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Soil Transmitted helminths
DR.HAMISI MKINDI,MD.
TO DOWNLOAD CONTACT: hermyc@live.com
CHANGING GLOBAL EPIDEMIOLOGY OF
HELMITHES
• There is a reduction in the prevalence of soil-transmitted helminths in
children aged 5–14 years in sub-Saharan Africa, from 44% in 2000 to
13% in 2018, driven by sustained delivery of preventive
chemotherapy, improved sanitation, and economic development.
• Nevertheless, 25% of implementation units still had an estimated
prevalence of moderate-to-heavy intensity infection exceeding the 2%
target threshold.
• In 2018, largely concentrated in nine countries ie Nigeria, Democratic
Republic of the Congo, Ethiopia, Cameroon, Angola, Mozambique,
Madagascar, Equatorial Guinea, and Gabon.
• Although helminth parasites infect over 25% of the world’s
population these infections are one of the most “neglected”
tropical diseases with no effective vaccines available for
humans.
HELMINTHS MODULATING IMMUNE SYSTEM
• Helminth parasites are masters at manipulating host immune
response by targeting of pattern recognition receptors (PRRs)
including
• toll-like receptors, C-type lectin receptors, and the inflammasome.
• These play a critical role in intracellular pathways and regulating innate
inflammatory responses as well as directing adaptive immunity toward Th1
and Th2 responses
• Helminths derived products ultimately converge host immunity
toward hyporesponsiveness and immunological tolerance.
TOLL LIKE RECEPTOR
• Stimulation of TRL receptors is done with helminth derived
products(HDPs), which trigger the mitogen activated protein kinase
pathway (MAP K) which is responsible for the production of
cytokines and dendritic maturation.
• Stimulation of MAP K it enhance stimulation of extracellular signal
related kinases 1 and 2 (ERK 1/2) which will enhance dendritic cell
maturation,cytokines, and it favour the Th2 respone which will reduce
the inflammatory process and favour parasite
• There is also other pathway which start from from stimulation of TRL
receptor which will stimulate MAP K pathway which lead to
stimulation of suppressor of cytokine signalling 3(SOCS3) which will
lead to the inhibition of signalling ofor cytokine production,
C-TYPE LECTIN
• HDPs once they bind to the C-type receptor they
 Induce Th2 suppression
 Induce Treg proliferation which will create a balance between Th1 and
Th2
 stimulation of both Th1 and Th2 will lead to the production of IL12 and
TNF which lead will to the production of T reg hence will reduce inflamatory
process hence favors parasite survival.
INFLAMMASOME
• It has a receptor called Node like receptor were by HDPs products
which will cause suppression of Th2 response by production of IL
18,IL1
NON PRR PATHWAYS
• Imparement of antigen presentation cell by blocking B cell receptor
which act by weaking signal to the naive T cell hence it cannot
recognise parasite
• IgE signalling interference the degranulation of mast cell
• Mimmicky key mediators like TGF alpha and PGE2, whichg lead to
conversion of Th1 and TH2
• Blocking pottasion gatted chanell causing dysfunction of t cells
EXTRACELLULAR VESICLE (EVs)
• These are vesicle released by the helminth which they contain
different materilas like protein,lipid, miRNA,RNA
• In host cells miRNA normally regulating post transcription gene
expression , but parasite miRNA block gene expression of host cells
products inculding cytokines.
• RNA inducing silencing complex og the host gene expession for the
products like cytokines.
INTERACTION BETWEEN HELMINTHIASIS AND
OTHER DISEASES
1.INTERACTION BETWEEN HELMINTH WITH TUBERCULOSIS AND BCG
Tuberculosis and helminth infections are coendemic in many parts of
the world, which raises the possibility of modulating tuberculosis
through host responses to helminths.
• A lower IFN-γ response and greater IL-10 response has been observed
in helminth-coinfected patients with tuberculosis than patients with
tuberculosis alone.
• Concurrent helminth infection in people exposed to M. tuberculosis
can increase their risk of becoming latently infected with M.
tuberculosis.
• Deworming of people before vaccination against BCG enhanced the
IFN-γ response, whereas the TGF-β response was lower than for
people who did not receive deworming treatment
• Sugesting that the poor immunogenicity of BCG in the helminth-
infected population could have been due to increased TGF-β
production.
2. INTERACTION BETWEEN HELMINTHS AND MALARIA
• Epidemiological studies suggest that helminth infection in humans
may alter the development of malaria not only by increasing the
replication of Plasmodium parasites but also by modulating the
severity of the pathological sequelae associated with malaria.
• Thus, by altering the TH2-TH1 balance, helminth infection may be a
substantial contributing factor to the delayed acquisition of clinical
immunity to malaria.
3. INTERACTION BETWEEN HELMINTHS AND HIV
• The helminth-induced immune response may have several
components that compromise the immune responses needed to keep
the HIV infection in check, including the production of TH2 cytokines
and impaired function of antigen-presenting cells.
• However, those same mechanisms through dampening the activation
of cells of the innate and adaptive immune systems may potentially
affect the early stages of HIV infection.
• Macrophages treated with IL-4 and IL-13 inhibited the entry of virus
by downregulating expression of the CCR5, CXCR4 and CD4 receptors
for viral entry.
• Thus, although the viral load of HIV may in some cases ultimately be
increased after helminth infection, those potential mechanisms that
decrease infectivity may offset the advantages of antihelminth
treatments.
4. METABOLIC DISEASES
• Epidemiological studies suggest that chronic helminth infections may
influence the development of metabolic diseases.
• Individuals with a previous or current helminth infection were 50%
less likely to have an outcome of metabolic dysfunction such as hyper
glycaemia or insulin resistance compared to those uninfected.
REFFERENCE
• Zakeri A, Hansen EP, Andersen SD, Williams AR and Nejsum P (2018)
Immunomodulation by Helminths: Intracellular Pathways and
Extracellular Vesicles available on www.fontersin.org

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HELMINTHIASIS-1-1.pptx

  • 1. Soil Transmitted helminths DR.HAMISI MKINDI,MD. TO DOWNLOAD CONTACT: hermyc@live.com
  • 2. CHANGING GLOBAL EPIDEMIOLOGY OF HELMITHES • There is a reduction in the prevalence of soil-transmitted helminths in children aged 5–14 years in sub-Saharan Africa, from 44% in 2000 to 13% in 2018, driven by sustained delivery of preventive chemotherapy, improved sanitation, and economic development. • Nevertheless, 25% of implementation units still had an estimated prevalence of moderate-to-heavy intensity infection exceeding the 2% target threshold.
  • 3. • In 2018, largely concentrated in nine countries ie Nigeria, Democratic Republic of the Congo, Ethiopia, Cameroon, Angola, Mozambique, Madagascar, Equatorial Guinea, and Gabon. • Although helminth parasites infect over 25% of the world’s population these infections are one of the most “neglected” tropical diseases with no effective vaccines available for humans.
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  • 5. HELMINTHS MODULATING IMMUNE SYSTEM • Helminth parasites are masters at manipulating host immune response by targeting of pattern recognition receptors (PRRs) including • toll-like receptors, C-type lectin receptors, and the inflammasome. • These play a critical role in intracellular pathways and regulating innate inflammatory responses as well as directing adaptive immunity toward Th1 and Th2 responses • Helminths derived products ultimately converge host immunity toward hyporesponsiveness and immunological tolerance.
  • 6. TOLL LIKE RECEPTOR • Stimulation of TRL receptors is done with helminth derived products(HDPs), which trigger the mitogen activated protein kinase pathway (MAP K) which is responsible for the production of cytokines and dendritic maturation. • Stimulation of MAP K it enhance stimulation of extracellular signal related kinases 1 and 2 (ERK 1/2) which will enhance dendritic cell maturation,cytokines, and it favour the Th2 respone which will reduce the inflammatory process and favour parasite
  • 7. • There is also other pathway which start from from stimulation of TRL receptor which will stimulate MAP K pathway which lead to stimulation of suppressor of cytokine signalling 3(SOCS3) which will lead to the inhibition of signalling ofor cytokine production,
  • 8. C-TYPE LECTIN • HDPs once they bind to the C-type receptor they  Induce Th2 suppression  Induce Treg proliferation which will create a balance between Th1 and Th2  stimulation of both Th1 and Th2 will lead to the production of IL12 and TNF which lead will to the production of T reg hence will reduce inflamatory process hence favors parasite survival.
  • 9. INFLAMMASOME • It has a receptor called Node like receptor were by HDPs products which will cause suppression of Th2 response by production of IL 18,IL1
  • 10. NON PRR PATHWAYS • Imparement of antigen presentation cell by blocking B cell receptor which act by weaking signal to the naive T cell hence it cannot recognise parasite • IgE signalling interference the degranulation of mast cell • Mimmicky key mediators like TGF alpha and PGE2, whichg lead to conversion of Th1 and TH2 • Blocking pottasion gatted chanell causing dysfunction of t cells
  • 11. EXTRACELLULAR VESICLE (EVs) • These are vesicle released by the helminth which they contain different materilas like protein,lipid, miRNA,RNA • In host cells miRNA normally regulating post transcription gene expression , but parasite miRNA block gene expression of host cells products inculding cytokines. • RNA inducing silencing complex og the host gene expession for the products like cytokines.
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  • 15. INTERACTION BETWEEN HELMINTHIASIS AND OTHER DISEASES 1.INTERACTION BETWEEN HELMINTH WITH TUBERCULOSIS AND BCG Tuberculosis and helminth infections are coendemic in many parts of the world, which raises the possibility of modulating tuberculosis through host responses to helminths. • A lower IFN-γ response and greater IL-10 response has been observed in helminth-coinfected patients with tuberculosis than patients with tuberculosis alone.
  • 16. • Concurrent helminth infection in people exposed to M. tuberculosis can increase their risk of becoming latently infected with M. tuberculosis. • Deworming of people before vaccination against BCG enhanced the IFN-γ response, whereas the TGF-β response was lower than for people who did not receive deworming treatment • Sugesting that the poor immunogenicity of BCG in the helminth- infected population could have been due to increased TGF-β production.
  • 17. 2. INTERACTION BETWEEN HELMINTHS AND MALARIA • Epidemiological studies suggest that helminth infection in humans may alter the development of malaria not only by increasing the replication of Plasmodium parasites but also by modulating the severity of the pathological sequelae associated with malaria. • Thus, by altering the TH2-TH1 balance, helminth infection may be a substantial contributing factor to the delayed acquisition of clinical immunity to malaria.
  • 18. 3. INTERACTION BETWEEN HELMINTHS AND HIV • The helminth-induced immune response may have several components that compromise the immune responses needed to keep the HIV infection in check, including the production of TH2 cytokines and impaired function of antigen-presenting cells. • However, those same mechanisms through dampening the activation of cells of the innate and adaptive immune systems may potentially affect the early stages of HIV infection.
  • 19. • Macrophages treated with IL-4 and IL-13 inhibited the entry of virus by downregulating expression of the CCR5, CXCR4 and CD4 receptors for viral entry. • Thus, although the viral load of HIV may in some cases ultimately be increased after helminth infection, those potential mechanisms that decrease infectivity may offset the advantages of antihelminth treatments.
  • 20. 4. METABOLIC DISEASES • Epidemiological studies suggest that chronic helminth infections may influence the development of metabolic diseases. • Individuals with a previous or current helminth infection were 50% less likely to have an outcome of metabolic dysfunction such as hyper glycaemia or insulin resistance compared to those uninfected.
  • 21. REFFERENCE • Zakeri A, Hansen EP, Andersen SD, Williams AR and Nejsum P (2018) Immunomodulation by Helminths: Intracellular Pathways and Extracellular Vesicles available on www.fontersin.org