Parasitology - Student Version PDF

PrinciPle of Parasitology Biol3061 By: saron fekadu  chaPter one PrinciPle of Parasitology 1. Basic Terminologies and Concept of Parasitology 1.1. The Concept of Parasitology 1.2. Classification of Parasites 1.3. The Hosts vs Vector 2. Parasitic Protozoa 2.1....

PrinciPle of Parasitology Biol3061 By: saron fekadu  chaPter one PrinciPle of Parasitology 1. Basic Terminologies and Concept of Parasitology 1.1. The Concept of Parasitology 1.2. Classification of Parasites 1.3. The Hosts vs Vector 2. Parasitic Protozoa 2.1. Intestinal Protozoa 2.2. Urogenital Protozoa 2.3. Tissue or blood protozoa definition of Parasites and Parasitism. q Parasitism is a form of association b/n organisms of d/t spps known as Symbiosis. q Symbiosis can be between any plant, animal or protist q The most common types of symbiosis:- Commensalism:- involves one-way benefit, but no harm Mutualism:- two-way (mutual) benefit and no harm. Parasitism:- one (the parasite) lives at the expense of the other (the host)  Parasites ?? Parasites are organisms that live on or within another organism, known as the Host. Parasites are dependent on their host for all or part of its life cycle and metabolic requirements. Examples: üProtozoan Parasites: Plasmodium species cause malaria in humans. üHelminth Parasites: Ascaris (a roundworm) infects the human intestines. üEctoparasites: Ticks and lice live on the surface of the host’s skin. Key Features of Parasites üSmaller than their host, üOutnumber the host, üShort life span than their host, and üHave greater reproductive potential than their host.  1.1. the concePt of Parasitology q Parasitology is the study of parasites, their hosts, and the relationship between them. Medical Parasitology focuses on parasites which cause diseases in humans, it’s clinical features and response generated by humans.  1.2. classification of Parasites Parasites can be Classified:- I. According to their habitat: 1. Ecto-parasites :- living on the body surface of the host. E.g. lice, tick, etc. 2. Endo-parasites :- living within the body of the host. E.g. Leishmania species, Ascaris lumbricoides, etc  ectoParasites Vs endoParasite FEATURE ECTOPARASITES ENDOPARASITES Live on the host’s surface (skin, Live inside the host’s body Location hair) (organs, blood) Ingestion, vectors (e.g., Direct contact or through the Transmission mosquitoes), or skin environment penetration Damage to Skin irritation, disease Organ damage, nutrient Host transmission depletion, severe diseases Tapeworms, roundworms, Examples Ticks, fleas, lice, mites protozoa (Plasmodium)  classification of Parasites cont... II. According to their dependence on the host: 1. Permanent (obligate) parasites: The parasite depends completely upon its host for metabolites, shelter, and transportation. This parasite can not live outside its host. E.g. Plasmodium species, Trichmonas vaginalis, etc. 2. Temporary (facultative) parasites: The parasite is capable of independent existence in addition to parasitic life. E.g. Strongyloids stercolaris, Naegleria fowleri, etc 3. Accidental parasites is an organism parasitizing an animal other than the usual (non-specific) host. For example, the dog or cat Ascaris can accidentally affect humans classification of Parasites cont... III. According to their Pathogenicity: 1. Pathogenic parasites It causes disease in the host. E.g., E. histolytica 2. Non-Pathogenic (commensal) parasite The parasite derives food and protection from the host without causing harm to the host. E.g. Entamoeba coli 3. Opportunistic parasites Parasites which cause mild disease in immunologically healthy individuals, but they cause severe disease in immuno-deficient hosts. E.g. Pneumocystis carnii, Toxcoplasma gondii, Isospora belli  terminologies in Parasitology Infective Stage:- The stage of parasite at which it is capable of entering the host and continue development within the host. Infection:- Invasion of the body by any pathogenic organism (except )arthropods and the reaction of the hosts tissue to the presence of the parasite or related toxins. Infestation:- The establishment of arthropods upon or within a host. Zoonosis:- Diseases of animals. Today this term is applied for those diseases that are transmittable to man. terminologies... Biological Incubation (Prepatent) Period:- It is time elapsing between initial infection with the parasite and demonstration of the parasites or their stages in excreta, blood, aspirate and other diagnostic material. Clinical Incubation Period:- It is the interval between exposure and the earliest manifestation or infestation. Autoinfection:- An infected individual acts as a source for hyperinfection to himself. Superinfection (Hyperinfection):- When an individual harboring the parasite is reinfected by the same parasite. Retroinfection:- A retrograde infection caused by the newly hatched larva of E. vermicularis from the perianal region to reach the colon, where the adolescent form of the parasite develop. 1.3. the hosts q The Host is a an organism to where the parasite can penetrate and reproduce q The different terms used to describe the host Definitive host – where parasite reproduces sexually The adult stage of parasite is present. Intermediate host – required by parasite to complete it’s asexual stage The larval stage is present in it. For example, the beef is intermediate host for beef tapeworm (larvae develop), and human is definitive host for that helminth (adults develop). the hosts Accidental host - An uncommon or rare host to a pathogenic microorganism. For example: a round worm of dogs Toxocara canis (dog Ascaris) may accidentally infect humans that are non-specific hosts for that parasite. Reservoir host - animals that serve as additional source of infection to humans. This host reserves and accumulates the parasite, and is a source for its spreading. the hosts Vs Vector cont… q Vectors. Arthropods (insects, ticks) that transfer the parasitic agents from one host to another are called vectors. Vectors are biological (specific) and mechanical. Biological vector is essential in the life cycle of parasite. It can be a definitive host (e.g. Anopheles mosquito for plasmodium) or an intermediate host (like the tse-tse fly for Trypanosoma brucei). Mechanical vector is unessential in life cycle of the parasite The insect (non-bloodsucking) mechanically transfers it, e.g. flies can transport cysts of amoeba, or eggs of Ascaris, etc 1.3.1. the host - Parasite relationshiP qWhen a parasite gains access to a host, The host has to compromise and The parasite has to adopt itself in host environment. q Series of events that occur in host – parasite relation Transmission of parasite from one host to another, Distribution and localization of parasite on or within the host, Growth or multiplication of parasite This stage includes the resistance of host to the parasite and the parasite adaptation to the host adaPtations of Parasites to Parasitism q Parasitic adaptations are responses to features in the parasite's environment (the body the host) qParasite adaptations help the parasite ü in staying within the host and i.e. Morphological adaptations ü spreading between hosts i.e. Life cycle adaptations morPhological adaPtation 1. Size Many parasites are large compared with their free-living relatives. This could be related to increased egg production 2. Shape Most parasites are dorso-ventrally flattened This is related to the need to cling on to the host. Fleas are laterally flattened and rely on escape through the hairs. 3. Loss of locomotory organs In multicellular parasites, particularly in endoparasites. morPhological adaPtation – size examPle Diphyllobothrium is a genus of tapeworms which can cause diphyllobothriasis in humans through consumption of raw or undercooked fish. morPhological adaPtation 4. Reduction of other organs For example: CNS and sense organs in many endoparasites are very primitive, degradation of gut and absorption of nutrients through the whole body surface (tapeworms). Helminthes tend either to loose their gut and absorb nutrients through their teguments, or else retain their gut and have a thick resistant cuticle (like round worms, e.g. Ascaris). morPhological adaPtation 5. Organs of attachment There are two types of attachment organs, ü Hooks or ü Suckers (organs specifically for absorption of nutrients) 6. Prolific reproductive organs In many parasites there is a tremendous elaboration of the reproductive system, associated with increased gamete production leading to high fertility. Parasites usually produce more eggs and sperm than their free-living relatives. Other adaptations, which increase egg production, are hermaphroditism (every individual produces eggs) and parthenogenesis at different stages. life cycle adaPtations 1. Development with alternation of hosts: Infection of definitive and intermediate hosts in many parasites This has the following advantages: üit increases range of the parasite in space and time. üthe parasite can survive periods when one host is temporarily scarce ü an intermediate host can direct the parasite towards its definitive host since the intermediate host is frequently part of the final host’s food chain or else closely related ecologically. life cycle adaPtations 2. Behavioral changes in hosts. These include: a) Behavioral responses of the host mediated by the parasite. For example, the roundworm Enterobius vermicularis (pin worm) causes intense itching of perianal skin when crawling out from anus for oviposition, and the eggs pass under finger nails when scratching and are again a source for re-infection. b) Changing the behaviour of the infected intermediate host to increase the chances of them being eaten by the definitive host e.g., the infected ants that are the second intermediate host of Dicrocoeleum lanceatum, change their behaviour, by running up, and attaching themselves, by their jaws, to the tops of blades of grass, where they can be accidentally ingested as their herbivorous definitive hosts graze. life cycle adaPtations 3. Synchronization (syn=together, chronos=time) of life cycles. How life cycle of a parasite becomes integrated (occurs simultaneously) with that of its host fall into two broad mechanisms: a. The oviposition of blood flukes (Schistosomes) occurs usually at hot daytime, when there is higher probability for swimming of humans in hot waters, so the eggs can be liberated from definitive host at this time and pass to the intermediate host, fresh water snail. b. Life cycle of some vectors matches with the periodicity of microfilaria (larvae of filarial roundworms), when they can be found in peripheral blood and be available for the insect vector when biting the host (for example, the black fly usually bites at daytime, when the microfilaria of Loa loa are found in the blood). effects of Parasites on their hosts A Parasite can affect the host in a number of ways such as:- 1. Consumption of the nutritive elements of the host E.g. Hookworm –sucks blood, Diphyllobothrium latum selectively remove V B12. 2. Obstruction of passages E.g., heavy infection with adult Ascaris may cause intestinal obstruction 3. Bleeding E.g. Schistosomes eggs 4. Destruction of tissues: E.g. Trophozoites of E. histolytica causes necrosis of liver, Leishmania donovani results marked destruction of marrow elements. effects of Parasites on their hosts 5. Compression of organs, E.g. Hydatid cysts in liver, brain cause pressure 6. Release of toxic substances, E.g., Rupture of E. granulosus cyst result anaphylactic shock 7. Opening path way to secondary infections E.g. Ulcer formed as a result of D. medinensis infection exposes to Bacterial, Viral infection 8. Allergy development, E.g., Bite of arthropode effects of Parasites on their hosts 9. Transmission of pathogens to man E.g., lice transmitting Rickettsia 10. Predisposition to malignancy E.g., Infection with bilharziasis predisposes to maliganacy (can develop to cancer) 11. Chronic immune stimulation leading to unresponsiveness to infections. host suscePtiBility factors Not all parasitic infection causes disease of clinical significance. Both host and parasitic factors are involved Parasite factors 1. Strain of the parasite and adaptation to human host 2. Parasite load ( number of parasite ) 3. Site (s) occupied in the body 4. Metabolic process of the parasite, particularly the nature of any waste products or toxins produced by the parasite during its growth and reproduction host suscePtiBility factors Host Factors 1. Genetic constitution 2. Age 3. Sex 4. Level of immunity: natural and acquired immunity. 5. Nutrition (malnutrition or under nutrition) 6. Intensity and frequency of infections 7. Presence of co-existing disease or conditions which reduces immune response. e.g. Pregnancy, HIV 8. Life style and occupation  host resPonse to Parasite v The responses of vertebrate host to the parasite express in two ways: resPonses of host non-sPecific - Reaction are not dependent on sPecific specific recognition of the non-self Is a response to a specific recognition of non-self - It is the first line of defence in most vertebrates sources of Parasitic infections A. Contaminated soil Soils polluted with human excreta is commonly responsible for exposure to infection with Ascaris lumbricoides, Strongyloides stercoralis , Trichuris trichuria and hook worms. B. Contaminated water Water may contain a. Viable cysts of Amoeba, flagellates and T. solium eggs, b. Cercarial stages of human blood fluke, c. Cyclops containing larva of Dracunculus medinesis, d. Fresh water fishes which are sources for fish tape worm, and intestinal flukes infection e. Crab or cray fishes that are sources for lung fluke f. Water plants which are sources for Fasciolopsis buski sources of Parasitic infections cont... C. Insufficiently cooked meat of pork and beef contains infective stage of the parasite E.g., Trichenilla spiralis, Taenia species. D. Blood sucking arthropods These are responsible for transmission of 1. Malaria parasites by female anopheles mosquito 2. Leishmania by phlebotomus 3. Trypanosoma by tsetse fly 4. Wuchreria by Culicine mosquito e.t.c  sources of Parsitic infections cont... E. Animals (domestic or wild animals harboring the parasite) Dogs are direct sources for human infection with (Echinococcus granulosus and Toxocara canis) Herbivores animals for human infection with Trychostrongylus species. F. Human beings Infected persons’ clothing, bedding or the immediate environment E.g. pathogenic amoeba E. histolytica, Enterobius vermicularis, Hymenolepis nana Sexual intercourse :- e.g., Trichomonas vaginalis H. Autoinfection :- e.g., S. stercoralis, E. vermicularis, and T. soliu mode of transmission 1. Direct mode of Transmission does not require biological vectors and/or intermediate hosts Horizontal Vertical Transmission is mainly effected through:- Feco- Transmission of the parasite is from the oral route: mother to child through: Most intestinal parasites transmitted in this way. oCongenital / transplacental oSexual intercourse oTransmammary (breast milk) oBlood transfusion oDirect skin penetration (soil transmitted helminthes) 2. Indirect Mode of Transmission The parasite has complex life cycle and Requires biological vectors and/or one or more intermediate hosts for transmission. route of transmission 1. By ingesting infective stage of parasites i. In food, water or from hands that have been contaminated with faeces, E.g. Entamoeba histolytica, Enterobius vermicularis ii. In raw or undercooked meat, e.g. Taenia saginata, Taenia solium, Trichinella spiralis iii. In raw or undercooked fish, crab, or water vegetation e.g. intestinal flukes iv. Water containing Cyclopes e.g., Dracunculus medinensis 2. Penetration of Skin When in Contact with i. Faecally polluted soil, e.g., Strongyloides stercoralis, Hook worms ii. Water containing infective stages of the parasite E.g., Cercaria of Schistosome species. route of transmission 3. Through Insect Bite e.g, filarial worms, Trypanosoma species, Plasmodium species , Leishmania species 4. Sexual Contact e.g., Trichomonas vaginalis 5. Transmammary e.g., Strongyloides stercoralis 6. Inhalation of contaminated air e.g., Enterobius vermicularis, Pneumocystis carnii 7. Transplacental e.g., Toxoplasma gondii 8. Kissing e.g., Trichomonas gingivalis, Trichomonas tena  taxonomy of Parasites The taxonomy of parasites involves classifying them into groups based on their biological characteristics. Parasites can be found across many branches of the tree of life Major taxonomic groups of medically parasites belongs to: 1. Kingdom: Protista (Protozoa) 2. Kingdom: Animalia (Metazoa)  major differences Between Parasitic Protozoa and metazoa Differences Protozoa Metazoa 1. Number of cells Unicellular Multicellular 2. Mode of multiplication Asexual (with exception) Sexual (with exception) 3. Rate of Multiplication Fast Slow 4. Longivity Short Long Amoeba, Flatworms, Tapeworms Examples Plasmodium, arthropods, Entamoeba, etc.  kingdom: Protista (Protozoa) Protozoan parasites are single-celled organisms Further classified into several phylums mainly: 1. Phylum: Apicomplexa 2. Phylum: Amoebozoa 3. Phylum: Euglenozoa 4. Phylum: Metamonada  kingdom: Protista (Protozoa) Phylum: Apicomplexa These are obligate intracellular parasites, Characterized by a unique structure called the apical complex, which they use to invade host cells. Examples: Plasmodium spp. (causes malaria), Toxoplasma gondii (causes toxoplasmosis), Cryptosporidium spp. (causes cryptosporidiosis).  kingdom: Protista (Protozoa) Phylum: Amoebozoa Amoeboid parasites move and feed using pseudopodia (temporary projections of the cell). Examples: Entamoeba histolytica (causes amoebic dysentery), Acanthamoeba spp. (causes amoebic keratitis).  kingdom: Protista (Protozoa) Phylum: Euglenozoa These parasites are flagellated protozoans. Examples: Trypanosoma spp. (causes sleeping sickness and Chagas disease), Leishmania spp. (causes leishmaniasis).  kingdom: Protista (Protozoa) Phylum: Metamonada These are flagellated protozoans, often associated with the digestive tracts of animals. Examples: Giardia lamblia (causes giardiasis), Trichomonas vaginalis (causes trichomoniasis).  kingdom: animalia (metazoa) Multicellular parasites in the animal kingdom include helminths and ectoparasites like arthropods. Further classified into several phylums mainly: 1. Phylum: Platyhelminthes (Flatworms) 2. Phylum: Nematoda (Roundworms)  chaPter two medical Protozoology  2.1. introduction to Protozoa q Protozoa (Greek - “proto” first, “zoa” animals) The fossil record shows ü Protozoa were present in the Pre-cambrian era i.e. 4 billion – 541 million years ago However, seen for the first time ü in 1674 ü by Anton van Leeuwenhoek ü by using microscope ü He described both free-living protozoa and several parasitic species Eg. Giardia lamblia from his own stools  2.1. introduction to Protozoa Protozoa found worldwide in most habitats. üMost species are free living, but all higher animals are infected with one or more species of protozoa ü The protozoa of medical importance to humans include:- Amoebas, Flagellates, Ciliates, Coccidia, Sporozoa and Microsporidia ü Many protozoan species are not pathogenic ü Protozoa may colonize or infect Intestinal tract, pharynx, and the uro-genital tract of humans.  introduction to Parasitic Protozoa Parasitic protozoa üsingle-celled microorganisms live as parasites, deriving their energy from a host organism. hosts including humans, animals, and even plants, and they can cause a wide range of diseases. üParasitic protozoa are eukaryotic meaning they have a well-defined nucleus and other membrane- bound organelles.  introduction to Parasitic Protozoa Key Characteristics of Parasitic Protozoa: 1. Unicellular Eukaryotes: They are single-celled organisms with complex cellular structures, including a nucleus. 2. Parasitic Lifestyle: They rely on a host organism to survive and reproduce, often causing disease or harm to the host. 3. Variety of Modes of Movement: Different groups of protozoa move using flagella, cilia, pseudopodia, or glide through host tissues.  introduction to Parasitic Protozoa 4. Complex Life Cycles: Many parasitic protozoa have complex life cycles involving multiple stages and often more than one host species, with stages in both the host and vector organisms. 5. Different in their feeding behavior ü Heterotrophic (feed on other organisms) ü Osmotrophy (simply absorb solutes from their media), ü Phagotrophy (ingest solid material) ü Autotrophic(convert light energy to chemical energy vMany protozoa are not restricted to a single feeding mechanism and can utilize combinations of the above (i.e., Mixotrophic).  2.2. medically imPortant Protozoa 1. Parasites of Mouth Parasitic Protozoa Lives in... Way of transmission Entamoeba Gingivalis Tartar of teeth and Kissing pockets of gums Trichomonas Tenax Pus pockets formed Kissing between teeth and gums Leishmania Brazxliensis The nasal mucous bite of sand-fly membrane  2. Parasites of Digestive tract Parasitic Protozoa Lives in... Way of transmission Entamoeba Histolytica the colon swallowing of cysts Trichomonas Hominis large intestine infective cysts Chilomonas large intestine infective cysts Giardia Intestinalis large intestine cyst in contaminated food or water Isopora Hominis large intestine occysts through contamination Sarocystis large intestine cysts Balantidium Coil colon of man infective cysts  3. Parasites of Blood and Lymph Parasitic Protozoa Lives in... Way of transmission Trypanosoma Sps: in the blood T. Gambiense “ " bite of tsetse fly, Glossina palpalis T. Rhodesiense “ " bite of tsetse fly, Glossina morsitans T. Cruzi: “ " bite of bug, Tritoma magista Leishmania Sps Leishmania endothelial cells of blood and bite of sand-fly, Phlebotomus. Donovani lymph capillaries leucocytes in the spleen, liver, bone marrow and lymph gland L. Tropica: endothelial cells of dermal tissues bite of sand-fly L Infentum spleen of children bite of sand-fly Plasmodium Sps intracellular parasites in red blood Female Anopheles mosquito 4. Parasites of Urogenital Tract Parasitic Protozoa Lives in... Way of transmission Trichomonas Vagina of female Direct inter-course Vaginalis Urethra of man  Phylum amoeBozoa The Phylum Amoebozoa is a diverse group of amoeboid organisms ü Characterized by their ability to move and feed using pseudopodia (temporary extensions of their cytoplasm) ü found in a variety of environments, including soil, freshwater, and marine habitats. ü Some are parasitic and can cause diseases in humans and animals.  amoeBa Amoebas can be found in various locations within the human body:- 1. Intestinal Tract Entamoeba histolytica Endolimax nana Entamoeba dispar Iodamoeba butschlii Entamoeba Coli vOnly E. histolytica is pathogenic to man, the others are commensals 2. Mouth (Oral Cavity) Entamoeba ginivalis amoeBa 3. Eyes Acanthamoeba - free living in normal circumstances Infection leads to a condition known as Acanthamoeba keratitis. 4. Nervous System Naegleria fowleri - free living in normal circumstances cause a severe brain infection known as primary amoebic meningoencephalitis (PAM). amoeBa q All human intestinal amoebae have: 1. Trophozoite form which is motile organism, feeding, and reproduce 2. Cystic form which is Non-feeding, non motile and dormant stage of protozoa. v But E. gingivalis has only a trophozoite from q Amoeba reproduce asexually by binnary fission  1. entamoeBa histolytica Entamoeba histolytica is a pathogenic amoeba üResponsible for causing amoebiasis, a serious intestinal disease in humans. Morphology: Under the microscope, Entamoeba histolytica can appear in two forms: 1. The trophozoite (the active, multiplying form) Trophozoites are typically larger and amorphous 2. The cyst (the dormant, resistant form) Cysts are spherical and have a protective outer layer.  entamoeBa histolytica Life cycle of E. histolytica Cysts in Contaminated Food/Water → Ingestion → Excystation in the Intestines → Trophozoites (Active Stage) → Multiplication (Binary Fission) → Invasion of Intestinal Mucosa (if pathogenic) → Encystation (Formation of Cysts) → Excretion in Feces of Cysts.  entamoeBa histolytica Transmission: üFecal-Oral Route: The primary mode of transmission is through ingestion of cysts present in contaminated food or water, often in areas with poor sanitation. üHuman to Human: The disease can spread from person to person if proper hygiene and sanitation practices are not maintained.  entamoeBa histolytica Pathogenesis: Intestinal Disease: ü Trophozoites that invade the intestinal wall, leading to ulceration and inflammation. This results in symptoms such as: Diarrhea (which may be bloody in severe cases), Abdominal pain, Cramping, Weight loss, Fever etc Extraintestinal Manifestations: ü In rare cases, the amoeba can enter the bloodstream and affect other organs, including the liver, lungs, and brain.  entamoeBa histolytica Diagnosis: Stool Examination: Diagnosis typically involves microscopic examination of stool samples to identify cysts or trophozoites. Serology and Imaging: Serological tests and imaging studies (like ultrasound or CT scans) may be used for detecting extraintestinal disease.  entamoeBa histolytica Treatment: Antimicrobial Medications: The standard treatment usually involves the use of medications such as metronidazole or tinidazole, followed by a luminal agent like iodoquinol or paromomycin to eliminate cysts in the intestine. Supportive Care: In cases of severe dehydration due to diarrhea, rehydration therapy may be necessary.  entamoeBa histolytica q Distribution of E. histolytica Cosmopolitan distribution (across all of the world) v mainly in the tropics and subtropics It is mainly related to üinadequate personal hygiene (environmental sanitation) ü lack of safe water supply and poor socioeconomic situation Quiz 1 List possible route of parasite into host What are the major site of parasitism for Amoeba spps in humans? Name the only pathogenic amoeba to hiuman? q Life cycle ü requires a single host ü mature tetra-nucleated cyst ingested ü it excysts in the small intestine ü produce metacystic trophozoite by binary fission ü immature trophozoites migrate to the colon and get mature ü invade the mucus membrane of the large intestine ü Some times it can perforate the intestinal wall causing extra-intestinal amoebiasis. ü After a period of growth and multiplication, encystment occurs in the large intestine entamoeBa gingiValis Entamoeba Ginivalis is found in the mouth ü inside the gingival pocket biofilm near the base of the teeth, and ü in periodontal pockets. Entamoeba gingivalis is found in 95% of people with gum disease and rarely in people with healthy gums. No Cyst formation therefore transmission is ü by kissing or ü by sharing eating utensils The trophozoiteare is usually 20 to 150 µm in diameter. Entamoeba gingivalis have pseudopodia ü It allow them to move quickly and ü Phagocytise the nucleus of polynuclear neutrophils (WBC) by exonucleophagy in periodontal disease.  2. free liVing Pathogenic amoeBa Free-living amoebae (FLA) are ubiquitous and opportunistic protozoa These FLAs inhabiting mostly in üfresh, brackish and salty water ümoist soil and üdecaying vegetation Four genera are responsible for opportunistic and non opportunistic infections in humans and other animals üAcanthamoeba üNaegleria üBalamuthia üGolbaly most reported cases are of Acanthamoeba and Naegleria üSappinia 2.1 acanthamoeBa sPP. Free-living single celled amoeba Cause severe infections of the eye, skin, and central nervous system. It is found worldwide in the water and soil. Acanthamoeba in... Can be transmitted to other host through Eyes contact lens use Skin skin wounds CNS being inhaled into the lungs Most people will be exposed to Acanthamoeba during their lifetime, but very few will become sick from this exposure. 2.1 acanthamoeBa sPP. The three diseases caused by Acanthamoeba Acanthamoeba keratitis ü An infection of the eye ü Occurs in healthy persons ü Can result in permanent visual impairment or blindness. Granulomatous Amebic Encephalitis (GAE) ü A serious infection of the brain and spinal cord ü Occurs in persons with a compromised immune system. Disseminated infection ü A widespread infection that can affect the skin, sinuses, lungs, and other organs independently or in combination. ü Common in persons with a compromised immune system.  2.2. naegleria found in warm fresh water (eg:- lakes, rivers, and hot springs) and soil. Only one species of Naegleria infects people: Naegleria fowleri ü Get into humans with water through the nose ü Then it travels up the nose to the brain, ü it destroys the brain tissue and causes a devastating infection called Primary amoebic meningoencephalitis (PAM).  2.2.1. Phylum metamonada It is a group of single-celled eukaryotic organisms that are primarily flagellates, (flagella for movement). Several medically important parasites belong to the Phylum Metamonada, most notably from the genera Giardia and Trichomonas  Phylum metamonada cont... General Characteristics 1. Anaerobic Metabolism: These parasites thrive in low-oxygen environments, such as the digestive or reproductive tracts. 2. They lack functional mitochondria and instead rely on alternative organelles like mitosomes or hydrogenosomes for energy production. 3. Uses flagellum as locomotory organell 4. Reproduce by simple binary fission 5. Complete their life cycles in a single host and a second host whom they infect is necessary for the continuation of the species. 6. Most are commensals except Giardia lamblia, Trichomonas vaginalis and Dientamoeba fragilis  1. dientamoeBa fragilis Dientamoeba fragilis üOriginally classified as an amoeba, but now defined as an amoeba like flagellate v Because electron microscopic studies have revealed that the internal structures are typical of flagellate Geographical Distribution: ü World wide Habitat: ü In the large intestine. Morphology: Diagrammatic representation of ü Has trophozoite stage only, No cyst a two-nucleated trophozoite  dientamoeBa fragilis Life cycle:- ühas feco-oral nature transmission. üIt reproduces asexually by binary fission. Laboratory Diagnosis:- ü Immediate examination of fresh stool vDue, the trophozoite stage is highly fragile and disintegrates explosively in water 2. giardia lamBlia Also called Giardia intestinalis and G.duodenale Habitat: ü Upper parts of the small intestine mainly in the duodenum and jejunum Geographical Distribution:- üCosmopolitan distribution in warm climate ümore prevalent in children than in adults. üIt is the most commonly diagnosed flagellate of the human intestinal tract Morphology: giardia lamBlia Trophozoite:- ü Size: 10-21 by 5-15μm ü Shape: pyriform (pear-shaped), i.e. rounded anteriorly and pointed posteriorly. § Anteriorly there are 2 sucking discs § Each contains a nucleus, § 4 pairs (8) flagella, § Parabasal body and axonemes giardia lamBlia Morphology: Cyst ü Size: 8-12μm, ü Shape: Oval shape with thick cyst wall. § Finely granular cytoplasm clearly separated from cyst wall. § 2-4 oval nuclei at one pole § Cytoplasm: clear when unstained; yellowish green or bluish in iodine solution.  giardia lamBlia Life Cycle üRequires a single host to complete its cycle üreproduces by a simple longitudinal binary fission Cyst ingested Move to the upper part of the Excystation i.e. with contaminated small intestine food, drink, finger, etc. i.e. to form flagellates Cyst in Encystation faeces ü some of the trophozoites undergo encystation Trophozoite ü attached to the intestinal Trophozoites wall by a sucking disc ü Trophozoites also get binary fission ü absorb nourishment out with the faeces through their body surface. giardia lamBlia giardia lamBlia Clinical Feature and Pathology:- üDuodenitis, üExcess secretion of mucus or malabsorption of fat (steatorrhoea), sugar and vitamins, üDehydration, Diarrhoea üWeight loss, Poor appetite, Vomiting, üLethargy bile passage obstruction Laboratory Diagnosis:- üFinding the trophozoite and cyst stages in stool specimen. üThe stool is usually offensive, bulky, pale, mucoid (fatty), diarrheic (watery) but there is no blood in the stool. trichomonas hominis Geographical Distribution: üNext to Giardia lamblia, it is probably the most common and most cosmopolitan of the intestinal flagellates of man. Habitat: üLarge intestine Morphology: üHas trophozoite stage only Trophozoite trichomonas hominis ü Size: 10-15μm, ü Sape: pyriform (oval with two pointed poles) ü Motility: whirls and turns (jerky) in all directions, seeming to vibrate. Undulating membrane and costa reach 2/3 or full length of the body ü Undulating membrane extension of the cytoplasmic membrane helping movements Single nucleus with central karyosome Flagellum: 3-5, usually ü 4 anterior free flagella and ü another flagellum on the margin of undulating membrane with a free trailing posterior end. Has semi-rigid axostyle (anchoring the parasite with the host)  trichomonas hominis Life Cycle ü The trophozoite stage reproduces by binary fission ü requires direct host to host transmission through contaminated food and/or drink. ü It has high prevalence in children and more common in warm climates Pathology: ü It is non-pathogenic Laboratory Diagnosis: but may cause ü Finding the trophozoite stage in fresh stool diarrhoea and infection specimen. trichomonas Vaginalis Geographical Distribution:- ü World wide distribution and mainly common in the temperate region. Habitat:- ü In the genital tract of male and commonly in female, ü especially the vagina, cervix, urinary bladder, prostate and seminal vesicles Morphology: ü Has trophozoite stage only.  trichomonas Vaginalis Trophozoite ü Size 15-25 by 5-12μm, is the largest Trichomonas. ü Shape: pyriform ü Moility: Jerky (on-spot), non-directional motility in fresh specimen. Short undulating membrane: extending along 1/3 of the body. Nucleus: Single with uniformly distributed chromatin granules Flagella: ü 4 anterior free flagella and ü one on the margin of the undulating membrane  trichomonas Vaginalis Life Cycle:- üThe trophozoite stage reproduces by longitudinal binary fission ütransmission is usually via sexual intercourse üalso by ü communal bathing, ü sharing of washclothes, ü toilet equipment seats and ü mother to daughter during birth.  trichomonas Vaginalis Pathology: üCauses Trichomoniasis üMajor symptoms are:- Vaginitis, Urethritis, Prostatitis, Chaffing of vulva, Cervical erosion, Burning Prevention and Controlsensation, Yellowish 1. Personal hygiene prulent discharge, and sanitation 2. Simultaneous treatment ofsterility Reversiable both partners. in male.  trichomonas tenax Geographical Distribution üWorld wide distribution with high incidence in warm climates. Habitat üOral cavity. Morphology üHas trophozoite stage only a. Dental plaque-induced gingivitis patient. B. Periodontitis patient Bottom: T. tenax trophozoites observed by microscopy in each patient are showed by arrows (× 400) Bracamonte-Wolf, C., 2019  trichomonas tenax Trophozoite üSize: 5-12μm üShape: pyriform üMotility: active jerky motility Undulating membrane: ü reaches two third of the body length. Nucleus: ü Single Flagella: ü four anterior free flagella and ü one flagellum on the undulating membrane. Thick axostyle ü extending a considerable distance behind the body.  trichomonas tenax Life Cycle:- üThe trophozoite stage reproduces by binary fission and üTransmission is direct from mouth to mouth through kissing or communal use of contaminated food and drinking utensils. Pathology:- ü It is non-pathogenic Laboratory Diagnosis:- ü Finding the trophozoites in unstained or stained smear in swab taken from the oral cavity trichomonas sPecies Trichomonas species. (A)T. vaginalis, (B)T. hominis, (C)T. tenax. 1. Undulating membrane 2. Costa 3. Flagella 4. Nucleus 5. Axostyle 2.2.3. Phylum euglenozoa They include both free-living (Euglenoids) and parasitic species (Kinetoplastids) Parasitic organisms within the phylum Euglenozoa (specifically the Kinetoplastea group), are often referred to as tissue flagellates Some of which are medically significant parasites for humans Eg. Trypanosoma spps. and Leishamania spp.  Blood and tissue flagellates The blood and tissue of humans are belonging to the family Trypomastidea There are six genera but only two of them cause disease to man These are ü Genus Leishmania ü Genus Trypanosoma All of these organisms have Leishmania developmental stages in blood Sandflies sucking arthropodes (intermediate host) and in humans (definitive host), and may have a non human Trypanosomes mammalian reservoir host. Triatomid bugs Tsetse fly  general characteristics 1. Reproduces by simple longitudinal binary fission 2. The infective stage is always the vegetative form. 3. Transmission occurs through biological insect vectors as intermediate hosts and man as definitive host 4. The species are morphologically indistinguishable, but they can be differentiated on the basis of their clinical features , geographical distribution, vectors, reservoir hosts, biochemical tests, immunological tests, etc. 5. Different developmental forms that can be differentiated on the basis of a) Presence or absence of free flagellum b) Presence or absence of undulating membrane c) Position of the kinetoplast relative to the nucleus. general characteristics of tissue flagellates: 1. Flagella for Locomotion: Tissue flagellates possess one or more flagella. Not all stages of their life cycle have flagella. For example, some intracellular stages (such as the amastigote form of Leishmania) are non-flagellated. 2. Parasites of Vertebrate and Invertebrate Hosts: They typically have complex life cycles involving both vertebrate (including humans) and invertebrate (arthropod) hosts, such as flies or bugs. They exist in different morphological forms in different hosts, often adapting their structure and behavior to suit their environment.  general characteristics cont... 3. Tissue or Bloodstream Inhabitants: Generally inhabit the tissues or bloodstream of their vertebrate hosts. Eg: Trypanosoma species live in the bloodstream or central nervous system, and Leishmania resides inside macrophages (immune cell). 4. Antigenic Variation: Some tissue flagellates, such as Trypanosoma brucei, are able to evade the host's immune system through antigenic variation. This means they can regularly change the proteins on their surface, preventing the host's immune system from mounting an effective response.  general characteristics cont... 5. Kinetoplast (in Kinetoplastids) Have a structure called the kinetoplast, which is a DNA-containing organelle associated with the mitochondrion and starting point for flagella 6. Intracellular and Extracellular Forms: Some tissue flagellates, like Leishmania, exist in both intracellular (inside host cells) and extracellular (outside host cells, in blood or tissue fluid) forms during different stages of their life cycle. 7. Transmission by Insect Vectors: These parasites are often transmitted by insect vectors (e.g., tsetse flies, sandflies, kissing bugs). The vector plays a critical role in their lifecycle by taking up the parasites from infected hosts and transmitting them to new ones.  tissue flagellates general life cycle Tissue flagellates When these The reside and reproduce vectors feed on a parasite within the gut of susceptible penetrates specific insect hosts vertebrate host at the feeding site Invades the Multiplies to blood and/or produce disease tissue of the new host  deVeloPmental forms of tissue flagellates Tissue flagellates pass through several distinct developmental forms during their life cycles. These forms differ in shape, structure, and the presence of flagella, depending on the host or vector they are in. Major developmental forms of tissue flagellates: Amastigote Promastigote Epimastigote Trypomastigote amastigote form Key Characteristics of Amastigotes: Shape: round or oval: Smaller than the other forms do not have the elongated, torpedo shape associated with motile forms. Lack of Flagellum: Therefore, they are non-motile. Intracellular: live and replicate inside host cell Inside host cells, amastigotes reproduce by binary fission. Found in Vertebrate Hosts: Amastigote is the only In diseases like leishmaniasis and Chagas disease, intracellular forms of all amastigotes are responsible for causing the symptoms leishmania species and of the disease, as they multiply inside cells, leading to Trypanosome cruzi. tissue damage.  Promastigote /lePtomonad/ forms Shape: Elongated (spindle like) Characteristic Size: Length = 15-20 microns Shape: Elongated, spindle-shaped (torpedo-like) Width = 1-2 microns Flagellum: Single flagellum at the anterior end equal or longer than the body length No undulating membrane Location: Found in sandfly vectors and introduced into the vertebrate host Function: Infective form transmitted by sandfly bites Replication: Multiplies by binary fission in the insect vector  ePimastigote /crithidial/ forms Shape: Elongated form Shape: Elongated, spindle-shaped Size: 15-20 microns long and Flagellum: Single flagellum attached to the slightly wider than promastigote, body, creating an undulating membrane Location: Found in the gut of triatomine bugs or salivary glands of tsetse flies Function: Replicative stage in the insect vector Development: Transforms into metacyclic trypomastigotes for transmission to vertebrate hosts  tryPomastigote /tryPanosomal/ forms Shape: ü Elongated form with highly polymorphism from rather short and stumpy Size: ü (15micron X 2-4micron) to a long slender (35micron X 2-4micron) Nucleus near middle kinetoplast is at the posterior end the flagellum and undulating membrane pass anteriorly along entire body length Free flagellum extends from anterior end when present stained blood film, Trypanosoma cruzi appears as C or U shape  tryPomastigote /tryPanosomal/ forms Size: ü (15micron X 2-4micron) to a Shape: Elongated, spindle-shaped (torpedo- long slender (35micron X 2- like) 4micron) Flagellum: Single flagellum at the posterior end Kinetoplast: Located at the posterior end of the cell Location: Found in the bloodstream of vertebrate hosts Function: Infective form responsible for disease symptoms Replication: Non-replicative in the bloodstream; infects host cells  comParison of deVeloPmental forms in tissue flagellates: Form Flagellu Kinetoplast Location Example Functions or m Position Diseases Amastigote No Central Intracellular (in tissues like Intracellular replication muscle or macrophages) (e.g., Chagas disease, leishmaniasis) Promastigote Yes Near anterior Insect vector (sandfly) Infective stage (e.g., leishmaniasis) Epimastigote Yes Near nucleus Insect vector (tsetse fly, Replicative stage in triatomine bug) vector Trypomastigote Yes Posterior Bloodstream of vertebrate Infective and circulating host; vector form (e.g., African sleeping sickness, Chagas disease)  leishmania sPecies Leishmania species cause a disease called Leishmaniasis There are 3 main forms of the disease: 1. Visceral leishmaniasis (VL), also known as kala-azar, is fatal if left untreated 2. Cutaneous leishmaniasis (CL) is the most common form and causes skin lesions, mainly ulcers, on exposed parts of the body. 3. Mucocutaneous leishmaniasis leads to partial or total destruction of mucous membranes of the nose, mouth and throat. leishmania sPecies life cycle leishmania troPica minor Geographical Distribution:- üWidely distributed in the urban area of Middle East, Europe, India, Eastern Mediterranean countries, Morocco, Algeria, Tunisia. Habitat: - üAmastigotes: In the endothelial cells of cutaneous tissues, lymph nodes, ulcers. üPromastigotes: In the gut of sandfly Morphology:- üIt has Amastigote and promastigote Stages only leishmania troPica minor Life Cycle:- ü Definitive host: Man ü Intermediate host: Female sandfly ü Reservoir host: Dog, cats, mice, etc. Mode of Transmission ü Inoculation by infected sandfly ü Direct contact with the ulcer Pathology Causes cuaneous leishmaniasis ü dry, urban, chronic, old world oriental sore At the site of bite - dry painless ulcer, 25-70mm in diameter, The infection is usually heals and confers long lasting immunity to reinfection. leishmania troPicam major Similar with Leishmania tropica minor except with the following differences: Geographical Distribution ü Wider distribution than Leishmania tropica minor and found in rural areas of sub-Saharan Africa from Senegal to central Sudan, Middle East, India, Pakistan, central Asia, North Africa. ü Infections are zoonotic (Disease Transmitted from Animals to Human) Clinical Feature and Pathology üCauses moist (wet), rural, acute, Old world cutaneous Leishmaniasis or oriental sore. leishmania aethioPica Similar with the previous leishmania except with the following differences Geographical distribution ü Southern Yemen, and the highlands of Ethiopia and Kenya Pathology: ü Causes old world coetaneous and diffuse cutaneous leishmaniasis.  l. troPica minor, l. troPica minor, l. aethioPica The three spps. have similar prevention and control, and laboratory diagnosis Prevention and Control Leishmania Species: 1. Avoid insect bites 2. Control of insect vectors 3. Protection of lesion from insect bites 4. Avoid auto-infection /self-infection 5. Treatment and health education Laboratory Diagnosis of Leishmania species:- 1. Amastigotes in stained smears taken from ulcers, lesions, nodules 2. Promastigotes in culture media. 3. Montenegroimmunologic/ leishmanin test. leishmania donoVani Geographical Distribution: ü India, Central Asia, China, Kenya, Sudan, Ethiopia, Somalia, Central and South America Habitat üAmastigotes: In the reticulo-endothelial cells of the visceral organs such as spleen, bone marrow, Lymph node, liver, kidney, lung, brain, CSF, whit blood cells, intestine, etc. üPromastigotes: In the gut of phlebotomus and Lytzomyia spps leishmania donoVani Pathology: vVisceral leishmaniasis or kala-azar. vMajor symptoms are üfever, chills, sweating, cough, diarrhoea, üvomiting, bleeding gums, weight loss, üsplenomegally, hepatomegally, ülemphadenopathy, hypopigmentation of skin  In Ethiopia, Ieishmaniasis is caused by four species of Leishmania, namely, Visceral leishmaniasis ü L. donovani, L.aethiopica, L.Major, L. Minor ü The former, L. donovoni, causes visceral leishmaniasis (VL) ü it is widely distributed throughout the lowlands of north-western Ethiopia (Asrat H and Frommel D, 1993). cutanceous leishmaniasis Cutanceous leishmaniasis (CL) with L. aethiopica prevailing in the highlands of Ethiopia.  tryPanosoma Geographical Distribution: üWest and western central Africa, extending from Senegal across to Sudan and down to Angola Trypanosoma brucei complex (group) üTrypanosoma brucei brucei - infective to animal but not humans üTrypanosoma brucei rhodesiense - causing acute Trypanosomiasis üTrypanosoma brucei gambiense - causing chronic Trypanosomiasis v All are morphologically indistinguishable. tryPanosoma gamBiense Habitat ü Trypomastigotes: In blood vessels and intercellular spaces of Lymph nodes, spleen, liver, Brain, CSF etc. ü Metacyclic trypomastigotes: In the mid and fore gut of the Glossina (tsetse flies) Life cycle ü It requires two hosts to complete its life cycle Glossina as an intermediate host Man and other animals as a reservoir host ü It reproduces asexually by binary fission. Life cycle of T. brucei complex tryPanosoma gamBiense Pathology Gambian trypanosomiasis or Chronic African sleeping sickness Major symptoms ü chancer, fever, haedache, sweating, ü post cervical enlargement of the lymph node(winter bottom’s sign), ü splenomegally, hepatomegally, meningoencephalilis, inability to speak, ü progressive mental dullness, excessive sleeping, weight loss, coma and death if untreated. tryPanosoma rhodesiense Geographical Distribution ü East Africa, Central Africa, and Southern Africa, extending from Ethiopia down to Botswana. Habitat üTrypomastigotes:- Mainly in the blood and CSF, also in lymphnodes, spleen, Brain etc üMetacyclic Trypomastigote:- In the mid and fore gut of the insect vector  tryPanosoma rhodesiense Pathology Rhodesiense trypanosomiasis or acute African sleeping sickness The major symptoms are similar to T.gambiense, But v Has short incubation period and rapid loss of weight v It is a zoonosis v Has low prevalence v Sporadic form of infection v More prevalent in male than in females  tryPanosoma cruzi Geographical distribution: üCentral and South America Habitat: üAmastigotes: Intracellular forms in the reticuloendothelial cells and tissues of brain, muscles, Lymph nodes, liver, Spleen, bone marrow, etc. üPromastigotes: Transitional stage üEpimastigotes: In the mid-gut of the insect vector (bug) üTrypomastige: In the mid-gut of the vector and; in the blood circulation and intercellular spaces of man. üMetacyclic Trypomastigote: In the mid gut and in the faeces of the insect vector  tryPanosoma cruzi Morphology ü Has all the developmental stages of haemoflagellates ü Amastigote stages are similar to amastigote stages of Leishmania species. ü The Trypomastigote are monomorphic forms about 2μm in size with “C” or “U” shape. Mode of Transmission of T. cruzi 1. Contact with the faeces of an infected blood sucking triatoma bug. 2. Blood transfusion. 3. Less commonly trans-placental transmission occurs with a fetus being infected from an asymptomatic mothers. 4. It can occur also if viable parasites (even very few) penetrate the skin, conjuctiva, or mucous membrane.  general life cycle of t.cruzi metacyclic (infective) trypomastigote trypomastgotes invade the contained in the faeces of an infected bug reticuloendothelial cells near the point (Triatoma) penetrate the skin at the bite of entry and multiply intracellularly site as amastigotes metacyclic trypomastigotes are amastigotes develop into formed in the hind gut of the bug. Trypomastigotes which are released into the blood when the cell ruptures Trypomastigotes transform in to triatomine bug vector ingests epimastigotes which multiply by circulating Trypomastigotes in a blood binary fission in the gut of the meal. vector  life cycle of tryPanosoma cruzi  tryPanosoma cruzi Pathology: ü Causes chaga’s disease Prevention and Control: üVector control, üimprovement of housing, ütreatment and health education. Laboratory Diagnosis: üBlood film -wet film for motility -thin and / or thick stained blood films üCulture of blood on blood agar slopes in the later stages of infection when facilities for xenodiagnosis is not available. üSerological diagnosis to detect anti- T.cruzi antibodies  grouP work 1. Relevance of Leishmaniasis in Ethiopia 2. Relevance of Trypanomiasis in Ethiopia 3. Relevance of Toxoplasmosis and Thrichomoniasis in Ethiopia 4. Relevance of Giardiasis in Ethiopia 5. Relevance of Malaria in urban areas of Ethiopia 6. Relevance of Malaria in rural areas of Ethiopia grouP work A review paper üStrictly follow the flow of a review paper format Presentation ü 10 slides within 5 minutes  class telosPoridea Do not possess any organells of the locomotion ü but they show change by sluggish amoeboid movement. They reproduce ü asexually by a process of sporulation called schizogony, ü sexually by union or syngamy called sporogony General Life Cycle Sporozoites → Trophozoites → Schizontes → Merozoites → Gametocytes → Gametes → Zygote → Ookinet → Oocyst  class telosPoridea Telosporidea Coccidiidea Haemosporidiidea Intestinal sprozoa Parasite of blood maturation oocyst occurs outside the body have sexual and asexual union in an in the passed faeces or in the soil insect & the definitive host infection of the host by contamination infection to man or other vertebrates by through the oral route. the bite of an insect vector, usually a The coccidiidea has the mosquito. ü family Eimeriidae Haemosporidiidea has three families: ü And two genera: ü Babasiidae, ü Eimearia ü Haemoproteidae and ü Isospora. ü Plasmociidae.  intestinal and tissue coccidian Parasites Isospora belli Cryptosporidium Parvum G. Distribution in the tropical and world wide subtropical countries Habitat: The epithelial cells of the small The epithelial cells of the intestine small intestine Life cycle complete its life cycle in a similar life cycle to I. single host. belli mature oocyst ingested, with man acquires infection contaminated food or drink from contaminated hand, food or drink. Pathology no disease or self limiting diarrheal disease in young gastroenteritis children  intestinal and tissue coccidian Parasites Cyclospora cayetanesis Pneumocystis carnii G.Distribution world wide world wide Habitat The epithelial cells of the small In the interstitial plasma cells of intestine the lung (alveoli, epithelial cells) of man and other animals Life Cycle It is transmitted by fecal-oral The complete life cycle of this route with infective oocyst parasite is unknown. being ingested. Pathology: prolonged diarrhea Causes a severe a typical interstitial plasma cell pneumonia, impaired ventilation, and death due to respiratory failure.  toxoPlasma gondii Geographical Distribution: ü World wide Habitat:- ü In the reticulo-endothelial cells of heart, lymph nodes, lung, spleen, bone marrow, mononuclear leukocytes, brain of man, domestic and wild animals Morphology: - There are five main developmental forms in the life cycle Trophozoite (toxoplasm) and cyst stages are found in man All other stages occur in the felines (cats).  toxoPlasma gondii Toxoplasm (trophozoite):-Two forms 1. Tachyzoite/endozoite ü occurs in the early acute stage of infection. ü Size: 3μm by 7 μm ü Shape: crescent or oval in shaped, one end is rounded and the other end is pointed ü Quickly multiplying forms that form pseudocyst (aggregation of a parasites inside a macrophage) 2. Bradyzoites/cryptozoites ü Occurs in the chronic stage of infection ü develops slowly and multiplies in the tissues to form a true cyst. Cyst:-10-100μm and may contain about 3,000 trophozoites  toxoPlasma gondii Life Cycle: ü Definitive host: Cat and Lynx ü Intermidiate host: Man and other animals ü The life cycle can be ü heteroxenous (requiring two hosts) monoxenous (one host). Both sexual and asexual reproduction occurs in cat But only sexual reproduction occurs in man. Mode of multiplication can be Endodyogony (repeated division in to two by internal budding), Ectomerogony (division in to several organisms simultaneously by external budding), Endopolygony (division into several organisms simultaneously by internal budding. toxoPlasma gondii Mode of Transmission 1. Ingestion of oocysts in food, drink, or hand contaminated with faeces of an infected cat. 2. Blood transfusion 3. Transplacental/congenital 4. Ingestion of cysts in raw or under cooked meat 5. Organ transplantation Pathology: Causes toxoplasmosis toxoPlasma gondii Major symptoms ü Fever, headache, splenomegally, lymphadenopathy, hydrocephales abortion, still birth. ü CNS toxoplasmosis is quite common in HIV/AIDS patient Prevention and Control 1. Avoid contamination of hand, food and water with the faeces of cat 2. Not eating raw or under cooked meat such as pork, mutton, beef 3. Screening of blood and organ of individuals for the parasites 4. Treatment and health education  haemosPoridia Malaria is the most important of all protozoan disease ü annually infects over 250 million individuals ü leading cause of illness and death in the developing world ü increasingly difficult to control because of Anopheline mosquito vector General Characteristics 1. Intracellular obligate parasites 2. Man is intermediate host. 3. Female Anopheles mosquitoes are the definitive hosts. 4. Those species which infect human being are P.vivax, P.falciparum, P.malariae, P.ovale and P. knowlesi 5. Infective stage to man from the insect vector is sporozoites and to the insect vector from man is gametocytes. haemosPoridia – Plasmodium Geographical Distribution ü Endemic to 85 countries ü 29 of the 85 countries accounted for 95% of malaria cases globally. P. falciparum in the hotter and more humid regions P.vivax in the temperate, subtropics and some parts of the tropics. Habitat Pre-erythrocytic - parenchyma cells of liver Erythrocytic phase - RBCs  haemosPoridia Morphology young troPhozoite (ring forms) P. falciparum P. vivax P. malariae P. ovale ü frequently found in ü Cytoplasm-circle, ü Cytoplasm - ü resemble blood film thin circle,thicker P.malariae ü Small rings ü Chromatin : fine ü Chromatin: one ü Chromatin : One ü double chromatin dot some times large red dot medium sized dot two ü Pigment: absent red dot ü Pigment: absent ü Pigment: absent. ü Pigment: absent  haemosPoridia morPhology mature troPhozoite P. falciparum P. vivax P. Malariae P. Ovale ü Rare in ü RBC enlarged ü RBC unaltered ü Size : Small peripheral blood ü Chromatin: Dots ü rounded shape ü Shape: Round ü RBC unaltered or threads of red ü Chromatin: round compact, very ü compact thin colour dot blue cytoplasm blue ring ü Pigment: Golden ü Pigment: dark ü Chromatin: One ü Chromatin: 1 or brown and brown or black, large red dot 2 red dots scattered often ü Pigment: -small ü Pigment: black concentrated at amount of brown or dense brown one edge pigment mass  haemosPoridia morPhology schizont P. falciparum P. vivax P. malariae P. ovale ü Not usually seen ü RBC much ü RBC unaltered ü small in peripheral enlarged ü Nearly fills RBCs ü segmented blood ü fills red blood ü Merozoites 6-12; ü Merozoites: 6- ü RBC unaltered cells average 8, 12; average 8 in ü Parasite about ü Amoeboid or ü Pigment: Brown a rosette 0.6RBC segmented aggregated in ü Pigment: Brown ü Merozoites: 8-32; ü Merozoites: 14- centre. average 24 24; average 16 ü Pigment: ü Pigment: Golden clumped black brown central loose mass  general life cycle of malaria Parasites Require two hosts to complete their life cycle vAnopheles mosquitoes - definitive host - sexual reproduction (sporogony) takes place vHuman being - intermediate host - asexual reproduction (schizogony) takes place. New Infection :- Sporozoites from infected female Anopheles mosquito with the saliva during blood meal Recrudescence :- Due to small number of erythrocytic parasites remaining in the blood after a previous attack - Occurs in Plasmodium falciparum and Plasmodium malariae Relapse :- Due to hypnozoite (dormant forms which precede schizont development in the liver) - Occur in vivax malaria and less commonly in Ovale malaria. 1. Anopheles mosquito inoculates sporozoites 2. Infection of the liver cells into the human host. Hepatocytes Schizont 3. Infection of RBCs 7. Transformation and Sporogenesis 5. mosquito ingests micro- and macro- 4. Production gametocytes of Gametes 6. Fertilization  modes of transmissions 1. Bite of infected female Anopheles mosquitoes. The main vectors in Ethiopia are An.gambiae, An.funestus, An.nili, An. arebiansis and An.pharonensis A. Infected person is bitten by B. Female Anopheles mosquito which then carry the Plasmodium parasites, in the form of sporozoites. C. The mosquito then bites a healthy person, (D, E) major symPtom The major symptom of malaria is fever usually that occurs in three stages, The malaria fever is due to the rupture of the infected red blood cells containing mature schizonte stage releasing ümalaria pigment, ütoxins, ümetabolic by products, üdebris of red blood cells and ümerozoites that can infect other red blood cells  leVel of Parasitaemia in the red Blood cells P.falciparum. üUp to 30-40% of the red blood cells can be infected, and üIt is considered as sever if more than 5% of RBC are infected. P.vivax. ü2% of the RBC can be infected P.ovale. ümore than 2% of the RBC can be infected P.malariae. Number of Merozoites § P.falciparum: 30,000 merozoites üup to 2% of the RBC can be infected Released From a Single § P.vivax: 10,000merozoites Pre-erythrocytic Schizonts § P.ovale : 15,000 merozoites § P.malariae : 15,000 merozoites Factors for Malignance of P.falciparum 1. Rapid multiplication 2. Infected red blood cells become "stick" 3. Infects all age group of red blood cells 4. A single red blood cell can be infected by more than one parasites 5. Erythrocytic schizogonic reproduction takes place in the deep capillaries of organs such as brain, lung, heart, spleen, bone marrow, placenta, intestine, etc  factors that ProVide Protection against malaria infections 1. Glucose-6-phosphate dehydrogenase deficiency , Scickle cell anemia Ovalocytosis and Adenosine tri-phosphate deficiency in non-immune black males provides protection against P.falciparum infection 2. Duffy blood group antigens (i.e., Fya and Fyb ) negative RBCs and Hemoglobin E provides protection against P.vivax infection. 3. Human fetal hemoglobin gives protection against all forms of malaria infection laBoratory diagnosis 1. Malaria parasites are detected in thin or thick blood films stained by wright’s stain, Giemsa stain, leishman stain or Field stain 2. Using a rapid immunodiagnostic tests 3. ELISA 4. PCR  PreVention and control 1. Avoid mosquito bites by ü Selecting healthy sites for houses and screening windows and doors with mosquito net. ü Using mosquito bed nets ü Wearing protective clothes such as long trouthers - Using mosquito repellents 2. Destroy adult mosquitoes by ü Indoor residual regular effective spraying 3. Preventing breeding of mosquitoes by ü Altering the habitat to discourage breeding ü Flooding or flushing of breeding places ü Drainage to remove surface water, filling in ponds, pot holes, etc. ü Spraying breeding places with effective chemicals particularly with larvicides Prevention Cont... 4. Using drugs to üPrompt diagnosis and treatment of malaria cases üPrevent infections using chemoprophilaxis, especially in non- immune persons visiting or going to malarious areas or in persons with reduced immunity such as pregnant women. 5. Health education. 6. Blood screening for malaria before providing for those who need blood BaBesia Parasites of domestic and wild animals vHumans are accidental hosts Transmitted by ixodid, or hard -bodied, ticks The organisms infect the red cells, they appear some what poleomorphic ring like structures. Most resembles ring stage of Plasmodia. The small parasites appearing much like P.falciparium It can be differentiated from malaria parasite by the absence of pigment in the infected erythrocytes. laBoratory diagnosis Human infection is diagnosed by üidentifying the intra-erythrocytic parasite in Giemsa -stained blood films. üalso diagnosed by serologic test with the indirect immunoflorescent antibody test; which is the most useful in diagnosis. class ciliatae (ciliates) Balantidium coil Geographical Distribution: üWorld wide being more commonly found amongst those who keep pigs, and uses pig faeces as fertilizer üIn Ethiopia it was reported from Debre Brahne Habitat: üTrophozoite and cyst in the large intestine of pig and rarely man  Balantidium coil - Morphology Trophozoite üSize: 50-200 μm by 40-70μm üShape: Oval, with one pole more rounded than the other. üMotility: Rapid motility, crossing the field in a definite direction and sometimes turning in circle. üCilia: Cover the whole body and many around the cytostome üNucleus: a large kidney shaped macronucleus and a small micronucleus.  Balantidium coil - Morphology Cyst üSize : 50-70μm, very large cyst /the size of a round worm egg. üShape: round üShell: thin double wall üNuclei: one large kidney shape macronucleus and one small Micronucleus beside the large nucleus. life cycle As soon as the thick wall cysts are excreted in the faeces, they are infective. Man acquires infection from contaminated food or drink or from hands contaminated with faeces. üFollowing ingestion, the cyst excyst in the intestine producing trophozoites veach cyst producing a single trophozoite. üThe ciliate multiply in the colon by simple binnary division Pig is the main reservoir host. Balantidium coil Pathogenicity:- ü It is the only ciliate that parasitize humans. üCauses balantidial dysentery Prevention and Control:- 1. Avoid contamination of food or drink. 2. Improving personal hygiene especially those who keep pigs. 3. Treatment and health education. Laboratory Diagnosis:- üFinding the tropozoites in dysenteric faecal specimens