General Parasitology PDF

General Parasitology Christine Alonzo Association between parasite and host: A parasite is a living organism, which takes its nourishment and other needs from a host; the host is an organism which supports the parasite. The parasites included in medical parasitology are protozoa, helminth...

General Parasitology Christine Alonzo Association between parasite and host: A parasite is a living organism, which takes its nourishment and other needs from a host; the host is an organism which supports the parasite. The parasites included in medical parasitology are protozoa, helminthes, and some arthropods. The hosts vary depending on whether they harbor the various stages in parasitic development.  Different Kinds of Parasites Ectoparasite – a parasitic organism that lives on the outer surface of its host, e.g. lice, ticks, mites etc. Endoparasites – parasites that live inside the body of their host, e.g. Entamoeba histolytica. Obligate Parasite - This parasite is completely dependent on the host during a segment or all of its life cycle, e.g. Plasmodium spp. Facultative parasite – an organism that exhibits both parasitic and non- parasitic modes of living and hence does not absolutely depend on the parasitic way of life, but is capable of adapting to it if placed on a host. E.g. Naegleria fowleri Accidental parasite – when a parasite attacks an unnatural host and survives. E.g. Hymenolepis diminuta (rat tapeworm). Erratic parasite - is one that wanders in to an organ in which it is not usually found. E.g. Entamoeba histolytica in the liver or lung of humans.  Different Kinds of Host Definitive host – a host that harbors a parasite in the adult stage or where the parasite undergoes a sexual method of reproduction. Intermediate host - harbors the larval stages of the parasite or an asexual cycle of development takes place. In some cases, larval development is completed in two different intermediate hosts, referred to as first and second intermediate hosts. Paratenic host – a host that serves as a temporary refuge and vehicle for reaching an obligatory host, usually the definitive host, i.e. it is not necessary for the completion of the parasites life cycle. Reservoir host – a host that makes the parasite available for the transmission to another host and is usually not affected by the infection. Natural host – a host that is naturally infected with certain species of parasite. Accidental host – a host that is under normal circumstances not infected with the parasite Three Common Symbiotic Relationship Mutualism an association in which both partners are metabolically dependent upon each other and one cannot live without the help of the other; however, none of the partners suffers any harm from the association. The protozoa, which depend entirely on a carbohydrate diet, acquire their nutrients from termites. In return they are capable of synthesizing and secreting cellulases; the cellulose digesting enzymes, which are utilized by termites in their digestion. Commensalism an association in which the commensal takes the benefit without causing injury to the host. E.g. Most of the normal floras of the humans’ body can be considered as commensals. Parasitism an association where one of the partners is harmed and the other lives at the expense of the other. E.g. Worms like Ascaris lumbricoides reside in the gastrointestinal tract of man, and feed on important items of intestinal food causing various illnesses. Effect of Parasites on the Host a. Direct effects of the parasites on the host Mechanical injury - may be inflicted by a parasite by means of pressure as it grows larger, e.g. Hydatid cyst causes blockage of ducts such as blood vessels producing infraction. Deleterious effect of toxic substances- in Plasmodium falciparum production of toxic substances may cause rigors and other symptoms. Deprivation of nutrients, fluids and metabolites -parasite may produce disease by competing with the host for nutrients. b. Indirect effects of the parasites on the host Immunological reaction: Tissue damage may be caused by immunological response of the host, e.g. nephritic syndrome following Plasmodium infections. Excessive proliferation of certain tissues due to invasion by some parasites can also cause tissue damage in man, e.g. fibrosis of liver after deposition of the ova of Schistosoma. Basic Concepts in Medical Parasitology Morphology includes size, shape, color and position of different organelles in different parasites at various stages of their development. This is especially important in laboratory diagnosis which helps to identify the different stages of development and differentiate between pathogenic and commensal organisms. For example, Entamoeba histolytica and Entamoeba coli. Geographical Distribution Even though revolutionary advances in transportation has made geographical isolation no longer a protection against many of the parasitic diseases, many of them are still found in abundance in the tropics. Distribution of parasites depends upon: Geographical Distribution a. The presence and food habits of a suitable host: Host specificity, for example, Ancylostoma duodenale requires man as a host where Ancylostoma caninum requires a dog. Food habits, e.g. consumption of raw or undercooked meat or vegetables predisposes to Taeniasis Geographical Distribution b. Easy escape of the parasite from the host- the different developmental stages of a parasite which are released from the body along with faeces and urine are widely distributed in many parts of the world as compared to those parasites which require a vector or direct body fluid contact for transmission. Geographical Distribution c. Environmental conditions favoring survival outside the body of the host, i.e. temperature, the presence of water, humidity etc. d. The presence of an appropriate vector or intermediate host – parasites that do not require an intermediate host (vector) for transmission are more widely distributed than those that do require vectors. Life Cycle of Parasites the route followed by a parasite from the time of entry to the host to exit, including the extracorporeal (outside the host) life. It can either be simple, when only one host is involved, or complex, involving one or more intermediate hosts. A parasite’s life cycle consists of two common phases one phase involves the route a parasite follows inside the body. This information provides an understanding of the symptomatology and pathology of the parasite. In addition, the method of diagnosis and selection of appropriate medication may also be determined. The other phase, the route a parasite follows outside of the body, provides crucial information pertinent to epidemiology, prevention, and control. Host Parasite Relationship Host parasite relationship - infection is the result of entry and development within the body of any injurious organism regardless of its size. Once the infecting organism is introduced into the body of the host, it reacts in different ways and this could result in: a. Carrier state - a perfect host parasite relationship where tissue destruction by a parasite is balanced with the host’s tissue repair. At this point the parasite and the host live harmoniously, i.e. they are at equilibrium. b. Disease state - this is due to an imperfect host parasite relationship where the parasite dominates the upper hand. It can result either from lower resistance of the host or a higher pathogenicity of the parasite. c. Parasite destruction – occurs when the host takes the upper hand. Laboratory Diagnosis a) Blood – in those parasitic infections where the parasite itself in any stage of its development circulates in the blood stream, examination of blood film forms one of the main procedures for specific diagnosis. For example, in malaria the parasites are found inside the red blood cells. In Bancroftian and Malayan filariasis, microfilariae are found in the blood plasma. Laboratory Diagnosis b) Stool – examination of the stool forms an important part in the diagnosis of intestinal parasitic infections and also for those helminthic parasites that localize in the biliary tract and discharge their eggs into the intestine. In protozoan infections, either trophozoites or cystic forms may be detected; the former during the active phase and the latter during the chronic phase. Example, Amoebiasis, Giardiasis, etc. In the case of helmithic infections, the adult worms, their eggs, or larvae are found in the stool. Laboratory Diagnosis c) Urine – when the parasite localizes in the urinary tract, examination of the urine will be of help in establishing the parasitological diagnosis. For example in urinary Schistosomiasis, eggs of Schistosoma haematobium are found in the urine. In cases of chyluria caused by Wuchereria bancrofti, microfilariae are found in the urine. Laboratory Diagnosis d) Sputum – examination of the sputum is useful in the following: In cases where the habitat of the parasite is in the respiratory tract, as in Paragonimiasis, the eggs of Paragonimus westermani are found. In amoebic abscess of lung or in the case of amoebic liver abscess bursting into the lungs, the trophozoites of E. histolytica are detected in the sputum. Laboratory Diagnosis e) Biopsy material - varies with different parasitic infections. For example spleen punctures in cases of kala-azar, muscle biopsy in cases of Cysticercosis, Trichinelliasis, and Chagas’ disease, Skin snip for Onchocerciasis. f) Urethral or vaginal discharge – for Trichomonas vaginalis Laboratory Diagnosis Indirect evidences – changes indicative of intestinal parasitic infections are: a. Cytological changes in the blood – eosiniphilia often gives an indication of tissue invasion by helminthes, a reduction in white blood cell count is an indication of kala-azar, and anemia is a feature of hookworm infestation and malaria. b. Serological tests – are carried out only in laboratories where special antigens are available. Treatment Many parasitic infections can be cured by specific chemotherapy. The greatest advances have been made in the treatment of protozoal diseases. For the treatment of intestinal helminthiasis, drugs are given orally for direct action on the helminthes. To obtain maximum parasiticidal effect, it is desirable that the drugs administered should not be absorbed and the drugs should also have minimum toxic effect on the host. Prevention and Control Measures may be taken against every parasite infectiving humans. Preventive measures designed to break the transmission cycle are crucial to successful parasitic eradication. Such measures include: Prevention and Control ƒReduction of the source of infection- the parasite is attacked within the host, thereby preventing the dissemination of the infecting agent. Therefore, a prompt diagnosis and treatment of parasitic diseases is an important component in the prevention of dissemination. ƒSanitary control of drinking water and food. ƒProper waste disposal – through establishing safe sewage systems, use of screened latrines, and treatment of night soil. ƒThe use of insecticides and other chemicals used to control the vector population. ƒProtective clothing that would prevent vectors from resting in the surface of the body and inoculate pathogens during their blood meal. ƒGood personal hygiene. ƒAvoidance of unprotected sexual practices. Classification of Medical Parasitology Parasites of medical importance come under the kingdom called protista and animalia. Protista includes the microscopic single-celled eukaroytes known as protozoa. Helminthes are macroscopic, multicellular worms possessing well differentiated tissues and complex organs belonging to the kingdom animalia. Medical Parasitology is generally classified into: Classification of Medical Parasitology Medical Protozoology - Deals with the study of medically important protozoa. Medical Helminthology - Deals with the study of helminthes (worms) that affect man. Medical Entomology - Deals with the study of arthropods which cause or transmit disease to man. PROTOZOA Protozoa Protozoan parasites consist of a single "cell-like unit" which is morphologically and functionally complete and can perform all functions of life. They are made up of a mass of protoplasm differentiated into cytoplasm and nucleoplasm. The cytoplasm consists of an outer layer of hyaline ectoplasm and an inner voluminous granular endoplasm. The ectoplasm functions in protection, locomotion, and ingestion of food, excretion, and respiration. In the cytoplasm there are different vacuoles responsible for storage of food, digestion and excretion of waste products. The nucleus also functions in reproduction and maintaining life. Protozoa The protozoal parasite possesses the property of being transformed from an active (trophozoite) to an inactive stage, losing its power of motility and enclosing itself within a tough wall. The protoplasmic body thus formed is known as a cyst. At this stage, the parasite loses its power to grow and multiply. The cyst is the resistant stage of the parasite and is also infective to the human host. Reproduction 1. Asexual multiplication: (a) Simple binary fission – in this process, after division of all the structures, the individual parasite divides either longitudinally or transversely into two more or less equal parts. (b) Multiple fission or schizogony – in this process more than two individuals are produced, e.g. asexual reproduction in Plasmodia. Reproduction 2. Sexual reproduction: (a) Conjugation – in this process, a temporary union of two individuals occurs during which time interchange of nuclear material takes place. Later on, the two individuals separate. (b) Syngamy – in this process, sexually differentiated cells, called gametes, unite permanently and a complete fusion of the nuclear material takes place. The resulting product is then known as a zygote. Occurrence of Protozoa Protozoa are found in all moist habitats. They are common in sea, in soil and in fresh water. These organisms occur generally as a single cell. Colonies of protozoa might also occur in which individual cells are joined by cytoplasmic threads and form aggregates of independent cells. Occurrence of Protozoa However, distinct types of protozoa, include a resistant cyst (non-motile) stage to survive adverse environmental conditions, such as desiccation, low nutrient supply, and even anaerobiosis. For example, the soil amoeba, Naegleria is a resistant cyst in dry weather, a naked amoeba in moist soil, and becomes flagellated when flooded with water. Morphology of Protozoa Protozoa are predominantly microscopic, ranging in size from 2 to more than 100μm. Morphologically, they are within a mass of protoplasm, consisting of a true membrane – bound nucleus and cytoplasm. The nucleus contains clumped or dispersed chromatin and central nucleolus or karyosome, which are useful structures to distinguish protozoan species from one another based on the shape, size and distribution of these structures. Importance of Protozoa Protozoa serve as an important link in the food chain and ecological balance of man communities in wetland & aquatic environments. They are also important in biological sewage treatment, which involves both anaerobic digestion and/or aeration. In addition, protozoa are important laboratory organisms in research areas, by which their asexual reproduction enables clones to be established with the same genetic make-up. These are useful in the study of cell cycles and nucleic acid biosynthesis during cell division. Transmission In most parasitic protozoa, the developmental stages are often transmitted from one host to another within a cyst. The reproduction process is also related to the formation of the cyst. Asexual reproduction of some ciliates and flagellates is associated with cyst formation, and sexual reproduction of Sporozoa invariably results in a cyst. Pathogenic protozoa can spread from one infected person to another by: Faecal – oral transmission of contaminated foods and water. Insect bit inoculums or rubbing infected insect faeces on the site of bite. Sexual intercourse Pathogenesis Protozoan organisms are virtually always acquired from an exogenous source, and as such, they have evolved numerous ways to enter the body of the human host. Factors that are important for pathogenicity include: Attachment to the host tissue followed by replication to establish colonization. Toxic products released by parasitic protozoa. Shifting of antigenic expression to evade the immune response and inactivate host defenses. Antiprotozoal Agents Generally the antiprotozoal agents target relatively rapidly proliferating, young, growing cells of the parasite. Most commonly, these agents target nucleic acid synthesis, protein synthesis, or specific metabolic pathways (e.g. folate metabolism) unique to the protozoan parasites. Amoebiasis Amoebas primitive unicellular microorganisms with a relatively simple life cycle which can be divided into two stages: Trophozoite – actively motile feeding stage. Cyst – quiescent, resistant, infective stage. Their reproduction is through binary fission, e.g. splitting of the trophozoite or through the development of numerous trophozoites with in the mature multinucleated cyst. Motility is accomplished by extension of pseudopodia (“false foot”) Entamoeba hystolica (Morphological Features) (a) Trophozoites Viable trophozoites vary in size from about 10-60μm in diameter. Motility is rapid, progressive, and unidirectional, through pseudopods. The nucleus is characterized by evenly arranged chromatin on the nuclear membrane and the presence of a small, compact, centrally located karyosome. The cytoplasm is usually described as finely granular with few ingested bacteria or debris in vacuoles. In the case of dysentery, however, RBCs may be visible in the cytoplasm, and this feature is diagnostic for E.histolytica. Entamoeba hystolica (Morphological Features) (b) Cyst Cysts range in size from 10-20μm. The immature cyst has inclusions namely; glycogen mass and chromatoidal bars. As the cyst matures, the glycogen completely disappears; the chromotiodials may also be absent in the mature cyst. Life Cycle Intestinal infections occur through the ingestion of a mature quadrinucleate infective cyst, contaminated food or drink and also by hand to mouth contact. It is then passed unaltered through the stomach, as the cyst wall is resistant to gastric juice. Life Cycle In terminal ileum (with alkaline pH), excystation takes place. Trophozoites being actively motile invade the tissues and ultimately lodge in the submucous layer of the large bowel. Here they grow and multiply by binary fission. Trophozoites are responsible for producing lesions in amoebiasis. Invasion of blood vessels leads to secondary extra intestinal lesions. Gradually the effect of the parasite on the host is toned down together with concomitant increase in host tolerance, making it difficult for the parasite to continue its life cycle in the trophozoite phase. A certain number of trophozoites come from tissues into lumen of bowel and are first transformed into pre-cyst forms. Pre-cysts secret a cyst wall and become a uninucleate cyst. Eventually, mature quadrinucleate cysts form. These are the infective forms. Both mature and immature cysts may be passed in faeces. Immature cysts can mature in external environments and become infective. Pathogenesis Trophozoites divide and produce extensive local necrosis in the large intestine. Invasion into the deeper mucosa with extension into the peritoneal cavity may occur. This can lead to secondary involvement of other organs, primarily the liver but also the lungs, brain, and heart. Extraintestinal amebiasis is associated with trophozoites. Amoebas multiply rapidly in an anaerobic environment, because the trophozoites are killed by ambient oxygen concentration. Epidemiology E.histolytica has a worldwide distribution. Although it is found in cold areas, the incidence is highest in tropical and subtropical regions that have poor sanitation and contaminated water. About 90% of infections are asymptomatic, and the remaining produces a spectrum of clinical syndrome. Patients infected with E.hisolytica pass non-infectious trophozoites and infectious cysts in their stools. Therefore, the main source of water and food contamination is the symptomatic carrier who passes cysts. Symptomatic amebiasis is usually sporadic. The epidemic form is a result of direct person-to-person faecal-oral spread under conditions of poor personal hygiene. Non-pathogenic protozoa 1. Entamoeba gingivalis- is a commensal living primarily on exudate from the margins of gums and thrives best on unhealthy gums. Can be transferred by kissing, using contaminated utensils, droplet spray of the mouth. Can be treated or prevented by proper care of the teeth and gums. 2. Entamoeba coli- transmitted through fecal contamination, personal hygiene Non-pathogenic protozoa 3. Endolimax nana- lumen dweller in the large intestine, results from ingestion of viable cyst in polluted water of contaminated food. 4. Iodamoeba buetschili- natural habitat is the lumen of the large intestine, the principal site probably being the caecum. Natural parasite of man and lower primates. Symptoms of Amoebiasis 1. Diarrhea/Dysentery 2. Nausea 3. Abdominal Pain 4. Vomiting Mastigophora (Pathogenic Flagellates) A phylum of protozoans comprising non-photosynthetic, chiefly free-living flagellates. This protist move with a whip like extension called flagella. Flagellates are unicellular microorganism. Three Groups of Flagellates 1. Luminal Flagellates- Giradia lambia, Dientamoeba fragilis 2. Hemoflagellates- Trypanosoma sp., Leishmania sp. 3. Genital Flagellates- Trichomonas vaginalis- causes trichomoniasis Trichomonas vaginalis - The trophozoite is found in the urethra and vagina of women and in the urethra and prostate gland of men. - After introduction by sexual intercourse, proliferation begins w/c results in the inflammation and large numbers of trophozoite in the tissues and secretions. Trichomonas vaginalis Symptoms: - Vaginal/vulval discharge is often sudden and occurs during or after menstruation as a result of increased vaginal acidity. - Vaginal secretions: greenish or yellowish and foul odor Trichomonas vaginalis Male: - Infection in the male may be latent, with no symptoms, or may be present as self limited, persistent, or recurring urethritis. Epidemiology - Sexual intercourse is the primary mode of transmission; - By using toilet articles, clothing or underwear; - Infants may be infected by passage through mother’s infected birth canal Clinical Disease Trichomoniasis - Women have a scanty, watery vaginal discharge; - Symptomatic cases vaginitis occurs with more extensive inflammation; - Erosion of epithelial lining; - Painful urination - Results to symptomatic vaginal discharge, vulvitis and dysuria Prevention 1. Both make and female sex partners must be treated to avoid reinfection. 2. Good personal hygiene, avoidance of shared toilet articles and clothing. 3. Safe sexual practice. Tryconympha - A symbiotic flagellate of many species of termites and of the wood-feeding cockroach. - Stays on the gut of termites.  COCCIDA (SPOROZOA) “Apicomplexa” - Are members of the class sporozoan, Phylum Apicomplexa - Protozoans with spores (spore forming protozoa) - Intracellular parasites - Majority are parasitic - Paracitized blood and other body fluids FOUR Species (Humans) of Malaria 1. Plasmodium falciparum 2. Plasmodium vivax 3. Plasmodium ovale 4. Plasmodium malariae Life Cycle of Malaria - The life cycle of malaria is passed in to two host (alteration of hosts) and has sexual and asexual stage (alteration of generations). - Vertebrate Host- man (intermediate host), where the asexual cycle takes place. The parasites multiplies by schizogony and there is formation of male and female gametocytes (gametogony). - Invertebrate Host- most (definitive host) where the asexual cycle takes place. Union of male and female gametes ends in the formation of sporozoites (sporogony) Four Stages of Life Cycle 1. Pre-erythrocytic Schizogony - Sporozoites reach the blood stream and within 30 minutes enter the parenchymal cells of the liver, initiating a cycle of schizogony. - Multiplication occurs in tissue schizonts to form thousands of tiny merozoites. - Merozoites are then liberated on rupture on schizonts about 7th-9th day of the bites and enter into the blood stream. - Invade the RBC’s or other parenchymal liver cells. 2. Erythrocytic Schizogony (Blood Phase) - Completed in 48 hours in P. vivax, P. ovale, and P. falciparum, 72 hours in P. malariae. - Merozoites reinvade fresh RBC’s repeating the schizogonic cycles. 3. Erythrocytic Merozoites - Do not reinvade the liver cells - Malaria transmitted by blood transfusion reproduces only erythrocytic cycle. - Gametogony- some merozoites that invade RBC’s develop into sexual stages (male and female gametocytes) - These undergo no further development until taken by the mosquito 4. Sporogony (extrinsic cycle in mosquito) - When a female Anopheles mosquito vector bites and infected person, it sucks blood containing the different stages of malaria parasite. - All stages other than gametocytes are digested in the stomach. Four Species of Malaria 1. Plasmodium falciparum - The most important Plasmodium spp.; - Known as the malignant tertian malaria; - Occurs almost exclusively in tropical and subtropical regions; - Weather ( rainfall, temperature , humidity) is the most obvious cause of seasonality in malaria transmission; - Drug-resistant infection in P. falciparum is a challenge; - The common cause of epidemic disease. Clinical Features - It has the shortest incubation period, which ranges from 7 to 10 days. - Rapidly produces daily chills and fever as well as severe nausea, vomiting, and diarrhea. - The period of attacks become tertian (36-48 hours) before disease develops. - Involvement of the brain (cerebral malaria) that can result to coma and death. - Kidney damage is also associated resulting in the illness called black water fever. - Liver involvement is characterized by abdominal pain, vomiting of bile, hepatosplenomegaly, severe diarrhea, and rapid dehydration. 2. Plasmodium vivax - Is selective in that it invades only young immature erythrocytes. - Characteristics of infections: - Infected RBC are usually enlarged and contain numerous pink granules of schuffner's dot. - The trophozoite is ring-shaped but ameboid in appearance. - More mature trophozoites a d erythrocytic schizonts containing up to 24 merozoites are present. - The gametocytes are round. Epidemiology - The most prevalent of the human plasmodia with the widest geographic distribution including the tropics, subtropic, and temperate regions. - The second most prevalent in Ethiopia following P. falciparum. Clinical Features - After incubation period (usually 10 to 17 days), the patient/s will experience vague flu-like symptoms: headache, muscle pain, photophobia, anorexia, nausea, and vomiting. - The paroxysms may remain relatively mild or may progress to severe attacks with hours of sweating, chills, shaking persistently, high temperatures (103°F to 106°F) and exhaustion. 3. Plasmodium ovale - Distributed primarily in tropical Africa. - It is also found in Asia and South America Clinical Features - The incubation period is 16-18 days but can be longer. - Clinically, P. ovale malaria resembles P. vivax with attacks reaccurring 48-50 hours. 4. Plasmodium malariae - In contrast with P. vivax and P. ovale, P. malariae can infect only mature erythrocytes with relatively rigid cell membranes. - The parasite’s growth must conform to the size and shape of RBC. - Benign tertian Malaria Epidemiology - Infection occurs primarily in the same sub-tropical and temperate regions as infections with the other plasmodia but is less prevalent. Clinical Features - The incubation period for P. malariae is the longest of the plasmodia. - Early symptoms are: - flu-like with fever patterns of 72 hours (quartan or malarial) in periodicity. Prevention 1. Chemoprophylaxis and prompt diagnosis and treatment. 2. Control of mosquito breeding. 3. Protection of insect bite by screening, netting and protective clothing. 4. Used of insect repellents. Other Coccidian Parasites Toxoplasma gondii - Causes toxoplasmosis - Definitive host is the domestic cat and other felines - Humans and other mammals are intermediate host. - Usually acquired by ingestion and transplacental transmission from an infected mother to the fetus can occur. - Human-to-human transmission other than transplacental transmission, does not occur. - After infection the intestinal epithelium, the organisms spread to other organs, especially in the brain, lungs, liver, and eyes. - Congenital infection can result in abortion, still birth, or neonatal disease with encephalitis, chorioretinitis, and hepatosplenomegaly. - Can cause mental retardation. Transmission/Prevention 1. Arthropods are natural transmitters like cockroach and housefly. 2. Avoid kissing, sleeping, eating food contaminated by cat faeces. 3. Can be acquired by eating raw meat. 4. Avoid drinking raw milk (cows milk) 5. Cook food properly. STAGES: CYST—OOCYST—TROPHOZOITE Life Cycle of Plasmodium spp. - Anopheles- mosquito that transmit malaria - Note: all species of malaria should go to the liver - Exoerythrocytic cycle- cycle growing outside the red blood cell - Only P. falciparum will go out the liver and will not go back, will invade RBC - Mosquito needs to suck blood for their egg production. - Chilling coincides with rupturing of RBC Gametocytogenesis - Production of male and female gametocytes. - It needs to suck male and female gametes to undergo gametocytogenesis. - Female mosquito- feeds on blood - Male mosquito- feeds on fruit juices - They bite from 9pm to 4am - They will rest of cling on the wall Pathogenic Flagellates Flagellates - Flagellates are unicellular microorganisms. - Their locomotion is by lashing a tail-like appendage called a flagellum or flagella; and - Reproduction is by simple binary fission. Three Groups of Flagellates: 1. Luminal flagellates Giardia lamblia Dientmoeab fragilis 2. Hemoflagellates Trypanosoma species. Leishmania species. 3. Genital flagellates Trichomonas vaginalis Giardia lamblia Important Features: - The life cycle consists of two stages, the trophozoite and cyst. - The trophozoite is 9-12 μm long and 5-15μm wide anteriorly. - It is bilaterally symmetrical, pear-shaped with two nuclei (large central karyosome), four pairs of flagella, two axonemes, and a suction disc with which it attaches to the intestinal wall. - The oval cyst is 8-12μm long and7-10μm wide, thick- walled with four nucleus and several internal fibera. - Each cyst gives rise to two trophozoites during excystation in the intestinal tract. - Transmission is by ingestion of the infective cyst. Life Cycle Pathogenesis Infection with G. lamblia is initiated by ingestion of cysts. Gastric acid stimulates excystation, with the release of trophozoites in duodenum and jejunum. The trophozoites can attach to the intestinal villi by the ventral sucking discs without penetration of the mucosa lining, but they only feed on the mucous secretions. In symptomatic patients, however, mucosa-lining irritation may cause increased mucous secretion and dehydration. Metastatic spread of disease beyond the GIT is very rare. Epidemiology Giardia lamblia has a worldwide distribution, particularly common in the tropics and subtropics. It is acquired through the consumption of inadequately treated contaminated water, ingestion of contaminated uncooked vegetables or fruits, or person-to-person spread by the faecal-oral route. The cyst stage is resistant to chlorine in concentrations used in most water treatment facilities. Infection exists in 50% of symptomatic carriage, and reserves the infection in endemic form. Clinical Features Clinical disease: Giardiasis Symptomatic giardiasis ranges from mild diarrhea to severe malabsorption syndrome. Usually, the onset of the disease is sudden and consists of foul smelling, watery diarrhea, abdominal cramps, flatulence, and steatorrhoea. Blood & pus are rarely present in stool specimens, a feature consistent with the absence of tissue destruction. Immunity The humoral immune response and the cellular immune mechanism are involved in giardiasis. Giardia – specific IgA is particularly important in both defense against and clearance of parasite. Laboratory Diagnosis Examination of diarrhoeal stool- trophozoite or cyst, or both may be recovered in wet preparation. In examinations of formed stool (e.g. in asymptomatic carriers) only cysts are seen. Giardia species may occur in “showers”, i.e. many organisms may be present in the stool on a given day and few or none may be detected the next day. Therefore one stool specimen per day for 3 days is important. Laboratory Diagnosis If microscopic examination of the stool is negative in a patient in whom giardiasis is highly suspected duodenal aspiration, string test (entero-test), or biopsy of the upper small intestine can be examined. In addition to conventional microscopy, several immunologic tests can be implemented for the detection of parasitic antigens. Figure 5; Giardia lamblia tphozoite (A), cyst (B) Treatment For asymptomatic carriers and diseased patients the drug of choice is quinacrine hydrochloride or metronidazole. Prevention - Asymptomatic reservoirs of infection should be identified & treated. - Avoidance of contaminated food and water. - Drinking water from lakes and streams should be boiled, filtered and/or iodine treated. - Proper waste disposal and use of latrine. Trichomonas vaginalis Important features- it is a pear-shaped organism with a central nucleus and four anterior flagella; and undulating membrane extends about two-thirds of its length. It exists only as a trophozoite form, and measured 7-23μm long & 5-15μm wide. Transmission is by sexual intercourse. Life Cycle Pathogenesis The trophozoite is found in the urethra & vagina of women and the urethra & prostate gland of men. After introduction by sexual intercourse, proliferation begins which results in inflammation & large numbers of trophozoites in the tissues and the secretions. The onset of symptoms such as vaginal or vulval pruritus and discharge is often sudden and occurs during or after menstruation as a result of the increased vaginal acidity. The vaginal secretions are liquors, greenish or yellowish, sometimes frothy, and foul smelling. Infection in the male may be latent, with no symptoms, or may be present as self limited, persistent, or recurring urethritis. Epidemiology This parasite has worldwide distribution, and sexual intercourse is the primary mode of transmission. Occasionally, infections can be transmitted by fomites (toilet articles, clothing), although this transmission is limited by liability of the trophozoite. Rarely, Infants may be infected by passage through the mother’s infected birth canal. The prevalence of this flagellate in developing countries is reported to be 5% –20% in women and 2% –10% in men. Clinical Features Clinical disease - trichomoniasis. Most infected women at the acute stage are asymptomatic or have a scanty, watery vaginal discharge. In symptomatic cases vaginitis occurs with more extensive inflammation, along with erosion of epithelial lining, and painful urination, and results in symptomatic vaginal discharge, vulvitis and dysuria. Immunity The infection may induce humoral, secretory, and cellular immune reactions, but they are of little diagnostic help and do not appear to produce clinically significant immunity. Laboratory Diagnosis In females, T.vaginalis may be found in urine sediment, wet preparations of vaginal secretions or vaginal scrapings. In males it may be found in urine, wet preparations of prostatic secretions or following massage of the prostate gland. Contamination of the specimen with faeces may confuse T.vaginalis with T.hominis. Treatment Metronidazole is the drug of choice. If resistant cases occur, re- treatment with higher doses is required. Prevention - Both male & female sex partners must be treated to avoid reinfection - Good personal hygiene, avoidance of shared toilet articles & clothing. - Safe sexual practice. Dientamoeba fragilis Dientamoeba fragilis was initially classified as an amoeba; however, the internal structures of the trophoziote are typical of a flagellate. No cyst stage has been described. The life cycle and mode of transmission of D. fragilis are not known. It has worldwide distribution. Dientamoeba fragilis Transmission by faecal- oral routes does occur. Most infection with D. fragilis is asymptomatic, with colonization of the cecum and upper colon. However, some patients may develop symptomatic disease, consisting of abdominal discomfort, flatulence, intermittent diarrhea, anorexia, and weight loss. The therapeutic agent of choice for this infection is iodoquinol, with tetracycline andparmomycine as acceptable alternatives. The reservoir for this flagellate and lifecycle are unknown. Thus, specific recommendation for prevention is difficult. However, infection can be avoided by maintenance of adequate sanitary conditions. Other Flagellates inhabiting the Alimentary Canal Trichomonas hominis Trichomonas hominis – The trophozoites live in the caecal area of the large intestine and feed on bacteria. It is considered to be non-pathogenic, although it is often recovered from diarrheic stools. Since there is no known cyst stage, transmission probably occurs in the trophic form. There is no indication of treatment. Trichomonas tenax Trichomanas tenax – was first recovered from the mouth, specifically in tartar from the teeth. There is no known cyst stage. The trophozoite has a pyriform shape and is smaller and more slender than that of T.hominis. Diagnosis is based on the recovery of the organism from the teeth, gums, or tonsillar crypts, and no therapy is indicated. Chilomastix mesnli Chilomastix mesnli – has both a trophozoite and cyst stage. It normally lives in the cecal region of the large intestine, where the organism feeds on bacteria and debris. It is considered to be a non-pathogenic, and no treatment is recommended. Hemoflagellates Leshmania Species Clinical disease - Veseral leishmaniasis - Cutaneous leishmaniasis - Mucocutaneous leishmaniasis The species of leishmania exist in two forms, amastigote (aflagellar) and promastigote (flagellated) in their life cycle. They are transmitted by certain species of sand flies (Phlebotomus & Lutzomyia) Visceral donovani Important features- the natural habitat of L.donovani in man is the reticuloendothelial system of the viscera, in which the amastigote multiplies by simple binary fission until the host cells are destroyed, whereupon new macrophages are parasitized. In the digestive tract of appropriate insects, the developmental cycle is also simple by longitudinal fission of promastigote forms. The amastigote stage appears as an ovoidal or rounded body, measuring about 2-3μm in length; and the promastigotes are 15- 25μm lengths by 1.5-3.5μm breadths. Pathogenesis In visceral leishmaniasis, the organs of the reticuloendothelial system (liver, spleen and bone marrow) are the most severely affected organs. Reduced bone marrow activity, coupled with cellular distraction in the spleen, results in anemia, leukopenia and thrombocytopenia. This leads to secondary infections and a tendency to bleed. The spleen and liver become markedly enlarged, and hypersplenism contributes to the development of anemia and lymphadenopathy also occurs. Increased production of globulin results in hyperglobulinemia, and reversal of the albumin-to-globulin ratio. Epidemiology L. donovani donovani, infection of the classic kala-azar (“black sickness”) or dumdum fever type occurs in many parts of Asia, Africa and Southeast Asia. Kala-azar occurs in three distinct epidemiologic patterns. In Mediterranean basin (European, Near Eastern, and Africa) and parts of China and Russia, the reservoir hosts are primarily dogs & foxes; in sub-Saharan Africa, rats & small carnivores are believed to be the main reservoirs. In India and neighborin countries (and Kenya), kala-azar is anthroponosis, i.e. there is no other mammalian reservoir host other than human. The vector is the Phlebotomus sand fly. Other variants of L. donovani are also recognized: L. donovani infantum with similar geographical distribution, reservoir host and vector; with L. donovani donovani. L. donovani chagasi is found in South America, Central America, especially Mexico, and the West Indies. Reservoir hosts are dogs, foxes, and cats, and the vector is the Lutzomiya sand fly. Clinical Features Symptoms begin with intermittent fever, weakness, and diarrhea; chills and sweating that may resemble malaria symptoms are also common early in the infection. As organisms proliferate & invade cells of the liver and spleen, marked enlargement of the organs, weight loss, anemia, and emaciation occurs. With persistence of the disease, deeply pigmented, granulomatous lesion of skin, referred to as post-kala-azar dermal leishmaniasis, occurs. Untreated visceral leishmaniasis is nearly always fatal as a result of secondary infection. Immunity Host cellular and humoral defense mechanisms are stimulated. Laboratory Diagnosis Examination of tissue biopsy, spleen aspiration, bone marrow aspiration or lymph node aspiration in properly stained smear (e.g. Giemsa stain). The amastigotes appear as intracellular & extra cellular L. donovan (LD) bodies. Culture of blood, bone marrow, and other tissue often demonstrates the promastigote stage of the organisms. Serologic testing is also available. Treatment The drug of choice is sodium stibogluconate, a pentavalent antimonial compound. Alternative approaches include the addition of allopurinol and the use of pentamidine or amphotercin B. Prevention Prompt treatment of human infections and control of reservoir hosts. Protection from sand flies by screening and insect repellents. Tripanosomiasis Tripanosomiasis Etiologic agents Trypanosoma brucei complex – African trypanosomiasis (sleeping sickness) Trypanosoma cruzi – American trypanosomiasis (Chagas’ disease) Important Features These species may have amastigote, promastigote, epimastigote, and trypomastigote stages in their life cycle. In human trypanosomes of the African form, however, the amastigote and promastigote stages of development are absent. Typical trypanosome structure is an elongated spindle-shaped body that more or less tapers at both ends, a centrally situated nucleus, a kinetoplast posterior to nucleus, an undulating membrane arising from the kinetoplast and proceeding forward along the margin of the cell membrane and a single free flagellum at the anterior end. African Tripanosomiasis Trypanosoma gambiense & Trypanosoma rhodesiene are causative agents of the African typanosomiasis, transmitted by insect bites. The vector for both is the tsetse fly. Pathogenesis The trypomastigotes spread from the skin through the blood to the lymph node and the brain. The typical somnolence (sleeping sickness) usually progresses to coma as a result of demyelinating encephalitis. In acute form, cyclical fever spike (approximately every 2 weeks) occurs that is related to antigenic variation. As antibody mediated agglutination and lysis of the trypomastigotes occurs, the fever subsides. With a few remains of antigenic variants new fever spike occurs and the cycle repeats itself over a long period. Clinical Features Although both species cause sleeping sickness, the progress of the disease is different. T.gambiense induced disease runs a low-grade chronic course over a few years. One of the earliest signs of disease is an occasional ulcer at the site of the fly bite. As reproduction of organisms continues, the lymph nodes are invaded, and fever, myalgia, arthralgia, and lymph node enlargement results. Swelling of the posterior cervical lymph nodes is characteristic of Gambian sleeping sickness and is called winter bottom’s sign. Clinical Features Chronic disease progresses to CNS involvement with lethargy, tremors, meningoencephalitis, mental retardation, and general deterioration. In the final stages, convulsions, hemiplegia, and incontinence occur. The patient becomes difficult to arouse or obtain a response from, eventually progressing to a comatose state. Death is the result of CNS damage and other infections, such as pneumonia. Clinical Features In T.rhodesiense, the disease caused is a more acute, rapidly progressive disease that is usually fatal. This more virulent organism also develops in greater numbers in the blood. Lymphadenopathy is uncommon, and early in the infection, CNS invasion occurs, resulting in lethargy, anorexia, and mental disturbance. The chronic stages described for T.gambiense are not often seen, because in addition to rapid CNS disease, the organism produces kidney damage & myocarditis, leading to death. Immunity Both the humoral and cellular immunity involve in these infections. The immune responses of the host to the presence of these parasites, however, is faced with antigenic variation, in which organisms that have changed their antigenic identity can escape the host immune response and initiate another disease process with increased level of parasitemia. Laboratory Examination of thin and thick films, in concentrated anticoagulated blood preparations, and in aspiration from lymph nodes and concentrated spinal fluid. Methods for concentrating parasites in blood may be helpful approaches including centrifugation of heparinized samples and an ion–exchange chromatography. Levels of parasitosis vary widely, and several attempts to visualize the organism over a number of days may be necessary. Treatment The same treatment protocol is applied for these parasites. For the acute stages of the disease the drug of choice is suramin with pentamidine as an alternative. In chronic disease with CNS involvement, the drug of choice is melarsoprol. Alternatives include trypars amide combined with suramin. Prevention Control of breeding sites of tsetse flies and use of insecticides. Treatment of human cases to reduce transmission to flies. Avoiding insect bite by wearing protective clothing & use of screen, bed netting and insect repellants. Medically Important Ciliates Balantidiasis The intestinal protozoan Balantidium coli is the only member of the ciliate group that is pathogenic for humans. Disease produced by B. coli is similar to amebiasis, because the organisms elaborate proteolytic and cytotoxic substances that mediate tissue invasion and intestinal ulceration. Life Cycle The life cycle of B. coli is simple, involving ingestion of infectious cysts, excystation, and invasion of trophozoites into the mucosal lining of the large intestine, caecum, and terminal ileum. The trophozoite is covered with rows of hair like cilia that aid in motility. Morphologically more complex than amebae, B. coli has a funnel-like primitive mouth called a cytostome, a large (macro) nucleus and a small (micro) nucleus involved in reproduction. Epidemiology B. coli are distributed worldwide. Swine and (less commonly) monkeys are the most important reservoirs. Infections are transmitted by the faecal-oral route; outbreaks are associated with contamination of water supplies with pig faeces. Person-to-person spread, including through food handlers, has been implicated in outbreaks. Risk factors associated with human disease include contact with swine and substandard hygienic conditions. Clinical Features As with other protozoan parasites, asymptomatic carriage of B. coli can exist. Symptomatic disease is characterized by abdominal pain, tenderness, tenesmus, nausea, anorexia, and watery stools with blood and pus. Ulceration of the intestinal mucosa, as with amebiasis, can be seen; a secondary complication caused by bacterial invasion into the eroded intestinal mucosa can occur. Extra intestinal invasion of organs is extremely rare in balantidiasis. Life Cycle Laboratory Diagnosis Microscopic examination of faeces for trophozoite and cysts is performed. The trophozoite is very large, varying in length from 50 to 200μm and in width from 40 to 70μm. The surface is covered with cilia. Treatment The drug of choice is tetracycline; iodoquinol and metronidazole are alternative agents. Medical Helminthology Introduction Medical helminthology is concerned with the study of helminthes or parasitic worms. Helminthes are trophoblastic metazoa (multi-cellular organisms). Helminthes are among the common parasitic causes of human suffering. They are the cause of high morbidity and mortality of people worldwide. They cause different diseases in humans, but few helminthic infections cause life- threatening diseases. Introduction They cause anemia and malnutrition. In children they cause a reduction in academic performance. Helminthes also cause economic loss as a result of infections of domestic animals. There is age dependent distribution of infections from geo- helminthes and schistosomes. As a result of predisposing behavioral and immunological status, children disproportionately carry the burden of schistosomes and geo-helminthes. The sources of the parasites are different. Exposure of humans to the parasites may occur in one of the following ways: 1. Contaminated soil (Geo-helminthes), water (cercariae of blood flukes) and food (Taenia in raw meat). 2. Blood sucking insects or arthropods (as in filarial worms). 3. Domestic or wild animals harboring the parasite (as in echinococcus in dogs). 4. Person to person (as in Enterobius vermicularis, Hymenolopis nana). 5. Oneself (auto-infection) as in Enterobius vermicularis. They enter the body through different routes including: mouth, skin and the respiratory tract by means of inhalation of airborne eggs. The helminthes are classified into three major groups. These are: 1. Trematodes (Flukes) 2. Nematodes (Round worms) 3. Cestodes (Tape worms) - The Trematodes and Cestodes are groups of flat worms. MEDICALLY IMPORTANT TREMATODES (FLUKES) Introduction Trematodes belong to the phylum platyhelminthes. They are found in a wide range of habitats. The great majority inhabit the alimentary canal, liver, bile duct, ureter and bladder of vertebrate animals. According to the sites they inhabit, there are four groups of flukes. These are: Blood flukes, Intestinal flukes, Liver flukes, and Lung flukes Blood Flukes These are flukes that reside mainly in the blood vessels of various organs and the schistosomes are the prototype and the commonest flukes in our country. SCHISTOSOMIASIS (BILHARZIASIS) It is estimated that about 600 million people in 79 countries suffer from schistosomiasis (Bilharziasis). The schistosomes cause intestinal, hepatosplenic, pulmonary, urogenital, cerebral and other forms of schistosomiasis. Schistosome is the only fluke with separate sexes. The female worm lies in the gynecophoral canal of the male. This condition is important for transportation. There are five medically important species: 1. Schistosoma mansoni: causes intestinal schistosomiasis. 2. Schistosoma haematobium: causes vesical (urinary) schistosomiasis. 3. Schistosoma japonicum: causes intestinal schistosomiasis. 4. Schistosoma intercalatum: causes intestinal schistosomiasis. 5. Schistosoma mekongi: causes intestinal schistosomiasis. This seems to cause milder disease in man. It causes disease in other vertebrate hosts. The first two schistosomes (S. mansoni and S. haematobium) are prevalent in Ethiopia. Schistosoma mansoni Habitat - This species lives in the veins of the intestine. Geographical distribution: It is found in Africa, South America, Middle East (some Arab countries) etc. Stream and lake-based transmission is common. The snail hosts that harbor S. mansoni are the genera: Biomphalaria (B. glabrata) and Trobicorbis. These have oval shells. Morphology Male: The male ranges in size from 1-1.4 cm in length and the body is covered by coarse tubercles. It has 6-9 testes Female:The female is 1.5-2.0 cm in length. The ovary is present in the anterior third and Vitelline glands occupy the posterior two-thirds. It lays about 100-300 eggs daily. The uterus is short containing few ova. URINARY SCISTOSOMIASIS Etiology - Schistosoma haematobium Habitat - The worm lives in the veins of the bladder of humans. The peak prevalence is the 10-14 year age group. The snail hosts that harbor S. haematobium are the genera Bulinus (Bulinus africanus, B. truncatus) and Physopsis. Male:The male ranges in size from 1-1.5 cm in length. The body is covered by fine tubercles. It has 4-5 testes. Female:The female ranges in size from 2-2.5 cm in length. The ovary is present in the posterior third. Vitelline glands occupy the posterior thirds. Uterus is long containing many ova. It lays about 20-200 eggs daily. URINARY SCISTOSOMIASIS Distribution: In Ethiopia, S. haematobium is found in the Lower Awash Valley in the east and in Benshangul-Gumuz (Assossa) regional state in the west in low altitudes below 1000 meters above sea level. SCHISTOSOMA JAPONICUM The female adult worm lays about 500-3500 eggs daily. The eggs are ovoid, bearing only a minute lateral spine or a small knob postero-laterally. It is found in Japan, China, and Philippines, etc. SCHISTOSOMA INTERCALATUM This is the rarest and least pathogenic schistosome that matures in man. It is found in Western and Central Africa. The daily egg output is about 300. The eggs have a terminal spine. LIFE CYCLE OF SCHISTOSOMES Adult worms reside in pairs: the female lying in the gynecophoral canal of the male. After fertilization, eggs are passed into the venules. A larval form – the miracidium - develops within the egg. Its lytic enzymes and the contraction of the venule rupture the wall of the venule liberating the egg into the perivascular tissues of the intestine (S. mansoni) or urinary bladder (S. haematobium). The eggs pass into the lumens and organs and are evacuated in the feces (S. mansoni) or the urine (S. haematobium). LIFE CYCLE OF SCHISTOSOMES On contact with fresh water the miracidia hatch from the eggs and swim about until they find the appropriate snail, which they penetrate. After two generations of sporocyst development and multiplication within the snail, the fork-tailed cercariae emerge. Infection to man takes place during bathing or swimming. The cercariae penetrate the skin, are carried into the systemic circulation and pass through to the portal vessels. Within the intrahepatic portion of the portal system, the worms feed and grow to maturity. Symptoms and complications Patients infected with S. haematobium suffer from terminal haematuria and painful micturition. There is inflammation of the urinary bladder (cystitis), and enlargement of spleen and liver. Patients infected with S. mansoni suffer from cercarial dermatitis (swimmers itch) and dysentery (mucus and blood in stool with tenesmus) as well as enlargements of the spleen and liver. S. haematobium causes squamous cell carcinoma in the bladder. Laboratory Diagnosis S. mansoni ♦ Microscopic examination of the stool for eggs after concentration by sedimentation method. The egg has characteristic lateral spine. ♦ Rectal snip Laboratory Diagnosis S. haematobium: ♦ Examination of the urine after allowing it to sediment in a conical urinalysis glass. A drop from the sediment is taken and examined for eggs. Egg has terminal spine. ♦ Biopsy from bladder Treatment Praziquantel: single oral dose of 40 mg/kg divided into two doses. Prevention 1. Health education: A. On use of clean latrines and safe water supply B. Avoid urination and defecation in canals, avoid contact with canal water 2. Snail control: A. Physical methods: i. Periodic clearance of canals from vegetations. ii. Manual removal of snails and their destruction. B. Biological methods: Use of natural enemies to the snails such as Marisa. C. Chemical methods: Molluscides are applied in the canals to kill the snails. e.g. Endod Intestinal Flukes ♦ Fasciolopsis buski: These giant intestinal flukes (2-7.5 cm in length) are found in some Asian countries. ♦ Heterophyids: Minute flukes acquired by ingestion of raw fresh water fish. They are found in Asian countries. Neither are found in Ethiopia. Liver Flukes ♦ Clonorchis sinensis: Chinese liver fluke - adult worms live in bile ducts. ♦ Faciola hepatica: Sheep liver fluke - is a common parasite, cosmopolitan in distribution. It is large (3 cm in length). Adult worms reside in the large biliary passages and gall bladder. ♦ Other: Faciola gigantica: lives in the liver of cattle. Human infections are very rare. Lung Flukes At least eight different species of lung flukes, all belonging to the genus Paragonimus, are known to infect man. Paragonimus westermani, best known species, affects man causing paragonimiasis (lung disease). It is found in Asia (China, India, Indonesia, Malaya etc) and some African countries. So far there is no report of it in Ethiopia.  Nematodes (Roundworms) All the important human parasites of the Phylum Nemathelminthes (Aschelminthes) belong to the Class Nematoda. General Characteristics They are un-segmented, elongated and cylindrical. They have separate sexes with separate appearances. They have a tough protective covering or cuticle. They have a complete digestive tract with both oral and anal openings. The nematodes are free living (Majority) or parasites of humans, plants or animals. Parasitic Nematodes The nematodes are generally light cream-white colored. Their life cycle includes: egg, larvae and adult. The parasitic nematodes are divided into: 1. Intestinal nematodes 1.1. Intestinal nematodes with tissue stage A. Ascaris lumbricoides B. Hookworms C. Strongyloides stercoralis The parasitic nematodes are divided into: 1.2. Intestinal nematodes without tissue stage A. Enterobius vermicularis B. Trichuris trichuira. 2. Tissue and blood dwelling nematodes 2.1. Filarial worms 2.2. Dracunculus medinensis 2.3. Trichinella 2.4. Larva migrans. INTESTINAL NEMATODES WITH TISSUE STAGE Ascaris lumbricoides These are common roundworms infecting more than 700 million people worldwide. Morphology: Male adult worm measures 15-20 cm in length. The posterior end is curved ventrally. The female worm measures 20-40 cm in length. Its posterior end is straight. Infective stage and modes of infection: The egg containing larva when ingested with contaminated raw vegetables causes ascariasis. Life Cycle Ingested eggs hatch in the duodenum. The larvae penetrate the intestinal wall and circulate in the blood. From the heart they migrate to the lungs, ascend to the trachea, descend to the esophagus and finally reach the small intestine to become adult. The female pass immature eggs which pass to the soil and mature in 2 weeks. Pathogenicity and Clinical Features Adult worms in the intestine cause abdominal pain and may cause intestinal obstruction especially in children. Larvae in the lungs may cause inflammation of the lungs (Loeffler’s syndrome) – pneumonia-like symptoms. Diagnosis 1. Examination of stool for eggs by direct saline smear method. The egg is ovoidal, 75x60 microns, covered by albuminous mamillatins. 2. Demonstration of adult worms Treatment: Mebendazole, Albendazole and Piperazine Hook Worm There are two species of hookworm: 1. Ancylostoma duodenale 2. Necator americanus The adults are found in the small intestines of man. Mixed infection is common. Both of the species are found in Ethiopia, but N. americanus is more common. Ancylostoma duodenale Grayish-white in color. The body is slightly ventrally curved. The anterior end follows the body curvature. The buccal cavity is provided ventrally with pairs of teeth and dorsally with a notched dental plate. Distribution: This species is found in the northern part of the world including China, Japan, Europe, North Africa and Ethiopia. Morphology Male: - The male measures 10 cm in length. - The posterior end is broadened into a membraneous copulatory bursa that is provided with two long spicules. Female: - The female measures 12 cm in length. The posterior end is straight. Necator americanus This species, so called American hookworm, is found in predominantly the tropics. The anterior end is hooked against the body curvature. The mouth is provided ventrally and dorsally with cutting plate. Morphology Male: The male measures 8 cm in length. The posterior end is broadened into a membranous copulatory bursa, which is provided with two long spicules fused distally. Female: The female measures 10 cm in length. The posterior end is straight Infective stage and methods of infection: The filariform larva infects by skin penetration. Life Cycle Adult male and female worms live in the small intestine. The female lays eggs (oval, 60x40 microns), which contain immature embryo in the 4 cell stage. When the eggs pass in the stool to the soil and under favorable conditions of temperature, moisture and oxygen, they hatch into larvae, which molt twice and become infective. When the filariform larvae penetrate the skin, they circulate in the blood, reach the lungs, ascend to the trachea, descend to esophagus to reach the small intestine and become adults. Pathogenicity Adult worms in the intestine feed on blood causing iron deficiency anemia. The larvae may cause inflammation of the lungs. Diagnosis: Examination of stool by direct saline smear to detect the eggs. Treatment Mebendazole: 1 tab 2x daily for 3 days.