Resolution of acute malaria (Plasmodium berghei in the rat): reversibility and spleen dependence
- PMID: 6986095
- DOI: 10.4269/ajtmh.1980.29.1
Resolution of acute malaria (Plasmodium berghei in the rat): reversibility and spleen dependence
Abstract
Six-week-old rats infected with Plasmodium berghei developed a peak parasitemia of 55.2 +/- 3.1% by day 15 of infection, followed by spontaneous resolution of the infection during a process referred to as crisis. Crisis was accompanied by the appearance in circulation of infected erythrocytes in which the parasites appeared abnormal ("crisis forms"). Rats splenectomized at different times during the crisis period experienced a sudden increase in parasitemia, with a marked decrease in the number of circulating crisis forms. Splenectomy in parasitemia, with a marked decrease in the number of circulating crisis forms. Splenectomy resulted in a 100% mortality, whereas all control and sham-operated rats survived their infection. Although P. berghei is restricted to developing within young erythrocytes, our observations could not be explained by the effects of splenectomy on the number of circulating reticulocytes. Indeed, the reticulocytosis which accompanies crisis was unaffected by splenectomy. Our observations therefore suggest that crisis is a reversible process and, specifically, that the spleen is necessary for its maintenance.
Similar articles
-
Intravascular clearance of parasitized erythrocytes in rodent malaria.J Clin Invest. 1979 Jun;63(6):1187-94. doi: 10.1172/JCI109413. J Clin Invest. 1979. PMID: 376554 Free PMC article.
-
Atypical reticulocytes in rats with malaria as a possible consequence of the pitting function of the spleen.Ann Trop Med Parasitol. 1981 Jun;75(3):363-5. doi: 10.1080/00034983.1981.11687452. Ann Trop Med Parasitol. 1981. PMID: 7030237 No abstract available.
-
Preferential invasion of reticulocytes during late-stage Plasmodium berghei infection accounts for reduced circulating reticulocyte levels.Int J Parasitol. 2006 Nov;36(13):1389-97. doi: 10.1016/j.ijpara.2006.07.009. Epub 2006 Sep 1. Int J Parasitol. 2006. PMID: 16979643
-
Relationship of alterations in splenic clearance function and microcirculation to host defense in acute rodent malaria.J Clin Invest. 1981 May;67(5):1400-4. doi: 10.1172/jci110168. J Clin Invest. 1981. PMID: 7014635 Free PMC article.
-
Studies on parasitic crisis in malaria: I. Signs of impending crisis in Plasmodium berghei infections of the white rat.Ann Trop Med Parasitol. 1977 Dec;71(4):429-33. doi: 10.1080/00034983.1977.11687208. Ann Trop Med Parasitol. 1977. PMID: 339858
Cited by
-
Murine malaria: blood clearance and organ sequestration of Plasmodium yoelii-infected erythrocytes.Infect Immun. 1982 Oct;38(1):162-7. doi: 10.1128/iai.38.1.162-167.1982. Infect Immun. 1982. PMID: 7141688 Free PMC article.
-
Failure of bacterial lipopolysaccharide to elicit a cytostatic effect on Plasmodium vinckei petteri in C3H/HeJ mice.Infect Immun. 1982 Jan;35(1):58-63. doi: 10.1128/iai.35.1.58-63.1982. Infect Immun. 1982. PMID: 7033142 Free PMC article.
-
In vivo compartmental kinetics of Plasmodium falciparum histidine-rich protein II in the blood of humans and in BALB/c mice infected with a transgenic Plasmodium berghei parasite expressing histidine-rich protein II.Malar J. 2019 Mar 13;18(1):78. doi: 10.1186/s12936-019-2712-3. Malar J. 2019. PMID: 30866956 Free PMC article.
-
Opsonic activity of human immune serum on in vitro phagocytosis of Plasmodium falciparum infected red blood cells by monocytes.Clin Exp Immunol. 1982 Mar;47(3):635-44. Clin Exp Immunol. 1982. PMID: 7044626 Free PMC article.
-
Demonstration of a lipopolysaccharide-induced cytostatic effect on malarial parasites.Infect Immun. 1981 Aug;33(2):343-7. doi: 10.1128/iai.33.2.343-347.1981. Infect Immun. 1981. PMID: 7275307 Free PMC article.
MeSH terms
LinkOut - more resources
Full Text Sources
Medical