Parasite density of Plasmodium falciparum malaria in Ghanaian schoolchildren: evidence for influence of sex hormones?

Landgraf, Barbara; Kollaritsch, Herwig; Wiedermann, G; Wernsdorfer, Walther H.

doi:10.1016/0035-9203(94)90505-3

Cited by 44 publications

(33 citation statements)

References 3 publications

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“…We failed to find any substantial epidemiologic explanation for this phenomenon but it is possible that gender might have an effect upon tumor necrosis factor (Kwiatkowski D, unpublished data), immune responses, 36,37 parasite density, 38 and thus on the course of clinical attacks.…”

Section: Discussionmentioning

confidence: 86%

Plasmodium falciparum clinical malaria in Dielmo, a holoendemic area in Senegal: no influence of acquired immunity on initial symptomatology and severity of malaria attacks.

Rogier¹,

Ly²,

Tall³

et al. 1999

Am J Trop Med Hyg

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Abstract. Six hundred eighty-nine Plasmodium falciparum malaria attacks were observed during a three-year period among 226 inhabitants of the village of Dielmo, Senegal, an area of high malaria transmission. Malaria attacks were defined as clinical episodes with fever (body temperature Ն 38.0ЊC) or reporting of fever or headache or vomiting, associated with a parasite:leukocyte ratio above an age-dependent pyrogenic threshold identified in this population. The symptom frequencies were tested against age, gender, and parasite density using a random-effect logistic regression model and the study of distinguishable clinical presentations was carried out by multi-correspondence analysis. There was little difference between the severity of symptoms during the initial course of attacks in young children and adults, and this severity was not correlated with the duration of the pathologic episode. It was not possible to distinguish objectively different malaria attack types according to the severity of clinical manifestations. In contrast, the duration of fever, symptoms, and parasite clearance were significantly longer among the youngest children than among the oldest children and adults. These findings suggest that of the two components of protective immunity, anti-parasite immunity and anti-toxic immunity, only the first would play a major role as age increases. They suggest also that the initial clinical presentation of malaria attacks is not predictive of the level of protective immunity.The main goal of the current malaria control strategies is to prevent malaria mortality by diagnosing and treating clinical manifestations of the disease as early as possible. 1 This depends not only on the availability of efficient health services but also on the knowledge and the attitude of the patients or of their parents and on their perception of the initial symptoms that influence their therapeutic approach at home. Although a number of studies have been published on the signs and symptoms of clinical malaria in endemic populations, almost all of these studies were conducted in hospitals or outpatient clinics. Few detailed data are available on the range of clinical manifestations of malaria at the community level, their relative frequency, and their value in diagnosing the disease and initiating treatment. Since access to health facilities is difficult for most rural populations of tropical Africa, a better knowledge of clinical malaria at the community level could help to develop simple rules that would be necessary for reducing malaria mortality in these populations.A better knowledge of the whole range of malaria morbidity would also determine whether different clinical forms of nonsevere malaria attacks exist. The distinction between forms of malaria attacks that differ in the severity of clinical expression could have implications for the evaluation of control methods. The assessment of the clinical efficiency of malaria drugs or vaccines could vary according to the clinical forms that have been chosen to evaluate them...

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Section: Discussionmentioning

confidence: 86%

Plasmodium falciparum clinical malaria in Dielmo, a holoendemic area in Senegal: no influence of acquired immunity on initial symptomatology and severity of malaria attacks.

Rogier¹,

Ly²,

Tall³

et al. 1999

Am J Trop Med Hyg

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“…In a recent prospective study of imported malaria cases in France, men reported more severe symptoms of malaria infection (e.g., chills, fever, and low platelet counts) than did women (7). Among Ghanaian school children, although the prevalence of P. falciparum infection does not differ between the sexes, the parasite density is significantly higher for boys than girls around puberty (i.e., from ages 8 to 16), suggesting that circulating sex steroids may influence this outcome (23). Although significantly more men die from infectious diseases than women (37), sex differences in mortality from Plasmodium infection are not consistently reported.…”

Section: Vol 74 2006 Sex Difference In Malaria Infection 3197mentioning

confidence: 90%

“…A few studies do, however, clearly illustrate that men are more susceptible than women. For example, several studies indicate that men tend to have higher parasitemia than women (23,32,52). In a recent prospective study of imported malaria cases in France, men reported more severe symptoms of malaria infection (e.g., chills, fever, and low platelet counts) than did women (7).…”

Section: Vol 74 2006 Sex Difference In Malaria Infection 3197mentioning

confidence: 99%

“…One genus of protozoan parasites that causes a pronounced sexual dimorphism in vertebrate hosts is Plasmodium. Among humans, although the incidence of infection is often similar between the sexes (see references 51 and 52), sex differences in the intensity of infection are reported in which men have higher parasitemia than women (23,32,52). The observation that P. falciparum (i.e., a human malaria parasite) density increases at puberty in men, but not in women, suggests that circulating sex steroids may influence this outcome (23).…”

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confidence: 99%

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Involvement of Gonadal Steroids and Gamma Interferon in Sex Differences in Response to Blood-Stage Malaria Infection

et al. 2006

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To examine the hormonal and immunological mechanisms that mediate sex differences in susceptibility to malaria infection, intact and gonadectomized (gdx) C57BL/6 mice were inoculated with Plasmodium chabaudi AS-infected erythrocytes, and the responses to infection were monitored. In addition to reduced mortality, intact females recovered from infection-induced weigh loss and anemia faster than intact males. Expression microarrays and real-time reverse transcription-PCR revealed that gonadally intact females exhibited higher expression of interleukin-10 (IL-10), IL-15R␣, IL-12R␤, Gadd45␥, gamma interferon (IFN-␥), CCL3, CXCL10, CCR5, and several IFN-inducible genes in white blood cells and produced more IFN-␥ than did intact males and gdx females, with these differences being most pronounced during peak parasitemia. Intact females also had higher anti-P. chabaudi immunoglobulin G (IgG) and IgG1 responses than either intact males or gdx females. To further examine the effector mechanisms mediating sex differences in response to P. chabaudi infection, responses to infection were compared among male and female wild-type (WT), T-cell-deficient (TCR␤␦ ؊/؊ ), B-cell-deficient (MT), combined T-and B-cell-deficient (RAG1), and IFN-␥ knockout (IFN-␥ ؊/؊ ) mice. Males were 3.5 times more likely to die from malaria infection than females, with these differences being most pronounced among TCR␤␦ ؊/؊ , MT, and RAG1 mice. Male mice also exhibited more severe weight loss, anemia, and hypothermia, and higher peak parasitemia than females during infection, with WT, RAG1, TCR␤␦ ؊/؊ , and MT mice exhibiting the most pronounced sexual dimorphism. The absence of IFN-␥ reduced the sex difference in mortality and was more detrimental to females than males. These data suggest that differential transcription and translation of IFN-␥, that is influenced by estrogens, may mediate sex differences in response to malaria.Males are more susceptible to many protozoan infections than females and field and laboratory studies link increased susceptibility to infection with circulating steroid hormones (17,18,39). One genus of protozoan parasites that causes a pronounced sexual dimorphism in vertebrate hosts is Plasmodium. Among humans, although the incidence of infection is often similar between the sexes (see references 51 and 52), sex differences in the intensity of infection are reported in which men have higher parasitemia than women (23, 32, 52). The observation that P. falciparum (i.e., a human malaria parasite) density increases at puberty in men, but not in women, suggests that circulating sex steroids may influence this outcome (23).Studies of rodent malarias have confirmed that males are more likely to die after blood-stage malaria infection than are females (2,3,(54)(55)(56)

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“…5 A correlation between pregnancy and human babesiosis has also been reported. 6 Males are more susceptible than females to infections with some protozoans such as Plasmodium berghei, 7 P. chabaudi, 8,9 P. falciparum, 10 Leishmania major, Leishmania mexicana,…”

Section: Introductionmentioning

confidence: 99%

Effect of Sex Steroids on Babesia microti Infection in Mice

Sasaki¹,

Fujii²,

Iwamoto³

et al. 2013

The American Society of Tropical Medicine and Hygiene

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Abstract. Sex-based-differences are known to affect susceptibility to protozoan infections, but their effects on parasitemia and clinical symptoms in Babesia infections remain unclear. We examined the sex-based susceptibility of various mouse strains to Babesia microti Munich strain infection. In all strains, male mice exhibited significantly higher peak parasitemia and more severe anemia than female mice. Testosterone and estradiol-17β treatment caused an increase in parasitemia and aggravation of anemia. Orchidectomized male mice receiving testosterone exhibited smaller splenic macrophage populations three days after infection, smaller B cell populations 10 days after infection, and reduced splenic tumor necrosis factor-α and interferon-γ mRNA expression than mice that did not receive testosterone. Mice receiving estradiol-17β did not exhibit immunosuppressive effects. Thus, a weakened and delayed innate immunity response may lead to acquired immunity failure. The results suggested that testosterone directly affects T or B cells, leading to delayed acquired immunity, dramatically increased parasitemia, and severe anemia.

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Parasite density of Plasmodium falciparum malaria in Ghanaian schoolchildren: evidence for influence of sex hormones?

Cited by 44 publications

References 3 publications

Plasmodium falciparum clinical malaria in Dielmo, a holoendemic area in Senegal: no influence of acquired immunity on initial symptomatology and severity of malaria attacks.

Plasmodium falciparum clinical malaria in Dielmo, a holoendemic area in Senegal: no influence of acquired immunity on initial symptomatology and severity of malaria attacks.

Involvement of Gonadal Steroids and Gamma Interferon in Sex Differences in Response to Blood-Stage Malaria Infection

Effect of Sex Steroids on Babesia microti Infection in Mice

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