Parasitology Course BIOL 2272. By Fred Opperdoes. Definition of parasitism. Parasitology describes the relationships between two organisms, i.e. the host organism and the parasite. When one organism gives shelter and food to another organism two totally different situations may exist:
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By Fred Opperdoes
Light microscopic picture of Trichomonas vaginalis
A trophozoite of Trichomonas vaginalis from culture. The four flagella and single nucleus are visible. The dark median rod is the axostyle which is characteristic of the trichomonads; approximate size = 26 µm.
Naegleria trophozoites in brain tissue
Acanthamoeba trophozoites in culture after immunofluorescence staining
Giardia, an intestinal parasite of beavers and man may contaminate fresh water lakes and rivers in the US. The drinking of this water may lead to intestinal infections in humans.
The trophozoites contain a dark transverse rod, the axostyle, which seems to be a supportive element. The cysts average about 13 µm in length, are oval, and contain two nuclei and remnants of the axostyle. Because of these unique characteristics, G. lamblia is one of the easiest intestinal protozoans of humans to diagnose.
Giardia trophozoites in the stool
Trichomonas vaginalis trophozoites Trypanosomes in blood Giardia lamblia trophozoites in the stool
Scanning EM of blood from an experimental animal (rat) infected with Trypanosoma rhodesiense with a very high parasitaemia (2-3 billion tryps / ml). There are almost as many trypanosomes as there are red blood cells.
Diagrammatic representation of a short stumpy bloodstream form trypanosome (from K. Vickerman with permission). A-the anterior flagellum. B-the underlying complex cytoskeleton. C-the nucleus. D-the mitochondrion. E-the kinetoplast (mitochondrial genome). F-glycosome (a unique organelle where glycolysis occurs). G-the flagellar pocket. H-the basal body. I-Golgi apparatus. J-endoplasmic reticulum. K-the undulating membrane. L-attachment of the flagellum to the undulating membrane. M-attachment of the flagellum directly to the cell body.
Life-cycle stages of trypanosomatidae. a, promastigote; b, ophistomastigote; c,epimastigote; d, trypomastigote; e, choanomastigote; f, amastigote; g, paramastigote; h,....K, kinetoplast; N, nucleus; F, flagellum.
The life-cycle of T. brucei is shown diagrammatically below. The procyclic is the stage which reproduces within the tsetse fly. Procyclics can be grown in vitro and have been very carefully studied as to their morphology, antigenicity, metabolic requirements and their mode of regulation of gene expression. The same is not true for the bloodstream stages, the stage which is actually responsible for disease in the human host. The constraint here is the development of a high yielding system for growing these stages in vivo, although recently a system for in vitro cultivation for the study of the genetics of differentiating trypanosomes has been described.
A life-cycle illustrating the morphology of the developmental stages of T. brucei is shown here:
Tsetse fly taking a blood meal.
Geographical distribution of tsetse in Africa
Prevalence of African Human Trypanosomiasis (HAT) or sleeping sickness
Course of parasitaemia
Mobile team visiting an African village
Collection of a drop of finger blood and the subsequent analysis of a wet drop for the presence of trypanosomes
Control (2) sleeping sickness
Differences in nutritional income between Africa and the European Union due to trypanosomiasis
Trypanosomiasis and nutrition (3) sleeping sickness
Influence of tsetse on cattle breeding in Africa
Rodent trypanosomes cause a rapid increase in parasitaemia, which comes to a halt when the host starts to produce a protein that has been called ablastin (for its growth inhibiting potency) and which has later been identified as immunoglobulin E (IgE). This IgE binds to a surface epitope on the trypanosome's plasma membrane which has been identified as a proton-pumping ATPase. The binding of IgE to this ATPase does not kill the parasite but prevents the parasites from dividing and multiplying. This situation may remain unchanged for several weeks, after which a new antibody, now an IgM is produced that recognizes the ablastine : H-ATPase complex on the trypanosome's surface leading to the activation of complement and resulting in the rapid lysis of the trypanosomes in the blood. When the host has recovered from this infection it has developed a solid immunity against subsequent infections with the same trypanosome.
Immunoglobulins directed against these VSGs recognise the trypanosomes. Binding of antibodies to the tryps will lead to lysis of the trypanosomes by complement and disappearance of the tryps from the blood. However, a minority will have changed its VSG and is not recognised by the circulating antibodies. This population will multiply and expand unlimited, until new antibodies will be produced against this variant, etc....
Schematic representation of the protein chain of a typical VSG. The N-terminus contains a signal peptide which is cleaved off from the mature protein. The variable region is different for each VSG and shows little or no identity with other VSGs. The hydrophobic tail contains a recognition signal for attachment to the glycolipid anchor (see below). When the anchor is attached the last 20 amino acids are cleaved off.
Structure of the glycolipid anchor for VSG.
The variable surface glycoprotein (VSG) is attached to the membrane via a glycolipid anchor consisting of ethanolamine, a glycan structure containing several mannose moieties, a glucosamine and a phosphoinositol that is linked to a 1,2-dimyristoylglycerol burried in the plasma membrane.
Linear map of the 22-kb maxicircle of T. brucei.
Orientation of genes on chromosomes
Trans-splicing of RNA
Glycosome sleeping sickness
Glycosomes of T. brucei bloodforms visualised by serial sectioning
From: Tetley and Vickerman, 1991
Immunogold localization of glycolytic enzymes sleeping sickness
The glycolytic enzyme PGK is inside glycosomes of T. brucei
Courtesy Marten Veenhuis
Compartmentation of glycolysis in bloodstream form trypanosomes
Distribution of Chagas ’ disease. Among an estimated population of 360 million inhabitants at least 90 million persons (25%) are considered at risk of infection and 16-18 million people are infected. It is generally expected that about 30% of the infected population will develop clinically overt disease. Thus it is expected that in total some 5 million people have the clinical symptoms of Chagas' disease.
Trypomastigotes in blood
The local inflammation caused by the entry of T. cruzi is called chagoma. Chagoma of the eye, Romaña ’s sign, is seen in 90 % of patients diagnosed as recently infected.
X-rays of two patients suffereing from the late stage of Chagas' disease, one with megacolon and the other with a severe weakening and widening of the hart muscle.