Sabtu, 09 Februari 2008

Medically Important Protozoa (3)

Cryptosporidiosis. Cryptosporidium parvum causes diarrhea disease mainly in infants and small children. It is normally self-limiting but in the immunocompromized host the disease can be severe. C. parvum is enzootic in young calves and is usually passed to man in water containing oocysts of the organism. Toxoplasmosis. Toxoplasma gondii causes the multi-organ infection of toxoplasmosis. The domestic cat is the definitive host for T. gondii from which man and other mammals can become infected. Infection commonly arises from the consumption of under cooked meat and in the healthy adult is usually asymptomatic. The most devastating form of toxoplasmosis is seen in congenital infection when a pregnant mother passes the organism to the fetus. This can result in severe abnormalities at birth. The life-cycle of T. gondii is complex, involving both sexual and asexual reproduction. Three main life forms of T. gondii occur: (i) the oocyst which is produced from the sexual cycle in the small intestine of the cat and contains sporozoites; (ii) the tachyzoite of the asexual invasive form found in secondary hosts which are derived from pseudocysts; and (iii) the tissue cyst that contains bradyzoites.
Microsporans
The medical importance of microsporidial infections has only recently been highlighted by the frequent recognition of these obligate intracellular parasites in material from patients with HIV infection and AIDS. Examples are: Encephalitozoon species, Nosema species and Septata intestinalis. Multi-organ infections occur and S. intestinalis is found in about 2% of all AIDS patients with chronic diarrhea.
Source: University of Leicester
References: Baker, J.R. and Muller, R (Eds). Advances in Parasitology. Academic Press, London. Knight, R. (1982). Parasites Diseases in Man. Churchill Livingstone, London. Peters, W. and Gilles, H.M. (1995) Colour Atlas of Tropical Medicine and Parasitology. Mosby-Wolfe.

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Jumat, 08 Februari 2008

Medically Important Protozoa (2)

Leishmania species cause leishmaniasis. The disease is spread by the bite of sandflies in which part of the organism's life cycle is completed. In man, the promastigotes from the bite of the sandfly become ingested by macrophages and multiply within them as amastigotes. Cutaneous
leishmaniasis occurs if the region of infection remains localized to the dermis as an open sore. In the Old World (Southern Europe, the Middle East, India, former USSR and parts of Africa) L. major, L. tropica, L. aethiopica and certain subtypes of L. infantum are responsible. In the New World (Mexico southwards and through South America) species responsible include L. braziliensis, L. mexicana and L. amazonensis. If the organism spreads, then mutocutaneous leishmaniasis can occur in which the nose, mouth and palate becomes destroyed. Infection with members of the L. donovani-L.infantum complex produce the systematic disease of visceral leishmaniasis often known as kala-azar that occurs with a global distribution seen in Old and New World leishmaniasis. The parasites multiply within the macrophages of the liver, spleen, bone marrow and other organs. Untreated, the disease is usually fatal. As with trypanosomiasis, leishmaniasis is a zoonosis as many mammals harbor the parasite.
Ciliates
These possess rows of cilia around the outside of the body that aid motility. The only member of this group known to infect man is Balantidium coli. This is a cyst forming parasite that is a commensal ("table-sharing" and meaning here a non-pathogenic parasite) of domestic and wild pigs. It does, however, cause severe diarrhea in humans.
Apicomplexa
This is a unique group because all members are parasitic. The group includes parasites causing malaria, cryptosporidiosis and toxoplasmosis. They lack any visible means of locomotion (most are intracellular) and have complex life cycles involving sexual and asexual reproduction.. The common feature of all members is the presence of an apical complex in one or more stages of the life cycle. Although the exact components of the apical complex varies among members, it contains enzymes used to penetrate host tissues.
Malaria. Plasmodium species cause malaria. The four principal species are P. falciparum, P. vivax, P. ovale and P. malariae. Malaria means "bad air" and dates from the time when the disease was thought to be spread from stagnant, foul smelling water. The disease is in fact transmitted by the female Anopheles mosquito that inhabits such environments. In the stomach of the female Anopheles male (micro-) and female (macro-) gametocytes fuse to form a zygote. This in turn forms a motile ookinete that penetrates the midgut wall and develops into an oocyst within which are many thousands of sporozoites. When mature, the sporozoites rupture the oocyst and penetrate the salivary glands. When the mosquito next feeds on man, the sporozoites are passed via the blood stream to infect parenchymal cells of the liver. Here they form pre-erythrocytic schizonts in which several thousand daughter cells, called merozoites. These merozoites enter red blood cells to start the asexual intraerythrocytic cycle and form new gametocytes. The asexual red cell stages are responsible for the pathological changes that occur in malaria (fever, chills, anemia, liver enlargement, encephalitis renal damage and death).


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Strongyloides westeri

Merupakan cacing nematoda. Terdapat diseluruh dunia pada mukosa usus halus kuda, keledai, dan zebra. Cacing ini biasanya tidak banyak. Mereka mempunyai oesophagus sangat panjang dan berbentuk hamper silindris, vulva pada bagian pertengahan tubuh posterior, ekor pendek berbentuk kerucut, uterus amfidelf (dengan cabang ke depan maupun ke belakang). Cacing betina panjangnya 8-9 mm dan berdiameter 80-95 mikron; mereka menghasilkan telur berembrio berbentuk elips, berkulit tipis, berukuran 40-52 x 32-40 mikron, masa prepaten sekitar 2 minggu. Hanya cacing betina yang bersifat partenogenetik.
Infeksi Strongyloides westeri dapat didiagnosa dengan cara menemukan telur-telurnya pada tinja atau nematode itu sendiri dengan pemeriksaan mikroskopik pada kerokan karena selaput lendir terutama dari duodenum pada saat pemeriksaan bedah bangkai. Akan tetapi, larva yang bermigrasi dapat menyebabkan radang paru-paru pada anak kuda, sebelum mereka menjadi dewasa dan mulai bertelur. Perlu ditekankan bahwa bagaimanapun telur yang banyak pada feses mungkin ditemukan juga pada hewan yang sehat.

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OOSISTA PADA KUDA

Eimeria leukarti
Eimeria leukarti biasanya berlokasi diusus halus kuda dan dapat menyebabkan diare intermiten. Eimeria leukarti mempunyai periode prepaten ± 15 hari. Oosista berisi 4 sporosista dengan tiap sporokista berisi 2 sporozoit. Ookista berbentuk oval atau piriform, sangat besar sekitar 80 x 60 µm dengan dinding kasar berlapis dua (gelap dan tebal) dan mempunyai mikropile berbeda. Patologi keradangan ditandai dengan adanya perubahan mukosa dan gangguan pada struktur vili. Hasil diagnosa sangat sulit, dan karena dinding oosista yang tebal maka harus dilakukan teknik sedimentasi, atau jika menggunakan taknik pengapungan maka diperlukan larutan gula jenuh.

Klossella
Klossiella equi terdapat pada ginjal kuda. Ookista yang telah tumbuh penuh berupa kantung berdinding tipis 50-90 x 35 µm mengandung sebanyak 40 sporokista seperti bentuk telur ± 8-10 x 4-5 µm, masing-masing dengan 8-12 sporozoit.

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Leucocytozoonosis

Leucocytozoonosis adalah penyakit yang disebabkan oleh parasit darah Leucocytozoon sp. yang dapat menyebabkan kematian dan terhambatnya pertumbuhan pada anak ayam. Penyakit ini untuk pertama kali dilaporkan oleh Dr. Theobold Smith (1895) pada seke­lompok kalkun yang terserang di Amerika Serikat bagian Timur. Pada ayam dewasa menimbulkan penurunan produksi telur dan pada kal­kun dapat menimbulkan penurunan daya tetas telur. Penyakit ini me­nyerang beberapa jenis unggas antara lain: itik dan angsa oleh Leuco­cytozoon neavei, Leucocytozoon numidae, Leucocytozoon costai dan Leucocytozoon simondi; kalkun oleh Leucocytozoon smithi; ayam oleh Leucocytozoon cauleryi, Leucocytozoon andrewsi; Leuco­cytozoon schoutedeni dan Leucocytozoon Sabrasezi.
Penularan terjadi melalui gigitan Sinulium sp (lalat hitam), Culi-coides sp dan Ornithophilous sp yang bertindak selaku perantara. Penyakit yang akut biasa terjadi pada waktu menjelang dan sewaktu musim panas pada saat populasi lalat hitam meningkat.
Gejala klinis dipengaruhi oleh umur dan jenis hewan yang terse­rang. Gejala klinis yang terlihat umumnya adalah terjadinya penurun­an nafsu makan, haus, depresi, bulu kusut dan pucat. Ayam kehi­langan keseimbangan, lemah, pernafasan cepat dan anemi. Kejadian penyakit berlangsung secara cepat. Ayam dapat mati atau sembuh dengan sendirinya. Angka kematian dapat mencapai 10% - 80%.
Perubahan paling menonjol adalah pembesaran limpa dan biasa­nya hati juga membengkak. Otot daging lembek, pucat dan terjadi perdarahan titik yang merata. Perdarahan kecil juga ditemukan pada lapisan luar usus.
Diagnosis secara klinis dilakukan berdasar gejala dan sejarah kejadian dalam kelompok. Diagnosis ini dapat diperteguh dengan pengujian sediaan ulas darah yang mengandung schizont protozoa sebagai agennya. Untuk keperluan ini sediaan ulas dikirim ke labo­ratorium dengan fiksasi kering udara. Potongan organ terutama paru, hati, limpa dan jantung dikirim dalam formalin 10% ke BPPH atau laboratorium yang terdekat.


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Medically Important Protozoa (1)

Protozoa means "first animal" and refers to simple eukaryotic organisms composed of a single cell (e.g. amoebae). Reproduction may be through simple cell division (e.g. the ameboflagellates) or sexual involving the fusion of gametes in part of the life cycle (e.g. the apicomplexa) as described below. Some protozoa can form a protective cyst stage capable of withstanding harsh environmental conditions.
Ameboflagellates
These use pseudopodia or flagella for locomotion.
Amoebae. These are characterized by a feeding and dividing trophozoite stage that can form a temporary resistant cyst stage.
Entamoeba histolytica is the cause of amoebic dysentery producing severe infection of the intestines that can spread to the liver. The organism is characterized by a trophozoite and cyst stage. E. histolytica is an example of a true parasite in that the organism cannot multiply outside of the host. Other amoebae occur naturally in soil and water environments which is their preferred habitat for feeding and replication. These amoebae are termed "free-living" as they have no natural host in which parasitism occurs. They can infect man opportunistically producing severe and often fatal disease. Such free-living amoebae are the Acanthameba, Naegleria fowleri and Balamuthia mandrillaris, all of which can infect the central nervous system. In addition, Acanthameba species can also invade the eye.
Flagellates
These organisms have flagella in the trophozoite stage. Trichomonas vaginalis is a common sexually transmitted organism causing trichomoniasis infection of the vagina and urethra. Giardia lamblia causes giardiasis producing symptoms of diarrhea and other intestinal disturbances. Infection arises from the ingestion of cysts, usually through contaminated water.
Trypanosoma brucei gambiense and T. brucei rhodesiense cause trypanosomiasis, more commonly known as African sleeping sickness. The disease is an arthropod (insect)-borne infections and is spread by the bite of the tsetse fly in which part of the trypanosome life cycle is completed. The eventual invasion of the central nervous system by the trypanosomes gives rise a comatosed state from which the common name for the disease is derived.
Trypanosoma cruzi causes Chagas' disease (American trypanosomiasis). The intermediate host in this case are triatomid bugs that feed off the blood of man. Infection results from the inoculation of the bug's feces that contains the organism into the bite wound. Individuals who survive the acute stage of the disease are frequently left with chronic and progressive neuronal and smooth muscle lesions in the heart and gastrointestinal tract. T. cruzi has an extensive reservoir in wild and domestic mammals and therefore Chagas' disease is a zoonosis.


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Soil-Mediated Helminthiases

Soil-transmitted helminthic infections are of two types: the hookworms, which undergo a cycle of development in the soil (the larvae being infective), and a group of nematodes that survive in the soil merely as eggs that have to be ingested in order for the cycle to continue.

Hookworms. The most common hookworms are Ancylostoma duodenale and Necator americanus. Adults attach to the walls of the jejunum and females lay large numbers of eggs that are passed out with the feces. The eggs hatch in the soil and infect man by usually burrowing through the soles of the feet. The larvae then migrate to infect the heart and lungs before passing into the tracheae, pharynx and then the small intestine.
Strongyloides stercoralis. Females live in the mucosal glands of the small intestine. Eggs hatch in these glands and the larvae are passed with the feces into the soil. As with other hookworms, infection results from the larvae burrowing into the skin. The rest of the life cycle is as for A. duodenale and N. americanus.
Ascariasis. Adult worms of Ascaris lumbricoides live in the small intestine where they lay large numbers of eggs that are passed out with the feces. Unlike the hookworms, the eggs are the infectious form in which the larvae develop. When ingested, the eggs hatch in the jejunum, penetrate the mucosa and are carried through the hepatic circulation to the heart and lungs. They again enter the stomach via the tracheae and oesophagus before growing to adulthood in the small intestine. Pneumonitis and intestinal obstruction may accompany heavy infestations.
Toxocariasis. The disease results from the accidental infection of man with eggs of the ascarid roundworm of the dog, Toxocara canis, and cat, T. cati. The life cycle is the same as that of Ascaris but the invasive larvae become arrested in various tissues where they are phagocytosed. In the process they induce marked eosinophilia and local tissue reaction commonly involving the liver and eye.
Trichurias. Trichuris trichiura ("whipworm") inhabits the caecum where they attach to the mucosa. Eggs from the mature worms are passed with the feces and develop in the soil. When swallowed, the eggs hatch in the small intestine and the developing larvae pass directly to their attachment sites in the large intestine. Heavy infections can cause abdominal pain and chronic bloody diarrhea that may result in rectal prolapse.


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Snail-Mediated Helminthiases

This important group of snail-transmitted helminthiases is all caused by trematodes (flukes) that undergo a complicated cycle involving various species of land or aquatic snails. The most significant of these fluke infections is schistosomiasis and over 200 million people are estimated to be infected world-wide. The three common species infecting man, Schistosoma mansoni, S. japonicum and S. haematobium have similar life cycles. Eggs are passed in the urine (S. haematobium) or feces (Schistosoma mansoni and S. japonicum) and hatch in natural waters. Miracidia hatch from the eggs, penetrate suitable snails and develop two generations of sporocysts. The last of these then produces fork-tailed cercariae. These cercariae penetrate the skin when a new host comes into contact with the contaminated water. Once through the skin the cercariae shed their tails and become schistosomulae that then migrate through the tissues to the liver. Here male and female flukes copulate and migrate to either the bladder or rectum where eggs are laid. Schistosomiasis can result in chronic liver, spleen and bladder damage.
Fascioliasis. Fasciola hepatica is found in most herbivores (but primarily sheep) that graze in wet pasturage where the intermediate host, snails of the genus Lymnaea, are found. F. hepatica eggs, shed from the infected primary host, mature into the embryonated form in the environment. These then hatch and release a motile miracidia that seeks out and penetrates the tissue of the intermediate snail host. Cercaria are produced in the snail that when released into the environment can encyst to produce metacercariae. In temperate climates man is often infected by eating wild watercress on which metacercariae have collected. After being ingested, the metacercariae pass through the duodenal wall and penetrate the liver capsule. Following maturation of the young flukes, the adults finally come to lie in the bile ducts or adjacent liver tissue. Here they cause severe damage to the biliary tract and eggs are passed with the bile into the feces to continue the cycle.

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PARASITIC DINOFLAGELLIDS

Species affected and geographical range
Parasitic dinoflagellids, the marine Amyloodinium ocellatum and the freshwater Piscinoodinium pillulare and P. limneticum, are not discriminatory in their choice of piscine hosts and have been implicated in mass mortalities of tropical marine and freshwater aquarium fish (Jacobs, 1946; Schaeperclaus, 1954; Paperna, 1980). A. ocellatum has infected sea water acclimatised Oreochromis mossambicus and Aphanius dispar in inland salt pans; some strains of this parasite survive in salinities as low as 10 ppt. Schaperclaus (1954) reports P. pillulare infection in 14 species of tropical ornamental freshwater fish of diverse families as well as in carp and crucian carp. Epizootic infections and mortalities were recently reported in farmed cyprinid fish in Malaysia, including grass carp (Ctenopharyngodon idella), bighead (Aristichthys nobilis), Leptobarbus hoevenii and Puntius gonionotus (Shaharom-Harrison et al., 1990). The presence of P. pillulare has never been established in Africa, but this ubiquitous parasite may eventually be found. If introduced with culture seed, it is likely to become established.
Diagnosis
Trophonts, when reaching the final stage of growth, are visible to the naked eye (80–100 μm diameter) as white spots (similar to that seen in ichthyophthiriasis) and turn dark blue when exposed to Lugol's-iodine. They are oval with a smooth wall and with inner aggregates of globules. In Malaysian fish, clinical signs of P. pillulare infection comprise both a rust-coloured appearance of the skin, indicating the presence of the parasite trophonts (20–75 × 14–50 μm), and a dense covering of mucus (Shaharom- Harrison et al., 1990).
Life cycle and biology
The life cycle of the dinoflagellid fish parasite is comprised of a parasitic feeding stage (trophont) which attaches to integumentary epithelial cells, and an encysted dividing stage (tomont) which is detached from the host. The trophonts of P. pillulare derive an essential part of their nutrition from photosynthesis. Trophonts dislodged at any time during their trophic stage will transform into a dividing tomont. Divisions yield a motile infective stage (dinospore) which attaches to a new host. There are several detailed studies of A. ocellatum (Paperna, 1984a), but comparable detailed data on the freshwater fish dinoflagellids are lacking. Data on P. limneticum growth and division (Jacobs, 1946), suggests that parasites reach a “maturation” prior to detachment. P. pillulare trophonts on the gills, at 23–25°C, develop from dinospore to detached tomont in three to four days. The tomont then completes division to the dinospore stage within 50–70 hours. At 15–17°C, the process of division is lengthened to 11 days (Schaperclaus, 1954).
Pathology and epizootiology
In larval fish, infections were limited to the skin, whereas in large fish the highest parasite densities occurred on the gill filaments and in the buccal-pharyngeal integument. Fish recovering from the epizootic infestation through a gradual decrease in infection, could not be reinfected (Paperna, 1980).
A. ocellatum is attached to and feeds from the host epithelial cell by means of rhizoids, which penetrate the host cell. The consumed cell gradually degenerates and collapses. Damage to infected cells leads to focal erosion of the epithelium. Prolonged infection exhausts a generation of mucus cells and leads to accelerated desquamation. Proliferation of the epithelium causes obliteration of the gill lamellae, while the inner strata of the epithelium become spongious and in some cases undergo complete lysis (Paperna, 1980). Attachment and penetration organelles of P. pillulare differ from those seen in A. ocellatum, in that the host cell is penetrated by nail-like extensions. However, damage to the host cell is similar (Lom & Schubert, 1983). Significant histopathological changes are only seen in the gills, where most of the infection occurs, namely a massive proliferation of the branchial epithelium which causes fusion of the lamellae by a confluent cellular mass (Shaharom-Harrison et al., 1990).
Piscinoodinium infection in Malaysia initially occurred among ornamental fish, but it spread eventually to pond farmed local and exotic cyprinids, causing mortality in fry of Puntius gonionotus in particular, although clinical signs were also apparent in a wider range of cyprinid fish species (Shaharom-Harrison et al., 1990).
Control
A. ocellatum is controlled by continuous application of copper sulphate, 0.75 ppm into infected tanks. A further option is a mixture of 5-hydrate copper sulphate with citric acid monohydrate, to yield 0.15 ppm copper ion concentration in the water (Hignette, 1981; Kabata, 1985). The same methodology will apparently effectively control Piscinoodinium infection, although concentrations should be adjusted to the freshwater medium and the fish targeted for treatment. In freshwater with a pH below 7.0 (in tropical aquaculture), concentrations above 0.3 ppm may be lethal to fish (e.g. Puntius gonionotus fry).

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ICHTHYOPHTHIRIASIS

Species affected and geographical range
Most species of freshwater fish are susceptible, although some may be more so than others. The world wide distribution of I. multifiliis (Hoffman, 1970) has apparently been facilitated by the widespread translocation of cultured and ornamental fish. The presence of this parasite in autochthonous fish, in remote areas of the world including, southern Venezuela (Ventura & Paperna, 1985) and Northern Transvaal in South Africa (Paperna, unpublished) may suggest, however, that many populations, particularly those in the tropics, are comprised of a mix of autochthonous and introduced parasites. Data available from Africa are limited to Southern Africa (in cichlids, carp, Barbus spp., trout and eels - Du Plessis, 1952; Lombard, 1968; Jackson, 1968; Van As & Basson, 1984) and Uganda (on native Barbus amphigramma and exotic Lebistes reticulatus from small streams at Kajansi - Paperna 1972). It is very common in Israel, in both farmed (Sarig, 1971; Hines & Spira, 1973a) and wild fish including cichlids (Ventura & Paperna, 1985).
Description and diagnosis
Gross signs - white spots on the skin and the gills, which under microscopic examination reveal (in skin and gill scrapings) uniformly ciliated organisms with a small cytostome, which may reach up to 1 mm in diameter. Staining with either haematoxylins or Giemsa (after adequate fixation, in such as Bouin) reveals a large crescent-shaped macronucleus and small micronucleus. Ichthyophthirius multifiliis is a monotypic genus of hymenostomatid ciliates.
Life history and biology
Trophonts (feeding stages) develop within the integumentary epithelium, always above the basal membrane (Ventura & Paperna, 1985; Ewing & Kocan, 1992). By maturity, which is reached in 2 days at ambient temperatures of 25–28°C (3–4 days at 21–24°C), the parasite evacuates the host tissue and settles within 2–6 hours on a substrate in the water to form a cyst-encapsulated tomont (dividing stage). Parasites evicted from the tissue before the scheduled time for their spontaneous departure, fail to develop into tomonts and eventually die (Ewing & Kocan, 1992; Paperna, unpublished observations). Within the cyst, tomonts undergo successive binary fissions with a resulting yield of 250–2000 tomites (infective, free swimming stages), which after release will seek a suitable host. The division of tomonts into tomites, in ambient temperatures of 25–28°C, is completed within 15–20 hours (Bauer, 1959; Meyer, 1969; Paperna, unpublished observations; 7–8 hours according to Hoffman, 1978).
Invasion of tomites (teronts) (30–45 μm long) into the host integument is facilitated by the excretion of a sticky substance from subpellicular crystalline organelles named mucocysts. Active penetration causes focal necrosis of the epithelial cells. It has been suggested that hyaluronidase and other enzymes may be produced by the penetrating parasite (Ewing et al., 1985). In the absence of a suitable host, tomites will lose their infective potential within 24 hours at 24–28°C (Ewing & Kocan, 1992). Higher temperatures hasten trophont maturation and tomont division, but at lower temperatures, slower development allows the growth of larger trophonts (0.8–1.0 mm in 5–10°C vs 0.5–0.7 mm in 20–24°C), yielding tomonts with higher numbers of tomite progeny (Ewing et al., 1986). In lower ambient temperatures the survival of the tomites is prolonged, thus, allowing more time to locate a host. Low temperatures do not interrupt propagation, a full cycle is completed at 20°C in 3–5 days, at 15°C in 7–14 days and at 10°C in 21–35 days (Bauer, 1959; Meyer, 1969). Data on the effect of other environmental parameters is less conclusive, although it has been suggested that dissolved oxygen levels below 1 mg/l affect parasite reproduction (Bauer, 1959).
Pathology
Ichthyophthiriasis is fatal to fish of all sizes. Chronic infection will cause serious damage to the skin, fin and gills; corneal infection impairs vision (Hines & Spira, 1973a, 1974a). The infective stage invades the integumentary epithelium and becomes established in the basal layer of the epithelium just above the basal membrane. Cellular damage in low to moderate infections remains restricted to the infected site. In addition to the damage caused to epithelial cells by the feeding and expanding parasites, in heavy infections mass exodus of parasites from the epithelial layer, having completed their scheduled growth, causes its erosion and detachment from the basal membrane. In some infections, parasites cause widespread lysis of the inner layer of the epithelium. Prolonged infection also induces epithelial proliferation and haemorrhagic inflammation, causing the integument to become severely disintegrated (Hines & Spira, 1974a; Ventura & Paperna, 1985; Ewing et al., 1986). Hines and Spira's (1973b, 1974a,b) haematological and clinical data from heavily infected fish reveal evident physiological dysfunction resulting apparently from both direct pathological damage induced by the parasite and as a by-product of the stress response.
Epizootiology
Ichthyophthirius multifiliis is one of the most common, troublesome and difficult to control of fish pathogens. Epizootic infections have been reported in cold water salmonid farms (also in Africa, Du Plessis, 1952; Lombard, 1968) and warm water farmed carp, eels, Clarias gariepinus and Ictalurus punctatus (channel catfish) (Meyer, 1970; Sarig, 1971; Hines & Spira, 1973a; Hine, 1975; Jackson, 1978; Khalifa et al. 1983; Paperna, unpublished). Fish may maintain low, subclinical (enzootic) infection (in preimmunity), while encysted tomonts may persist in the habitat. Enzootic infections in native fish have been found in Lebistes reticulatus in Uganda (Paperna, 1972), in cichlids and cyprinids native to the Lake Kinneret system in Israel (Paperna, unpublished), in glass eels, cyprinids and cichlids in native habitats of South Africa (Jackson, 1978; Van As & Basson, 1984), and in a variety of native fish in the southern United States (Allison & Kelly, 1963). Transition from nonclinical enzootic to epizootic clinical infection is usually stress-mediated, prompted by adverse growth conditions such as overcrowding, poor feeding and excess nitrogenous waste. Epizootic infection, however, never occurs in overwintering tilapia or Clarias gariepinus in Israel, or southern Africa, but rather, coincides (also in southern USA - Meyer, 1970) with the warming of the water in early spring when fish are still kept in overcrowded conditions after winter storage. In South Africa, 6.4% of wild glass eels in the Southern Cape are infected. Via these, fish infection has been introduced into eel nurseries where elvers, especially those not completely acclimated, succumbed to severe infestations (Hine, 1975; Jackson, 1978).
Spontaneous recovery has been observed in both natural infections in natural habitats and in holding facilities, and even in experimental infections in aquaria (Paperna, 1972; Lahav & Sarig, 1973). The potential for spontaneous recovery varied with fish species. Infection in scaled fish, notably cichlids, regressed faster than in smooth skinned fish (eels, Clarias spp. and other siluriforms, mirror and leather carp) (Paperna, 1972 and unpublished observations). After recovery, fish were refractory to reinfection or retained a merely subclinical chronic infection (Hines & Spira, 1974c; Wahli & Meier, 1985; Paperna, unpublished observations). The observed interspecific variation in susceptibility to infection could, however, also result from differential compatibility of various fish species to man-made habitats and variable vulnerability to stress.
Spontaneous recovery from infection and resistance to reinfection of recovered fish indicate that fish are capable of developing defence mechanisms against I. multifiliis (Hines & Spira, 1974c). Spontaneous recovery observed in carp at temperatures as low as 10°C (Lahav & Sarig, 1973) implies some protective responses other than via humoral antibody production, which becomes suppressed in carp below 12°C (Avtalion, 1981).
Hines & Spira (1974c) demonstrated immobilisation of free swimming tomites with sera taken from carp after their recovery from infection. The infective stages were also shown to be unable to penetrate the skin of resistant carp. Immobilisation tests with trophonts showed that in infected trout anti-parasitic activity of the mucus increases quickly after infection and decreases soon after the infection has disappeared. The anti-parasitic activity of the serum, in the same fish, increases slowly but remains at a higher level for at least 7 months (Wahli & Meier, 1985). Fish immunised with Tetrahymena spp. developed a resistance to a challenge of lchthyophthirius infection (Goven et al., 1981).
Carp were immunised following controlled exposure to the infective tomite (teront) stage, and survived challenges with high infective doses, but lost protection after being immunosupressed by the administration of corticosteroids. These results could have simulated a stress mediated situation. Levels of humoral antibodies in immunosuppressed fish, however, remained the same as in the immunised group, which further confirms the involvement of other than humoral type immune systems in the protection processes against l. multifiliis infections (Houghton & Matthews, 1990).
Immunisation with killed vaccines gave less satisfactory results, although better protection was obtained through intraperitoneal inoculation of live teronts (Burkart et al., 1990). Oreochromis aureus mothers vaccinated through the latter method, passively transferred a protective immunity to their fry (Subasinghe & Sommerville, 1989). Additionally to immunity passed from mothers via eggs, demonstrable by antibodies in the soluble extracts of fry tissues, a protective immunity was acquired directly from the parent mouth during the brooding period (Sin et al., 1994).
Control
Both trophonts, localised beneath the epithelial layer of the integument, and the encysted tomonts, attached to substrates in the aquatic habitat, are resistant to practically all externally applied usable antiparasitic agents.
Infection can be effectively controlled only by destruction or elimination of the free dividing tomonts or the tomites they release. In warm water systems (24–28°C), three to four daily transfers of fish to clean tanks will effectively reduce infection, while enabling the fish to develop tolerance to reinfections. Tomonts can be effectively removed from large circulating tanks by repeated brushing with vacuum suction. Spontaneous recovery and transition into a refractory state will be further promoted by management techniques which alleviate stressing conditions (improving water flow, accelerating aeration and reducing stocking densities). Chemical parasiticides will be effective only through continuous or repeated daily application. Of the many listed (Meyer, 1969), the only cost-effective remedy for large scale farming systems is Malachite green at a dose of 0.05 ppm for continuous application (3–4 days) or up to 0.15 ppm (depending on the specific fish tolerance which varies with species - siluriforms are particularly susceptible). Formalin will dislodge some of the trophonts and is often applied mixed with Malachite green (50 ppm with 0.05 ppm) (Sarig, 1971).
Systemic therapy seems to be the only means of effective control. Elimination of tissue trophozoites was reported in several species of ornamental aquarium fish fed medicated food (Tetra, MA 100/50) containing Malachite green in a non-water soluble formulation for 4 days (neither drug concentration in the food, nor daily rations are given; Schmahl et al., 1992). For use in commercial food-fish culture for human consumption, the cost efficiency of Malachite medicated feed formulations and their toxicity to humans must be considered.


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Helminth infections acquired through the gastrointestinal tract

Trichinosis. Trichinella spiralis is the cause of trichinosis in man. The nematode circulates between rats and pigs with man becoming infected from eating raw or inadequately cooked pork products. Encysted larvae in the meat excyst (hatch) in the intestine and develop into minute adults in the mucosa. These mature and the females deposit larvae that then migrate through the tissues to reach skeletal muscles in which they encyst. Human infections may be asymptomatic but can include fever, orbital oedema, myalgia and eosinophilia. In the extreme, infection can be fatal through myocarditis or encephalitis.
Enterobiasis. Enterobias vermicularis is a small thread-like "pinworm" mainly infecting young children. The female emerges to the perianal region usually at night and lays some 10,000-15,000 eggs and then dies. In the process they cause severe pruritis (itching). The embryonated eggs are infectious on ingestion and hatch in the duodenum. The larvae pass to the caecum where they mature into adults. Because of the pruritis, children often re-infect themselves from eggs under their fingernails. Bedding is also a source of infection and can be a means of spreading the organism in families and institutions such as orphanages and boarding schools.
Taenia solium (pork tapeworm). The adult lives in the small intestine of man that is the definitive host. Segments of the worm pass through the anus and release large numbers of eggs that can survive for long periods outside of the body. When ingested by pigs, the eggs hatch and each releases an onchosphere that migrates through the intestinal wall and blood vessels to reach striated muscle where encystment occurs. When inadequately cooked pig meat is eaten by man, excystment occurs in the small intestine and an adult cestode (worm) develops. If the eggs are released into the upper intestine of man (e.g. through regurgitation) they can invade the host setting up a potentially dangerous larval infection known as cysticercosis in muscle and other sites.
Taenia saginata (beef tapeworm). This also infects man through cattle. The life cycle is similar to T. solium and in both species the adult tapeworm can grow up to 10 meters in length.
Hydatidosis. This is caused by the tapeworm Echinococcus granulosus. The adult worm inhabits the small intestine of dogs from which the eggs of the species are passed. These eggs can be ingested by herbivorous animals and hatch in the duodenum. The embryos enter the circulation where they are carried to various sites to develop into cysts. Dogs become infected when they eat contaminated offal. Humans are infected if they accidentally ingest eggs from infected dogs and the liver is the most common site of infection in which hydatid cysts form.

References: Baker, J.R. and Muller, R (Eds). Advances in Parasitology. Academic Press, London. Knight, R. (1982). Parasites Diseases in Man. Churchill Livingstone, London. Peters, W. and Gilles, H.M. (1995) Colour Atlas of Tropical Medicine and Parasitology. Mosby-Wolfe.

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Echinococcosis (hydatid)

Echinococcus granulosus and E. multilocularis are causative agents of hydatid cysts

Echinococcus granulosus
Epidemiology
The organism is common in Asia, Australia, Eastern Africa, southern Spain, southern parts of South America and northern parts of North America. The incidence of human infection about 1 to 2 per 1000 population and may be higher in rural areas of affected regions.
Morphology
This is the smallest of all tapeworms (3 to 9 mm long) with only 3 proglottids.
Life cycle
The adult worm lives in domestic and wild carnivorous animals. Eggs, passed by infected animals, are ingested by the grazing farm animals or man, localize in different organs and develop into hydatid cysts containing many larvae (proto-scolices or hydatid sand) (Figure 8). When other animals consume infected organs of these animals, proto-scolices escape the cyst, enter the small intestine and develop into adult worms (Figure 7). Echinococcus eggs, when swallowed by man, produce embryos that penetrate the small intestine, enter the circulation and form cysts in liver, lung, bones, and sometimes, brain. The cyst is round and measures 1 to 7 cm in diameter, although it may grow to be 30 cm. The cyst consists of an outer anuclear hyaline cuticula and an inner nucleated germinal layer containing clear yellow fluid. Daughter cysts attach to the germinal layer, although some cysts, known as brood cysts, may have only larvae (hydatid sand). Man is a dead end host.
Symptoms
The symptoms, comparable to those of a slowly growing tumor, depend upon the location of the cyst. Large abdominal cysts produce increasing discomfort. Liver cysts cause obstructive jaundice. Peribronchial cysts may produce pulmonary abscesses. Brain cysts produce intracranial pressure and Jacksonian epilepsy. Kidney cysts cause renal dysfunction. The contents of a cyst may produce anaphylactic responses.
Diagnosis
Clinical symptoms of a slow-growing tumor accompanied by eosinophilia are suggestive. Intradermal (Casoni) test with hydatid fluid is useful. Pulmonary cysts and calcified cysts can be visualized using x-rays. Antibodies against hydatid fluid antigens have been detected in a sizable population of infected individuals by ELISA or indirect hemagglutination test.
Treatment and control
Treatment involves surgical removal of cyst or inactivation of hydatid sand by injecting the cyst with 10% formalin and its removal within five minutes. It has been claimed that a high dose of Mebendazole results in some success. Preventive measures involve avoiding contact with infected dogs and cats and elimination of their infection

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Diphyllobothrium latum (fish or broad tapeworm)

Epidemiology
Fish tapeworm infection is distributed worldwide, in the subarctic and temperate regions; it is associated with eating of raw or improperly cooked fresh water fish.
Morphology
This is the longest tapeworm found in man, ranging from 3-10 meters with more than 3000 proglottids. The scolex resembles two almond-shaped leaves and the proglottids are broader than they are long, a morphology reflected in the organism's name. Eggs are 30 x 50 micrometers in size and contain an embryo with 3 pairs of hooklets.
Life cycle
Man and other animals are infected by eating uncooked fish that contains plerocercoid larvae (15 x 2 mm) which attach to the small intestinal wall and mature into adult worms in 3 to 5 weeks. Eggs discharged from gravid proglottids in the small intestine are passed in the feces. The egg hatches in fresh water to produce a ciliated coracidium which needs to be ingested by a water flea (Cyclops) where it develops into a procercoid larva. When infected Cyclops are ingested by the freshwater fish, the procercoid larva penetrates the intestinal wall and develops into a plerocercoid larva, infectious to man (figure 3).
Symptoms
Clinical symptoms may be mild, depending on the number of worms. They include abdominal discomfort, loss of weight, loss of appetite and some malnutrition. Anemia and neurological problems associated with vitamin B12 deficiency are seen in heavily infected individuals.
Diagnosis
Diagnosis is based on finding many typical eggs and empty proglottids in feces (Figure 3). A history of raw fish consumption and residence in an endemic locality is helpful.
Treatment and control
Praziquantel is the drug of choice. Freezing for 24 hours, thorough cooking or pickling of fish kills the larvae. Fish reservoirs should

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