PROTOZOA

*INTESTINAL PROTOZOAN
protozoan Portal of entry Mode of transmission Entamoeba histolytica Balantidium coli mouth mouth Contaminated water, food, vegetables with infective feces Hands of contaminated food handlers Direct transmission by cyst carrier Homosexuals Night soil cultivation Oral-anal intercourse (Giardia lamblia) Giardia lamblia mouth Trichomonas vaginalis genital Sexual intercourse Contaminated toilet articles. Seats Infection in babies through infected birth canal Cryptosporidium parvum mouth Contaminated water, food, vegetables with infective feces

characteristics

Trophozoite

Trophozoite

Trophozoite

Trophozoite

Oocyst

-wide clear refractile hyaline cytoplasm separated from the endoplasm -granular cytoplasm may include RBC -clearly defined nuclear membrane, lined with uniform -closely packed fine granules of chromatin as rods Cyst

-largest intestinal protozoan -shaped like sac -enclosed in a delicate protective pellicle -covered with spiral longitudinal rows of cilia -2 contracted vacuoles Cyst

-bilaterally symmetrical -pear-shaped/tear drop shaped flagellate -broad rounded anterior -tapering posterior extremity -dorsal surface is convex -an avoid, concave sucking disk at the flat ventral surface -2 large nuclei with large central karyosome -2 axonemes -4 pairs of flagella Cyst

-3-5 anterior flagella -undulating membrane -an axosystole and usually a cytostome -colourless pyriform flagella no cyst

spherical in shape 4-5 um in diameter 4 sporozoites 4-6 granules within oocyst stained by acid fast stain

-round/oval -smooth refractile non-staining wall -cytoplasm contains vacuole with glycogen -chromatin bodies contain ribonucleic acid -1-4 nuclei

-unstained greenish yellow spherical/oval cyst -macronucleus, contractile vacuoles and cilia -thick wall -multiply by binary fission and conjugation

-smooth well-defined wall -2-4 nuclei -4 median bodies -cytoplasm granular

Life cycle

disease

Clinical symptoms

diagnosis

Treatment and management

-ingestion of contaminated food/water containing infective cysts -on ingestion, only the mature cysts which are resistant to the acidic digestive juice of the stomach pass to the lower part of intestine -under the influence of the alkaline juice, the cyst wall disintegrates liberating 4-nucleated metacystic amoeba that ultimately divides into 8 small trophozoites (excystation) -the trophozoites inhabit the large intestine and live in the intestinal lumen -may invade the mucosal crypts where they feed on RBC and form flask-shape ulcers -ulceration of intestinal wall give rise to amoebic dysentery -invading amoeba find its way to capillaries to be transported via blood stream to liver and other organs -amoeba may re-enter the lumen of the gut and passed in liquid/semiformed stools as trophozoites/rounded cysts (encystations) Amoebiasis Amoebic dysentery Amoebic hepatitis Amoebic liver abscess Depends on location and severity -abdominal discomfort, irregular colicky abd pain -severe dysentery with stools containing mucus, mild diarrhea -malaise, weakness, fever, dehydration -constipation -chronic liver damage, abscess -pulmonary amoebiasis -brain abscess/tumor Stool examination Concentration method Trichrome staining Sigmoidoscope examination Culture of stool Serology assay-ELISA Metronidazole Screen food handlers Clean and proper hygiene Cover food, boil water Proper sewage disposal Public education Do not use feces as fertilizer

Life cycle similar to E.histolytica Found mostly in the lumen but also in the mucosa and submucosa on the large intestine especially in the cecal region Form superficial ulcers

Life cycle similar to E.histolytica -do not penetrate the mucosa but attached to the intestinal epithelium by its ventral sucker -causes shortening and blunting of the villi and deepened the crypts -causes cellular infiltration of lamina propria of mucus membrane -inhabits the duodenum, upper jejunum, bile ducts and gallbladder

Moves rapidly, rotating through debris by the lashing of the anterior flagella and by the action of the undulating membrane Found in the urine, vagina, urethra, epididymis, prostate

-Ingestion of oocyst containing 4 sporozoites via contaminated water/food -Excystation occurs in small intestine & releases 4 sporozoites. -Sporozoites invade intestinal epithelial cells where it multiplies by means of asexual intracellular multiplication -Differentiate into micro and macrogametocytes -Development of oocysts (infective stage) -Oocysts passed out in faeces (thick and thin walled oocyst) -Thin walled oocyst reinfects internally while thick walled oocysts are passed out in faeces

Balantidiasis

Giardiasis Malabsorption Epigastric pain Flatulence Steartorrhea Weight loss Foul-smelling and bulky stool Impaired absorption of carotene, folate and B12

Vaginitis Urethritis Low grade inflammation fever Creamy, frothy yellowish discharge Itching and burning

Cryptosporidiosis

Acute infection dysentery

-Chronic diarrhoea 4-8 stools/ day with loss of fluid & electrolytes -Malabsorption -Bloating, Nausea & anorexia -Flatulence/ epigastric pain

Stool examination looking for trophozoite/cysts

Duodenal aspiration Stool examination String test

Microscopic examination Culture of the organism

Duodenal/jejunal fluid (lavage/aspirates) for oocysts Stool exam- Modified Trichome Stain

*BLOOD PROTOZOA
protozoa Portal of entry MOT Plasmodium vivax Plasmodium malariae Skin Plasmodium falciparum Babesiosis Bite of hard ticks (zoonotic infection) tropics Not enlarged Double chromatin dots in 1 ring Delicate ring/ameboid form No schizont (trophozoite only) No pigment A cluster composed of 4 small merozoites is called tetrad Bite of infected Anopheles mosquito Transfusion of blood from infected people Contaminated needles/syringe Congenital (mother to newborn) Temperate zone Temperate zone enlarged Fine dot on chromatin ring Signet ring Not enlarged Compact ring

distribution Morphology Parasitized RBC Trphozoite

Schufners dots Vacuole at the center

Zymans dots Black pigments in cytoplasm Band form No of merozoites : 8

Very delicate ring Mutiple infections (>1ring) Maurers clefts No of merozoites : 24

Mature schizont

No of merozoites : 16

Gametocytes

Small, round/oval

Banana/crescent shape

Shape is rounded Chromatin at its periphery and center Solid, no vacuole Macro : compact chromatin mass Micro : diffuse nucleus stained pink

Micro : diffuse chromatin Macro : thickened chromatin

Life cycle

Incubation period disease Clinical symptoms

complications

diagnosis

In man/intermediate host Bite of infected female Anopeheles mosquito, release sporozoites (needle shape) Sporozoites enter blood circulation and enter liver cells (round form) Mature : liver schizont Merozoites circulate in peripheral blood circulation and enter RBC : ring form/trophozoites Become mature trophozoites : young schizont Mature schizonts infect RBC Schizonts rupture and releasing merozoites, then enter ciculation and become gamotecytes or infect other RBC In mosquitoes/definitive host Mosquito ingests contaminated blood Maturation of macrogametocytes by reduction division Exflagellation of microgametocytes Fertilization and form zygote Elongation and development of zygote, form ookinete Penetration of stomach wall by ookinete Development of oocyts and sprozoites Rupture of oocysts liberating sporozoites into body cavity Localization in many sporozoites in salivary glands The mosquito now gets infection 2 weeks weeks 2 weeks Benign. Tertian, 48 hours fever Quartian malariae Malignant tertian, pernicious, 48 hours fever Depends on the no. of parasites in the body Fever, chills, rigors Sweats Headache Jaundice Blood coagulation defects Shock Kidney/liver failure *Plasmodium falciparum = more severe, found in deep organs, short duration of multiplication, highest no. of merozoites produced, tendency for multiple parasites in a single RBC Cerebral malaria Renal failure : black water fever Quartan malarial nephropathy Tropical spenomegaly syndrome Malarial anaemia Congenital malaria Hypoglycaemia hyperparasitaemia Thick/thin blood smears Culture Serology - ELISA Iv quinine, chloroquine, primaquine, fansidar, tetracycline, qinghaosu Recrudescence chloroquine/amodiaquine/quinine Relapse - primaquine

Found in RBC and causes hemolysis Mutiply by binary fission/budding

1-2 weeks babesiosis Fever, chills Sweats Myalgia Arthralgia Mental depresseion Nausea, vomiting Jaundice Haemoglobinaemia, haemoglobinuria, anemia Due to hemolysis of RBC and an allergic reaction to merozoites released from parasitized RBC

Treatment and prevention

Bone marrow Peripheral blood film Liver/spleen aspiration Inoculation of patients blood Quinine + clindamycin Atovaquone + azithromycin

TISSUE PROTOZOAN I
species disease vector MOT Leishmania donovani Leishmaniasis Phlebotomy sandfly : old world Lutzomyla sandfly : old world Bite of infected sandfly Blood transfusion from infected people Congenital infection Amastigote Trypanosoma cruzi America Trypanosomiasis Kissing bug (reduviid bugs) Bite of infected bugs (killing bugs) Blood transfusion from infected people Congenital infections Laboratory accidents Trypanosoma brucei gambiense Trypanosoma brucei rhodiense African Trypanosomiasis Tsetse fly (Glossina sp.) Bite of infected tsetse fly Blood transfusion from infected people Congenital infection Laboratory accidents

morphology

round or oval bodies, kinetoplast adjacent to it Promastigote

Life cycle

spindle shape with posterior end gradually tapering to a point, flagellum, nucleus centrally placed, kinetoplast lies close to anterior end, flagellum emerges from anterior end In human Bite of infected sandfly and releases promastigotes into blood circulation Parasites pseudopodia gradually surround the parasites and engulf it Within macrophage, parasites loose their flagella, becoming amastigotes lying inside a parastiphorous vacuole Amastigotes multiply by binary fission Macrophages rupture and release amastigotes Amastigotes then ingested by other macrophages In sandfly The sandfly feeds on human blood causes amastigotes transferred to them Inside its gut, amastigotes develop into promastigotes to become its infective metacyclic promastigote Promastigotes multiply by binary fission becoming elongated parasites with a single spindle shaped

Infectious/metacyclic forms are passed in the feces of the infected vector, deposited at the site of the bite wound Parasites move into the blood stream via the bite or through contaminated of mucus membrane They penetrate into mesenchymal cells origin, mainly the cardiac muscles Inside the muscle, they change to the amastigotes, epimastiogotes and trypomastigotes form Replication occurs only as amastigote Trypomastigotes emerge from the muscle cells and enter the blood circulation They may re-invade the muscle cells or circulate without division Trypomastigotes picked up by vector, and change to epimastigote before becoming metacyclic (monomorphic form)

Inside Glossina sp. Trypanosomes are initially confined to an area surrounded by peritrophic membrane and rapidly change to elongated forms Move into the space between the peritrophic membrane and gut wall They enter the main food channel by penetrating the peritrophic membrane Turn back to hypopharynx to enter the salivary gland and become epimastigote form In salivary gland, they develop into metacyclic form Inside human Divide by binary fission Pleomorphic with slender, intermediate and stumpy form (polymorphic form)

disease Clinical symptoms

Black fever/dumdum fever Kala azar Acute Prolonged, irregular fever with chill, rigors hepatosplenomegaly Lymphadenopathy Pancytopenia Progressive anaemia Hypergammaglobulinaemia Hypoalbuminaemia Chronic Cachetic Febrile with heavily parasitized Post kala azar dermal leishamaniasis Histiocytes in the skin as macules, papules and nodules Advanced lepromatous leprosy

Chagas disease Acute Erythema and swelling lesion Romanas sign : unilateral painless oedema (palpebrae, periocular tissue) Fever, malaise, oedema of the face Lymphadenopathy, hepatomegaly Intermediate Postive IgG/present of parasite Absence of signs and symptoms Absence of ECG abnormalities Regular size of heart, eosophagus and colon Chronic Cardiomyopathy Heart failure, arrythmias, thromboembolism Increase in ECG alteration Digestive form Megaoesophagus (dysphagia, regurgitation of food) Megacolon : constipation, intestinal obstruction and rupture Direct examination of blood Polymerase chain reaction Xenodiagnosis Hemoculture Nifurtimox/benznidazole Allopurinol/fluconazole blood screening Treatment of homes with residual insecticides Healthy education

Sleeping sickness Stage 1/hemolymphatic stage Fever Lymphadenopathy Discrete, rubbery and non-tender nodule Winterbottoms sign Cervival lymphadenopathy Stage 2/encephalitic stage Neuropsychiatric Motor and sensory abnormalities Severe post-treatment reactive encephalopathy

diagnosis

Demonstration by microscopy (amastigote) Isolation (culture) : promastigote Species identification Serodiagnosis DNA detection Parenteral agents Sodium stibogluconate (Sbv) Pentamidine isethionate Paramomycin Oral agents Miltefosine Azoles Sitamaquine Combination Sbv + paramomycin Miltefosine + paramomycin Vector control (bed beds/curtains) Health education

Treatment and prevention

Staining and microscopic Serodiagnosis Lymph node/bone marrow aspiration Lumbar puncture (CSF findings) Animal inoculation Serum proteomic signature Suramin Pentamidine Eflornithine Arsenic melarsoprol Insecticides Treatment for infected people Health education