CS3 - NTD Schistosomiasis 2 Flashcards
(50 cards)
What are the later symptoms of schistosomiasis depending on parasite species and location in the host?
A:
Frequent, painful, or bloody urine (especially in urogenital schistosomiasis)
Abdominal pain and bloody diarrhea (intestinal schistosomiasis)
Anaemia due to chronic blood loss
Chills and muscle aches
Inflammation and scarring of the bladder (leading to urogenital issues)
Lymph node enlargement
Secondary blood disorders in cases of colon damage
Bladder cancer may develop in some cases (due to chronic infection)
Children with repeated infections can develop anaemia, malnutrition, and learning disabilities
Katayama fever (manifestation of acute schistosomiasis):
Fever
Urticarial rash (swimmer’s itch)
Enlarged liver and spleen
Bronchospasm
What are the stages of pathogenesis in schistosomiasis?
Acute
Established active
Late chronic
What happens during the acute phase (Katayama Fever) of schistosomiasis?
Cercarial Dermatitis: After cercarial skin penetration, some larvae die in the skin, while others enter the bloodstream.
What immune response occurs during the acute phase of schistosomiasis?
Type 1 hypersensitivity: Immune reactions to dying larvae cause a pruritic maculopapular rash (swimmer’s itch) due to mast cell degranulation and histamine release.
What happens during the acute phase (Katayama Fever) of schistosomiasis?
A:
Cercarial Penetration: Penetrating cercariae mature into schistosomula.
Timing: Symptoms appear 2 weeks to 3 months after exposure.
Immune Response: Symptoms are due to T helper type 1 (Th1) hypersensitivity and the formation of immune complexes in response to schistosomula antigens/secretions released during migration.
What are the immune and inflammatory responses in the acute phase of schistosomiasis (Katayama Fever)?
Cell-driven Inflammatory Response: Involves TNF, interleukins, and cytokines, leading to febrile illness.
Eosinophilia: Increased eosinophil count is commonly observed.
Pulmonary Infiltrates: Transient infiltrates occur, causing bronchospasm due to substances denser than air (e.g., oedema, blood, eosinophils) accumulating in the lung parenchyma.
What immune response is involved in the transition from acute to established schistosomiasis?
Th-1 Response: Initial response to egg antigens triggers proinflammatory cytokine production.
How does the immune response shift during the transition from acute to established schistosomiasis?
Th-1 to Th-2 Shift: Th-1 cells secrete interferon gamma, prompting a switch to a Th-2 response with anti-inflammatory cytokines, antibody production, and eosinophil recruitment.
What is the role of granulomas in established schistosomiasis?
Granulomas form in a Th-1 environment, leading to hepatocellular microvesicular changes, inflammation, and necrosis in the liver. Activated hepatic stellate cells (HSC) contribute to liver fibrosis.
What is the role of adult schistosome worms in established active infection?
A:
Adult worms in blood vessels usually do not stimulate local inflammation. They bind host antigens and regenerate their protective tegument, hiding worm antigens from the immune system.
What causes the symptoms and organ-related lesions in established schistosomiasis?
Symptoms are caused by inflammatory responses to eggs. Eggs actively secrete antigenic glycoproteins that facilitate their passage through blood vessels to the intestine or bladder and induce inflammation.
How do granulomas form around eggs in established schistosomiasis?
A:
Soluble egg antigens induce granuloma formation around eggs trapped in tissues. Hepatic granulomas during the Th-2 response limit egg secretion spread with minimal parenchymal inflammation.
How do organ-specific symptoms correlate with schistosomiasis infection intensity?
Organ-specific symptoms are mediated by egg-induced inflammation and granulomatous reactions, and often positively correlate with infection intensity.
Children in endemic areas are commonly affected.
Symptoms are reversible after treatment and removal of adult worms.
What happens during the late chronic infection phase of schistosomiasis?
Worm burden declines due to partial immunity and natural death of worms.
Egg excretion decreases, and new granulomas are smaller with less inflammation due to immunological downregulation.
Previous granulomas are replaced by fibrous tissue (scarring), reducing symptoms but potentially causing permanent pathology.
What are the consequences of the chronic inflammatory reaction to eggs in schistosomiasis?
Continuous inflammation leads to tissue destruction, fibrosis, and the formation of granulomata.
This results in fibrotic nodules known as sandy patches.
Chronic S. haematobium infection can lead to squamous cell carcinoma of the bladder.
How does schistosomiasis affect different stages of human growth and development?
Schistosomiasis has effects at various life stages, with associated health problems like growth impairment, developmental delays, and reduced cognitive function.
Systematic reviews (SR), meta-analyses (MA), randomized controlled trials (RCT), cohort studies (C), and cross-sectional studies (CS) provide varying levels of evidence for these associations.
What are the control measures in place for schistosomiasis at different life stages?
Red: Some interventions are in place, but neglected in endemic areas.
Yellow: More interventions, but no wide-scale Mass Drug Administration (MDA) in place.
Green: School-based MDA programmes target school-age children.
Grey: First 1000 days of life are not covered by current MDA programmes, which focus on children.
How does schistosomiasis impact children, and why is it considered a barrier to development?
Children are the primary targets of schistosomiasis infection.
The disease compromises physical and cognitive development, affecting their growth and ability to learn.
Schistosomiasis is not only a disease of poverty but also acts as a barrier to development in endemic countries.
How does praziquantel work in the treatment of schistosomiasis, and what are its limitations?
Praziquantel kills adult schistosomes, reducing morbidity in treated patients.
It is ineffective against juvenile worms and does not prevent reinfection.
The overall effect on disease transmission is transient, as prevalence quickly returns to baseline levels after treatment.
What are the challenges in developing a vaccine for schistosomiasis, and why is it a priority?
Funding issues and the complex immunology pathway make vaccine development difficult.
The human host oscillates between fighting off infection and managing tissue egg pathology from previous infections.
A schistosomiasis vaccine is considered one of the 10 most important vaccines that needs immediate and successful development due to its feasibility and high need.
How does the complex life cycle of Schistosoma affect vaccine development?
The complex life cycle of Schistosoma is a major barrier to vaccine development.
The parasite’s life cycle involves multiple stages, each requiring different immune responses, complicating the creation of a single effective vaccine.
How have schistosomes evolved to survive and enter the human host?
Schistosomes have developed sophisticated survival tactics over their evolution.
These tactics allow them to successfully navigate multiple, vastly different conditions in their life cycle, enabling effective entry into the human host.
What is the major reason for the spread of schistosomiasis?
The major reason for schistosomiasis spread is the inability of the immune system to effectively recognize and eliminate migrating larvae and adult worms.
What is the goal of developing a vaccine for schistosomiasis, and how would partial efficacy impact disease transmission?
The goal is not to achieve sterile immunity, as schistosomes do not replicate in their hosts.
A vaccine with even partial protective efficacy would significantly reduce disease burden and subsequent transmission.
