PHYLUM SARCOMASTIGOPHORA.
PHYLUM APICOMPLEXA. PHYLUM CILIOPHORA
Parasitology is the study of parasites and as such that does not include bacterial, fungal or viral parasites.
Human parasites are separated into intestinal and blood borne parasites. For a parasite to be defined as intestinal it must have an intestinal life cycle stage, though it may have life-cycle stages in the heart, blood vessels, and lungs in the humans, other animals or the environment.
The association between two organisms may be one of the following:
• Mutualism: mutual benefit is derived from the association. Mutual benefit, but the two organisms cannot live independently.
• Commensalism: one partner benefits (commensal) while the other (host) is unaffected. It may be called a non-pathogenic parasite.
• Parasitism: when an animal lives on another organism from which it receives food and shelter without any compensation to it. The animal, which enjoys advantages, is the parasite. all animals have parasites; hence there are more parasites than free-living animals. The habitat occupied by a parasite is very different from the environment of its free-living ancestors, hence it has either to adapt itself to this new habitat or perish.
Parasitism: one organism (parasite) lives at the expense of the other (host). The latter usually suffers from the association with pathogenic parasite). Parasitism is the form of mutual relations between organisms of various kinds, from which one (parasite) uses another (host) as environment for living, and from which it obtains food causing him damage (disease).
Parasitology is a complex biological science studying the phenomena of parasitism. There are mutual relations between the parasite and host, their dependence on the factors of external environment, and also diseases, caused by the parasites, and methods of fighting with them in man, animals and plants.
Parasite is an organism that lives upon or within another living organism (host) at whose expense it obtains some advantage. External parasite is an ectoparasite that lives on skin or hair of host. Internal parasite is an endoparasite that lives in body organs, body tissues, in cells or in cavity of host’s body.
Host is an organism that harbours or nourishes another organism (parasite). The hosts are divided into definitive hosts and intermediate hosts. Definitive host (final h.) harbours the adult or sexually mature parasite. Intermediate host harbours the immature or asexual stages of the parasite; usually designated first and second, if there is more than one.
Diseases that are caused by animals are known as invasive diseases. Protozoan diseases are caused by protozoa.
Diseases which are characteristic for human, (e.g. amoebiasis) called Anthroponotic.
Diseases which are characteristic for animals (e.g. malaria of birds) called Zoonotic.
Anthropozoonotic diseases are characteristic for humans and animals, for example, leishmaniasis.
There are four ways of agent transmission of invasive diseases:
1) contagious (by skin contact, sexual contact);
2) alimentary or faecal-oral (ingestion of raw or undercooked food or use of drinking water containing the infective stage of the parasite);
3) by blood (by bite of vectors containing the infective stage, blood transfusion). Vector is an arthropod that carries a parasite to host (e.g. Anopheles mosquito);
4) congenital (transplacental).
Medical parasitology consists of 3 parts:
· Medical protozoology
· Medical helminthology
· Medical entomology.
Classification of parasites
Each parasite belongs to a phylum, class, order, family, genus and species; the scientific designation of a parasite is binomial, a generic name (genus) and a specific name (species).
The parasites of humans in the kingdom Protozoa are now classified under 3 phyla:
Sarcomastigophora (containing the amoebae and flagellates);
Apicomplexa (containing the sporozoan);
Ciliophora (containing the ciliates).
The important human parasites are found within these great groups.
1. Class Lobozea (Sarcodina) is typically amoeboid and in represented in humans by class of Entamoeba, Endolimax, lodamoeba, Naegleria, and Acanthamoeba.
2. Class Zoomastigophora, the flagellates, have one or more whip-like flagella and, in some cases, an undulating membrane (e.g., trypanosomes). These include intestinal and genitourinary flagellates (Giardia, Trichomonas, Dientamoeba, Chilomastix) and blood tissue flagellates (Trypanosoma, Leishmania).
3. Class Sporozoa undergoes a complex life cycle with alternating sexual and asexual reproductive phases, usually involving two different hosts (e.g., arthropod and vertebrate, as in the blood forms). The subclass Coccidia contains the human parasites Isospora, Toxoplasma, and others. One of these, Cryptosporidium, has been implicated as a cause of intractable diarrhea among the immunosuppressed. Among the Haemosporina (blood sporozoan) are the malaria parasite (Plasmodium species) and the subclass Piroplasmia, which includes Babesia species. Pneumocystis has recently been shown to be a member of the Fungi rather than the Protozoa. It is another opportunistic parasite of immunosuppressed individuals.
4. Class Litostomatea is a complex protozoan bearing cilia distributed in rows or patches, with two kinds of nuclei in each individual. Balantidium coli, a giant intestinal ciliate of humans and pigs, is the only human parasite representative of this group.
The Parasitic Worms, Or Helminths, Of A Human Being, Belong To Two Phyla:
1. Platyhelminths (Flatworms) lack a true body cavity (celom) and are characteristically flat in dorsoventral section. Medically important species belong to the classes Cestoda (tapeworms) and Trematoda (flukes).
The tapeworms of humans are band-like and segmented; the flukes are typically leaf-shaped, and the schistosomes are narrow and elongate.
The important tissue and intestinal cestodes of humans belong to the genera diphyllobothrium, spirometra, taenia, echinococcus, hymenolepis, and dipylidium. medically important trematode genera include schistosoma, paragonimus, clonorchis, opistorchis, heterophyes, metagonimus, fusciolopsis, and fasciola.
2. Nemathelminthes (worm-like, separate-sexed, insegmented roundworms) include many parasitic species that infect humans.
Phylum Arthropoda includes 3 Classes Of Medical Importance:
1. Class Crustacea: Cyclops, Etc.
2. Class Arachnida (Octapoda): Scorpions, Ticks And Mites.
3. Class Insecta (Hexapoda): Mosquitoes, Flies, Bugs, Lice And Fleas.
Types of parasites
• Endoparasite: lives within the body of the host (infection).
• Ectoparasite: lives on the outside of the body of the host (infestation).
• Obligate parasite: completely dependent upon its host and cannot lead a free life.
• Facultative parasite: capable of leading both a free-living and a parasitic existence.
• Incidental parasite: can establish itself in a host in which it does not ordinarily live.
• Accidental parasite: a free-living organism that may live as a parasite in a host.
• Permanent parasite: remains all or most of its life in or on its host.
• Temporary parasite (occasional or intermittent): free-living but seeks its host from time to time for food.
• Periodic parasite (transitory): passes a definite part of its life cycle as a parasite.
• Specific parasite: occurs in one particular host.
• Pseudoparasite: an artifact mistaken for a parasite.
Types of hosts
• Final host or definitive host: harbours the adult or sexually mature parasite (female mosquito Anopheles for Plasmodium malaria)
• Reservoir host: an animal that harbours the same species of parasites as man and constitute a source of infection to him. Usually these animals are not affected by infection. The reservoir host serves as a potential source of human reinfection and as means of sustaining the parasite when it is not infecting man. Diseases of animals that are transmissible to man are called zoonotic diseases.
• Intermediate host: harbours the immature or asexual stages of the parasite (cow for beef tapeworm).
Vector: an arthropod that carries a parasite to its host.
Source and mode of parasitic infection or infestation
1. Food and drink:
Ingestion of raw or undercooked food or drinking water or other beverages containing the infective stage of the parasite.
2. Soil, dust and water (canals and streams)
a) Ingestion of food or drink contaminated with soil or dust containing the infective stage of the parasite.
b) Inhalation of dust.
c) Direct contact with soil (handling, walking barefooted); the infective stage penetrates the skin.
d) Using water streams (washing, swimming, wading, irrigation, etc.); the infective stage penetrates the skin or mucous membrane.
3. Vector
a) Bite of vector inoculating the infective stage.
b) Feces of vector containing the infective stage contaminate the skin (intact or wounded).
c) Ingestion of vectors containing the infective stage.
d) Direct penetration of an arthropod into the skin.
4. Direct contact:
a) Skin contact.
b) Sexual contact.
c) Autoinfection or direct infection.
5. Congenital infection (toxoplasmosis).
Effect of the parasite on the host (Pathogenicity)
The effect depends on the number, size and shape of the parasite; its activity (movement and migration); site (habitat); specific toxin and host reaction.
The effect may be due to:
1. The parasite abstracting nourishment from the host.
2. Mechanical effect leading to tissue destruction as a result of trauma, pressure, compression or obstruction; feeding on tissues or irritation of tissues leading to inflammatory or neoplastic reactions.
3. Toxic effects from toxins secreted or waste products excreted by the parasite, leading to poisoning or allergic reactions.
4. Secondary infection with other organisms as bacteria. The host reaction to the invading parasite may be:
a) Generalized in the form of fever, anaemia, leucocytosis, leucopaenia, eosinophilia, allergic reactions, weakness, etc.
b) Localized according to the tissue or organ affected, e.g. gastro-intestinal disturbances (colic, dyspepsia, diarrhea, and dysentery), itching, ulceration, hepatomegaly, splenomegaly, etc.
PROTOZOAN TAXONOMY
Taxonomy is concerned with the classification and denomination of organisms. In addition to nomenclature, taxonomy also places organisms into groups, sharing common features, and presumably evolutionary relationships. However, taxonomic criteria are often arbitrary, and taxonomy is always changing to reflect new discoveries and interpretations.
Protozoa are usually classified within the Kingdom Protista (Haeckel, 1866), which includes other unicellular eukaryotes.
Historically protozoa were divided into four major groups: the amoebae, the flagellates, the sporozoa and the ciliates. The distinguishing features between the groups were based on motility (i.e., amoeboid, flagella, cilia). The sporozoa were a heterogeneous group that produced spores during one stage of their life cycles and exhibited “gliding” motility.
In addition, some members within these two groups share some common features and therefore the amoebae and flagellates can be grouped together (e.g., sarcomastigophora).
So, the parasites of humans in the subkingdom PROTOZOA are now classified under 3 phyla: SARCOMASTIGOPHORA (containing the amoebae and flagellates); APICOMPLEXA (containing the sporozoans); and CILIOPHORA (containing the ciliates). The important human parasites are found within these great assemblages.
Medical protozoology
Protozoa are single celled organisms. There are four classes of Protozoa commonly found in concentrated faecal samples. These are differentiated by the method of motility. Protozoa include Entamoeba, Giardia, Trichomonas, Cryptosporidium, Isospora, Pneumocystis and Balantidium. There are two diagnostic life-cycle stages commonly seen in parasites – the cyst and the adult trophozoite stage. The trophozoite stage is analyzed directly on a slide without concentration. Cysts require concentration. The key diagnostic factor is that Protozoan cysts are typically 5-30 microns in diameter, and as such that are smaller than most Helminths eggs. Due to the size they are particularly difficult to see under the microscope if the sample clarity is bad.
The other major groups of parasites are known as blood-borne parasites where they are transmitted by an arthropod vector. Far more important arthropods for transmitting parasitic infections are the mosquitoes. Mosquitoes are known to carry malaria and filarial nematodes. Different types of biting flies transmit African trypanosomiasis, leishmaniasis and several kinds of filariasis.
Protozoa exhibit a wide variety of morphologies. There is no one shape or morphology, which would include a majority of protozoa. Shapes range from the amorphous and ever-changing forms of amoeba to relatively rigid forms dictated partially by highly ordered cytoskeletons or secreted walls or shells. Many protozoan species exhibit complex life cycles with multiple stages. Sometimes the different life cycle stages are so dissimilar that they have been mistaken for completely different species.
The vast majority of protozoa are microscopic. However, they do exhibit an incredibly large range of sizes. Extant species range in size from < 1 μm (10-6 meter) to several mm. Fossilized Forminiferida of several cm have been identified. Most of the organisms discussed in Parazitology will be 3 – 50 μm. This small size necessitates the use of a microscope to detect protozoa. An electron microscope is needed for detailed morphological studies.
Protozoa are conveniently divided into free-living and symbiotic with a few that are facultative symbionts. Generally free-living organisms are found in the soil or aqueous environments, whereas symbionts live in close association with another organism. Symbiosis implies a physiological dependency on another organism for its nutrition.
General morphology of Protozoa
1. Protozoa are unicellular organisms (single cell) sometimes called non-cellular or acellular, being not divided into cells.
2. Each protozoon performs all vital functions.
3. The protozoon is made of a mass of protoplasm differentiated into cytoplasm and nucleoplasm.
4. The cytoplasm consists of outer thin hyaline ectoplasm and inner voluminous granular endoplasm.
5. The ectoplasm perfoms the following: protection, locomotion, and ingestion of food, excretion and respiration.
6. The endoplasm is concerned with metabolism. It encloses:
a) food vacuoles: containing food during digestion,
b) volutin granules: stored food in the form of carbohydrate (glycogen vacuoles) or protein (chromatoid bodies),
c) excretory vacuoles: collect waste products and discharge them to the exterior by bursting through the ectoplasm or by an anal opening (cytopyge),
d) the nucleus.
7. The nucleus is important in reproduction and maintaining life. It is made of nuclear membrane, nuclear sap, and chromatin. In the vesicular nucleus chromatin is concentrated in a mass (the karyosome) or distributed between the karyosome and the inner surface of the nuclear membrane (peripheral chromatin). In the massive nucleus chromatin is distributed diffusely.
General biology of protozoa
1. Nutrition is perfomed either by: absorption of liquid food through the body surface, or ingestion of solid particles by means of pseudopodia or through the cytostome.
2. Excretion is perfomed either by: diffusion through the body surface, or excretory vacuoles.
3. Secretion: digestive enzymes, toxins, and material for cyst wall, enzyme to liquefy tissues.
4. Respiration is either: aerobic or anaerobic.
5. Locomotion can be carried by:
a) Pseudopodia (amoeboid movement);
b) Flagella: whip-like filaments arise from the kinetoplast+ blepharoplast + parabasal body);
c) Cilia: like flagella but smaller and more numerous covering most of the body.
6. Cyst formation: encystment of some protozoa is essential for survival outside the body of the host and during transmission from host to host.
7. Reproduction may be asexual or sexual.
a) Asexual reproduction (simple fission): division of the nucleus by amitosis (simple division) or mitosis (differentiation of chromatin into chromosomes); division of the cytoplasm by simple fission into two (binary fission) or more (multiple fission).
b) Sexual reproduction: the formation of 2 cells (male and female gametes) by reduction division, and their union (or syngamy) resulting in the formation of a zygote.
Class Lobozea. These organisms move with the help of pseudopodia. Reproduction is by binary fission. The production of a cyst is one of the stages in the life cycle.
Among the pathogenic species for man is Entamoeba histolytica, the causative agent of human intestinal amoebiasis, or amoebic disentery. Morphology. E. histolytica occurs in the human body in such forms:
1) Entamoeba histolytica forma magna – vegetative large tissue form which feeds on the erythrocytes and does not become encysted;
2) Entamoeba histolytica forma minuta – vegetative small commensal encysted form which lives in the lumen of the large intestine; 3) cysts which develop from the forma minuta.
Entamoeba histolytica
The trophozoites of E. histolytica / dispar, extracted from dysenteric stools, exhibit ingested red blood cells and clear pseudopodia.
Those of E. dispar will have no ingested red blood cells. They can be up to 60µm in diameter, and their motility is rapid and unidirectional. On a permanently stained faecal smear e.g. Trichrome or Iron haematoxylin, the morphological features are more visible. When using Trichrome staiuclei, chromidial bars, chromatin, red cells and bacteria stain red, cytoplasm stains blue-green and background and yeasts stain green. The presence of a small centrally placed karyosome is clearly visible. With Iron haematoxylin, nuclear chromatin and the karyosome will be stained immensely black. The remainder will be varying shades of grey/black.
Cysts of E. histolytica / dispar are 10 – 15µm in diameter and contain 1 – 4 nuclei.
Chromatoid bodies are usually present in young cysts as elongated bars with bluntly rounded ends. Glycogen is usually diffuse, but in young cysts it is often present as a concentrated mass, staining reddish brown with iodine.
Clinical signs of disease
Amoebiasis is an infection usually caused by the pathogenic Entamoeba histolytica / dispar, and is commonly an infection of the colon. It has a world wide distribution where environmental sanitation is poor. The parasite may behave as a commensal (causing no harm to the host) or it may act as a parasite (doing harm to the host). It is a disease of human beings, although some monkeys can become infected and the infection is then transmitted to humans.
Intestinal disease
Patients with intestinal disease may exhibit a number of symptoms including profuse diarrhoea with blood and mucus, fever and dehydration. Amoebic ulcers may develop in the large colon and can also be found in the rectal area. The ulcers are usually “flask shaped” with a small opening on the mucosal surface and a larger area below the surface.
Extra- intestinal amoebiasis: abscess of liver, lungs, brain, skin.
Microscopy
Where amoebic dysentery is suspected, the laboratory should be informed that a “hot stool” is being delivered so that it can be examined within twenty minutes. On cooling the amoebae stop moving and become very difficult to be identified. Direct microscopy should be done by mixing a small amount of the specimen in 0.9% sodium chloride solution. This permits detection of motile trophozoites of Entamoeba histolytica / dispar and can also provide information on the content of stool i.e. the presence of leucocytes and red blood cells. If one searchs e.g. primarily for cysts, not for amoebae, several stool samples are required to be examined, by direct microscopy and a sensitive concentration technique. Three negative stool samples are required before it can be found that there is no amoebic infection. Microscopic examination of an amoebic abscess aspirate, e.g. in the liver or lungs, may reveal haematophagous trophozoites. It must be examined immediately by mixing a drop of warm saline with some aspirated pus on a microscope slide.
Entamoeba coli
Entamoeba coli is a non-pathogenic amoeba with world wide distribution. Its life cycle is similar to that of E. histolytica but it does not have an invasive stage and does not ingest red blood cells.
The trophozoite is larger than that of E. histolytica ranging from 15-50 µm in diameter. It exhibits blunt pseudopodia with sluggish movement. A permanently stained preparation shows a nucleus with a moderately large eccentric karyosome with chromatin clumped on the nuclear membrane. The cytoplasm appears to be granular containing vacuoles with ingested bacteria and other food particles.
Cysts of E. coli are 15 – 30 µm in diameter and contain 1 – 8 nuclei with irregular peripheral chromatin: karyosomes not central. Chromatoid bodies are not frequently seen but, when present, they are usually splinter-like with pointed ends. Glycogen is usually diffuse but in young cysts is occasionally found as a well-defined mass, which is stained reddish brown with iodine.
Laboratory Diagnosis
Laboratory diagnosis is made by finding the characteristic cysts in iodine stained, formol-ether concentration method or by detecting the characteristic trophozoites in a wet preparation or a permanent stained preparation.
Prophylaxys. All patients are transferred to a hospital and adequately treated. Preventive measures against amoebiasis also include protection of foodstuffs and water from flies and contamination with faeces. The staff of catering establishments must be examined for cysts carriage. Health education of the population.
Non-pathogenic amoebas can parasitize the human gastrointestinal tract. These include Entamoeba gingivalis (oral cavity), Entamoeba coli (large intestine). E. coli larger than E. histolytica. Their cytoplasm is granular and the vacuoles contain bacteria, leucocytes, food particles, and glycogen, but no erythrocytes. E.coli forms cysts with 8 nuclei. E. gingivalis doesn’t form cysts.
Entamoeba gingivalis
Entamoeba gingivalis is an Entamoeba histolytica-like amoeba that lives in/on the teeth, gums, and sometimes tonsils. It measures 10-35 micrometers in length. Endocytotic vacuoles are ofteumerous and the parasite will ingest bacteria, leukocytes, and erythrocytes (dark circles in trophozoites, above) although it is not itself invasive. No cysts are formed and transmission is entirely by oral-oral contact. Multiple samplings reveal the parasite to colonize the oral cavity of nearly all adult humans.
Class Zoomastigophorea.
Movement is effected by means of one or several long flagella. They are oval, elongate or spherical in shape. Reproduction of parasites is generally by longitudinal fission (asexual), sexual reproduction rarely occurs. Type representatives are trypanosomes, leishmaniaes, tricomonas and lamblias.
Giardia lamblia (giardiasis)
Giardia lamblia is a flagellate of world wide distribution. It is more common in warm climates than moderate climates. It is the most common flagellate of the intestinal tract, causing Giardiasis. Humans are the only important reservoir of infection. Infection is most common in parts of the world where sanitation levels are the lowest. Giardiasis is an infection of the upper small intestine, which may cause diarrhoea. Only Giardia spreads disease.
The trophozoites of G. lamblia are flattened pear shaped and are of an average size of 15 µm long, 9 µm wide and 3 µm thick. When stained, the trophozoite is seen to have 2 nuclei, 2 slender median rods (axostyles), and 8 flagella arising from the anterior end. They have been described as looking like tennis rackets without the handle (they are often seen having a comical face-like appearance when observing at the front view).
The movement of the trophozoites is described as tumbling leaf motility, using their 4 pairs of flagella for locomotion. They attach themselves to the surface of the jejunal or duodenal mucosa by their disc-like suckers, which are found on their ventral surface. They multiply in the gut by binary fission. Once the trophozoites drop off the mucosal surface they are normally carried in the intestinal contents down the gut where they usually encyst.
The cysts of G. lamblia are 8 – 12 µm in length and are elliptic in shape. They contain 4 nuclei, which tend not to be obvious. Longitudinal fibrils consisting of the remains of axonemes and parabasal bodies may also be seen. Cysts may appear to shrink from the cell wall. Cysts are infective as soon as they are passed.
Clinical signs of disease
Giardia lamblia colonizes the small intestine where the trophozoites adhere to the mucosal surface by means of their sucking discs. Cysts are produced as the parasites descending the intestinal tract, although trophozoites can pass in feces in severe infections. G. lamblia is transmitted through ingestion of cysts in contaminated water or food. Cysts can survive outside the body for several weeks under favourable conditions. The main symptoms are abdominal pain, flatulence, and episodic diarrhoea with steatorrhea and periodical soreness in severe cases. No blood or mucus is normally seen. Although, however, 50% of G. lamblia infections are symptomless, severe infections may develop in immunocompromised hosts. What determines susceptibility is poorly understood. After swallowing cysts for the first time, symptoms commonly develop 2-6 weeks later.
Normally illness lasts for 1 to 2 weeks, but there are cases of chronic infections lasting months to years. Chronic cases, both those with defined immune deficiencies and those without, are difficult to treat. The disease mechanism is unknown, with some investigators reporting that the organism produces a toxin while others are unable to confirm its existence. The organism has been demonstrated inside host cells in the duodenum, but most investigators think this is such an infrequent occurrence that it is not responsible for disease symptoms. Mechanical obstruction of the absorptive surface of the intestine has been proposed as a possible pathogenic mechanism, as has a synergistic relationship with some of the intestinal flora.
Thus, no matter what it looks like, stream water should be treated before drinking. Boiling will kill Giardia cysts, and there are commercially available filters that will remove the cysts from water.
Cysts can be found by examination of the deposit of a formol-ether concentrate of a stool preparation. The oval cysts with thick walls serve as characteristic features for these organisms. The flagella disintegrate and form a central “streak” which becomes visible when stained with iodine or MIF (merthiolate-iodine-formaldehyde). Cysts may be excreted intermittently; therefore it is important to examine more than one stool. Stools are usually passed 3-8 times / day and are usually pale, offensive, rather bulky and accompanied by much flatus.
Trophozoites are found by examination of saline wet preparations of fresh, diarrhoeic stool, duodenal or jejunal aspirate or in a permanently stained fecal preparation.
Trophozoites can also be found in the jejunal aspirate. These can be recovered by the String Test or Enterotest capsule and the material examined microscopically for motile trophozoites.Trophozoites and cysts can be found to be scarce in chronic infections.
Pathogenesis and disease in man. The source of infection is people who discharge cysts with the faeces. The chitin membrane of the cyst dissolves in small intestine. The vegetative forms (trophozoites) of lamblias multiply in the small intestine and penetrate into the duodenum and gall-bladder. The liver and intestine are involved (chronic duodenitis, enterocolitis). Cholecystitis and hepatitis develop quite frequently.
Laboratory diagnosis is made by microscopic examination of the duodenal contents or faeces.
Prophylactic measures are similar to those carried out in prevention of intestinal infection.
Trichomonas vaginalis (trichomoniasis, “trich” or “trick”)
Trichomonas vaginalis is a sexually transmitted disease (STD), although transmission by other routes (such as soiled towels) has been documented. There is no cyst in the life cycle, so transmission is via the trophozoite stage. Most people infected with trichomoniasis are asymptomatic.
Multiplication and Life Cycle. The trophozoite, the only form of this organism,divides by binary fission in the urogenital tract. Transfer of trophozoite is usually directly from person to person.
Clinical Manifestations. Trichomoniasis is a common urogenital disease in women. Vaginitis, with discharge may be present, frequent and painful urination are common. This infection is usually asymptomatic in men. The organisms are transferred during sexual intercouse.
Diagnosis. Trichomonas organisms can be demonstrated in vaginal fluid, scrapings, or washing. Trichomonas hominis (large intestine) is non-pathogenic, doesn’t form cysts.
Symptomatic infections are characterized by a white discharge from the genital tract and itching. Diagnosis depends on finding trophozoites in secretions of the genital tract from men or women. In cases where the numbers of organisms are very low, the trophozoites can be cultured to increase their numbers.
Trypanosoma species
Trypanosomes are haemoflagellates and three species of the genus Trypanosoma are responsible for disease in humans such as sleeping sickness.
Trypanosomes occur in the blood of the majority of vertebrate animals. The life cycle involves intermediate host, which usually is an insect. Many species of trypanosomes can live in harmony with their hosts producing no pathogenic effect, but the best known species are those that are pathogenic to their definitive hosts. The disease caused by the pathogenic types is called trypanosomiasis.
Trypanosoma brucei rhodesiense and Trypanosoma brucei gambiense – these metacyclic trypanosomes are found in the proboscis of the insect vector – infection is therefore inoculative. The above are the aetiological agents of African trypanosomiasis, it is a zoonotic species in the fact that it multiplies in the blood of a range of animals, domestic and wild animals as well as a man.
Trypanosoma brucei rhodesiense causes an acute form of sleeping sickness in East Africa, while T. b. gambiense causes chronic sleeping sickness in West Africa.
These are known as salivarian trypanosomes as they complete their development in the salivary system (anterior portion of the vector). Transmission takes place by innoculation of the metacyclic stage.
Trypanosoma cruzi – the metacyclic trypanosomes occupy a posterior position in the gut of the insect vector and are passed out in the faeces – infection is therefore contaminative. This is the aetiological agent of South American trypanosomiasis.
These trypanosomes are known as stercocarian as they complete their development in the posterior region of the vector, so that the infective forms appear in the insects’ feces. Hosts are infected by a contaminative route.
African Trypanosomiasis
Transmission from one vertebrate to another is carried out by blood-sucking invertebrates, usually an insect. The vector for African Trypanosomes is the Tsetse fly, Glossina, and the species which cause the disease are T. b. gambiense and T. b. rhodesiense.
Metacyclic (infective) trypomastigotes are inoculated through the skin when a tsetse fly takes a blood meal.
The parasites develop into long slender trypomastigotes, which multiply at the site of inoculation where ulceration occurs. The trypanosomes continue to develop and then may invade the lymphatic tissue, the heart, various organs and in later stages, the central nervous system. Trypomastigotes are taken up by the tsetse fly (male and female) during a blood meal. The parasites develop in the midgut of the fly where they multiply. 2-3 weeks later the trypomastigotes move to the salivary glands transforming from epimastigotes into metacyclic (infective) trypomastigotes. The tsetse fly remains infective for all their life i.e. about 3 months.
The mode of transmission mentioned above, metacyclic transmission, requires to be separated from mechanical transmission, a process in which trypanosomes survive, for a short time, on and about oral region of an insect and are inoculated into a new host when the vector bites again, without undergoing any developmental cycle.
Metacyclic transmission requires a lapse of time to allow the trypanosomes to reach an infective stage by a particular developmental sequence in the vector, usually a period of several days.
Morphology
The parasite is an elongated cell with single nucleus, which usually lies near the centre of the cell. Each cell bears a single flagellum, which appears to arise from a small granule – the kinetoplast. The kinetoplast is a specialised part of the mitochondria and contains DNA. The length and position of the trypanosome’s flagellum are variable. In trypanosomes from the blood of a host the flagellum originates near the posterior end of the cell and passes forward over the cell surface, its sheath is expanded and forms a wavy flange called an undulating membrane.
Development is characterised by the occurrence of three types of blood forms (polymorphic), these are:
1) Slender forms: long and thin, about 29mm long, free flagellum.
2) Stumpy forms: thick and short, average length 18mm, typically no free flagellum, but a short one may be present.
3) Intermediate forms: about 23mm long with a moderately thick body and a free flagellum of medium length.
Clinical signs of disease
The early stages of African trypanosomiasis may be asymptomatic and there is a low grade parasitiaemia. This period may last for several weeks to several months. The disease may terminate untreated at this stage or go on to invade the lymph glands. Invasion of the lymph glands is usually accompanied by a high irregular fever with shivering, sweating and an increased pulse rate. The lymph glands near the bite often become swollen, in T. b. gambiense the glands at the back of the neck and T. b. rhodesiense usually the glands under the jaw are affected (Winterbottoms sign). As the disease progresses oedema of the eyelids, face and sleeplessness are features along with increasing lethargy and listlessness.
Trypanosomes may invade the central nervous system giving symptoms of meningoencephalitis, confusion, apathy, excessive sleeping and incontinence. At this stage, the cerebro-spinal fluid (CSF) usually contains mononuclear cells and a few trypanosomes may be detected. If untreated, character changes, mental deterioration and coma develop, finally resulting in death. Such signs are more commonly seen with gambiense than in rhodesiense in which patients often die before these symptoms develop completely.
Laboratory diagnosis of African trypanosomiasis
Laboratory diagnosis of African trypanosomiasis is by:
1. Examination of blood for the parasites
2. Examination of aspirates from enlarged lymph glands for the parasites
3. Examination of the CSF for the parasite
4. Detection of trypanosomal antibodies in the serum
Prophylaxis is ensured by a complex measures which include recognition and treatment of patients, protection of the population from the bites of tsetse flies (Glossina palpalis), the use of insect repellents, extermination of vector flies.
South American trypanosomiasis
Trypanosoma cruzi occurs throughout South and Central America, especially in Brazil, Argentina and Mexico causing the disease known as Chagas’ disease.
It is estimated that over 24 million people are infected with this species. It is a zoonotic parasite with over 150 species of wild animals known to harbour the parasites, for example opposums, dogs, rates, pigs and cats.
It is transmitted to man by brightly coloured bugs belonging to the Reduviidae family, subfamily Triatominae. All stages of these bugs are known to become infected.
The bugs live in the crack of the walls and vegetal roofs of the poorly maintained houses, coming out at night to feed on the exposed parts of the host’s body.
Metacyclic trypomastigotes are deposited in feces on the skin as the triatomine bug (reduviid bug) feeds. The bug usually bites round the edges of the mouth and eyes. The trypomastigotes are either rubbed into the skin by scratching the irritated area or penetrate the conjunctiva or membranes of the nose and mouth. Trypomastigotes become amastigotes in localised reticular endothelial cells and multiply. The amastigotes develop into trypomastigotes, which are released into the blood when the cell ruptures. No multiplication of the parasite takes place in the blood in its trypomastigote stage. The trypomastigotes reach tissue cells especially heart muscle, nerves, skeletal muscle and smooth muscle of the gastrointestinal system through the blood and lymph. The trypomastigotes become amastigotes and multiply forming pseudocysts. Within the pseudocyst some amastigotes become elongated and develop first into epimastigotes and then trypomastigotes. When the cell ruptures the trypomastigotes are released into the blood and continue to circulate whilst others invade further tissue cells. The life cycle completes when a triatomine bug vector ingests circulating trypomastigotes. In the vector the trypomastigotes transform and develop into epimastigotes, multiply by binary fission in the gut of the bug. After about 10 – 15 days, metacyclic trypomastigotes are formed and can be found in the hindgut of the bug.
Morphology
Trypanosoma cruzi has a single form (monomorphic), about 20mm in length, and characteristically curved. The kinetoplast is large, considerably larger than the Trypanosoma bruceii species already discussed. They sometimes appear as a bulge at the posterior end. The flagellum is medium in length.
Clinical signs of disease
Many people infected with T. cruzi remain asymptomatic and free from Chagas’ disease or experience only an acute infection without progressing to the chronic stage. The most severe form of the disease is most commonly seen in children younger than 5 years of age. Multiplication of T. cruzi at the site of infection can produce an inflamed swelling (chagoma) which persists for weeks. Trypomastigotes or amastigotes may be seen in the aspirate of the chagoma.
Regional lymph nodes may become infected which frequently involve one side of the face. Unilateral oedema of the upper and lower eyelid may occur along with conjuctivitis. This is known as Romana’s sign.
In the acute stage of infection trypomastigotes can be found in the blood. Symptoms may pass unnoticed, but there may be fever, malaise, increased pulse rate and enlargement of the lymph glands, liver and possibly spleen. Muscle aches and pains are characteristic at this stage and parasites may be seen in blood films. The acute form is most often seen in young children and occasionally can cause serious damage to the heart and other complications leading to death caused by central nervous system involvement.
Chronic manifestations include signs of cardiac muscle damage with a weak and irregular heartbeat, oedema, heart enlargement leading to heart failure. Dilation of the digestive tract resulting in megaoesophagus and megacolon may also occur. About 10% of persons infected with T. cruzi develop chronic Chagas cardiopathy.
Laboratory Diagnosis of South American trypanosomiasis is made by:
1. Examination of blood;
2. Xenodiagnosis;
3. Blood culture;
4. Serology.
Leishmania species
Leishmaniasis is caused by parasites of the genus Leishmania and is endemic in many parts of Africa, Asia and South America. It is transmitted by Phlebotomus species, sandfly. Leishmania species are mainly parasites of man and other animals, especially dogs and rodents. They cause diseases collectively known as Leishmaniasis; causing 3 types of disease i.e. visceral leishmaniasis, cutaneous leishmaniasis and muco-cutaneous leishmaniasis. These are all debilitating and disfiguring diseases, which occur throughout the Old and New World. The parasites are unusual in that they live entirely within the cells of the reticulo-endothelial cells; they have become perfectly adapted as the proteolytic enzymes, which attack other foreign bodies in the blood stream, do not destroy them.
Prophylaxis is achieved by extermination of bugs (the vectors of the causative agent). Chemoprophylaxis with special preparations is carried out in endemic areas.
Visceral leishmaniasis
Human visceral leishmaniasis (VL), sometimes known as Kala-azar, is caused by Leishmania donovani complex; L. donovani and L. donovani infantum in the Old World and L. donovani chagasi in the New World. The clinical features –azar caused by these species are similar, but they have different epidemiological features. The parent species L. donovani occurs in Asia (Northeastern China, India and Iran) and Africa (primarily Sudan, Kenya and Ethiopia) and can affect people of all ages. The parasite (L. d. infantum), which causes VL in countries bordering the Mediterranean, (Southern Europe as well as North Africa) affects young children as well as infants. It is now being seen in the immunocompromised. In the New World also, VL is mainly a disease of young children, with the causative organism L. d. chagasi being closely related to, but slightly different from, L. donovani. The main geographical foci of VL in Latin America are iorthern and northeastern Brazil. Small foci are found in northern Argentina, Columbia and Venezuela. Sporadic cases are found in Central American countries, including Mexico.
Cutaneous leishmaniasis
Cutaneous leishmaniasis is caused by L. tropica, L. major and L. aethiopica in the Old World and L. mexicana complex in the New World. Leishmania tropica is widely distributed around the Mediterranean basin, Afghanistan, Kenya, Armenia, Azerbaijan, Turkmenistan and Uzbekistan. Leishmania aethiopica is seen in the highlands of Ethiopia and L. major occurs in the Middle East, West Africa, North Africa and Kenya. Leishmania mexicana complex is found in Central America and the Amazon Basin.
Life cycle
All forms of infection starts when a female sandfly (Phlebotomus species) takes a blood meal from an infected host. Small amounts of blood, lymph and macrophages infected with Leishmania amastigotes are ingested. Once ingested the amastigotes transform to promastigotes in the sandfly, the non-infective promastigotes divide and develop into infective metacyclic promastigotes. These are formed in the midgut of the sandfly and migrate to the proboscis. When the sandfly bites the extracellular inoculated promastigotes at the site of the bite is phagocytosed by macrophages. After phagocytosis, transformation to dividing amastigotes occurs within 24 hours. Reproduction at all stages of the lifecycle is believed to occur by binary fission. No sexual stage has been identified.
Morphology
Leishmania exist as flagellated extracellular promastigotes in the Sandfly vector and as a flagellar obligate intracellular amastigotes within mononuclear phagocytes of their vertebrate hosts
.
The various species are not distinguishable morphologically from one another. When stained with Romanowsky stains such as Giemsa, amastigotes appear as round or oval bodies ranging from 2 – 3mm in diameter with a well defined nucleus and kinetoplast, a rod shaped specialized mitochondrial structure that contains extranuclear DNA. The flagellated promastigote is spindle shaped, measuring 10 – 20mm in length, not including the length of the flagellum. As in the amastigote form a nucleus and kinetoplast are clearly visible.
Clinical signs of disease – Visceral Leishmaniasis
VL has been documented in India, Pakistan, southern Russia, China, Africa, the countries bordering the Mediterranean, and South and Central America. Systemic infection results from parasitization of cells of the reticuloendothelian system with L. donovani. The incubation period of kala-azar (caused by Leishmania donovani) varies from several weeks to 2-3 months. It is followed by fever and long-term remissions. The temperature is moderately elevated, the spleen and liver become enlarged, and progressive anaemia develops. The skin turns a dark colour. Kala-azar is characterized by a chronic course and lasts for many years. Death rate ranges from 20 to 30 per cent. The reservoirs of infection are man and domestic animals (dogs, cats).
The incubation period of VL may vary between 2 weeks and 18 months. The onset of VL is usually insidious with fever, sweating, weakness and weight loss. The most prominent findings are fever, hepatosplenomegaly and anaemia. The sites mainly affected are the liver, spleen and bone marrow. Enlargement of the liver is due to hyperplasia of Kupffer cells which are packed with amastigotes. The bone marrow is infiltrated with parasitised macrophages.
Some organs, notably the kidneys, may show pathological changes secondary to deposition of immune complexes. In advanced cases, ascites and oedema can develop. Deaths are usually due to secondary bacterial infections such as pneumonia, tuberculosis or dysentery.
Laboratory Diagnosis of Visceral Leishmaniasis
1. Microscopy
2. Culture
3. Serodiagnosis
Prophylaxis of VL comprises the following measures: early diagnosis, opportune treatment, rodent control, and extermination of sandflies and of dogs infected with leishmaniasis.
Clinical signs of disease – Cutaneous Leishmaniasis
Following a bite from an infected sandfly, a small red papule appears at the site of the bite about 2-8 weeks later. The papule increases in size centrifugally.
The patient then mounts either a hypersensitive response or an anergic response. In a hypersensitive response, the papule eventually ulcerates, becomes depressed and then eventually heals through scarring. The patient is now immune from subsequent bites. In an anergic response, the nodule grows and spreads over large areas of the skin. This resembles leprosy.
Laboratory Diagnosis of Cutaneous Leishmaniasis
1. Slit skin smear.
2. Polymerase chain reaction
Prophylaxis of CL: early diagnosis, extermination of sandflies and dogs and rodents infected with leishmaniasis, and vaccination.
Apicomplexa, Sporozoae
The over 5,500 described members of phylum Apicomplexa are all endoparasites in animals. At two stages in the life cycle, all individuals possess a structurally complicated grouping of microtubules and organelles at one end of the cell; the phylum name formally acknowledges this “apical complex”. Adult sporozoans are highly specialized for existence as endoparasites and completely lack locomotory organelles. Sporozoans life cycles are complicated affairs, including sexual reproduction by means of gamete fusion, asexual reproduction through fission, and the production of resistant or infective spores.
The malaria parasites of man include four species: Plasmodium vivax, the causative agent of tertian malaria, Plasmodium malariae, the causative agent of quartan malaria, Plasmodium falciparum, the causative agent of tropical (falciparum) malaria, Plasmodium ovale, the causative agent of tertian ovale-malaria.
Toxoplasma gondii
Toxoplasma gondii, the causative organism of toxoplasmosis, was first observed in 1927 in the gondii, a North African rodent. The first human case of toxoplasmosis was also reported that year. The organism is a coccidian protozoa belonging to the subphylum Apicomplexa and has a world wide distribution occurring in all warm-blooded animals.
Cats are the definitive hosts and they become infected by ingesting oocysts or cysts in tissues of paratenic hosts, such as mice, or transplacentally. Man becomes infected either by direct ingestion of oocysts from a cat or by eating raw or undercooked meat. Those who handle raw meat are particularly at risk. Infection can be transmitted transplacentally.
Morphology.
1) Pseudocysts (intracellular collection of trophozoites in cells in the acute stage of infection);
2) Trophozoites (intracellular parasites, about 6 × 2 micro;m, crescent-shaped with central nucleus and multiply by binary fission forming pseudocysts);
3) Cysts (collection of trophozoites enclosed in a true tissue cyst, in the chronic stage or latent infection);
4) Oocysts (oval, 10 × 12 micro; m, contains two sporocysts each containing four sporozoites, and found in stool of infected cats).
Life cycle
The development of the entereoepithelial (sexual) cycle in the cat’s intestine is brought about by the ingestion of sporulated oocysts of a mouse with cysts. The pre-patent period up to the shedding of the oocysts varies with the stage of T. gondii ingested, for example only 3-10 days if the cat has ingested a mouse containing cysts, but about 19-20 days or longer after direct infection with oocysts or ingestion of a mouse containing only tachyzoites.
The final host is the cat in which the oocyst-producing sexual stage of Toxoplasma can occur.
Mammals, including humans, birds are in which parasite reproduces asexually are intermediate hosts.
Transmitted to humans
1. Oocysts pass from cat intestine to cat feces.
2. Oocysts sporulate in soil and are viable for longer than one year.
3. Humans ingest oocysts either from soil or cat raw tissue infected with cysts. The alimentary route of infection takes place on ingestion of meat, milk, and dairy products of animals sick with toxoplasmosis, uncooked eggs of affected birds, and water contaminated by sick animals.
4. Transmitted via placenta when mother develops infection during gestation-congenital infection.
5. Toxoplasma gondii invades intestinal wall after entering host (usually orally) and disseminate via lymphatics and bloodstream forming trophozoites. T. gondii can spread to many host cells (the histophagocytic system, nerve tissue, liver, placenta, etc).
Women most at risk of delivering an infected infant are those who acquire the infection just prior to gestation.
Humans can acquire infection by:
1) Accidental ingestion of the oocyst shed in the cat’s feces;
2) Ingestion of the tachyzoite in infected milk or transplacentally;
3) Ingestion of the tissue cyst in undercooked or raw meat;
4) Transplant of an infected organ in a seronegative recipient.
Clinical Signs of Disease
Serological evidence has shown that approximately one third of the world’s population has Toxoplasma antibodies. This suggests that the majority of infections are benign with most people exhibiting few or no symptoms, but fever and swelling may be seen. However Toxoplasma gondii can cause severe illness in congenital infections, acquired infections and in immunocompromised patients. This may lead to ocular toxoplasmosis and ultimately to fatal CNS disorders such as encephalitis.
Typical manifestations are pneumonia, enterocolitis, nephritis, hepatitis, myocarditis, and a high or subfebrile temperature. Infection is often asymptomatic. Congenital toxoplasmosis is characterized by hydro- or microcephalus, lesions in the organs of the vision (chorioretinitis), cirrosis of the liver and enlargement of the spleen. Asymptomatic toxoplasmosis in the mother leads to infection of the foetus and this results in abortion or birth of a dead child.
Congenital toxoplasmosis
This occurs approximately in 1 per 1000 pregnancies. It can cause severe damage to and even death of the fetus. Proliferation of tachyzoites leads to intracellular calcification, corioretinitis, hydrocephaly, psychomotor disturbances and convulsions.
A small proportion of babies who are asymptomatic at birth develop retinocoroiditis or mental retardation becoming children or young adults. When a mother is first exposed to the parasite in later pregnancy the infant is likely to be less severely damaged or asymptomatic.
Acquired infections
Infections with T. gondii are often mild with flu-like symptoms, thus they often go unnoticed. However lympadenopathy is the most easily recognized symptom and it can be accompanied by fever, headache and myalgia. Toxoplasmosis may also produce infectious mononucleosis-like symptoms. Ocular toxoplasmosis is also a common sign, however, it is not yet proved whether this is due to congenital or acquired infections. Other manifestations of Toxoplasma infections are meningoencephalitis, hepatitis, pneumonitis and myocarditis.
Immunocompromised patients
Toxoplasmosis has been shown to occur as an opportunistic pathogen in immunocompromised patients and can cause severe complications. Toxoplasmosis in immunocompromised patients almost always arises from a reactivation of latent infections. Conditions, which can predispose to toxoplasmosis are malignancies, organ transplants, leukaemias and patients with acquired immune deficiency syndrome (AIDS). In immunocompromised patients, the central nervous system is primarily involved with diffuse encephalopathy, meningoencephalitis or cerebral mass lesions. Toxoplasma encephalitis has been reported as a life threatening among patients with AIDS.
Laboratory Diagnosis
Microscopic examination of fluids and organs of sick man (presence of T. gondii).
Biological tests with susceptible animals (mice, white rats, guinea pigs).
Serology of blood and cerebrospinal fluid.
Prophylaxis: washing of hands before meals and after handling animals and animal products, and the prohibition of preparing food from insufficiently cooked meat products, in particular liver. All women with a history of spontaneous abortion must be examined by laboratory methods for prevention of congenital toxoplasmosis.
Malaria
Red blood cells offer parasites an excellent environment for invasion and survival. Haemosporina are the only protozoan parasites, which can invade the red blood corpuscles of vertebrates. Most of them, if not all, have multiplicative phases in the reticulo-endothelial system.
The red blood cells are thin-walled and constantly moving, with the result that absorption of food materials and elimination of waste products of metabolism are relatively easy to achieve. In addition, they also contain rich supplies of protein and oxygen.
Malarial parasites are knowot actually to penetrate the red blood cell but, in fact, enter the cell membrane by endocytosis and enclosed in a parasitophorous membrane.
Malaria is the most important tropical disease known to mankind, causing many deaths and much morbidity throughout the world. It remains a significant problem in many tropical areas especially in sub-Saharan Africa. In many areas of the world we have the situations, deteriorating as a result of environmental changes, including global warming, civil disturbances, increasing travel and drug resistance. (Greenwood, B.M, 1997) There are approximately 100 million cases of malaria worldwide with about 1 million of these proving fatal.
Malaria is caused by protozoa of the Plasmodium species. There are 4 species which infect both humans and aniamls; Plasmodium malariae (quartian malaria), Plasmodium vivax (benign tertian malaria), Plasmodium falciparum (malignant tertian malaria, subtertian malaria) and Plasmodium ovale (ovale tertian malaria).
All Plasmodium species undergo the general haemosporina developmental cycle, which can be summarised as:
1. Initial or continual schizogny in the vertebrate host with initiation of gametogeny;
2. Formation of gametes in the arthropod host and subsequent fertilization and formation of a zygote;
3. Formation of sporozoites from the zygote by repeated nuclear division followed by cytoplasmic divisions (Smyth, J.D, 1994)
Morphology of plasmodia.
Blood stages of Plasmodium:
1) young trophozoites (ring forms);
2) growing trophozoites;
3) mature trophozoites;
4) mature schizonts;
5) macrogametocytes;
6) microgametocytes.
The merozoite is the youngest form of the parasite, appearing as the result of the splitting of a mature schizont. It is spherical or oval and small in size (1-2 micro;m). The merozoites consist of cytoplasm and a nucleus. Merozoites penetrate into the erythrocytes and give rise to asexual forms of the parasites. The young trophozoite (ring-form stage) grows larger and a vacuole appears in its cytoplasm. At this stage the malarian parasite has irregular contours and resembles a ring. The semimature schizont is capable of amoeboid movement. As it grows, a pigment appears within it (a product of haemoglobin breakdown) in the form of dark-brown spots.
The mature schizont becomes rounded and pulls in its pseudopodia by the time of complete merulation, occupying almost the entire erythrocyte.
The nucleus and cytoplasm divide and form from 6 to 24 merozoites (it depends from the species of the parasite). The pigment accumulates in the centre in a compact clump. The erythrocytes are destroyed by merozoites. The merozoites release into the blood plasma. Some of them again penetrate into erythrocytes. The gametocytes are sex cells and are subdivided into female (macrogametocytes) and male (microgametocytes) cells. The macrogametocytes are 12-14 micro;m, their nuclei are small. The microgametocytes are smaller, their nuclei are large.
Life cycle involves sexual stage (sporogony) in the mosquito (Anopheles) and asexual stage (schizogony) in humans. Man is an intermediate host and mosquito is a definitive host.
The life cycle passes 3 stages: two in man:
“Exoerythrocytic schizogony (liver phase)” and “Erythrocytic schizogony (blood phase)”; one in mosquito: “Sporogony”.
Exoerythrocytic schizogony (liver phase)
1. Mosquito bites man, takes blood meal and injects sporozoites from its salivary gland into the blood.
2. Sporozoites travel through blood to the liver, multiply asexually to form merozoites, which upon liver cell rupture. Merozoites are released into the bloodstream and infect erythrocytes.
Erythrocytic schizogony (blood phase)
1. Merozoites enter the erythrocytes, forming a ring-like trophozoite. Mature trophozoites asexually divide to form schizonts.
2. Schizont develops into merozoites, then lyse the erythrocytes membrane, leading to periodic paroxysms of disease due to resultant parasitemia. P. ovale, P. vivax, P. falciparum—membrane lysis in 48 hours, P. malariae—membrane lysis in 72 hours.
3. Some merozoites are developed into macrogametocytes and microgametocytes.
Sporogony
1. Mosquito ingests gametocytes with blood meal.
2. Gametocytes enter mosquito gut.
3. Zygote, formed from fertilization, invades gut wall to form an oocyst within 24 hours following ingestion.
4. Sporozoites are formed, released into the stomach, migrate to salivary glands, then injected into human with blood meal.
There is no requirement for resistant stages since the transfer of parasites between the vertebrate and invertebrate hosts is made by withdrawal or injection during the bloodsucking act, there is little or no exposure to the hazards of the outside world; thus by blood transfusion or inoculation, via the blood stages of the parasite.
Malaria is transmitted by the female Anopheline mosquito. The life cycle of all species of human malaria parasites is essentially the same. It comprises an exogenous sexual phase (sporogony) with multiplication in certain Anopheles mosquitoes and an endogenous asexual phase (schizogony) with multiplication in the vertebrate host. The latter phase includes the development cycle in the red cells (erythrocytic schizogony) and the phase taking place in the parenchyma cells in the liver (pre-erythrocytic schizogony).
Infection with all four strains of malaria has many clinical features in common. These are related to the liberation of fever-producing substances, especially during schizogony.
The common features of malaria are:
• fever: often irregular. The regular pattern of fever does not occur until the illness has continued for a week or more. It depends on synchronised schizogony;
• anaemia: anaemia is haemolytic in type. It is more severe in infections with P. falciparum because in this infection cells of all ages can be invaded. Also, the parasitaemia in this infection can be much higher than in other malarias;
• splenomegaly: the spleen enlarges early in an acute attack of malaria. When a patient has been subjected to many attacks, the spleen may be of an enormous size and lead to secondary hypersplenism;
• jaundice: mild jaundice due to haemolysis may occur in malaria. Severe jaundice only occurs in P. falciparum infection, and is due to liver involvement.
Diagnosis of malaria parasites
Thick Blood Films
In examining stained thick blood films, the red blood cells are lysed, so diagnosis is based on the appearance of the parasite. In thick films, organisms tend to be more compact and denser than in thin films.
Parasitology is the study of parasites and as such that does not include bacterial, fungal or viral parasites.
Human parasites are separated into intestinal and blood borne parasites. For a parasite to be defined as intestinal it must have an intestinal life cycle stage, though it may have life-cycle stages in the heart, blood vessels, and lungs in the humans, other animals or the environment.
Prophylaxis. Malaria may be prevented by chemoprophylaxis and personal protective measures against the mosquito vector (Anopheles).
Class Ciliata
Move by cilia, which are numerous and cover most of the body
2) Have 2 nuclei, macronucleus containing vegetative chromatin and micronucleus containing generative chromatin
3) Reproduce by transverse binary fission, and sometimes by conjugation.
The protozoa Balantidium coli is the only infusorial parasite of man, which belongs to the class Ciliata and is responsible for human balantidiasis.
Distribution. B. coli has a wordwide distribution. It has most commonly been reported from various parts of Latin America, the Far East, and New Guinea, but such reports are rare. Incidence is highest in areas of poor hygiene and nutrition and where pigs and man have close contact.
Morphology. The balantidia range from 75 to 200 µm in length. The parasite has an asymmetrical oval body covered with cilia. Its anterior end is more pointed than the posterior end and has a mouth aperture (cytostome (1)) which leads into a short oesophagus (2). Large cilia arranged close to the cytostome form a peristome which directs food into the oesophagus together with a flow of fluid. The posterior end of the body has an anal pore (6). The balantidia has the macronucleus (4), the micronucleus (5), food vacuole (3) and there are two contractile vacuole (7). The parasites multiply by horizontal fission. Within the human intestine the parasite is encysted in a double-layer membrane, losing its covering of cilia. The cysts are from 30 to 60 µm in diameter.
Transmission. Infection is particularly common in pigs, and are the main source of transmission to man.
More then 50 % of human cases had contact with pigs. The handling and slaughtering of pigs and the use of pig excrement for fertilizing vegetables favor increased transmission. Person-to-person contact occurs through fecal contamination.
Cysts are the infective stage and may remain viable for weeks in moist feces. Excystation occurs in the bowel, and the trophozoites live in the large intestine, where they either remain in the lumen or invade the intestinal mucosa. Encystation occurs either as fecal material is being moved down the bowel or after passage of semiformed stool.
Clinical manifestations. Balantidia cause lesions in the colon through the action of its cilia and through the production of lytic hyaluronidase-type enzymes, producing ulcers, abscesses, and colitis characterized by the presence of blood and mucus in the stool. Diarrhea, abdominal colic, nausea, loss of appetite, and loss of weight may occur with heavy infection.
Laboratory diagnosis. Fresh stools are examined. Through the microscope the vegetative forms and cysts can seen (seldom).
Prevention: protection of foodstuffs and water from contamination with swine faeces and observation of individual hygiene when taking care of the animals (domestic swines).
