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The infectious state of Entamoeba histolytica may be symptomatic or asymptomatic or both in irregular ways. Entamoeba histolytica causes two types of amoebiasis: Invasive amoebiasis or extra-intestinal amoebiasis in chronic conditions and Non-invasive amoebiasis or intestinal amoebiasis in both acute and chronic conditions). Entamoeba histolytica trophozoites invade the intestinal mucosa causing swelling of colon (also called as amoebic colitis) resulting necrosis of colon and cause dysentery characterized by mucous and blood in diarrheal stools. Other sysmptoms are constipation for long time, weakness, dehydration along with malaise, loss of appetite, abdominal pain,appendicitis, pseudo-polyps etc. In chronic stage, the parasite's trophozoites reach to the bloodstream to travel into the reproductive organs, respiratory organs (pneumonitis in lungs), digestive organs (hepatitis in livers), urinary system, genital system (orchitis of testes), muscular system and nervous system (encephalitis in brain). These migratory trophozoites cause the 'abscess' in the organs where they live for long period of time. It is a potent pathogen secreting proleinases that dissolve host tissues; killing host cells on contact and engulfing RBCs. Besides, the secondary infection can occur in these organs because of the routes or holes made by these trophozoites for bacteria.
B) Giardia lamblia
History: Giardia lamblia was first discovered by Leeuwenhoek in 1681 while examining own stool.
Distribution: It is worldwide in distribution.
Morphology: It is confined in its distribution to the small intestine particularly the duodenum and upper part of Jejunum occasionally invading the bile ducts. It exists in two forms, trophozoite and cyst. Trophozoite is a 'tear drop' or pear-shaped shaped with convex dorsal surface and concave ventral one and with 8 flagella and 2 axostyles arranged in a bilateral symmetry. (Smyth, 1996). The ventral surface possesses two depressions called adhesive discs (large suction discs), which make contact with the intestinal cells of the host. The cytoplasm contains two nuclei and two parabasal bodies. Its size is 12 to 15 micrometer long by 7mm broad. It is feeding phex.Cyst is a fully formed cyst is oval or ellipsoidal in shape with thick wall and measures 9 to 12 micrometer broad. The cytoplasm contains four nuclei and many of the structures seen in the trophozoite. It is infective phase. Cysts are passed in the faeces. Transmission is through faecal-oral route i.e. Giardia cysts passed in the faeces of one person result in a new infection when swallowed by another person.
Lifecycle: Humans are infected when they consume the food or drink water or milk containing infective stages (cysts) of Giardia lamblia. Excystation occurs in the duodenum and from each cyst, two trophozoites are produced. These trophozoites mostly stay in the upper small intestine where they may swim freely or attach to the sub-mucosal epithelium via the ventral suction disc. They divide binary fission and produce many offsprings. The free trophozoites encyst as they move down stream. The cysts are passed in the stool.
Symptoms and pathogenicity: Disease caused by G. lamblia is called as giardiasis or flagellate diarrhoea. It is identified cause of water-borne disease associated with breakdown of water purification systems, drinking from contaminated streams, travel to endemic areas and day care centers. There are two types of Giardiasis: Intestinal Giardiasis which is characterized by disturbance in intestinal functions, leading to malabsorption of fats, persistent looseness of bowels and mild steatorrhoea and Exta-intestinal Giardiasis which is characterized by allergic manifestation, fever, anaemia, enteritities and chronic cholecytopathy accompanied by production of toxins by parasites.
C) Cryptosporidium parvum
History: Cryptosporidium was first described by E.E. Tyzzer in 1907 in the gastric glands of a mouse. He described this pathogen as Cryptosporidium muris and classified as possibly in the family Asporocystidae.
Morphology: Cryptosporidium (hidden spores or Latin: underground spores) is a small round parasite measuring 3 to 5 micrometers. It is a polymorphic coccidian parasite consisiting more than one morphologic structures in its lifecycle. The oocyst consists of 4 sporozoites. These sporozoites are infective in humans, animals. So, it is unique that coccidia have usullay sporozoites encased in smaller spores (or sporocyst), exclusively absent in this species. Molecular studies show that the genus is more closely related to the gregarines than to eimerians or even the malaria.
Lifecycle: Humans are infected when they consume the sporulated oocysts (resistant stage found in the environment) contaminated food or water or they can be directly infected while oral sex, or oral sex followed by anal sex or anal to anal sex. Each sporozoites release from a suture located along one side of the oocyst and infect the luminal surface of the cells. These sporozoites multiply by multiple fission or merogony or schizogony giving rise to formation of 8 merozoites within the meront. These meronts are termed Type I meronts and rupture releaseing free merozoites. These merozoites penetrate new cells and undergo merogony to produce numerous meronts. Type I merozoites undergo merogony indefinitely. Some type I merozoites produce another type meront called Type II meront which contains only 4 merozoites. Type II merozoites are liberated and undergo sexual stages. These merozoites enter cells, grow to form macrogamerocyte, and some undergo multiple fission once inside cells forming microgametocytes containing 16 non-flagellated microgametes. Microgametes and macrogametes fusion coccur and zygote develops. A resistant wall is formed around zygote inside which meiosis occurs and 4 sporozoites are formed by sporogony. These oocysts are passed in the stools into the environment.
Some of the oocysts produced in the intestine doesn't produce wall around the oocyst, called thin walled oocysts. So, cryptosporidium can have autoinfective cycles because the first by continuous recycling of Type I meronts and second through sporozoites rupturing from thin-walled oocysts.
Symptoms and pathogenicity: The disease caused by Cryptosporidium is called Cryptosporidiosis. The symptoms are characterised by acute and chronic diarrhea. The diarrhea is chronic type and watery type followed by weight loss, cramping and flatulence in children, olders and immunocompromised patients, whereas, it is acute type in immunocompetent patient. Even in AIDS patients, the organisms may invade gallbladder, gallbladder, biliary tract and the lung epithelium leading extra-intestinal pathogenesis.
D) Isospora belliÂ
History: I. belli is a rare infection of normal humans, although it is being seen in increasing numbers. Woodcock and wenyon found the first positive case of Isospora infection in humans, but didn't name the etiology. Dobell in 1919 named and described Isospora hominis which was changed into Isospora belli by Wenyon
Morphology: The infective stage is the oocyst with 2 sporocysts, each sporocyst with 4 sporozoites. The merogonous stages not disseminated extraintestinally in mononuclear cells, can infect invertebrates and vertebrates including humans.
Lifecycle: Humans are infected when they consume the contaminated food and water contaminated with oocysts of this parasite. Lifecycle is similar to Cryptosporidium. Humans are infected when they feed on the sporulated oocyst infected food or water. The sporozoites are released from the oocysts and sporocysts and attach the intestinal linings. They undergo asexual reproduction to produce many merozoites. The merozoites produce gametes which undergo fertilisation to produce zygote. Zygote divides by meiotic division producing 4 haploid spores. A resistant wall is formed around the zygote called oocysts which are passed through the stools in the environment.
Symptoms and pathogenicity: Disease caused by Isospora belli is called Isosporiasis. The symptom is similar to Giardiasis or Cyclosporiasis. The state of infection may be asymptomatic in normal individuals as well as symptomatic in AIDS patients. In the immunocompromised patients, symptoms are chronic with lots of volume of diarrheal stools.
E) Cyclospora cayetanensis
History- Cyclospora cayetanensis was first reported in the medical literature in 1979 in Papua New Guinea as an oocyst like body found in three patients with intestinal infection cases began being reported more often in the middle 1980s.
Morphology- Cyclospora cayetanensis is a coccidian protozoan parasite measuring 8 - 10 mm in diameter. The infective stage is the sporulated oocyst containing two sporocyst, each with two sporozoites.
Lifecycle: Humans are infected with Cyclospora when they consume the food or drink water contaminated with the sporulated oocysts of Cyclospora. Direct person to person has not been reported. Human excrete unsporulated cysts or oocysts into the environment. Sporocysts excyst in the gastro-intestinal tract and sporozoites are released into the gut. The sporozoites invade small intestinal epithelial cells. They have been reported in extra-intestinal sites such as respiratory tract. The sporozoites multiply robustly and they are sorrounded by oocysts wall from the outside. These oocysts are released into the outside through stools. On the environment, they undergo further development. The development and maturation of spores or sporulation occurs. During sporulation, the sporant divides into two sporocysts and each contain two sporozoites. Cyclospora infection affects both immunocompetent and immunocompromised individuals, the latter potentially more severely.
Symptoms and pathogenicity: Disease caused by Cyclospora is called cyclosporiasis. It may be asymptomatic as in many healthy or immunocompetent individuals or symptomatic to healthy and immunocompromised patients. It may be acute causing watery diarrhea or chronic long term watery diarrhea followed by constipation. The chronic diarrhea is the characteristic feature of diarrhea in immunocompromised patients. Other symptoms are frequent (sometimes explosive) bowel movements, other symptoms can include loss of appetite, substantial loss of weight, bloating, increased gas, stomach cramps, nausea, vomiting, muscle aches, low-grade fever and fatigue.
F) Endolimax nana
Morphology: It is a dimorphic parasite having cyst and trophozoite stage in the lifecycle. Cysts are spherical to ellipsoidal. Mature cysts contain 4 nuclei, immature cysts are rarely seen. They are 5-10 micrometer in size.Chromatid bodies are absent sometimes, small granules or inclusions bodies may occur in the cytoplasm. Trophozoites are 6-12 micrometer in size. They are sluggish. It has onliny one nucleus. The karyosome is large and is irregular shape. The cytoplasm is granular and highly vacuolated and may contain bacteria.
Lifecycle: Lifecycle is direct. But mechanical vectors may occur. Humans are infected when they ingest the food or drink water contaminated by cysts of Endolimax nana. The uninucleated cysts get excysted in the intestine and simple binary fission occurs with nuclear division producing trophozoite inside the gut. The trophozoites invade the intestinal tissues and in adverse conditions, the trophozoites become developed. Cysts which are unineculated are released into the stools outside the body. They undego matureation in the environment.
Symptoms and pathogenicity:Previously endolimax nana was thought be a non-pathogenic commensal but studies suggest that it causes intermittent or chronic diarrhea.
G) Balantidium coli
Morphology: Balantidium coli is a ciliate protozoan containing two stages in lifecycle. The cyst is spherical or ellipsoid with the 30-200 micrometerX20-120micrometer size. It contains 1 macronuclus and one meganucleaus. Cilia are found in immature cysts where they are slowly rotating. In mature cyst, no cilia is observed. The trophozoites are about 30-150 micrometerX25-120 micrometer or more. They are oval and covered by short cilia. The cytostome is funnel-shaped at the anterior portion.
Lifecycle: Humans are infected when they consume food or drink water contaminated with cysts of Balantidium coli. The cyst wall gets ruptured in the wall of intestine and trophozoites get developed.
Symptoms and pathogenicity: Disease caused by Balantidium coli is called Balantidiosis. The symptoms are charancterised by diarrhea. The parasites can penetrate the mucosa layer of the intestine resulting ulcerations. Extra-intesinal infection is rare.
H) Hymenolepis nana
History- This helminth species was discovered by Bilharz in 1851 in the small intestine of a native boy in Cairo Grassi and Rovelli (1887, 1892) first worked on the life cycle and demonstrated that no intermediate host was required.
Geographical Distribution- The worm is practically cosmopolitan in its distribution but is more common in warmer than in colder climate.
Morphology: - Hymenolepis nana is also known as dwarf tapeworm, as the entire worm is small, measuring up to 25mm to 40 mm in length by a maximum of 1 mm diameter. Scolex is rhomboidal with four hemispherical suckers and a short rostellum armed with 20-30 spines in one ring. Proglottids are 200 in numbers. Eggs are oval or spherical in shape with two distinct membranes. The outer membrane is thin and colorless and inner embryophore encloses an oncosphere with three pains of lancet-shaped hooklets. The adult worm lives in the small intestine of human.
Lifecycle: The infection occurs through ingestion of food contaminated with eggs of Hymenolepis nana..
Hymenolepiasis: - The clinical symptoms are restless, irritability, abdominal pain and diarrhoea.
I) Ascaris lumbricoides
History: - This worm was observed and reported as a parasite of man by many ancient people (Craig & Faust, 1943). It has undoubtedly been one of man's most faithful and constant companion from time immemorial (Chandler, 1961).
Geographical Distribution- Ascaris lumbricoides is the most cosmopolitan and most common of all helminths. It flourishes in warm moist climates or in moist temperate regions where personal hygiene and environmental conditions combine to favor embryonation of the eggs in polluted soil.
Habitat- The adult worm lives in the small intestine of human beings.
Morphology- It is elongated, cylindrical nematode, tapering bluntly at the anterior end and somewhat more attenuated at the posterior end. Lateral lines can easily be seen. The head is provided with conspicuous lips. Sexes are separate. The size of male is 15 to 25 cm in length with a maximum diameter of 3 to 4 mm and female is 25-40 cm in length with diameter of 5 mm.
Mode of Infection- Faecal-oral route infection occurs by the ingestion of food or water contaminated with embryonated eggs of the parasite. The infection occurs by ingestion ofÂ food contaminated with infective eggs which hatch in the upper small intestine. The larvae (250 x 15 micrometers) penetrate the intestinal wall and enter the venules or lymphatics. The larvae pass through the liver, heart and lung to reach alveoli in 1 to 7 days during which period they grow to 1.5 cm. They migrate up the bronchi, ascend the trachea to the glottis, and pass down the esophagus to the small intestine where they mature in 2 to 3 months. A female may live in the intestine for 12 to 18 months and has a capacity of producing 25 million eggs at an average daily output of 200,000 (figure 2). The eggs are excreted in feces, and under suitable conditions (21 to 30 degrees C, moist, aerated environment) infective larvae are formed within the egg. The eggs are resistant to chemical disinfectant and survive for months in sewage, but are killed by heat (40 degrees C for 15 hours). The infection is man to man. Auto infection can occur.
Symptoms and pathogenicity: Ascaris lumbricoides is an important parasite of human, it often occurs in high levels in population living under conditions of poor hygiene (Smyth, 1996). It has been estimated that there are about 1000 million cases of ascariasis worldwide; with average prevalence in the range of 32-60% (Crompton et al., 1989). In some surveys of children between the ages of six and twelve years, the infection rate was as high as 90%. The infection results in malnutrition and retardation of growth in children but other symptoms associated with both the larval (tissue) and adult (intestinal) stages include pneumonitis, asthma, diarrhea, nausea, abdominal pain and anorexia.
J) Trichuris trichiura
History- This worm was first described by Linnaeus in 1771. The life cycle was first studied by Grassi (1887) and letter by Fulleborn (1923) and Hagegawa (1924) (Craig and Faust 1943). It is also known as whipworm.
Geographical Distribution- It is cosmopolitan in distribution but is more common in the warm moist regions of world. The whipworm infection is more or less co-extensive with ascariasis.
Habitat- The adult worm lives in the large intestine particularly the caecum and also found in the vermiform appendix.
Morphology- They are so called whip-worms, a term derived from the whip like form of the body. The anterior three-fifth of body is very thin and hair like and the posterior two-fifth is thick and stout. Male measures 3-4 cm in length with ventrally curved tail. Female measures 4-5 cm in length with arc or comma shaped. Eggs are brown in color with the size about 50 mm in length by 25mm in breath, barrel shaped with a mucous plug at each pole.
Mode of Infection- Human is infected by swallowing embryonated eggs with food or water.
Symptoms and pathogenicity: This species is a much more common human parasite than is generally appreciated and it is reported to infect up to 800 millions people throughout the tropical and temperate areas (Smyth, 1996). There is now evidence that children are especially prone to intestinal disorder like loss of appetite, abdominal pain, nausea, vomiting emaciation, dysentery with blood tinged mucous, acute appendicitis and prolapsis of rectum. Trichuris dysentery, rectal prolapse, anaemia, poor growth and clubbing of the fingers constitute an important public health problem (Stephenson et al, 2000).
K) Trichinella spiralis (Trichinosis)
The adult female measures 3.5 mm x 60 micrometers. The larvae in the tissue (100 micrometers x 5Â micrometers) are coiled in a lemon-shaped capsule.
Infection occurs by ingestion of larvae, in poorly cooked meat, which immediately invade intestinal mucosa and sexually differentiate within 18 to 24 hours. The female, after fertilization, burrows deeply in the small intestinal mucosa, whereas the male is dislodged (intestinal stage). On about the 5th day eggs begin to hatch in the female worm and young larvae are deposited in the mucosa from where they reach the lymphatics, lymph nodes and the blood stream (larval migration). Larval dispersion occurs 4 to 16 weeks after infection. The larvae are deposited in muscle fiber and, in striated muscle, they form a capsule which calcifies to form a cyst. In non-striated tissue, such as heart and brain, the larvae do not calcify; they die and disintegrate. The cyst may persist for several years. One female worm produces approximately 1500 larvae. Man is the terminal host. The reservoir includes most carnivorous and omnivorous animals (Figure 3 and 4).
Symptoms and pathogenicity: Trichinosis symptoms depend on the severity of infection: mild infections may be asymptomatic. A larger bolus of infection produces symptoms according to the severity and stage of infection and organs involved (Table 1).
Trichinella pathogenesis is due the presence of large numbers of larvae in vital muscles and host reaction to larval metabolites. The muscle fibers become enlarged edematous and deformed. The paralyzed muscles are infiltrated with neutrophil, eosinophils and lymphocytes. Splenomegaly is dependent on the degree of infection. The worm induces a strong IgE response which, in association with eosinophils, contributes to parasite death.
Diagnosis is based on symptoms, recent history of eating raw or undercooked meat and laboratory findings (eosinophilia, increased serum creatine phosphokinase and lactate dehydrogenase and antibodies to T.Â spiralis).
Treatment and Control
Steroids are use for treatment of inflammatory symptoms and Mebendazole is used to eliminate worms. Elimination of parasite infection in hogs and adequate cooking of meat are the best ways of avoiding infection.
L) Ancylostoma duodenale
History- The parasite was first discovered in 1838 by an Italian physician Angelo Dubini. The pathogenesis and mode of entrance of the larvae into human was worked out by Looss in 1898.
Geographical Distribution- It is widely distributed in all tropical and sub-tropical countries extending from parallel 360 North to parallel 300 South.
Habitat- The adult worm lives in the small intestine of human, particularly in the jejunum, less often in the duodenum and rarely in the ileum.
Morphology- It is commonly known as hookworm. The adult worms are somewhat cylindrical in shape, are slightly constricted anteriorly and have a cervical curvature. The large conspicuous buccal capsule is lined with a hard substance provided with six teeth, four hooks on ventral side and two knobs like on dorsal side. A male measure 8-11 mm x 0.4 mm while female is 10-12 mm x 0.6 mm (Craig and Faust, 1943). Male bears copulatory bursa at posterior end. Eggs are oval or elliptical in shape measuring 65mm x 40mm colorless with a thin transparent hyaline shell membrane.
Lifecycle: Infection occurred by the entry of filariform larva, the infective stage through the penetration of skin. Ancylostoma duodenale can infect man successfully by oral, transmammery and (probably) transplacental routes (Smyth, 1996). The life cycle of hookworms is identical to that of threadworms, except that hookworms are not capable of a free-living or auto-infectious cycle. Furthermore, A. duodenale can infect also by oral route.
Symptoms and pathogenicity: Hookworm must be classified as one of the most destructive of human helminth parasites with estimates of some 900 million cases worldwide (Compton, 1969). Hookworms were essentially blood suckers and can cause severe blood loss (i.e. hookworm anemia). They insidiously undermine the health of their hosts causing stunting of growth and general laziness accompanied by acute mental distress.
M) Strongyloides stercoralis (Threadworm)
History: Strongyloides stercoralis was first found by Normand in 1876 in the faeces of French colonial troops.
Geographical Distribution: - It is worldwide in distribution. It is adapted to warm climate but it has been reported sporadically in temperate regions (Craig and Faust, 1943).
The size and shape of threadworm varies depending on whether it is parasitic or free-living. The parasitic female is larger (2.2 mm x 45 micrometers) than the free-living worm (1 mm x 60 micrometers) (figure 10). The eggs, when laid are 55 micrometers by 30 micrometers. In the parasitic phase, the females are readily discovered but not the male. The parasitic female measures 2.5 mm in length and 40 -50 mm in diameter. Males are shorter and broader than females. Eggs are thin shelled, transparent and oval and measures 50mm x 30mm.
Infection occurs by the entry of filariform larvae which penetrate directly through skin coming in contact with soil. Strongyloides can undergo 'autoinfection'; this infection has been reported to last more than 30 years in untreated human. Also, infection with these parasites can be transmitted via breast milk (Stephenson et al. 2000). The infective larvae of S. stercoralis penetrate the skin of man, enter the venous circulation and pass through the right heart to lungs, where they penetrate into the alveoli. From there, the adolescent parasites ascend to the glottis, are swallowed, and reach the upper part of the small intestine, where they develop into adults. Ovipositing females develop in 28 days from infection. The eggs in the intestinal mucosa, hatch and develop into rhabditiform larvae in man. These larvae can penetrate through the mucosa and cycle back into the blood circulation, lung, glottis and duodenum and jejunum; thus they continue the auto infection cycle. Alternatively, they are passed in the feces, develop into infective filariform larvae and enter another host to complete the direct cycle. If no suitable host is found, the larvae mature into free-living worm and lay eggs in the soil. The eggs hatch in the soil and produce rhabditiform larvae which develop into infective filariform larvae and enter a new host (indirect cycle), or mature into adult worms to repeat the free-living cycle.
Symptoms and pathogenicity
Light infections are asymptomatic. Skin penetration causes itching and red blotches. During migration, the organisms cause bronchial verminous pneumonia and, in the duodenum, they cause a burning mid-epigastric pain and tenderness accompanied by nausea and vomiting. Diarrhea and constipation may alternate. Heavy, chronic infections result in anemia, weight loss and chronic bloody dysentery. Secondary bacterial infection of damaged mucosa may produce serious complications.
N) Enterobius vermicularis (pinworm)
Enterobiasis is by far the commonest helminthic infection in the US (18 million cases at any given time). The worldwide infection is about 210 million. It is an urban disease of children in crowded environment (schools, day care centers, etc.). Adults may get it from their children. The incidence in whites is much higher than in blacks.
The female worm measures 8 mm x 0.5mm; the male is smaller. Eggs (60 micrometers x 27 micrometers) are ovoid but asymmetrically flat on one side.
Infection occurs when embryonated eggs are ingested from the environment, with food or by hand to mouth contact. The embryonic larvae hatch in the duodenum and reach adolescence in jejunum and upper ilium. Adult worms descend into lower ilium, cecum and colon and live there for 7 to 8 weeks. The gravid females, containing more than 10,000 eggs migrate, at night, to the perianal region and deposit their eggs there. Eggs mature in an oxygenated, moist environment and are infectious 3 to 4 hours later. Man-to-man and auto infection are common (Figure 7 and 8). Man is the only host.
Symptoms and pathogenicity
Enterobiasis is relatively innocuous and rarely produces serious lesions. The most common symptom is perianal, perineal and vaginal irritation caused by the female migration. The itching results in insomnia and restlessness. In some cases gastrointestinal symptoms (pain, nausea, vomiting, etc.) may develop. The conscientious housewife's mental distress, guilt complex, and desire to conceal the infection from her friends and mother-in-law is perhaps the most important trauma of this persistent, pruritic parasite.
O) Toxocara canis and T. catti (visceral larva migrans)
These are roundworms of dogs and cats but they can infect humans and cause damage of the visceral organs. Eggs from feces of infected animals are swallowed by man and hatch in the intestine. The larvae penetrate the mucosa, enter the circulation and are carried to liver, lungs, eyes and other organs where they cause inflammatory necrosis. Symptoms are due to the inflammatory reaction at the site of infection. The most serious consequence of infection may be loss of sight if the worm localizes in the eye. Treatment includes Mebendazole to eliminate the worm and prednisone for inflammatory symptoms. Avoidance of infected dogs and cats is the best prevention (figure 14 and 15).