Plasmodium PDF

Plasmodium Dr : Ebrahim Magdy Plasmodium  Malaria is a mosquito-borne disease caused by 4 species of obligate intracellular protozoan parasites of the genus Plasmodium People with malaria often experience fever, chills, and flu-like illness Plasmodium vivax...

Plasmodium Dr : Ebrahim Magdy Plasmodium  Malaria is a mosquito-borne disease caused by 4 species of obligate intracellular protozoan parasites of the genus Plasmodium People with malaria often experience fever, chills, and flu-like illness Plasmodium vivax Benign tertian malaria Plasmodium falciparum Malignant tertian malaria Plasmodium malariae Benign quartan malaria Plasmodium ovale Benign tertian malaria. Malaria is a life-threatening infectious disease, with approximately 200 million cases and 400,000 deaths annually worldwide Definitive host (vector): female mosquito Intermediate host: human M ode of transmission: 1. Bite of female mosquitoes (Anopheles) 2. Blood transfusion causes erythrocytic schizogony only 3. Congenital transmission (from mother to baby across the Placenta) 4. The use of common syringes Asexual reproduction by schizogony in liver and RBCs of human rounded body having a vacuole in the center with the cytoplasm pushed to the periphery and the nucleus at one pole (ring stage) it enlarges in size becoming irregular in shape and shows ameboid motility. This is called the ameboid form or late trophozoite A mature schizont contains 8-32 merozoites and hemozoin pigment The mature gametocytes are round in shape, except in P. falciparum, in which they are crescent-shaped.  Hepatic stage Erythrocytic stage  Pathogenesis Multiplication of parasite within RBCs results in: 1.Hemolytic anemia 2.Release of toxins that cause malarial attack 3.Liberation of pigment, engulfed by R.E.C resulting in enlarged liver and spleen, dark pigmentation of viscera 4. P. falciparum , infected RBCs develop knob like protrusions on their surface. These knobs responsible for adherence of infected RBCs to each other and to vascular endothelium , blocking capillaries lead to tissue anoxia, necrosis , hemorrhage Every attack passes into 3 stages: 1. Cold stage: shivering 2.Hot stage : high fever 3.Sweating stage: profuse sweating Latent stage: In P. vivax and P. ovale, two kinds of sporozoites are seen, some of which multiply inside hepatic cells to form schizonts and others persist and remain dormant (resting phase). Relapse: The resting forms are called hypnozoites. From time to time, some are activated to become schizonts and release merozoites, which go on infecting RBCs producing clinical relapse. Recrudescence: In P. falciparum and P. malariae, small numbers of erythrocytic parasites persist in the bloodstream and when patient immunity is lowered, they multiply to reach significant numbers resulting in clinical disease  Differences between recrudescence and relapse Recrudescence Relapse Seen in P. falciparum and P. malariae Seen in P. vivax and P. ovale Due to persistence of the parasite at a subclinical Due to reactivation of hypnozoites present in level in circulation liver cells Occurs within a few weeks or months of a Occurs usually 24 weeks to 5 years after the previous attack primary attack Can be prevented by adequate drug therapy or use Can be prevented by giving primaquine to of newer antimalarial drugs in case of drug eradicate hypnozoites resistance  Pathology Malaria is often classified as uncomplicated or complicated/severe. Uncomplicated malaria can be caused by all four species and is characterized by periodic fever and chills, mild anemia and splenomegaly. Uncomplicated malaria is rarely fatal unless it is left untreated and it progresses to severe disease Severe or complicated malaria is almost exclusively caused by P. falciparum infections  Complications of malaria P. Falciparum causes serious complications due to: 1.Number of infected RBCs reaches very high level 2 Blockage of capillaries of internal organs. Cerebral malaria : convulsions, paralysis  Algid malaria : shock, hypothermia  Dysenteric malaria: loose stool with blood  Gastric malaria: vomiting 3.  Black water fever: massive hemolysis of RBCs Congenital malaria may result in abortion, stillbirth, low birth weight infants Death may occur due to  Liver damage Pulmonary oedema Renal failure  Cerebral oedema Hemolytic anemia Hypotension and shock  Disease Erythrocytic cycle duration Or Periodicity ( hours ) P. Vivax Benign tertian malaria 48 P. ovale Benign tertian malaria 48 P. falciparum Malignant malaria 48 P. malariae Quartan malaria 72 Fever , chills, sweats, rigors, headache, nausea and vomiting, body aches and general malaise Fever( which may be periodic), chills, sweating, hemolytic anemia an splenomegaly Every attack passes into 3 stages: 1. Cold stage: sensation of cold, shivering 2.Hot stage : high fever 3.Sweating stage: profuse sweating  Table : Comparison of the characteristics of plasmodia causing human malaria P. vivax P. falciparum P. malariae P. ovale Hypnozoites Yes No No Yes Erythrocyte preference Reticulocytes Young erythrocytes, but can Old erythrocytes Reticulocytes infect all stages Stages found in peripheral blood Rings, trophozoites, Only rings and gametocytes As in vivax As in vivax schizonts, gametocytes Ring stage Large, 2.5 μm, usually Delicate, small, 1.5 μm, Similar to vivax, but thicker Similar to vivax, more single, prominent chromatin double chromatin, and compact multiple rings common, accole forms found Late trophozoite Large irregular, actively Compact, seldom seen in Band form characteristic Compact, coarse pigment amoeboid, prominent blood smear vacuole Schizont Large filling red cell Small, compact, seldom Medium size Medium size seen in blood smear Number of merozoites 12- 24 in irregular grape-like 8-24 grape-like cluster 6-12 in daisy-head or rosette 6-12 irregularly arranged cluster pattern Microgametocyte Spherical, compact, pale Sausage or banana-shaped As in vivax As in vivax (male gametocyte) pale blue or pink cytoplasm, blue cytoplasm, diffuse large diffuse nucleus nucleus Macrogametocyte Large, spherical, deep blue Crescentic, deep blue As in vivax As in vivax (female gametocyte) cytoplasm, compact nucleus cytoplasm, compact nucleus Infected erythrocyte Enlarged, pale, stippled Normal, stippled with Normal, occasionally Enlarged, oval fimbriated, with numerous fine pink Maurer's dots bigger and Ziemann's stippling prominent Schuffner's dots Schuffner's dots densely stained  Diagnosis Thin film Thick film Microscopic diagnosis Antigen Detection : HRP II antigen Molecular Diagnosis can detect less than 10 parasites/ μl of blood Antibodies detection: not differentiate between an active and past infection Hematology : anemia, thrombocytopenia Treatment Treatment Prevention and control 1. Treatment of patients 2. Mosquito control 3. Insect repellent, mosquito net, clothing covering body 3. Chemoprophylaxis Babesia Babesia is intraerythrocytic parasites They are called piroplasms because they have pear-shaped merozoites Babesia spp. Cause babesiosis or priroplasmosis (a malarial-like disease without the periodicity) Babesiosis is a worldwide tick-borne disease. Opportunistic parasite Species: Medically important Babesia species are:  B. microti (rodent strain)  B. divergens (cattle strain)  B. bovis ( cattle strain) Morphology 2x 1.5 um Babesia micoti Tetrad form Merozoites Intracellular , pear shaped , round or oval Found in pairs No pigments No gametocytes Babesia divergens 1.5 x 0.5 um  1 2 3 4 Infection through tick bite, blood transfusion, organ transplantation, or transplacentally. Habitat: The parasite is present in erythrocytes Definitive Host: hard ticks. Intermediate Host: Man or other mammals Reservoirs: Rodents and cattle  Symptoms  Incubation period 1-4 weeks  Self limited in immunocompetent  Disease is sever and fatal in immunosuppressed patients, signs include Fever , fatigue, anorexia, headache, cough, shaking chills, profuse sweating, nausea, dark urine, vomiting, abdominal pain, hemolytic anemia, Pain in muscles and joints, jaundice, hemoglobinuria  Babesia microti Diagnosis Microscopy : blood film PCR: babesial 18S rRNA Serology : Antibody Detection IgM, IgG Hematology : 1. Hemolytic anemia 2. Thrombocytopenia Biochemical : Babesia divergens 1. Liver function tests 2. Renal function Urine analysis : detect hemoglobinuria, excess urobilinogen and proteinuria.  Treatemnt I. Atovaquone 750 mg twice daily, along with azithromycin 500 mg- 1 g/day for a period of 7- 10 days is effective. II. Alternatively, clindamycin (300- 600 mg, 6 hourly) along with quinine (650 mg 6-8 hourly) may be given intravenously.  Prophylaxis 1. Hard tick control 2. Individuals who reside or travel in endemic areas, should wear protective clothing and apply tick repellents. 3. Individuals with history of symptomatic babesiosis or with positive antibody titer should be indefinitely deferred from donating blood Flagellates  Flagellates Blood flagellates Genital flagellates Enteric flagellates Trypanosoma Leishmania Trichomonas vaginalis Giardia Blood flagellates General characters:  Live in blood and tissue Move by one flagellum  Need vector for transmission  Require 2 hosts (vertebrate and invertebrate) Exist in 2 or more of 4 morphological stages. These forms were called leishmanial, leptomonad, crithidial and trypanosomal stages. Trypanosomes  Trypanosomes African Trypanosomes American trypanosomes Trypanosoma gambiense Trypanosoma rhodesiense Trypanosoma cruzi  African trypanosomes or Old World trypanosomes  African trypanosomes are extracellular protozoan parasites that cause lethal infections in humans  Vector born disease   Two subspecies of Trypanosoma brucei T. b. gambiense, causes chronic African trypanosomiasis (West African sleeping sickness) T. b. rhodesiense, causes acute African trypanosomiasis (East African sleeping sickness)   Transmission by Glossina (tse tse fly)  Multiplication by binary fission  Morphology Trypanosome is elongated spindle-shaped, 15-40 um in length, with central nucleus, a posterior kinetoplast, and long-undulating membrane Pleomorphic 1 long slender form,. short broad form without free flagellum 2 intermediate form with short free flagellum. 3. Pathogenesis and Symptoms Trypanosomal chancre (painful nodule) Haemolymphatic stage Fever  Lymphadenopathy, The posterior cervical nodes (winter bottom’s sign). Hepatosplenomegaly Thrombocytopenia and anemia Meningoencephalitic stage  Progressive daytime somnolence (sleeping  sickness), with restlessness and insomnia at night  mental (hallucinations, delirium)  motor (motor weakness, ataxia) Neurologic (abnormal reflexes, seizures, coma)  Diagnosis Microscopic examination wet film, stained and unstained smear from blood, lymph node aspirates, chancre fluid, and CSF to detect trypanosomes. Centrifugation methods of blood , examine buffy coat layer Antibody detection tests Antigen detection tests: detect circulating trypanosomal antigens in patients' blood Molecular diagnosis : trypanosome detection in both CSF and blood Imaging: CT scan of the brain shows cerebral edema  Treatment Early stage treatment (haemolymphatic stage) a. Suramin b. Pentamidine Late stage treatment (cerebral stage) a. Melarsoprol b. Tryparasmide c. eflornithine  Prevention  Treatment of patients  Control of vector  Chemoprophylaxis: injection of pentamidine every 6 months