DOCSLIB.ORG

Anopheles Freebornifreeborni Courtesycourtesy Plasmodia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

AnophelesAnopheles freebornifreeborni CourtesyCourtesy Plasmodia seen with the microscope M. Lontie, MCH, Leuven, 2012 Diagnosis of malaria • Thin film (better for species identification). •Thick film (more sensitive). • QBC (quantitative buffy coat, BD). • Antigen-detection. • Molecular methods (New Microbiol. 2001. 24:69.). • Serology. • (Platelet count: low in case of severe P. falciparum infection). Thick film • Blood (finger, tube), no anticoagulants. • Immediately after sampling. • Defibrination (at least during one minute). •Not too thick. • Allow drying. • Quality of the water (pH). • Also for Babesia, Borrelia, Trypanosoma, filaria … (last pictures). U.S. Department of Health, Education, and Welfare. Courtesy Peters W. & Gilles H.M. Thick film Only with disposable fingerstick devices (Acta Clinica Belgica. 2005. 60:63-69.). Can also be made with blood with anticoagulants (EDTA). Allow then much longer drying. Thick film made with EDTA blood Diagnosis of malaria • 1 parasite / 100 000 rbc = fever (non- immune person). • 100 000 rbc in a thin film = 30 min. • Thick film = concentration technique. • Thick film = 10 to 30 times more sensitive than thin film. • Thick film = 3 to 5 (10) min. U.S. Department of Health, Education, and Welfare. Diagnosis of malaria • 1 parasite / 100 000 rbc = fever (non-immune person) = 25 - 50 parasites / μl. • Tolerance in immune persons = 5 000 - 10 000 (100 000) parasites / μl. • Cerebral malaria in children (P. falciparum): 1 000 000 parasites / μl associated with fatal issue. (Wéry, 1995). Thick - thin film, objective 100 x 10 000 wbc, 5 000 000 rbc Giemsa May-Grünwald-Giemsa 100 fields 100 fields 0.25 μl / 10 min 0.01 μl / 10 min 2500 wbc 100 wbc 1 250 000 rbc 50 000 rbc one = 4 parasites / μl one = 100 parasites / μl 50 / μl = fever in non- 50 / μl = fever in non- immune = 12.5 / film immune = 0.5 / film Wéry M. 1995. Protozoologie Médicale. Diagnosis of malaria • Geographical distribution of different species should be taken into account. • Plasmodium falciparum limited to (sub-) tropical areas (summer isotherm of 20°C, altitude < 2000 m). • Mixed infections are not uncommon (eg P. falciparum + P. ovale in West Africa). Duffy blood group system = receptor P. vivax West & Central Africa East Africa Duffy bg: absent Duffy bg: present Plasmodium ovale Plasmodium vivax Wéry M. 1995. Protozoologie Médicale. MALARIA (vivax) (malariae) (falciparum) vivax (vivax) falciparum malariae malariae vivax falciparum ovale falciparum ovale vivax malariae According to M. Wéry, 1995 Malaria: antigens • HRP-2: watersoluble histidine-rich protein from axesual stages and young gametocytes of P. falciparum (related to knob-associated HRP-1 and HRP-3). • Pan-malarial antigen: pLDH or aldolase, present in all four Plasmodium spp. A. Moody. 2002. CMR, 15:66-78. Malaria antigen (HRP2) detection Sensitivity: 50-100 (and less) parasites / µL. False negatives due to very high parasitemias. Diagnosis of malaria antigen- detection • Persistent positivity with gametocytes (JCM, 2001, 1025). • PMA is expressed by P. malariae (JCM, 2001, 2035). • Moody A. 2002. CMR, 15:66-78. Rapid diagnostic tests for malaria parasites (review). Lee N. et al. 2006. JCM., 44:2773-2778. Effect of sequence variation in Plasmodium falciparum histidine-rich protein 2 on binding of specific monoclonal antibodies: implications for rapid diagnostic tests for malaria. • Sequence variation can help to explain the variations in the performance of HRP-based RDTs and point toward possible solutions. Prozone in 16 of 17 HRP-2 based RDTs P. Gillet. 2011. Dissertation at the Maastricht University. Malaria antigen detection Prozone:Prozone how to avoid? Always have a look at the thick film Perform always HRP2 & LDH or aldolase If low platelets look a “secondsecond” time at the thick film Species-specific PCR diagnosis of malaria (CDC) 1. P. vivax 2. P. malariae 3. P. falciparum 4. P. ovale Two step nested PCR using the primers of Snounou et al. CDC, 2001. Detection of four Plasmodium species in blood from humans by 18S rRNA gene subunit-based and species-specific real time PCR assays Rougemont M. et al. 2004. JCM, 42:5636-5643. Malaria serology • Only P. falciparum cultivated in vitro. • To exclude malaria e.g. among travellers. • Blood donation from travellers. • For epidemiological reasons. Wéry M., 1995. Malaria: staining procedures used • Thick film: Giemsa staining. • Thin film: May-Grünwald staining. Inexpensive method of diluting Giemsa stain • Petithory J.C. et al. 2005. JCM, 43:528. 29 bottles of Evian water. pH: 7.36 Ready to use and stable for weeks. pH 7.2 = optimal pH 6.4 – 6.8: less coloured parasites and stippling pH 7.6: stronger coloured parasites and stippling UK NEQAS Parasitology on the web • Why is malariology so difficult? I firmly believe that knowledge and experience arises from constant practice and exposure to a wide variety of different forms of the parasites. • The other problem is that no two strains of the same parasite are identical; intra-species variation is a characteristic of the malarial parasite. Diagnosis of malaria • Percentage of infected red blood cells. • Ring stage. • Trophozoite (growing ring stage). • Schizont: number of merozoites: 2 (young) -24. • Gametocytes: shape (crescentic ot rounded). • Dots: James, Schüffner, Maurer. • Pigment: P. malariae, P. ovale ... • Atypical elements. U.S. Department of Health, Education, and Welfare. Parasitized RBC • All: Plasmodium falciparum. • Young (reticulocytes, larger rbc): Plasmodium ovale and Plasmodium vivax. • Old (smaller rbc): Plasmodium malariae. Gentilini & Duflo. 1986. Plasmodium falciparum vivax ovale malariae RBC + > 40 % 2 % 2 % 1 % RBC normal enlarged enlarged smaller Maurer’s Schüffner’s Schüffner’s spots dots dots, oval fimbriated Ring 1, 2 / rbc 1 / rbc 1 (2) / rbc 1 / rbc with two nuclei Trofozoite not in ameboid ameboid band shape peripheral pigment pigment blood Schizont not in (2), 16-24 (2), 8-10 (2), 6-8 peripheral merozoites merozoites merozoites blood Gametocyte crescentic rounded rounded rounded Courtesy Tulane Sharing Plasmodium knowlesi? • White N. 2004. Sharing malarias. Lancet:1006. •Singh B. et al. 2004. Lancet: 1017-1024. Monkey malaria in 120 humans in 2000-2002 in Malaysian Borneo by PCR (by microscopy P. malariae). Plasmodium knowlesi: the fifth human malaria parasite. N. J. White. 2008. CID 46:172-173. Island of Borneo, Malaysia. Plasmodium falciparum in thick film Courtesy U.S. Department of Health, Education and Welfare. 1960. Plasmodium falciparum: thick film with numerous small rings. Plasmodium falciparum: thick film with numerous rings. Plasmodium falciparum: ring in a thick film. Plasmodium falciparum: ring and crescentic gametocyte in a thick film. Plasmodium falciparum: two crescentic gametocytes in a thick film. Plasmodium falciparum in thin film Courtesy U.S. Department of Health, Education and Welfare. 1960. Courtesy Lamy L.H. Plasmodium falciparum: two rings and Maurer’s spots in a thin film. Plasmodium falciparum: four rings in a thin film. Plasmodium falciparum: small young ring in a thin film. Plasmodium falciparum: two « accolé » forms in one cell in a thin film. Plasmodium falciparum: several rings, two in one red blood cell in a thin film. Plasmodium falciparum: three rings in one red blood cell, ring with two nuclei, « accolé » form, two red blood cells with small rings in a thin film. Plasmodium falciparum: numerous rings, three in one red blood cell in a thin film. Plasmodium falciparum: numerous rings, four in one red blood cell in a thin film. Plasmodium falciparum: numerous rings in a thin film. Plasmodium falciparum: two small, and one « accolé-like » rings in a thin film. Plasmodium falciparum: with very dark pigment collected in one small, dense block in a thin film. Plasmodium falciparum: with very dark pigment collected in one small, dense block and in the process of initial chromatin division in a thin film. Plasmodium falciparum: schizont in cord blood in a thin film. Plasmodium falciparum: schizont with clumped pigment in peripheral blood. This is seen only in heavy infections (thin film). Plasmodium falciparum: two rings and one gametocyte (thin film). Plasmodium falciparum: one crescentic gametocyte, about 1.5 times diameter of erythrocyte in length (thin film). Plasmodium falciparum: two crescentic gametocytes (thin film). Plasmodium vivax in thin film Courtesy U.S. Department of Health, Education and Welfare. 1960. Courtesy Lamy L.H. Plasmodium vivax: ring with Schüffner’s stippling (thick film). Plasmodium vivax: trophozoite with Schüffner’s stippling (thick film). Plasmodium vivax: young schizont, ameboid trophozoites and rings (thin film). Plasmodium vivax: older ring and ameboid trophozoite (thin film). Plasmodium vivax: older ring and ameboid trophozoite both with Schüffner’s stippling (thin film). Plasmodium vivax: three ameboid trophozoites in a thin film. Plasmodium vivax: ameboid (vivax) trophozoite (thin film). Plasmodium vivax: ameboid trophozoite, gametocyte and Schüffner’s dots (thin film). Plasmodium vivax: gametocyte (thin film). Plasmodium vivax: three gametocytes (thin film). Plasmodium vivax: schizont with many merozoites in an enlarged red blood cell (thin film). Plasmodium vivax: schizont with many merozoites (thin film). Plasmodium vivax: schizont with many merozoites (thin film). Plasmodium vivax: mature schizont with many (19) merozoites (thin film). Plasmodium vivax: disrupted schizont with many merozoites (thin film). Plasmodium vivax: disrupted schizont (thin film).
Recommended publications
  • Basal Body Structure and Composition in the Apicomplexans Toxoplasma and Plasmodium Maria E

    Basal Body Structure and Composition in the Apicomplexans Toxoplasma and Plasmodium Maria E

    Francia et al. Cilia (2016) 5:3 DOI 10.1186/s13630-016-0025-5 Cilia REVIEW Open Access Basal body structure and composition in the apicomplexans Toxoplasma and Plasmodium Maria E. Francia1* , Jean‑Francois Dubremetz2 and Naomi S. Morrissette3 Abstract The phylum Apicomplexa encompasses numerous important human and animal disease-causing parasites, includ‑ ing the Plasmodium species, and Toxoplasma gondii, causative agents of malaria and toxoplasmosis, respectively. Apicomplexans proliferate by asexual replication and can also undergo sexual recombination. Most life cycle stages of the parasite lack flagella; these structures only appear on male gametes. Although male gametes (microgametes) assemble a typical 9 2 axoneme, the structure of the templating basal body is poorly defined. Moreover, the rela‑ tionship between asexual+ stage centrioles and microgamete basal bodies remains unclear. While asexual stages of Plasmodium lack defined centriole structures, the asexual stages of Toxoplasma and closely related coccidian api‑ complexans contain centrioles that consist of nine singlet microtubules and a central tubule. There are relatively few ultra-structural images of Toxoplasma microgametes, which only develop in cat intestinal epithelium. Only a subset of these include sections through the basal body: to date, none have unambiguously captured organization of the basal body structure. Moreover, it is unclear whether this basal body is derived from pre-existing asexual stage centrioles or is synthesized de novo. Basal bodies in Plasmodium microgametes are thought to be synthesized de novo, and their assembly remains ill-defined. Apicomplexan genomes harbor genes encoding δ- and ε-tubulin homologs, potentially enabling these parasites to assemble a typical triplet basal body structure.
  • Plasmodium Evasion of Mosquito Immunity and Global Malaria Transmission: the Lock-And-Key Theory

    Plasmodium Evasion of Mosquito Immunity and Global Malaria Transmission: the Lock-And-Key Theory

    Plasmodium evasion of mosquito immunity and global malaria transmission: The lock-and-key theory Alvaro Molina-Cruz1,2, Gaspar E. Canepa1, Nitin Kamath, Noelle V. Pavlovic, Jianbing Mu, Urvashi N. Ramphul, Jose Luis Ramirez, and Carolina Barillas-Mury2 Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852 Contributed by Carolina Barillas-Mury, October 15, 2015 (sent for review September 19, 2015; reviewed by Serap Aksoy and Daniel L. Hartl) Plasmodium falciparum malaria originated in Africa and became for the parasite to evade mosquito immunity. The implications global as humans migrated to other continents. During this jour- of P. falciparum selection by mosquitoes for global malaria ney, parasites encountered new mosquito species, some of them transmission are discussed. evolutionarily distant from African vectors. We have previously shown that the Pfs47 protein allows the parasite to evade the mos- Results quito immune system of Anopheles gambiae mosquitoes. Here, we Differences in Compatibility Between P. falciparum Isolates from investigated the role of Pfs47-mediated immune evasion in the Diverse Geographic Origin and Different Anopheline Species. The adaptation of P. falciparum to evolutionarily distant mosquito species. compatibility between P. falciparum isolates from different continents We found that P. falciparum isolates from Africa, Asia, or the Americas and mosquito vectors that are geographically and evolutionarily have low compatibility to malaria vectors from a different continent, distant was investigated by simultaneously infecting major malaria an effect that is mediated by the mosquito immune system. We iden- vectors from Africa (A. gambiae), Southeast Asia (Anopheles dirus), tified 42 different haplotypes of Pfs47 that have a strong geographic and the New World (A.
  • Non-Invasive Surveillance for Plasmodium in Reservoir Macaque

    Non-Invasive Surveillance for Plasmodium in Reservoir Macaque

    Siregar et al. Malar J (2015) 14:404 DOI 10.1186/s12936-015-0857-2 METHODOLOGY Open Access Non‑invasive surveillance for Plasmodium in reservoir macaque species Josephine E. Siregar1, Christina L. Faust2*, Lydia S. Murdiyarso1, Lis Rosmanah3, Uus Saepuloh3, Andrew P. Dobson2 and Diah Iskandriati3 Abstract Background: Primates are important reservoirs for human diseases, but their infection status and disease dynamics are difficult to track in the wild. Within the last decade, a macaque malaria, Plasmodium knowlesi, has caused disease in hundreds of humans in Southeast Asia. In order to track cases and understand zoonotic risk, it is imperative to be able to quantify infection status in reservoir macaque species. In this study, protocols for the collection of non-invasive samples and isolation of malaria parasites from naturally infected macaques are optimized. Methods: Paired faecal and blood samples from 60 Macaca fascicularis and four Macaca nemestrina were collected. All animals came from Sumatra or Java and were housed in semi-captive breeding colonies around West Java. DNA was extracted from samples using a modified protocol. Nested polymerase chain reactions (PCR) were run to detect Plasmodium using primers targeting mitochondrial DNA. Sensitivity of screening faecal samples for Plasmodium was compared to other studies using Kruskal Wallis tests and logistic regression models. Results: The best primer set was 96.7 % (95 % confidence intervals (CI): 83.3–99.4 %) sensitive for detecting Plasmo- dium in faecal samples of naturally infected macaques (n 30). This is the first study to produce definitive estimates of Plasmodium sensitivity and specificity in faecal samples= from naturally infected hosts.
  • Babesia Species

    Babesia Species

    Laboratory diagnosis of babesiosis Babesia species Basic guidelines A. Capillary blood should be obtained by fingerstick, or venous blood should be obtained by venipuncture. B. Blood smears, at least two thick and two thin, should be prepared as soon as possible after col- lection. Delay in preparation of the smears can result in changes in parasite morphology and staining characteristics. In Babesia infections, infected red blood cells (rbcs) are normal in size. Typically rings are seen, and they may be vacuolated, pleomorphic or pyriform. Extracellular or tetrad-forms may also be present. Unlike Plasmodium spp., Babesia organisms lack pigment. Rings Rings of Babesia spp. have delicate cytoplasm and are often pleomorphic. Infected rbcs are not enlarged; multiple infection of rbcs can be common. Rings are usually vacuolated and do not produce pigment. Oc- casional classic tetrad-forms (Maltese Cross) or extracellular rings can be present. Rings of Babesia sp. in thick blood smears. Thin, delicate rings of Babesia sp. in a Babesia sp. in a thin blood smear, Thin blood smear showing a cluster of thin blood smear. showing pleomorphic rings and multiply- extracellular rings. infected rbcs. Laboratory diagnosis of babesiosis Babesia species Babesia microti in a thin blood smear. Note Babesia microti in thin blood smears. Notice the vacuolated and pleomorphic rings and multi- the classic “Maltese Cross” tetrad-form in ply-infected rbcs. Notice also there is no pigment present in any of the parasites. the infected rbc in the lower part of the image. Babesia sp. in a thin blood smear stained with Giemsa, showing pleomorphic rings and Babesia sp.
  • Comparison of the Plasmodium Species Which Cause Human Malaria

    Comparison of the Plasmodium Species Which Cause Human Malaria

    Comparison of the Plasmodium Species Which Cause Human Malaria Plasmodium Stages found Appearance of Erythrocyte species in blood (RBC) Appearance of Parasite normal; multiple infection of RBC more delicate cytoplasm; 1-2 small chromatin Ring common than in other species dots; occasional appliqué (accollé) forms normal; rarely, Maurer’s clefts seldom seen in peripheral blood; compact Trophozoite (under certain staining conditions) cytoplasm; dark pigment seldom seen in peripheral blood; mature Schizont normal; rarely, Maurer’s clefts = 8-24 small merozoites; dark pigment, (under certain staining conditions) clumped in one mass P.falciparum crescent or sausage shape; chromatin in a Gametocyte distorted by parasite single mass (macrogametocyte) or diffuse (microgametocyte); dark pigment mass normal to 1-1/4 X,round; occasionally fine Ring Schüffner’s dots; multiple infection of RBC large cytoplasm with occasional not uncommon pseudopods; large chromatin dot enlarged 1-1/2–2 X;may be distorted; fine large ameboid cytoplasm; large chromatin; Trophozoite Schüffner’s dots fine, yellowish-brown pigment enlarged 1-1/2–2 X;may be distorted; fine large, may almost fill RBC; mature = 12-24 Schizont Schüffner’s dots merozoites; yellowish-brown, coalesced P.vivax pigment round to oval; compact; may almost fill enlarged 1-1/2–2 X;may be distorted; fine RBC; chromatin compact, eccentric Gametocyte Schüffner’s dots (macrogametocyte) or diffuse (micro- gametocyte); scattered brown pigment normal to 1-1/4 X,round to oval; occasionally Ring Schüffner’s dots;
  • And Toxoplasmosis in Jackass Penguins in South Africa

    And Toxoplasmosis in Jackass Penguins in South Africa

    IMMUNOLOGICAL SURVEY OF BABESIOSIS (BABESIA PEIRCEI) AND TOXOPLASMOSIS IN JACKASS PENGUINS IN SOUTH AFRICA GRACZYK T.K.', B1~OSSY J.].", SA DERS M.L. ', D UBEY J.P.···, PLOS A .. ••• & STOSKOPF M. K .. •••• Sununary : ReSlIlIle: E x-I1V\c n oN l~ lIrIUSATION D'Ar\'"TIGENE DE B ;IB£,'lA PH/Re El EN ELISA ET simoNi,cATIVlTli t'OUR 7 bxo l'l.ASMA GONIJfI DE SI'I-IENICUS was extracted from nucleated erythrocytes Babesia peircei of IJEMIiNSUS EN ArRIQUE D U SUD naturally infected Jackass penguin (Spheniscus demersus) from South Africo (SA). Babesia peircei glycoprotein·enriched fractions Babesia peircei a ele extra it d 'erythrocytes nue/fies p,ovenanl de Sphenicus demersus originoires d 'Afrique du Sud infectes were obto ined by conca navalin A-Sepharose affinity column natulellement. Des fractions de Babesia peircei enrichies en chromatogrophy and separated by sod ium dodecyl sulphate­ glycoproleines onl ele oblenues par chromatographie sur colonne polyacrylam ide gel electrophoresis (SDS-PAGE ). At least d 'alfinite concona valine A-Sephorose et separees par 14 protein bonds (9, 11, 13, 20, 22, 23, 24, 43, 62, 90, electrophorese en gel de polyacrylamide-dodecylsuJfale de sodium 120, 204, and 205 kDa) were observed, with the major protein (SOS'PAGE) Q uotorze bandes proleiques au minimum ont ete at 25 kDa. Blood samples of 191 adult S. demersus were tes ted observees (9, 1 I, 13, 20, 22, 23, 24, 43, 62, 90, 120, 204, by enzyme-linked immunosorbent assoy (ELISA) utilizing B. peircei et 205 Wa), 10 proleine ma;eure elant de 25 Wo.
  • Cerebral and Plasmodium Ovale Malaria in Rhode Island

    Cerebral and Plasmodium Ovale Malaria in Rhode Island

    CASE REPORT Cerebral and Plasmodium ovale Malaria in Rhode Island JOSHUA KAINE, MD; JOSEPH MORAN-GUIATI, MD; JAMES TANCH, MD; BRIAN CLYNE, MD 64 67 EN ABSTRACT mortality. While the CDC currently reports a stable inci- We report two cases of malaria diagnosed in Rhode Is- dence of malaria in the US, climate change is predicted to land. First, a 21-year-old female who presented with 5 affect disease dynamics, and it remains unclear how the US days of fevers, chills, headache, and myalgias after return- incidence will be affected by climate change in the future.2,3 ing from a trip to Liberia, found to have uncomplicated Given the potentially fatal consequences of a missed malaria due to P. ovale which was treated successfully diagnosis of malaria and the relative inexperience of US with atovaquone/proguanil and primaquine. Second, a clinicians with the disease, we review two cases of malaria chronically ill 55-year-old male presented with 3 days of recently diagnosed in Rhode Island that are representative of headache followed by altered mental status, fever, and the spectrum of the disease one could expect to encounter in new-onset seizures after a recent visit to Sierra Leone, the US. The first is a classic, uncomplicated presentation of found to have P. falciparum malaria requiring ICU ad- malaria in a 21-year-old female and the second is an example mission and IV artesunate treatment. The diagnosis and of severe malaria in a chronically ill 55-year-old male. management of malaria in the United States (US), as well as its rare association with subdural hemorrhage are subsequently reviewed.
  • Malaria History

    Malaria History

    This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike License. Your use of this material constitutes acceptance of that license and the conditions of use of materials on this site. Copyright 2006, The Johns Hopkins University and David Sullivan. All rights reserved. Use of these materials permitted only in accordance with license rights granted. Materials provided “AS IS”; no representations or warranties provided. User assumes all responsibility for use, and all liability related thereto, and must independently review all materials for accuracy and efficacy. May contain materials owned by others. User is responsible for obtaining permissions for use from third parties as needed. Malariology Overview History, Lifecycle, Epidemiology, Pathology, and Control David Sullivan, MD Malaria History • 2700 BCE: The Nei Ching (Chinese Canon of Medicine) discussed malaria symptoms and the relationship between fevers and enlarged spleens. • 1550 BCE: The Ebers Papyrus mentions fevers, rigors, splenomegaly, and oil from Balantines tree as mosquito repellent. • 6th century BCE: Cuneiform tablets mention deadly malaria-like fevers affecting Mesopotamia. • Hippocrates from studies in Egypt was first to make connection between nearness of stagnant bodies of water and occurrence of fevers in local population. • Romans also associated marshes with fever and pioneered efforts to drain swamps. • Italian: “aria cattiva” = bad air; “mal aria” = bad air. • French: “paludisme” = rooted in swamp. Cure Before Etiology: Mid 17th Century - Three Theories • PC Garnham relates that following: An earthquake caused destruction in Loxa in which many cinchona trees collapsed and fell into small lake or pond and water became very bitter as to be almost undrinkable. Yet an Indian so thirsty with a violent fever quenched his thirst with this cinchona bark contaminated water and was better in a day or two.
  • Download the Abstract Book

    Download the Abstract Book

    1 Exploring the male-induced female reproduction of Schistosoma mansoni in a novel medium Jipeng Wang1, Rui Chen1, James Collins1 1) UT Southwestern Medical Center. Schistosomiasis is a neglected tropical disease caused by schistosome parasites that infect over 200 million people. The prodigious egg output of these parasites is the sole driver of pathology due to infection. Female schistosomes rely on continuous pairing with male worms to fuel the maturation of their reproductive organs, yet our understanding of their sexual reproduction is limited because egg production is not sustained for more than a few days in vitro. Here, we explore the process of male-stimulated female maturation in our newly developed ABC169 medium and demonstrate that physical contact with a male worm, and not insemination, is sufficient to induce female development and the production of viable parthenogenetic haploid embryos. By performing an RNAi screen for genes whose expression was enriched in the female reproductive organs, we identify a single nuclear hormone receptor that is required for differentiation and maturation of germ line stem cells in female gonad. Furthermore, we screen genes in non-reproductive tissues that maybe involved in mediating cell signaling during the male-female interplay and identify a transcription factor gli1 whose knockdown prevents male worms from inducing the female sexual maturation while having no effect on male:female pairing. Using RNA-seq, we characterize the gene expression changes of male worms after gli1 knockdown as well as the female transcriptomic changes after pairing with gli1-knockdown males. We are currently exploring the downstream genes of this transcription factor that may mediate the male stimulus associated with pairing.
  • Package 'Malariaatlas'

    Package 'Malariaatlas'

    Package ‘malariaAtlas’ June 1, 2020 Title An R Interface to Open-Access Malaria Data, Hosted by the 'Malaria Atlas Project' Version 1.0.1 Description A suite of tools to allow you to download all publicly available parasite rate survey points, mosquito occurrence points and raster surfaces from the 'Malaria Atlas Project' <https://malariaatlas.org/> servers as well as utility functions for plot- ting the downloaded data. License MIT + file LICENSE Encoding UTF-8 LazyData true Imports curl, rgdal, raster, sp, xml2, grid, gridExtra, httr, dplyr, stringi, tidyr, methods, stats, utils, rlang Depends ggplot2 RoxygenNote 7.0.2 Suggests testthat, knitr, rmarkdown, palettetown, magrittr, tibble, rdhs URL https://github.com/malaria-atlas-project/malariaAtlas BugReports https://github.com/malaria-atlas-project/malariaAtlas/issues VignetteBuilder knitr NeedsCompilation no Author Daniel Pfeffer [aut] (<https://orcid.org/0000-0002-2204-3488>), Tim Lucas [aut, cre] (<https://orcid.org/0000-0003-4694-8107>), Daniel May [aut] (<https://orcid.org/0000-0003-0005-2452>), Suzanne Keddie [aut] (<https://orcid.org/0000-0003-1254-7794>), Jen Rozier [aut] (<https://orcid.org/0000-0002-2610-7557>), Oliver Watson [aut] (<https://orcid.org/0000-0003-2374-0741>), Harry Gibson [aut] (<https://orcid.org/0000-0001-6779-3250>), Nick Golding [ctb], David Smith [ctb] Maintainer Tim Lucas <[email protected]> 1 2 as.MAPraster Repository CRAN Date/Publication 2020-06-01 20:30:11 UTC R topics documented: as.MAPraster . .2 as.MAPshp . .3 as.pr.points . .4 as.vectorpoints . .5 autoplot.MAPraster . .6 autoplot.MAPshp . .7 autoplot.pr.points . .8 autoplot.vector.points . 10 autoplot_MAPraster . 11 convertPrevalence . 13 extractRaster .
  • A Comparative Genomic Study of Attenuated and Virulent Strains of Babesia Bigemina

    A Comparative Genomic Study of Attenuated and Virulent Strains of Babesia Bigemina

    pathogens Communication A Comparative Genomic Study of Attenuated and Virulent Strains of Babesia bigemina Bernardo Sachman-Ruiz 1 , Luis Lozano 2, José J. Lira 1, Grecia Martínez 1 , Carmen Rojas 1 , J. Antonio Álvarez 1 and Julio V. Figueroa 1,* 1 CENID-Salud Animal e Inocuidad, Instituto Nacional de Investigaciones Forestales Agrícolas y Pecuarias, Jiutepec, Morelos 62550, Mexico; [email protected] (B.S.-R.); [email protected] (J.J.L.); [email protected] (G.M.); [email protected] (C.R.); [email protected] (J.A.Á.) 2 Centro de Ciencias Genómicas, Universidad Nacional Autónoma de México, AP565-A Cuernavaca, Morelos 62210, Mexico; [email protected] * Correspondence: fi[email protected]; Tel.: +52-777-320-5544 Abstract: Cattle babesiosis is a socio-economically important tick-borne disease caused by Apicom- plexa protozoa of the genus Babesia that are obligate intraerythrocytic parasites. The pathogenicity of Babesia parasites for cattle is determined by the interaction with the host immune system and the presence of the parasite’s virulence genes. A Babesia bigemina strain that has been maintained under a microaerophilic stationary phase in in vitro culture conditions for several years in the laboratory lost virulence for the bovine host and the capacity for being transmitted by the tick vector. In this study, we compared the virulome of the in vitro culture attenuated Babesia bigemina strain (S) and the virulent tick transmitted parental Mexican B. bigemina strain (M). Preliminary results obtained by using the Basic Local Alignment Search Tool (BLAST) showed that out of 27 virulence genes described Citation: Sachman-Ruiz, B.; Lozano, and analyzed in the B.
  • A New Malaria Vector in Africa: Predicting the Expansion Range of Anopheles Stephensi and Identifying the Urban Populations at Risk

    A New Malaria Vector in Africa: Predicting the Expansion Range of Anopheles Stephensi and Identifying the Urban Populations at Risk

    A new malaria vector in Africa: Predicting the expansion range of Anopheles stephensi and identifying the urban populations at risk M. E. Sinkaa,1, S. Pirononb, N. C. Masseyc, J. Longbottomd, J. Hemingwayd,1, C. L. Moyesc,2, and K. J. Willisa,b,2 aDepartment of Zoology, University of Oxford, Oxford, United Kingdom, OX1 3SZ; bBiodiversity Informatics and Spatial Analysis Department, Royal Botanic Gardens Kew, Richmond, Surrey, United Kingdom, TW9 3DS; cBig Data Institute, Li Ka Shing Centre for Health Information and Discovery, University of Oxford, Oxford, United Kingdom, OX3 7LF; and dDepartment of Vector Biology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom, L3 5QA Edited by Nils Chr. Stenseth, University of Oslo, Norway, and approved July 27, 2020 (received for review March 26, 2020) In 2012, an unusual outbreak of urban malaria was reported from vector species in the published literature and found an equal Djibouti City in the Horn of Africa and increasingly severe out- number of studies (5:5) reported An. arabiensis in polluted, turbid breaks have been reported annually ever since. Subsequent inves- water as were found in clear, clean habitats, with a similar result tigations discovered the presence of an Asian mosquito species; for An. gambiae (4:4). Nonetheless, urban Plasmodium falciparum Anopheles stephensi, a species known to thrive in urban environ- transmission rates are repeatedly reported as significantly lower ments. Since that first report, An. stephensi has been identified in than those in peri-urban or rural areas (7, 10). Hay et al. (10) Ethiopia and Sudan, and this worrying development has prompted conducted a meta-analysis in cities from 22 African countries and the World Health Organization (WHO) to publish a vector alert reported a mean urban annual P.