I. The influence of parasitemia].

During eight years (1982-1990) the evolution of chronic chagasic cardiopathy and its relation to parasitemia was evaluated in 279 patients, 85 men and 194 women, studied by resting electrocardiography and xenodiagnosis. All patients were residents in Virgem da Lapa, State of Minas Gerais, Brazil and their ages varied from 7 to 76 years (average 42.6 y). According to the results of the electrocardiograms the evolution of chagasic cardiopathy was classified as a) unchanged--when there was no change of the initial pattern off the ECG, b) progressive--when there was deterioration of the ECG pattern and c) regressive-when there was normalization or regression of the ECG alterations. Regarding xenodiagnosis 120 were considered with positive parasitemia, one or more xenodiagnoses positive, and 159 with negative parasitemia--all xenodiagnoses negative. The results showed: a) chagasic cardiopathy unchanged in 172 (61.6%) patients, b) progressive in 99 (35.5%) patients and c) regressive in 8 (2.9%). There was no relation between the evolution of chagasic cardiopathy and parasitemia. Independent from parasitemia, the cardiopathy was progressive according to the age of the patients and significantly greater in males. In conclusion we can state that evolution of chronic chagasic cardiopathy is associated with the age and with the male sex, but not with parasitemia, and this may suggest that parasitemia is not related to the development of the chronic chagasic cardiopathy.

Adolescent↗
PubMed1983

Non-antibody-mediated control of parasitemia in acute experimental Chagas' disease.

There appear to be two phases in the control of parasitemia in acute Chagas' disease in the mouse. The first phase occurs during the first few weeks after infection and control is achieved through a thymus-dependent, antibody-independent mechanism. Challenge of B cell-suppressed C3H and F1 (C57BL/6 X C3H) mice with the Brazil strain of Trypanosoma cruzi led to a course of parasitemia for the first 3 wk after infection similar to that seen in normal C3H or F1 mice and markedly lower than the parasite levels observed in the blood of nu/nu mice. Challenge of BXH-2 recombinant inbred mice resulted in a course of parasitemia similar to that seen in nu/nu mice up to day 16 despite the production of normal levels of antibody. The BXH-2 mice lack the ability to effect the early control of parasitemia. The second phase begins several weeks after infection with the rise in antibody titer, and the control is exerted through an antibody-mediated mechanism. In all B cell-suppressed mice, an inexorable rise in parasitemia occurred up to the time of death, which suggests that antibody is important for the eventual clearance of parasites from the blood. A comparison of the IgM and IgG antibody titers to T. cruzi in a series of resistant and susceptible strains showed that there was no correlation between the appearance of specific antibody or antibody titers and the levels of parasitemia observed. The level of parasitemia attained in the late acute phase may be primarily determined by the extent of parasite proliferation in the early acute phase.

Acute Disease↗
PubMed1997

Lack of association between falciparum malaria parasitemia and acute diarrhea in Nigerian children.

It is widely believed that malaria causes diarrhea. Yet, national and international diarrheal diseases control programs are silent about the overlap between these two major public health problems that coexist in most tropical countries. To test the hypothesis that malaria is associated with diarrhea and to define the role of malaria in morbidity due to diarrhea, 522 children 6-60 months of age presenting with acute diarrhea to the Children's Emergency Ward of the University College Hospital in Ibadan, Nigeria were routinely screened by means of thin and thick blood films for malaria parasitemia. Controls, without diarrhea, were studied in parallel. Detailed clinical features were recorded for every patient. Sixty-eight (13%) of the 522 diarrhea patients screened had malaria parasitemia. Among the controls (who had similar distributions of admission temperature, hemoglobin types, glucose-6-phosphate dehydrogenase deficiency, and prior treatment with antimalarial drugs), parasitemia was not significantly different, occurring in 56 (17.9%) of 313. In the dry season, however, a significantly higher prevalence of parasitemia was observed among the control group (15.5%) than in the diarrhea group (7.0%) (P = 0.004). Parasitemia was significantly more common in the dehydrated diarrhea patients than their well-hydrated counterparts (25% of 56 versus 11% of 466; P < 0.005). There were no significant differences in admission temperature, the presence of vomiting, or the home use of oral rehydration fluids between the dehydrated and the well-hydrated subsets of diarrhea patients. Consideration of parasite densities did not alter any of the foregoing relationships. These data contradict the widely held view that diarrhea is a symptom of malaria or that malaria causes diarrhea. They do, however, provide support for examining blood smears at least in dehydrated children with diarrhea in malaria-endemic areas and giving immediate antimalarial therapy to those who have malaria parasitemia.

Antimalarials↗
PubMed1989

The parasitemia of cloned Trypanoplasma borreli Laveran and Mesnil, 1901, in laboratory-infected common carp (Cyprinus carpio L.).

The course of parasitemia of cloned Trypanoplasma borreli in laboratory-infected common carp was investigated. In 25-42-g carp kept at 20 C, the prepatent period was 8 days; after a phase of exponential growth, the parasitemia peaked at day 39 postinjection (PI) at a level of about 10(3) T. borreli/microliters blood. This maximum was followed by a chronic phase of about 6 wk with large numbers of T. borreli. At 20 wk PI, T. borreli was absent in infected carp. In 2.2-g carp kept at 20 C, the prepatent period was 4 days only, and the parasitemia peaked at day 23 PI. At 30 C, T. borreli was present in the blood only for 12 wk, and the number of T. borreli did not exceed 162 trypanoplasms/microliters blood. Carp kept at 8 and 15 C showed retarded development of parasitemia. The prepatent period lasted longer and the generation time was increased, but the level of parasitemia was not affected. Carp, inoculated at 8 C and then warmed to 20 C on days 27 and 55 PI, developed a parasitemia of 10(4) flagellates/microliters blood and showed high mortalities. During the prepatent period, T. borreli was found in the muscle tissue of the inoculation area but in no other tissue. In the kidney, T. borreli was found 27 hr PI, whereas in the circulating blood it was manifest at day 3 PI. At the same time it was manifest in the liver and spleen.

Animals↗
PubMed1996

Control of parasitemia and survival during Trypanosoma brucei brucei infection is related to strain-dependent ability to produce IL-4.

We studied non-MHC gene-dependent expression of a number of cytokines in relation to host defense and survival during Trypanosoma brucei brucei (Tbb) infection in mice. In particular, the role of IL-4 was explored with use of genomically IL-4-disrupted mice and in vivo Ab blocking. Splenocytes from MHC-identical B10.Q (relatively resistant) mice showed day 5 postinfection higher numbers of IL-4 mRNA expressing cells than C3H.Q (highly susceptible). A trypanosome-derived lymphocyte triggering factor, which is released by Tbb to polyclonally activate CD8+ T cells, stimulated naive splenocytes in vitro to a higher IL-4 response in B10.Q than in C3H.Q mice. The C3H.Q mice developed an extremely high parasitemia, showed a low Ab response against the variant surface glycoprotein (VSG), and had a mean survival time of 42 days. Conversely, B10.Q mice had lower parasitemia, mounted higher anti-VSG response, and had a mean survival time of 56 days. Deletion of the IL-4 gene had no influence on the infection in C3H.Q mice, while in B10.Q mice the deletion was associated with lower anti-VSG Ab levels and higher parasitemia. Paradoxically, B10.Q mice with disrupted IL-4 gene survived longer than the wild type. Anti-IL-4 Ab-blocking experiments in vivo displayed an enhanced parasitemia and prolonged survival in infected B10.Q mice. We conclude that 1) a non-MHC gene-related and CD8+-dependent ability to produce IL-4 partly determines the susceptibility to Tbb infection; and 2) IL-4, although involved in controlling the levels of parasitemia by its effects on immunoglobulin synthesis, also can have toxic effects on the animals.

Animals↗
PubMed1993

Plasmodium berghei: recombinant interferon-gamma and the development of parasitemia and cerebral lesions in malaria-infected mice.

Mice infected with Plasmodium berghei K173-parasitized erythrocytes develop severe hypothermia followed by death as a consequence of murine cerebral malaria early in the second week after infection. A single intraperitoneal injection of 10(5) Units of IFN-gamma given between Day 4 and Day 6 postinfection results in a transient decrease of body temperature. No effect on parasitemia and cerebral malaria is obtained by this treatment. Daily injections of relatively low doses of IFN-gamma delays the patency of the infection for 2 days. Furthermore the proliferation rate of the parasites is reduced and the development of cerebral malaria is also delayed for 2 days. The reduction of body temperature, as found in untreated infected mice, is absent. Administration of IFN-gamma by means of a continuous delivery from intraperitoneally inserted osmotic pumps (1.2 x 10(4) Units of IFN-gamma/24 hr) also delays patency and inhibits parasitemia. Body temperature decreases during infection but mice are protected against the development of cerebral malaria. In nude mice, this treatment inhibits parasitemia to the same extent. However, reduction of body temperature was also prevented. High doses of IFN-gamma delivered by osmotic pumps (2.5 x 10(4) or 10(5) Units of IFN-gamma/24 hr) appear to be lethally toxic in conventional as well as in nude mice, independently of infection. Cerebral malaria-like symptoms are found in these mice. Treatment of infected C57BL/6J mice with antibody to IFN-gamma 4 days before and after infection as well as on the day of infection enhances parasitemia but does not affect the development of murine cerebral malaria. Single injections of anti-IFN-gamma-antibody 6 hr prior to infection or 7 days after infection have no effect. In CBA/Ca mice, treatment with anti-IFN-gamma-antibody enhances parasitemia; furthermore protection against cerebral malaria was obtained in part of the mice.

Animals↗
PubMed1983

Interrelationships of immunoconglutinin, immune complexes, and complement in anemia, thrombocytopenia, and parasitemia of acute and chronic malaria in rats.

Anemia, thrombocytopenia and reduction in parasitemia in P. chabaudi infection of rats were associated with appearance in blood of soluble immune complexes, immunoconglutinin (IK), and by reductions in titers of lytic complement. With reduction of parasitemia to subpatent levels, anemia, but not thrombocytopenia, persisted and erythrocyte counts did not return to preinfection levels for several weeks. This chronic anemia was accompanied by elevated amounts of soluble immune complex, depressed titers of lytic complement and persistence of IK. Evidence was presented indicating that the infections of the rats persisted in a chronic form. It was thus indicated that immune interactions, related to anemia and clearance of parasitemia, persisted in absence of microscopically evident parasitemia, and may have been in part responsible for the persistent anemia. Based on the evidence cited, it is suggested that complement-fixing immune complexes attach to blood cells, infected as well as uninfected, and that these cells are sequestered and phagocytized in the spleen after immunoconglutination by IK. It is also suggested that this interaction continued after the clearance of patent parasitemia and accounted for the persistence of anemia in the chronic phase of infection.

Acute Disease↗
PubMed1983

Influence of parasitemia level at feeding on development of Anaplasma marginale Theiler in Dermacentor andersoni Stiles.

Four splenectomized dairy calves were inoculated with a Virginia isolate of Anaplasma marginale Theiler and served as an infective source (donor) for laboratory-reared Dermacentor andersoni Stiles nymphs. Two donor calves developed higher parasitemias during tick feeding than did the 2 other donor calves. One month after molting, adult ticks were incubated at 37 C for 2.5 days to stimulate development of colonies of A marginale, and homogenates of gut were made from ticks fed on each donor calf. Eight susceptible, splenectomized dairy calves (2 per donor calf) were each inoculated IV with the gut homogenates collected from 50 adult ticks and were monitored for patent A marginale infection. Gut tissues from these same groups of ticks were processed for histologic studies. Homogenates from ticks infected on donor calves with lower parasitemias caused infections with longer prepatent periods (av, 43.25 days) than did similar homogenates made from ticks infected by feeding on donor calves with higher parasitemias (av, 31.0 days). Also, sections of gut tissues from ticks infected at the lower parasitemias contained fewer (av, 0.65) colonies/0.001 mm2 of tissue examined than did those from ticks infected at higher parasitemias (av, 6.31).

Anaplasma↗
PubMed1996

[Experimental infection of mice with Babesia microti: characterization of parasitemia].

The apicomplexa parasites of the genus Babesia, the etiologic agents of the disease not only in domestic and wild mammals but also in humans, live and reproduce in erythrocytes of the host. Transmission of Babesia species is by tick (Ixodidae) bite. In natural conditions, trans-stadial and trans-ovarian passage occurs in Ixodes ricinus infected with some species of Babesia, e.g. B. divergens. However, there is apparently trans-stadial passage of B. microti in Ixodes sp. only from larvae to nymphs, but trans-stadial passage from nymphs to adults or trans-ovarian passage has not been reported. The present study was undertaken to compare the parasitemia of B. microti infection in BALB/c and F1 (B10 x CBA) mice by two different methods: intraperitoneal injection of parasites or infection by the oral route. In both groups, experimental mice were inoculated with 5 x 10(7) infected erythrocytes in 100 microliters of blood. Babesia infection was acquired by all mice infected intraperitoneally with maximum 57% of parasitemia on day 6 post infection (pi) in F1 (B10 x CBA) mice and 40% of parasitemia on day 8 and 10 pi in BALB/c mice. Ten of 27 (37%) BALB/c mice infected by oral route showed low parasitemia (9%) during first two weeks pi. In this group of mice the pick of parasitemia (26%) was observed on day 22 pi. In both groups of infected mice the period of prepatency ended between days 35 and 40 pi. Experiments have confirmed that the maintenance of babesiosis may be continued in the absence of a tick vector. Demonstration, under experimental conditions, of infection of Babesia by oral route may suggest that in nature cannibalism of rodents, occurring under certain circumstances, can be considered as a natural way of oral transmission of B. microti.

Animals↗
PubMed1999

Comparison of a rapid field immunochromatographic test to expert microscopy for the detection of Plasmodium falciparum asexual parasitemia in Thailand.

We assessed a rapid, Plasmodium falciparum histidine rich protein 2 (PfHRP2)-based immunochromatographic test (ICT Malaria Pf Test), for detection of asexual P. falciparum parasitemia in 551 subjects in three groups: (1) symptomatic patients self-referring for diagnosis, (2) villagers in a screening survey, and (3) patients recently treated for P. falciparum malaria. Expert light microscopy was the reference standard. ICT test performance was similar for diagnostic and screening modes. Four findings emerged: (1) test sensitivity correlated directly with parasite density, (2) test band intensity correlated directly with parasite density, (3) persistent test positivity after parasite clearance precludes its use for monitoring early therapeutic responses, and (4) a false negative test at 18,000 parasites/microl is unexplained. We conclude that a strong positive ICT test is highly predictive of falciparum asexual parasitemia for the diagnosis of new cases of falciparum malaria in Thailand, but a negative test result is inadequate to exclude parasitemia < 300/microl, and in some instances, even a higher parasitemia.

Adult↗