Filariasis pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
m (Bot: Removing from Primary care)
 
(18 intermediate revisions by 6 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Filariasis}}
{{Filariasis}}
{{CMG}} {{AE}} {{KD}} {{AEL}}  
{{CMG}}; {{AE}} {{KD}}, {{AEL}}  


==Overview==
==Overview==
Filariasis [[infection]] occurs when a larva carrying [[mosquito]] bites individual [[skin]] introducing these larvae into the skin. The larvae then enter the patient [[blood]] through the skin [[wound]] and spread to the different sites such as [[lymphatic vessels]], [[Subcutaneous tissue|subcutaneous tissues]] or the [[Serous cavity|serous cavities]]. At these sites, the larvae tend to mature in a six to twelve months process to be adult [[Filaria|filariae]] which can live up to fifteen years. Reproduction takes place between the male and female adult worms producing microfilariae which are premature organisms with sheath that circulate the blood in case they are settled in the [[lymphatic vessels]]. During another [[blood]] meal, the mosquito takes up the microfilariae, then these microfilariae lose their sheath within two weeks to be larvae that enter the human body. When a human being is bitten by a mosquito, the cycle restarts again. Pathogenesis of the [[disease]] depends on number of factors including [[immune response]] of the patient, the number of secondary [[bacterial infections]], the accumulation of the [[Antigen|worm antigens]], release of [[Wolbachia]] [[bacteria]] from the worm and the [[genetic predisposition]].<ref name="pmid21803313">{{cite journal| author=Chandy A, Thakur AS, Singh MP, Manigauha A| title=A review of neglected tropical diseases: filariasis. | journal=Asian Pac J Trop Med | year= 2011 | volume= 4 | issue= 7 | pages= 581-6 | pmid=21803313 | doi=10.1016/S1995-7645(11)60150-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21803313  }} </ref>
Filariasis [[infection]] occurs when a larva carrying [[mosquito]] bites an individual, introducing these larvae into the skin. The larvae then enters the patient's [[blood]] through the [[Wound|skin wound]] and spread to the different sites such as [[lymphatic vessels]], [[Subcutaneous tissue|subcutaneous tissues]] or the [[Serous cavity|serous cavities]]. At these sites, the larvae matures in a six to twelve months period into the adult [[Filaria|filariae]] which can live up to fifteen years. [[Reproduction]] takes place between the [[male]] and [[female]] adult [[Worm|worms]] producing microfilariae which are premature [[organisms]] with sheath that circulate the [[blood]] in case they are settled in the [[lymphatic vessels]]. During another [[blood]] meal, the [[mosquito]] takes up the microfilariae, then these microfilariae lose their sheath within two weeks to be larvae that enter the [[human body]]. When a [[human]] is bitten by a [[Mosquitoes|mosquito]], the cycle restarts again. Pathogenesis of the [[disease]] depends on number of factors including [[immune response]] of the [[patient]], the number of [[secondary]] [[bacterial infections]], the accumulation of the [[Antigen|worm antigens]], release of [[Wolbachia]] [[bacteria]] from the [[worm]] and the [[genetic predisposition]].


==Pathophysiology==
==Pathophysiology==
===Pathogenesis===
===Pathogenesis===
*Pathogenesis of developing [[lymphedema]] and its progression to [[elephantiasis]] has been controversial to understand as host related or worm related. A study conducted to completely understand the pathogenesis of the disease showed that some factors have an obvious impact in development of the filariasis clinical manifestations. These factors include the following:<ref name="pmid12041732">{{cite journal| author=Taylor MJ| title=A new insight into the pathogenesis of filarial disease. | journal=Curr Mol Med | year= 2002 | volume= 2 | issue= 3 | pages= 299-302 | pmid=12041732 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12041732  }} </ref><ref name="pmid12543723">{{cite journal| author=Lammie PJ, Cuenco KT, Punkosdy GA| title=The pathogenesis of filarial lymphedema: is it the worm or is it the host? | journal=Ann N Y Acad Sci | year= 2002 | volume= 979 | issue=  | pages= 131-42; discussion 188-96 | pmid=12543723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12543723  }} </ref><ref name="pmid23053393">{{cite journal| author=Babu S, Nutman TB| title=Immunopathogenesis of lymphatic filarial disease. | journal=Semin Immunopathol | year= 2012 | volume= 34 | issue= 6 | pages= 847-61 | pmid=23053393 | doi=10.1007/s00281-012-0346-4 | pmc=3498535 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23053393  }} </ref><ref name="pmid11741630">{{cite journal| author=Cross HF, Haarbrink M, Egerton G, Yazdanbakhsh M, Taylor MJ| title=Severe reactions to filarial chemotherapy and release of Wolbachia endosymbionts into blood. | journal=Lancet | year= 2001 | volume= 358 | issue= 9296 | pages= 1873-5 | pmid=11741630 | doi=10.1016/S0140-6736(01)06899-4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11741630  }} </ref>  
The pathogenesis of [[lymphedema]] and its progression to [[elephantiasis]] is controversial. Factors involved in the clinical manifestations of filariasis include:<ref name="pmid21803313">{{cite journal| author=Chandy A, Thakur AS, Singh MP, Manigauha A| title=A review of neglected tropical diseases: filariasis. | journal=Asian Pac J Trop Med | year= 2011 | volume= 4 | issue= 7 | pages= 581-6 | pmid=21803313 | doi=10.1016/S1995-7645(11)60150-8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21803313  }} </ref><ref name="pmid12041732">{{cite journal| author=Taylor MJ| title=A new insight into the pathogenesis of filarial disease. | journal=Curr Mol Med | year= 2002 | volume= 2 | issue= 3 | pages= 299-302 | pmid=12041732 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12041732  }} </ref><ref name="pmid12543723">{{cite journal| author=Lammie PJ, Cuenco KT, Punkosdy GA| title=The pathogenesis of filarial lymphedema: is it the worm or is it the host? | journal=Ann N Y Acad Sci | year= 2002 | volume= 979 | issue=  | pages= 131-42; discussion 188-96 | pmid=12543723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12543723  }} </ref><ref name="pmid23053393">{{cite journal| author=Babu S, Nutman TB| title=Immunopathogenesis of lymphatic filarial disease. | journal=Semin Immunopathol | year= 2012 | volume= 34 | issue= 6 | pages= 847-61 | pmid=23053393 | doi=10.1007/s00281-012-0346-4 | pmc=3498535 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23053393  }} </ref><ref name="pmid11741630">{{cite journal| author=Cross HF, Haarbrink M, Egerton G, Yazdanbakhsh M, Taylor MJ| title=Severe reactions to filarial chemotherapy and release of Wolbachia endosymbionts into blood. | journal=Lancet | year= 2001 | volume= 358 | issue= 9296 | pages= 1873-5 | pmid=11741630 | doi=10.1016/S0140-6736(01)06899-4 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11741630 }} </ref><ref name="pmid8337737">{{cite journal| author=Kar SK, Mania J, Kar PK| title=Humoral immune response during filarial fever in Bancroftian filariasis. | journal=Trans R Soc Trop Med Hyg | year= 1993 | volume= 87 | issue= 2 | pages= 230-3 | pmid=8337737 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8337737 }}</ref>  
**[[Immune response]] of the patient
*[[Immune response]] of the [[patient]]
**The number of filarial and [[bacterial infection]]  
*The number of [[filarial]] and [[bacterial infection]]  
**The accumulation of the [[Antigen|worm antigen]] in the [[lymphatic vessels]]
*The accumulation of the [[Antigen|worm antigen]] in the [[lymphatic vessels]]
**The release of [[Wolbachia]] bacteria following death of the worm
*The release of [[Wolbachia]] [[bacteria]] following death of the [[worm]]


{| class="wikitable"
{| class="wikitable"
Line 20: Line 20:
|[[Immune response]] of the host
|[[Immune response]] of the host
|
|
* In several studies, it has been noticed that there is a strong correlation between the host [[immune response]] and [[lymphoedema]] development. The [[immune response]] is higher in the lymphedema patients more than the patients with microfilariae just circulating in the blood.  
* There is a strong correlation between the host [[immune response]] and [[lymphoedema|lymphedema]] development.
* Hence, it is believed the role of the immune response in the development of the lymphedema as it leads to [[inflammation]] and obstruction of the [[lymphatic vessels]].  
* Patients with [[lymphedema]] mount a higher immune response when compared to those with [[Microfilaria diurnal|microfilariae]] just circulating in the [[blood]].  
* [[Infection]] by filariasis induces [[cell mediated immunity]] in response to the filarial [[antigens]]. This will lead to the production of [[cytokines]] and [[interleukins]].   
* It is believed that the role of the [[Immune system|immune response]] in the development of the lymphedema leads to [[inflammation]] and [[obstruction]] of the [[lymphatic vessels]].  
* High levels of [[immunoglobulins]] ([[Immunoglobulin G|IgG]]1,2,3) has been detected in patients with [[lymphedema]] which increases the evidence of the role of the immune response in pathogenesis of the disease.  
* [[Infection]] by filariasis induces [[cell mediated immunity]] in response to the filarial [[antigens]].  
* This leads to the production of [[cytokines]] and [[interleukins]].   
* High levels of [[immunoglobulins]] ([[Immunoglobulin G|IgG]]1,2,3) have been detected in [[patients]] with [[lymphedema]] which increases the evidence of the role of the immune response in pathogenesis of the disease.  
|-
|-
|Secondary bacterial infections  
|[[Bacterial infections|Secondary bacterial infections]]
|
|
* Adenolymphangitis is a result of the inflammation induced by the filarial infection and the immune response. It is believed that it worsens the disease and leads to morbidity.  
* Adenolymphangitis is a result of the [[inflammation]] induced by the [[filarial infection]] and the [[immune response]].  
* It affects the [[lower limbs]] resulting in cord like lesion of the lymphatic vessels and worsening of the filariasis.  
* It is believed that it worsens the disease and leads to [[morbidity]].  
* It affects the [[lower limbs]] resulting in [[cord]] like lesion of the [[lymphatic vessels]] and worsening of the filariasis.  
|-
|-
|Wolbachia bacteria
|Wolbachia [[bacteria]]
|
|
* [[Nematodes|The round worms]] causing filariasis are carriers of a kind of bacteria called [[Wolbachia]] that is released after the death of the worms.  
* [[Nematodes|The round worms]] causing filariasis are carriers of a kind of [[bacteria]] called [[Wolbachia]] that is released after the death of the [[Worm|worms]].  
* It has been found that there is a correlation between Wolbachia [[bacteria]] and the inflammatory reactions in cases of filariasis especially in the phase of treatment by [[chemotherapy]] that ends with [[lymphedema]].  
* There is a correlation between [[Wolbachia]] [[bacteria]] and the [[inflammatory]] reactions in cases of filariasis especially in the phase of treatment by [[chemotherapy]] that ends with [[lymphedema]].  
* Immunologically, serum [[antibodies]] may be released against Wolbachia surface protein may also play role in the development of the lymphedema.  
* Immunologically, [[serum]] [[antibodies]] released against Wolbachia [[Protein|surface protein]] may also play a role in the development of the [[lymphedema]].  
|}
|}


===Genetics===
===Genetics===
*Studies have been held to detect the genetic predisposition probability in patients developing [[lymphedema]].<ref name="pmid12543723">{{cite journal| author=Lammie PJ, Cuenco KT, Punkosdy GA| title=The pathogenesis of filarial lymphedema: is it the worm or is it the host? | journal=Ann N Y Acad Sci | year= 2002 | volume= 979 | issue=  | pages= 131-42; discussion 188-96 | pmid=12543723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12543723  }} </ref>  
*A mutation in the [[Vascular endothelial growth factor|vascular endothelial growth factor receptor 3 (VEGFR-3)]] is associated with development of [[primary lymphedema]] secondary to [[dysfunction]] of the [[endothelial cells]] and [[impairment|impaired]] [[lymphangiogenesis]].<ref name="pmid12543723">{{cite journal| author=Lammie PJ, Cuenco KT, Punkosdy GA| title=The pathogenesis of filarial lymphedema: is it the worm or is it the host? | journal=Ann N Y Acad Sci | year= 2002 | volume= 979 | issue=  | pages= 131-42; discussion 188-96 | pmid=12543723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12543723  }} </ref><ref name="pmid10835628">{{cite journal| author=Karkkainen MJ, Ferrell RE, Lawrence EC, Kimak MA, Levinson KL, McTigue MA et al.| title=Missense mutations interfere with VEGFR-3 signalling in primary lymphoedema. | journal=Nat Genet | year= 2000 | volume= 25 | issue= 2 | pages= 153-9 | pmid=10835628 | doi=10.1038/75997 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10835628  }} </ref>
*It is found that patients who develop [[primary lymphedema]] has a mutation in gene of the [[Vascular endothelial growth factor|vascular endothelial growth factor receptor 3 (VEGFR-3)]]. This will lead to dysfunction of the [[endothelial cells]] and impairment [[lymphangiogenesis]].<ref name="pmid10835628">{{cite journal| author=Karkkainen MJ, Ferrell RE, Lawrence EC, Kimak MA, Levinson KL, McTigue MA et al.| title=Missense mutations interfere with VEGFR-3 signalling in primary lymphoedema. | journal=Nat Genet | year= 2000 | volume= 25 | issue= 2 | pages= 153-9 | pmid=10835628 | doi=10.1038/75997 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10835628  }} </ref>
*Mutation in the [[FOXC2|forkhead transcription factor (FOXC2)]] also leads to [[hereditary lymphedema]].  
*Mutation in the [[FOXC2|forkhead transcription factor (FOXC2)]] also leads to [[hereditary lymphedema]] and forms impaired protein.
*The last two [[genetic mutations]] increase the possibility of filarial lymphedema to be genetically related and increase the risk of disease occurrence among the same family members.  


====Life cycle of filariasis nematodes====  
====Life cycle of filariasis nematodes====  
In order to understand how filariasis could occur, it is important to know the life cycles of different [[nematodes]] causing the disease. Through this table the important steps in the worms life cycle is discussed as well as the vectors responsible for disease transmission.<ref name="Mansonellosis">CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017 </ref><ref name="Lymphatic filariasis">CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017 </ref><ref name="Lymphatic filariasis">CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_b_malayi.html Accessed on June 27, 2017 </ref><ref name="Loiasis">CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017 </ref><ref name="Onchocerciasis">CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017 </ref>
In order to understand how filariasis could occur, it is important to know the [[Life cycle|life cycles]] of different [[nematodes]] causing filariasis. Through this table the important steps in the worms life cycle is discussed as well as the vectors responsible for disease transmission.<ref name="Mansonellosis">CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017 </ref><ref name="Lymphatic filariasis">CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017 </ref><ref name="Loiasis">CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017 </ref><ref name="Onchocerciasis">CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017 </ref>


{| class="wikitable"
{| class="wikitable"
Line 50: Line 51:
!Causative nematode
!Causative nematode
!Vectors
!Vectors
!Life cycle
!Life Cycle
!Illustrative image
!Distinctive features
|-
|-
| rowspan="2" |Lymphatic filariasis
| rowspan="2" |Lymphatic filariasis
|[[Wuchereria bancrofti]] 
|[[Wuchereria bancrofti]] 
|
|
* Culex as C. pipiens
* Culex as ''C. pipiens''
* [[Aedes]] as A. aegypti
* [[Aedes]] as ''A. aegypti''
*  [[Anopheles]] as A. arabinensis
*  [[Anopheles]] as ''A. arabinensis''
* Coquillettidia.as C. juxtamansonia
* Coquillettidia.as ''C. juxtamansonia''
| rowspan="2" |
| rowspan="2" |[[Image:W bancrofti LifeCycle.gif|500px|thumb|center|Source: https://www.cdc.gov/]]
* Infected [[mosquito]] bite introduces the third stage larva onto the [[skin]] and then enters to the [[blood]] through the wound.
* The larvae develop to adult which reside in the '''[[lymphatic vessels]]'''.
* Adult worm produce sheathed microfiliae that migrate to [[lymph]] and [[blood]]. They have '''nocturnal periodicity'''.
* Another [[mosquito]] ingests the microfiliae.
* The microfilariae lose their sheaths and work their way through the wall of the proventriculus and [[cardiac]] portion of the [[midgut]] to reach the thoracic [[muscles]].
* Microfiliae mature inside the mosquito till third stage larvae.
* In another bite to a host [[skin]] the mosquito introduces the larvae onto the skin.
| rowspan="2" |[[Image:W bancrofti LifeCycle.gif|350 px|center]]
| rowspan="2" |
* The difference between the nematodes causing lymphatic filariasis is in the shape and size of the worm.
* The Brugia worms are similar to the W. bancrofti but smaller.  
|-  
|-  
|[[Brugia timori]] and [[Brugia malayi]]
|[[Brugia timori]] and [[Brugia malayi]]
Line 83: Line 71:
|
|
* Chrysops  
* Chrysops  
* C. silacea
* ''C. silacea''
* C. dimidiata
* ''C. dimidiata''
| rowspan="4" |
| rowspan="4" |[[Image:L loa LifeCycle.gif|500px|center|thumb|Source: https://www.cdc.gov/]]
* Infected fly bite introduces the third stage larva onto the [[skin]] and then enters to the [[blood]] through the [[wound]].
* The larvae develop to adult which reside in the '''[[subcutaneous tissue]]'''.
* Loa Loa adult worm produce sheathed microfilariae that are found in the blood during day and in the [[lungs]] during the non circulating phase. They have '''diurnal periodicity'''.
* Another fly ingests the microfiliae.
* After ingestion, the microfilariae lose their sheaths and migrate from the fly's [[midgut]] through the [[hemocoel]] to the thoracic muscles of the [[arthropod]].
* Microfilariae mature inside the fly till third stage larvae.
* The third-stage infective larvae migrate to the fly's proboscis and in another bite the cycle restarts.
| rowspan="4" |[[Image:L loa LifeCycle.gif|350 px|center]]
| rowspan="4" |
* Unlike Loa Loa filaria, Mansonella streptocerca , Mansonella ozzardi and Onchocerca volvolus produce '''unsheathed non-periodic microfilariae'''.
* Mansonela streptocerca adults residue in the dermis.  
* Onchocerca volvulus adults residue mainly in the subcutaneous nodules. Their microfilariae can be found in the peripheral [[blood]], [[urine]], and [[sputum]] but are typically found in the [[skin]] and in the [[Lymphatic|lymphatics]] of connective tissue.
|-
|-
|[[Mansonella streptocerca]]
|[[Mansonella streptocerca|''Mansonella streptocerca'']]
|
|
* Midge (genus Culicoides)
* Midge (genus Culicoides)
|-
|-
|[[Mansonella ozzardi]]
|[[Mansonella ozzardi|''Mansonella ozzardi'']]
|
|
* Midge (genus Culicoides)
* Midge (genus Culicoides)
Line 111: Line 87:
* Blackfly (genus Simulium)
* Blackfly (genus Simulium)
|-
|-
|Serous cavity filariasis
|[[Serous cavity|Serous cavity filariasis]]
|[[Mansonella perstans]]
|[[Mansonella perstans]]
|
|
* Midge (genus Culicoides)
* Midge (genus Culicoides)
* Blackfly (genus Simulium)  
* Blackfly (genus Simulium)  
|
|[[Image:M perstans LifeCycle.gif|500px|center|thumb|Source: https://www.cdc.gov/]]
* Infected midge bite introduces the third stage larva onto the skin and then enters to the blood through the wound.
* The larvae develop to adult which reside in the different body cavities like [[peritoneal cavity]], [[pleural cavity]], and less frequently in the [[pericardium]].
* Adult worm produce unsheathed subperiodic microfilariae that reaches the [[blood stream]].
* Another midge ingests microfilariae during a [[blood]] meal.
* After [[ingestion]], the microfilariae migrate from the midge's [[midgut]] through the [[hemocoel]] to the thoracic muscles of the [[arthropod]].
* Microfiliae mature inside the midge till third stage larvae.
* The third-stage infective larvae migrate to the midge's proboscis and in another bite the cycle restarts.
|[[Image:M perstans LifeCycle.gif|350 px|center]]
|
|}
|}


Line 134: Line 101:
==References==
==References==
{{reflist|2}}
{{reflist|2}}
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}
[[Category:Parasitic diseases]]
[[Category:Parasitic diseases]]
[[Category:Neglected diseases]]
[[Category:Neglected diseases]]
[[Category:Infectious disease]]
[[Category:Disease]]
[[Category:Disease]]
[[Category:Needs overview]]
[[Category:Needs overview]]
 
[[Category:Emergency mdicine]]
{{WikiDoc Help Menu}}
[[Category:Up-To-Date]]
{{WikiDoc Sources}}
[[Category:Infectious disease]]
[[Category:Vascular medicine]]
[[Category:Urology]]
[[Category:Gastroenterology]]

Latest revision as of 21:46, 29 July 2020

Filariasis Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Filariasis from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

X Ray

CT Scan

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Filariasis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

slides

Images

American Roentgen Ray Society Images of Filariasis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Filariasis pathophysiology

on Filariasis pathophysiology

Filariasis pathophysiology in the news

Blogs on Filariasis pathophysiology

Directions to Hospitals Treating Filariasis

Risk calculators and risk factors for Filariasis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2], Ahmed Elsaiey, MBBCH [3]

Overview

Filariasis infection occurs when a larva carrying mosquito bites an individual, introducing these larvae into the skin. The larvae then enters the patient's blood through the skin wound and spread to the different sites such as lymphatic vessels, subcutaneous tissues or the serous cavities. At these sites, the larvae matures in a six to twelve months period into the adult filariae which can live up to fifteen years. Reproduction takes place between the male and female adult worms producing microfilariae which are premature organisms with sheath that circulate the blood in case they are settled in the lymphatic vessels. During another blood meal, the mosquito takes up the microfilariae, then these microfilariae lose their sheath within two weeks to be larvae that enter the human body. When a human is bitten by a mosquito, the cycle restarts again. Pathogenesis of the disease depends on number of factors including immune response of the patient, the number of secondary bacterial infections, the accumulation of the worm antigens, release of Wolbachia bacteria from the worm and the genetic predisposition.

Pathophysiology

Pathogenesis

The pathogenesis of lymphedema and its progression to elephantiasis is controversial. Factors involved in the clinical manifestations of filariasis include:[1][2][3][4][5][6]

Factor Role in pathogenesis
Immune response of the host
Secondary bacterial infections
Wolbachia bacteria

Genetics

Life cycle of filariasis nematodes

In order to understand how filariasis could occur, it is important to know the life cycles of different nematodes causing filariasis. Through this table the important steps in the worms life cycle is discussed as well as the vectors responsible for disease transmission.[8][9][10][11]

Type of filariasis Causative nematode Vectors Life Cycle
Lymphatic filariasis Wuchereria bancrofti 
  • Culex as C. pipiens
  • Aedes as A. aegypti
  • Anopheles as A. arabinensis
  • Coquillettidia.as C. juxtamansonia
Source: https://www.cdc.gov/
Brugia timori and Brugia malayi
  • Mansonia
  • Aedes
Subcutaneous filariasis Loa loa filaria
  • Chrysops
  • C. silacea
  • C. dimidiata
Source: https://www.cdc.gov/
Mansonella streptocerca
  • Midge (genus Culicoides)
Mansonella ozzardi
  • Midge (genus Culicoides)
Onchocerca volvulus
  • Blackfly (genus Simulium)
Serous cavity filariasis Mansonella perstans
  • Midge (genus Culicoides)
  • Blackfly (genus Simulium)
Source: https://www.cdc.gov/

Microscopic pathology

This video gives a brief explanation on the possible histopathological findings of soft tissue sample of case of filariasis: {{#ev:youtube|67zC7mXigpY}}

References

  1. ↑ Chandy A, Thakur AS, Singh MP, Manigauha A (2011). "A review of neglected tropical diseases: filariasis". Asian Pac J Trop Med. 4 (7): 581–6. doi:10.1016/S1995-7645(11)60150-8. PMID 21803313.
  2. ↑ Taylor MJ (2002). "A new insight into the pathogenesis of filarial disease". Curr Mol Med. 2 (3): 299–302. PMID 12041732.
  3. ↑ 3.0 3.1 Lammie PJ, Cuenco KT, Punkosdy GA (2002). "The pathogenesis of filarial lymphedema: is it the worm or is it the host?". Ann N Y Acad Sci. 979: 131–42, discussion 188-96. PMID 12543723.
  4. ↑ Babu S, Nutman TB (2012). "Immunopathogenesis of lymphatic filarial disease". Semin Immunopathol. 34 (6): 847–61. doi:10.1007/s00281-012-0346-4. PMC 3498535. PMID 23053393.
  5. ↑ Cross HF, Haarbrink M, Egerton G, Yazdanbakhsh M, Taylor MJ (2001). "Severe reactions to filarial chemotherapy and release of Wolbachia endosymbionts into blood". Lancet. 358 (9296): 1873–5. doi:10.1016/S0140-6736(01)06899-4. PMID 11741630.
  6. ↑ Kar SK, Mania J, Kar PK (1993). "Humoral immune response during filarial fever in Bancroftian filariasis". Trans R Soc Trop Med Hyg. 87 (2): 230–3. PMID 8337737.
  7. ↑ Karkkainen MJ, Ferrell RE, Lawrence EC, Kimak MA, Levinson KL, McTigue MA; et al. (2000). "Missense mutations interfere with VEGFR-3 signalling in primary lymphoedema". Nat Genet. 25 (2): 153–9. doi:10.1038/75997. PMID 10835628.
  8. ↑ CDC https://www.cdc.gov/dpdx/mansonellosis/index.html Accessed on June 27, 2017
  9. ↑ CDC https://www.cdc.gov/parasites/lymphaticfilariasis/biology_w_bancrofti.html Accessed on June 27, 2017
  10. ↑ CDC https://www.cdc.gov/parasites/loiasis/biology.html Accessed on June 27, 2017
  11. ↑ CDC https://www.cdc.gov/parasites/loiasis/biology.htmlhttps://www.cdc.gov/parasites/onchocerciasis/biology.html Accessed on June 27, 2017

Template:WikiDoc Sources

Retrieved from "https://www.wikidoc.org/index.php?title=Filariasis_pathophysiology&oldid=1638261"