PARA & ENTO FOR NURSING STUDENTS LECTURE NOTE 5 2024.pdf

C. INTRODUCTION TO PARASITOLOGY AND ENTOMOLOGY DEFINITION OF TERMS Parasitology: This is the area of biology concerned with the phenomenon of dependence of one living organism on another in which one benefits and the other one hurts. Medical parasitology: “the study and medical implications of parasites that infect humans” Veterinary parasitology:” the study and medical implications of parasites that infect animals” A parasite is an organism that is entirely dependent on another organism, refers to its host for all or part of life cycle and metabolic requirements. A parasite: “a living organism that acquires some of its basic nutritional requirements through its intimate contact with another living organism”. Parasites may be simple unicellular protozoa or complex multicellular metazoan Classification PROTOZOA (Single-celled Organisms) SARCOMASTIGOPHORA CILIOPHORA COCCIDIA Amoebae Ciliates Sporozoa Entamoeba histolytica Balantidium coli Plasmodium falciparum Naegleria species Plasmodium vivax Flagellates Plasmodium malariae Giardia lamblia Plasmodium ovale Trichomonas vaginalis Toxoplasma gondii 1 Haemoflagellates Cryptosporidium Trypanosoma cruzi Trypanosoma b. gambiense Trypanosoma b. rhodesiense Leishmania donovani Leishmania spp HELMINTHS (Worms) PLATYHELMINTHES NEMATHELMINTHES (Filariform) (Cylindrical Worms) TREMATODA CESTODA NEMATODA Flukes Tapeworms Roundworms Schistosoma haematobium Taenia solium Ascaris lumbricoides Schistosoma mansoni Taenia saginata Enterobius vermicularis Schistosoma spp Diphylobothrium latum Strongyloides stercoralis Fasciola hepatica Hymenolepis nana Trichuris trichiura Heterophyes heterophyes Echinococcus granulosus Ancylostoma duodenale Paragonimus spp Necator americanus Toxocara canis Wuchereria bancrofti Trichinella spp Onchocerca volvulus 2 Dracunculus medinensis Brugia spp TERMS USED IN PARASITOLOGICAL STUDIES Microparasite: it is small, unicellular and multiplies within its vertebrate host, often inside cells. E.g. Viruses, bacteria, and protozoan Macroparasite: it is large, multicellular and has no direct reproduction within its vertebrate host. This category include: helminths Based on location of the adults parasite: An endoparasite: “a parasite that lives within another living organism” – e.g. malaria, Giardia An ectoparasite: “a parasite that lives on the external surface of another living organism” – e.g. lice, ticks Ectoparasite: these are organisms the live on the surface of the skin and superficial tissues. The infection by these parasites is referred to infestation. Endoparasite: these are organisms that live within the body the host. The infection by this organism is referred to as infection. E.g. include helminths. Endo parasites are further divided into:- Obligate parasite: These are organisms that cannot exist without a host. Facultative parasites: these are organisms that under favorable conditions may live either as parasitic or free living. E.g. Naeglaria fowleri, Acantamoeba sp. Accidental parasites: These are organisms that attack an unusual host. Aberrant parasites: organism that attack host where they cannot live or develop further. Parasitic host:-This is defined as an organism which harbors the parasite and provides the nourishments and shelter. It is of the following types: 3 Definitive host:- This is the host in which sexual reproduction of the parasite take place or in which the most highly developed form of the parasite occurs. Intermediate host:- This is the host which alternate with the definitive host and in which the larval or asexual stage of the parasite are found. Paratenic host:- This is the host in which larval stage of the parasite survives but does not develop further.it is often not necessary parts of the life cycle. Reservoir host:- It is an animal host which harbors a parasite which infects humans and serves as an important source of infection to other susceptible host. HOST PARASITE RELATIONSHIP Symbiosis:- This is an association in which both the host and parasite are so dependent upon each other that one cannot live without the help of the other. Commensalism:- This is an association in which only the parasite derives benefit without causing any injury to the host. Parasitism :- This is the relationship in which the parasite benefits and the host provide the benefit. The host gets nothing in return and always suffers from some injuries. SOURCES OF INFECTION Parasites may be transmitted from :- - animals to humans, - from humans to humans, or - from humans to animals. This transmission from host to host is:- - through consumption of contaminated food and water, - by putting anything into your mouth that has touched the stool (faeces) of an infected person or animal. Parasitic infections originate from the following sources: 1. Contaminated soil and water: Soil polluted with human excreta acts as a source of infection with Ascaris lumbricoides, Trichuris trichiura, Ancylostoma duodenale, Necator americanus and Strongyloides stercoralis. These are known as soil transmitted helminthes. Water polluted with human excreta may contain viable cysts of Entamoeba histolytica, Giardia lamblia (intestinalis), Balantidium coli, eggs of Taenia solium, 4 Hymenolepis nana, and the infective cercarial stage of Schistosoma haematobium, S. mansoni, and S. japonicum. 2. Freshwater fishes: constitute the source of Diphyllobothrium latum and Clonorchis sinensis. 3. Crab and crayfishes are the sources of Paragonimus westermani. 4. Raw or undercooked pork is the source of Trichinella spiralis, T. solium, T. saginata asiatica and Sarcocystis suihominis. 5. Raw or undercooked beef is the source of T. saginata, Toxoplasma gondii and S. hominis. 6. Dog is the source of Echinococcus granulosus and Toxocara canis (visceral larva migrans). 7. Cat is the source of T. gondii. 8. Blood-sucking insects transmit Plasmodium spp., Wuchereria bancrofti, Brugia malayi, Onchocerca volvulus, Trypanosoma brucei, T. cruzi, Leishmania spp. and Babesia spp. 9. Housefly (mechanical carrier) is the source of E. histolytica. 10. Man is the source of E. histolytica, G. lamblia, Enterobius vermicularis and H. nana. 11. Watercress is the source of Fasciola hepatica. PORTALS OF PARASITE ENTRY INTO THE BODY 1. Mouth a) The commonest portal of entry of parasites is oral. i. Through contaminated food, water, or soiled fingers. This mode of transmission is referred to as fecal-oral route. ii. Many intestinal parasites, e.g. E. histolytica, G. lamblia, B. coli, E. vermicularis, T. trichiura, A. lumbricoides, T. spiralis, T. solium, T. saginata, T. saginata asiatica, D. latum, F. hepatica, Fasciolopsis buski, C. sinensis and P. westermani enter the body in this manner. 2. By the parasite penetrating the Skin when in contact with faecally polluted soil:- 5 a) Infection with A. duodenale, N. americanus and S. stercoralis is acquired when filariform larvae of these nematodes penetrate the unbroken skin of an individual walking over faecally contaminated soil. b) Schistosomiasis caused by S. haematobium, S. mansoni and S. japonicum is acquired when the cercarial larvae, in water, penetrate the skin. c) Blood-sucking arthropods introduce e.g. Plasmodium spp., W. bancrofti, B. malayi, O. volvulus, T. brucei gambiense, T. b. rhodesiense, T. cruzi, Leishmania spp. and Babesia spp. 3. By Sexual contact:- Trichomonas vaginalis is transmitted by sexual contact. E. histolytica and G. lamblia may also be transmitted by anal-oral sexual practices. 4. Kissing:- E. gingivalis is transmitted by kissing or from contaminated drinking utensils. 5. Congenital :- Infection with T. gondii and Plasmodium spp. may be transmitted from mother to fetus trans- placentally. 6. Inhalation:- Airborne eggs of E. vermicularis may be inhaled. 7. Latrogenic infection:- Malaria parasites in blood of donors containing asexual forms of erythrocytic schizogony. This is known as trophozoite induced malaria or transfusion malaria. Malaria parasites may result from the use of contaminated syringes and needles by drug addicts. GENERAL CHARACTERISTICS OF MEDICALLY IMPORTANT PARASITES 6 Medically important protozoa, helminthes, and arthropods, which are identified as causes and propagators of disease have the following general features. These features also differ among parasites in a specific category. (1) 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. 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 – the methods of reproduction or multiplication among the parasitic protozoa are of the following types: 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. 2. Sexual reproduction: 7 (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 known as a zygote. Protozoa are divided into 4 types classified based on their organs of locomotion. The classification are amoebas, ciliates, flagellates and sporozoa. Table 1: Classification of the pathogenic protozoa S/No Protozoa Organ of locomotion Important human pathogens 1. Rhizopoda (Amoeba) Pseudopodia Entamoeba histolytica 2. Mastigophora Flagella Trypanosoma (flagellates) Leishmania Trichomonia Giardia 3. Sporozoa None exhibit a slight Plasmodium spp amoeboid movement 4. Ciliates Cilia Balantidium coli (2) HELMINTHS: The heliminthic parasites are multicellular, bilaterally symmetrical animals having three germ layers. The helminthes of importance to human beings are divided into three main groups with the peculiarities of the different categories described in table 2. Table 2: Differentiating features of helminthes Cestode Trematode Nematode Shape Tape like, Leaf like, Elongated, segmented Unsegmented Cylindrical Sexes Not separate Not separate Separate (monoecious) (monoecious) (dioecious) except blood 8 flukes which are dioecious) “Head” End Suckers: with Suckers: no hooks No suckers and hooks hooks Alimentary canal Absent Present but Present and incomplete complete Body cavity Absent Absent Present (3) ARTHROPODS Arthropods, which form the largest group of species in the animal kingdom, are characterized by having a bilaterally symmetrical and segmented body with jointed appendages. They have a hard exoskeleton, which helps enclose and protect the muscles and other organs. An open circulatory system, with or without a dorsally situated heart pumps the blood (hemolymph) via arteries to the various organs and body tissues. Blood is returned to the heart through body spaces known as hemocoeles. In addition, respiratory, excretory and nervous systems are present. Arthropods affect the health of humans by being either direct agents for disease or agents for disease transmission. The arthropods of medical importance are found in Classes Insecta, Arachnida, and Crustacea which have their own distinguishing features. In Class insect, the body is divided into head, thorax, and abdomen, with one pair of antennae. Diseases like malaria, yellow fever, onchocerciasis, and trypanosomiasis are primarily transmitted by insects. CLASSIFICATION OF ARTHROPODS Kingdom Animalia Phylum Arthropoda Class Crustacea e.g Scorpion; Class Arachnida e.g Ticks.; Class Chilopoda e.g Centipede and Class Insecta e.g Mosquito. N.B. Crustacia, Arachnida, and Insecta are the three most common classes of arthropods of medical significance. 9 A. MEDICAL PROTOZOLOGY LEARNING OBJECTIVES: At the end of the lesson, the student should be able to: Discuss the classification of medically important protozoa. Discuss the pathogenesis and clinical aspects of infections. Describe the general epidemiological aspects and transmission patterns of diseases caused by protozoa. Identify the methods and procedures of laboratory diagnosis of pathogenic protozoa in clinical specimens. Discuss treatment options for protozoan infections. Implement the preventive and control measures of protozoan infection. INTRODUCTION Protozoa (singular, protozoan), from the Greek ‘protos’ and ‘zoon’ meaning “first animal”, are members of eukaryotic protists. They may be distinguished from other eukaryotic protists by their ability to move at some stage of their life cycle and by their lack of cell wall. 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. 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. 10 Importance of protozoa Protozoa serve as an important link in the food chain and ecological balance of many communities in wetland & aquatic environments. They are also important in biological sewage treatment, which involves both anaerobic digestion and/or aeration. These are useful in the study of cell cycles and nucleic acid biosynthesis during cell division. Medical concern of protozoa Protozoa are ubiquitous in moist areas, including the human alimentary canal. From an ecological standpoint, protozoa may be divided into free-living forms and symbiotic forms. Some of the symbiotic ones are parasitic and may cause disease. Although most amoebas are free-living, several are found as commensal inhabitants of the intestinal tract in humans. One of these organisms Entamoeba histolytica may invade tissue and produce disease. Majority of ciliates are free living and seldom parasitize humans. Flagellates of the genus Trypanosomes and Leishmania are capable of invading the blood & tissue of humans, where they produce severe chronic illness. Others such as Trichomonas vaginalis and Giardia lamblia, inhabit the urogenital and gastrointestinal tracts and initiate disease characterized by mild to moderate morbidity but no mortality. Sporozoan organisms, in contrast, produce two of the most potentially lethal diseases of humankind: malaria and toxoplasmosis. With the advent of HIV a new and important chapter has been opened; i.e. ‘opportunistic’ parasitosis. Most of the parasitic incidents belong to endocellular protozoa of different genera or species. Reproduction and regeneration of protozoa As a general rule, protozoa multiply by asexual reproduction. This is not to say that sexual processes are absent in the protozoa. Some parasitic forms may have an asexual phase in one host and a sexual phase in another host. 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 11 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 pathogenecity 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 defences. 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. CLASSIFICATION OF PROTOZOA Protozoa of medical importance are classified based on their morphology and locomotive system as described below: Amoebas - Entamoeba histolytica Flagellates - Giarda lamblia, Trichomonas vaginalis, Trypanosoma spp, Leishmania spp Cliliophora - Balantidium coli Coccidian - Isospora belli, Cryptosporidium parvum, Toxoplasma gondii, Plasmodium species. Protozoan pathogens can also be grouped according to the location in the body where they most frequently cause disease. AMOEBIASIS INTRODUCTION 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 within the mature 12 multinucleated cyst. Motility is accomplished by extension of pseudopodia (“false foot”). Entamoeba histolytica 1.1. 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. 1.2. (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 1.3. 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. 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 are 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. 13 Fig 1 : Life cycle of Entamoeba histolytica 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 trophozites 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. Patients infected with E. hisolytica pass non-infectious trophozotes and infectious cysts in their stools. Therefore, the main source of water and food contamination is the symptomatic carrier who passes cysts. Symptomatic 14 amebiasis is usually sporadic. The epidemic form is a result of direct person-to- person faecal-oral spread under conditions of poor personal hygiene. Clinical features The outcome of infection may result in a carrier state, intestinal amebiasis, or extraintestinal amebiasis. diarrhoea, flatulence, and cramping are complaints of symptomatic patients. More severe disease is characterised by the passing of numerous bloody stools in a day. Systemic signs of infection (fever, leukocytosis, rigors) are present in patients with extraintestinal amebiasis. The liver is primarily involved, because trophozoites in the blood are removed from the blood by the portal veins. The right lobe is most commonly involved, thus pain over the liver with hepatomegaly and elevation of the diaphragm is observed. Immunity E. histolytica elicits both the humeral and cellular immune responses, but it is not yet clearly defined whether it modulates the initial infection or prevents reinfection. Laboratory diagnosis in intestinal amoebiasis: Examination of a fresh dysenteric faecal specimen or rectal scraping for trophozoite stage. (Motile amoebae containing red cells are diagnostic of amoebic dysentery). Examination of formed or semiformed faeces for cyst stage. Diagnosed by the use of scanning procedures for liver and other organs. Specific serologic tests, together with microscopic examination of the abscess material, can confirm the diagnosis. Treatment Acute, fulminating amebiasis is treated with metrondiazole followed by iodoquinol. The cysticidal agents are commonly recommended for asymptomatic carriers who handle food for public use. Metronidazole, chloroquine, and diloxanide furoate can be used for the treatment of extra intestinal amoebiasis. Prevention 15 Introduction of adequate sanitation measures and education about the routes of transmission. Avoid eating raw vegetables grown by sewerage irrigation and night soil OTHER AMOEBAE INHABITING THE ALIMENTARY CANAL Most of these amoebae are commensal organisms that can parasitize the human gastrointestinal tract. Entamoeba hartmanni in all of its life–cycle stage, E. hartmanni resembles E. histolytica except in size, yet there is a slight overlap in the size range. The trophozoites do not ingest red blood cells, and their motility is generally less vigorous than that of E. histolytica. As in other amoebae, infection is acquired by ingestion of food or water contaminated with cyst-bearing faeces. Identification is based on examination of small amebae in unstained or iodine-stained preparations. Usually no treatment is indicated, measures generally effective against faecal-borne infections will control this amoebic infection. Entamoeba coli the life cycle stages include; trophozoite, precyst, cyst, metacyst, and metacystic trophozoite. Typically the movements of trophozoites are sluggish, with broad short pseudopodia and little locomotion, but at a focus the living specimen cannot be distinguished from the active trophotozoite of E. histolytica. However, the cysts are remarkably variable in size. Entamoeba coli is transmitted in its viable cystic stage through faecal contamination. Ε.coli as a lumen parasite is non-pathogenic and produces no symptoms. The mature cyst (with more than four nuclei) is the distinctive stage to differentiate E.coli from the pathogenic E. histolytica. Specific treatment is not indicated since this amoeba is non-pathogenic. The presence of E. coli in stool specimen is evidence for faecal contamination. Prevention depends on better personal hygiene and sanitary disposal of human excreta. Entamoeba polecki- a relatively cosmopolitan parasite of hog and monkey. It can cause human disease but is rarely isolated. The disease is manifested as mild, transient diarrhoea. The diagnosis of E. polecki infection is confirmed by the microscopic detection of cysts in stool specimens. Treatment is the same as for E. histolytica infection. Prevention is achieved by good personal hygiene. Endolimax nana is a lumen dweller in the large intestine, primarily at the cecal level, where it feeds on bacteria. The life cycle is similar to E.histolytica. Motility is typically sluggish (slug-like) with blunt hyaline pseudopodia, Projects shortly. Human infection results from ingestion of viable cysts in polluted water or contaminated 16 food. Typical ovoid cysts of E.nana are confirmative. Prevention can be achieved through personal cleanliness and community sanitation. Iodamoeba buetschlii: - the natural habitat is the lumen of the large intestine, the principal site probably being the caecum. The trophozoite feeds on enteric bacteria; it is a natural parasite of man and lower primates. It is generally regarded as a nonpathogenic lumen parasite. Prevention is based on good personal hygiene and sanitation in the community. Entamoeba gingivalis - only the trophozoite stage presents, and encystation probably does not occur. E. gingivalis is a commensal, living primarily on exudate from the margins of the gums, and thrives best on unhealthy gums. No specific treatment is indicated. However the presence of E. giingivalis suggests a need for better oral hygiene. The infection can be prevented by proper care of the teeth and gums. Blastocystis hominis- is an inhabitant of the human intestinal tract previously regarded as non-pathogenic yeast. Its pathogenecity remains controversial. The organism is found in stool specimen from asymptomatic people as well as from people with persistent diarrhoea. B. hominis is capable of pseudopodia extension and retraction, and reproduces by binary fission or sporulation. There are thin – walled cysts involved in autoinfection, and thick–walled cysts responsible for external transmission via the faecal-oral route. The presence of large numbers of these parasites (five or more per oil immersion microscopic field) in the absence of other intestinal pathogens indicates disease. The organism may be detected in wet mounts or trichome –stained smears of faecal specimens. Treatment with iodoquinol or metronidazole has been successful in eradicating the organism from intestine and alleviating symptoms. However, the definitive role of B. hominis in disease remains to be demonstrated. PATHOGENIC FREE-LIVING AMOEBAE Among the numerous free-living amoebae of soil and water habitats, certain species of Naegleria, Acanthamoeba and Balamuthia are facultative parasites of man. Most human infections of these amoebae are acquired by exposure to contaminated water while swimming. Inhalation of cysts from dust may account for some infections. Naegleria fowleri- the trophozoites occur in two forms. Amoeboid forms with single pseudopodia and flagella forms with two flagella which usually appear a few hours 17 after flooding water or in CSF. Naegleria trophozoites in a section of spinal cord from a patient with amoebic meningoecephalitis Acanthamoeba species- the trophozoites have an irregular appearance with spine- like pseudopodia, and acanthopodia. Balamuthia species- the trophozoite extends a broad, flat lamellipodia or sub pseudopodia from it. The trophozoite may be bi-nucleated. Unlike most amoebae the nuclear envelope breaks down during mitosis. Naegleria, Acanthamoeba, Balamuthia organisms are opportunistic pathogens. Naegleria fowleri causes acute primary amoebic meningoencephalitis. Acantamoeba & Balamuthia organisms are responsible for granulomatous amoebic encephalitis and single or multiple brain abscesses, primarily in immunocompromised individuals. Keratitis (eye) and skin infection by Acanthamoeba may also occur. For the diagnosis of Naegleria, Acanthamoeba, and Balamuthia infections, specimens of nasal discharge and cerebrospinal fluid; and in cases of eye infections corneal scraping should be collected. The clinical specimen can be examined with saline wet preparation and Iodine stained smear. PATHOGENIC FLAGELLATES INTRODUCTION 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. There are three groups of flagellates: Luminal flagellates:- Giardia lamblia, Dientmoeaba fragilis Hemoflagellates:- Trypanosoma species, Leishmania species. Genital flagellates:- Trichomonas vaginalis Luminal flagellates 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 18 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 Cyst & 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. 19 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 20 symptomatic patients, however, mucosa-lining irritation may cause increased mucous secretion and dehydration. 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 streatorrhoea. Blood & pus are rarely present in stool specimens, a feature consistent with the absence of tissue destruction. Immunity 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. 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. 21 Diagram of Trichomonas vaginalis Life cycle Of T. vaginalis 22 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. 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 23 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. Haemoflagelates Leishmania Species Clinical disease - Visceral 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 leishmaniasis Leishmania donovani Important features- the natural habitat of L. donovani in man is the reticuloendothelial system of the viscera, in which the amastigote multiplies by 48 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 anaemia, 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 anaemia 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 India and neighboring countries (and Kenya), kala-azar is anthroponosis, i.e. there is no 24 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. 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. 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. 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. Old World Cutaneous Leishmaniasis (Oriental sore) Clinical disease L.tropica minor - dry or urban cutaneous leishmaniasis L.tropica major - wet or rural cutaneous leishmaniasis L.aethiopica - cutaneous leishmaniasis. Important features:- These are parasites of the skin found in endothelial cells of the capillaries of the infected site, nearby lymph nodes, within large mononuclear cells, in neutrophilic leukocytes, and free in the serum exuding from the ulcerative site. Pathogenesis; In neutrophilic leukocytes, phagocytosis is usually successful, but in macrophages the introduced parasites round up to form amastigote and multiply. In the early stage, the lesion is characterized by the proliferation of macrophages that contain numerous amastigotes. There is a variable infiltration of lymphocytes and plasma cell. The overlying epithelium shows acanthosis and hyperkeratosis, which is usually followed by necrosis and ulceration. 51 Epidemiology Cutaneous leishmaniasis produced by L. tropica 25 complex is present in many parts of Asia, Africa and Mediterranean Europe. The urban Cutaneous leishmaniasis is thought to be an anthroponosis while the rural cutaneous leishmaniasis is zoonosis with human infections occurring only sporadically. The reservoir hosts in L. major are rodents. L. aethopica is endemic in Ethiopia and Kenya. The disease is a zoonosis with rock & tree hyraxes serving as reservoir hosts. The vector for the old world cutaneous Leishmaniasis is the Phlebotomus sand fly. Clinical features The first sign, a red papule, appears at the site of the fly’s bite. This lesion becomes irritated, with intense itching, and begins to enlarge & ulcerate. Gradually the ulcer becomes hard and crusted and exudes a thin, serous material. At this stage, secondary bacterial infection may complicate the disease. In the case of the Ethiopian cutaneous leishmaniasis, there are similar developments of lesions, but they may also give rise to diffuse cutaneous leishmaniasis (DCL) in patients who produce little or no cell mediated immunity against the parasite. This leads to the formation of disfiguring nodules over the surface of the body. Treatment The drug of choice is sodium stibogluconate, with an alternative treatment of applying heat directly to the lesion. Treatment of L. aethopica remains to be a problem as there is no safe and effective drug Prevention – Prompt treatment & eradication of ulcers - Control of sand flies & reservoir hosts. New World Cutaneous and Mucocutaneous Leishmaniasis (American cutaneous leishmaniasis) Clinical disease: Leishmania mexicana complex- Cutaneous leishmaniasis. Leishmania braziliensis complex- mucocutaneous or cutaneous leishmaniasis. Important features: The American cutaneous leishmeniasis is the same as oriental sore. But some of the strains tend to invade the mucous membranes of the mouth, nose, pharynx, and larynx either initially by direct extension or by metastasis. The metastasis is usually via lymphatic channels but occasionally may be the bloodstream. Pathogenesis The lesions are confined to the skin in cutaneous leishmaiasis and to the mucous membranes, cartilage, and skin in mucocutaneous leishmaniasis. A 26 granulomatous response occurs, and a necrotic ulcer forms at the bite site. The lesions tend to become superinfected with bacteria. Secondary lesions occur on the skin as well as in mucous membranes. Nasal, oral, and pharyngeal lesions may be polypoid initially, and then erode to form ulcers that expand to destroy the soft tissue and cartilage about the face and larynx. Epidemiology Most of the cutaneous & mucocutaneous leishmaniasis of the new world exist in enzootic cycles of infection involving wild animals, especially forest rodents. Leishmania mexicana occurs in south & Central America, especially in the Amazon basin, with sloths, rodents, monkeys, and raccoons as reservoir hosts. The mucocutaneous leishmaniasis is seen from the Yucatan peninsula into Central & South America, especially in rain forests where workers are exposed to sand fly bites while invading the habitat of the forest rodents. There are many jungle reservoir hosts, and domesticated dogs serve as reservoirs as well. The vector is the Lutzomyia sand fly. Clinical features:- The types of lesions are more varied than those of oriental sore and include Chiclero ulcer, Uta, Espundia, and Disseminated Cutaneous Leishmaniasis. Laboratory diagnosis Demonstration of the amastigotes in properly stained smears from touch preparations of ulcer biopsy specimen. Serological tests based on fluorescent antibody tests. Leishman skin test in some species. Treatment:- The drug of choice is sodium stibogluconate. Prevention Avoiding endemic areas especially during times when local vectors are most active. Prompt treatment of infected individuals. Trypanosomiasis 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 27 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 trypanosomiasis Trypanosoma gambiense & Trypanosoma rhodesiene are causative agents of the African typanosomiasis, transmitted by insect bites. The vector for both is the tsetse fly. Life cycle of Trypanosoma brucei Pathogenesis 28 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. Epidemiology:- T.burcei gambiense is limited to tropical west and central Africa, correlating with the range of the tsetse fly vector. The tsetse flies transmitting T. b. gambiense prefer shaded stream banks for reproduction and proximity to human dwellings. People who work in such areas are at greatest risk of infection. An animal reservoir has not been proved for this infection. T. burcei rhodeseinse is found primarily in East Africa, especially the cattle- raising countries, where tsetse flies breed in the brush rather than along stream banks. T. b. rhodeseines also differs from T. b. gambiense in that domestic animal hosts (cattle and sheep) and wild game animals act as reservoir hosts. This transmission and vector cycle makes the organism more difficult to control than T. b. gambiense. Clinical features 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 winterbottom’s sign. 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. 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 29 rapid CNS disease, the organism produces kidney damage & myocarditis, leading to death. Laboratory Examination of thin and thick films. Levels of parasitosis vary widely, and several attempts to visualize the organism over a number of days may be necessary. Trypomastigote stage of Trypanosoma burcei complex 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. American trypanosomiasis Trypanosoma cruzi is a pleomorphic trypanosome that includes an additional form of amastigote in its life cycle. The vector for transmission are reduviid bugs. Pathogenesis During the acute phase, the organism occurs in blood as a typical trypomastigote and in the reticuloendothelial cells as a typical amastigote. The amastigotes can kill cells and cause inflammation, consisting mainly of mononuclear cells. Cardiac muscle is the most frequently and severely affected tissue. In addition, neuronal damage leads to cardiac arrhythmias and loss of tone in the colon (megacolon) and esophagus (megaesophagus). In the chronic phase, the organism persists in the amastigote form. Epidemiology T.cruzi occurs widely in both reduviid bugs and a broad spectrum of reservoir animals in North, Central, and South America. Human disease is found most often among children in South and Central America, where there is direct correlation between infected wild animal reservoir hosts and the presence of infected bugs whose nests are found in human dwellings. Clinical features Chagas’ disease may be asymptomatic acute or chronic disease. One of the earliest signs is development at the site of the bug bite of an 30 erythematous and indurated area called a chagoma. This is often followed by a rash and edema around the eyes and face; in young children frequently an acute process with CNS involvement may occur. Acute infection is also characterized by fever, chills, malaise, myalgia, and fatigue. The chronic Chagas’ disease is characterized by hepatosplenomegaly, myocarditis, and enlargement of the esophagus and colon as a result of the destruction of nerve cells (E.g. Auerbach’s plexus) and other tissues that control the growth of these organs. Involvement of the CNS may produce granulomas in the brain with cyst formation and a meningoencephalitis. Death from chronic Chagas’ disease results from tissue destruction in the many areas invaded by the organisms, and sudden death results from complete heart block and brain damage. Laboratory diagnosis Examine thin or thick stained preparations for trypomastigotes. Wet preparations should also be examined to look for motile organisms that leave the blood stream and become difficult to find. Biopsy of lymph nodes, liver, spleen, or bone marrow may demonstrate organisms in amastigote stage. ; Amastigote stage of Trypanosoma cruzi in skeletal muscle. 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 31 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. 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. COCCIDIA (SPOROZOA) INTRODUCTION Coccidia are members of the class sporozoa, Phylum Apicomplexa. Apical complex is present at some stage and consists of elements visible with electron microscope. The life cycle is characterized by an alternation of generations, i.e. sexual (gametogony) and asexual (schizogony) reproduction and most members of the group also share alternative hosts. The locomotion of a mature organism is by body flexion, gliding, or undulation of longitudinal ridges. There are four species normally infecting humans, namely, Plasmodium falciparum, Plasmodium vivax, Plasmodium ovale, and Plasmodium malariae. Life cycle:- The life cycle of malaria is passed in two hosts (alternation of hosts) and has sexual and asexual stage (alternation of generations). Vertebrate host - man (intermediate host), where the asexual cycle takes place. The parasite multiplies by schizogony and there is formation of male and female gametocytes (gametogony). Invertebrate host - mosquito (definitive host) where the sexual cycle takes place. Union of male and female gametes ends in the formation of sporozoites (sporogony). The life cycle passes in four stages: Three in man:- Pre - erythrocytic schizogony - Erythrocytic schizogony - Exo- erythrocytic schizogony One in mosquito - Sporogony Introduction into humans - when an infective female Anopheles mosquito bites man, it inoculates saliva containing sporozoites (infective stage). 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 32 occurs in tissue schizonts, to form thousands of tiny merozoites. Merozoites are then liberated on rupture of schizonts about 7th – 9th day of the bites and enter into the blood stream. These merozoites either invade the RBC’s or other parenchymal liver cells. In case of P. falciparum and possibly P. malariae, all merozoites invade RBC’s without re-invading liver cells. However, for P. vivax and P. ovale, some merozoites invade RBC’s and some re-invade liver cells initiating further Exo-erythrocytic schizogony, which is responsible for relapses. Some of the merozoites remain dormant (hypnozoites) becoming active later on. Erythrocytic schizogony (blood phase) is completed in 48 hrs in P. vivax, P. ovale, and P. falciparum, and 72 hrs in P. malariae. The merozoites reinvade fresh RBC’s repeating the schizogonic cycles Erythrocytic merozoites do not reinvade the liver cells. So 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. Sporogony (extrinsic cycle in mosquito) When a female Anopheles mosquito vector bites an infected person, it sucks blood containing the different stages of malaria parasite. All stages other than gametocytes are digested in the stomach. The microgametocyte undergoes ex-flagellation. The nucleus divides by reduction division into 6-8 pieces, which migrate to the periphery. At the same, time 6-8 thin filaments of cytoplasm are thrust out, in each passes a piece of chromatin. These filaments, the microgametes, are actively motile and separate from the gametocyte. The macrogametocyte by reduction division becomes a macrogamete. Fertilization occurs by entry of a micro gamete into the macro gamete forming a zygote. The zygote changes into a worm like form, the ookinete, which penetrates the wall of the stomach to develop into a spherical oocyst between the epithelium and basement membrane. The oocystes increase in size. Thousands of sporozoites develop inside the oocysts. Oocysts rupture and sporozoites are liberated in the body cavity and migrate everywhere particularly to the salivary glands. Now the mosquito is infective The sporogonous cycle in the mosquito takes 8-12 days depending on temperature. 33 Life cycle of Plasmodium falciparum 34 35 Plasmodium falciparum Plasmodium falciparum demonstrates no selectivity in host erythrocytes, i.e. it invades young and old RBCs cells. The infected red blood cells also do not enlarge and become distorted. Multiple sporozoites can infect a single erythrocyte, and show multiple infections of cells with small ring forms. The trophozoite is often seen in the host cells at the very edge or periphery of cell membrane at accole position. Occasionally, reddish granules known as Maurer’s dots are observed Mature (large) trophozoite stages and schizonts are rarely seen in blood films, because their forms are sequestered in deep capillaries, liver and spleen. Peripheral blood smears characteristically contain only young ring forms and occasionally crescent shaped gametocytes. Epidemiology:- P.falciparum occurs almost exclusively in tropical and subtropical regions. Weather (rainfall, temperature & humidity) is the most obvious cause of seasonality in malaria transmission. To date, abnormal weather conditions are also important causes of significant and widespread epidemics. Moreover, drug-resistant infection of P.falciparum is the commonest challenge in many parts of the world. In Ethiopia, even though all the four species of plasmodium infecting man have been recorded, P.falciparum is the one that most causes the epidemic disease and followed by vivax and malariae. P.ovale is rare. Infection rates in Ethiopia are 60%, 40%, 1%, and Clinical features Of all the four Plasmodia, P. falciparum has the shortest incubation period, which ranges from 7 to 10 days. After the early flu-like symptoms, P. falciparum rapidly produces daily (quotidian) chills and fever as well as severe nausea, vomiting and diarrhea. The periodicity of the attacks then becomes tertian (36 to 48 hours), and fulminating disease develops. Involvement of the brain (cerebral malaria) is most often seen in P. falciparum infection. Capillary plugging from an adhesion of infected red blood cells with each other and endothelial linings of capillaries causes hypoxic injury to the brain that can result in coma and death. Kidney damage is also associated with P. falciparum malaria, resulting in an illness called “black water” fever. Intravascular hemolysis with rapid destruction of red blood cells produces a marked hemoglobinuria and can result in acute renal failure, tubular necrosis, nephrotic 36 syndrome, and death. Liver involvement is characterized by abdominal pain, vomiting of bile, hepatosplenomegally, severe diarrhea, and rapid dehydration. Treatment Because chloroquine – resistant stains of P. falciparum are present in many parts of the world, infection of P. falciparum may be treated with other agents including mefloquine, quinine, guanidine, pyrimethamine – sulfadoxine, and doxycycline. If the laboratory reports a mixed infection involving P. falciparum and P. vivax, the treatment must eradicate not only P. falciparum from the erythrocytes but also the liver stages of P. vivax to avoid relapses provided that the person no longer lives in a malaria endemic area. Other Coccidian parasites Toxoplasma gondii – causes toxoplasmosis. The definitive host is the domestic cat and other felines. Humans and other mammals are intermediate hosts. T. gondii is 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 of the intestinal epithelium, the organisms spread to other organs, especially the brain, lungs, liver, and eyes. Most primary infections in immunocompetent adults are asymptomatic. Congenital infection can result in abortion, stillbirth, or neonatal disease with encephalitis, chorioretinitis and hepatosplenomegaly. Fever, jaundice, and intracranial calcifications are also seen. For the diagnosis of acute and congenital infections, an immunofluorescence assay for detection of antibody is used. Microscopic examination of Giemsa– stained preparations shows crescent–shaped trophozoite. Cysts may be seen in the tissue. Treatment is with a combination of sulfadiazine and pyrimethamine. Life cycle of Toxoplasma gondii. 37 Review Questions 38 1) What are the two distinctive characteristics that differentiate protozoa from other Eukaryotic protists? 2) What are the ecological advantages of protozoa? 3) Explain the reproductive process, transmission route and pathogenesis of protozoan parasites. 4) How are medically important protozoa classified? 5) Describe the pathogenesis of E.histolytica. 6) Explain the clinical features of Giardia lamblia. 7) What are the drugs of choice for treatment of Trichomoniasis vaginalis? 8) What is the hemoflagellate responsible for causing kala-azar? 9) What are the protozoal species responsible for old world cutaneous leishmaniasis? 10) Explain the pertinent clinical syndrome of Leishmania aethiopica. 11) What are the causative protozoa for African tryponosomiasis? 12) Explain the immune systems involved and the immune phenomenon in the infection of African trypanosomiasis. 13) What are the common characteristics of the class sporozoa? 14) Which of the plasmodia parasite has the shortest incubation period 15) List and describe the pathogenesis of parasitic protozoa frequently found in immunocompromized individuals. B. MEDICAL HELMINTHOLOGY 39 LEARNING OBJECTIVES At the end of this session, students should be able to: Understand medically important helminthes including their life cycles, modes of transmissions, clinical features, diagnosis, treatment and prevention. Describe blood, intestinal, liver and lung flukes. Understand common round worms. Understand different species of Cestodes. 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. 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: 40 1. Trematodes (Flukes) 2. Nematodes (Round worms) 3. Cestodes (Tape worms) The Trematodes and Cestodes are groups of flat worms. Helminth is a term derived from a Greek word that simply means worm. Characteristics - Multicellular, bilaterally symmetrical, elongated, flat or round animals. - Most helminthic worms are macroscopic in size and often visible to naked eye. - All helminths with a few exceptions produce eggs which are excreted in different secretions of the body. - The outer covering (cuticle or integument) is resistant to intestinal digestion and may be armed with spines or hooks. - Nervous system and excretory system are primitive. - Digestive system is either complete, partially lost (rudimentary) or completely absent. - Reproductive system is very well developed. - They may be monoecious or dioecious. - Both self-fertilization and cross-fertilization may take place. Helminth which occur as parasites in human belong to two phyla:- Phylum Platyhelminthes belong to two classes: Class Trematoda and Cestoda. Phylum Nematoda belong to two classes: Class Adenophorea and Secernentea. Examples of Cestodes include: Diphyllobotrium latum, Taenia solium, T. saginata, H nana and Echinococcus granulosus. Examples of Trematodes include: Fasciola hepatica, Clonorchis sinensis, Schistosoma haematobium (blood flukes) and Paragonimus westermani. Examples of Secementheans include: Ancylostoma duodenale (hookworm), Ascaris lumbricoides(roundworm), Enterobius vermicularis(pinworm), Strongyloides stercoralis. Example of Adenophoreans include: Trichuris trichiura Life cycle 41 The Life cycle of helminths may be completed in one or more hosts. Cestode with the exception of Hymenolepis nana (single host), D. latum (three host) completes their life cycle in two different hosts. Trematode complete their life cycle in one intermediate host and one definitive, but Dicrocoelium dendriticum utilizes two intermediate host that involves an ant. Nematodes complete their life cycle in one host except in filarial nematodes and Dracunculus medinenses which complete their life cycle in man and insect vector as second host for the former and Cyclops as second host for the latter. Larval stages:- The Larval forms include:- - Rhabditiform, filariform, and microfilaria in nematodes. - Cysticercus , Cysticercoid, Coenurus, A and Hydatid cyst, in cestodes. - Miracidium, sporocyst, redia, cercaria and metacercaria in trematodes. 42 - Phylum Platyhelminthes Characteristics Dorsoventrally flattened hence called flat worm, Endoparasite of vertebrate or free living, Bilaterally symmetrical, Incomplete alimentary system or entirely lacking, Mostly hermaphrodites (monoecious) and Triploblastic (3 germ layer). Human pathogenic helminthes belong to two classes:- Cestoda and Trematoda. Cestode Classification 1. Order: Pseudophyllidea (Genus: Dipylidium, Diphyllobothrium, and Spirometra) 2. Order: Cyclophyllidea (Genus: Taenia, Echinococcus and Hymenolepis) Class Cestoda General characters of Cestodes Phylum: Platyhelminthes Class: Cestoda Order: Cyclophyllidea Family Taeniae 43 Species: Taenia saginata and T. solium This group include the most important cestode parasites of man, the adults of these species occur only in man but are usually of minor medical importance. The larval stage are always in mammals and consist of a fluid filled cyst which may contain a single or many protoscoleces. Geographical Distribution Taenia saginata and T. solium are worldwide in distribution. Taenia solium is more prevalent in poorer communities where humans live in close contact with pigs and eat undercooked pork. s Morphology The scolex of T. saginata is pear shaped with four prominent round suckers with no rostellum and hooks. The adult worm is long sometimes exceeding 20 meters and contain 1000-2000 proglottids. The scolex of T. solium on the other hand is globular and contain four large suckers and a conspicuous rostellum with two rows of alternating large and small hooks. The adult is short and contains 800-1000 segments. Location in the host The scolex of the adult worm is embedded in the mucosa of the wall of the ileum, with rest of the tape extending through the lumen. Characteristics Majority are long, segmented and tape-like, hence called tape-worms. Sizes vary from a few millimeters to several meters. Adult worms are found in the intestinal canal of man and animal. Head is provided with suckers (cup like) and sometimes with hooks which serves as organs of attachment. Adult is divided i) a head (scolex), ii) a neck (iii) a strobila (a body or trunk) consisting of a series of segments called (proglottids). Each individual worm is a hermaphrodite. Newly formed proglottids are small and immature. Mature proglottids contain fully developed reproductive organs (several 44 testes, bilobed ovary, and a uterus which may be coiled or consist of a central stem with side branches). Proglottidis that contain eggs are called gravid segments. Body cavity is absent. There is no mouth or digestive system. Alimentary canal is entirely absent. Excretory and nervous systems are present. Reproductive system is highly developed and complete in each segment. Fertilization takes place between the segments; it may be a self- fertilization or a cross-fertilization. According to maturity of the reproductive organs three types of segments of the strobila can be recognized from the front backwards: immature: male and female organs not differentiated; mature: male and female organs have become differentiated; gravid: uteri are filled with eggs. In cyclophyllidean csetodes, the egg is not operculated and has two coverings; the inner which surrounds the embryo is known as embryophore and the outer is thin and is known as egg-shell. The egg, when first laid contains a six-hooked (hexacanth) embryo known as onchosphere. It does not have ciliated epithelium. Order:- Cyclophyllidea;e.g Taenia spp (tapeworms) LIFE CYCLE of Taenia saginata T. saginata complete its life cycle in two different hosts. Man is the definitive host who harbours the adult worms. The intermediate host is cattle. Eggs or gravid segments are passed out with the faeces on the ground; when ingested by cows while grazing. On reaching the duodenum, the embryophore of the eggs ruptures and liberates oncospheres, with the help of the hooklets, they penetrate the wall of the intestine and enters into portal vessels or mesenteric lymphatic 45 LIFE CYCLE OF Taenia saginata L LIFECYCLE OF Taenia solium (pork tapeworm) 46 They pass through the general circulation ( heart, lungs) and are filtered out in the striated muscles; they develop into bladder worm known as cycticercus bovis within 10-12 weeks. The mature cysticerci are ovoid in shape milky-white in colour. They have unarmed scolices (scolices without hooklets) invaginated in them. The cysticerci can live in flesh of cattle for about 8 months, but can develop further only when ingested by man its definitive host. Man acquires infection by eating raw or under-cooked beef containing encysted larval stage (Cysticercus bovis). The larvae hatch out in the small intestine, the scolices exvaginate and anchor to the mucosal surface by means of their suckers and develop into adult worms. They grow to sexual maturity in 2-3 months, lay eggs which are passed out in faeces along with the gravid segments and the cycle is repeated. Clinical Presentation/pathogenicity Taenia saginata :-Taeniasis produces only mild abdominal symptoms. The most striking feature consists of the passage (active and passive) of proglottids. Occasionally, appendicitis or cholangitis can result from migrating proglottids. Taenia solium taeniasis is less frequently symptomatic than Taenia saginata taeniasis. The main symptom is often the passage (passive) of proglottids.The most important feature of Taenia solium taeniasis is the risk of development of cysticercosis. Laboratory Diagnosis, Prophylaxis , Treatment Laboratory diagnosis:- Microscopic identification of eggs and proglottids in faeces is diagnostic for taeniasis, Microscopic identification of gravid proglottids (or, more rarely, examination of the scolex) allows species determination. Prophylaxis:- Avoid eating raw or undercooked pork or beef and Proper waste disposal Treatment:- Niclosamide, Paromomycin 47 Phylum: Platyhelminthes Class: Cestoda Order: Pseudophyllidea Species: Diphyllobothrium latum D. latum This parasite is usually referred to as fish tapeworm or broad tapeworm. D. latum belong to the pseudophyllidean tapeworm group which is characterised by having a scolex with two bothria rather than suckers. The distribution of this parasite is worldwide. Infection is acquired by ingestion of raw, poorly cooked or pickled fresh water fish. D latum is the longest tape worm found in man. It measures up to 10 meters or more in length with as many as 3000 or more proglottids consisting of immature, matured and gravid segments. A single worm may discharge as many as 1,000,000 eggs daily. Location in the host The adult worm inhabits the lumen of the small intestine with the scolex embedded in the mucosa. The longest tapeworm found in man. LIFE CYCLE:- The host passes its life cycle in one definitive host and two intermediate hosts. The adult worm consists of scolex, neck and strobila. The adult worm which resides in the ileum or jejunum (small intestine) lays operculated eggs which are passed along with faeces in water. The egg develops into first, second, and third stage larva. The first stage larva is known as Coracidium. It develops from the egg in water. A spherical ciliated embryo containing three pairs of hooklets. Coracidium develops within each egg shell in one to two weeks. Coracidium swims about in water are ingested by a small copepod. The ciliated coracidium shed off its cilia within the intestine of the copepod (first intermediate host) and penetrate the body cavity and develop to a second larva called onchosphere which later transformed in to procercoid larva within the body of the copepod. When a copepod with infective procercoid larva are eaten by a suitable second intermediate host (fresh water fish); the procercoid penetrate the intestine of the fish and comes to lie free between the muscle fibre where it grows into plerocercoid larva. Humans become infected when they eat undercooked, raw or lightly salted infective fresh water fish. 48 LIFE CYCLE OF Diphyllobothrium latum Inside the intestine of man the plerocercoid larva develops in to an adult worm and after having attained sexual maturity begin to lay egg which are passed along with faeces. PATHOGENICITY: -Infection is usually asymptomatic. Infected persons may develop weakness, mechanical obstruction of the bowel, abdominal pain, fatigue, vomiting, diarrhoea, and weight loss. In severe infections there may be vitamin B12 deficiency and anaemia. DIAGNOSIS:- Identification of egg and segments in stool. PROPHYLAXIS:- 1.Through cooking of fish. 2. Prevent contamination of lakes, ponds, rivers etc. 3. Treatments of infected persons. 49 TREATMENTS:- Niclosamide and praziquantel. Class Trematoda General characters of trematodes (digenetic) These are leaf-shaped, unsegmented flat worms, called flukes. Size varies from 1 mm to several cm in length. The organs of attachment are two strong muscular cup- shaped depressions, called suckers. Oral and ventral (acetabulum). All are hermaphrodite (monoecious) except the Schistosomes. Body cavity is absent. The alimentary canal is present but incomplete. The anus is absent. Excretory and Nervous systems are present. Excretory system consists of “flame cells” and collecting tubules which opens posteriorly, in to excretory pore. Reproductive system is highly developed and complete in each individual. The genital organ lie between the two branches of the intestine. The worm is oviparous, since eggs are liberated. Eggs are all operculated (with lid) (except those of Schistosomes) Examples are Schistosoma, Gastrodiscoides, Fasciolopsis, Fasciola, Clonorchis, Heterophyes, etc. Class Trematoda Phylum: Platyhelminthes Class: Trematode Subclass: Digenea Genus: Schistosoma Species: S. haematobium, S. mansoni, S. japonicum, S.intercalatum Schistosomes Schistosomiasis, also known as bilharzia, is a parasitic disease caused by trematodes from the genus Schistosoma. There are four main species that infect humans. S.mansoni, S.Japonicum, S. intercalatum and S. haematobium. URINARY SCISTOSOMIASIS Etiology - Schistosoma haematobium Habitat - The worm lives in the veins of the bladder of humans. 50 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. Geographical distribution:- They have a world wide distribution and affect about 77 countries including Africa and China. Morphology of the adult parasite:- The sexes are separate (dioecious). In all species the male worm is boat shaped with a gynaecophoric canal in which females live. The cuticle of the male is smooth (S. japonicum) or has tuberculation (other species). There are two small suckers and a varying number of testes. The female is longer than the male but thinner, and circular in cross section. The two suckers of the female are small and weak. MORPHOLOGY OF THE EGGS:- Schistosoma haematobium eggs are elongated, has a thin smooth shell, rounded anterior end, a characteristic terminal spine from the tapered posterior end. Adult worm reside in the portal system venules, primarily those of the urinary bladder. Eggs work their way through vessels and mucosa of urinary bladder. The intermediate snail host and definitive host are Bulinus spp and Man respectively. Schistosoma mansoni eggs are elongated, has a thin smooth shell with a prominent lateral spine near the more rounded posterior end. Anterior end tends to be pointed and curved. Adult worm resides in the large intestine. The intermediate snail host and definitive host are Biomphalaria spp and 51 Above is the LIFE CYCLE OF Schistosoma spp Man respectively. Schistosoma japonicum eggs are oval, has a smooth thick shell. Adult resides in the ileo-caecal region of the large intestine. The intermediate snail host and definitive host are Oncomelania spp and Man respectively. 52 LIFE CYCLE OF SCHISTOSOME The life cycle of all the species follows a common pathway. Eggs are eliminated with faeces (S. mansoni, japonicum, S.intercalatum) or urine (S. haematobium). Under optimal conditions the eggs hatch and release miracidia, which swim and penetrate specific snail intermediate hosts. The stages in the snail include 2 generations of sporocysts and the production of cercariae. Upon release from the snail, the infective cercariae swim, penetrate the skin of the human host, and shed their forked tail, becoming schistosomulae. The schistosomulae migrate through several tissues and stages to their residence in the veins. Adult worms in humans reside in the mesenteric venules in various locations, which at times seem to be specific for each species. S. japonicum, S. mansoni, and S. intercalatum are more frequently found in the superior mesenteric veins draining the small intestine. S. haematobium most often occurs in the venous plexus of bladder, but it can also be found in the rectal venules. The females (size 7 to 20 mm; males slightly smaller) deposit eggs in the small venules of the portal and perivesical systems. The eggs are moved progressively toward the lumen of the intestine (S. mansoni and S. japonicum) and of the bladder and ureters (S. haematobium), and are eliminated with feces or urine, respectively. Symptoms and signs:- Urinary Schistosomiasis: S. haematobium, Gross haematuria, Dysuria, Bladder, ureters and kidneys damaged. Cancer of the bladder is common Intestinal schistosomiasis: S. mansoni, S. japonicum:- Gradual enlargement of liver and spleen, abdominal blood vessels begin to bleed then Blood in the stools. PATHOGENICITY:- Pathology of S. mansoni and S. japonicum includes: Katayama fever, hepatic perisinusoidal egg granulomas, Slimmer’s’ pipe stem periportal fibrosis, portal hypertension, and occasional embolic (blockage of artery) egg granulomas in brain or spinal cord. Pathology of S. haematobium includes:- Haematuria (blood in urine), scarring, calcification, squamous cell carcinoma (tumor) , and occasional embolic egg granulomas in brain or spinal cord. 53 Pathology and clinical symptoms Acute Manifestations i. Cercarial dermatitis, also known as swimmer's itch, is an allergic reaction caused by the penetration of cercariae in persons who have been exposed to cercariae in salt water or fresh water. Cercarial dermatitis manifests as petechial haemorrhages with oedema and pruritus, followed by maculopapular rash, which may become vesicular. The process is usually related to avian schistosomal species of the genera Trichobilharzia, Gigantobilharzia, and Orientobilharzia, which do not develop further in humans. ii. Katayama syndrome corresponds to maturation of the fluke and the beginning of oviposition. This syndrome is caused by high worm load and egg antigen stimuli that result from immune complex formation and leads to a serum sickness –like illness. This is the most severe form and is most common in persons with S. mansoni and S. japonicum infections. Symptoms include high fever, chills, headache, hepatosplenomegaly, lymphadenopathy, eosinophilia, and dysentery. A history of travel in an endemic area provides a clue to the diagnosis. Chronic Manifestations i. Symptoms depend on the Schistosoma species that causes the infection, the duration and severity of the infection, and the immune response of the host to the egg antigens. ii. Terminal haematuria, dysuria, and frequent urination are the main clinical symptoms of urinary schistosomiasis. iii. The earliest bladder sign is pseudotubercle, but, in long-standing infection, radiography reveals nests of calcified ova (sandy patches) surrounded by fibrous tissue in the submucosa. iv. Dysentery, diarrhoea, weakness, and abdominal pain are the major symptoms of intestinal schistosomiasis. v. A reaction to schistosomal eggs in the liver causes a periportal fibrotic reaction termed Symmers clay pipestem fibrosis. vi. Haemoptysis, palpitation, and dyspnea upon exertion are the symptoms of schistosomal cor pulmonale that develops as a complication of hepatic schistosomiasis. 54 vii. Headache, seizures (both generalised and focal), myeloradiculopathy with lower limb and back pain, paresthesia, and urinary bladder dysfunction are the noted symptoms of CNS schistosomiasis due to S.japonicum infection. Diagnosis Intestinal schistosomes Laboratory confirmation of S. mansoni and S. japonicum infection can be made by finding the eggs in the faeces. When eggs cannot be found in the faeces, a rectal biopsy can be examined. Serological tests are of value in the diagnosis of schistosomiasis when eggs cannot be found. Urinary schistosome The definitive diagnosis of urinary schistosomiasis is made by finding the characteristic ova of S. haematobium in urine. Terminal urine should be collected as the terminal drops contain a large proportion of the eggs. The urine can then be centrifuged and the deposit examined microscopically for ova. Eggs can sometimes be found in seminal fluid in males. A bladder biopsy is seldom necessary to make the diagnosis. A rectal snip may show the presence of ova as they sometimes pass into the rectal mucosa. Serological tests can be of value when eggs cannot be found in clinical samples. An enzyme linked immunosorbent assay using soluble egg antigen to detect antischistosome antibody is most sensitive. Note: There is a marked periodicity associated with the time when most eggs are passed out. Higher numbers of eggs are encountered in urine specimens passed between 10 am and 2pm, presumably as a result of changes in the host’s metabolic and physical activities. Epidemiology of Schistosomiasis The following factors are of epidemiological importance in the transmission of schistosomiasis: - The presence of water bodies such as rivers, streams, lakes, dams suitable for the breeding of the snail intermediate hosts. 55 - Presence of appropriate snail hosts necessary for the developments of the asexual stages and transmission of the infective stage to the human definitive host. - Contamination of natural water bodies with infected human urine and faeces. - Human water contact activities including swimming, laundry and fetching. - Factors that promote intramolluscan development of parasite and subsequent transmission to man. - Socio-economic status of the people such as good sanitary system and water supply. Control - Reduction of human-water contact. - Improved sanitation by proper waste disposal. - Attacking the adult forms of parasite through chemotherapy to reduce the worm burden or egg production. - Eradication or reduction of snail population through the use of molluscicides. - Development of vaccine to induce immunity. - Modification of the ecology of the snail habitat. - Biological control through the introduction of competitors’ snails into the snail habitat. - Education. TREATMENT:- Praziquantel: effective against all species. S. haematobium: single dose (40 mg/kg), S. mansonia and S. japonicum: 2-3 doses of 30mg/kg. PROPHYLAXIS Ovoid water pollution with human faeces Eradication of Molluscan host. Avoid swimming, bathing, wadding, or washing in infected water. Treatment of infected persons. Educate people to not urinate or defecate in fresh water supplies. Provide piped water to avoid direct contact with cercariae. Prevention: 1. Health education: 56 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 FASCIOLA HEPATICA (a trematode) Common names: The sheep liver fluke; the liver fluke. F. hepatica was the first trematode found in sheep with “liver rot”. Geographical distribution:- Human infections with F. hepatica are found in areas where sheep and cattle are raised, and where humans consume raw watercress. Habitat:- Adult worms reside in the biliary passage (i.e bile duct) of the liver of sheep, goat, cattle and man. Morphology:- It is a large leaf-shaped fluke and brown in colour. It is dorsoventrally flattened, bilaterally symmetrical with three body layers, and no true body cavity. The anterior end is conical in shape while the posterior end is broadly pointed. The oral sucker is situated in the conical projections at the anterior end, while the ventral sucker is situated nearby in a line with two shoulders. Life span of the adult worm is around 10 years. Eggs:- Eggs are large, oval, operculate (have a lid), light yellowish-brown in colour; with thin shell with a smooth surface. Each egg contains an immature larva, the miracidium, which extends to the shell margins without leaving a clear space. Infective form:- Metacercariae encysted on water plants that are ingested by humans. Life cycle:- F. hepatica passes its life cycle in one definitive and two intermediate hosts. 57 Definitive hosts:- Sheep, goat, cattle and man. They are reservoir hosts of F. hepatica. Intermediate hosts First intermediate host: Snails of the genus Lymnae. Second intermediate host: Aquatic vegetation e.g watercress. Life cycle The adult worms reside in the biliary passages of the liver of the definitive host. Eggs are laid in the biliary passages of the host, reach the intestine and are passed out in the faeces, into the freshwater (lakes, canals and the likes) releasing a free- swimming miracidium which burrows into the flesh of an appropriate snail within 8 hours. As it penetrates the snail’s tissue, the miracidium sheds its ciliated cover. The miracidium passes through the stages of sporocyst, first-generation (mother) rediae, second-generation (daughter) rediae, and finally lead to the release of hundreds of free-swimming, straight-tailed cercariae. 58 Life cycle of Fasciola hepatica 59 The cercariae escape from the snail into water, attach to aquatic vegetation and encyst as infective metacercariae. Herbivorous animals and occasionally humans acquire infection by ingesting uncooked aquatic plants thus infected. The matacercariae excyst in the duodenum and migrate through the duodenal wall into the peritoneal cavity, penetrate the capsule of the liver, traverse its parenchyma and settle in the biliary passages and grow to sexual maturity. The migration takes 6-7 weeks. The adult worms begin producing eggs which exit in the faeces 3-4 months after ingestion of metacercariae. Pathogenicity F. hepatica infection occurs mainly in rural area and is most common among sheep and cattle herders. The metacercarial larvae of F. hepatica that escape from cysts in the duodenum normally produce no significant damage as they migrate through the duodenal wall into the peritoneal cavity but traumatic and necrotic lesions 1 cm or more in diameter and heavily infiltrated with eosinophils are formed in the liver parenchyma by the young migrating flukes. These are accompanied by fever, mild to severe abdominal pain, urticarial, hepatosplenomegaly, and jaundice. The larvae develops into adult after arrival in the bile ducts, at this stage, the patient is generally asymptomatic or may develop gastrointestinal symptoms. Some patients may develop chronic cholecystitis accompanied by biliary colic, epigastric pain, nausea, pruritis. In heavy infections, the young worms may wander back into the liver parenchyma producing abscesses. Laboratory diagnosis:- Detection of eggs in stool or in bile obtained by duodenal intubation. Treatment:- Drugs used for this infection are bithionol, triclabendazole and dehydroemetine. Prophylaxis: Prevention can be carried out by:- Sanitation improvement and health education. Avoidance of eating raw or undercooked aquatic vegetation. Eradication of the disease in mammals by treatment of infected animals and destruction of molluscan hosts by use of molluscicides. 60 NEMATODES (ROUND WORMS) All the important human parasites of the Phylum Nemathelminthes (Aschelminthes) belong to the Class Nematoda. GENERAL CHARACTERISTICS OF NEMATODES 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. The 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 with tissue stage:- Ascaris lumbricoides, Hookworms and Strongyloides stercoralis 2. Intestinal nematodes without tissue stage:- Enterobius vermicularis and Trichuris trichuira. Tissue and blood dwelling nematodes:- Filarial worms:- Dracunculus medinensis, Trichinella spiralis and 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. Life cycle of Ascaris lumbricoides 61 Pathogenecity 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 62 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 WORMS 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. 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 membraneous 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

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