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Home , Dientamoeba fragilis, Kinetoplastida

تابع 2

أ.د / فاطمة إبراهيم سنبل أستاذ الميكروبيولوجيا الصيدلية • (Plate 2) • Life cycle of Balantidium coli

Mastigophora • General characters : • This subphylum includes those that move actively by means of a (or several flagella) during all or part of their life. In addition, the body has a definite form (not irregular as in amoebae) maintained by a firm pellicle on its outer surface. Some are devoid of a mouth opening but some have an opening or through which food is ingested. They reproduced by longitudinal binary fission (not transverse fission as in case of B. coli). • Some have undulating membrane which appear to consist of highly modified flagellum. Flagellates have vesicular type of nucleus . • The parasitic flagellated protozoa fall into two categories with respect to the type of disease produced in humans : • a) Intestinal and genital flagellates : these are found only in the intestinal or genital tracts and their transmission does not require a biological vector and so pass directly from man to man usually enclosed in a cyst. They include : • - intestinalis (lamblia) • - Enteromonas hominis • - hominis • - Trichomonas tenax • - • - (-like ) • The parasites are nearly all harmless commensals but two species, Giardia intestinalis and Trichomonas vaginalis are associated with inflammatory lesions in heavy infections and for practical purposes may be regarded as pathogenic . • b) Blood and tissue flagellates (haemoflagellates) : these infect the vascular system and various tissues and their transmission requires a biological vector. usually an arthropod (insect) in which they undergo a fresh cycle of alteration and multiplication before they can again infect man. This class contains : • -Genus . • -Genus . • (A) Intestinal and genital flagellates • Giardia intestinalis • Geographical distribution: Universal • Morphology : The trophozoite is bilaterally symmetrical, pear shaped with a broad rounded anterior end and a tapering posterior end. The usual length is 12-15u. The dorsal surface is convex, the sucking disc appears as an ovoid concavity with raised margins and used for attachment. There are two nuclei (containing central karyosome but no chromatin), two axostyles, four pairs of flagella and two median (parabasal) bodis . There is no mouth .

• The cyst is ovoid with highly refractile wall. It measures about 12μ in length. Two or four nuclei may be detected (according to the stage of maturity), 4 median bodies and also parts of flagella . • Life cycle : (Plate 3) • Man is infected by swallowing the cyst which pass safely through the stomach and hatches in the upper part of the small intestine liberating 2-4 trophozoites. The organism starts dividing into two by longitudinal division, and attach to the mucosa by their suckers. They become encysted in the lower part of the small intestine. Cysts are passed in the faeces and the cycle is repeated . • Plate (3) • Giardia intestinalis life cycle • Pathogenicity : • is transmitted through food and water containing cysts after contamination by sewage, flies or by food handlers. The parasite is weakly pathogenic but its attachment to the intestinal mucosa may cause • -Irritation and inflammation with consequent Epigastric pain and acute or chronic diarrhea and digestive disturbances. • -Steatorrhoea (fatty diarrhea- Stool is light-coloured and greasy due to malabsorption of vitamin A and fats, and • - Flatulence • - Occasionally, the parasites are found in the bile ducts and even in the • gall bladder leading to cholangitis and cholecystitis . • Predisposing Factors: that determine disease severity • 1- Hypogammaglobulinaemia. • 2- Achlorhydria. • Laboratory diagnosis : • Microscopical examination of faeces to find the characteristic cysts or more rarely the trophozoites Duodenal biopsy may be necessary for diagnosis by demonstrating trophozoites . • N.B. : In giardiasis the stools are usually greasy or fatty (steatorrhoea) due to malabsorption of fats and there is no blood or mucus . • Treatment : • -Metronidazole OR Tinidazole • -Recently Albendazole. • -Correction of the resulting nutritional deficiency from • malabsorption . • Giardiasis is often a family infection, (because it doesn't need intermediate host) so other members should be screened and treated as necessary . • Prevention & control : • Transmission depends on the swallowing of mature cysts (in feaces). Prevention therefore depends on a high level of sanitation • Trichomonas vaginalis • Geographical distribution : Cosmopolitan. • Habitat : • The genital tract of man, both in the male and in the female but particularly the latter . • Morphology : • It is the largest trichomonad found in human being. The parasite is fusiform or oval, 20 u x l0u and has 4 flagella. However, the number of flagella vary from 3-5. The nucleus is elongated. An originates near the nucleus and extends to the posterior end. An undulating membrane is also present which does not extend beyond two thirds of the body length. There is a well developed parabasal body lying close to the nucleus. Cysts are not known .

• Transmission : (Plate 4 ) • T. vaginalis lives in the vagina and urethra of women and in the prostate, seminal vesicles and urethra of men. It is transmitted primarily by sexual intercourse. • Its presence occasionally in young children including virginal females suggests that the infection can be contracted from soiled washcloths, towels & clothing. • Pathogenicity : • The acidity of the normal vagina (pH4-5) ordinarily discourages infection, but once established, the organism itself cause a shift toward alkalinity (pH 5-6) which further encourages its growth. A few days after infection, there is a degeneration of the vaginal epithelium followed by an intense inflammation which lead to itching and a copious white discharge (characteristic) containing trophozoites. Infection of men is usually asymptomatic but there may be an irritating urethritis or prostitis . • Laboratory diagnosis : • Microscopical : depends on recognizing the trichomonad in secretions which may be vaginal, prostatic or urethral or sedimented urine . • The vaginal secretions are likely to be more alkaline than normal, we may use a strip of pH paper. The pH is likely to exceed 5.0. • Treatment : • - Systemic treatment using oral drugs such as Metronidazol cure infection in about 5 days. Treatment of both partners simultaneously is necessary to avoid reinfection . • - Local treatment by (a) promoting an acid pH of the vagina using lactic acid douche or douche containing 4 tablespoons of vinegar (b) Flagyl vaginal insert (c) Clotrimazole (canestine) vaginal cream or tablets . • Plate ( 4) • Trichomonas vaginalis • Prevention & control : • - Personal hygiene. • - Disinfection of W C. seats. • - Boiling of underwear . • - Treating cases and both partners simultaneously . • -Condom use • (B) The blood and tissue flagellates • (Haemoflagellates) • These parasites include two genera : Leishmania and Trypanosoma which belong to an order of protozoa called as they are characterized by the presence of a structure unique to the order, the , which contain the mitochondrial DNA . • General characters of order kinetoplastida : • 1- The flagellum of these flagellates arises from the kinetosome. The kinetoplast and kinetosome are always closely associated, sometimes so close that they appear as a single body under the light microscope. However, most electron micrographs show no physical connection between kinetosome and kinetoplast . • 2- These species are heteroxenous. Part of their life cycle is spent in the gut of a fly where they assume the form of a promastigote and the remainder of their life cycle is completed in vertebrate tissues (amastigate). • 3- The species of kinetoplastida usually pass through different morphological stages, depending on the phase of their life cycle and the host they are parasitizing. These stages include

• Genus Trypanosoma • Members of this genus have been found parasitizing all types of vertebrates, both worm and cold - blooded and have a world-wide distribution (Cosmopolitan). • General characters • 1- A trypanosome (Tripomastigote form) is elongated, flattened organism having a single nucleus of the vesicular type and containing a large central karyosome near the kinetosome there is a round or rod-shaped organelle known as kinetoplast. There are a single flagellum and undulating membrane both serve to propel the trypanosome in the same way as a fin propel a fish.

• 2- Multiplication of trypanosomes is asexually by longitudinal binary fission . • 3- All trypanosomes are divided into two broad categories or "Sections:" based on characteristics of their development in their invertebrate host. When a species develops in the front portions of the digestive tract it is said to undergo anterior station development and is placed under section salivaria. In this case transmission is inoculative through insect saliva. On the other hand when a species develops in the hind gut of its invertebrate host (insect), it is said to undergo posterior station development and is placed under section . Stercoraria In this case transmission of infection is contaminative through the insect faeces. • 4- Some trypanosomes e.g. those occurring in animals in temperate countries cause only unapparent infection and appear to cause little disturbances to their hosts. On the other hand some or many trypanosomes are highly pathogenic e.g. Trypanosoma gambiense and T. rodesiense which cause a widespread endemic disease called "Sleeping sickness" or African and T. cruzi which is the cause of American trypanosomiasis or "Chaga's disease ." • (Sleeping sickness) • A hemoflagylate found only in Africa, a zoonosis with a resevoir, in the East African form of disease, where it is transmitted from resevoir animal (cattle) to man by the vector tsetse fly (e.g. Glossina palpalis). In west African form it is transmitted by tsetse from human to human . • 2 species: Trypanosoma gambiense (west Africa) Trypanosoma rhodesiense (east Africa) • Morphology : • Both T. gambiense and T. rhodesiense have the characters of trypanosomal form. However the kinetoplast is short and rod shaped and the undulating membrane is wide. In the blood of the infected person these species present in three different forms (polymorphic) : – long slender form which is the most common and is actively motile using the long free flagellum, – intermediate form with smaller size and short free flagellum. – short stumpy form which is the smallest in size and more stouter and have no free flagellum . • Plate ( 5) • Life cycle of Trypanosoma gambiense & T. rhodesianse • Life cycle: (Plate 5) : • The trypanosomal form is found in the blood of man. It does not invade tissue cells but multiplies in the connective tissue spaces of various organs (e.g. spleen, lymph nodes and brain). When the trypamosomes are ingested by Tsetse flies they multiply within the intestine of the fly. Then, they migrate to salivary glands where they transform to epimastigote forms which multiply and become infective metacyclic form within few days. These may be injected back into man by the fly at the next blood meal . • Pathogenesis • Tsetse bites man and injects saliva containing trypanosomes into the wound. These multiply locally producing a local lesion and then invade • intravascular space where the trypanosome multiplies by binary fision extracellularly producing fever and lymphadenopathy and then eventually reaches the central nervous system producing a meningoencephalitis. • Symptoms can be minor in the beginning but usually become apparent within the first months of the infection. African trypanosomiasis has three symptomatic stages, the last one being the most dangerous eventually leading to death, if left untreated. • 1. In 1–3 weeks after the bite a chancre (a red sore skin lesion) can develop on the bite area. • 2. Several weeks or months later Trypanosoma parasites in the blood, spinal and lymphatic fluid (hemolymphatic stage) can cause: • anemia • cardiac dysfunction • pruritus (itching) • fatigue • irregular fever • headache • muscle and joint pain • renal failure • skin rash • splenomegaly (enlargement of the spleen) • swelling of the lymph nodes (most prominently in the back of the neck and in the groin), hands and face • thrombocytopenia (low level of platelets, thrombocytes) • weight loss. • 3. The disease reaches its final stage when the parasites get through the blood-brain barrier entering the brain. The central nervous system involvement can occur as early as within a month in some cases. This meningoencephalitic stage (inflammation of the central nervous system) causes (in addition to the above second stage symptoms) some of the following symptoms: • severe headache • mental dullness • confusion and abnormal behaviour • insomnia (sleeping troubles) • personality changes • restlessness and sleeping which develop even during eating or standing • coma • death (within months or years) • Also trypanosomiasis causes a degree of immune suppression to bacterial infection which often" complicate the late stage of the disease and may lead to death. • Laboratory diagnosis : • Microscopical examination of fresh or stained film of blood, CSF or the juice obtained by puncture of enlarged lymph gland for detection of the trypanosomal forms of the parasites . • Serological tests: Detection of trypanosome-specific antibodies can be used for diagnosis, but the sensitivity and specificity of these methods are too variable to be used alone for clinical diagnosis. • high levels of protein (IgG and IgM) in CSF lymphocytosis in CSF • antigen capture or PCR. • Treatment : • Acute disease – Suramin – Pentamidine • Chronic (CNS) disease – Melarsoprol (arsenic) • Major problems - how to control Tsetse fly (killing off all wild animal reservoirs?) - vaccine production very difficult because of antigenic variation of trypanosome • Prevention & control : • - Mass treatment of cases . • - Control of Tse tse fly . • American Trypanosomiasis • (Chaga' s disease) • This is caused by . • Geographical distribution : South and Central America and Southern North America . • Morphology : • In tissue sections typical leishmanial forms are seen while the trypanosomal forms are seen in blood. The kinetoplast is egg-shaped and very large and the nucleus is central. In stained films the parasite appear as question mark-shape . • Transmission: • - by reduvid bug bite - vertical (in utero) - blood transfusion • Life cycle : (plat 6) • Metacyclic trypanosomal forms derived from the winged bug (Triatoma) penetrate the tissue cells (of the heart or CNS), lose their flagellum, round up into the amastigote form and then divide repeatedly. The infected cells burst liberating amastigote (leishmanial) forms which invade new. cells or transform to trypanosomal forms that circulate in blood . • The bug acquires the infection by biting an infected person. The trypanosomal form in its gut change into crithidial forms and multiply. The epimastigote (crithidial) forms migrate to the hind gut of the insect and transform to trypanosomes. These are infective and are passed out of the hind gut of the insect with the faeces. They contaminate the wound made by the biting, and so produce infection in man . • Plate (6) • Life cycle of Trypanosoma cruzi • Pathogenicity : • There will be a local multiplication at the site of bit producing an erythematic swelling known as Chagoma. The lesion occurs usually on the face but may occur else-where on the body. The organisms spread rapidly • to regional lymph nodes which become enlarged, hard, and tender. Similar lesions of hard edema may develop in various parts of the body. Later the parasites make their way to the blood stream causing generalized infection. The systemic infection may take an acute or chronic form or may pass from acute to chronic states. • Clinical Picture • In acute stage local inflammation at site of innoculation (chagoma) The patient may suffer from anemia, loss of strength, nervous disorders, muscle and bone pain and varying degrees of heart failure and death may occur 3-4 weeks after infection. • The symptom of the chronic stage (up to several decades after acute stage ) depends on the organ affected. So cardiomegally, myocarditis heart failure , megaoesophages & megacolon when heart & G.1. T. are affected respectively . • Laboratory diagnosis : • - blood smear for trypanosomes (Giemsa stain) - serology, PCR - biopsy - xenodiagnosis • Treatment: - Nifurtimox (Lampit) a nitrofurone, is most effective early in the course of infection, but it is poorly effective in the chronic phase . • Control: - Concrete walls and floors prevent reduvid bug infestations - antiparasitic agents added to transfused blood products • Genus Leishmania • Like the trypanosomes, the leishmanias are heteroxenous . • Part of their life cycle is spent in the gut of a fly, where they assume the form of a promastigote; the remainder of their life cycle is completed in vertebrate tissues where only the amastigote form is found. Tradionally the amastigote is also know as a Leishman-Donovan body (L-D body). The commonly infected vertebrate host are humans, dogs, and several species of rodents. Sand flies of the genus Phlebotomas is the invertebrate host and thereby the primary vector of . • Human leishmaniasis may take three forms : • 1- (Kala-azar): caused by . It is a form of generalized and often fatal infection . • 2- (Tropical sore). : caused by L. tropica. The infection is confined to the skin producing ulceration . • 3- Mucocutaneous leishmaniasis (Espundia). • It is a local lesion which affects chiefly the mucous membrane of the nasal and buccal cavities and caused by . • Visceral Leishmaniasis • (Kala-azar) • Geographical distribution : India, Central Asia, China, Trophical Africa and South America . • Morphology : • The stage present in human tissue is the amastigote form which is 2-5 urn spheroid to avoid bodies. In stained preparations only, the nucleus and a very large kinetoplast can be seen . • Life cycle: (plat 7). • Plate (7) • The parasite' is found in man as amastigote (leishmanial) form and it multiplies by binary fission within the mononuclear and polymorph nuclear macrophages of blood cells and the endothelial cells of the reticuloendothelial system. The cells rupture releasing the parasites which invade new cells. When these amastigote forms are ingested by a female sand fly they transform into the promastigote form in the insect intestine. These promastigotes multiply and eventually travel to the buccal cavity of the fly, where they may be injected into man. Then, they loose their flagella and assume amastigote forms. • Pathogenicity : • Visceral leishmaniasis is generally a disease of the reticuloendothelial system (RES). Once inoculated, the parasite is immediately engulfed by a macrophage in which it divides rapidly by binary fission killing the host cell Escaping from the dead macrophage, the protozoa are engulfed by another macrophage which they also kill and by this means severe damage of the RES occur, one of the host defense mechanisms against disease. So the patient manifest fever, splenomegally, hepatomegally, loss of weight, anemia and death may occur due to invasion of a secondary pathogen that the body is unable to combat . • Laboratory diagnosis : • 1- The only confirmatory diagnosis depends on finding the amastigote forms in blood, secretions or tissues from spleen, liver, lymph nodes and bone marrow. This is performed by microscopical examination using Leishman's stain . • 2- Immunodiagnosis is sensitive but cannot differentiate -between current and cure cases . • Treatment : • Antimonial compounds are the traditional treatments for leishmaniasis Resistance to the antimonials is prevalent in some parts of the world, and the most common alternative is amphotericin B or Paromomycin , good nursing care and adequate diet with high protein and vitamins to combat nutritional deficiency . • Cutaneous Leishmaniasis • (Tropical sore) • Geographical distribution The Far East, Middle East, Mediterranean basin and Central and South America . • Morphology : As L. donovani. • Life cycle : • As in Kala-azar but multiplication and infection is limited to a small area of skin . • Pathogenicity : • The leptomonad parasite injected into man are transformed into leishmanial forms and taken by the phagocytic cells lying just beneath the skin. The parasites remain in the skin. Single or multiple sores develop on the exposed parts of the body. At first a papule appears, continues to enlarge, and acquires a glazed purplish appearance. It becomes covered with brownish scales and by the 3rd- 4th month forms ulcer which discharges a thin offensive pus. Secondary bacterial infection may follow and regional lymph nodes may be infected. • Uncomplicated sores heal within 2-10 months but leave depigmented retracted scars which are often disfiguring . • Diagnosis : Detection of the Leishmania parasites in cells of skin • • 1- If the skin is unbroken, a smear is made from the lesion after scarification . • 2- If the skin is ulcerated the smear is made from the deeper parts at the growing edge of the ulcer and stained with Leishman's or Giemsa stain . • 3- Intradermal test: using culture of Leishmania as antigen . • Treatment : • The scabs must be removed and the sores cleaned and treated with antibiotics if secondary infection is present. Multiple or chronic sores are best treated by injections of antimony compounds . • Mucocutaneous Leishmaniasis • (Espundia) • Geographical distribution : South America and Sudan. • Morphology : As L. danovani . • Life cycle : • As in tropical sore but the parasites invade also the mucus membranes of nose and mouth . • Pathogenicity : • A lesion develops on the skin and it resembles that caused by L. tropica but has the tendency to invade mucous membranes of : the nose, mouth, and pharynx causing destruction of bone and cartilage of nose and mouth. Secondary infection may follow and the disease could be fatal . • Laboratory diagnosis : • The smears are made from nasal mucosa, stained and examined . • Treatment : • Injection of antimony compounds. Also removal of scabs from ulcers and cleansing to get red of bacterial infections . • Prevention and control of leishmaniasis. • 1- Treatment of cases . • 2- Control of sand flies and reservoir animals . • 3- Active immunization with living organism or material from an active ulcer which produce life long protection. • III) Phylum • Class sporozoea • General characters : • - All members are parasitic . • - Their life cycle include the production of spores. Have no organelles for locomotion as cilia or flagella . • - They show alternation of generation in which a single sexual generation is followed by a series of asexual generations. The sexual reproduction is known as gametogony which results in the formation of gametes that fuse to form zygote then divides by sporogony to produce the infective spores. The asexual reproduction is known as "Schizogony" and during such reproduction, the parasite reproduce by binary or multiple fission . • - They often show alternation of hosts with the sexual cycle in one host and the asexual cycle in another . • - The most common genus in this class is the genus which produce a disease in humans known as "Malaria " • Genus Plasmodium • Four species of this genus may give rise to malaria in man . • These are : • 1- Plasmodium vivax: which cause tertian malaria. • 2- P. malaria: which cause quartian malaria . • 3- P. ovale: which cause tertian malaria . • 4- P. falciparum : which cause malignant tertian malaria . • The word tertian and quartian indicate the frequency of the fever in days .The fever is associated with the release of merozoites and their metabolic products from the infected erythrocytes . • Geographical distribution : Tropics and subtropics and some parts of temperate regions . • Spread • - Bite of Anopheles female - blood transfusion - vertical - transmission mother/child at time of birth • Habitat : • 1- In the bodies of anopheline mosquitoes during the sexual cycle of the parasite . • 2- In the cells of liver and in the red blood cells of man during the asexual cycle . • Life cycle : (plate 8) • 1- The asexual cycle (Schizogony)" • The bite of an infected mosquito results in the injection of many spindle shaped cells (sporozoites) into the blood stream. These sporozoites rapidly disapear to enter the parenchyma cell of the liver. Here, the exo-erythrocytic cycle is initiated. The nucleus and cytoplasm of each sporozoite increase in size producing a Schizont. The nucleus of the schizoan divides into small fragments each surrounded by a small amount of the cytoplasm imerozoites). Then, the liver cells rupture releasing the merozoites. • Most of the merozoites are phago cytosed but some enters new liver cells to repeat the process while others invade red blood cells. P. falciparum undergoes only one exoerythrocytic cycle whereas the other species may continue this cycle and hence relapses could occur .

Exoerythrocytic cycle inhepatic cells • The cycle in the R.B. Cs. is termed (the erythrocytic cycle). When the merozoite enters the R.B. C. a vacuole is formed in the cytoplasm of the parasite pushing the nuclear chromatin to one side. This gives ring shaped trophozoite. The trophozoite starts to grow and its cytoplasm begins to develop pigments till it almost fills the erythrocyte. At this stage it is called a Schizont. The nucleus of the schizont undergoes the process of schizogony to produce merozoites . • The R.B.Cs burst releasing the merozoites in the blood stream to repeat the cycle in fresh red cells. This cycle is completed in 72 hrs. in P. malaria and in 48 hrs in case of other species . Genus Plasmodium life cycle Genus Plasmodium life cycle • It takes place in the body of female Anopheles mosquito . Some merozoites of the erythrocytic cycle will develop into two forms of gametocytes which may be distinguished : the male (microgametocyte) and the female (macrogametocyte). The blood containing the malaria parasite (merozoites, gametocytes, ....) passes to the stomach of the mosquito where all stages of the parasite are digested except the gametocytes. Each macrogametocyte matures to give a macrogamete ready for fertilization. At the same time, the nuclear chromatin of the microgametocyte develops into • 4-8 slender sperm like cells attached to the mother cell. These sperm-like c. us are called the microgametes and will be detached from parent cells to fertilize macrogametes. The fertilized gamete known as the zygote which develops into an elongated and motile ookinete. The ookinete penetrates the mosquito's stomach wall and produces a round oocyst just beneath the basement membrane. The nucleus of the oocyst divides repeatedly to give hundreds of spindle-shaped sporozoites. After 1-3 weeks, the oocyst bursts releasing the sporozoites into the body cavity. Some of the sporozoites reach the salivary glands to be injected into the blood of the next person to be bitten by the mosquito . • Pathogenicity : • The classic symptoms of malaria is directly related to the cyclic release of the parasite from the R.B.Cs. Thus, three stages are present which are : cold, hot and sweating stages . • a) Cold stage (10 minets-1 hour) : • The patient has a sensation of intense cold with teeth chattering although his temperature is above normal. These symptoms appear soon after rupture of R.B.Cs . • b) Hot stage (3-4 hours) : • Appeared where more than 90% of the merozoites are released from the R.B.Cs. The skin is hot and dry, the face flushed, the temperature elevated, headache and vomiting . • c) Sweating stage (1-3 hours) : • By this time the parasites entered the R.B. Cs. and are actively growing. The temperature drops rapidly and the patient rests until the next attack . • The parasites entered the R.B.Cs. and are actively growing. The cyclic occurrence of these symptoms continues until the infected individual develops immunity. As a result of infection, anemia results due to destruction of R.B.Cs . • Thrombosis is produced due to accumulation 01 the parasite within blood capillaries. Relapses may occur due to the persistence of the parasite in liver cells (except in case of P. falciparum). • Black water fever is another grave condition associated with falciparum malaria, but its clinical picture is distinct from the foregoing. It is an acute massive lysis of erythrocytes, marked by high levels of free hemoglobin and its breakdown products in the blood and urine and by renal insufficiency. Because of the presence of hemoglobin and its products in the urine, the fluid is quite dark, hence the name of the condition. A prostrative fever, jaundice, and persistent vomiting occur. Renal failure is usually the immediate cause of death . • Pathophysiology • - only RBC trophozoites and schizonts cause disease - no liver pathology caused by hepatic schizonts or sporozoites - disease caused by: 1. RBC destruction: - by parasite - immune hemolysis - splenic pooling 2. antigen-antibody complexes in kidney 3. schizonts of P. falciparum sticking to post- capillary venules' (esp. cerebral) endothelial cells 4. cytokines and other ill-defined shock, proinflammatory and capillary leakage producing products • Acute clinical picture: complications • Fever , headache, , anemia , splenomegaly • cerebral malaria (P.falciparum only) adult respiratory distress syndrome (ARDS)(P.falciparum) black water fever (severe hemolysis)(P.falciparum only) acute renal failure • Chronic clinical picture: - nephrotic syndrome (P. malariae only) - big spleen syndrome (hypertrophic malarial splenomegaly) • Laboratory diagnosis : • 1- Microscopical examination of blood films stained with Giemsa's stain (rings, trophozoites, schizonts and gametocytes). • 2- Serological tests as complement fixation and fluorescent antibody tests when the parasites are difficult to be detected . • Treatment : • The ideal treatment should : • 1- Destroy all forms of the parasite in blood to cure the clinical attack e.g. by Quinine, Chloroquine, Paludrine and Atebrin . • 2- Destroy all exoerythrocytic forms in order to prevent replases by using Primaquine and Pyrimethamine . • 3- Destroy all gametocytes so that mosquito infections will be prevented by Plasmoquine . • No single drug will answer these three objectives but combination of two drugs will often meet the need . • Prevention and control : • Removing breeding sites, larvacides, insecticides - Chemoprophylaxis - Avoidance (nets, clothing) • Toxoplasma gondii • Worldwide • Zoonotic parasite; Toxoplasma is an opportunistic pathogen. • Infects animals, cattle, birds, rodents, pigs, and sheep. • and humans. • Causes the disease Toxoplasmosis. • Toxoplasmosis is leading cause of abortion in sheep and goats. • Intracellular parasite. • Final host (Felidae family, cat) • Intermediate host (mammals ) • Toxoplasmosis • All parasite stages are infectious. • Risking group: Pregnant women, meat handlers (food preparation) or anyone who eats the raw meat • Morphology : • 1- Trophozoite: intracellular, crescent-shaped with central nucleus, invade all cells except RBCs (non nucleated) and multiply by binary fission forming pseudocyst . • 2- Pseudocyst: Intracellular collection of trophozoites (tachyzoites) in macrophages and R.E.S. cells (in acute stage). • 3- Cysts: Collection of trophozoites (cystozoites, bradyzoites) enclosed in a true tissue cyst (in chronic stage or latent infection when immunity develops). • 4- Oocysts : Oval, contain 2 sporocysts each containing four sporozoites and found in stool of infected cats .

• Life cycle: (Plate 9). • 1- Sexual or enteric cycle occur when a cat or other host ingests pseudocys, cysts or oocysts. Schizogony and gametogony takes place in intestinal epithelium and occysts are produced and pass in faeces . • 2- Asexual cycle occure in intermediate hosts (man, rodents, chickens, pigs. and other animals). Ingestion of pseudocysts, cysts or oocysts the parasite develops extraintestinally forming pseudocysts and cysts in viscera, muscles and brain . • (Plate 9) • Toxoplasma gondii • Sources of infection : • - Contaminated water or food by oocysts • - Undercooked meat , Ingestion of tachyzoites and bradyzoite (cysts) in flesh of infected host. • - Mother to fetus. • - Organ transplant (rare). • - Blood transfusion (rare). • Pathogenicity • In immunocompetent adults • 1- Most infections benign ,toxoplasmosis, may produce flu-like symptoms, sometimes associated with lymphadenopathy • 2- Rarely severe :hepatitis, encephalomyelitis, myocarditis .Few cases of retinochoroiditis which can progress to blindness • In immunodeficiency • 1- Serious or fatal infection occurs as in AIDS, transplant and cancer patients; • 2- presents with specific organ involvement e.g. encephalitis, pneumonitis. generalized parasitemia involvement of brain, liver lung and other organs, and often death. • Congenital toxoplasmosis : transmission from mother to fetus • when mother has developed acute toxoplasmosis during pregnancy - increased transmission rate in third trimester, but increased severity of fetal disease in first trimester. Presents as hydrocephalus, hepatomegaly, cerebral calcifications, mental retardation with death at one end of spectrum and mental retardation or just later choreoretinitis at the other end of spectrum. • Laboratory diagnosis : • Sabin-Feldman dye test (DT): is carried out by staining the parasites with alkaline methylene blue in the presence of the patient's serum. In the absence of specific antibodies, the organisms are stained by the dye. If antibodies are present (+ve test) the dye is excluded from the organisms. • Enzyme immunoassay for T. gondii specific IgM (EIA) • Immunsorbent agglutination assay (ISAGA) • Enzyme immunoassay for IgG avidity • Isolation and culture of parasite (isolation of organism from tonsil or lymph gland biopsy). • Direct detection by microscopy and PCR • Animal inoculation with biopsy material e.g. lymph node and then identification of the parasite in specimen from the intrapritoneal region. • Treatment : • Only accepted treatment pyrimethamine with trisulfapyrimines for one month • Intravenous clindamycin used to treat encephalitis in AIDS patients • spiramycin has been used to treat toxoplasmosis in pregnancy • Prevention and control : • 1-Avoid consumption of raw or undercooked meat • 2-Litterpans should be changed daily –Wash hands after handling raw meat, litter pans & soil –Pregnant women should avoid contact with cats –Issue of prenatal screening • Medically important protozoa

Location Species Mode of Disease transmission Skin Sand fly cutaneous (Blood and L. braziliensis leishmaniasis tissue) mucocutaneous leishmaniasis

Intestine Giardia lamblia Ingestion of cysts in gardiasis (Intestinal tract) Entamoeba food amebiasis histolytica Liver Entamoeba - - Leishmania

Blood Plasmodium Anopheles malaria vivax, P.ovale sleeping P. malariae mosquito sickness Trypanosom Tsetse fly a gambiense CentraL Toxoplasma Ingestion toxoplasmo Nervous gondii of cyst in raw sis System Entamoeba meat amebae Plasmodiu malaria m trypanosom Trypanoso es ma