12 Makhluk Halus dalam Tubuh Babi !!!

Posted Kamis, 24 Mei 2012 by bunga

12 Makhluk Halus Dalam Tubuh BABI (WASPADALAH)


Mari membuka pikiran..buka mata dan hatimu..Lihatlah makhluk2 halus yg bersarang dalam tubuh babi..

Babi adalah kontainer (tempat penampung) penyakit. Beberapa bibit penyakit yang dibawa babi :

1. Cacing pita Taenia solium

Spoiler for Taenia solium:

2. Cacing spiral Trichinella spiralis
Spoiler for cacing:

3. Cacing tambang Ancylostoma duodenale
Spoiler for Ancylostoma duodenale:

4. Cacing paru Paragonimus pulmonaris
Spoiler for Paragonimus pulmonaris:

5. Cacing usus Fasciolopsis buski
Spoiler for Fasciolopsis buski:

6. Cacing Schistosoma japonicum
Spoiler for Schistosoma japonicum:

7. Bakteri Tuberculosis (TBC)
Spoiler for Tuberculosis:

8. Bakteri kolera Salmonella choleraesuis
Spoiler for Salmonella choleraesuis:

9. Bakteri Brucellosis suis
Spoiler for Brucellosis suis:

10. Virus cacar (Small pox)
Spoiler for Small pox:
 Penyakitnya kayak gini:
Spoiler for cacar:

11. Virus kudis (Scabies)
Spoiler for Scabies:
 penyakitnya kayak gini
Spoiler for kudis:

12. Parasit protozoa
A. Parasit protozoa Balantidium coli

Spoiler for Balantidium coli:
B. Parasit protozoa Toxoplasma gondii
Spoiler for Toxoplasma gondii:

Giardia lamblia

Posted Senin, 21 Mei 2012 by bunga

Giardia lamblia

Clasass: Flagelata
Family: Hexamitidae
Genus Giardia
Species: Giardia lalmblia
Protozoa ini ditemukan pertama kali oleh Leuwenhoek pada tahun 1681, yang ia temukan pada fesesnya sendiri. Spesies protozoa ini banyak ditemukan didaerah yang beriklim panas. Anak-anak peka terhadap infeksi penyakit ini, dimana G. Lamblia adalah flagellata yang paling sering dijumpai pada saluran pencernaan manusia.

Daur hidup
Giardia lamblia hidup dalam usus halus orang yaitu bagian duodenum, jejenum dan bagian atas dari ileum, melekat pada permukaan epithel usus. Protozoa dapat berenang dengan cepat menggunakan flagellanya. Pada seorang yang menderita berat penyakit ini , ditemukan 14 milyard parasit dalam fesesnya, sedangkan pada infeksi sedang ditemukan sekitar 300 juta cyste.
Dalam usus halus dimana isi usus berbentuk cairan, parasit ditemukan dalam bentuk trophozoit, tetapi setelah masuk kedalam colon parasit akan membentuk cyste.. Pertama-tama flagella memendek, cytoplasma mengental dan dinding menebal, kemudian cyste keluar melalui feses. Pada awal terbentuknya cyste, ditemukan dua nukleoli, setelah sejam kemudian ditemukan 4 nukleoli.. Bila cyste tertelan hospes maka cyste tersebut langsung masuk kedalam duodenum, flagella tumbuh dan terbentuk trophozoit kembali.
Kebanyakan kasus infeksi tidak menunjukkan gejala infeksi, biasanya ada orang yang lebih peka terhadap penyakit ini daripada lainnya. Pada suatu kasus terjadi sekresi cairan mukosa berlebihan sehingga terjadi diaree, dehydrasi, sakit perut dan berat badan menurun. Feses terlihat berlemak tetapi tidak ditemukan darah. Protozoa tidak merusak sel hospes, tetapi memakan cairan mukosa pada epithel usus, sehingga menghambat absorpsi lemak dan unsur nutrisi lain, hal ini memacu terjadinya gejala penyakit tersebut diatas. Cairan empedu dapat terserang sehingga menyebabkan jaundice (penyakit kuning/icterus) dan sakit perut (colic). Penyakit tidak menyebabkan fatal, tetapi sangat mengganggu.
Diagnosis dan pengobatan
Dengan menemukan trophozoit dan cyste dalam feses dapat dijadikan pedoman diagnosis. Pengobatan dilakukan dengan pemberian Quinacrin atau metronidazole, biasanya sembuh dalam beberapa hari.

Plasmodium vivax

Posted by bunga

Plasmodium vivax

Plasmodium vivax
Mature P. vivax trophozoite
Scientific classification
Kingdom: Chromalveolata
Superphylum: Alveolata
Phylum: Apicomplexa
Class: Aconoidasida
Order: Haemosporida
Family: Plasmodiidae
Genus: Plasmodium
Species: P. vivax
Binomial name
Plasmodium vivax
Grassi & Feletti 1890
Plasmodium vivax is a protozoal parasite and a human pathogen. The most frequent and widely distributed cause of recurring (Benign tertian) malaria, P. vivax is one of the four species of malarial parasite that commonly infect humans. It is less virulent than Plasmodium falciparum, which is the deadliest of the four, and is seldom fatal. P. vivax is carried by the female Anopheles mosquito, since it is only the female of the species that bites.




P. vivax is found mainly in the United States, Latin America, and in some parts of Africa. P. vivax can cause death due to splenomegaly (a pathologically enlarged spleen), but more often it causes debilitating – but non-fatal – symptoms.[1][2] Overall it accounts for 65% of malaria cases in Asia and South America.


Chloroquine remains the treatment of choice for vivax malaria,[3] except in Indonesia's Irian Jaya (Western New Guinea) region and the geographically contiguous Papua New Guinea, where chloroquine resistance is common (up to 20% resistance). Chloroquine resistance is an increasing problem in other parts of the world, such as Korea,India.[4]
When chloroquine resistance is common or when chloroquine is contraindicated, then artesunate is the drug of choice, except in the U.S., where it is not approved for use.[5] Where an artemisinin-based combination therapy has been adopted as the first-line treatment for P. falciparum malaria, it may also be used for P. vivax malaria in combination with primaquine for radical cure.[3] An exception is artesunate plus sulfadoxine-pyrimethamine (AS+SP), which is not effective against P. vivax in many places.[3] Mefloquine is a good alternative and in some countries is more readily available.[6] Atovaquone-proguanil is an effective alternative in patients unable to tolerate chloroquine.[7] Quinine may be used to treat vivax malaria but is associated with inferior outcomes.
Thirty-two to 100% of patients will relapse following successful treatment of P. vivax infection if a radical cure (eradication of liver stages) is not given.[8][9][10] Eradication of the liver stages is achieved by giving primaquine, after checking the patients G6PD status to reduce the risk of haemolysis.[11] However, in severe G6PD deficiency, primaquine is contraindicated and should not be used.[3] Recently, this point has taken particular importance for the increased incidence of vivax malaria among travelers.[12] At least a 14-day course of primaquine is required for the radical treatment of P. vivax.[3]

Eradication efforts in Korea

P. vivax is the only indigenous malaria parasite on the Korean peninsula. In the years following the Korean War (1950–53), malaria-eradication campaigns successfully reduced the number of new cases of the disease in North Korea and South Korea. In 1979, World Health Organization declared the Korean peninsula vivax malaria-free, but the disease unexpectedly re-emerged in the late 1990s and still persists today. Several factors contributed to the re-emergence of the disease, including reduced emphasis on malaria control after 1979, floods and famine in North Korea, emergence of drug resistance and possibly global warming. Most cases are identified along the Korean Demilitarized Zone. As such, vivax malaria offers the two Koreas a unique opportunity to work together on an important health problem that affects both countries.[13][14]


P. vivax can reproduce both asexually and sexually, depending on its life cycle stage.
Asexual forms:
  • Immature trophozoites (Ring or signet-ring shaped), about 1/3 of the diameter of a RBC.
  • Mature trophozoites: Very irregular and delicate (described as amoeboid); many pseudopodial processes seen. Presence of fine grains of brown pigment (malarial pigment) or hematin probably derived from the haemoglobin of the infected red blood cell.
  • Schizonts (also called meronts): As large as a normal red cell; thus the parasitized corpuscle becomes distended and larger than normal. There are about sixteen merozoites.
Sexual forms: Gametocytes: Round. The gametocytes of P. vivax are commonly found in the peripheral blood at about the end of the first week of parasitemia.
It has been suggested that P. vivax has horizontally acquired genetic material from humans. [15]

Life cycle

The incubation period for the infection usually ranges from ten to seventeen days and sometimes up to a year. Persistent liver stages allow relapse up to five years after elimination of red blood cell stages and clinical cure.

Human infection

The infection of Plasmodium vivax takes place in human when an infected female anopheles mosquito sucks blood from a healthy person. During feeding, the mosquito injects saliva to prevent blood clotting (along with sporozoites), thousands of sporozoites are inoculated into human blood; within a half-hour the sporozoites reach the liver. There they enter hepatic cells, transform into the tropozoite form and feed on hepatic cells, and reproduce asexually. This process gives rise to thousands of merozoites (plasmodium daughter cells) in the circulatory system and the liver.

Liver stage

The P. vivax sporozoite enters a hepatocyte and begins its exoerythrocytic schizogony stage. This is characterized by multiple rounds of nuclear division without cellular segmentation. After a certain number of nuclear divisions, the parasite cell will segment and merozoites are formed.
There are situations where some of the sporozoites do not immediately start to grow and divide after entering the hepatocyte, but remain in a dormant, hypnozoite stage for weeks or months. The duration of latency is variable from one hypnozoite to another and the factors that will eventually trigger growth are not known; this explains how a single infection can be responsible for a series of waves of parasitaemia or "relapses".[16] Different strains of P. vivax have their own characteristic relapse pattern and timing.[17] The earlier stage is exo-erythrocytic generation.

Erythrocytic cycle

P. vivax preferentially penetrates young red blood cells (reticulocytes). In order to achieve this, merozoites have two proteins at their apical pole (PvRBP-1 and PvRBP-2). The parasite uses the Duffy blood group antigens (Fy6) to penetrate red blood cells. This antigen does not occur in the majority of humans in West Africa [phenotype Fy (a-b-)]. As a result P. vivax occurs less frequently in West Africa.[19]
The parasitised red blood cell is up to twice as large as a normal red cell and Schüffner's dots (also known as Schüffner's stippling or Schüffner's granules) is seen on the infected cell's surface, the spotted appearance of which varies in color from light pink, to red, to red-yellow, as coloured with Romanovsky stains. The parasite within it is often wildly irregular in shape (described as "amoeboid"). Schizonts of P. vivax have up to twenty merozoites within them. It is rare to see cells with more than one parasite within them. Merozoites will only attach to immature blood cell (reticulocytes) and therefore it is unusual to see more than 3% of all circulating erythrocytes parasitised.

Sexual stage

The sexual stage includes following processes by which P. vivax reproduces sexually:
  1. Transfer to mosquito
  2. Gametogenesis
    • Microgametes
    • Macrogametes
  3. Fertilization
  4. Ookinite
  5. Oocyst
  6. Sporogony

Mosquito stage

the life cycle in mosquitoes include:
Formation of gametes
Development of gametes from gametocytes is known as gametogony. When a female Anopheles mosquito bites an infected person, gametocytes and other stages of the parasite are transferred to the stomach where further development occur.
The microgametocytes becomes very active and its nucleus undergoes fission to give 6-8 daughter nuclei which becomes arranged at the periphery. The cytoplasm develops long thin flagella like projections, then a nucleus enter into each one of these extensions. These cytoplasmic extensions later break off as mature male gametes (microgametes). This process of formation of flagella like microgametes or male gametes is known as exflagellation. Macrogametocytes show very little change. It develops a cone of reception at one side and becomes mature as female gamete / macrogameto cytes.
Male gametes move actively in the stomach of mosquito in search of female gamete. Male gamete then enters into female gamete through the cone of reception and the complete fusion of 2 gametes result in the formation of zygote. (synkaryon). Process of fusion of male and female gamete is called as syngamy. Fusion of 2 dissimilar gametes is known as anisogamy. The zygote remains inactive for sometime but it soon elongates, becomes vermiform (worm-like) and motile. It is now known as ookinete. The pointed ends of ookinete penetrate the wall of stomach and comes to lie below its outer epithelial layer. Here it becomes spherical and develops a cyst wall around itself. The cyst wall is derived partly from the stomach tissues and partly produced by the zygote itself. At this stage, it is known as the oocyst. The oocyst absorbs nourishment and grow in size. These oocyst protrude (bulge) from the surface of stomach giving it a kind of blistered appearance. In a highly infected mosquito, as many as 1000 oocyst may be seen.
The nucleus of oocyst divides repeatedly to form large number of daughter nuclei. At the same time, the cytoplasm develops large vacuoles and forms numerous cytoplasmic masses. These cytoplasmic masses then elongate and a daughter nuclei migrates into each one of them. The resulting sickle-shaped bodies is known as sporozoites. This phase of asexual multiplication is known as sporogony and is completed in about 10–21 days. The oocyst then burst and sporozoites are released into the body cavity of mosquito from where they eventually reach the salivary glands of mosquito through blood. The mosquito now becomes infectiv . Salivary glands of a single infected mosquito may contain as many as 200,000 sporozoites. When the mosquito bites a healthy person, thousands of sporozoites are infected into the blood along with the saliva and the cycle starts again.

Laboratory considerations

P. vivax and P. ovale that has been sitting in EDTA for more than half-an-hour before the blood film is made will look very similar in appearance to P. malariae, which is an important reason to warn the laboratory immediately when the blood sample is drawn so they can process the sample as soon as it arrives. Blood films are preferably made within half-an-hour of the blood being drawn and must certainly be made within an hour of the blood being drawn. Diagnosis can be done with the strip fast test of antibodies,


P. vivax can be divided into two clades one that appears to have origins in the Old World and a second that originated in the New World.[20] The distinction can be made on the basis of the structure of the A and S forms of the rRNA. A rearrangement of these genes appears to have occurred in the New World strains. It appears that a gene conversion occurred in an Old World strain and this strain gave rise to the New World strains. The timing of this event has yet to be established.
At present both types of P. vivax circulate in the Americas. The monkey parasite - Plasmodium simium - is related to the Old World strains rather than to the New World strains.
A specific name - Plasmodium collinsi - has been proposed for the New World strains but this suggestion has not been accepted to date.

Trichomonas vaginalis

Posted by bunga

Trichomonas vaginalis

Trichomonas vaginalis
T. vaginalis phase contrast microscopy
Scientific classification
Domain: Eukarya
Phylum: Metamonada
Class: Parabasalia
Order: Trichomonadida
Genus: Trichomonas
Species: T. vaginalis
Binomial name
Trichomonas vaginalis
(Donné 1836)
Trichomonas vaginalis is an anaerobic, flagellated protozoan, a form of microorganism. The parasitic microorganism is the causative agent of trichomoniasis, and is the most common pathogenic protozoan infection of humans in industrialized countries.[1] Infection rates between men and women are the same with women showing symptoms while infections in men are usually asymptomatic. Transmission takes place directly because the trophozoite does not have a cyst. The WHO has estimated that 160 million cases of infection are acquired annually worldwide.[2] The estimates for North America alone are between 5 and 8 million new infections each year, with an estimated rate of asymptomatic cases as high as 50%.[3] Usually treatment consists of metronidazole and tinidazole.[4]



Mechanism of Infection

Trichomonas vaginalis, a parasitic protozoan, is the etiologic agent of trichomoniasis, and is a sexually transmitted disease.[5][2] More than 160 million people worldwide are annually infected by this protozoan.[2]


Pap smear, showing infestation by Trichomonas vaginalis. Papanicolaou stain, 400x.
Trichomoniasis, a sexually transmitted infection of the urogenital tract, is a common cause of vaginitis in women, while men with this infection can display symptoms of urethritis.[6]


Some of the complications of T. vaginalis in women include: preterm delivery, low birth weight, and increased mortality as well as predisposing to HIV infection, AIDS, and cervical cancer.[7] T. vaginalis has also been reported in the urinary tract, fallopian tubes, and pelvis and can cause pneumonia, bronchitis, and oral lesions. Condoms are effective at reducing, but not wholly preventing, transmission.[8] Ten percent of women with the infection will have a "strawberry" cervix or vagina on examination.[citation needed]
Recent research also suggests a link between T. vaginalis infection in males and subsequent aggressive prostate cancer.[9]


Classically, with a cervical smear, infected women have a transparent "halo" around their superficial cell nucleus. It is unreliably detected by studying a genital discharge or with a cervical smear because of their low sensitivity. T. vaginalis was traditionally diagnosed via a wet mount, in which "corkscrew" motility was observed. Currently, the most common method of diagnosis is via overnight culture,[10][11] with a sensitivity range of 75-95%.[12] Newer methods, such as rapid antigen testing and transcription-mediated amplification, have even greater sensitivity, but are not in widespread use.[12] The presence of T. vaginalis can also be diagnosed by PCR, using primers specific for GENBANK/L23861.[13][14]


Infection is treated and cured with metronidazole or tinidazole, usually as a single-dose therapy, and should be prescribed to any sexual partner(s) as well because they may be asymptomatic carriers.[15][6]


The T. vaginalis trophozoite is oval as well as flagellated, or "pear" shaped as seen on wet-mount slide. It is slightly larger than a white blood cell, measuring 9 X 7 μm. Five flagella arise near the cytostome; four of these immediately extend outside the cell together, while the fifth flagellum wraps backwards along the surface of the organism. The functionality of the fifth flagellum is not known. In addition, a conspicuous barb-like axostyle projects opposite the four-flagella bundle; the axostyle may be used for attachment to surfaces and may also cause the tissue damage noted in trichomoniasis infections.[16]
While T. vaginalis does not have a cyst form, organisms can survive for up to 24 hours in urine, semen, or even water samples. It has an ability to persist on fomites with a moist surface for 1 to 2 hours.[citation needed]

Protein function

T. vaginalis has enzymes that catalyze many chemical reactions making the organism relevant to the study of protein function. T. vaginalis lacks mitochondria and other necessary enzymes and cytochromes to conduct oxidative phosphorylation. T. vaginalis obtains nutrients by transport through the cell membrane and by phagocytosis. The organism is able to maintain energy requirements by the use of a small amount of enzymes to provide energy via glycolysis of glucose to glycerol and succinate in the cytoplasm, followed by further conversion of pyruvate and malate to hydrogen and acetate in an organelle called the hydrogenosome.[17]


One of the hallmark features of Trichomonas vaginalis is the adherence factors that allow cervicovaginal epithelium colonization in women. The adherence that this organism illustrates is specific to vaginal epithelial cells (VECs) being pH, time and temperature dependent. A variety of virulence factors mediate this process some of which are the microtubules, microfilaments, adhesins (4), and cysteine proteinases. The adhesins are four trichomonad enzymes called AP65, AP51, AP33, and AP23 that mediate the interaction of the parasite to the receptor molecules on VECs.[18] Cysteine proteinases may be another virulence factor because not only do these 30 kDa proteins bind to host cell surfaces but also may degrade extracellular matrix proteins like hemoglobin, fibronectin or collagen IV.[19]

Genome sequencing and statistics

The T. vaginalis genome was found to be approximately 160 megabases in size[20] – ten times larger than predicted from earlier gel-based chromosome sizing [21] (The human genome is ~3.5 gigabases by comparison.[22]) As much as two-thirds of the T. vaginalis sequence consists of repetitive and transposable elements, reflecting a massive, evolutionarily-recent expansion of the genome. The total number of predicted protein-coding genes is ~98,000, which includes ~38,000 'repeat' genes (virus-like, transposon-like, retrotransposon-like, and unclassified repeats, all with high copy number and low polymorphism). Approximately 26,000 of the protein-coding genes have been classed as 'evidence-supported' (similar either to known proteins, or to ESTs), while the remainder have no known function. These extraordinary genome statistics are likely to change downward as the genome sequence, currently very fragmented due to the difficulty of ordering repetitive DNA, is assembled into chromosomes, and as more transcription data (ESTs, microarrays) accumulate. But it appears that the gene number of the single-celled parasite T. vaginalis is, at minimum, on par with that of its host H. sapiens.
In late 2007 TrichDB.org was launched as a free, public genomic data repository and retrieval service devoted to genome-scale trichomonad data. The site currently contains all of the T. vaginalis sequence project data, several EST libraries, and tools for data mining and display. TrichDB is part of the NIH/NIAID-funded EupathDB functional genomics database project.[23]

Increased susceptibility to HIV

The damage caused by Trichomonas vaginalis to the vaginal endometrium increases a woman's susceptibility to an HIV infection. In addition to inflammation, the parasite also causes lysis of epithelial cells and RBCs in the area leading to more inflammation and disruption of the protective barrier usually provided by the epithelium. Having Trichomonas vaginalis also may increase the chances of the infected woman transmitting HIV to her sexual partner(s).[24][25]

Oxyuris vermicularis

Posted Sabtu, 19 Mei 2012 by bunga

      Oxyuris vermicularis


Posted Jumat, 18 Mei 2012 by bunga


From Wikipedia, the free encyclopedia
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Classification and external resources

Skin vesicles on the forearm, created by the penetration of Schistosoma. Source: CDC
ICD-10 B65
ICD-9 120
MeSH D012552
Schistosomiasis (also known as bilharzia, bilharziosis or snail fever) is a parasitic disease caused by several species of trematodes (platyhelminth infection, or "flukes"), a parasitic worm of the genus Schistosoma. Snails serve as the intermediary agent between mammalian hosts. Individuals within developing countries who cannot afford proper sanitation facilities are often exposed to contaminated water containing the infected snails. [1]
Although it has a low mortality rate, schistosomiasis often is a chronic illness that can damage internal organs and, in children, impair growth and cognitive development. The urinary form of schistosomiasis is associated with increased risks for bladder cancer in adults. Schistosomiasis is the second most socioeconomically devastating parasitic disease after malaria.[2]
This disease is most commonly found in Asia, Africa, and South America, especially in areas where the water contains numerous freshwater snails, which may carry the parasite.
The disease affects many people in developing countries, particularly children who may acquire the disease by swimming or playing in infected water.[2] When children come into contact with a contaminated water source, the parasitic larvae easily enter through their skin and further mature within organ tissues. As of 2009, 74 developing countries statistically identified epidemics of Schistosomiasis within their respective populations. [1]



[edit] Classification

Species of Schistosoma that can infect humans:
Avian schistosomiasis species cause swimmer's itch and clam digger itch
Species of Schistosoma that can infect other animals:
S. bovis — normally infects cattle, sheep and goats in Africa, parts of Southern Europe and the Middle East
S. mattheei — normally infects cattle, sheep and goats in Central and Southern Africa
S. margrebowiei — normally infects antelope, buffalo and waterbuck in Southern and Central Africa
S. curassoni — normally infects domestic ruminants in West Africa
S. rodhaini — normally infects rodents and carnivores in parts of Central Africa

[edit] Signs and symptoms

Above all, schistosomiasis is a chronic disease. Many infections are subclinically symptomatic, with mild anemia and malnutrition being common in endemic areas. Acute schistosomiasis (Katayama's fever) may occur weeks after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include:
Occasionally central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid paraplegia.
Calcification of the bladder wall on a plain x-ray image of the pelvis, in a sub-Saharan man of 44 years old. This is due to urinary schistosomiasis.
Continuing infection may cause granulomatous reactions and fibrosis in the affected organs, which may result in manifestations that include:
Bladder cancer diagnosis and mortality are generally elevated in affected areas.

[edit] Pathophysiology

[edit] Life cycle

Schistosoma life cycle. Source: CDC
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive host.

[edit] Snails

The life cycles of all five human schistosomes are broadly similar: parasite eggs are released into the environment from infected individuals, hatching on contact with fresh water to release the free-swimming miracidium. Miracidia infect fresh-water snails by penetrating the snail's foot. After infection, close to the site of penetration, the miracidium transforms into a primary (mother) sporocyst. Germ cells within the primary sporocyst will then begin dividing to produce secondary (daughter) sporocysts, which migrate to the snail's hepatopancreas. Once at the hepatopancreas, germ cells within the secondary sporocyst begin to divide again, this time producing thousands of new parasites, known as cercariae, which are the larvae capable of infecting mammals.
Cercariae emerge daily from the snail host in a circadian rhythm, dependent on ambient temperature and light. Young cercariae are highly mobile, alternating between vigorous upward movement and sinking to maintain their position in the water. Cercarial activity is particularly stimulated by water turbulence, by shadows and by chemicals found on human skin.

[edit] Humans

Penetration of the human skin occurs after the cercaria have attached to and explored the skin. The parasite secretes enzymes that break down the skin's protein to enable penetration of the cercarial head through the skin. As the cercaria penetrates the skin it transforms into a migrating schistosomulum stage.
Photomicrography of bladder in S. hematobium infection, showing clusters of the parasite eggs with intense eosinophilia, Source: CDC
The newly transformed schistosomulum may remain in the skin for 2 days before locating a post-capillary venule; from here the schistosomulum travels to the lungs where it undergoes further developmental changes necessary for subsequent migration to the liver. Eight to ten days after penetration of the skin, the parasite migrates to the liver sinusoids. S. japonicum migrates more quickly than S. mansoni, and usually reaches the liver within 8 days of penetration. Juvenile S. mansoni and S. japonicum worms develop an oral sucker after arriving at the liver, and it is during this period that the parasite begins to feed on red blood cells. The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the shorter male. Adult worms are about 10 mm long. Worm pairs of S. mansoni and S. japonicum relocate to the mesenteric or rectal veins. S. haematobium schistosomula ultimately migrate from the liver to the perivesical venous plexus of the bladder, ureters, and kidneys through the hemorrhoidal plexus.
Parasites reach maturity in six to eight weeks, at which time they begin to produce eggs. Adult S. mansoni pairs residing in the mesenteric vessels may produce up to 300 eggs per day during their reproductive lives. S. japonicum may produce up to 3000 eggs per day. Many of the eggs pass through the walls of the blood vessels, and through the intestinal wall, to be passed out of the body in feces. S. haematobium eggs pass through the ureteral or bladder wall and into the urine. Only mature eggs are capable of crossing into the digestive tract, possibly through the release of proteolytic enzymes, but also as a function of host immune response, which fosters local tissue ulceration. Up to half the eggs released by the worm pairs become trapped in the mesenteric veins, or will be washed back into the liver, where they will become lodged. Worm pairs can live in the body for an average of four and a half years, but may persist up to 20 years.
Trapped eggs mature normally, secreting antigens that elicit a vigorous immune response. The eggs themselves do not damage the body. Rather it is the cellular infiltration resultant from the immune response that causes the pathology classically associated with schistosomiasis.

[edit] Diagnosis

High powered detailed micrograph of Schistosoma parasite eggs in human bladder tissue.
S. japonicum eggs in hepatic portal tract.
Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. The stool exam is the more common of the two. For the measurement of eggs in the feces of presenting patients the scientific unit used is eggs per gram (epg). Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected.
Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Since eggs may be passed intermittently or in small amounts, their detection will be enhanced by repeated examinations and/or concentration procedures (such as the formalin-ethyl acetate technique). In addition, for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique.
Eggs can be found in the urine in infections with S. japonicum and with S. intercalatum (recommended time for collection: between noon and 3 PM). Detection will be enhanced by centrifugation and examination of the sediment. Quantification is possible by using filtration through a nucleopore membrane of a standard volume of urine followed by egg counts on the membrane. Investigation of S. haematobium should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection.
Recently a field evaluation of a novel handheld microscope was undertaken in Uganda for the diagnosis of intestinal schistosomiasis by a team led by Dr. Russell Stothard from the Natural History Museum of London, working with the Schistosomiasis Control Initiative, London.[7]
Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium) may demonstrate eggs when stool or urine examinations are negative.
The eggs of S. haematobium are ellipsoidal with a terminal spine, S. mansoni eggs are also ellipsoidal but with a lateral spine, S. japonicum eggs are spheroidal with a small knob.
Antibody detection can be useful in both clinical management and for epidemiologic surveys.

[edit] Prevention

[edit] Eliminating or avoiding the snails

Prevention is best accomplished by eliminating the water-dwelling snails that are the natural reservoir of the disease. Acrolein, copper sulfate, and niclosamide can be used for this purpose. Recent studies have suggested that snail populations can be controlled by the introduction of, or augmentation of existing, crayfish populations; as with all ecological interventions, however, this technique must be approached with caution.
In 1989, Aklilu Lemma and Legesse Wolde-Yohannes received the Right Livelihood Award for their research on the sarcoca plant, as a preventative measure for the disease by controlling the snail. Concurrently, Dr Chidzere of Zimbabwe researched the similar gopo berry during the 1980s and found that it could be used in the control of infected freshwater snails. In 1989 he drew attention to his concerns that big chemical companies denigrated the gopo berry alternative for snail control.[8] Gopo berries from hotter Ethiopia climates reputedly yield the best results. Later studies were conducted between 1993 and 1995 by the Danish Research Network for international health.[9][10] For many years from the 1950s onwards, civil engineers built vast dam and irrigation schemes, oblivious to the fact that they would cause a massive rise in water-borne infections from schistosomiasis. The detailed specifications laid out in various UN documents since the 1950s could have minimized this problem. Irrigation schemes can be designed to make it hard for the snails to colonize the water, and to reduce the contact with the local population.[11]
This has been cited as a classic case of the relevance paradox because guidelines on how to design these schemes to minimise the spread of the disease had been published years before, but the designers were unaware of them.[12]

[edit] Treatment

Schistosomiasis is readily treated using a single oral dose of the drug praziquantel annually.[13] As with other major parasitic diseases, there is ongoing and extensive research into developing a schistosomiasis vaccine that will prevent the parasite from completing its life cycle in humans. In 2009, Eurogentec Biologics developed a vaccine against bilharziosis in partnership with INSERM and researchers from the Pasteur Institute.[14][15][16]
The World Health Organization has developed guidelines for community treatment of schistosomiasis based on the impact the disease has on children in endemic villages:[13]
  • When a village reports more than 50 percent of children have blood in their urine, everyone in the village receives treatment.[13]
  • When 20 to 50 percent of children have bloody urine, only school-age children are treated.[13]
  • When less than 20 percent of children have symptoms, mass treatment is not implemented.[13]
The Bill & Melinda Gates Foundation has recently funded an operational research program---the Schistosomiasis Consortium for Operational Research and Evaluation (SCORE) to answer strategic questions about how to move forward with schistosomiasis control and elimination. The focus of SCORE is on development of tools and evaluation of strategies for use in mass drug administration campaigns.
Antimony has been used in the past to treat the disease. In low doses, this toxic metalloid bonds to sulfur atoms in enzymes used by the parasite and kills it without harming the host. This treatment is not referred to in present-day peer-review scholarship; praziquantel is universally used. Outside of the U.S., there is a drug available exclusively for treating Schistosoma mansoni (oxamniquine) and one exclusively for treating S.hematobium (metrifonate). While metrifonate has been discontinued for use by the British National Health Service, a Cochrane review found it equally effective in treating urinary schistosomiasis as the leading drug, praziquantel.[17]
Mirazid, an Egyptian drug made from myrrh, was under investigation for oral treatment of the disease up until 2005.[18] The efficacy of praziquantel was proven to be about 8 times than that of Mirazid and therefore Mirazid was not recommended as a suitable agent to control schistosomiasis.[19]

[edit] Epidemiology

Disability-adjusted life year for schistosomiasis per 100,000 inhabitants.
  no data
  less than 50
  more than 500
The disease is found in tropical countries in Africa, the Caribbean, eastern South America, Southeast Asia and in the Middle East. Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the Middle East; S. haematobium in Africa and the Middle East; and S. japonicum in the Far East. S. mekongi and S. intercalatum are found locally in Southeast Asia and central West Africa, respectively.
Among human parasitic diseases, schistosomiasis (sometimes called bilharziasis) ranks second behind malaria in terms of socio-economic and public health importance in tropical and subtropical areas. The disease is endemic in 74-76[verification needed] developing countries, infecting more than 207 million people, 85% of whom live in Africa. They live in rural agricultural and peri-urban areas, and placing more than 700 million people at risk.[20]
Of the infected patients, 20 million suffer severe consequences from the disease.[21] Some estimate that there are approximately 20,000 deaths related to schistosomiasis yearly.[citation needed] In many areas, schistosomiasis infects a large proportion of children under 14 years of age. An estimated 600 million people worldwide are at risk from the disease.
A few countries have eradicated the disease, and many more are working toward it.[citation needed] The World Health Organization is promoting these efforts. In some cases, urbanization, pollution, and/or consequent destruction of snail habitat has reduced exposure, with a subsequent decrease in new infections. The most common way of getting schistosomiasis in developing countries is by wading or swimming in lakes, ponds and other bodies of water that are infested with the snails (usually of the genera Biomphalaria, Bulinus, or Oncomelania) that are the natural reservoirs of the Schistosoma pathogen.

[edit] History

Schistosomiasis is known as bilharzia or bilharziosis in many countries, after Theodor Bilharz, who first described the cause of urinary schistosomiasis in 1851.
The first doctor who described the entire disease cycle was Pirajá da Silva in 1908.
It was a common cause of death for Ancient Egyptians in the Greco-Roman Period.