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__NOTOC__ | __NOTOC__ | ||
{{Schistosomiasis}} | {{Schistosomiasis}} | ||
{{CMG}} | {{CMG}} ; {{AE}} {{ADG}} | ||
==Overview== | ==Overview== | ||
The pathogenesis of acute human schistosomiasis is mainly related to egg deposition and liberation of antigens of adult worms and eggs. A strong inflammatory response characterized by high levels of pro-inflammatory cytokines, such as interleukins 1 | The pathogenesis of acute human schistosomiasis is mainly related to egg deposition and liberation of [[antigens]] of adult worms and eggs. A strong [[inflammatory response]] characterized by high levels of pro-inflammatory [[cytokines]], such as [[IL-1|interleukins 1]], [[Interleukin 6|6]], [[TNF-α|tumor necrosis factor-α]], and circulating [[immune complexes]] participates in the pathogenesis of the acute phase of the [[disease]]. Schistosomes have a typical [[trematode]] vertebrate-invertebrate lifecycle, with humans being the definitive host. The life cycles of all five human schistosomes are broadly similar. Infection can occur by penetration of the human skin by [[cercaria]] or following the handling of contaminated soil. [[Cercaria]] gets transformed into migrating schistosomulum stage in the skin. The incubation period for acute schistosomiasis is usually 14-84 days. Both the early and late manifestations of schistosomiasis are [[Immunological|immunologically]] mediated. The major pathology of infection occurs with chronic schistosomiasis in which retention of eggs in the host tissues is associated with chronic [[granulomatous]] injury. | ||
==Pathophysiology== | ==Pathophysiology== | ||
===Life Cycle=== | ===Life Cycle=== | ||
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive host. The life cycles of all five human schistosomes are broadly similar. | Schistosomes have a typical [[trematode]] [[Vertebrate|vertebrate-invertebrate]] lifecycle, with humans being the [[definitive host]]. The life cycles of all five human schistosomes are broadly similar.<ref name="urlSchistosomes and Other Trematodes - Medical Microbiology - NCBI Bookshelf">{{cite web |url=https://www.ncbi.nlm.nih.gov/books/NBK8037/ |title=Schistosomes and Other Trematodes - Medical Microbiology - NCBI Bookshelf |format= |work= |accessdate=}}</ref><ref name="urlCDC - DPDx - Schistosomiasis Infection">{{cite web |url=https://www.cdc.gov/dpdx/schistosomiasis/index.html |title=CDC - DPDx - Schistosomiasis Infection |format= |work= |accessdate=}}</ref> | ||
===Snail cycle=== | ===Snail cycle=== | ||
* | *Schistosomal eggs are released into the environment from infected individuals. | ||
*The schistosomal eggs hatch on contact with fresh water to release the free-swimming [[miracidium]]. | |||
*Miracidia infect fresh-water snails by penetrating the snail's foot. | *Miracidia infect fresh-water snails by penetrating the snail's foot. | ||
*After infection, the miracidium transforms into a primary | *After infection, the [[miracidium]] transforms into a primary [[sporocyst]]. | ||
*Germ cells within the primary sporocyst will then begin dividing to produce secondary | *[[Germ cells]] within the primary [[sporocyst]] will then begin dividing to produce secondary [[Sporocyst|sporocysts]], which migrate to the snail's hepatopancreas. | ||
*Once at the hepatopancreas, germ cells within the secondary sporocyst begin to divide producing thousands of new parasites, known as cercariae, which are the larvae capable of infecting mammals. | *Once at the hepatopancreas, [[germ cells]] within the secondary [[sporocyst]] begin to divide producing thousands of new parasites, known as [[Cercaria|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. | *[[Cercaria|Cercariae]] emerge daily from the snail host in a [[circadian]] rhythm, dependent on ambient temperature and light. | ||
*Young cercariae are highly motile, alternating between vigorous upward movement and sinking to maintain their position in the water. | *Young [[Cercaria|cercariae]] are highly motile, 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. | *Cercarial activity is particularly stimulated by water turbulence, by shadows and by chemicals found on human skin. | ||
[[Image:Schistosomiasis Life Cycle.jpeg|center|thumb|350px|Schistosomiasis life cycle. Source: CDC]] | [[Image:Schistosomiasis Life Cycle.jpeg|center|thumb|350px|Schistosomiasis life cycle. - [https://www.cdc.gov/parasites/schistosomiasis/biology.html Source: CDC]]] | ||
===Human cycle=== | ===Human cycle=== | ||
*Penetration of the human skin occurs after the cercaria have attached to and explored the skin. | *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. | *The [[Parasites|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. | *As the [[cercaria]] penetrates the skin it transforms into a migrating schistosomulum stage. | ||
*The newly transformed schistosomulum may remain | *The newly transformed schistosomulum may remain inside the skin for 2 days before locating a post-capillary [[venule]]. | ||
*The schistosomulum travels from the skin 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 sinusoid]]s. | *Eight to ten days after penetration of the skin, the parasite migrates to the [[liver sinusoid]]s. | ||
*The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the male. | *The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the male. | ||
* | *''[[Schistosoma haematobium|S. haematobium]]'' schistosomula ultimately migrates 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. | *Parasites reach maturity in six to eight weeks, at which time they begin to produce eggs. | ||
*''[[Schistosoma haematobium|S. haematobium]]'' eggs pass through the [[ureteral]] or [[Bladder|bladder wall]] and into the urine. | |||
*Only mature eggs are capable of crossing into the [[Gastrointestinal tract|digestive tract]], possibly through the release of [[proteolytic]] enzymes, but also as a function of [[Immune response|host immune response]], which fosters local tissue ulceration. | |||
*''S. haematobium'' eggs pass through the ureteral or bladder wall and into the urine. | *Up to half the eggs released by the worm pairs become trapped in the [[Mesenteric|mesenteric veins]], or will be washed back into the [[liver]], where they will become lodged. | ||
*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. | *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. | |||
*Trapped eggs mature normally, secreting [[antigens]] that elicit a vigorous [[immune]] | |||
*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. | |||
===Pathogenesis=== | ===Pathogenesis=== | ||
====Transmission==== | ====Transmission==== | ||
Infection can occur by | Infection can occur by: | ||
* Penetration of the human skin by [[cercaria]] | |||
* Handling of contaminated soil | |||
* Consumption of contaminated water or food sources (e.g, unwashed garden vegetables) | |||
====Dissemination==== | ====Dissemination==== | ||
Cercaria gets transformed into migrating schistosomulum stage in the skin. | * [[Cercaria]] gets transformed into migrating schistosomulum stage in the skin. | ||
* Migrating schistosomulum are transported via the [[blood stream]] to respective organ system. | |||
====Incubation period==== | ====Incubation period==== | ||
The incubation period for acute schistosomiasis is usually 14-84 days. | * The incubation period for acute schistosomiasis is usually 14-84 days. | ||
====Infective stages==== | ====Infective stages==== | ||
*Cercaria are the infective stage of schistosomiasis to humans | * [[Cercaria]] are the infective stage of schistosomiasis to humans. | ||
====Diagnostic stages==== | ====Diagnostic stages==== | ||
*Miracidium | * [[Miracidium]] is diagnostic for schistosomiasis. | ||
====Pathogenesis==== | ====Pathogenesis==== | ||
*The pathogenesis of acute human schistosomiasis is | *The pathogenesis of acute human schistosomiasis is related to egg deposition and liberation of [[antigens]] of adult worms and eggs.<ref name="pmid1580585">{{cite journal |vauthors=Capron A, Dessaint JP |title=Immunologic aspects of schistosomiasis |journal=Annu. Rev. Med. |volume=43 |issue= |pages=209–18 |year=1992 |pmid=1580585 |doi=10.1146/annurev.me.43.020192.001233 |url=}}</ref> | ||
*A strong inflammatory response characterized by high levels of pro-inflammatory cytokines, such as interleukins 1 and 6 and tumor necrosis factor-α, and by circulating immune complexes participates in the pathogenesis of the acute phase of the disease. | *A strong inflammatory response characterized by high levels of pro-inflammatory [[cytokines]], such as [[IL-1|interleukins 1]] and [[Interleukin 6|6]] and [[TNF-α|tumor necrosis factor-α]], and by circulating [[immune complexes]] participates in the pathogenesis of the acute phase of the disease. | ||
====Immune response==== | ====Immune response==== | ||
*Both the early and late manifestations of schistosomiasis are immunologically mediated.<ref name="pmid25142505">{{cite journal |vauthors=Colley DG, Secor WE |title=Immunology of human schistosomiasis |journal=Parasite Immunol. |volume=36 |issue=8 |pages=347–57 |year=2014 |pmid=25142505 |pmc=4278558 |doi=10.1111/pim.12087 |url=}}</ref><ref name="pmid25685450">{{cite journal |vauthors=Barsoum RS, Esmat G, El-Baz T |title=Human schistosomiasis: clinical perspective: review |journal=J Adv Res |volume=4 |issue=5 |pages=433–44 |year=2013 |pmid=25685450 |pmc=4293888 |doi=10.1016/j.jare.2013.01.005 |url=}}</ref> | *Both the early and late manifestations of schistosomiasis are immunologically mediated.<ref name="pmid25142505">{{cite journal |vauthors=Colley DG, Secor WE |title=Immunology of human schistosomiasis |journal=Parasite Immunol. |volume=36 |issue=8 |pages=347–57 |year=2014 |pmid=25142505 |pmc=4278558 |doi=10.1111/pim.12087 |url=}}</ref><ref name="pmid25685450">{{cite journal |vauthors=Barsoum RS, Esmat G, El-Baz T |title=Human schistosomiasis: clinical perspective: review |journal=J Adv Res |volume=4 |issue=5 |pages=433–44 |year=2013 |pmid=25685450 |pmc=4293888 |doi=10.1016/j.jare.2013.01.005 |url=}}</ref> | ||
*The major pathology of infection occurs with chronic schistosomiasis | *The major pathology of infection occurs with chronic schistosomiasis. | ||
*Eggs may be trapped at sites of deposition (urinary | *Eggs may be trapped at sites of deposition ([[Urinary bladder|urinary bladde]]<nowiki/>r, [[ureters]], [[Intestines|intestine]]) or be carried by the [[Bloodstream|bloodstream t]]<nowiki/>o other organs, most commonly the [[liver]] and less often the [[lungs]] and [[central nervous system]]. | ||
*The host response to these eggs involves local as well as systemic manifestations. | *The host response to these eggs involves local as well as systemic manifestations. | ||
*The cell-mediated immune response leads to granulomas composed of lymphocytes, macrophages, and eosinophils that surround the trapped eggs and add significantly to the degree of tissue destruction. | *The [[cell-mediated immune response]] leads to granulomas composed of [[lymphocytes]], [[macrophages]], and [[eosinophils]] that surround the trapped eggs and add significantly to the degree of tissue destruction. | ||
*Granuloma formation in the bladder wall and at the ureterovesical junction results in the major disease manifestations of schistosomiasis haematobia (hematuria, dysuria, and obstructive uropathy). | *Granuloma formation in the bladder wall and at the ureterovesical junction results in the major disease manifestations of schistosomiasis haematobia ([[hematuria]], [[dysuria]], and [[obstructive uropathy]]). | ||
*Intestinal as well as hepatic granulomas underlie the pathologic sequelae of the other schistosome infections( ulcerations and fibrosis of intestinal wall, hepatosplenomegaly, and portal hypertension) due to pre-sinusoidal obstruction of blood flow. | *Intestinal, as well as hepatic granulomas, underlie the pathologic sequelae of the other schistosome infections( [[ulcerations]] and [[fibrosis]] of [[Intestinal wall|intestinal wall,]] [[hepatosplenomegaly]], and [[portal hypertension]]) due to pre-sinusoidal obstruction of blood flow. | ||
* | *Anti-schistosome inflammation increases circulating levels of proinflammatory [[cytokines]]. | ||
*These responses are associated with hepcidin-mediated inhibition of iron uptake and use, leading to anemia of chronic inflammation. | *These responses are associated with [[hepcidin]]-mediated inhibition of iron uptake and use, leading to [[anemia]] of chronic inflammation. | ||
*Schistosomiasis-related undernutrition may be the result of similar pathways of chronic inflammation. | *Schistosomiasis-related undernutrition may be the result of similar pathways of chronic inflammation. | ||
*Acquired partial protective immunity against schistosomiasis has been demonstrated in some animal species and may occur in humans. | *Acquired partial protective immunity against schistosomiasis has been demonstrated in some animal species and may occur in humans. | ||
==Associated conditions== | ==Associated conditions== | ||
*Recurrent Salmonella infections can occur in patients with schistosomiasis. Salmonella bacteria live in symbiosis within the parasite's integument, allowing them to evade eradication by many antibiotics.<ref name="pmid21711539">{{cite journal |vauthors=Barnhill AE, Novozhilova E, Day TA, Carlson SA |title=Schistosoma-associated Salmonella resist antibiotics via specific fimbrial attachments to the flatworm |journal=Parasit Vectors |volume=4 |issue= |pages=123 |year=2011 |pmid=21711539 |pmc=3143092 |doi=10.1186/1756-3305-4-123 |url=}}</ref> | *Recurrent [[Salmonella infections]] can occur in patients with schistosomiasis. Salmonella bacteria live in symbiosis within the parasite's integument, allowing them to evade eradication by many antibiotics.<ref name="pmid21711539">{{cite journal |vauthors=Barnhill AE, Novozhilova E, Day TA, Carlson SA |title=Schistosoma-associated Salmonella resist antibiotics via specific fimbrial attachments to the flatworm |journal=Parasit Vectors |volume=4 |issue= |pages=123 |year=2011 |pmid=21711539 |pmc=3143092 |doi=10.1186/1756-3305-4-123 |url=}}</ref> | ||
*Chloramphenicol-sensitive Salmonella | *[[Chloramphenicol]]-sensitive [[Salmonella enterica Serovar Typhi|Salmonella entericaserovar Typhi]] has been shown to be refractory to [[chloramphenicol]] therapy in patients coinfected with Schistosoma. | ||
*Patients coinfected with hepatitis C virus and Schistosoma have increased progression of liver fibrosis compared to patients with hepatitis C alone.<ref name="pmid15724383">{{cite journal |vauthors=el-Kady IM, el-Masry SA, Badra G, Halafawy KA |title=Different cytokine patterns in patients coinfected with hepatitis C virus and Schistosoma mansoni |journal=Egypt J Immunol |volume=11 |issue=1 |pages=23–9 |year=2004 |pmid=15724383 |doi= |url=}}</ref> | *Patients coinfected with [[hepatitis C virus]] and Schistosoma have increased progression of [[Liver Failure|liver fibrosis]] compared to patients with [[hepatitis C]] alone.<ref name="pmid15724383">{{cite journal |vauthors=el-Kady IM, el-Masry SA, Badra G, Halafawy KA |title=Different cytokine patterns in patients coinfected with hepatitis C virus and Schistosoma mansoni |journal=Egypt J Immunol |volume=11 |issue=1 |pages=23–9 |year=2004 |pmid=15724383 |doi= |url=}}</ref> | ||
*Urogenital schistosomiasis is a co-factor in the spread and progression of human immunodeficiency virus (HIV) infection and other sexually transmitted infections, especially in women, and also is associated with female infertility.<ref name="urlwww.who.int">{{cite web |url=http://www.who.int/schistosomiasis/Urogenital_Schistosomiasis_HIV_Nov2011.pdf |title=www.who.int |format= |work= |accessdate=}}</ref> | *Urogenital schistosomiasis is a co-factor in the spread and progression of [[Human Immunodeficiency Virus|human immunodeficiency virus]] ([[HIV]]) infection and other [[Sexually transmitted disease|sexually transmitted infections]], especially in women, and also is associated with female [[infertility]].<ref name="urlwww.who.int">{{cite web |url=http://www.who.int/schistosomiasis/Urogenital_Schistosomiasis_HIV_Nov2011.pdf |title=www.who.int |format= |work= |accessdate=}}</ref> | ||
===Microscopic Findings=== | ===Microscopic Findings=== | ||
*Adult worms are about 10 mm long | *Adult worms are about 10 mm long | ||
{{#ev:youtube|X0eQxiwecIA}} | {{#ev:youtube|X0eQxiwecIA}} | ||
{{#ev:youtube|9VpqxnPRvL8}} | {{#ev:youtube|9VpqxnPRvL8}} | ||
==References== | ==References== | ||
| Line 93: | Line 95: | ||
[[Category:Hepatology]] | [[Category:Hepatology]] | ||
[[Category:Neglected diseases]] | [[Category:Neglected diseases]] | ||
Latest revision as of 18:44, 18 September 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
The pathogenesis of acute human schistosomiasis is mainly related to egg deposition and liberation of antigens of adult worms and eggs. A strong inflammatory response characterized by high levels of pro-inflammatory cytokines, such as interleukins 1, 6, tumor necrosis factor-α, and circulating immune complexes participates in the pathogenesis of the acute phase of the disease. Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive host. The life cycles of all five human schistosomes are broadly similar. Infection can occur by penetration of the human skin by cercaria or following the handling of contaminated soil. Cercaria gets transformed into migrating schistosomulum stage in the skin. The incubation period for acute schistosomiasis is usually 14-84 days. Both the early and late manifestations of schistosomiasis are immunologically mediated. The major pathology of infection occurs with chronic schistosomiasis in which retention of eggs in the host tissues is associated with chronic granulomatous injury.
Pathophysiology
Life Cycle
Schistosomes have a typical trematode vertebrate-invertebrate lifecycle, with humans being the definitive host. The life cycles of all five human schistosomes are broadly similar.[1][2]
Snail cycle
- Schistosomal eggs are released into the environment from infected individuals.
- The schistosomal eggs hatch on contact with fresh water to release the free-swimming miracidium.
- Miracidia infect fresh-water snails by penetrating the snail's foot.
- After infection, the miracidium transforms into a primary sporocyst.
- Germ cells within the primary sporocyst will then begin dividing to produce secondary sporocysts, which migrate to the snail's hepatopancreas.
- Once at the hepatopancreas, germ cells within the secondary sporocyst begin to divide 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 motile, 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.
Human cycle
- 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.
- The newly transformed schistosomulum may remain inside the skin for 2 days before locating a post-capillary venule.
- The schistosomulum travels from the skin 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.
- The nearly-mature worms pair, with the longer female worm residing in the gynaecophoric channel of the male.
- S. haematobium schistosomula ultimately migrates 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.
- 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.
- 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.
Pathogenesis
Transmission
Infection can occur by:
- Penetration of the human skin by cercaria
- Handling of contaminated soil
- Consumption of contaminated water or food sources (e.g, unwashed garden vegetables)
Dissemination
- Cercaria gets transformed into migrating schistosomulum stage in the skin.
- Migrating schistosomulum are transported via the blood stream to respective organ system.
Incubation period
- The incubation period for acute schistosomiasis is usually 14-84 days.
Infective stages
- Cercaria are the infective stage of schistosomiasis to humans.
Diagnostic stages
- Miracidium is diagnostic for schistosomiasis.
Pathogenesis
- The pathogenesis of acute human schistosomiasis is related to egg deposition and liberation of antigens of adult worms and eggs.[3]
- A strong inflammatory response characterized by high levels of pro-inflammatory cytokines, such as interleukins 1 and 6 and tumor necrosis factor-α, and by circulating immune complexes participates in the pathogenesis of the acute phase of the disease.
Immune response
- Both the early and late manifestations of schistosomiasis are immunologically mediated.[4][5]
- The major pathology of infection occurs with chronic schistosomiasis.
- Eggs may be trapped at sites of deposition (urinary bladder, ureters, intestine) or be carried by the bloodstream to other organs, most commonly the liver and less often the lungs and central nervous system.
- The host response to these eggs involves local as well as systemic manifestations.
- The cell-mediated immune response leads to granulomas composed of lymphocytes, macrophages, and eosinophils that surround the trapped eggs and add significantly to the degree of tissue destruction.
- Granuloma formation in the bladder wall and at the ureterovesical junction results in the major disease manifestations of schistosomiasis haematobia (hematuria, dysuria, and obstructive uropathy).
- Intestinal, as well as hepatic granulomas, underlie the pathologic sequelae of the other schistosome infections( ulcerations and fibrosis of intestinal wall, hepatosplenomegaly, and portal hypertension) due to pre-sinusoidal obstruction of blood flow.
- Anti-schistosome inflammation increases circulating levels of proinflammatory cytokines.
- These responses are associated with hepcidin-mediated inhibition of iron uptake and use, leading to anemia of chronic inflammation.
- Schistosomiasis-related undernutrition may be the result of similar pathways of chronic inflammation.
- Acquired partial protective immunity against schistosomiasis has been demonstrated in some animal species and may occur in humans.
Associated conditions
- Recurrent Salmonella infections can occur in patients with schistosomiasis. Salmonella bacteria live in symbiosis within the parasite's integument, allowing them to evade eradication by many antibiotics.[6]
- Chloramphenicol-sensitive Salmonella entericaserovar Typhi has been shown to be refractory to chloramphenicol therapy in patients coinfected with Schistosoma.
- Patients coinfected with hepatitis C virus and Schistosoma have increased progression of liver fibrosis compared to patients with hepatitis C alone.[7]
- Urogenital schistosomiasis is a co-factor in the spread and progression of human immunodeficiency virus (HIV) infection and other sexually transmitted infections, especially in women, and also is associated with female infertility.[8]
Microscopic Findings
- Adult worms are about 10 mm long
{{#ev:youtube|X0eQxiwecIA}} {{#ev:youtube|9VpqxnPRvL8}}
References
- ↑ "Schistosomes and Other Trematodes - Medical Microbiology - NCBI Bookshelf".
- ↑ "CDC - DPDx - Schistosomiasis Infection".
- ↑ Capron A, Dessaint JP (1992). "Immunologic aspects of schistosomiasis". Annu. Rev. Med. 43: 209–18. doi:10.1146/annurev.me.43.020192.001233. PMID 1580585.
- ↑ Colley DG, Secor WE (2014). "Immunology of human schistosomiasis". Parasite Immunol. 36 (8): 347–57. doi:10.1111/pim.12087. PMC 4278558. PMID 25142505.
- ↑ Barsoum RS, Esmat G, El-Baz T (2013). "Human schistosomiasis: clinical perspective: review". J Adv Res. 4 (5): 433–44. doi:10.1016/j.jare.2013.01.005. PMC 4293888. PMID 25685450.
- ↑ Barnhill AE, Novozhilova E, Day TA, Carlson SA (2011). "Schistosoma-associated Salmonella resist antibiotics via specific fimbrial attachments to the flatworm". Parasit Vectors. 4: 123. doi:10.1186/1756-3305-4-123. PMC 3143092. PMID 21711539.
- ↑ el-Kady IM, el-Masry SA, Badra G, Halafawy KA (2004). "Different cytokine patterns in patients coinfected with hepatitis C virus and Schistosoma mansoni". Egypt J Immunol. 11 (1): 23–9. PMID 15724383.
- ↑ "www.who.int" (PDF).